Midterm Study Notes

Mechanics of Ventilation
Muscles of inspiration
- Increase vertical dimensions:
o Diaphragm
The major muscle of inspiration (phrenic nerve C3, 4, 5)
Resting inspiration descends ~1 cm; can move up to 10 cm
Also increases A-P & M-L dimensions (with the assistance of the external
intercostals)
Resting expiration passive, diaphragm relaxes and elastic recoil of lungs
forces air out
Abdominal muscles are accessory for expiration
Movements of the rib cage
- Increase A-P dimensions
o Ribs move forward & upward pump handle motion
o Primarily ribs 3-6
o Extension of thoracic spine (t-spine problems can limit excursion)
- Increase transverse dimensions
o Ribs move up & out bucket handle motion
o Primarily lower ribs
o Costochondral junction increases, elongating ribs & further increasing volume cavity
o Lowest 2 ribs (floating ribs not attached to sternum) can only open outwards caliper
motion
Costovertebral joints
- 2-9 articulate with vertebral body of same level and the level above (demi-facets) and the
corresponding IVD
- 1, 10-12 articulate only with vertebral body of same level
Costotransverse joints
- Articulation changes shape as you move inferiorly
- Higher in thorax roll
o Joint centres lie more in coronal (frontal) place
o Pump handle motion
- Lower in thorax glide
o Joint centres lie more in sagittal plane
o Bucket handle motion
Relationship of lungs to chest wall
- Pleural membranes cover the lungs and inner surface of the chest wall
- These membranes glide over one another
- Remember we have muscular control over the chest wall only, not the lungs
Pleura
- The inside pleural membrane lines the lungs termed the visceral pleura
- The outside pleural membrane lines the inside of the chest wall termed the parietal pleura
- The pleural space is a potential space between the two pleura. A very thin film of fluid is found
between the two pleura

Negative pressure (vacuum) in the pleural space holds lungs to chest wall
Pleura is serous membrane
Parietal layer
o Lines cavity (chest wall, diaphragm, mediastinal surface)
o Sensitive to pain
- Visceral layer
o Covers lung (invaginates lobes, reflects off root of lung to become parietal layer)
o Insensitive to pain
- Pleural cavity
o Pleural fluid (lubricant, about 2-5mL)
o Forms thin film between layers of pleura
o Allows slightly slimy lungs slither & slide within thorax
o Constant drainage of serious fluid by lymphatic system creates this negative pressure
Ventilation
- Ventilation is not the same as respiration (alveolar-capillary interface respiration and tissuecapillary interface respiration gas exchange)
- Ventilation is defined as the exchange of air between the atmosphere and alveoli
- In order to inspire air, our chest cavity volume must increase to create a low pressure environment
in the alveoli. Then, since the pressure in the chest is lower than the atmosphere, air flows in
from an area of higher pressure to an area of lower pressure
Recoil of lung
- Forces pulling lung inwards
- 2/3 due to surface tension
- 1/3 due to elastin
o Pathology due to loss of elastin
o E.g., emphysema (causes difficulties with respiration), alpha1-antitrypsin deficiency
(predisposed to destruction of connective tissues)
Pressures
- All pressures described in the respiratory system are relative to atmospheric pressure. The
pressure within the lungs (alveolar pressure) between breaths is described as 0 mmHg, that is, the
same as atmospheric pressure (~760 mmHg)
- Intrapleural pressure (IPP) is created by the tendency of
o Chest wall pulling out (also has recoil properties)
o Lung recoiling inwards
- Average IPP between breaths is around -4 mmHg (less than atmosphere)
- Transpulmonary pressure (TP)
o Is the difference between pressure in the lung and the pleural cavity
o TP = Palv IPP [ 0 (-4) = 4 mmHg]
o It is the pressure required to hold the lungs open
o Always present; without it, lungs would collapse
- Due to weight of lung
o IPP is less negative at base than apex
o Base is more compressed
o Note:
Base expands more on inspiration in an UPRIGHT lung (therefore dimensions
increase more in lower thorax than upper)

More increase in capacity in the base of the lung than at the apex at rest
Tendency to have air trapping in apices of lungs due to higher IPP

Volumes, Capacities, and Blood Flow of the Lungs

Normal breathing
- Inspiration happens actively because of muscle contraction
- Quiet expiration happens passively because of the recoil forces on the lung
o Elastic tissue
o Surface tension
- 3-5% of total energy expended by body goes to breathing
o Heavy exercise can increase 50-fold
- In obstructive lung disease, up to 30% of bodys energy expenditure is for breathing even at rest
Lung volumes and capacities
- Lung volumes
o Refer to the volume of air associated with different phases of the respiratory cycle
o Can be measured directly
- Lung capacities
o Based on the addition of two or more lung volumes
o Unlike volumes, which are directly measured, capacities are inferred from the sum of
certain lung volumes
Lung volumes
- 4 in total
- Non-overlapping
- Subdivisions of the total lung volume
- Measured by a spirometer
Tidal and residual volume
- The average total lung capacity of an adult human male is about 6 L of air (4.2 L in females)
- Only a small amount of this capacity is used during normal breathing
- Tidal volume
o Tidal breathing is normal, resting breathing
o The tidal volume is the volume of air that is inhaled or exhaled in only a single such
breath (normal, healthy individual)
o Normally 500 mL
- Residual volume
o The volume of gas in the lungs at the end of a full forced expiration
o The stiffness of the chest wall limits further decrease in volume by expiratory muscle
force
o Prevents lungs from collapsing (cant collapse chest wall)
o Hard to measure involves helium
o Normally 1200 mL
Reserve volumes
- Reserve volumes represent the maximum amounts of air you can inhale or exhale beyond normal,
passive tidal respiration
- Must be inhaled or exhaled actively/full-forced
- Two types

Expiratory reserve volume: The maximal volume of air that can be exhaled from the endexpiratory position
I.e., emptying out your lungs as much as you can
Whatever remains in your lungs is your residual volume
Normally 1200 mL
Inspiratory reserve volume: The maximal volume that can be inhaled from the endinspiratory level
I.e., breathing in as much air as you can hold
Normally 3100 mL

Lung capacities
- Total capacity
o The total capacity of air in your lungs (add up all 4 volumes)
The total volume of gas your lungs can possible hold (i.e., the sum of gas in your
lungs following a full forced inspiration)
Inspiratory muscle force stretches the chest wall and the lungs beyond their
resting positions
The stiffness of the lungs limit further expansion by inspiratory muscle force
Total lung capacity is around 6000 mL
o Tidal volume + residual volume + expiratory reserve volume + inspiratory reserve
volume
- Functional residual capacity
o Volume of lungs after normal passive expiration (during tidal expiration)
o At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and
there is no exertion by the diaphragm or other respiratory muscles
o The tendency of the chest to expand is balanced by the tendency of the lungs to collapse
o Calculated as
FRC = expiratory reserve volume + residual volume
2400 mL = 1200 + 1200
o A lowered or elevated FRC is often an indication of some form of respiratory disease
- Inspiratory capacity
o The total amount of air that can be actively inspired
IC = tidal volume + inspiratory reserve volume
3600 mL = 500 + 3100
- Vital capacity
o The total amount of air that can be expired after fully inhaling
o Approximately 80% of TLC
o VC = tidal volume + inspiratory reserve volume + expiratory reserve volume
o About 4800 mL
o Variations in VC occur with
Height/weight/surface area VC is proportional to height (reason for variation
between genders)
Age decreased VC with age
Posture VC decreases when supine
o Changes in lung volumes or capacities can be used to diagnose pathological conditions
In restrictive diseases (pulmonary fibrosis, weak respiratory muscles), flow is
normal, but volumes are decreased

In obstructive diseases (asthma, COPD, emphysema), flow rates are impeded

Increased residual volume, air trapping

FVC and FEV1

- FVC = forced vital capacity, the maximum amount of air forcibly expired after maximum
inspiration
- FEV1 = forced expiratory volume in the first second of forced vital capacity maneuver
- FEV1 and FVC help differentiate obstructive and restrictive lung disorders
Lung volumes/capacities of restricted diseases
- Compliance of the lung is reduced
- Increased stiffness of the lung and limited expansion (difficulty inhaling to full capacity)
- A greater pressure than normal is required to give the same increase in volume
- Causes of restrictive disorder: pulmonary fibrosis (reduced space in alveoli due to thickening, as
well as overall stiffness), pneumonia and pulmonary edema, stiffness of the chest wall, weak
muscles (e.g., Duchennes muscular dystrophy)
- IRV and ERV are decreased (TLC is decreased)
Lung volumes/capacities of obstructive diseases
- Obstructive difficulty exhaling normal amount
- Airway obstruction causes an increase in resistance. During normal breathing, the pressure
volume relationship is no different from in a normal lung. However, when breathing rapidly,
greater pressure is needed to overcome the resistance to flow, and the volume of each breath gets
smaller
- Common obstructive diseases include asthma, bronchitis, emphysema, cystic fibrosis
- Overall TLC is increased and RV is increased
Not always limited to one type!
- Combination of obstructive and restrictive disorders
o E.g., smoker with emphysema that later in life develops a neuromuscular disorder
o Reduced TLC with reduction in flow
Blood in the lungs
- Pulmonary blood supply
o Blood through the lungs for gas exchange
- Systemic blood supply
o Blood to the lung tissue/cells
Blood flow through the lungs from the pulmonary artery
- High flow (5 L/min), low pressure (15 mmHg), low resistance (1-2 mmHg/L/min) circuit
- Initially arteries, veins, and bronchi run together
- Toward the periphery:
o Veins outside of lobe segments
o Arteries centre of lobe segments
o Capillaries between arteries and veins
~ 7 micrometers diameter and are short large surface area 50-100 m2

RBCs travel the capillary bed in ~0.75 seconds, lung in 4-5 seconds
Small capillary diameter squishes RBCs increases contact between RBCs
and capillary wall and therefore increases gas exchange

Blood supply to lung tissue: Bronchial arteries

- In addition to pulmonary circulation, there are also branches from the systemic circulation
- Bronchial arteries
o Arise from the thoracic aorta
o Supply blood to the bronchi and connective tissue of the lungs
o Travel with and branch with the bronchi, end at the level of the respiratory bronchioles
o There are also bronchial veins, but the majority of bronchial arteries are drained by
pulmonary veins
Blood volume of lungs
- Normal blood volume of lungs is 450 mL (70 mL in capillaries)
- Pulmonary vessels act as reservoir, accommodate up to twice as much blood volume
- Volume of blood in lungs varies with intrathoracic pressure
o High intrathoracic pressure (expiration) expels blood from lungs
o Low intrathoracic pressure (inspiration) increases blood volume
Left ventricular failure can cause pooling of blood in lungs and rise in pulmonary
pressure
Blood pressures in the lung
- Mean pulmonary arterial pressure is 15 mmHg
- Only need enough pressure maintained to lift blood above the heart to the top of lung
o Therefore, work required of right ventricle is much less than left
o RV is less muscular than LV
Pressures in the pulmonary circulation
- Larger pulmonary arteries and veins
o Subjected to much lower pressures than alveolar vessels
o Pulled open as lung expands on inspiration
- Pulmonary capillaries
o Small and surrounded by gas
o Subjected to pressure shifts occurring within the thorax during ventilation
If alveolar pressure is higher than pressure in capillary, it will cause the capillary
to collapse stops perfusion, and leads to the creation of alveolar dead space
Tends to occur in upper regions of lung because of increased alveolar pressure
combined with lower intracapillary pressure
Regional differences
- Lower regions of lung are better perfused than upper zones when an individual is upright
- Gravity is primary determinant, as it creates a hydrostatic pressure gradient
o Lowest point in lung is 30 cm below highest point

o
o

Regional arterial blood pressure is typically in the range 5 mmHg near the apex of the
lung to 25 mmHg at the base
It takes less energy to pump blood to the bottom of the lung than to the top

Ventilation-Perfusion Matching (VA/Q)

Perfusion
- Does not consider systemic circulation that supplies the lungs
Tracheobronchal tree
- Conducting zone not available for gas exchange
- Transit and respiratory zone areas where gas exchange takes place
Useful information
- At rest a normal healthy person breathes ~500 mL of air at a frequency of 12-16 breaths/min.
Therefore minute ventilation (VE) = 6-8 L/min
- Tidal volume or VT is composed of
o VD (dead space) + VA (alveolar NEW air ~1/7)
We replace about 1/7 of alveolar air with each breath
- Dead space:
o Proportions of the tidal volume that are not used for gas exchange
o Anatomical dead space is that area of the tracheobronchal tree not involved in gas
exchange. This includes all the conducting airways including the larynx, pharynx, and so
on
o This represents ~ 150 mL in a normal person so that 30% of a tidal volume of 500 mL is
wasted
o In disease states there are areas of the lung which receive adequate ventilation but are
under (or not) perfused. Therefore it is more accurate to term all of this as physiological
dead space
- Alveolar volume
o It is that volume of air participating in gas exchange (only 1/5-1/7 of air in alveoli is fresh
air from last breath)
Bohr equation
- The Bohr equation is used for calculating physiologic dead space and uses the principle that
increasing amounts of dead space ventilation augment the difference between PCO 2 in arterial
blood and expired gas
- The equation is written as VD/VT = [PaCO2 PECO2]/PaCO2
Introduction to gas exchange
- Oxygen enters the pulmonary capillaries to be utilized at the cellular level
- CO2 entering at the cellular level will move into the capillaries and then into the alveoli
Compliance
- Recoil of lungs is 2/3 due to surface tension and 1/3 due to elastin
- Chest wall has recoil forces pulling in the opposite direction

Surface tension
- Surface tension is the force acting across an imaginary line 1 cm long in the surface of a liquid. It
is there because the attractive forces between adjacent molecules of the liquid are much stronger
than those between the liquid and gas with the result that the liquid surface becomes as small as
possible
- Fluid molecules lining alveoli want to pull the alveoli in on itself due to surface tension
- Drop of water on non-wetable surface
o At air-water interface, water molecules are strongly attracted to each other so they act
like an elastic membrane, drawing water into a sphere (minimizing surface area)
o Add detergent (or surfactant)
Molecules at surface are no longer as strongly attracted to each other and water
flows across surface
Reduces surface tension so that water flows
Surfactant
- Function:
o Decreases surface tension, decreases recoil & decreases work required for inhalation
- Consequences of low surfactant:
o Stiff lungs (low compliance therefore hard to inhale)
o Areas at atelectasis (decreased or absent air in the entire or part of a lung resulting in loss
of lung volume)
o Alveoli fill with transudate (fluid moving from capillary to alveoli; likely plasma)
- Without surfactant
o Surface tension collapse alveoli
o Fluid drawn into alveoli
- With surfactant
o Surface tension decreased (NOT eliminated)
o Surface tension still responsible for 2/3 of recoil during exhalation
- Surfactant is a phospholipid, a constituent of which is DPPC (dipalmitoyl phosphatidyl choline),
and is produced by type II alveolar epithelial cells
- Without surfactant, small alveoli tend to empty into large alveoli, because the smaller alveolus
generates a larger pressure
o Surfactant stabilizes alveoli by reducing surface tension
o This helps to maintain surface area
Compliance
- Is the change in lung volume produced by change in transpulmonary pressure
- Compliance = change volume/change pressure
- The larger the ratio, the greater the compliance (distensibility/stretchability)
- Compliance of both lungs averages 200 mL/cm of water (normal)
- Compliance is not elasticity!
Pressure-volume curve (compliance curve)
- Note that the curve is non-linear is that it is stiffer at higher volumes
- Hysteresis the inflation curve is not the same as the deflation curve (due to air trapping)

Compliance is the slope (change in volume/change in pressure)

The compliant behaviour of the lung depends on collagen, elastin, and surface tension
Saline-filled lung is more stretchable than air-filled lung

Low lung volumes

- Note that the normal distribution of ventilation is inverted in very low lung volumes (transient
situation)
Compliance Curve
- Compliance of the respiratory system depends on the combination of lung compliance and chest
wall compliance
- Compliance of chest wall includes costal cartilage, movement in thoracic spine, musculature, etc.
- Compliance decreases with age due to a variety of factors
- Patients with restrictive lung disease (fibrosis) have lower than normal compliance
- Patients with obstructive lung disease (emphysema) have higher than normal compliance
FEV1/FVC ratios in disease
- Normal ratio is 80%
- Lower ratios indicate obstructive disease
- Higher ratios indicate restrictive disease
Regional differences in perfusion (in the upright lung)
- Note that blood flow per unit volume is better at the bottom of the lung than the top
- It decreases quite steeply as we move past the middle of the lung and towards the top
- Blood is heavy/air is light
Pressure gradients
- PA is alveolar pressure
- Pa is the pressure at the arterial end of the capillary bed
- Pv is pressure at the venous end of the capillary bed
- Top of lung: PA > Pa > Pv
- Middle of lung: Pa > PA > Pv
- Bottom of lung: Pa > Pv > PA
- Note how the pressures preferentially allow for better perfusion at the bases in this upright lung
Graphical VA/Q relationship
- Note that both ventilation and perfusion are better at the bottom than at the top
- This holds true for resting lungs or when the demand is not high
- This changes with activity
- Note that the decline is steeper for perfusion (blood flow) than it is for ventilation when moving
towards the top of the lungs
Regional differences in VA/Q matching
- Note that VA/Q approaches infinity at the top of the lung (higher ventilation but no perfusion)
- Best VA/Q matching is middle and base of lung

Shunt and dead space

- Shunt is defined as an area of adequate perfusion but no ventilation (low VA/Q)
- Dead space is defined as an area of adequate ventilation but no perfusion (high VA/Q)
Adjustment of airflow to blood flow via CO2 induced change in the airway
- Initial state left alveolus is receiving too much air for its blood supply
- Right alveolus is receiving too little air for its blood supply
- Therefore low alveolar CO2exposure of left bronchiole and high alveolar CO 2exposure of right
bronchiole
- Local compensation low alveolar CO2 causes airway constriction, and high alveolar CO 2causes
airway dilation. Thus airflow is now matched to blood flow
- Note: Airways are constricted by parasympathetic nerves and dilated by sympathetic nerves as
well as by local CO2 concentrations
Adjustment of blood flow to airflow via H+ and O2 induced changes in the arteries
- Initial state left alveolus is receiving too little blood supply for its airflow and therefore arterial
H+ is low and arterial O2 is high. Right alveolus is receiving too much blood supply for its airflow
and therefore arterial H+ is high and arterial O2 is low
- Local compensation low arterial H+ and high arterial O2 causes arterial dilation. High arterial
H+ and low arterial O2 causes arterial constriction. This acts to shift the blood away from the
poorly ventilated alveolus and to the well-ventilated alveolus
- Note: This is exactly the opposite of the local control events occurring in the systemic circulation
Gas Exchange and Physiology of Blood Gases
Definitions:
- Diffusion is the net movement of a molecule from an area of high concentration to an area of low
concentration
- Pressure is the total exerted force of molecules against a surface
Partial Pressures
- Mixtures of gases in atmospheric air, oxygen, nitrogen, carbon dioxide
- The pressure created by an individual gas is directly proportional to the concentration of the gas
molecule
- Sum of partial pressures = total pressure
Partial Pressures of Inspired Air
o H2O variable
o CO2 0.003 mmHg
o O2 159 mmHg
o N2 601 mmHg
o Total pressure 760 mmHg
Air Humidification
- As soon as respiratory air enters the respiratory passages, it is humidified by the fluids on the
surfaces of the respiratory passages
- Humidification causes dilution
Partial Pressures of Alveolar Air (after Humidification)
- H2O 47 mmHg

CO2 40 mmHg (CO goes up as it exiting the bloodstream, higher concentration than in
atmospheric air)
- O2 105 mmHg
- N2 568 mmHg
- Total pressure 760 mmHg
Replacing Alveolar Air
- The volume of alveolar air replaced by atmospheric air is only about 1/7 th of the total residual
volume
- It takes about 16-17 breaths to replace most of the original alveolar air with atmospheric air
O2 and CO2 in the Alveoli
- The concentration of O2 and CO2 is controlled by
o The amount of alveolar ventilation
o The rate of absorption or excretion of each gas into the blood
Diffusion of Gases: Respiratory Membrane
1. Fluid + surfactant in the alveolus
2. Alveolar epithelium
3. Epithelial basement membrane
4. Thin interstitial space
5. Capillary basement membrane often fused with alveolar basement membrane
6. Capillary endothelial membrane
- Thin membrane allows easier/faster diffusion
Respiratory Membrane
- Total surface area = 70 square metres
- Total quantity of blood in the lung at a given instant is 60-140 mL
- Average diameter of a capillary is about 5 micrometers which is smaller than a red blood cell
- Red blood cell must squeeze through the capillary causing the red blood cell wall to contact the
capillary wall further facilitating gas exchange
Factors Affecting Diffusion
1. Thickness of the membrane
a. Occasionally increases edema, fibrotic lungs increased thickness in parts of
membrane
2. Surface area of the membrane
a. Decreased surface area: Removal of lung or parts of lung, emphysema loss of alveolar
walls
3. Diffusion coefficient of the gas
a. CO2 diffuses 20x more rapidly than O2
4. Pressure difference of the gas between the two sides of the membrane
a. Net diffusion of oxygen into the blood
b. Net diffusion of oxygen into the tissues
c. Net diffusion of CO2 into the alveolus
Blood Gases & Acid-Base Balance
Oxygen Transport
- Small amount is dissolved in blood ~0.3 mL/100 mL of blood
- The remainder is transported by hemoglobin (iron-containing oxygen-transporter in RBC)
~15g/100 mL
Oxygen Dissociation Curve

Oxygen combines with hemoglobin to form a reversible combination oxyhemoglobin

o O2 + Hb HbO2
- 4 O2 can bind to 1 Hb (to each heme/iron group)
- Primary factor that determines how much O2 is bound to hemoglobin is the PO2
Oxygen Dissociation Curve Definitions
- Oxygen capacity the maximum amount of oxygen that can be combined with Hb (~20.8 mL
oxygen/100 mL blood)
- Oxygen saturation the percentage of oxygen actually bound to Hb compared to the total oxygen
capacity
o E.g., in arteries - O2 saturation ~97.5% at a PO2 of 100 mmHg
- The actual amount of circulation oxygen is dependent on the amount bound to the Hb and the
amount of Hb in the bloodstream
- Under normal conditions, about 5 mL of oxygen is transported from Hb to the peripheral tissues,
leaving about 15 mL still bound to Hb in reserve
o O2 saturation ~75% in veins
Oxygen Dissociation Curve
- The flat upper portion changes in PO2 lead to minimal changes in loading of oxygen onto
hemoglobin
- The steep lower part represents the ability of the tissues to remove large amounts of oxygen for
small changes in capillary PO2 maximizes the exchange
- Arteries PO2 = 100 mmHg, which gives a 97.5% saturation
- Veins PO2 = 40 mmHg, which gives a 40% saturation
- Tissues PO2 = 20 mmHg
Influences on the Curve
- Factors shifting to the right (e.g., exercise)
1. Decrease pH (increase H+)
2. Increase temperature
3. Increase CO2
4. Increase DPG (diphosphoglycerate)
- A shift to the right causes greater O 2 removal from Hb for a given PO2
- This increases unloading of oxygen at tissues due to the rightward shift (reflects increased
demand for oxygen)
CO2
- CO2 is constantly formed in the body by intracellular metabolic process
- Increasing metabolic rate increase PCO2 in blood
- Decreasing metabolic rate decrease PCO 2 in blood
CO2 Transport
- Transported three ways
o Dissolved in solution ~7%
o Bound to proteins ~23%
o Bicarbonate ion ~70%
Bicarbonate Buffering System
- Maintains blood pH
- CO2 in the red blood cell is quickly converted to carbonic acid by the enzyme carbonic anhydrase
o CO2 + H2O H2CO3 H+ + HCO3- Carbonic acid dissociates into hydrogen ions and bicarbonate ions

H+ binds to the Hb molecule (which can induce a conformational change in Hb) and HCO 3diffuses into the blood stream
Acid/Base Balance
- Acid molecules containing hydrogen atoms that can freely release H + into solution, e.g., HCl,
H2CO3
- Base an ion or molecule that can readily accept H + e.g., HCO3- or some proteins like Hb
- Regulation of H+ in the body is important because almost all enzyme activity in the body is
influenced by H+
Buffer System
- A buffer is any substance that can reversibly bind H+
o Buffer + H+ HBuffer
- Increased H+ forces the reaction to the right (provided the buffer is in excess)
- Decreased H+ forces the reaction to the left
Regulation of pH, e.g., Acidosis
- CO2 + H2O H2CO3 H+ + HCO3- Acidosis forces the reaction to shift towards the left, increasing carbon dioxide
- Respiratory rate increases to blow off excess carbon dioxide, decreasing blood pH
-

Regulation of Blood Pressure via Kidney Heart Axis

Purpose of Lecture
- You are likely to come across patients with hypertension
- The kidney plays a significant role in BP regulation
- There are many drugs which work by altering kidney function to lower BP
o Common side effect = orthostatic hypotension
The Urinary System
- Two kidneys, two ureters, a bladder, and a urethra
o Ureters are high in sensory nerve endings (think kidney stones)
- Filter system for the blood that produces about 180 L of filtrate/day, but only excretes 1.5 L
urine/day
- Regulates blood volume
- Eliminates metabolic waste produces
o Excretes excess ions
E.g., acid-base balance (homeostasis), when potassium levels get too high
(hyperkalemia) cardiac arrest occurs
- Other functions
o Regulates blood pressure renin
o Secretes vitamin D
o RBC production (erythropoietin)
So What?
- If the kidneys fail then salts and waste products like urea build up and pH of the blood goes down
- Massive pitting edema results from the salt retention
- Academia results from the inability to excrete acids
- Therefore, we cannot stop blood flow to the kidneys EVER (even though with activity, some
blood flow to kidney and GI tract is shunted to muscles)
o Renal artery stenosis leads to increased BP at all costs because we MUST maintain
blood flow to kidney

Gross Anatomical Features

- Cortex (more pathology will result in a thinner cortex)
- Medulla (all the renal pyramids)
- Renal pelvis
- Minor calyx
- Major calyx
- Nephron collecting duct
- Renal pyramid
- Renal column
- Renal papilla
- Renal hilum
Polycystic Kidney
- Most healthy people have some renal cysts after age 30-50, but many cysts is pathologic
- Kidney can become 80-90% damaged before acute renal failure
- Other problems include hydroureter and hydronephrosis, as well as horseshoe kidneys and
supernumary renal arteries
o Problem with multiple renal arteries is that one may grow over ureter and constrict it
The Big Picture of Renal Function The Nephron
- Afferent arteriole glomerulus efferent arteriole peritubular capillaries
- Glomerulus contained within Bowmans capsule is the renal corpuscle (filtrate making machine)
- Filtrate drains into the proximal convoluted tubule, travels through the loop of Henle, and into the
distal convoluted tubule
o Along the way, filtrate is made into urine by reabsorption of material from the filtrate in
the tubule to the blood, and secretion of material from the blood to the tubule
- Collecting duct concentrates the urine
- Urine goes to the renal calyces then ureters and then the bladder
- Blood goes back to the venous circulation
Filtration and Podocytes
- Capillary fenestrations and pedicels of a foot process in a podocyte form filtration slits
- All small molecules can pass into the capsular space and form filtrate, but large molecules (>
albumin size) cannot and stay in the blood
How Does the Kidney Regulate BP?
1. Renin-Angiotensin-Aldosterone System (RAAS)
2. Natriuretic Peptide (ANP & BNP)
The RAAS
1. Sensing of low BP/low volume in afferent arteriole/systematic circulation
2. Sympathetic nerve stimulation
3. Low sodium levels and low flow in macula densa of the distal convoluted tubule
- All of these things cause an increase in release of renin by the juxtaglomerular apparatus
Angiotensin II and Blood Pressure
- Renin converts angiotensinogen into angiotensin I
- ACE converts angiotensin I into angiotensin II
- Angiotensin II acts to cause constriction of systemic and glomerular afferent arterioles, causing
blood pressure to increase

Angiotensin II also causes the release of aldosterone from the adrenal cortex (causes fluid
retention) and the release of anti-diuretic hormone (ADH, also called vasopressin) from
the posterior pituitary (causes fluid retention)
Diabetes inspidus caused by a lack of ADH or a lack of sensitivity to ADH
- ACE inhibitors, the most common medication for high blood pressure, prevent angiotensin I from
becoming angiotensin II and shut down these effects
Natriuretic Peptides
- High blood pressure in the atrium causes distension of the atrium and release of atrial natriuretic
peptide (ANP) by atrial myocytes
- Similarly, distension of the ventricles causes release of brain natriuretic peptide (BNP)
- These cause increased urine excretion
ANP
- Distension of the atrium of the heart leads to the release of ANP
- The ANP causes relaxation of the mesangial cells between the glomerular capillaries
- Once the mesangial cells relax, the glomerular capillaries are more spread out and relaxed so
more filtration can occur
- ANP also relaxes the afferent arteriole of the glomerulus and increases sodium loss
- Total effect is a decrease in blood volume and therefore a decrease in blood pressure
Other Types of Medication for HBP
- After ACE inhibitors, diuretics are most common (especially thiazides)
- Osmotic agents (mannitol)
- Loop agents (e.g., furosemide)
- Thiazides
- Aldosterone antagonists
- ADH antagonists
Summary
- The kidney plays a fundamental role in regulating blood pressure
- The RAAS acts to raise BP via the heart/kidney axis
- NP acts to lower pressure via the heart/kidney axis
- Many drugs will attempt to alter BP by altering kidney function
o

Control of Breathing (Ventilation)

Respiratory Centre
- Consists of a series of bilateral paired nuclei in the reticular formation of the brain stem
o Paired nuclei indicates they have a reciprocal connection (they cycle)
- Dorsal Respiratory Group (DRG) major driving input to rate of breathing
o Rhythmic activity via pacemaker neurons but has many inputs (limbic system, cortical
areas)
o It is a ramp signal therefore a series of impulses which increase the contraction of
respiratory muscles then stops
o Input to diaphragm via phrenic nerve
- Ventral Respiratory Group (VRG)
o Interacts with DRG when demand goes up. Note powerful drive to both inspiration and
expiration

Note: The output of the DRG and VRG would be delivered to the muscles via their respective
peripheral nerves through increased activation of respective motor neuron pools e.g., phrenic
motor neurons supplying diaphragm

Input to DRG and VRG

- Peripheral chemoreceptors
o Sensitive to partial pressures (e.g., of CO2 and O2)
o Aortic bodies via the vagus nerve
Afferent and efferent connections to DRG and VRG
o Carotid body via the glosspharyngeal nerve
Located at the bifurcation of external and internal carotid arteries
- Chemosensitive centre
o Baroreceptors (pressure) and other lung receptors (stretch receptors)
Respiratory Center
- Pneumotaxic centre (P Centre)
o Limits inspiration by inhibiting apneustic centre
o This then increases rate
- Apneustic centre
o In balance with P Centre to fine tune the rate during activities such as exercising
o Potential mechanism is to modulate ramp signal of inspiration
o Communicates mostly with the DRG but also with the VRG
- Hering Breuer Inflation Reflex
o Mediated via stretch receptors in the lung afferents input via vagus nerve
o Prevents over-inflation of the lung
- The P Centre and the apneustic centre are actually paired nuclei which cycle. They contribute to
the function of the DRG in the medulla
- The apneustic center has an excitatory effect on inspiration and will tend to prolong inspiration
(decreasing RR)
- The P centre is inhibitory and switches inspiration off (increasing RR). This will then assist in the
control of respiratory rate and inspiratory volume
- Damage to the connections between these centres as a result of brain injury will result in an
irregular breathing pattern consisting of prolonged inspiratory gasps interrupted by expiratory
efforts
Chemical Control of Ventilation
- Driven by H+ (pH), CO2, and O2
o Hypercapnia (CO2 and H+) contributes the most to drive to breathe
o Oxygen has a smaller effect
Central Chemosensitive Area
- Central chemoreceptor thought to be located in the ventrolateral medullary surface
- Sensitive to H+ only
o H+ does not cross the blood-brain barrier into the ESF or CSF
o CO2 on the other hand crosses readily

Hence the reaction where carbonic acid very rapidly dissociates into bicarbonate
and H+
o Therefore, blood CO2 has a greater effect than blood H+ (pH)
Effect of CO2 decreases after 1-2 days
o This is due to the buffering capacity in the blood via the increase in blood bicarbonate
Oxygen has NO EFFECT in this area!

Peripheral Chemoreceptors
- Very sensitive to decreases in O2
- Also sensitive to H+ and CO2
What is Important to Know as PTs
- Know that there exists neural oscillators in the medulla that support inspiration and expiration
- Have to be under some automatic control because, for example, we dont stop breathing when we
are asleep! So these areas have to have pacemaker cells
- However these areas are finely modulated (tuned) to generate respiratory-related motor activities
like talking, singing, eating, etc.
Control of the Heart
Skeletal Muscle and Cardiac Muscle
- Compare and contrast
o Both have contractile elements
o Cardiac muscle has elements of both smooth and striated muscle
Can generate action potentials that spread to adjacent cells. Note intercalated
discs
Can observe gap junctions
o Can contract to produce force
o Cardiac muscle, unlike skeletal muscle has automaticity
o The heart is a functional syncytium a syncytium is a multinucleated protoplasmic
mass formed by the secondary union of originally separate cells funny way to describe
a heart but note functional
Basically, a mass of cells that functionally behave all together
Histology
- Purkinje cells part of the conducting system of the heart (they conduct rather than contract).
Are in fact modified cardiac muscle
o Note no T-tubules
o Note no gap junctions and no intercalated discs
- SA node
o Intrinsic pacemaker of the heart (because it has the fastest rate of firing)
o Has both sympathetic and parasympathetic drive/input
Cardiac Action Potential
- Partial repolarization is due to closing of fast sodium channels
- Plateau is due to slow sodium and calcium channels

Repolarization due to increased activation of potassium channels and closing of slow sodium and
calcium channels

Relationship of AP to Twitch
- There is an overlap between the action potential and muscle twitch in cardiac muscle (unlike in
skeletal muscle)
Ion Currents
- Notice differences in ionic flow in different cardiac cells
- Note pacemaker potential in SA nodal cell
o Slow leaking potassium = automaticity
- Pacemaker current depends on extra ionic current
- Provides nodal cell with automaticity
Conducting System
- Notice the presence of the SA node and AV node
- Notice the intemodal pathways
- The significant of the AV delay = allows time for ventricular filling
The ECG Signal
- Is a cumulative sum of APs (not a single AP)
- P wave = depolarization of atria
- QRS = depolarization of ventricles
- T wave = rapid depolarization of ventricles
- U wave = usually very small but reflects the final phase of the Purkinje fiber repolarization
- P-R interval ~ 0.12-0.20 seconds
o Delay between SA and AV node
o Problems indicate alterations in ventricular filling
- S-T segment is the plateau initial phase of ventricular repolarization
o Pathology if above or below the isoelectric line
o The time when the entire ventricular muscle is depolarized
- The T wave is the rapid phase of ventricular repolarization
- Q-T interval is the period of electrical systole of ventricles
Myocardial Infarction Triad
1. Ischemia
o Characteristic sign of ischemia is an inverted T wave (caused by reduced supply from the
coronary arteries)
o May see these transiently (e.g., during a stress test or in angina patients)
2. Injury
o Elevation of S-T segment signifies acute injury (MI is new/acute)
3. Infarction
a. Necrosis
Abnormal Q wave indicates necrosis cell death in left ventricle
Significant Q wave 1 mm or greater wide (40 msec duration)
Abnormal Q wave = electrical void of necrotic infarct

S-T Segment Depression

- Can be caused by
o Subendocardial (partial thickness) MI
o Positive stress test
o Digitalis medication
Ventricular Fibrillation
- Normally, ventricular contraction starts with the inner lining of the muscle and progresses to the
outer layer
- Ventricular fibrillation disturbs this mechanism and causes random firing (outside muscle
contracts before inside, and is ineffective)
Autonomic Control of the Heart
- Sympathetic drive increases both HR and force of contraction (efferents to SA and AV node, and
cardiac muscle)
- Parasympathetic drive decreases HR (efferents to SA and AV node only)
- Notice that the vagus nerve delivers parasympathetic impulses
- Resting HR is a reflection of the balance between these two systems
Mechanics and Physiology of Breathing
- Respiratory tract
Nasal cavity mouth pharynx larynx trachea main bronchus lobar
bronchus segmental bronchus conducting bronchiole terminal bronchiole
respiratory bronchiole alveolar duct alveolar sac alveolus
- Lungs can be expanded and contracted in two ways
By downward and upward movement of the diaphragm to lengthen or shorten the chest
cavity
By elevation and depression of the ribs to increase and decrease the anteroposterior
diameter of the chest cavity
- Normal quiet breathing is accomplished almost entirely by movement of the diaphragm
During inspiration, contraction of the diaphragm pulls the lower surfaces of the lungs
downward
During expiration, the diaphragm relaxes, and the elastic recoil of the lungs, chest wall,
and abdominal structures compresses the lungs and expels the air
- During heavy breathing, the elastic forces are not powerful enough to cause rapid expiration
Extra force is achieved by contraction of the abdominal muscles, which pushes the
abdominal contents upward against the bottom of the diaphragm, thereby compressing
the lungs
- All the muscles that elevate the chest cage are classified as muscles of inspiration
When the rib cage is elevated, the ribs project almost directly forward, so that the
sternum also moves forward, away from the spine, increasing the anteroposterior
diameter of the chest cavity

Most important = external intercostals

Others include sternocleiomastoid (which lift upward on the sternum), serratus anterior
(which lift many of the ribs), and scalenes( which lift the first two ribs)
All the muscles that depress the chest cage are classified as muscles of expiration
Most important = rectus abdominus (pulling down on lower ribs at same time as pressing
abdominal contents upward against the diaphragm) and internal intercostals
Lung is an elastic structure that collapses whenever there is no force to keep it inflated
Lung is attached to the walls of the chest cage only at the hilum
Lung floats in the thoracic cavity, surrounded by a thin layer of pleural fluid that
lubricates movement of the lungs within the cavity
Continual suction of excess fluid into lymphatic channels maintains a slight suction between the
visceral pleural surface and the parietal pleural surface
Slightly negative pleural pressure

Therefore, the lungs are held to the thoracic wall as if glued there, expect that they are
well lubricated and can slide freely as the chest expands and contracts
During inspiration, expansion of the chest cage pulls outward on the lungs with greater
force and creates more negative pressure = increase in lung volume
Alveolar pressure is the pressure inside the lung alveoli
To cause inward flow of air during inspiration, the pressure in the alveoli must fall to a
value slightly below atmospheric pressure to pull air into the lungs
During expiration, the alveolar pressure must rise to slightly above atmospheric pressure
to force the inspired air out of the lungs
Transpulmonary pressure = pressure difference between alveolar pressure and plural pressure
A measure of the elastic forces in the lungs; recoil pressure
Airways are lined with goblet cells that produce mucous, as well as cilia, that continually beat
upwards
This creates a mucous elevator that is very effective at trapping and removing inspired
particles

Role of CV System in Gas Transport

- Heart is two separate pumps (divided by septum)
A right heart that pumps blood through the lungs (right AV valve = tricuspid)
A left heart that pumps blood through the peripheral organs (left AV valve =
mitral/bicuspid)
Each of these hearts is a pulsatile two-chamber pump composed of an atrium and a
ventricle
- Each atrium is a weak primer pump for the ventricle, helping to move blood into the ventricle
- Ventricles then supply the main pumping force that propels the blood either through the
pulmonary circulation by the right ventricle, or through the peripheral/systemic circulation by the
left ventricle
- Function of the arteries (more elastic, more muscular) is to transport blood under high pressure to
the tissues

Function of the capillaries is to exchange fluid, nutrients, electrolytes, hormones, and other
substances between the blood and the interstitial fluid
The veins function as conduits for transport of blood from venules back to the heart
Pulmonary circulation contains approximately 9% of total blood volume at any given time

Gas Transport by Blood

- Diffusion of oxygen from the alveoli into the pulmonary blood and diffusion of carbon dioxide in
the opposite direction, out of the blood
- Gases diffuse from areas of high concentration to areas of low concentration
- Partial pressure of the gas is directly proportional to the concentration of the gas
- The partial pressure of oxygen is generally greater in the gas phase in the alveoli than in the
dissolved state in the pulmonary blood = net diffusion of oxygen into the blood
Normal alveolar PO2 is 104 mmHg
- The partial pressure of carbon dioxide is generally greater in the dissolved state in the pulmonary
blood than in the gas phase in the alveoli = net diffusion of carbon dioxide out of the blood
Normal alveolar PCO2 is 40 mmHg
Carbon dioxide diffuses about 20 times as rapidly as oxygen because it is much more
soluble in water
- Alveolar walls are extremely thin, and between the alveoli is an almost solid network of
interconnecting capillaries
Flow of blood can be described as a sheet of flowing blood
Alveolar gases are in very close proximity to the blood of the pulmonary capillaries
- Respiratory membrane is very thin (averages 0.6 micrometers), and total surface area of
respiratory membrane is 70 square meters
Total quantity of blood in the capillaries of the lungs at any given instant is 60-140 mL
Looking at these two factors = easy to understand how fast oxygen and carbon dioxide
can be exchanged
- Must consider: some areas of the lungs are well ventilated but have almost no blood flow,
whereas other areas may have excellent blood flow but little or no ventilation
Normal VA/Q ratio is 0.8
Mismatch occurs to some degree in a healthy lung, but especially in lung diseases
This mismatch of ventilation and perfusion seriously impairs gas exchange through the
respiratory membrane
When ventilation/perfusion ratio is below normal = inadequate ventilation to provide the
oxygen needed to fully oxygenate the blood flowing through the alveolar capillaries
A certain fraction of the venous blood passing through the pulmonary capillaries does not
become oxygenated = shunted blood
Total amount of shunted blood per minutes = physiologic shunt
The greater the physiologic shunt, the greater the amount of blood that fails to be
oxygenated as it passes through the lungs

When ventilation/perfusion ratio is greater than normal = far more available oxygen in
the alveoli than can be transported away from the alveoli by the flowing blood
Ventilation of these alveoli is said to be wasted
Ventilation of anatomical dead space areas is also wasted
The sum of these two types of wasted ventilation is called the physiologic dead space
When the physiologic dead space is great, much of the work of ventilation is wasted
effort because so much of the ventilating air never reaches the blood
About 97% of oxygen transported from the lungs to the tissues is carried in chemical combination
with hemoglobin in the red blood cells
Remaining 3% is transported in the dissolved state in the water of the plasma and blood
cells
Oxygen molecule combines loosely and reversibly with the heme portion of hemoglobin
When PO2 is high, as in the pulmonary capillaries, oxygen binds with the hemoglobin
When PO2 is low, as in the tissue capillaries, oxygen is released from the hemoglobin
Bohr effect: increase in carbon dioxide in the blood causes oxygen to be displaced from
hemoglobin
Increases in blood carbon dioxide and hydrogen ions has a significant effect by
enhancing the release of oxygen from the blood in the tissues
As the blood passes through the tissues, carbon dioxide diffuses from the tissue cells into
the blood
This increases the blood PCO2, which in turn raises the blood carbonic acid and
hydrogen ion concentration
These effects shift the oxygen-hemoglobin dissociation curve to the right, forcing oxygen
away from the hemoglobin and therefore delivering increased amounts of oxygen to the
tissues
Carbon dioxide diffuses out of the tissue cells in the dissolved molecular carbon dioxide form
A small portion (7%) of the carbon dioxide is transported in the dissolved state to the
lungs
About 70% of the dissolved carbon dioxide in the blood reacts immediately with water to
form carbonic acid (catalyzed by enzyme carbonic anhydrase, found in red blood cells)
Carbonic acid formed in the red blood cells dissociates into hydrogen and bicarbonate
ions
Most of the hydrogen ions then combine with the hemoglobin in the red blood cells
(hemoglobin is a powerful acid-base buffer)
Many of the bicarbonate ions diffuse from the red blood cells into the plasma, while
chloride ions diffuse into the red blood cells to take their place (bicarbonate-chloride
carrier protein in the red blood cell membrane)
Reversible reaction
More than 20% of the dissolved carbon dioxide reacts directly with amine radicals of the
hemoglobin molecule to form the compound carbaminohemoglobin

Reversible reaction with a loose bond, so that the carbon dioxide is easily released into
the alveoli, where the PCO2 is lower than in the pulmonary capillaries
Haldane Effect: binding of oxygen with hemoglobin tends to displace carbon dioxide from the
blood
Combination of oxygen with hemoglobin in the lungs causes the hemoglobin to become a
stronger acid
The more highly acidic hemoglobin has less tendency to combine with carbon dioxide to
form carbaminohemoglobin, thus displacing much of the carbon dioxide that is present in
the carbamino form in the blood
The increased acidity of the hemoglobin also causes it to release an excess of hydrogen
ions, and these bind with bicarbonate ions to form carbonic acid; this then dissociates into
water and carbon dioxides, and the carbon diode is released from the blood into the
alveoli

PPENDERS for Abdominal Aortic Aneurysm

- Pathophysiology
o Abnormal dilation of abdominal aorta resulting in diameter > 30 mm (or 1.5 times
expected normal diameter)
Aortic wall loses elasticity through loss of elastic fibers and degradation of
collagen
Proteolytic process enzymes that degrade (MMP) increase while inhibitors
decrease
o True aneurysm = dilation involves all 3 layers of artery wall (intima, media, and
adventitia)
o False aneurysm = communication of blood between layers of artery wall and arterial
lumen, so not all 3 layers are dilated
o Most common location is infrarenal
o Shape can be fusiform (widening all around diameter of aorta) or saccular (bulging on
one side of the aorta)
o Types
Atherosclerotic or nonspecific aneurysm
Most common type
Strongly associated with progressive atherosclerosis and atherosclerotic
risk factors
Congenital aneurysm
AAA may be more frequent in individuals with genetic predisposition to
connective tissue disorders (e.g., Marfan syndrome)
Inflammatory aneurysm
Variant of atherosclerotic aneurysm
Wall of aneurysm thickened with dense, shiny, white fibrosis and
adherence to surrounding tissues
Tends to be more symptomatic than noninflammatory aneurysms
Infectious (mycotic) aneurysm
Bacterial inflammation of arterial wall, sometimes of existing aneurysm

Most commonly Staphylococcus or Salmonella in primary aortic

infections
o AAA rupture is an immediate surgical emergency
Should be considered as a possibility until ruled out in any patient with
hypotension, abdominal pain, and palpable mass
o Other concerns of an AAA are compression of neighbouring structures and increased
clotting
Prognosis
o AAA > 5-5.5 cm has high rupture rate if untreated
o 65% of those who have a rupture will die
o Risk factors for rupture include current smoking, increased blood pressure, larger AAA
diameter, and female sex
o Poor preoperative lung and renal function are associated with postoperative mortality
Epidemiology
o Most affected:
Men > 65 years old
Caucasians and Native Americans have higher risk of AAA than Blacks,
Hispanics, and Asians
Natural History
o Some aneurysms are dormant for months to years then suddenly grow
o Large aneurysms usually grow more rapidly
o Growth rate of small AAAs may increase with increasing baseline diameter
o Growth rate higher in smokers
o Aneurysm size is a strong predictor of risk of rupture
6-6.9 cm = 10-20%
Differential Diagnosis
o AAA associated with increased incidence of coronary artery disease, peripheral arterial
disease, hernia (in surgical patients), COPD, polycystic kidney disease, and obstructive
sleep apnea
o Often asymptomatic and usually discovered incidentally by physical exam, abdominal
ultrasound, or other imaging
o AAA rupture may mimic
Nephrolithiasis (kidney stones)
Diverticulitis (formation of pouches within the bowel wall)
Gastrointestinal hemorrhage (blood loss from the GI tract)
Etiology
o In most cases associated with atherosclerosis
Build-up of plaque within arteries from excess fat, cholesterol, calcium, etc.
Over time causes hardening and narrowing of arteries
Risk Factors
o Smoking
o Clinical vascular disease/cardiovascular disease
o Male
o Older age
o Hypertension
o Hyperlipidemia

o Atherosclerotic disease
o Family history of AAA
o Previous aortic aneurysm
o Excess weight
Signs and Symptoms
o Usually asymptomatic until rupture
o If present, symptoms can include
Vague, chronic abdominal pain
Low back pain
Mid-abdominal or flank pain which may radiate to back, groin, or scrotum
Potential palpable pulsatile nontender mass
But, clinical exam not reliable to rule out AAA, especially in obese
patients
o Rupture can present with acute abdominal or flank pain with fainting or shock

Surgery for an AAA

- Surgery recommended for AAA > 5.5 cm, or symptomatic AAA of any diameter
- Indications for AAA repair:
o Ruptured AAA
o Symptomatic AAA
o Rapidly expanding aneurysm (>1 cm/year)
o Asymptomatic aneurysms > 5.5 cm
o Thromboembolism
o Complicated aneurysms
- Relative contraindications to AAA repair
o Advanced age
o Class III or IV angina
o Heart failure
o Pre-existing renal impairment
o COPD
- Open surgery or endovascular aneurysm repair (EVAR)
o EVAR entry through femoral artery
o EVAR has lower perioperative mortality than open repair, but similar all-cause mortality
at 2-4 years and increased risk for additional surgical intervention
o Open surgery is associated with a longer hospital stay
o ACCF/AHA recommendations:
Open or EVAR of infrarenal AAAs indicated in patients who are good surgical
candidates
Open aneurysm repair reasonable to perform in patients who are good surgical
candidates but who cannot comply with periodic long-term surveillance required
after endovascular repair
General Anesthesia
- Anesthesia = condition in which sensations, principally pain and anxiety, are blocked
- To allow patients to undergo invasive procedures, such as major surgery, without pain or distress

Allows health care professionals to perform an indicated procedure without the additional
impediments associated with an excited, combative, and mobile patient
Patients who undergo general anesthesia cannot control or protect their airway, may require
assisted ventilation, and often have depressed cardiovascular function
Cause peripheral vasodilation and inhibit sympathetic autonomic regulation
o Patient can no longer autoregulate the circulation and tissue perfusion
o Also results in redistribution of blood flow to the skin and loss of thermoregulation with
resultant heat loss, a decrease in core temperature, and hypothermia
Aggressive monitoring and hemodynamic control are essential to achieve the best outcomes
Data does indicate that general anesthesia is associated with relative depression of diaphragmatic
function after aortic surgery (potential cause = overactive inhibitory reflexes of phrenic activity
arising from the abdominal wall and/or viscera)
Anesthesia causes nausea, vomiting
Those under general anesthesia will have atelectasis of the lower lobes 90% of the time post-op
Anesthesia also increases the VA/Q mismatch as well as depresses the sigh reflex (which leads to
atelectasis)

Smoking
- Smoking is the leading cause of preventable premature morbidity and mortality in the United
States and many other countries
- A lifelong smoker has a one in three chance of dying prematurely from a complication of
smoking
- Current smokers have a life expectancy shortened by 10 years
- Smoking is the major cause of lung cancer and COPD in developed countries
- Smoking is also a substantial causative factor in respiratory infections, including pneumococcal
pneumonia, influenza, and tuberculosis
- Tobacco use is a major cause of death from cancer, cardiovascular disease, and pulmonary disease
o Cardiovascular disease:
Sudden death
Acute myocardial infarction
Unstable angina
Stroke
Peripheral arterial occlusive disease
Aortic aneurysm
o Pulmonary disease
Lung cancer
Chronic bronchitis
Emphysema
Asthma
- Smoking is also a major risk factor for osteoporosis, reproductive disorders, and fire-related and
trauma-related injuries
- COPD
o More than 80% of COPD is attributable to cigarette smoking
o Causes loss of cilia, mucous gland hyperplasia, increased number of goblet cells in the
central airways, inflammation, goblet cell metaplasia, squamous metaplasic, mucus
plugging of small airways, destruction of alveoli, and a reduced number of small arteries

Also consider the carbon monoxide in cigarette smoke reduced capacity of hemoglobin
to carry oxygen and impairs oxygen release at the tissues
Cardiovascular disease
o Cigarette smoking accounts for about 20% of CV deaths in the United States
o Smoking accelerates atherosclerosis and promotes acute ischemic events
o Mechanics are believe to include
Hemodynamic stress (nicotine increases heart rate and transiently increases blood
pressure)
Endothelial injury and dysfunction (nitric oxide release and resultant vasodilation
are impaired)
Developed of an atherogenic lipid profile
Enhanced coagulability
Arrhythmogenesis
Relative hypoxemia because of the effects of carbon monoxide
Overall increase in inflammatory agents
o

Inactivity
- Inactivity can cause increased work of breathing
- Decreased chest wall compliance
- Weaker respiratory muscles
PT Pre-Op Assessment
- Become aware of other comorbidities/diagnoses as well as past medical history
- Learn about current symptoms (get baseline to compare)
- Become aware of medications
- Risk factors for heart disease: hypertension, smoking, elevated serum cholesterol or dietary
cholesterol intake, family history of heart disease, stress, sedentary lifestyle, older age, male
gender, obesity, diabetes
- Relevant social history: long-term smoking
- Baselines for clinical laboratory data, radiologic studies, oxygen therapy, PFT, vital signs, etc.
- Gain consent for post-op assessment/intervention
- Learn about home environment and family situation
- Able to run through exercises ahead of time
- If able to do a pre-op intervention
o Smoking cessation
o Increase strength of respiratory/coughing msucles
PT Post-Op
- Because of the invasiveness of this procedure throughout the abdomen, patients undergoing this
procedure are at high risk for pulmonary complications
- Incisional pain and the use of the abdominal musculature in coughing discourage the patients
from full inspirations as well as effective forceful coughing or huffing
- Appropriate bronchial hygiene techniques are essential for decreasing the incidence of pulmonary
complications, especially in patients with chronic pulmonary disease
- Assess for pulmonary symptoms:

o Shortness of breath
o Dyspnea on exertion
o Audible wheezing
o Cough
o Increased work of breathing
o Sputum production
o Look for rapid breathing rate, shallow depth, associated with accessory muscle activity
Inspection
o General appearance
LOC
Body type
Posture/positioning
Skin tone
Need for external support equipment
o Facial characteristics
Distress = nasal flaring, sweating, paleness, enlarged pupils
o Evaluation of the neck
Accessory muscle activity
Jugular venous distension
o Evaluation of the chest
Breathing patterns
Breathing rates
Inspiratory to expiratory ratios
Symmetry of chest wall motion
o Phonation
o Cough
o Cough production
o Appearance of extremities
Palpation
o Tracheal position
o Fremitus
o Muscle activity of chest wall and diaphragm
o Chest wall pain or discomfort
o Pulses
Percussion
Ausculation
Activity evaluation
o Assess response to situations: rest (supine), sitting, standing, ADL, ambulation of some
distance
Heart rate
Heart rhythm
Blood pressure
Oxygen saturation

Hb and WBC
- Normal range of hemoglobin is 12-16 g/100 mL for females and 13-17 g/100 mL for males

Many facilities use a cut-off value for Hb of <8 g/100 mL as a red flag for out-of-bed activities
<7 g/100 mL is usually when a transfusion will occur
Andrews hemoglobin is 7.4 g/100 mL
He therefore has an extremely low oxygen-carrying capacity and therefore is performing a lot of
work even with bed and activities of daily living
He also will have an elevated heart rate due to low Hb and be performing a lot of work with
breathing
Normal range of WBC is 4.0 - 10.0 x 109/L
Andrews WBC is 11.6 (elevated)
WBC <0.5 should avoid activity because of the extremely high risk for fatal infection
Elevated levels of WBCs are found in response to infectious diseases
This could be due to leukemia, bacterial infection, or polycythemia (secondary to bone marrow
stimulation)

Arterial Lines/CVP Lines/PCA/Morphine

- An arterial line is most commonly inserted through the radial artery but can also be inserted
through the femoral artery
- It allows for continuous measurement of arterial blood pressure and allows blood draw access for
arterial blood gas measurement
- The monitoring via the arterial line provides and displays a continuous measurement of systolic,
diastolic, and mean arterial pressures
- The MAP reading does not very significantly with motion artifact or movement on the catheter
site
- It is useful clinically because it yields one number that relates to cardiac output and the systemic
vascular resistance
- An MAP of less than 60 mmHg may indicate inadequate tissue perfusion
- Normal values are between 70-110 mmHg
- The central line is a central venous catheter inserted most commonly through the subclavian or
jugular vein; however, the femoral access is also used at times
- Catheter rests in the proximal superior vena cava allowing central venous pressures to be
measured directly to assess cardiac function and intravascular fluid sampling
- It also allows IV access for medication administration and other procedures
- Elevations in CVP may result from fluid overload, right ventricular failure, tricuspid
insufficiency, or chronic left ventricular failure. Low CVP may be indicative of hypovolemia
(decrease in blood plasma volume) and dehydration.
- The use of morphine in the treatment of severe heart failure has proved invaluable for both its
analgesic and its hemodynamic effects
- Morphine has a similar effect on the respiratory system as general anaesthesia (depression of sigh
reflex, increases VA/Q mismatch, etc.)
- Morphine is very addictive
- Common side effects: drowsiness, dizziness, constipation, stomach pain, nausea, vomiting,
headache, tired feeling, anxiety, mild itching
- 1-2 mg per PCA dose, 30 minutes after IV dose of 5-20 mg; lock out of 6-15 minutes between
PCA doses
Sputum

A productive cough, which was preceded by an earlier, painful, non-productive cough associated
with an upper respiratory tract infection, is indicative of lobar pneumonia
A dry or productive cough, with acute bronchitis, may indicate bronchopneumonia
Mucoid or bloodstained sputum with a paroxysmal cough, in a patient exhibiting flu-like
syndrome is indicative of mycoplasma or viral pneumonia
Purulent sputum, when sputum was formally mucoid, is indicative of acute exacerbation of
chronic bronchitis
Foul-smelling, copious, layered purulent sputum, which is a long-standing problem, is indicative
of bronchiectasis
Blood-tinged sputum which has lasted for a month is indicative of tuberculosis or fungal infection
Frothy sputum which worsens in supine position, accompanied by dyspnea, indicates heart failure
or pulmonary edema
In Andrews case- yellow sputum may indicate some sort of respiratory infection, such as
pneumonia

Auscultation Results- Post-Op Abdominal Surgery

- A decrease in lung tissue density, as in the emphysematous lung, would cause decreased sound
transmission.
- Decreased sound transmission also occurs if only shallow breaths are taken, or if distance of
transmission between the airways and the stethoscope is increased (obesity, pleural effusion,
barrel chest)
- In Andrews case, diminished breath sounds bilaterally in the anterior, lateral, and posterior basal
segments of lower lobes is likely due to only shallow breaths being taken, or to hypoinflation due
to atelectasis
- Crackles are discontinuous adventitious lung sounds that sound like brief bursts of popping
bubbles
- Crackles are more commonly heard during inspiration
- They may result from the sudden opening of closed airways (more fine) or as the result of the
movement of secretions during inspiration and expiration (more coarse)
- Peripheral airways can collapse owing to atelectasis, pulmonary edema, fibrosis, or compression
from pleural effusion, and often crackles ausculated with these pathologic conditions are in the
latter half of inspiration
- Crackles due to the movement of fluid or secretions in the lungs are often described as lowpitched and may be found on either inspiration or expiration or both
- Andrews crackles are likely due to secretions because they are coarse and clear with coughing
o Dependent areas close more easily lower lobes atelectasis
o Fluid accumulates here
- Normal respiratory rate is 12-16
o >20 = tachypnea
MRSA
- Methicillin-resistant Staphylococcus aureus
- Any strain of Staphylococcus aureus carrying genes conferring resistance to penicillinaseresistant penicillins, such as methicillin or oxacillin
- Rates of MRSA infection in the United States vary geographically but appear to be declining
since 2005, except in pediatric populations where rates appear to be stable or increasing

Most common is healthcare-acquired community-onset infections

Comprised 8.5% of hospital-acquired infections in the United States in 2009 and 2010
Risk factors:
o Advanced age
o Male gender
o Previous hospitalization
o Prolonged hospitalization
o ICU admission
o Chronic medical illness
o Prior and prolonged antibiotic treatment
o Presence and size of wound
o Exposure to colonized or infected patient
o Presence of invasive indwelling devices
o Residents in long-term care facility
Treated with antibiotics; culture and susceptibility testing should guide antibiotic selection

Atelectasis Post-Op
- Atelectasis: incomplete expansion of the lung or loss of volume of part (or all) or a lung
- In Andrews case, post-op atelectasis occurs which leads to the complication of lobar or
segmental pneumonia
- The main contributing factor is the inability or unwillingness (often because of pain or mental
confusion) of the patient to cough effectively and to take deep breaths throughout the day
- This type of atelectasis could be prevented with good pulmonary hygiene
- Acute atelectasis can respond to deep breathing or incentive spirometry exercises as well as
coughing
- Other airway clearance techniques may help with improving atelectasis
- If simple measures do not improve the lung collapse, fiberoptic bronchoscopy can be performed
to suction secretions that may be causing the atelectasis
Discharge from PT Services
- Restoration of pre-admission functioning
- Independently mobile with transfers and ambulation
- Restored normal breathing patterns (normal diaphragmatic excursion; reduced use of respiratory
muscles; normal respiratory rate)
- Pain under control
- Patient understands exercises and can perform them correctly
- Strong cough
Pulmonary Post-Surgical Complications
- The pulmonary dysfunction that results from surgical therapy is due to three primary factors
o The anesthetic agent
o The surgical incision or procedure itself
o The pain caused by the incision or procedure
- The anesthetic agent causes a decrease in the pulmonary arterial vasoconstrictive response to
hypoxia
- This increases ventilation-perfusion mismatching and decreases pulmonary gas exchange

Anesthesia also depresses the respiratory control centres so that ventilatory response to
hypercapnia and hypoxia is reduced
Placement of an endotracheal tube increases airway resistance
Placing the patient in a supine position reduces the functional residual capacity by 20%
During surgery, the shape and configuration of the thorax changes shape
o The anterioposterior diameter decreases
o The lateral diameter increases
o The vertical diameter decreases
With the diaphragm moving in a caudal direction owing to the effect of general
anesthesia on central nervous system innervation of diaphragmatic tone
These changes further reduce the FRC by another 15%
The surgical incision will cause a significant, although temporary, restrictive impairment
o Following upper abdominal surgery, the VC is decreased by 55% and the FRC by 30%
o These decreases in lung volumes reach their greatest values 24-48 hours following
surgery
o Lung volumes then return to relatively normal values in 5 days, although full recovery
may take 2 weeks
o Diaphragmatic dysfunction has been demonstrated in some abdominal surgery patients
Because of the pain, the tone in the muscles of the thorax and the abdominal will increase,
thereby decreasing the chest wall compliance (known as muscular splinting)
Contributes to decrease lung volumes and increased work of breathing post-op
Signs
o Pulmonary function tests
Decrease in all lung volumes
Decreased VC by 55% and FRC by30%
Flow rates normal
o Chest radiograph
Atelectasis (in approximately 95% of patients following abdominal and thoracic
surgery)
May also show pneumonia, especially of lower lobes, or even pulmonary
embolism
o Arterial blood gases
Decreased PaO2
SpO2<90% found in 35% of postop patients
o Breath sounds
Decreased breath sounds
May have rhonci or rales
o Cardiovascular
May have myocardial infarction, arrthymias, and possible cardiac arrest
Symptoms
o Altered breathing patterns, decreased VT and increased RR
o Cough reflex suppressed due to anesthesia
o Cough productive of blood-streaked sputum if patient was intubated
Treatment
o Hypoxia can be treated with inflation-hold breathing techniques, PEEP, CPAP, and
occasionally with increased oxygen concentrations

o
o
o
o

To treat postop atelectasis, deep breathing exercises, early mobilization of the patient out
of bed, incentive spirometers, and CPAP
Nosocomial pneumonias following surgery are not uncommon following upper
abdominal surgery, and 12-20% of patients experience this complication
Treated with an appropriate antibiotic and possibly with postural drainage, percussion,
and vibration if the patients secretion clearance mechanisms are impaired
Prevention of venous thromboembolism may include simple leg exercises (ankle dorsi
and plantar flexion), low-dose subcutaneous or adjusted-dose heparin, external pneumatic
compression devices, and gradient compression stockings

Problem List for Andrew

Body Structure/Function Impairments
- AAA; now repaired- large incision from xiphoid process to pubic symphysis
- Weak cough producing yellow sputum
- Breathing pattern altered
o Excessive use of accessory respiratory muscles
o Reduced lateral-costal expansion bilaterally
o Very limited diaphragmatic excursion
- Chest radiograph indicates left lower lobe triangular retrocardiac atelectasis
Activity Limitations
- Able to walk to the bathroom but requires moderate assistance of one person
- Able to transfer from supine to sitting and standing but requires moderate assistance of one
person
Participation Restrictions
- Limited ability to perform ADLs restricts ability to fulfill role as independent member of society
Personal Factors
- Moderate smoker
- 69 years old
- Widower
- Retired
- Sedentary
Environmental Factors
- Roommate has MRSA
- Lives alone in a two-story house
Short and Long-Term Goals- Andrew
- STG: Restoration of normal breathing patterns/diaphragmatic excursion in three days
- LTG: Achieve independent ambulation of 20 m in five days
Treatment Plan- Andrew
- Hb is low; check with doctors before getting patient out of bed
- Deep breathing/diaphragmatic exercusion
- Coughing
o First line of intervention is positioning and teaching proper coughing technique
Position the patient to allow for trunk flexion and extension

Maximize the inspiratory phase via verbal cues, positioning, and active arm
movements
Improve the inspiratory hold by giving verbal cues and by positioning
Maximize intrathoracic and intraabdominal pressures with muscle contractions or
trunk movement
Orient the patient to respective timing and trunk movements for expulsion
o Surgical patients will need to be instructed in how to splint their incision by applying
pressure over it with a pillow or blanket roll during the expiratory phase of the cough
o If pain is inhibiting the patients ability to perform proper coughing techniques, pain
medication should be administered in time for it be effective during the patients session
with the physical therapist
Deep breathing 10 times every hour plus a cough
Early mobilization
Postural drainage
o Assumption of one or more body positions that allow gravity to assist with draining
secretions from each of the patients lung segments
o Need an adjustable bed, pillows or blanket rolls, and enough personnel to assist in
moving the patient safely
o Tissues, a sputum cup, airway suctioning equipment, and body substance barriers should
be available to safely collect any secretions that are produced
o Patients face should always be visible
o Good lung down
o Hold position for 2-10 minutes
Ankle pumps- prevention of venous thromboembolism 10 times every hour

PPENDERS for COPD

Pathophysiology
- Pulmonary disease characterized by persistent airflow limitation associated with a chronic
inflammatory response (to noxious particles or gases) in airways and lungs resulting in
destruction of lung tissue and often long-term decline in lung function
- COPD exacerbation defined as an acute event characterized by worsening of respiratory
symptoms beyond normal day-to-day variations and leading to change in medication
o Following exacerbation, patients rarely return to baseline function
- Airflow limitation results from:
o Inflammation-induced structural changes, including
Small airway remodeling and narrowing
Parenchymal destruction
o Decreased elastic recoil in patients with emphysema
o Subsequent reduction in ability of airways to remain open during expiration
- FEV1/FEV < 70% for diagnosis
Prognosis
- Chronic airflow limitation is usually progressive
- Dyspnea typically persistent and slowly progressive
- Chronic cough may be intermittent

Factors associated with increased COPD mortality include:

o Cigarette smoking
o Low FEV1
o Low FVC
o Breathlessness with limited activity
o Poor exercise tolerance (assessed by walking distance or peak oxygen consumption)
o Weight loss
o Reduction in PaO2
o Comorbidities
o Higher BODE index
Etiology
- Chronic abnormal inflammatory response of lung to noxious particles or gases (for example,
cigarette smoking) resulting in small airway disease (obstructive bronchiolitis) and parenchymal
destruction (emphysema)
- Bronchitis = blue bloaters
- Emphysema = pink puffers
Natural History
- COPD progression associated with small airway changes with accumulation of inflammatory
mucous exudate in lumen and inflammatory infiltrate (including lymphoid follicles) in wall
- Narrowing and disappearance of small conducting airways appears to occur before onset of
emphysematous destruction in patients with COPD
Differential Diagnosis
- Associated conditions:
o Cardiovascular disease, including
Hypertension
Coronary artery disease
Atrial fibrillation
Heart failure
o Lung cancer
o Osteoporosis
o Depression and anxiety
o Arthritis
o Diabetes
o Metabolic syndrome
o Infections, especially respiratory infections
o Gastroesophageal reflux disease
o Bronchiectasis
Persistent or progressive suppurative lung disease characterized by irreversibly
dilated bronchi and chronic or recurrent bronchial inflammation and infection
- Indicators for diagnosis of COPD
o Dyspnea
o Chronic cough

o Chronic sputum production

o Hx of exposure to risk factors
o FEV1/FEV ratio <70% required for definitive diagnosis
Epidemiology
- Overall under-recognized and under-diagnosed
- Most affected are smokers, men, and people aged >40 years
- Fourth leading cause of mortality worldwide
- Estimated 4%-10% prevalence of COPD worldwide
- Prevalence of COPD among smokers about 15%
Risk Factors
- Cigarette smoking is most common risk factor worldwide
- Occupational exposures (including organic and inorganic dusts, chemical agents, and fumes)
- Alpha-1 antitrypsin deficiency
- Indoor air pollution, particularly biomass smoke from burning biomass fuels in confined spaces,
especially in women and children
- Exposure to passive smoke (secondhand smoke, environmental tobacco exposure)
- Other types of tobacco smoke and marijuana
- Outdoor pollution
- Other possible risk factors:
o Poverty
o History of severe childhood respiratory infection
o Tuberculosis
o Suboptimal lung development during gestation or childhood
o Asthma
o IV drug use
Signs and Symptoms
- Chronic and progressive symptoms of
o Dyspnea
o Cough
o Sputum production
- Although symptoms are chronic and progressive, symptoms can be variable from day to day
- Chronic cough and sputum production may be present years prior to airflow limitation
- Physical signs of airflow limitation may not manifest until lung function substantially impaired
- Muscle wasting or cachexia may occur with severe disease or comorbidities
- Hemodynamic instability with disease exacerbation
- Reduced alertness possible with disease exacerbation
- Central cyanosis
o New onset or worsening of central cyanosis may indicate disease exacerbation
- Barrel chest associated with COPD but not sensitive or specific
- Use of accessory respiratory muscles (scalenes or SCM)
- Pursed-lip breathing
- Reduced chest expansions

Reduced breath sounds

Expiratory time > 4 seconds
Wheezing

Orthopnea
- Orthopnea = difficulty breathing in postures over than erect
- Often indicates pulmonary edema
Hoover Sign
- Some patients with advanced disease have paradoxical inward movement of the rib cage with
inspiration (Hoovers sign), the result of alteration of the vector of diaphragmatic contraction on
the rib cage as a result of chronic hyperinflation
- Flattened diaphragm
- This sign rules in obstruction as a potential cause of respiratory distress
Tracheal Tug
- One type- the dilated aorta may produce a tracheal tug by pulsating against the left bronchus
- Second type- flattened diaphragm pulls entire mediastinum down during inspiration
Pitting Edema
- When the skin and underlying soft tissues of a leg with edema are compressed with fingers, the
impressions remain
- This type of edema is most commonly associated with heart failure and is usually a transudate
- Commonly associated with left-sided congestive heart failure and occurs most often in the lower
extremities
- Associated with kidney function/failure
Two Minute Walk Test
- This test is adapted from the American Thoracic Societys 6-Minute Walk Test Protocol
- This test measures sub-maximal cardiovascular endurance by recording the distance that the
participant is able to walk on a 50-foot (out and back) course in 2 minutes
- The participants raw score is the distance in feet and inches walked in 2 minutes
- Norm for males between 70-85 years is 81 feet
- Assistive devices can be used but should be kept consistent from test to test
- Individual should be able to ambulate without physical assistance
- MDC for older adults = 40 feet (12.2 m)
Medications
Lasix
- A sulfonamide, loop-type diuretic and antihypertensive agent
- Uses:
o Management of edema associated with CHF, hepatic cirrhosis, and renal disease
o Considered a diuretic of choice for most patients with CHF

IV management of acute pulmonary edema (in combination with oxygen and a cardiac
glycoside)
o Management of hypertension (along or in combination with other classes of
antihypertensive agents)
o Not considered a preferred agent for initial management of hypertension; however, may
be useful in selected patients with renal impairment or heart failure
- Common adverse effects
o Orthostatic hypotension, dizziness, electrolyte imbalance (hyponatremia, hypokalemia,
hypochloremia), tinnitus, photosensitivity
Prednisone
- Synthetic glucocorticoid; minimal mineralocorticoid activity
- Treatment of a wide variety of diseases and conditions; used principally for glucocorticoid effects
as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic
systems in the palliative treatment of various diseases
- For severe exacerbations of COPD, a short (e.g., 1-2 weeks) course of oral glucocorticoids can be
added to existing therapy
- Much less dramatic effects in stable COPD than in asthma, and the role of glucocortioids is
limited to very specific indications
- Common adverse effects:
o Associated with long-term therapy: bone loss, cataracts, indigestion, muscle weakness,
back pain, bruising, oral candidiasis
Ventolin
- Bronchodilator; relatively selective, short-acting, beta-2-adrenergic agonist
- Uses in COPD:
o Symptomatic management of reversible bronchospasm associated with COPD in patients
who continue to have evidence of bronchospasm despite regular use of an orally inhaled
bronchodilator and who require a second bronchodilator
o Symptomatic management of reversible bronchospasm associated with COPD when
given on an as-needed or regular (e.g., 4 times daily) basis, either alone or concomitantly
with other inhaled bronchodilators
o Regular use of a selective, short-acting inhaled beta-2-adrenergic agonist in the
management of COPD, in contrast to that in asthma, does not appear to be detrimental
- Common adverse effects:
o Asthma exacerbation, bronchospasm, nervousness, tremor, shakiness, otitis media,
nausea, cough, bronchitis, headache, tachycardia/palpitations, muscle cramps,
hypokinesia, insomnia, weakness, dizziness, excitement, hyperactivity, increased
appetite, flu syndrome, lymphadenopathy, skin/appendage infection, urticaria
o

Percussion
- A tympanic sound is loud, long, and hollow, and may be heard over an empty stomach or a
hyperinflated chest
- In Bens case, his lungs are likely hyperinflated throughout

Auscultation- COPD
- A decrease in lung tissue density, as in the emphysematous lung, would cause decreased sound
transmission.
- Decreased sound transmission also occurs if only shallow breaths are taken, or if distance of
transmission between the airways and the stethoscope is increased (obesity, pleural effusion,
barrel chest)
- Crackles are discontinuous adventitious lung sounds that sound like brief bursts of popping
bubbles
- Crackles are more commonly heard during inspiration
- They may result from the sudden opening of closed airways or as the result of the movement of
secretions during inspiration and expiration
- Peripheral airways can collapse owing to atelectasis, pulmonary edema, fibrosis, or compression
from pleural effusion, and often crackles ausculated with these pathologic conditions are in the
latter half of inspiration
- Crackles occurring in the early half of inspiration often result from the popping open of more
proximal airways
- Crackles due to the movement of fluid or secretions in the lungs are often described as lowpitched and may be found on either inspiration or expiration or both
- Wheezes are continuous adventitious sounds with a constant pitch and varying duration
- Wheezes on expiration are most common and are often associated with airway constriction, as
found in bronchospasm or when secretions are narrowing the airway
Chest X-Ray- COPD
- Hyperinflated lung fields or bullous changes point to a chronic pulmonary disorder with
secondary pulmonary hypertension
- In dominant emphysematous disease, radiographs demonstrate signs of hyperaeration, such as
increased anteroposterior chest diameter, flattened diaphragms, increased parenchymal lucency,
and attenuation of pulmonary arterial vascular shadows
- Blood flow redistributes to upper lung fields due to pulmonary edema in lower lung fields
o Common cause of pulmonary edema = left-sided heart failure
Pulmonary Function Tests
- Based on the results of PFTs, pulmonary diseases may be classified into three basic categories:
obstructive, restrictive, or combined
- Tests that measure airflow rates during forced breathing maneuvers provide important
information relating to the actual function of the lungs, the degree of impairment, and often the
general location (large airways, small airways, etc.) of the problem
- FVC is the maximum volume of gas the patient can exhale as forcefully and as quickly as
possible
- The FVC is generally reduced in both obstructive and restrictive diseases
o Individuals with obstructive deficits will demonstrate large lung volumes, but reduced
FVC because of inability to get the air out forcefully (as in asthma or emphysema)

Individuals with restrictive defects will demonstrate small lung volumes, and possibly
reduced FVC because of the lack of muscle strength (as in a patient with pneumonia or
severe pulmonary fibrosis)
FEV1 is the volume of air that is exhaled during the first second of the FVC and reflects the
airflow in the large airways
The utility of the FEV1 measurement is exemplified by the simple relationship between it and the
associated degree of obstruction
o Little or no obstruction: FEV1 above 2.0 L to normal
o Mild to moderate obstruction: FEV1 between 1.0 and 2.0 L
o Severe obstruction: FEV1 less than 1.0 L
This volume may also be expressed as a percentage of the FVC exhaled in 1 second
Normally, 75% of the FVC should be exhaled within 1 second
A FEV1% of more than 80% or 90% indicates restrictive disease, while a reduced FEV 1%
indicates airway obstruction
o

Arterial Blood Gas Analysis

- Blood gas analysis is crucial to the assessment of problems related to acid-base balance,
ventilation, and oxygenation
- Normal ranges of arterial blood gas values
o pH = 7.35-7.45 (normal = 7.4)
o PCO2 = 35-45 (normal = 40 mmHg)
o PO2 = >80 (normal = 97 mmHg)
o HCO3- = 22-28 (normal = 24 mEq/L)
- If a patients PO2 is between 60-80 mmHg, the patient is said to be mildly hypoxemic
Oxygen Titration (Authorized Act)
- Within a regulated scope of practice, a health care professional may be permitted to perform a
variety of authorized activities
- Authorized activities are procedures with an element of higher risk
- This potential for harm means that public protection is required and performance is restricted to
certain professionals with the skill, competence, and accountability to perform them
- In other words, appropriate authorization is needed to perform these activities
- There are two main ways to receive the authority to perform an authorized activity
o Members of a profession can be directly authorized to perform an activity (by law or
regulation under a law)
o Individuals can received indirect authority most commonly by a transfer of authority
from another authorized health professional but also by exemption or exception to the
rules
- The Physiotherapy Act provides direct authority for Ontario physiotherapists to perform he RHPA
controlled acts
o This includes administering a substance by inhalation

Administering a substance by inhalation has also been authorized to rostered physiotherapists, but
comes with the additional provision that the substance must be ordered by a member of the
College of Physicians and Surgeons of Ontario, or by a member of another College who is
authorized to order the substance
The substance that most physiotherapists would administer is oxygen

Home Oxygen for Ben

- Ben has a qualifying diagnosis of COPD
- He has a PO2 > 60 mmHg (72 mmHg)
- He does have SpO2 of 88% or less (80%) with exertion on room air
- We would have to assess whether his exercise tolerance improves with O2
- If yes, he would qualify for Hypoxemia During Exertion Funding
o Respirologist/internist with respiratory medicine expertise must agree to sign HOPA
o Independent facility is responsible for HOP requalification testing at 90 days and 12
months after initial HOP application
Analysis Statement for Ben
71-year-old male presenting with acute exacerbation of COPD, c/o dyspnea/orthopnea. On 2L/min O 2
delivered by nasal cannulas. Breathing patterns altered (increased accessory muscle use and decreased
lateral costal expansion). Reduced FEV1/FVC% consistent with obstructive lung disease. Reduced PO2
consistent with mild hypoxemia. Minimal assistance required with ambulation and transfers from bed to
chair.
Pack-Year
A way to measure the amount a person has smoked over a long period of time. It is calculated
by multiplying the number of packs of cigarettes smoked per day by the number of years the
person has smoked. For example, 1 pack year is equal to smoking 1 pack per day for 1 year, or 2
packs per day for half a year, and so on.
- Odds ratio for COPD with a 40 or greater pack year history is 4.58
MMRC Dyspnea Scale
- Purpose is to assess the level of physical activity necessary to precipitate breathlessness (NOT
level of actual dyspnea)
- Self-administered scale consisting of five descriptive statements regarding levels of physical
activity that precipitate shortness of breath
- The patient is asked to select the grade (0-4) that best describes their shortness of breath (0 = least
severe, 4 = most severe)
- Has been validated in individuals with COPD
- MMRC score of 0 in healthy individuals is to be expected
- Bens MMRC score is 3
6MWT- COPD
- Normative data from Hill (2011) sets Bens predicted distance at 586 m

o Ben only walked 175 m

MCID of 30 m (ATS/ERS 2014)
Data from Solway et al. (2002) indicates that Ben may need a gait aid (subjects who walked <300
m)
o He is currently using a non-wheeled walker
<200 m is predictive of mortality and hospitalization in those with COPD

BODE Index
- BODE index assesses clinical risk
- Risk of respiratory-related mortality increases 60% with each additional level of the BODE
index
- Bens BODE Index score is 7
- Better predictor of all-cause mortality and respiratory disorder-mortality than FEV 1 alone
- MCID = 1
- Score between 7 and 10 = 18% survival over four years
Treatment Plan In-Hospital
- Pursed-lip breathing PRN (functional)
o Reduces dyspnea
o Keeps airways open longer during expiration (back pressure inside airways to splint them
open, so expiration takes less work)
- Ankle pumps 10x hour
- Coughing every hour
o If ineffective, postural draining (10-15 min per position) with potential addition of
percussion or vibration
- Mobilization ambulating, stair training, potential new gait aid training
- Strength training
o Shoulder flexion
o Leg bed exercises (quads over roll, bridging)
- If dietician hasnt been referred educate on avoiding sodium
o There may also be a fluid restriction for patients with acute heart failure (1 L/day)
- Educate on tripod position for dyspnea
- Also consider active cycle of breathing (ACB)
Treatment Plan In-Community
- Pursed-lips breathing
- Walking 10-30 min, 3-5 days, 60-80% intensity
- Resistance training
o 10 reps @ 50% 1-RM to start; progress to 12-24 reps
o 2 days a week
- Balance
o Stance (1 minute each, 2x day, 7 days/week)
o Transition sit-to-stand (30 seconds each, 5 days/week)
o Gait parallel bars, sideways, backwards (10 min, 2xday, 7 days/week)
o Functional strength toe/heel raises, squats, step ups (10x per day, 7 days/week)

Education
o Energy conservation
To increase efficacy of exercise program (for moderate-severe COPD)
o Supplemental oxygen
o 4WW (as opposed to 4 point walker)
o Water-based exercise can be an alternative if available and preferred by patient

Problem List for Ben

Body Structure/Function
- Dyspnea/orthopnea
- Diagnosis of COPD
- O2 delivered by nasal cannulas (2L/min)
- Barrel-shaped chest
- Using accessory muscles at rest, loss of bucket-handle rib movement, Hoover sign present
- Resting heart rate 92 bpm
- Chest excursion decreased
- Tracheal tug
- Bilateral pitting edema
- Hyper-resonant thorax
- Diminished breath sounds all lung fields; inspiratory and expiratory crackles at the bases,
bilateral; expiratory wheezes throughout both lungs
- Chest x-ray shows hyperinflated lungs, flattened diaphragms, and pulmonary vascular
redistribution upper lung fields
- Reduced FEV1, FVC, and FEV1/FVC%
- Reduced PO2
- Low BMI
Activity Limitations
- Unable to lie flat (uses 3 pillows)
- Needs minimal assistance to move from bed to chair
- Needs minimal assistance to ambulate to the bathroom
- Unable to ambulate for two minutes without oxygen saturation dropping to 80% on room air
Participation Restrictions
- Unable to meet his friends at community centre (social)
Personal Factors
- 71 years old
- 100 pack/year smoking history (has stopped smoking, for the third time, four months ago)
- Retired
- Lives with his wife
- Has had pneumonia several times in the past few years (most recent 4 months ago)
- Risk of developing heart failure
- Taking lasix, prednisone, and ventolin inhaler
Environmental Factors
- Former steelworker

Lives in a two-storey home

PPENDERS for Acute Inferior Myocardial Infarction

- Pathophysiology
o Symptoms of myocardial ischemia accompanied by persistent elevation of ST segment
on ECG and subsequent release of biomarkers of myocardial necrosis
o Types
Type 1 spontaneous MI
Related to atherosclerotic plaque rupture, ulceration, fissuring, erosion,
or dissection with resulting intraluminal thrombus in at least one
coronary artery resulting in decreased myocardial blood flow or distal
platelet emboli with ensuing myoctye necrosis
Patients may have or not have underlying CAD
Type 2 MI secondary to ischemic imbalance
Myocardial injury with necrosis due to condition other than CAD
contributing to imbalance between myocardial oxygen supply and/or
demand
Causes include coronary endothelial dysfunction, coronary artery spasm,
coronary embolism, tachyarrhythmias, bradyarrhythmias, anemia,
respiratory failure, hypotension, and hypertension with or without left
ventricular hypertrophy
Type 3 MI resulting in death when biomarker values are unavailable
Type 4 MI associated with percutaneous coronary intervention (type 4a) or with
stent thrombosis (type 4b)
Type 5 MI associated with coronary artery bypass grafting
o Most commonly, atherosclerotic plaque rupture resulting in occlusion of coronary artery
o Resulting decrease in myocardial blood flow may cause myocyte necrosis after >2-4
hours, depending on
Presence of collateral circulation to ischemic zone
Intermittment or persistent coronary occlusion
Sensitivity of myocytes to ischemia
Preconditioning
Demand for oxygen and nutrients
o Entire process from myocyte necrosis to healed infarction may take >5-6 weeks
- Prognosis
o Mortality 4.6% in-hospital and 4.5% at 6 months in patients admitted with STEMI
o 11% of in-hospital patients developed heart failure or pulmonary edema
- Epidemiology
o Most affected are adults with coronary artery disease
o 70% of patients with STEMI are men
o Incidence of myocardial infarction appears to be decreasing in United States
o 70% STEMIs, 30% NSTEMIs
o Theres a heart attack every 7 minutes in Canada
- Differential Diagnosis

o Thoracic aortic aneurysm and dissection

o Unstable angina
o Pulmonary embolism
o Esophageal rupture
o Tension pneumothorax
o Perforating ulcer
o Myocarditis
o Rib fracture
o Anxiety disorder
o Panic attack
Diagnosis
o Chest discomfort (intense pressure)
o ECG changes
o Elevated biomarkers
o Atypical presentation common in older adults, women, and patients with diabetes
Etiology/Natural History
o Atherosclerotic plaque due to CAD may rupture resulting in thrombus occluding the
coronary artery (most common cause)
o Less commonly, plaque erosion characterized by disrupted or absent endothelium on top
of plaque with abundant smooth muscle cells and proteoglycans may cause coronary
obstructions via thrombi development on dysfunctional intima
o Nonatherosclerotic causes include
Emboli
Mechanical obstruction (e.g., chest trauma, dissection of coronary arteries)
Increased vasomotor tone (e.g., variant angina pectoris, nitroglycerin withdrawal)
Arteritis
Aortic stenosis
Cocaine abuse
Coronary vasospasm
Risk Factors
o Major risk factor is coronary artery disease
o CAD major risk factors
Tobacco exposure
Includes cigarette or cigar smoking, or spit or chewing tobacco
Passive (second-hand) cigarette smoke also increases risk
Dyslipidemia
Elevated triglyceride levels; elevated total LDL or non-HDL cholesterol
levels; low HDL cholesterol levels
Hypertension
Diabetes
Hyperglycemia in people without diabetes also associated with increased
risk
Obesity
Metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance)
Family history of cardiovascular disease in first-degree relative
Elevated high-sensitivity C-reactive protein (CRP) levels

Atherosclerosis in non-coronary arteries

Low ankle-brachial pressure index
Carotid bruits
Transient ischemia attack or ischemic stroke
o Potential triggering events
Anger
Unemployment status and cumulative job loss
Exposure to traffic
Acute infection (e.g., acute respiratory infection)
Episodic physical and/or sexual activity
Death of loved one
Shift to and from daylight saving time
Viewing World Cup soccer (in Germany)
o Atrial fibrillation
o Medication/drug use
Cocaine
NSAIDs
Inhaled beta-2 agonists
o HIV positive
Signs and Symptoms
o Chest pain or pressure frequently in substernal region, which may radiate to neck, jaw,
left shoulder, or left arm
o Dyspnea
o Nausea and vomiting
o Diaphoresis (sweating)
o Fatigue
o Palpitations
o Denial
Myocardial infarction is a major risk factor for heart failure
He should be aware of most common symptoms
o Dyspnea
o Fatigue
o Edema
Likely risk factors that he can modify are hypertension, obesity, metabolic syndrome, diet
(increase sodium intake results in increased risk for heart failure), smoking

Acute Coronary Syndrome

- Spectrum of acute myocardial ischemia and/or necrosis usually secondary to reduction in
coronary blood flow, including
o Unstable angina
Differentiated from NSTEMI by absence of cardiac biomarkers indicating
ischemic myocardial necrosis
o Non-ST-elevation myocardial infarction
Suggested by absence of persistent ST-segment elevation
Elevated cardiac biomarkers
o ST-elevation myocardial infarction

Creatine Kinase
- Creatine phosphokinase is a marker that is diagnostic of cardiac injury
- CPK has been used as a cardiac marker for more than 35 years; however, it has been shown to be
elevated after cardiac surgery and cardiopulmonary resuscitation (especially if the person was
defibrillated), and has been shown to be abnormally elevated in patients undergoing thrombolysis
with streptokinase or tissue plasminogen activator
- False-elevated CPK levels in patients without MI was evidenced in 43.3% of elective hip surgery
patients
- CPK-MB (the isoenzyme which is most conclusive for myocardial injury) > 3% is considered
abnormal
- Normal values for CPK-MB are 0-3%
- Normal values for CPK are 55-71
- Onset of rise is within 3-4 hours, time of peak rise is about 33 hours, and return to normal is
within 3 days
Troponin I
- Troponin is a marker that is diagnostic of cardiac injury
- Now considered the gold standard
- Elevated levels of troponin occur earlier and may last for up to 5-7 days in plasma
- Normal range = 0-0.1 ng/mL (not detectable by normal blood test)
- Levels > 0.3 ng/L indicate potential risk of MI
- Onset of rise is within 4-6 hours, time of peak rise is within 12-24 hours, and return to normal is
within 4-7 days
- Three tests are usually done acutely
PTT
-

INR
-

Partial Thromboplastin Time

Looks at how long it takes for blood to clot
In general, clotting should occur between 28-38 seconds
If a person is taking blood thinners (such as Juusi) clotting takes up to two-and-a-half times
longer (1.5-2.5 times longer when therapeutic)

International Normalized Ratio, developed to standardize prothrombin time values, so that test
results from different thromboplastins and coagulation analyzers become equivalent
Post-MI patients have a target INR of 3 (2.5-3.5)
Normal values are 0.9 to 1.2 (in the general population)
INR values > 4.5 increase the risk of major haemorrhage
INR < 2 increases the risk of thromboembolism

Heparin
- Heparin is an anticoagulant that acts as a thrombin inhibitor
o Thereby prevents the influence of thrombin on fibrinogen
- It is used prophylactically to prevent blood clot formation

May also be used when a thrombus is already formed to prevent emboli

Prevention of an impending acute myocardial infarction includes the emergency use of
anticoagulants and antiplatelet agents as part of acute coronary syndrome management

Nitroglycerin
- One of the oldest anti-ischemic medications
- Nitrates are converted in the vessels to nitric oxide, which increases the action of the secondary
messenger cGMP
- This seems to stimulate a kinase enzyme that decreases the sensitivity of the contractile proteins
to calcium and relaxes the blood vessels
- This group of drugs is unusually selective in that it almost exclusively acts on smooth muscle
cells, in particular on vascular smooth muscle cells
o As a venodilator, nitrates decrease venous return (preload)
o As an arteriodilator, nitrates decrease afterload
o As a relaxant for coronary artery smooth muscle, nitrates possibly increase coronary
artery blood supply
- These factures decrease myocardial oxygen demand
- Can be taken in different forms (sublingual, spray, percutaneous ointment, oral, intravenous,
transdermal patch)
- Side effects include headache, hypotension and dizziness, reflex tachycardia, flushing of the skin,
nausea and vomiting
- Contraindications include pregnant women, breast feeding, and consuming alcohol while on
nitroglycerin
- Effect of nitroglycerin may be diminished by heparin
Angiogram
- Invasive coronary angiography remains the standard for identifying coronary artery narrowing
related to coronary artery disease
- Angiography is performed under local anesthesia with small-diameter catheters introduced
through a transarterial sheath
- In the majority of cases, either the femoral or the radial route is used
- Through the catheters, iodinated contrast media is injected selectively into the left and right
coronary arteries
- A few angiographic projections are used to enable visualization of the whole coronary tree
- Used to establish or rule out the presence of coronary stenoses, define therapeutic options, and
determine prognosis
- In patients with STEMI, guidelines recommend coronary angiography in the acute phase
- No absolute contraindications, but relative contraindications include febrile untreated infection,
severe anemia, severe electrolyte imbalance, active bleeding, acute renal failure, and ongoing
stroke
Cardiac Rehab
- Cardiac rehab is a program of exercise, education, and counselling designed to help you recover
from a heart attack or other heart conditions
- Help you to regain your strength, prevent your condition from getting worse, and reduce your risk
of having heart problems in the future

Open to those who have had a heart attack, heart surgery, or have heart disease
Cardiac rehab team may include physicians, exercise physiologists, nurses, occupational
therapists, physical educators, dieticians, psychiatrists, physiotherapists, and/or social workers
Generally include a medical assessment, physical activity, lifestyle education, and psychosocial
support
Phases of cardiac rehab
o Phase I: Acute phase or monitoring phase
Beings when patient medically stable following an MI, CABG, PTCA, valve
repair, heart transplantation, or CHF
o Phase II: Subacute phase of rehab or conditioning phase
Begins as early as 24 hours after discharge and lasts up to 6 weeks. Frequency of
visits depends on the patients clinical needs. Initiate secondary prevention of
disease
o Phase III: Training or intensive rehabilitation
Beings at end of Phase III and extends indefinitely. Patients exercise in larger
groups and continue to progress in their exercise program. Resistance training
often begins in this phase
o Phase IV: Ongoing conditioning (maintenance) phase or prevention phase
Candidates are individuals who are at high risk for infarction because of their risk
factor profile, as well as those who want to continue to be followed by
supervision of trained personnel
Physician referral may be needed
Progressive activity for 5-day length of stay (Phase I)
o Day 1, CCU (MET level 1-2)
Bedrest until stable, use of bedside commode, out of bed to chair if stable
o Day 2, step-down unit (MET level 2-3)
Full assessment
Sitting warm-ups, walking in room, self-care activities
Education: explanation of event, treatment plan
o Day 3-5
Out of bed as tolerated if stable, walk 5-10 minutes in hall (supervised as needed)
(MET level2-3)
Shower with seat, walk 5-10 minutes 2-3 times/day, up/down one half flight of
stairs (MET level 3-4)
Education:
Assess readiness to learn
Teach signs/symptoms
Nitroglycerin use
Emergency response to symptoms
Safety factors
Dos and donts for home activity
Introduce Phase II

ECG Interpretation

Ischemia is classically demonstrated on the 12-lead ECG with T-wave inversion or ST-segment
changes
The T wave may vary from a flat configuration to a depressed inverted wave
o However, T-wave becoming sharp and peaked is the most acute sign
The location of the ST segment is another indication of ischemia or injury
Elevation of the ST segment above the baseline indicates acute injury
o In the presence of an acute infarction, the ST segment elevates and then later returns to
the level of baseline (within 24-48 hours)
o Indicates early repolarization of the ventricles
During myocardial injury, alterations in the initial portion of the QRS complex occur
o The presence of a significant Q wave is also diagnostic for infarction
o Typically due to previous MI absence of electrical activity
o Occurs hours after MI

Cardiac Output
- Volume of blood pumped from the right or left ventricle per minute
- CO = SV x HR
- Stroke volume is determined by the preload, myocardial distensibility, myocardial contractility,
and afterload
Preload
- The end-diastolic muscle fibre length of the ventricles before systolic ejection
- On the left side it reflects the left ventricular end-diastolic volume
o Dependent on venous return, blood volume, and left atrial contraction
- An increase in ventricular volume stretches the myocardial fibres and increases the force of
myocardial contraction (Starling effect) and stroke volume
o Starling effect is limited by the physiologic limits of distension of the myocardium
o Excessive stretching (fluid overload) leads to suboptimal overlap of the actin and myosin
filaments, impairing rather than enhancing contractility
Afterload
- The resistance to the ejection of blood during ventricular systole
- Afterload of the left ventricle is determined primarily by four factors
o Distensilbity of the aorta
o Vascular resistance
o Patency of the aortic valve
o Viscosity of the blood
Valsalva
- The normal physiological response consists of four phases.
1. Initial pressure rise
o On application of expiratory force, pressure rises inside the chest forcing blood out of the
pulmonary circulation into the left atrium. This causes a mild rise in stroke volume.
2. Reduced venous return and compensation
o Return of systemic blood to the heart is impeded by the pressure inside the chest. The
output of the heart is reduced and stroke volume falls. This occurs from 5 to about 14

seconds in the illustration. The fall in stroke volume reflexively causes blood vessels to
constrict with some rise in pressure (15 to 20 seconds). This compensation can be quite
marked with pressure returning to near or even above normal, but the cardiac output and
blood flow to the body remains low. During this time, the pulse rate increases
(compensatory tachycardia).
3. Pressure release
o The pressure on the chest is released, allowing the pulmonary vessels and the aorta to reexpand causing a further initial slight fall in stroke volume (20 to 23 seconds) due to
decreased left atrial return and increased aortic volume, respectively. Venous blood can
once more enter the chest and the heart, cardiac output begins to increase.
4. Return of cardiac output
o Blood return to the heart is enhanced by the effect of entry of blood, which had been
dammed back, causing a rapid increase in cardiac output (24 seconds on). The stroke
volume usually rises above normal before returning to a normal level. With return of
blood pressure, the pulse rate returns towards normal.
Activity Restrictions Prior to Starting Cardiac Rehab
- Activities during weeks 1-3 at home
o Sit outside
o Do light housework
o Engage in hobbies or activities you can do sitting down (reading, crafts)
o Climb one flight of stairs slowly
o Walk around your house or yard (or as instructed by your doctor or cardiac rehab team)
o Ride in a car as a passenger (short trips of about half an hour)
o Lift up to 5 lbs.
o Make a few social visits
- Weeks 3-6
o Continue walking as instructed by your doctor or cardiac rehab team
o Climb two flights of stairs
Resume sexual relations once you can climb two flights (but avoid if you have
had a large meal or alcohol in the past two hours or are feeling tired)
o Make more social visits
o Garden, grocery shop, or housework (lightly)
o Lift up to 10 lbs.
o Ride in a car for up to one hour, or, if approved by your doctor, driving
o Dance (slowly), fish, sail a small boat, cycle at medium speed, play table tennis or 5-pin
bowling
- Weeks 6+
o Resume all normal levels of activity for you such as walking at a brisk pace, swimming,
cycling, skating (go at your own pace and rest when necessary)
o Lift or carry up to 20 lb
o Return to work, with your doctors approval (usually 8-16 weeks)
o Golf
Start with 9 holes and play during the cooler parts of the day in the summer
months

Use a cart to carry your clubs

Be careful of
o Very hot or very cold water
o Lifting heavy weights
o Pushing or pulling actions that cause you to hold your breath
o Working for long periods with you arms above your head
o Repetitive arm work such as raking, digging, grass cutting or vacuuming
o Snow shovelling
o Activity after meal
o Driving (for at least 4-6 weeks)
o Sexual relations (for usually around 2-3 weeks)
o Air travel

Criteria for Discharge from PT Services

- Able to perform ADLs
- Able to ambulate independently
- Able to climb stairs independently
- Independent with transfer
- Safety all of this with no symptoms
Cardiorespiratory Examination and Assessment
Assessing Respiratory Function
- IPPA system
o Inspection (observation)
Lung location reflected onto chest wall (surface anatomy)
Chest expansion/Thoracic excursion
Position
Posture
Body structure
Height, shape of chest , adipose tissue
Scars
Skin color
Cyanosis, pallor
Digital clubbing
Breathing pattern
At tidal volume or at maximal inspiratory effort; apical/diaphragmatic
Shortness of breath- dyspnea, orthopnea (SOB in supine)
Effort of breathing
Nasal flaring, accessory muscle use
Jugular vein distension (if the vein is distended above the level of the clavicle)
Peripheral vascular changes
o Palpation
Temperature of skin
Symmetry of chest movement
Chest excursions/diaphragmatic excursions
Trachea (position/movement)

Pulses: carotid, brachial, radial, femoral, popliteal, tibialis posterior, dorsalis

pedis
Peripheral edema
Capillary refill (press nail beds)
Percussion (Mediate Percussion)
When might you not want to percuss?
Open wounds
Fractures
Implanted devices
Subcutaneous ports
Consolidation = dull
Pleural effusion = dull
Pneumothorax = hyperresonant
Atelectasis = dull
Procedure for mediate percussion
Seek a quiet place
Client sitting or supine
Identify any areas to avoid percussing at this time
Middle finger on non-dominant hand is placed firmly on the chest wall in
intercostal space and parallel to ribs (keep rest of hand off chest)
Middle finger of dominant hand strikes the middle or distal phalanx of
the other had with quick, sharp motion
Feel and listen to all aspects of chest in systematic way
Compare left and right, upper and lower
Note quality of the sound is it normal, dull, or tympanic
(hyperresonant)?
May need to have client take a deep breath to listen to the lower lobes
Auscultation
Basics
Quiet environment, warm room, warm stethoscope
Proper position
o If possible, client should be sitting
o Position yourself so you can monitor your clients face
Bare skin
Systematic method (R/L, upper/lower)
o Compare side to side before upper/lower
Patient comfort (draping, position, time)
Patient safety
o Watch sitting balance if patient is weak prevent from falling
o Avoid hyperventilation patient can become dizzy allow
patient to rest every few breaths
Use diaphragm of stethoscope, press firmly
Listen to one complete respiratory cycle at each site

Client breaths in and out through their mouth, taking deep breaths as
consistently as possible
Note the intensity and length of breath sounds
Note the presence or absence of adventitious sounds
Always clean your stethoscope after each use!
Common errors in auscultating lung sounds
Listening through the patients gown
Allowing the stethoscope tubing to rub against sheets, bed rail, gown
Interpreting chest hair sounds as adventitious lung sounds
Auscultating only the convenient areas
What are we looking for?
Is the intensity of breath sounds increased, normal, or decreased?
Is the character of breath sounds normal or abnormal?
Are there any abnormal or adventitious sounds?
Need to document these sounds and specify lobe/segment
Normal breath sounds
Vesicular
o Soft
o Low-pitched
o Primarily heard during inspiration and minimally heard in the
first 1/3 of expiration
o Flow from inspiration to expiration, no break
o Heard over most of the lung/thorax areas
Bronchial
o Loud (tubular, hollow)
o High-pitched
o Equal inspiratory/expiratory duration
o Pause between inspiratory and expiratory components
o Heard normally over the manubrium (trachea) not a standard
area for auscultation
o If present in other lung areas = abnormal (consolidation)
Abnormal breath sounds
Absent or diminished vesicular breath sounds
o Shallow breaths, frail/elderly
o Decrease in lung tissue density
Emphysema
Fibrosis
o Pleural effusion
o Pneumothorax
o Atelectasis (collapse) absent unless its in the upper lobes
Adventitious sounds
Crackles
o Fine (high pitched, very brief)
o Coarse (low pitched, brief)
o Mechanism

Sudden opening of small, previously closed airways

Air bubbling through secretions
o Causes
Pulmonary edema, consolidation, atelectasis, COPD, etc.
Wheezes
o Continuous, high-pitched, musical, expiratory
o Monophonic (suggestive of one airway obstruction)
o Polyphonic (if inspiratory static bronchoconstriction tumours,
foreign bodies)
o Mechanism
Air flowing through narrowed airways
o Causes
Asthma
Acute or chronic bronchitis
o Other considerations
Paroxysmal nocturnal dyspnea (PND) sudden onset of SOB at night in supine
Fluid balance sudden weight gain may be related to fluid retention (they
measure fluid in and out in the ICU)
Intermittent claudication
Disabling pain during walking
Caused by
Systemic complication of artherosclerosis
With or without overt ischemic heart disease
Intercostal indrawing = skin pulling in between ribs on inspiration (sign of
respiratory distress)
Assessment/diagnostic tests and procedures
o Spirometry (FVC, FEV6, FEV1)
o Oxygen saturation of the blood (SpO2)
o Walking tests (self-paced walking test)
o Blood pressure measurement

Pulses
- Use tips of middle and index fingers (not thumb)
o Press firmly and gently
- Assess
o Rate
o Strength
o Regularity
- Carotid either side of trachea
- Brachial medial aspect of antecubital fossa
- Radial anterolateral wrist
- Femoral between iliac crest and groin
- Popliteal behind knee
- Tibialis posterior behind medial malleolus
- Dorsalis pedis dorsal aspect of foot

Anatomy of the Bronchopulmonary Segments

- Left
o Upper
Apicoposterior
Posterior parallel with T2
Anterior
Anterior above 2nd rib AND below 2nd rib
Superior lingula
Anterior under 4th rib, lateral to nipple
Inferior lingula
Cannot be ausculatated
o Lower
Superior
Posterior parallel with T4/T5
Lateral basal
Posterior/lateral just anterior to mid-axillary line parallel with xiphoid
process (below 6th rib)
Anteromedial basal
Cannot be auscultated
Posterior basal
Posterior parallel with T7/8
- Right
o Upper
Apical
Posterior parallel with T1/2
Anterior
Anterior above 2nd rib AND below 2nd rib
Posterior
Posterior parallel with T2/T3 and more lateral
o Middle
Lateral
Anterior under 4th rib, lateral to nipple
Medial
Cannot be auscultated
o Lower
Superior
Posterior parallel with T4/5
Lateral basal
Lateral just anterior to mid-axillary line parallel with xiphoid process
(below 6th rib)
Medial basal
Cannot be auscultated
Posterior basal
Posterior parallel with T7/8

Anterior basal
Anterior lateral under 6th rib

Basic Principles of Chest X-Ray Interpretation

- Metal or contract material very white
- Bone/calcium white
- Soft tissues whitish
- Fat slightly black
- Air black
A Structured Approach to CXR Interpretation
1. Trachea and bronchi
2. Heart
3. Mediastinum
4. Hila
5. Lungs
6. Pleura
7. Chest wall
Additional Key Anatomical Structures
- Clavicles
- Ribs
- Diaphragm
Atelectasis incomplete expansion or volume loss in lung
Consolidation blood, pus, water, and sometimes tumor in airspaces
- On x-ray, can still see border of diaphragm (cannot in atelectasis)
Pleural effusion fluid in pleural space
- No sharp lines on x-ray
Pneumothorax lung collapse. Air between outside surface of lung and inside surface of chest wall
30 Second Sit to Stand
- Number of times sit to stand completed in 30 seconds
- Predictive equations available for specific ages
Respiratory Adjuncts and Supplemental Oxygen
Respiratory Therapy Adjuncts
- Therapies used to correct pulmonary problems
o Aerosol and humidity therapy
o Bronchodilator therapy
o Oxygen therapy
o Bronchial hygiene therapy
o Lung expansion therapy
o Airway management
o NIPPV
o Mechanical ventilation
Lung Volume Recruitment
- Also referred to as breath stacking

Used when patients have difficulty with deep breathing, or have persistent atelectasis
o Patient is bed-ridden, weak diaphragm
- Sometimes used in combination with in-exsufflation in patients with neuromuscular diseases
- Uses a one-way valve to prevent exhalation
- Subsequent breaths are delivered and stacked onto each other
- Device is removed and patient exhales
In-Exsufflation
- Used to facilitate secretion removal in patients with ineffective cough/clearance of secretions
- Objective measurements:
o Recommended when patients have peak cough flow < 270 L/min
- Provides positive pressure during inspiration
- Applies negative pressure during exhalation to facilitate secretion clearance
- Timing is key:
o In-2-3, Out-2-3
Peak Cough Flow
- Measures peak flow during a cough maneuver
- Important monitor in patients with muscle weakness
- Guidelines: PCF > 270 L/min
Oscillating Positive Expiratory Pressure
- Designed to aid in the loosening and removal of mucus build-up in the lungs
- Valves cause oscillating pressure in the airways which helps to loosen secretions
- Patients usually instructed to perform various breathing/coughing exercises with use
- Has started to replace manual chest physiotherapy
Oxygen Therapy
Normal Healthy Range for SpO2
- Normal range for healthy young adults
o 96-98%
- Slight fall with advanced age
o Mean SpO2 of 96.7% in patients > 70 years of age
Effects of Sudden Hypoxia
- Impaired mental function begins at 84%
- Loss of consciousness occurs at <55%
Concerns with Oxygen Therapy
- There are dangers to delivering oxygen routinely and without clinical implications
o Renders pulse oximetry worthless as a measure of ventilation
o May prevent early diagnosis & specific treatment of hypoventilation
Over-oxygenated patient may cause delayed response to hypoventilation
Minimum SpO2
- For patients requiring oxygen a minimum SpO2 greater than 92% should be acceptable
- Critical care patients are managed with lower oxygenation targets
o Critical care consensus guidelines
Minimum 90%
o Surviving sepsis campaign
Aim at 88-95%
Risk of Type II Respiratory Failure with High Dose Oxygen
- SpO2 maintained at 88-92%

Chronic hypoxic lung disease

COPD
Bronchiectasis
Cystic fibrosis
o Neuromuscular disease
o Obesity hypoventilation
Effects of Hypercarbia on Oxygenation (Alveolar Air Equation)
- Inspired O2 = O2 in the atmosphere exhaled CO2
- Hypoxic drive theory
o 10-15% of drive due to oxygen when healthy (rest due to CO2 and pH)
o These ratios approach 50:50 as patients get sicker
- Increasing O2 in the atmosphere causes an increase in the already elevated CO2
- Worsens respiratory acidosis
- Therefore we must keep these patients slightly hypoxic to maintain respiratory drive and keep
blowing off CO2/balancing pH (avoid respiratory acidosis)
Generalized Approach
- What is normal and safe
o Most patients
92-98%
o Risk of hypercapnic respiratory failure
88-92%
O2 Therapy Devices
Nasal Cannula
- Flow rate
o 1-6 L/min (max)
- 24-44% oxygen
- Very unreliable
o Depends on breath rate and depth
Venti/Vickers Mask
- Flow rate
o Wall 2-15 L/min
o Total flow to patient 30-52 L/min
o 24-50%
- Reliable
o Will provide total flow that is higher than the patients inspired flow rate
- Caution!
o Vickers mask and Venti-mask have different colours that correspond to % of oxygen
and these colours are not consistent between systems
Venturi Masks
- High flow devices
Non-Rebreather Mask
- Flow rate
o Flush!
- >80% oxygen
o Unreliable
o

o Total flow depends on the flow meter or oxygen tank

Humidity Therapy
The Effect of Dry Gas
- The medical gas in a hospital has not water content
o To protect medical equipment
- When the air we breathe is extremely dry, the mucus layer of the airways may become thick and
tenacious
- Coughing is less productive
Cold Humidity Therapy
- Uses air-entrainment device
- Provides large nebulized humidity
- Particles are larger than bacteria and viruses
o Can transmit infection
- Equipment needs regular changing
Heated Humidity Therapy
- Devices provide heated pass-over humidity
- Particles are smaller than bacteria and virus
- Equipment changed as needed or at planned intervals
- Different temperature options for optimizing humidification
- 31 degrees C for non-invasive application (face)
- 37 degrees C for invasive application (endotracheal)
High-Flow Nasal Cannula
- Designed to deliver high flow oxygen
- Large cannula fill approximately 50% of the nares
- Flow rates (depends on device):
o Adult 35-55 L/min
Benefits to HFNC
- Improved comfort
- Can meet inspiratory flow demand
- Deliver up to 100% oxygen accurately
- Washout of anatomical deadspace
- Optimized mucocillary clearance
- Constant flow rate at all oxygen levels
Airway Clearance and Oxygenation
Chest Physiotherapy as Airway Clearance: Oxygenation
- CPT:
o Postural drainage, percussion, and vibration
- Evidence regarding benefit in oxygenation and gas exchange is lacking
- Devices such as a Flutter and Intrapulmonary Percussive Ventilation (IPV) have proven
beneficial
Physical and Respiratory Therapy
- Traditionally the link between respiratory and physical therapy practice was surrounding airway
clearance techniques
- Over the years, airway clearance techniques with various devices have outperformed chest
physiotherapy in certain areas of patient care

Currently the strongest benefit for what the physiotherapist and respiratory therapist provides
occurs in the critical care an d rehabilitation settings
o Evidence of CPT reduce risk of ventilator associated pneumonia
o Mobilization of ICU patients
o Strength training with COPD patients
Room for improvement:
o Recognizing patients whom which humidity therapy would be beneficial and discussing
the options available

Managing, Monitoring, and Mobilizing the Post-Op Patient

The Nurse-Physiotherapist Relationship
- Both focused on a common goal: Assisting the patient in their recovery to return to previous or
optimal level of functioning
- Knowledge and expertise is mutually beneficial
- Should be a mutually respectful relationship
Approach to Communication with Nursing Staff
- Perceived barriers
- Do your homework
- Have you formulated a plan based on information gathered?
Questions to ask the Nurse
- How is the patient this morning?
- How was his/her night?
- Has their pain been well controlled?
- Do you think he/she needs anything for pain before we get them up?
- Is there anything I need to know before I go in to see him/her?
After mobilizing...
- Report back to the RN with pertinent info when you are finished
- Leaving the patients as you found them is really helpful and considerate
- High fives all around if they still have all the tubes/lines they started with
Pain Management for the Post-Op Patient
Understanding Pain Management in the Post-Op Patient
- Patients report that some of the most painful surgeries are intrathoracic surgeries, gastric
surgeries, and abdominal surgeries, with pain lasting from 2 to 8 days
- Analgesics treat pain by either reducing the capacity of the nerve fibers to sense pain or by
reducing pain recognition by higher centres in the brain
- Opioids- most commonly used analgesics for post operative pain management
Opioids prescribed for early post-op pain management
- Morphine
o Onset of action: 5-10 min
- Hydromorphine (Dilaudid)
o Onset of action: 5 min
o More potent than morphine
- Fentanyl
o Onset of action: 1-5 min but shorter duration of action than morphine
- Side effects:

Sedation, respiratory depression, hypotension, N&V, pruritus (itchiness), urinary

retention, constipation
Administration of Opioids for Post-Op Pain Management
- Three most common ways to administer pain medications in the first few days after surgery
o IV morphine, hydromorphine, or fentanyl administered by the RN
o IV opioid by Patient Controlled Analgesia device (PCA)
o Epidural administration of an opioid and local anesthetic solution via epidural catheter
IV bolus
- Medication mixed and administered by RN as needed for pain
- In critical care areas med may be given direct IV push
Patient Controlled Analgesia
- Continuous dose of analgesia delivered (basal rate)
- Patient can administer bolus dose of medication as needed
- Lock out between patient administered doses
- Very important that no one expect the patient (e.g., visitors) push the button!
Epidural Analgesia
- Catheter sits in epidural space at the desired level
- Opioids and local anesthetics administered close to site of action (CNS)
- Lower doses of opioids required and effects last longer
Pain Management: Applications and Considerations for Physiotherapy
- Assessment:
o Neuro/Cognitive
Awake, alert and responsive? Following commands?
Pain level
Motor and sensory function
o Cardio-Resp
Vital signs (heart rate, resp rate and effort, and blood pressure)
Introduction: Monitoring, Indwelling Lines, Tubes, and Catheters
Introduction to Monitoring
- Beside monitoring most commonly seen in Intensive Care Units or Step-Down Units (Medical
and Surgical)
- Depending on acuity of patient, all or some components of monitoring will be present and
required when mobilizing patient
Components of bedside monitoring
- ECG monitoring heart rate and rhythm
- Blood pressure monitoring:
o Continuous via arterial catheter /line
o Intermittent using a non invasive blood pressure cuff (NIBP)
- Central Venous Pressure monitoring: (intermittent or continuous) via central venous catheter
inserted in neck (internal jugular) or just under collarbone (subclavian access)
- Oxygen saturation: SpO2 measured continuously via finger probe or ear probe
- Respiratory rate: Red lead from 5 lead ECG monitoring detects respiratory effort/rate
Lines/Tubes/Catheters: The systems based approach
- Lines, catheters, and tubes are present for the purpose of monitoring, sampling, collecting,
draining, and infusing
o

Presence can be related to or affiliated with a particular body system

A systematic approach to assessing these multiple attachments can be helpful to understanding
their purpose and function

Neuro
- Epidural catheter
o Purpose: Delivery/administration of analgesia
o Location: Catheter inserted into epidural space (thoracic or lumber)
o Tubing from catheter is attached to a med syringe and administered via pump (similar to
IV pump)
o Special considerations:
Catheter is typically taped and secured well
Important that catheter does not become dislodged when boosting in bed or
when mobilizing
Always check sensory and motor function before mobilizing!
Cardiovascular
- ECG monitoring:
o Purpose: To monitor cardiac rate and rhythm
o 3-5 wires or leads from chest attached to a telemetry device or monitor
o Special considerations: Artifact, loose connections can affect tracing and trigger alarms
look at other waveforms BUT always look at the patient first!
o Percussion treatment can alter ECG readings let nurse know ahead of time
- Central Venous Pressure
o Purpose: To measure pressure created by volume in right side of heart used to guide
fluid replacement/volume status
o Location: Top of the bed pressure bag and tubing with transducer attaches to distal port
of central line (usually at neck or chest area)
o Cable from transducer attaches to monitor
o Special considerations: Not always continuously monitored
- Arterial line
o Purpose: Continuous blood pressure monitoring; sampling port for arterial blood gases
and other blood tests
o Location: Radial (wrist), brachial (interior elbow), femoral (groin), or pedal (top of foot )
catheter attaches to pressure tubing/transducer (like CVP)
o Special considerations: Kinked catheter = poor waveform; false high/low BP with
mobilizing
- Central line
o Purpose: Administer IV fluids and medications; central venous pressure monitoring;
access for intermittent or continuous hemodialysis/hemofiltration
o Location: internal jugular or subclavian vein, femoral vein, basilic vein (PICC)
o Special considerations: Some ports may be capped; check local policy re: mobilizing with
femoral
- Peripheral IV
o Purpose: To administer IV fluid and medications
o Location: Arms, hands, feet
o Special considerations: May or may not have fluid infusing; may have multiple sites

Respiratory
- Chest Tube
o Purpose: For the removal or drainage of air, blood, or fluid from the intrapleural or
mediastinal space
o Location: Inserted through the ribs into the chest
Gastrointestinal-Nasogastric Tube
- Purpose: Drain fluid/air from stomach, potentially decompress bowel, administer tube feedings
- Location: Inserted through nose and terminates in the stomach or the duodenum
- Special considerations: Extra vigilance for protection with esophagectomy patients; may or may
not be attached to suction or may be clamped
Urinary
- Nephrostomy Tube
o Purpose: To drain urine directly from the kidney
o Location: Inserted through skin at flank area into kidney
- Foley Catheter
o Purpose: Provides continuous drainage of urine from bladder
o Location: Inserted through urethra into bladder
Other drains, devices, machines
- Surgical site drains
- Sequential compression device (Moonboots)
- VAC dressings/suction devices
- Warming or cooling devices
- Feeding pumps (attached to NG tube or PEG tube)
Where can you find information about lines, catheters, and tubes?
- Medical record
- Bedside nurse
- Observe the patient
Where to start?
- Start by observing below the bed
- Observe above the beside the bed
- Look at the monitor
- Look at the patient
Summary
- Team based collaboration and communication benefits everyone...but most importantly the
patient
- Pain management: Consider time route and timing of pain control before mobilizing
- Relating tubes, catheters, and lines to their respective systems and purpose will make the whole
mess seem more manageable
Post-Operative Abdominal Surgery Assessment
Clinical Decision-Making
- A complex, cyclic process where decisions and actions were intertwined, building on and
informing each other in an evolving process specific to each patients care
- Also a contextual process requiring integration of factors surrounding the decision
Clinical decision-making in acute care integrates many factors

Reason for admission

o Emergent vs. elective
- Previous medical history
o Previous functional status; previous home environment
- Reason for PT consult/involvement
o Mobility orders (bed rest, activity as tolerated)
o Other restrictions (weight bearing, other)
- Current status
o Recent chart notes, including current medications
o Recent laboratory values and trends
o Recent vital signs and trends
Practical approach to initial acute care assessment
- Chart review
- Start to write the patients story
o Reason for admission
o Previous medical history
o Previous functional history gait aid? Endurance?
o Social history type of residence, living alone or with help, primary caregiver?
o Current medications, lab values
- Start to develop a plan for you r assessment
o Respiratory status, mobility, need for PT
- Communicate with team
Selected Key Acute Care Lab Values
- Hematocrit (HCT)
o < 25%-35% = essential ADLs, assistance PRN for safety; light aerobics, light weights (12 lbs.)
o < 25% = essential ADLs, assistance PRN for safety
- Hemoglobin (Hb)
o < 80 g/L = light ADLs
o 80-100 g/L = avoid heavy exercise (monitor HR and SpO2)
- Platelets (Plt)
o < 20,000 = no exercise; increased risk of bleeding
o Normal = 150 400 x 10*9/L
- Potassium (K)
o > 5.1 = no exercise; increased risk of arrhythmia; potentially life-threatening
- Troponin (Troponin I HS)
o > 30 ng/L = high values potential risk of MI; need to correlate w/ECG and clinical
symptoms; potentially life-threatening
- Glucose
o < 5.5 mmol/L = risk of hypoglycemia; determine need for carbohydrate with team
Overall Appearance
- Quick look
o ? alert
o Breathing pattern/rate
o Catheters/tubes/monitoring
Mechanical ventilation

 Dialysis intermittent/continuous; location of catheter

Arterial line, chest tube, others
o Current vitals/ventilator settings/medications
Criteria for Initiating a PT Mobility Session
- Respiratory
o SpO2 > 88% (or per team; e.g., COPD may be lower)
o Respiratory rate < 35 bpm
o FiO2 < 60%
- Cardiovascular
o HR > 50 or < 140 bpm
o Systolic BP > 90 or < 180 mmHg
o MAP > 65 or <120 mmHg
o No new onset chest pain
o No new arrhythmia
- Patient consent
- If in doubt, communicate and clarify individual patient considerations with the team
Planning for mobility activities
- Decide which side of the bed you will mobilize
o Prioritize the most important connection to the patient and move towards it
Airway endotracheal tube or tracheostomy
Circulation active dialysis
Others...
- Prepare the environment before you mobilize
o Untangle lines
o Ensure sufficient slack in all lines
o Move equipment towards one side of the bed
o Prepare equipment, chairs, etc.
Criteria for Terminating a PT Mobility Session
- Respiratory
o Respiratory rate < 5 or > 40 bpm
o Tenuous airway
o SpO2 < 90% (or per team values; e.g., COPD may be lower)
- Cardiovascular
o 20% decrease in HR; HR < 40 or > 130
o New onset dysrhythmia
o Systolic BP > 180 mmHg
o > 20% decrease in systolic or diastolic BP
o MAP < 65 or > 110 mmHg
o New onset chest pain
- Patient requests to stop
- If in doubt, communicate and clarify individual patient considerations with the team before the
PT session
Safety of physical therapy interventions in critically ill patients: A single-center prospective evaluation of
1110 intensive care unit admissions
- 1,787 admissions
o 1,110 (62%) participated in 5,267 PT sessions

60% receiving mechanical ventilation

34 sessions with physiologic abnormality or potential safety event
Cardiac arrhythmias: 10 occurrences (0.2%)
MAP > 140 mmHg: 8 occurrences (0.2%)
MAP < 55 mmHg: 5 occurrences (0.1%)
Falls: 3 occurrences (2 assisted, 1 unassisted)
- 34 potential safety events in 25 admissions
o 0.6% of PT sessions (i.e., 6 per 1000 PT treatments)
80% of events = transient physiological changes
- Only 4 occurrences (0.08% of all PT treatments) required minimal additional treatment or cost,
but no associated increased length of stay
o Removal of 2 oral gastric tubes, 1 radial arterial line, 1 chest tube, & 1 fall with small
laceration & sutures
- Most common activities for a physiologic abnormality or potential safety event (n = 34)
o Sitting at the edge of the bed: 18 (53%)
o Transfer from bed to chair: 5 (15%)
o Standing: 5 (15%)
o Walking: 4 (11%)
- No incidence of cardiopulmonary arrests or removal of any airways, central, or dialysis lines in
over 5200 PT interventions
After mobilizing...
- Write down post-treatment vitals
- Report back to the RN with pertinent info
- Leaving the patients as you found them is really helpful and considerate
- Complete your PT note
o
o

The Thoracic Surgery Patient

- What do they look like POD#1
o Usually supine in bed if all goes well, they are also alert and awake
o Lines/tubes
Chest tubes (typically 2 but can be 1-4 depending on situation)
Epidural
Foley catheter
Art line
IV
o Whats monitored
HR, SpO2, RR, ABP, NBP
o Types of chest tubes you may see
Topaz dont drop it
Atrium
Sahara
For both Atrium and Sahara dont tip the chest tube, dont raise and
maintain the chest tube above the patients chest, dont drop it, and dont
pull the tube out
o Common complaints
Incisional pain

Pain with coughing

Pain in the shoulder on the side of the surgery
Referred from incision area
Positioning of that arm during surgery
Fatigue
Itchiness/nausea/vomiting
Fear of movement due to all the lines/tubes
Standard exercises
A ankle pumps
B breathing (deep)
C coughing
S shoulder flexion exercises
Get this person moving
What type of chest drainage system does patient have?
Can the patient come off suction to mobilize?
Are there any restrictions?
Did they remove or crack any ribs when doing the surgery?
Are all the lines/tubes connected properly (especially epidural)?
Do you know where all the lines/tubes are (dont lower the bed on top of the
chest tube!)?
Did you share you r plan with the patient?
Physiotherapy Carepath
Patient is up to chair night of surgery or early morning
Patient is ambulating first day at least once; twice by day 2
Deep breathing and coughing exercises/manual chest PT as needed starting day 1
Discharge home with or without PT follow-up by day 3-5

Postural Drainage/Percussions/Vibrations/Kolaczkowski Techniques

- In general, affected side/lobe/segment is placed up for postural drainage
- Vibrations
o Make sure you are above the 11th and 12th ribs (floating)
o Applying pressure to fibs and following movement of ribs with breathing, but not
actually moving hands
o Fine vibrations for people who cant tolerate coarse
o Coarse vibrations bigger amplitude and less frequency
o If vibrating on front (not as well tolerated) change movement to correlate with more
pump-handle motion of ribs
- Kolaczkowski
o Squeezing expiration (can be done alone)
o Springing helps with inspiration (needs to be done along with squeezing during
expiration)
Technique

Postural drainage

(Treatment) Percussions

Purpose

Get secretions out using

Loosen secretions

Vibrations/Kolaczkowski
techniques
Utilized in PD positions

gravity in different
positions

Indications

Precautions

Contraindications

Impaired mucocilliary
transport
Impaired/ineffective
cough
Pulmonary edema
Hemoptysis
Massive obesity
Large pleural effusion

Increased ICP or head

trauma, NG/OG tube, or
bad reflux no head
down positions
Hemodynamically
unstable
Recent spinal fusion
surgery
Recent head trauma
Recent eye surgery
Diaphragmatic function

Impaired mucocilliary
transport
Impaired/ineffective
cough
Rib fracture
Decreased bone density
Uncontrolled
bronchospasm
Metastatic cancer to
ribs
Anxiety
Pulmonary embolism
Open wounds, burns in
thoracic cavity
Untreated
pneumothorax
Platelet count <20,000
Subcutaneous
emphysema
Recent skin grafts or
flaps on thorax
Hemoptysis

to mobilize and clear

secretions from affected
lung segments (better
than PD alone for
mobilizing secretions)
Impaired mucocilliary
transport
Impaired/ineffective
cough
Tumour obstruction of
airway
Recent pacemaker
placement
Convulsive or seizure
disorders
Pulmonary embolism
Open wounds, burns in
thoracic cavity
Untreated pneumothorax
Platelet count <20,000
Subcutaneous
emphysema
Recent skin grafts or
flaps on thorax
Hemoptysis

Spirometry
- Spirometry measures airflow in L/min, while respiratory muscle testing measures muscle strength
in cm H2O
- Spirometry is a volitional test results are dependent on test technique and participant motivation
- Lung volumes should be standardized when measuring spirometry at total lung capacity
- A practice effect may be observed, thus learning trials may be needed before performing
spirometry effectively
Patient Preparation for Spirometry Testing
- Assess for contraindications
o Absolute: recent severe cardiac problems (myocardial infarction, angina), pulmonary
embolus, ascending aortic aneurysm (risk of rupture due to increased pressure)
o Relative: surgery (abdominal, thoracic, or ocular), pneumothorax (if untreated could
potentially make it worse), hemoptysis (could indicate something more serious),
contagious respiratory infection. Also consider unhealed or fractured ribs, and
ears/nose/throat (be cautious). Also acute diarrhea risk of infection to you and
embarrassment

Have the patient sit upright in a chair

Explain and demonstrate procedure to patient
Instruct patient to insert mouthpiece into the mouth and check that the patients lips have a good
seal around the mouthpiece
- If the patient has difficulty in maintaining an airtight seal, perioral leak may be prevented by
holding the lips firmly around the mouthpiece with both hands
Measure FEV1, FVC, FEV6
- Before the test
o Assemble the equipment
o Assess for contraindications
o Collect and enter required information
COPD6 = age, height (cm), sex
Spirodoc = age, height (cm), weight (kg), sex
o Explain the test
We are going to do a test of your lung function. We will repeat this test a few
times to get the information we need. I will ask you to take a quick, deep breath
in, then blast it out hard and fast. When I ask you to take in a deep breath, please
take in as much air as you can. When I ask you to blast it out, please blow out as
hard and fast as you can for at least 6 seconds, and keep on blowing out until you
cannot get anymore air out.
- During the test
o Apply the noseclip and give the patient a tissue for the end of the test. Test for leaks with
the noseclip by asking the patient to gently blow against the noseclip.
o Ensure there is a tight seal around the mouthpiece at the start of the test.
o Ask the patient to inhale maximally (to total lung capacity, TLC)
o As soon as the patient has reached TLC, quickly ask the patient to expire maximally
o Listen for the beep
- Assess quality of the test
o No hesitation at start of inspiration, no coughing
o Ensure patient understands directions and provides maximum effort
o Patient sitting up straight in bed or chair
o No air leaks around mouthpiece
- Allow a rest period (at least 30 seconds to 1 minute) between each measurement
- Repeat measurements 3 times (and up to 8 times) with the goal of obtaining at least 2
measurements of FEV1 within 150 mL of the maximum value obtained
o Record FEV1, FEV6, and the ratio of FEV1/FEV6
- Calculating the final measurement
o Identify any values where FEV6 is <80% predicted, and/or FEV1/FEV6 <0.75
Regaining Breath Control
- After taking the straw out first reaction is to breath out fully to expel the air (and carbon
dioxide) trapped during exercise
- Techniques to teach patients how to regain breath control when SOB
o Tripod position
Allows use of more accessory muscles (bracing arms reverses the
origin/insertion)

 Facilitates diaphragm movement due to gravity

Pursed lip breathing
Increases back-pressure in lungs so that alveoli do not collapse, allowing
movement of carbon dioxide out more efficiently
o Deep diaphragmatic breathing
Steps to regaining breath control when SOB
o First assume tripod position, ideal is seated in chair, leaning forward with arms on lap
1. Pant naturally (as quickly as you want to)
2. Start to slow breathing down, especially with expiration
3. Breathe in through nose and out through mouth
4. Pursed-lip breathing
o This is a mental exercise, and needs to be practiced so it is automatic
o Start these steps as soon as breathlessness begins
o Have family member learn these steps so they can coach them through it when patient is
panicking due to SOB
o

Energy Conservation
- Any activity that can be done it sitting vs. standing can save 25% of energy
- Six Ps
o Pacing
o Planning
o Priorities
o Positioning
o Practice
o Physical fitness
Mechanical Ventilation and Arterial Blood Gas Interpretation
Alveolar Air Equation
- Inspired oxygen = oxygen in the atmosphere - exhaled carbon dioxide
- Elevated carbon dioxide (due to COPD or respiratory failure) = decrease in inspired oxygen due
to alveolar air equation
o This causes an increase in the already elevated carbon dioxide
o Worsens respiratory acidosis
- Mechanical ventilation is used mainly for carbon dioxide elimination (most difficult part)
Diffusion
- Resting conditions: pulmonary capillary blood is fully equilibrated with the alveoli after 0.25
seconds
o Pulmonary capillary blood is in contact with the alveolus for about 0.75seconds
o When diffusion is impaired there is additional time for gas exchange
- Carbon dioxide diffuses 20x faster than oxygen
- Note: when a patient is in distress pulmonary blood flow is quicker and shortens the time
available for gas exchange
Ventilation and Perfusion
- Anatomical deadspace
- True alveolar deadspace:

Due to pulmonary embolism or compression of capillaries due to over-inflation of lungs

(can be a mechanical ventilation error due to an increase in pressure)
- Relative alveolar deadspace
- Ideal V/Q matching
- Relative capillary shunt
- True capillary shunt
o Can be due to consolidation (collapsed alveoli)
Work of Breathing
- (Elastance x Volume) + (Flow x Resistance)
o Settings we can adjust on ventilator = pressure, volume, flow
Elastance
- The quality of recoil when distending pressure is removed
- Affected by
o Pulmonary fibrosis
o Consolidation
o ARDS
o Fluid overload/resuscitation
o COPD (emphysema)
o Ascites
- Change in pressure/change in volume
- Cm H2O/L
o Inverse of compliance
mL/cmH2O
- Depending on their elastance can help keep their lungs inflated with PEEP (overcome airway
collapse, keeps airways open during exhalation)
Resistance
- Opposing force to airflow within the lungs
- Affected by:
o ETT
o Bronchospasm
o Mucosal edema
o PEEP (expiratory resistance)
- Depending on their resistance, can try medication, suctioning
- If patient airway has too much resistance (swelling, upper airway obstruction) must intubate
Mechanical Ventilation
- We control everything except resistance and compliance (time constant)
o Peak inspiratory pressure
o End expiratory pressure
o Pressure gradient
o Tidal volume
o Inspiratory time and frequency are set
Determine IE ratio and expiratory time
o Minute ventilation
Time Constant
- Compliance x resistance = time constant
o Time constant x 3 = 95% lung filling
o

o Time constant x 5 = 99% lung emptying

Mechanical Ventilator
- Most important waveform is next to tidal volume (represents flow)
o Flat line is bad!
o Pushing 100% oxygen button to suction can disconnect alarms be careful
o If it looks choppy (sawtooth) secretions or water in the airway tube
- Getting rid of carbon dioxide on ventilator often requires a slower respiratory rate
Modes Simplified
- Assist controlled
o Patient is not required to breath
o All aspects of the breath delivery are controlled
Minimum rate
Pressure or volume
Time or flow
o PEEP and FiO2 set
- Supportive
o Patient is required to breath
o Some aspects of the breath may be controlled
Pressure or volume
Flow cycling (changes length of breath delivery)
o PEEP and FiO2 set
Positive End-Expiratory Pressure and FiO2
- PEEP/CPAP/EPAP
o Pressure left in the lung at the end of exhalation
o Used to maintain an open and compliant lung
Prevent atelectasis
o Optimal setting depends on recruitable lung units and presence of external forces
(elevated pleural pressure)
o Biggest use of CPAP in-community is for sleep apnea
- FiO2
o Fraction of oxygen delivered to the patient (0.21-1.0)
o Adjusted to maintain appropriate oxygenation
Flow Cycling
- Delayed cycling will deteriorate diaphragm over time
o Decrease in expiratory time causes a decrease in lung emptying
o Increases dynamic hyperinflation/PEEPi
o Increases trigger delay and trigger workload, increases non-triggering breaths, increases
respiratory muscle workload
- Most common form of asynchrony in the ICU
Types of Asynchrony
- Triggering
o Auto triggering
o Reverse triggering
o Double triggering
o Delayed triggering

Effort
o Ineffective efforts
o Flow asynchrony (air hunger)

The Art of Mechanical Ventilation

- Complicated patients require a more thorough evaluation of whether correcting an arterial blood
gas value can cause more harm than good
- Patients with Acute Respiratory Distress Syndrome are normally ventilated with a goal of
protecting the lung from damage while accepting abnormal blood gas values
o Permissive hypercarbia
o Permissive hyoxemia
Summary of Ventilator Adjustment
- Carbon dioxide management
o Ensure tidal volume is appropriate for patient
Adjust pressure or volume
o Ensure lung filling and emptying is optimal
Adjust time or flow
o If patient is not breathing adjust respiratory rate
- Oxygen management
o Adjust FiO2
o Assess if PEEP is appropriate
Too high can cause compression of vessels, alveolar strain, and impairment of
gas exchange
Too low can cause atelectasis, alveolar strain, and impairment of gas exchange
Arterial Blood Gas Interpretation
- pH 7.35-7.45
o <7.35 = acidosis
o >7.45 = alkalosis
- PCO2 35-45
- PO2 80-100
- HCO3 22-26
- SaO2 95%-100%
- BE 0 +/- 2
Steps to Interpretation
- pH classification
- Determine primary disturbance
o Respiratory disturbances
Alters the arterial PaCO2
Normal value 35-45
o Metabolic disturbances
Alters the serum HCO3
Normal value 22-26
- Compensation evaluation
o Patients will not overcompensate when looking at blood gases
o Disturbance refers to a value out of normal range
o Respiratory disturbance = CO2

o Metabolic disturbance = HCO3

o One disturbance = primary disturbance
o Two disturbances = compensation
- Oxygenation classification
- Complete acid-base classification
Uncompensated
- One disturbance
o CO2 or HCO3
o The disturbance is the primary cause
- Abnormal pH
Partial Compensation
- Two disturbances
o CO2 and HCO3
- Increase or decrease in the same direction
- pH is not normal
Fully Compensated
- Two disturbances
o CO2 and HCO3
- Increase or decrease in the same direction
- pH is normal
Mixed Disorder (Abnormal pH)
- Two disturbances
o CO2 and HCO3
- Increase or decrease in opposite direction
- pH is not normal
Oxygen Classification
- Hyperoxemia
o >100 mmHg
- Normoxemia
o 80-100 mmHg
- Mild hypoxemia
o 60-79 mmHg
o 90-94 SpO2
- Moderate hypoxemia
o 40-59 mmHg
o 75-80% SpO2
- Severe hypoxemia
o <40 mmHg
o 30mmHg = loss of consciousness
o 20 mHg = anoxia- brain injury likely
o <75% SpO2

Introduction to Suctioning
Structure

Approximate Spinal Level

Cricoid cartilage
Vocal cords
Suprasternal notch
Trachea
Carina
Right mainstem bronchus
Left mainstem bronchus
Esophagus
Xiphoid process

C5
C5
T2
C5 to T4
Intervertebral disk b/t T4 & T5
Intervertebral disk b/t T4 & T5
Intervertebral disk b/t T4 & T5
C5/6 to T11
T9

Endotracheal tube
- Cuff inflated helps to keep it in place
- May also be taped in place or tube holders
- Always respect the airway as a PT nothing pulling on the tube (sufficient slack in lines, etc.)
Nasalpharangeal Airway
Tracheostomy
- Cuff as well as inner cannula (which can be changed to prevent secretion buildup)
- Same precautions no tugging, etc.
Tracheostomy components
1. Pilot balloon
2. Inflation line
3. Flange/neck plate
4. Outer cannula
5. Trach cuff
6. Inner cannula
7. Obturator
Procedure for Closed System or In-Line Suctioning
- Education
1. Explain the procedure to the patient. Encourage the patient to cough to assist with secretion
clearance (if feasible).
2. Be prepared to provide the patient with support and explanation throughout the procedure.
- Preparation
3. Wash hands before patient contact.
4. Put CLEAN gloves on both hands.
5. Organize and check all equipment
a. Ensure there is an ambu bag at bedside (similar to bag valve mask for resuscitation)
b. Find the hyperoxygenation (100% O2) button on the ventilator
c. Set the wall suction to ~80-120 mmHg, or maybe higher. The in-line system gives
30% less suction. Ensure the suction is working properly by occluding the suction
tubing.
d. Attach the suction tubing to the port at the end of the catheter sleeve. Turn the
suction valve to the open position.
e. Confirm that the suction catheter is connected to the correct vacuum canister
f. Find saline for post-suction flushing of tubing

6. Turn OFF ventilator alarms. Please note, some ventilator alarms cannot be silenced until they
are activated (i.e., you may need to provide 100% O2 and then silence alarm as it recognizes
the hyperoxygenation from the ventilator)
Suctioning
7. Provide hyperoxygenation using the 100% O2 feature on the ventilator for 30-60 seconds
8. Support the endotracheal tube with your non-dominant hand. Gently pass the catheter down
the tube with your dominant hand until you stimulate a cough or contact the carina. Do not
force past obstructions. DO NOT SUCTION DURING INSERTION.
9. Apply suction by closing valve with thumb. Wait for 2-3 seconds for the suction to build up
in the system before starting to withdraw the catheter
10. Withdraw the catheter using continuous suctioning only (intermittent will cause the system to
lose its suction). Pull the catheter straight out to avoid kinking, holding onto the valve at the
end of the catheter. Ensure that you hold the endotracheal tube securely with your nondominant hand. Do not pull catheter out too far or you risk breaking the seal or tearing the
plastic sleeve (Note: if the seal is broken or the plastic sleeve is torn, the plastic sleeve will
collect moisture and/or balloon out)
11. Complete suctioning within 10-15 seconds (try holding your own breath to estimate this time)
12. Allow patient to settle between suction passes. Maintain 100% O2 during this time
13. Repeat procedure if necessary
Post-Suctioning
14. Turn ventilator alarms on when finished (if necessary)
15. Flush the catheter with saline. Insert disposable saline bottle into flushing port. Squeeze a
small amount of saline into tip of catheter while applying suction. Try to avoid having the
saline drip into the endotracheal tube. This may trigger the ventilator alarms. Reset if
necessary.
16. Remove the suction tubing. Ensure that the suction valve is closed.
17. Dispose of the CLEAN gloves.
18. Wash hands after patient contact.

Authorized Activities and Rostering

- Authorized activities that you need to roster for:
o Tracheal suctioning
o Spinal manipulation
o Acupuncture (including dry needling)
o Treating a wound below the dermis
o Assessing or rehabilitating pelvic musculature
o Administering a substance by inhalation
o Please note that communicating a diagnosis is also an authorized activity, but you do not
have to roster for it because it is considered an essential competency
- Rostering
o Rostering is the process where physiotherapists add their names to a list indicating they
have the required training, education, and experience to safely perform the higher risk
activity
o Physiotherapists must roster for each of the authorized activities they perform in their
practice

o
o

Rostering is mandatory for any physiotherapists doing these authorized activities under
their own authority
Suctioning:
In order to deep suction patients you must be rostered
If you are rostered you must:
Be able to prove you have the training, education, and experience to
safely perform the higher risk activity
If you are not rostered, you must ensure a safe environment
I.e., ensure RN or RT are available when secretion clearance assistance is
anticipated
O2 titration
Using the 100% O2 button is titration
When using medical directives or delegation to titrate, you do NOT need to roster
for O2 titration
In a hospital setting O2 titration still falls under the Hospital Act which does
not allow PTs to titrate. Ensure that there is a directive or a delegation for you in
the facility you are working in.

Courseware
Jette AM. Toward a common language for function, disability, and health. Phys Ther 2006;86:726-734.
- Disablement model has been useful in PT as a language to discuss the consequences of disease
and injury
- The World Health Organizations ICF has the potential of becoming a standard for disablement
language that looks beyond mortality and disease to focus on how people live with their
conditions
- The ICF framework (if adopted) could provide the rehabilitation field with a common,
international language
o Facilitate communication across disciplines and national boundaries
o Stimulate interdisciplinary research to improve clinical care
o Better inform health policy and management
- Three main models of disablement
o Medical model disability as a characteristic of the person, directly caused by disease or
trauma, requires some time of intervention to correct or compensate for the problem
o Social model disability as a socially created problem, not as an attribute of the person;
problem is created by an unaccommodating environment, due to attitudes or features of
the social and physical environment, calls for a political solution
o Biopsychosocial model attempts to integrate both models
- Crucial area of research is to improve the ICFs ability to differentiate clearly among concepts and
categories within the framework and to develop assessment instruments that can be used to
measure the various domains outlined in the ICF framework
National Public Health Partnership (2006). The Language of Prevention. Melbourne: NPHP
- Prevention = efforts of society to promote, protect, and sustain the health of the population

Primary prevention goal is to limit the incidence of disease and disability in the population by
measures that eliminate or reduce causes or determinants of departures from good health, control
exposure to rosk, and promote factors that are protective of health
Secondary prevention aims to reduce progression of disease through early detection, usually by
screening at an asymptomatic stage, and early intervention
Tertiary prevention - goal is to improve function and includes minimisation of the impact of
eastablished disease, and prevention or delay of complications and subsequent events through
effective management and rehabilitation
Public health = the organized response by society to protect and promote health, and to prevent
injury, illness, and disability
o Usually public health focuses on primary prevention, but occasionally secondary
prevention as well

Rimmer JH. Use of the ICF in identifying factors that impact participation in physical
activity/rehabilitation among people with disabilities. Disabil Rehabil 2006;28(17):1087-1095.
- Many health professionals have expressed difficulty finding ways to keep people with disabilities
engaged in community-based physical activity/rehabilitation programs
- Major reason for low adherences = recommended intervention does not match well with the
specific needs of the individual
- Personal and environmental factors along with the persons level of functioning can impede
participation
- The ICF can be a useful tool for identifying key factors associated with participation in
community-based physical activity
- The ICF allows health professionals to identify the level of functioning at the body, person, and
societal level, and understand the person-environment contextual factors that may impede or
enhance participation
- Body function
o Mental functions
o Sensory functions and pain
o Voices and speech functions
o Functions of the cardiovascular, hematological, immunological and respiratory systems
o Functions of the digestive, metabolic, and endocrine systems
o Genitourinary and reproductive functions
o Neuromusculoskeletal and movement-related functions
o Functions of the skin and related structures
- Activity limitations/participation restrictions
o Learning and applying knowledge
o Communication
o Mobility
o Self-care
- Environmental factors
o Products and technology
o Natural environments and human made changes to environment
o Support and relationships
o Attitudes
o Services, systems, and policies

Personal factors
Broad recommendations to engage in exercise or become more physically active are likely to fail
without a systematic framework for identifying key problem areas

Dolmage TE, Goldstein RS. Principles of aerobic testing and training. Physiother Can 2006;58:820.
- Small changes in the physiologic capacity of patients with limited reserve (cardiovascular,
respiratory, or neuromuscular) often have a substantial impact on their symptoms and ability to
perform daily activities
- The primary outcome measure of an exercise test is aerobic capacity (oxygen uptake), the main
determinant of the ability to sustain the power requirements of repetitive physical activity
- The test protocol is designed to enable a wide range of exercise intensity (power) to be presented
over a short time, under controlled conditions
o They stimulate the physiologic demands of everyday activities that involve rhythmic
contractions of large muscles
- Cardiopulmonary exercise tests can be used to identify exercise limitations, quantify reserves,
and evaluate the effects of interventions (medications, surgery, rehabilitation)
o Can also be used to establish exercise training protocols
- The incremental exercise test, used to determine maximum oxygen uptake, is a widely accepted
evaluation of cardiopulmonary health, fitness, and exercise capacity
- Key indicators of the appropriateness of the systemic response include an increase in HR and
ventilation
- Aerobic training will enhance peak oxygen uptake and therefore have a substantial impact on
physical performance
Nordon-Craft A, Moss M, Quan D, Schenkman M. Intensive care unit-acquired weakness: implications
for physical therapist management. Phys Ther. 2012; 2(12):1494-506.
- Patients admitted to the ICU can develop a condition referred to as ICU-acquired weakness
o Characterized by profound weakness that is greater than might be expected to result from
prolonged bed rest
o Often accompanied by dysfunction of multiple organ systems
- Individuals with ICU-acquired weakness typically have significant activity limitations
o Often require physical assistance for even the most basic activities associated with bed
mobility
- Many of these individuals have activity limitations months to years after hospitalization
- Rehabilitation can be implemented with very few adverse effects
- Respiratory strategies
o Costophrenic assisted cough
o Pursed-lip breathing
o Diaphragmatic breathing
o Scoop technique
- ROM
o Passive ROM
o Active ROM
o Active-assistive ROM
o Resisted ROM
o PNF diagonals

Patient education
o Pacing of activities
o Safety awareness to prevent falls
o Compensatory strategies to increase efficiency of movements
Functional mobility training
o Bed mobility
o Balance
o Transfer training
o Gait
o Stair negotiation
Exercise prescription and training
o Borg RPE scale
o PFIT (Physical Function in the ICU Test)
o 2MWT
o 6MWT
PTs play an important role in the restoration of function of people who have ICU-acquired
weakness

Dean E. Chapter 2. Oxygen Transport: the basis of cardio-pulmonary physical therapy. In: Frownfelter D
and Dean E, editors. Cardiovascular and Pulmonary Physical Therapy. 4th edition, Mosby Elsevier, 2006.
- Oxygen transport is essential to life, activity, and participation in life consistent with the ICF
o Maximizing the efficiency of oxygen transport promotes optimal obility and
independence, which are the cornerstones of quality of life and well-being
- Oxygen transport (deficits and threats to it) is the concern of PTs, irrespective of the primary
clinical area of their practice
o Especially true give the trend toward PTs direct access to patients and the prevelance of
dieases affecting oxygen transport
- Oxygen delivery = arterial oxygen context X cardiac output
- Oxygen consumption = (arterial oxygen content venous oxygen content) X cardiac output
- Oxygen extraction ratio = oxygen consumption/oxygen delivery (usually 23% at rest)
- Steps in the oxygen transport pathway
1. Inspired oxygen and quality of the ambient air
2. Airways
3. Lungs and chest wall
4. Diffusion
5. Perfusion
6. Myocardial function
7. Peripheral circulation
8. Tissue extraction and use of oxygen
9. Return of partially desaturated blood and CO2 to the lungs
- Factors that normally perturb oxygen transport are gravitational stress (secondary to changes in
body position), exercise stress (secondary to the increased oxygen demand of working muscles),
arousal, and emotional stress
- Factors that can impair and threaten oxygen transport include underlying pathophysiology,
restricted mobility, recumbency, factors related to the patients care, and factors related to the
individual

Hill K, Patman S, Brooks D. Effect of airway clearance techniques in patients experiencing an acute
exacerbation of chronic obstructive pulmonary disease: a systematic review. Chron Respir Dis.
2010;7(1):9-17.
- Airway clearance techniques did not improve measures of resting lung function or produce any
consistent change in measures of gas exchange
- The application of 5 min of continuous chest wall percussion reduced FEV1
o Should administer a bronchodilator beforehand, or limit application to less than 5 minutes
- In people with copious secretions, mechanical vibration and non-oscillating PEP mask therapy
increased sputum expectoration
- In patients with hypercapnic respiratory failure, intrapulmonary percussive ventilation and PEP
mask therapy reduced the need for, and duration of, NIPPV
- With the exception of continuous chest wall percussion, airway clearance techniques were safe in
patients during an AECOPD
Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Can Respir J
2006;13(4):203-209.
- Major respiratory complications of obesity include a heightened demand for ventilation, elevated
work of breathing, respiratory muscle inefficiency, and diminished respiratory compliance
- Decreased functional residual capacity and expiratory reserve volume, with a high closing
volume to functional residual capacity ratio, are associated with the closure of peripheral lung
units, ventilation to perfusion ratio abnormalities, and hypoxemia, especially in the supine
position
- Conventional respiratory function tests are only mildly affected by obesity, except in extreme
cases
- Major circulatory compensations are increased total and pulmonary blood volume, high cardiac
output, and elevated left ventricular end-diastolic pressure
- Patients with obesity commonly develop hypoventilation and sleep apnea syndromes with
attenuated hypoxic and hypercapnic ventilatory responsiveness
- Final result is hypoxemia, pulmonary hypertension, and progressively worsening disability
- Increased dyspnea and decreased exercise capacity (affects quality of life)
- Decreased muscle, increased joint pain, and skin friction also play a role in decreased exercise
capacity
- Effects of obesity on mortality in heart failure and COPD have not been resolved
o Also unknown whether obesity contributes to asthma and airway hyper-responsiveness
- Weight reduction and physical activity are effective to reverse the respiratory complications of
obesity
Reid WD, Kelm C, Hopkins-Rosseel D, Brooks D. The Canadian Thoracic Society Recommendations for
Management of Chronic Obstructive Pulmonary Disease: Implications for physiotherapists. Physiother
Can 2007;59:218-228.
- PTs, as direct access practitioners or members of a multidisciplinary team, should play a major
role in the health care of persons with COPD, a serious health condition that affects 4% of adult
Canadians

The main responsibilities that PTs should assume to optimize prevention of COPD and
management of persons with COPD are to
o Recommend and support smoking cessation for all patients who are smokers
o Prescribe exercise programmes for patients with COPD
Prescription of aerobic and resistance exercise as well as education and
behaviour modification activities
o Ensure that people with COPD resume activity after an acute exacerbation
o Refer patients to physicians for appropriate evaluation and care if not yet diagnosed with
COPD or if the management of the patients symptoms is not optimal or consistent with
COPD guidelines
PTs should consider referring a patient for diagnosis when there is a substantial
history of smoking (one package per day for more than 20 years) along with one
or more of the following
40 years of age or older
Persistent cough and sputum production
Frequent respiratory tract infections
Progressive SOB related to activities
o Facilitate adherence to pharmacotherapy
o Participate actively in ongoing evaluation and education about all aspects of care for
patients with COPD and their caregivers (facilitate adherence to pharmacotherapy)
o Support patients with COPD and their caregivers with end-of-life issues

Vestbo J, Hurd SS, Agust AG, Jones PW, Vogelmeier C, et al. Global strategy for the diagnosis,
management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J
Respir Crit Care Med. 2013 Feb 15;187(4):347-65.
- GOLD recommends that spirometry is required for the clinical diagnosis of COPD to avoid
misdiagnosis and to ensure proper evaluation of severity of airflow limitation
o Post-bronchodilator FEV1/FEV < 0.7
o Diagnosis should be considered in patients with dyspnea, chronic cough, and/or sputum
production, and a history of exposure to risk factors for the disease; but spirometry is
required for a definitive diagnosis
- Assessment of the patient with COPD should always include assessment of
o Symptoms (MMRC)
o Severity of airflow limitation
o History of exacerbations
o Comorbidities
- Nonpharmacologic and pharmacologic management of COPD to relieve symptoms and reduce
risk of exacerbations
o Smoking cessation is a key therapeutic measure (pharmacotherapy and nicotine
replacement)
o Regular physical activity is recommended for all patients with COPD
o All patients with COPD with breathlessness when walking at their own pace on level
ground benefit from rehabilitation and maintenance of physical activity, improving their
exercise tolerance and quality of life, and reducing symptoms of dyspnea and fatigue

Diagnosis of an exacerbation relies exclusively on the clinical presentation of the patient

complaining of an acute change of symptoms that is beyond normal day-to-day variation
o Leads to a change in medications

American College of Sports Medicine and American Heart Association. Joint Position Statement.
Exercise and Acute Cardiovascular Events: Placing the Risks into Perspective. Medicine and Science in
Sports and Exercise 2007;39(5):886-897.
- Habitual physical activity reduces coronary heart disease events, but vigorous activity can also
acutely and transiently increase the risk of sudden cardiac death and acute MI in susceptible
persons
- Exercise-associated acute cardiac events generally occur in individuals with structural cardiac
disease
- Hereditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac
events among young individuals, whereas atherosclerotic disease is primarily responsible for
these events in adults
- The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in
the study population
- The incidence of both acute MI and sudden death is greatest in the habitually least physically
active individuals
- Maintaining physical fitness through regular physical activity may help to reduce events because
a disproportionate number of events occur in least physically active subjects performing
unaccustomed physical activity
- Other strategies, such as screening patients before participation in exercise, excluding high-risk
patients from certain activities, promptly evaluation possible prodromal symptoms, training
fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear
prudent but have not been systematically evaluated
- Benefits of regular physical activity outweigh its risk
o Physical activity should be encourage for most individuals in accordance with the
Centers for Disease Control and Prevention recommendations for >30 minutes of
moderate-intensity physical activity such as brisk walking on most, preferably all, days of
the week
o Vigorous exercise, however, transiently increases the risk of AMI and SCD, even in
exercise-conditioned individuals
Healthcare professionals should know the pathological conditions associated with
exercise-related events so that physically active children and adults can b
appropriately evaluated
Active individuals should know the nature of cardiac prodromal symptoms and
seek prompt medical care if such symptoms develop
High school and college athletes should undergo pre-participation screening by
qualified professionals
Athletes with known cardiac conditions should be evaluated for competition
according to published guidelines
Healthcare facilities should ensure that their staffs are trained in managing
cardiac emergencies, have a specified plan, and have appropriate resuscitation
equipment

Active individuals should modify their exercise programs in response to

variations in their exercise capacity, their habitual activity level, and the
environment
Janssens JP. Ageing of the respiratory system: impact on pulmonary function tests and adaptation to
exertion. Clin Chest Med 2005;26(3):469-84
- Most of the age-related functional changes in the respiratory system result from three physiologic
events: progressive decrease in compliance of the chest wall, in static elastic recoil of the lung,
and in strength of respiratory muscles
- Compliance of the chest wall and the respiratory system and lung elastic recoil decrease with
aging, resulting in static air trapping (increased RV), increased FRC, and increased work of
breathing
- Respiratory muscle function also is affected by again, either as a consequence of geometric
changes in the rib cage, nutritional status (lean body mass, body weight), cardiac function, or
through the age-related reduction in peripheral muscle mass and function (sacropenia)
- In subjects over 80, values of MIP may reach critically low values; this may result in alveolar
hypoventilation or respiratory failure in clinical situations such as left-sided heart failure or
pneumonia
- Expiratory flow rates also decrease with aging, with characteristic changes in the flow-volume
curves suggesting increased collapsibility of peripheral airways
- Gas exchange is remarkably well preserved at rest and during exertion in spite of a reduced
alveolar surface area and increased V/Q heterogeneity
o In older athletes who have regular physical training respiratory system remains capable
of adapting to high levels of exercise
o In sedentary individuals VO2max decreases regularly with aging, whereas work of
breathing increases
- Decreased sensitivity of respiratory centers to hypoxia or hypercapnia may result in a diminished
ventilatory response in case of acute disease, such as heart failure, infection, or aggravated airway
obstruction
- Blunted perception of added resistive loads (i.e, bronchoconstriction) and diminished physical
activity may result in a lesser awareness of respiratory disease and delay diagnosis