Respiratory System

Paramedic Anatomy Review

Upper Respiratory Tract:
The sequence of Organs that comprise the upper

conducting pathway:
Nasal cavity and sinuses
Pharynx
Larynx
Trachea

Nasal Cavity:
The nasal cavities are separate from each other
by the nasal septum.
Vascular membrane on the Nasal Septum
Most nose bleeds in young people originate at
the anterior nasal septum
Most nose bleeds in older people are from the
posterior nasal structures
The Cribriform plate is the thin layer of bone that
separates the brain from the nasal cavity.
Lungs:
Right Lung 3 lobes
Left lung 2 lobes
Bronchioles:
Smallest airways
Walls consist entirely of smooth muscle (No
cartilage present)
*Constriction increases resistance to airflow

 *Dilation reduces resistance to airflow

Alveoli:
Surrounded by surfactant, allows alveoli to not
collapse Allows to expand
Thin, semi-permeable
Air Sacs
Site of carbon dioxide exchange with blood
Gas exchange allows oxygenation of surrounding
capillaries
Diaphragm:
Phrenic Nerve
Frontal
Vagus
Extends thorax
#1 breathing muscle
Ribs Intercostal: C-3, C-4 allow muscle to expand
Pleura:
Double walled membrane
Visceral layer covers lung (surrounds organs)
Parietal layer lines inside of chest wall,
diaphragm (Surrounds Cavity)
Potential space fluid it, to reduce pain
Trauma: allows negative pressure, collapse lung,
blunt, penetration due to pressure.
Atmosphere pressure: 760mg TORR
Tidal volume: 500 ml
Pleuritis: Infection, Chest pain- press down on
chest non-ischemic chest pain

Respiratory System Physiology:

Inspiration
Active process
Chest cavity expands
Intrathoracic pressure falls
Air flows in until pressure equalizes
*Needs to make PEEP (Positive end
expiatory pressure)
Create 5 tor/mg to maintain PEEP

Expiration
Passive process
Chest cavity size decreases
Intrathoracic pressure rises
Air flows out until pressure equalizes

Neurotoxic center- Exhale

Abnosic Center
Respiratory System:
Automatic Function (Hypoxic Drive)
Primary Drive: Increase in arterial CO2
Secondary (hypoxic) Drive: decrease in
arterial O2

 * Normally we breathe to remove CO2

from the body NOT to get oxygen in
#1 Co2 Required to breath in to
simulate Chemoreceptors
To stretch, put up hydrogen Ions
COPD Pt.:
Hypoxic Drive level changed/switched
Medulla & Pons change
Dependent on O2
Hypoxic Drive change: Apnea:
NRB- due to change
Drive level change- Reverse take NRB
off
*Never deprive anyone of Oxygen
Getting O2
If not sating well take off, put on
Sources of Pulmonary Impairment:
Pulmonary diseases
Disorders of the Pulmonary system
Non-pulmonary disorders/disease
impairing ventilation or respiration
Sources of Pulmonary Impairment:
VENTILATION:

 Upper Airway:
Trauma
Epiglottis
FBAO
Inflammation of tonsils
Lower Airway:
Trauma
Obstructive lung disease
Mucus accumulation
Smooth Muscle spasm
Airway edema
Chest Wall Impairment:
Trauma
Hemothorax
Pneumothorax
Empyema
Pleural
Inflammation
Neuromuscular diseases
Neurological Control:
Brainstem dysfunction- Coning
Phrenic or spinal nerve dysfunction

Sources Of Pulmonary Impairment:

Diffusion:
Inadequate FIO2 (Smoke Inhalation)
Carbon Monoxide 250X stronger than
Oxygen (Remove from area EMCA-P)
Diseased Alveoli: Cant Expand
Asbestosis
COPD
Inhalation Injury
Capillary Bed Disease:
Atherosclerosis (No gas exchange,
hardening of artery)

Interstitial Space Disease:

High Pressure Pulmonary Edema
High Permeability Pulmonary Edema
(Pressure on alveoli: at fluid squeezes more
fluid)

Perfusion:
Inadequate blood volume or
hemoglobin
Hemmorging

 Hypovolemia
Anemia
Impaired Blood Flow:
Pulmonary Embolus

Capillary Wall Pathology:

Trauma

Thoracic: (Ventilation)
Chest Trauma:

Flail Chest
Simple Rib Fracture
Pneumothorax
Hemothorax
Sucking Chest Wound
Diaphragmatic Hernia
Pleural effusion
Spinal Cord Trauma
(High C-spine lesion)
Morbid Obesity

Neurological/Neuromuscular Disease

Poliomyelitis
Myasthenia
Muscular dystrophy
Guillain-Barre Syndrome

Respiratory Pathophysiology:
Drive system (Decreased Respiratory
Drive)

 Head Trauma
CVA- (Stroke) Around Pons & Maddule

Depressant drug Toxicity

Narcotics- Bradypena

Sedatives- Hypnotics
Ethyl Alcohol

Initial Assessment:
Airway
Anticipate airway problems with
Decreased LOC
Head Trauma
Maxillofacial Trauma
Neck Trauma
Chest Trauma
OPEN-CLEAR-MAINTAIN
Respiratory Sounds:
Respiration Requires:
Ventilation, the mechanical process of

moving air or gases into and out of the

lungs
Perfusion, or movement of blood though
the lungs and capillaries

 Diffusion of gas between the lungs and the

blood

Ventilation:
Tracheobronchial tree: involved in
ventilation but does not participate in gas
exchange.
Gas Exchange: Takes place in the
respiratory of the lungs, where gas
diffuses across the alveolar-capillary
membrane as they are exchanged
between the lungs and the blood that
flows through the pulmonary capillaries.
Regulation Of Respirations:
DEPENDS ON 5 COMPONENTS:
1.

Respiration Rate: The number of

breath a person breaths in a minute
2. Nervous Impulses from the
Respiratory Center: Main respiratory
center lies in the Medulla Oblongata in the
brainstem
3. Stretch Receptors: During inspiration,
the lungs become distended, activating
stretch receptors. These impulses send to
the brainstem to inhibit the medullary cells,
decreasing inspiratory stimulus. Thus

respiratory muscles relax allowing elastic

lungs to recoil and expel air from the body.
4. Chemoreceptors: Involuntary
respiration controls central chemical
receptors in the medulla and peripheral
chemoreceptors in the carotid bodies and
in the arch of the aorta. They are
stimulated by decreased oxygen and
increased carbon dioxide.
5. Hypoxic Drive: The mechanism that
increases respiratory stimulation when
blood oxygen falls and inhibits respiratory
stimulation when blood oxygen climbs.

Normal Respirations:
Vesicular: Low pitched (soft) breath
sounds that consist of a quiet. Wispy
inspiration phase with a shortened and
softer expiratory phase. They are
heard over the periphery of the lung
field.
Bronchovesicular: Louder (more
harsh), breath sounds consists of full
inspiratory phase with a shortened and
softer expiratory phase. They may be
heard throughout the full lung field and
are often louder than tracheal breath
sounds.

 Bronchial: Highest pitched (course),

breath sounds consists of a full
inspiratory and expiratory phase
usually being louder. They are normally
heard over the Trachea and Larynx.
Abnormal Respirations:
Absent-no air entry
Diminishing: Are caused by an
obese/thick walled chest
Adventious: Sounds heard in addition
to normal sounds. Such as Crackles,
Wheezing, Rhonchi, Stridor.
Crackles: Are also known, as Rales are
discontinuous, explosive, popping,
sounds that originate within the
airways. They are heard when an
obstructed airway suddenly opens and
the pressures on either side of the
obstruction suddenly equilibrates
resulting in transient, distinct
vibrations in the airway wall. Crackles
can be heard on both inspiratory and
expiratory, but are more often heard
on inspire.
Two Types:

 Course crackles: Sound wet, low

pitched
Fine Crackles: Sound dry, high
pitched
Wheezing: Continuous, musical sounds
similar to a whistle sound. It results when
air moves though the partially obstructed
airways. Their causes include asthma,
bronchospasms, and foreign body
obstruction. You may hear them without a
stethoscope or by auscultating the chest
during any or all phases of the respiratory
cycle. They often originate by the small
bronchioles and first appear at the end of
exhalation. The closer to the end of
inspiration they appear, the worse your
patients condition is.
Rhonchi: Continuous, rumbling or rattling
lower pitched sound that has a snoring
quality. They are heard in the larger
airway when large secretions,
inflammation, fluid or other materials,
obstruct airway. This is often found in the
patients suffering from bronchitis &
pneumonia. Rhonchi usually appear in the

early exhalation but may occur in early

inspiration as well.
Stridor: bark like sound that tends to be
accentuated during inspiration when extra
thoracic airways collapse due to lower
lumen pressure. They can often be heard
without a stethoscope. It is often a sign
characteristic of an upper airway
obstruction, Such as croup.
Pleural Friction Rub: Are the squeaking
or grating sounds of the pleural linings
rubbing together. They occur where the
pleural layers are inflamed and have lost
their lubrication. Pleural rubs are common
in pneumonia and pleurisy (inflammation
of the pleura). Because these sounds are
heard whenever a patients chest wall
moves. They appear during the entire
respiratory cycle.
Respirations:
Apnea: Not breathing. It is an ominous
findings and indictor of a serious
problem with the airway, Breathing or
both.

 Bradypnea: Slow, regular respirations

with a rate that is slower than 12
breaths per minute.
Eupena: Normal, Regular full
respirations with a rate fluctuating
between 12-20 breaths per minute,
with the expiratory phase that lasts 34 times longer than the inspiratory
phase.
Tachypnea: Fast, rapid respirations
with a rate that exceeds 20 breaths
per minute.
Dyspnea: Difficult breathing, with
sensation of shortness of breath.
Orthopnea: Dyspnea while laying
supine
Paroxysmal Nocturnal Dyspnea:
Short attacks of dyspnea that occurs at
night and interrupt sleep.
Agonal: Shallow, slow or infrequent
breathing. Inactive of brain anoxia.

Normal Respiration Rates:

Age

Low Rate

High Rate

New BornInfant (<1 yrs)

30

60

Toddler (1-2
yrs)

24

40

Preschooler
(3-5 yrs)

22

34

School age
(6-12 yrs)

18

30

Adolescent
(13-18 yrs)

12

26

Adult (>18 yrs)

12

20

Ataxic (Biots): Repeated episodes of

gasping ventilations separated by periods
of apnea. This pattern is seen in patients
with increased ICP.
Central Neurogenic Hyperventilation:
Depp & Rapid breaths caused by stroke or
an injury to the brainstem. In this case,
this is a loss of regulatory of ventilatory

controls and respiratory alkalosis is often

seen.
Cheyne Stokes: Progressively deeper
and faster respirations alternating with
slow and shallow breathing possibly apnea
at the end of expiration. This pattern is
typically seen in older patients with
terminal illness or brain injury. (Cushings)
Kussmauls: Deep, slow OR rapid GASPING
that results as a corrective measure
against such conditions as diabetic
ketoacidosis that produce metabolic
acidosis
PRESENT PROBLEMS:
Abdominal/back pain
Allergic reaction
Chest Pain
Electrocution
Inhalation of toxic gases: e.g. Carbon
Dioxide
Major/Multiple Trauma
Near-Drowning
Overdose
Vision

BLS Respiratory RATES (Adult):

Assist Ventilation if breathing is
deemed inadequate; i.e. respiratory
rates <8-10 or respiratory rates <2830 bpm
Breathing Appears shallow, patient
is cyanosed or decreased LOA.
PA)
ABG:
PH: Normal: 7.35-7.45Homeostasis
CO2: (Acidotic): Normal: 35-45
Respiratory
HCO3: (Alkalytic): Normal: 22-26
Metabolic
Partial Pressure of Oxygen and
Carbon Dioxide
PCO2: Always the Opposite to PH
Norm: 35-45%
PAO2: 80-100%
Buffering: Homeostasis

Respiratory System:

Tachypnea/Bradypnea:
Orthopedic?
Signs of Respiratory Distress:
Nasal Flaring (Opening up Airway as

much as possible)
Tracheal Tugging
Reactions
Accessory Muscle use
Use of abdominal muscle on exhalation
Tripod Positioning
Sniffing position- angle

Respiratory Assessment:
Cyanosis (Late, unreliable sign of
Hypoxia)
OXYGENATE Immediately! Especially if:
Decreased LOC (first Sign)
Possible Shock
Possible severe Hemorrhage
Chest Pain
Chest Trauma
Respiratory Distress or Dyspnea

 Hx of any kind of Hypoxia

Helpful Respiratory Terminology
Hypoxia: Inadequate Oxygen at the
cellular level
Hypoxemia: Deficiency of oxygen in
the arterial blood
Anoxia: lack of Oxygen
Respiratory Patterns:
Agonal: pattern of gasping followed by
apnea
Ataxic Respirations: Cluster, breathing
or irregular characterized by a series of
inspirations & expirations (lesions in
the medulla)
Biots: irregular respirations
characterized by varying depths of
apnea. (this pattern lacks repetitive
such as cheyne-stokes) Usually
indicates ICP changes or head injuries.

 Cheyne-Stokes: Regular periodic

pattern of breathing with equal
intervals of apnea. Followed by
crescendo-ascendo sequence of
respirations, also seen in cortical head
injuries or dysfunction, or possibly
sleep patterns in some adults.
Kussmauls: Abnormally deep pattern of
respirations with sighing sequences,
usually indicated DKA (Diabetic) (2630)
Nervous System Effect on
Ventilation:
Medulla: Stimulation to initiate
ventilation
Phrenic: Innervation of the
diaphragm
Spinal Nerves at Thoracic Levels:

 Innervation of intercostal muscles

Hering-Breuer Reflex:
Prevents overinflation
MEDICAL RESPIRATORY PATHOLOGIES:
Pleurisy:
Inflammation of pleura caused by
friction rub
Layers of Pleura rubbing together
Commonly associated with another
respiratory disease
Infection
Layers Rub together
Presentation Of Pleurisy:
Sharp, sudden and intermittent chest

pain with related dyspnea

Possibly referred to the shoulder
May
or
with respirations
Pleural friction rub may be audible
May have effusion (Fluid) or be dry

Pulmonary Embolism:

 50,000 deaths/year
5% of all sudden deaths
10% of PE result in death

Pulmonary Embolism (PE)

Pathophysiology:
Something (Fat, bone, air) moving now
embolis) with flow of blood passes
through right heart into pulmonary
circulation
It reaches an area to narrow to pass
though the lodges there
Part of pulmonary circulation blocked
Blood:
Does not pass Alveoli
Does not exchange gases
A disorder of perfusion
Embolis if mobile
Fracture opens up fat, vessel gets into
venous system causing PE

 Combination of factors increase

probability of occurrence:
Hypercoagulability: Higher risk of
clotting
Platelet Aggregation- thicken blood
Deep Vein Stasis (possibility of blood
clots due to deeper veins with poor
blood flow)
Embolus usually originates in lower
extremities or pelvis
V: Q mismatch (Cant Perfuse well)
ABG:
Acidotic CO2
PH
(Acidic)
RISK FACTOR:
Vein stasis or DVT (enlarged Trachea
Veins)
Recent surgery or trauma
Long bone fractures (lower)
Oral Contraception
Pregnancy
Smoking

 Cancer
Long flights
*Polycythemia: Increase in Red Blood
Cells
Anemia due to poor perfusion
Training lower partial pressure in
certain states
Training: Anticoagulability given
Other Causes:
Air
Amniotic Fluid (mom can leak
fluid into vascular)
Fat Particles (long bone fracture)
Particles from substance Abuse
Venous Catheter
Signs & Symptoms Of PE:
RAPID ONSET
DYSPNEA
TACHYCARDIA
TACHYPNEA
FEVER (SOMETIMES)
EPISODIC (SHOWERS)

 EVIDENCE OR HISTORY OF
THROMBOPHLEBITS (Plaque)
CONSIDER EARLY WHEN NO OTHER
CARDIORESPIRTORY FITS
V:
VERY LARGE EMBOLI
Preceded by s/s of small & larger
emboli:
Central Chest Pain
JVD
ACUTE RIGHT HEART FAILURE:
Blockage right heart failure
Shock
Cardiac Arrest
ARDS:
A condition that results in severe
illness or injury and associates
with a high mortality rate
Increased permeability
Pulmonary Edema
Surfactant Destruction

 Atelectasis
Decreased compliance
Hypoxemia (severe Hypoxemia)
Blood O2 low
ADULT RESPIRTORY DISTRESS
SYNDROME:
AKA: NON-Cardiogenic Pulmonary

edema
A Complication Of:
Severe Trauma/Shock
Severe infection/sepsis
Bypass Surgery
Multiple Transfusion
Drug Overdose
Aspiration
Decreased compliance
Hypoxemia: Fluid in alveoli, gas
exchange is embedded, cannot
perfuse, alveoli

ARDS MANAGEMENT:
Airway Management:
Endotracheal Intubation

Suction
MECANICAL VENTALTION:
PEEP
ECG Monitoring:
Treat Under lying Causes:
May require Vasopressors for shock
C-PAP
B-PAP
Splint Alveoli PEEP Ventilation

PNEUMONIA:

Fifth leading cause of death in US

Group of specific infections
Risk Factors
Cigarette smoking
Exposure to Cold
Extremes of age
Young
Old

PNEUMONIA:
Inflammation of Bronchioles and
Alveoli
Products of inflammation (secretions,
pus) add to respiration difficulty

Gas Exchange is impaired

Work of breathing increased
May Lead to:
Atelectasis
Sepsis
VQ mismatch
Hypoxemia

Presentation Of Pneumonia:
Shortness of breath, Dyspnea
Fever, Chills
Pleuritic Chest Pain, Tachycardia
Cough
Green/Brown Sputum
May have crackles, rhonchi,
wheezing in peripheral lung fields
Consolidation
Egophony
Management Of Pneumonia:

Treatment mostly based on symptoms:

O2
Rarely is intubation required
IV Access & rehydration

 B2 Agonosit may be useful

Antibiotics
Antipyretics
Obstructive Airway Disease:
Asthma (Air hungry: breathing guppy)
Emphysema
Chronic Bronchitis
ASTHMA:
Experienced by 4-5% of US Population
Mortality Rate increasing
FACTORS leading to Obstructive Airway
Disease:
Smoking
Exposure to environment agents
Genetic Preposition
Exacerbation Factors:
INTRINISIC:
Stress (Especially in Adults)
URI
Exercise
EXTRNSTIC:
Cigarette Smoke

 Allergens
Drugs
Occupational Hazards
General Pathophysiology:
Specific pathophysiology varies by
disease
Obstruction in Bronchioles
Smooth muscle spasm (beta0
Mucus accumulation (Goblet cells get
irritated and mucus)
Inflammation
Obstruction may be reversible or
irreversible
Obstruction results in air trapping
Bronchioles usually dilate on
INSPIRATION
Dilation allows air to enter even in
presence or obstruction
Bronchioles tend to CONSTRICT on
expiration

 Air becomes trapped distal to

obstruction
Cyanotic late sign (very ill)
Ph.
Acidotic CO2
CHRONIC OBSTRUCTIVE
PULOMNARY DISEASE:
Emphysema
Chronic Bronchitis
Sometimes Asthma
Emphysema:
Adelectics: loss of elastic recoil with

alveoli/muscles
Destruction of Alveolar walls
Distention of pulmonary air space
Destruction of gas exchange surface
Alveoli get stretched due to air

trapping, losing expansion

Etiology:
Smoking:
90% of all cases

 Smokers 10X more likely to die od

COPD than non-smokers

Environmental Factors
Alpha- 1 antitrypsin deficiency
Hereditary
50,000 to 100,00 cases
Most people of Northern European

Descent
Geriatrics Disease
PATHOPHYSIOLOGY:
Decreased surface area leads to
decreased gas exchange with blood
Loss of pulmonary capillaries &
Hypercarnia Leads to:
Increased resistance to blood flow
which leads to:
Pulmonary HTN
Right Heart Failure (Cor Pulmonale)
Loss of elastic recoil leads to increase
in residual volume and CO2 retention
Air trapping

 Hyperinflation
Hypercapnia
Vasoconstriction

Pulmonary
V/Q

mismatch
SIGNS AND SYMPTOMS:
Increased Thoracic AP Diameter (Barrel
Chest)
Decreased Lung sounds/ heart (size of
surface area increased
Hyperresonant chest
LIP PURSING: Air Trapping to increase
PEEP levels (exhalation)
Alerted blood gases
Normal or decreased PaO2
Elevated CO2
Clubbed fingers
Still perfusing
Cyanosis is a late sign of disease
PINK PUFFER!
Treatment:
BLS:
Ventilate

 O2 mask
Cardiac Monitor Irregular (PVC)
Monitor Breathing
Chronic Bronchitis:
Increased mucus production for more
then 3 months for 2 consecutive years.
Recurrent productive cough
Etiology:
Smoking
Environmental irritants
Pathophysiology:
Mucus plugging/inflammation edema
Increase airflow resistances leads to
alveolar hypoventilation
Alveolar Hypoventilation leads to:
Hypercardia
Hypoxemia
Dont air trap
Hypoxemia leads to: Increase in red
blood cell production without O2
causing Cyanosis: Barrel and
Chemoreceptors tell to increase/ not
getting enough red blood cells,

creating more causing Polycythemia

(not getting oxygenated by Alveoli)
Hypercarbia leads to pulmonary
vascular constriction: increased right
ventricular which leads Right sided
heart failure which can lead to
enlargement of right side (Cor
Pulmonale)
SIGNS & SYMPTOMS
Increasing dyspnea on exertion
Frequent colds of increasing duration
Productive cough
Weight Gain, edema (right hear failure)
Bluish-red skin (polycythemia): DUE TO
UNOXYGENATED BLOOD
Rales, Rhonci, Wheezing
Headache, drowsiness (increase in
CO2)
Unintelligence
Over weight due to SOB

PITTING EDEMA
Personality Change
Hyperocarbia
Hypoxia
Fluid Backs up, Inferior and Superior
become semi-permeable, blood leaks
out into interstitial space
Treatment: * Antibiotics
CYANOSIS IS AN EARLY COURSE OF

DISEASE
BLUE BLOATER!!
COPD Assessment Findings:
Chronic Condition
Acute
Episode
S&S of

work of breathing

and/or hypoxemia
Use of accessory muscles
Increased expiratory effort
Tachycardia
Cyanosis
Wheezing, Rhonli

 Decreased Lung Sounds

Thin, red/pink appearance
SATURATION USUALLY NORMAL IN
EMPHYSEMA
Management:
Airway and Breathing:
Sitting position or position of comfort
Calm & Reassuring
Encourage Cough
Avoid Excretion
OXYGEN
Maintain O2 Saturation above 90%
TRUE HYPOXIC DRIVE IS VERY RARE!

Understand Difference!

ARDS: (SEVERE ACUTE

RESPIRTORY FAILURE)

 Respiratory Failure:
Inability of the lungs to meet metabolic
demands of the body
Cant take in enough O2 & Cant
eliminate enough CO2 fast enough
Ventilation Failure: Imbalance between
load on the lungs and the ability of the
bellows to compensate
Failure of Oxygenation: PaO2 <60
mmhg
Failure to Ventilation: PaCO2 >50
mmhg
ARDS:
Leaky Alveolar capillaries
Plasma fluid and Leukocytes leak into
the airspace
Shunt
Hypoxemia
CAUSES OF ARDS:
Pneumonia
Aspiration of Gastric contents

 Pulmonary Contusion
Near-Downing
Inhalation Injury (CO-Smoke)
Reperfusion Pulmonary Edema
After Lung Transplant or
Pulmonary Embolectomy
INDIRECT LUNG INJURY:
Non-Pulmonary sepsis
Severe trauma with SHOCK
Cardiopulmonary Bypass
Acute Pancreatitis
Drug Reaction (ARA-C)
FAT, Amniotic Fluid
Embolism, bypass
PATHOPHYSIOLOGY:
Increase alveolar permeability due
to direct neutrophil-mediated
injury to the alveolar epithelium.
Always ends in some form of
fulminating Edema.
End result:

 Severe HYPOXEMIA
BLS THEARPHTIC GOALS:
Maintain Reasonably Oxygen
Delivery
FIND & FIX PRIMARY CAUSE
THORACIC TRAUMA:
Second leading cause of trauma
deaths after head injuries
Causes of about 10-20% of all auma
death
Many deaths due to thoracic trauma
are preventable
PREVENTION STRATEGIES:
Gun Safety Education
Sports Training & Protective
Equipment
Seat Belts & Air Bag Use
Mechanism Of Injury
Blunt Injury
Deceleration
Compression

 Penetrating Injury
Both
Anatomical Injuries:
Thoracic Cage (Skeletal)
Cardiovascular (Lethal Dysrhythmia)
Pleural and Pulmonary Mediastinal
Diaphragmatic
Espogheal
Penetrating Cardiac (Grave TOR)
Often Results in:
Hypovolemia
Pulmonary V/P mismatch
In intrathroxic pressure relationships
(external signs breathing, JVD, angle
stretcher 30 degrees, pressure up,

jugs come up)

Hypercarbia:
In intrathoracic pressure relationships
Altered/decreased LOC
Acidosis: Hypoperfusion of tissue
(Metabolic)

How & Why do we ventilate?

Perfusion & Ventilation
General Pathophysiology:
Impairment to Cardiac Output
Blood loss
Increased intrapleural pressure
(Pnemo)
Blood in Pericardial Sac
Myocardial Valve Damage
Vascular Disruption
Impairments in Ventilation:
Chest excursion compromise:

Pain
Air in pleural sac
Asymmetrical movement
Bleeding in Pleural Space
Ineffective Diaphragm contraction
Impairment in Gas Exchange:
Atelectasis
Pulmonary Contusion
Respiratory Tract disruption
Initial Exam directed towards

Life Threatening Injuries:

Open Pneumothorax
Flail Chest
Tension Pneumothorax
Massive Hemothorax
Cardiac Tamponade
Conditions:
Apnea
Respiratory Distress
ASSESSMENT FINDINGS:
Mental Status (decreased)
Pulse (Absent, Brady, Tachy)
BP (Narrow PP, Hyper/Hypotensive)
Pulsus Paradoxus: Alteration in BP in
inspiration
Ventilation rate & effort (Tachy, or
Brady, Labored, retractions)
Skin (Diaphoresis, pallor, Cyanosis, open
injury, ecchymosis)
Neck (Tracheal position, SQ
emphysema, JVD, Open Injury)
Chest (contusions, tenderness,
asymmetry, absent or decreased lung
sounds, abnormal percussion, open

injury, impaled object, crepitus,

hemoptysis (coughing up of blood)
Heart Sounds (muffled, distant,
regurgitant murmur)
Upper Abdomen (Contusion, open
injury)
ECG (ST segment abnormalities,
dysrhythmias)
History:
Dyspnea
Pain
Past hx of Cardiovascular disease
Restraint device used
Item/weapon involved in injury

THORACIC TRAUMA: SPECIFIC

INJURIES:
Rib Fracture:
Most common chest wall fracture
from direct trauma
More common in adults then
children

Especially common in Elderly (falls)

Ribs form rings
Possible break in 2 places (8th)
Most commonly 5th-9th
Poor Protection
Fractures of the 1st and 2nd require

high force
Frequently have injury to aorta or
bronchi
Occur in 90% of patients with
Tracheo-Bronchial rupture
Subcutaneous emphysema)
May injure Subclavian artery/vein
(nerve under Clavicle)
May result in Pneumothorax
30% will die
Fractures to the 9th to 12th ribs
can cause damage to underlying
abdominal solid organs:
Liver
Spleen
Kidney (Blood in Urine)

 Short & Stocky

Lateral Impact MVC
ASSESSMENT FINDINGS:
Localized pain, tenderness
Increase on palpation or when
Patient:
Coughs
Moves
Breaths
Splinted Respirations (Guarding,
short tidal volume) (Pillow Splint:
Cleansing breathing, long as
possible resp.)
Instability in chest wall, Crepitus
Deformity and discoloration
Associated with Pneumo &
Hemothorax
MANAGEMENT:
High Conc. O2
Positive Pressure Ventilation C-PAP
Splint using Pillow or swath
Encourage Pt. to breath deeply
Helps prevent Atelectasis

 Analgesics for isolated trauma

(Morph.)
Non-circumferential splinting
(Isolate to that Region)
Monitor Elderly pt. & COPD
patients Closely:
Broken Ribs can cause
decompensation
Pt. will fail to breath deeply and
cough, resulting in poor clearance of
secretions
Usually Non-Emergent Transport
STERNAL FRACTURE:
Uncommon, 5-8% in blunt chest
trauma
Large traumatic force
Direct blow to front of chest by
Deceleration:
Steering wheel
Dashboard
Other object

 25%-45% mortality due to

associated trauma:
Disruption of thoracic aorta
Tracheal or Bronchial tear
(Subcutaneous Emphysema)
Diaphragm Rupture
Myocardial Trauma
High Incidence of myocardial
Contusion, Cardiac Tamponade or
pulmonary contusion
ASSESSMENT FINDINGS:
Localized Pain
Tenderness over sternal
Crepitus
Tachypnea, Dyspnea painful
ECG changes with associated
Myocardial Contusion
Hx/Mechanism of blunt chest
trauma
MANAGEMENT:
Establish Airway

 High Concentration O2 (12-15, 95%

SO2)
Assist ventilations with BVM as
needed
IV NS/LS
Restrict Fluids
Emergent Transport: TRAUMA
CENTER
C-SPINE
FLAIL CHEST:
Two or more adjacent ribs fractured
in two or more places producing a
free floating segment of the chest
wall
Life Threatening
O2 levels (Hypoperfusion) (Cap
delayed)
CTAS 2, Priority 4
Usually secondary to Blunt Trauma
Most commonly MVC

Also results from:

Falls from heights
Industrial Accidents
Assault
Birth Trauma
MORE COMMON IN OLDER PT.
Mortality rates 20-40% due to

associated injuries
Mortality increased with:
Seven or more ribs fractured
Three or more associated injuries
Shock
Head Injuries
CONSEQUENCES OF FLAIL

CHEST:
Respiratory Failure due to:
Pulmonary Contusion
Intrathoracic Injury
Inadequate diaphragm movement
PARADOXICAL MOVEMENT:
Must large to compromise

ventilation
Increased work of breathing

 PAIN, Decreased Chest

expansion:
Leading to decreased ventilation
Hypoxic, Hypoperfused
Contusion of Lung:
Decreased lung compliance
Intra-alveolar-capillary hemorrhage
Decreased Ventilation;
Hypercapnea Co2 increase
Hypoxia
ASSESSEMENT FINDINGS:
Chest wall contusion
Respiratory Distress
Pleuritic Chest Pain
Splinting effected side
Crepitus
Tachypnea, Tachycardia
Paradoxical Movement (possible)
MANAGEMENT:
Suspect Spinal Injuries
Establish Airway
High Conc. O2
Assist ventilation with BVM

 Treat hypoxia from underlying

contusion
Promote full lung expansion
Consider need for Intubation and
PEEP
ANIXETY Reduces, Pain, Tidal
Volume Increase
Mechanically Stabilize Chest Wall
(Questionable value) (Bulk
dressings, Cravats)
IV of LR/NS (lactated RingersTrauma) NS- Normal Saline 0.9%
Sodium, Isotonic Fluid remains
inside vessels
Avoid rapid replacement in
hemodynamically stable patient
Contused lung cannot handle fluid
overload
MONITOR EKG:
Chest Trauma and cause
dysrhythmias

 EMERGENT TRANSPORT:
TRUAMA CENTER
SIMPLE Pneumothorax:
Pleural wall
Incidence:
10-30% in blunt chest trauma
almost 100% with penetrating chest
trauma
Morbidity & Mortality depends on:
Extent of atelectasis
Associated Injuries
CAUSES:
Commonly a fx rib lacerates lung
Paper bag effect
May Occur spontaneously in tall,
thin, young males following:
Exertions
Coughing
Air Travel
Spontaneous may occur with
Marfans Syndrome (Elongated
Lungs)
PATHOPHYSOLOGY:

 Air enters pleural space causing

partial lung collapse
Small tear self-seal
Larger tears may progress
Usually well tolerated in the
young & Healthy
Severe compromise can occur in
the elderly or patients with
pulmonary disease
Degree of distress depends on
amount & speed of collapse
ASSESSMENT FINDINGS:
Tachypnea, tachycardia
Difficulty breathing or respiratory
distress
Pleuritic Pain (chest pain that is not
cardiac pain)
May be referred to shoulder or arm
pain on affected side
Decreased or absent breath
sounds:

Not always reliable

If pt. is standing, assess apices first
If supine assess anteriorly first
Patients with Multiple rib fractures
may splint injured side by not

breathing deeply
MANAGEMENT:
Establish airway,
Trend Vitals
Dont leave patient alone
High Conc. O2
Assist with BVM
Decreased or rapid respirations
Inadequate Tidal Volume (TV)
IV or LS/NS
Monitor Progression
Monitor ECG
Usually non-emergent transport
Acidotic
Open Pneumothorax:
Hole in chest wall that allows
air to enter pleural space

 Larger the hole the more likely

air will enter through there than
the Trachea
If trauma pt. does not ventilate well
with an open airway, look for hole
Maybe subtle
Abrasion with deep punctures
Pathophysiology:
Results of penetrating trauma
Profound hypoventilation may occur
Allows communication between
pleural space & Atmosphere
Prevents development of negative
intrapleural pressure
Results in Ipsilateral lung collapse

(One Side)
Inability to ventilate affected lung
V/Q mismatch:
Shunting
Hypoventilation
Hypoxia
Large functional dead space

 Hypotensive during venous returnCO-Reduce- Reduced BP

ASSESSMENT FINDINGS:

Opening in the chest wall

Sucking sound on inhalation
Tachycardia
Tachypnea
Respiratory Distress
SQ emphysema
Decreased Lung sounds on affected
side
MANAGEMENT:
Cover chest opening with occlusive
dressing (ACS- Asherman Chest
Seal)
High CO2
Assist with positive pressure
ventilations
Monitor for progression of tension
Pneumothorax
IV with LR/NS
Monitor EKG

 EMERGANT TRANSPORT-TRAUMA
CENTER
TENSION PNEUMOTHORAX:
Incidence:
Penetrating trauma
Blunt Trauma
Morbidity/Morbidity: High
Severe Hypoventilation
Immediate Life-threat if not
managed early
Cant treat this
Recognize
30 minute transport-Heli- Rapid
Pathophysiology:
One-way Valve forms in lung or
chest wall Air enters Pleural Space,
but cannot leave
Air is trapped in pleural space
Pressure collapses lung on affected
side
Mediastinal shift contralateral side

 Reduction in Cardiac OutputVenous return reduced

Increased intrathroxic pressure
Deformed Vena Cava reducing
preload
Positive pressure building more &
more
760 mm- suppose to be 5
Pressure on heart
Deviated trachea
Starling Law: greater stretch,
greater elastic recoil
Pressure on superior, inferior, aorta
JVD
Hypotensive- BP
ASSESSEMENT FINDINGS: - (MOST
LIKELY)
Severe Dyspnea- Extreme resp.
distress
Restlessness, anxiety, agitation

 Absent/decreased breath sounds

Absent/reduced air entry
Worsening or severe shock/
cardiovascular collapse
Tachycardia
Weak Pulse: volume less on arteries

(arterial collapse with Narrow PP

Hypotensive
Narrow PP
Deviates to unaffected side
ASSESSMENT FINDINGS (usually

late)
JVD
Absent if hypovolemic
Hyperresonance to percussionIntercostal in-between ribs (tap)
SQ emphysema
TRACHEAL SHIFT AWAY FROM
INJURED SIDE (late)
Cyanosis (late)
MANAGEMENT:
Recognize & Manage early
Establish Airway

 High O2
Positive pressure ventilation with

BVM
Needle thoracostomy
Iv of LR/NS
Monitor ECG
EMERGENT TRANSPORT
Consider need to intubation
Trauma center

Needle Thoracostomy Review:

Decompress with 14g (large
bore), 2-inch needle
Midclavicular line: 2nd intercostal
Midaxillary Line; 4th or 5th
intercostal space
Go over superior margin of rib to
avoid blood vessels
Be careful not kink or bend needle
If available attach one way valve

 Hemothorax:
PATHOPHYSIOLOGY:
Blood in Pleural space
Most common as a result of major
chest trauma to the chest wall
Present in 70-80% of penetrating
and major non-penetrating trauma

cases
Associated with Pneumothorax
Rib fractures are frequent causes
Blood vessels ruptures
Blood in 1000cc-3000cc
Flat Neck Veins
*Kinematics Higher
Each can hold up to 3000cc of blood
Life-threatening often requiring

chest tube and or/ surgery

If associated with Great/ Vessel or
cardiac injury:
50% die immediately
25% die 5 to 10 minutes
25% may live 30 minutes or longer

BLOOD LOSS RESULTS IN:

Hypovolemia
Decreased ventilation affected lung
Accumulation of blood in Pleural

Space
Penetrating or blunt trauma
Chest wall vessels
Intercostal vessel
Myocardium
MASSIVE hemothorax indicates

great vessel or cardiac injury

Intercostal Artery can bleed
50cc/min
Results in Collapse lung
Accumulation of blood eventually
producing a tension hemothorax
shifting the mediastinum producing:
Ventilation impairment
Cardiovascular collapse
ASSESSMENT FINDINGS:

 Tachypnea or Respiratory
Distress
Shock
Rapid, weak pulse
Hypotensive, Narrow PP
Restlessness, Anxiety
Cool, Pale, Clammy Skin
Thirst
Pleuritic Chest Pain
Decreased Lung sounds
Collapsed neck veins
Dullness on Percussion
MANAGAEMENT:
Establish Airway
High Conc. O2
Assist ventilations with BVM
MAST in Profound Hypotension
Needle Thoracostmy if tension &
unable to differate from Tension
Pneumothorax
IVs X2 with LR/NS
Monitor ECG

 EMERGENT TRANSPORT to TRAUMA

CENTER
PULMONARY CONTUSION:
PATHOPHYSIOLOGY:
Blunt Trauma to the Chest
Rapid deceleration forces cause
lung to strike chest wall
High energy shock wave from
explosion
Low velocity as with Ice pack
MOST Trauma from blunt thoracic

trauma:
30-75% of blunt trauma
Mortality 14-20%
Rib fx in many but not all cases
Alveolar rupture with hemorrhage 7

Edema
Increased capillary membrane
permeability
Large vascular shunt develop
Gas exchange disturbances
Hypoxemia

 Hypercarbia
ASSESSMENT FINDINGS:
Tachypnea or Respiratory distress
Tachycardia
Evidence of blunt chest trauma
Cough and/or Hemoptysis
Apprehension
Cyanosis
MANAGEMENT:
Supportive Therapy
Early use of Positive Pressure
Ventilation, reduces ventilator
therapy duration
Avoid aggressive crystalloid therapy
Severe cases may require Ventilator
therapy
EMERGENT TRANSPORT: TRAUMA
Center
CARDIOVASUCLAR TRAUMA:
Any patient with significant
Blunt Trauma or Penetrating
Trauma to Chest has Heart/

Great Vessel injury until proven

otherwise
MYOCARDIAL CONTUSION:
Most common blunt trauma to heart
Usually due to Steering wheel
Significant cause of morbidity and
Mortality in the blunt trauma patient
PATHOPHYSIOLOGY:
Behaves like an Acute MI
Hemorrhage with Edema
Cellular injury
Vascular damage
Hemopericardium may occur from
Lacerated epicardium or endocardium
(blood Pericardium Sac)
May produce Arrhythmias (Ectopic
Foceye, extra beats)
May cause unresponsive Hypotension
to fluid and drug therapy
ASSESSMENT FINDINGS:

 Cardiac Arrhythmias following blunt

chest trauma
Angina-like pain unresponsive to
Nitroglycerin
Precordial discomfort indepence of
respiratory movement
Pericardial friction rub (late)
ECG Changes:
Persistent Tachycardia
ST elevation, T wave Inversion
RBBB
Atrial Flutter, Atrial Fibrillation
PVCs
PACs
MANAGEMENT:
Establish Airway
High Conc. O2
IV LR/NS
Cautious fluid administration due to
injured myocardium
ECG:
Standard drug therapy for arrhythmias
12 Lead ECG if time permits

 Consider vasopressors for

hypotension
Emergent Transport- Trauma
Pericardial Tamponade:
Usually associated with
Penetrating trauma
Rare with Blunt trauma
Occurs in 2% of chest trauma
GSW have greater morbity than
stab wounds
Lower Mortality rate if isolated
Tamponade
PATHOPHYSIOLOGY:
Space normally filled with 30-50
ml straw-colored fluid.
Lubrication
Lymphatic Discharge
Immunologic protection of the heart
RAPID ACCUMULATION OF BLOOD IN
the INELASTIC PERICARDIUM

 Heart is compressed decreased blood

entering heart:
Decreased diastolic expansion and
filling
Hinders venous return - preload
Myocardial Perfusion decreased due to:
Pressure effects on walls of heart
Decreased diastolic pressures
Ischemic dysfunction may result in
injury
Removal of as little as 20ml may
increase CO drastically
Stroke Volume- Left ventricle- ejection
fraction= 60-85% of stroke volume
Fluid around cant pump as well
SIGNS & SYMPTOMS:
BECK TRIAD:
Resistant Hypotension Boles no
change
Increased Central Venous
Pressure: Blood thats draining

get collected and causes JVD

(Distended neck/arm veins in
presence of decreased arterial BP)
Small Quiet Heart (Decreased
Heart Sounds) Narrow PP
Fluid goes into lungs
Hydrostatic Osmatic pressure fluid
will go into Alveoli due to pressure
semi-permeable
Pulsus Paradoxus:
Radial pulse becomes weak or
disappears when patient inhales10mm systolic
Increased intrathoracic pressure on
inhalation causes blood to be trapped
in lungs temporarily
PEA- LETHAL DYSRHYMTMA
LOC
MANAGEMENT:
Secure Airway
High CONC. O2 Mask

 Pericardiocentesis
Out of hospital primarily reserved for
Cardiac Arrest
Rapid Transport
IVs of LR/NS
Definitive treatment is
Pericardiocentesis followed by surgery
Pericardial window
Tamponade is Hard to diagnosis
Hypotension is common in chest
injury
Heart sounds difficult to hear
Bulging neck veins may be absent
if Hypovolemia is present
High Index of Suspicion required
Traumatic AORTIC
DISSECTION/RUPTURE:
Caused by:
MVC
Falls from Heights
Crushing Chest Trauma
Animal Kicks
Blunt Chest Trauma

 15% of all blunt chest trauma deaths

1 in 6 people who die in MVC has
Aortic Rupture
85% die instantaneously
10-15% survive to hospital
1/3 die with in six hours
1/3 die with in 24 hours
1/3 survive 3 days or longer
MUST HAVE HIGH SUPSION
Separation of aortic intima and media
Tear 2 degree high speed deceleration
at points of relative fixation
Blood enters media through a mall
intima tear-Thinned layer may rupture
Descending Aorta at the Isthmus distal
to left subcalvian artery most common
site of rupture- Ligamentum Arterisom
ASSESSMENT FINDINGS:
Retrosternal or interscapular Pain
Pain in lower back or one leg: not
getting perfused well
Respiratory Distress

 Asymmetrical arm BPs

Upper Extremity hypertension with
Decreased Femoral Pulses or Absent
Femoral Pulses
Dysphagia (Swollen)
MANAGEMENT:
Establish Airway
High Conc. Mask
C-SPINE
Maintain Minimal BP in dissection
IV LR/NS Minimize fluid administration
Avoid PASG
EMERGENT TRANSPORT:
Trauma Center with Vascular Surgery
Capability
TRAUMATIC ASPHYSIXA:
Look they have been hung or
strangled
PATHOPHYSIOLOGY:
Blunt force to chest causes:
Increased intrthoracic pressure

 Backward flow of blood out of right

heart into vessels of upper chest and
back
JVD
Capillaries rupture
ASSESSMENT FINDINGS:
Purplish-reddish discoloration of:
Head
Neck
Shoulders
Blood shot, protruding eyes
JVD
Sternal Facture or central flail
Shock when pressure released
MANAGEMENT:
Airway with C-spine control
Assist in Ventilation
Spinal Stabilizations
IV of LR
Monitor EKG
MAST in severely Hypotensive pts.
Rapid Transport

 Consider Early Sodium Bicarbonate in

Arrest (HCO3)
Diaphragmatic Rupture:
Usually due to blunt trauma but
may occur with penetrating
trauma
Usually life threatening
Likely to be associated with other
severe injuries
JVD
Abdominal Contents in Pleural
Space
PATHOPHYSIOLOGY:
Compression to abdomen results
in increased intra-abdominal
Pressure:
Abdominal contents rupture through
diaphragm into chest
Bowel Obstruction and strangulation
Restriction of lung expansion
Mediastinal shift

 90% occur on the left side due to

protection of right side by liver
ASSESSMENT FINDINGS:
Decreased Breath Sounds
Usually unilateral
Dullness on percussion
Dyspnea or Respiratory Distress
Scaphoid Abdomen (hollow
appearance)
Usually impossible to hear bowl sounds
MANAGEMENT:
Establish Airway
Assist Ventilations with High Conc. O2
IV of LR
Monitor EKG
NG tube if possible
Avoid
MAST
Trendelenbrug Position
Diaphragmatic Penetration:
Suspect intra-abdominal trauma
with any injury below 4th ICS

 Suspect Intrathoraic trauma with

any abdominal injury above
Umbilicus
Esophageal Injury:
Rare Blunt Trauma
Can perforate Spontaneously
Violent emesis
Carcinoma (Tears)
ASSESSMENT FINDING:
Pain, local tenderness
Hoarseness, Dysphagia
Resp. Distress
Resistance of neck on passive motion
Mediastinal esophageal perfection
Mediastinal emphysema/medistinal
crunch
SQ Emphysema
Splinting of Chest wall
SHOCK
MANAGEMENT:
Establish Airway
Consider early intubation
IV LR/NS titrated to BP 90-100 mm hg

 EMERGENT TRANSPORT
TRACHEOBRONICAL RUPTURE:
Uncommon injury
Less than 3% of chest trauma
Occurs with Penetrating trauma or
blunt
High Morbity rate
May involve fracture or upper ribs
Losing air into pleural space
Carina splint common
PATHOPHYSIOLOGY:
Majority (80%) occur near Carina
\Rapid movement of air into the Pleural
Space
Continuous flow of air flow from needle
of decompressed chest
ASSESSEMENT FINDINGS:
Respiratory Distress:
Dyspnea
Tachypnea
Obvious SQ Emphysema
Hemoptysis
Bright Red colour

 Signs of Tension Pneumothorax

unresponsive to needle decompression
MANAGEMENT:
Establish Airway and Ventilations
Consider Early intubation
Maybe life saving
EMERGENT TRANSPORT

INTRODUCTION TO CARDIOLOGY:
CARDIOVASCULAR DISEASE:
Single greatest cause of death and
disability in the US
Includes heart disease and Vascular
Disease
2 Million People diagnosed with as
ACS/yr.
1.5 million will experience an Acute MI
Of these 0.5 million will die

 Almost half of these (250,00) will

sudden and within the first hour of
onset of symptoms
500,00 people will suffer a stroke each
year in the US
Nearly of these will die

ATHEROSCLEROSIS:
Plaque accumulation within the
lumen of the artery resulting in:
Decreased Lumen inner diameter
Increase Vascular resistance
Potential for Thrombus or Embolus
formation
ASSOCIATED WITH:
HTN
STROKE
ANGINA, HEART ATTACK
RENAL FAILURE
RISK FACTOR:
Age
Family History
Hypertension
Hypercholesterolemia
Male
Smoking
Diabetes

 CONTRUBTING FACTORS:
Diet
Obesity
Oral Contraceptives
Sedentary Lifestyle
Personality Type

EMS ROLE:
Original was the need for rapid response
to identify emergency care of victims of
Sudden cardiac death (paramedics have
been prove to make difference in survival
and Acute Myocardial Infraction,
Contributions to being reconized in acute
coronary syndromes
Looking for ST Elevation in 3 or more
leads Cardiac Artery is then Splinted or
Stented
Bypass ER Department

Weak Vs. Strong Chain of

Survival:

Outcome is low with delayed CPR

Good quality CPR is GOOD
If we dont have good CPR
then we can perfuse heart
with Hemoglobin
TO substance Ventricular
Fibulation (Rhythm)
With ventricular Fibulation
there is no rhythmic reaction
on pulse.
Life:
V-Fib
Pulseless V-Tach

 PEA- Pulseless
Pulseless V-Tach
Asystoli (Flat line)
Anatomy & Physiology:
When heart must conducts
first
Functionally sypthom
Autocontratility: we can
contract our own
Pulmonary Edema: LCHF:
Conductive SYSTEM:
SA-NODE: (PACEMAKER)
60-100 bpm (RA- Anterior
inferior wall of Atrium)
AV NODE: 40-60 BPM
PERkinjie Fibers: 20-40bpm
Perkinje system
AV JUNCTION- Junctinal
Rhythm

Look for GAP JUCTIONS

Parietalpericardialsac
Pericardialfluid

Blood Flow:

(Mitral
valve)

CONDUCTION OF PATHWAY OF THE

HEART:

CARDIAC CYCLE:

DIASTOLIC

SYSTOLIC

PERIPHERAL VASCULAR SYSTEM

VENOUS RETURN:
SKELETAL MUSCLE PUMP:
Muscular contraction squeezes
adjacent veins causing a milking action
Valves prevent opposite flow
RESPIRTORY MOVEMENTS:
Diaphragm contraction exerts pressure
in abdomen and decreases pressure in
thoracic cavity

 Blood moves to area of lower pressure

in thorax
VENOUS RETURN:
Constriction of Veins
Sympathetic stimulation causes
contraction of the smooth muscles
walls of veins
Gravity

 Negative Effects on Venous

Return:
Increased intrathoracic Pressure
PEEP/CPAP/BiPAP

ARTERIAL RESISTANCE (Afterload)

BP:
Cardiac Output X Systemic Vascular
Resistance
(Stoke Volume x Heart Rate) X
Systemic Vascular Resistance
Starlings Law: The Greater the
Stretch the greater the recoil
SYSTEMIC VASCULAR RESISTANCE:
Vasoconstriction:
Sympathetic NS effects
Medications (prescription, nonprescription, recreational)
Renin-Angiotensin-Aldosterone
Mechanism
Atherosclerosis
Anatomical Dead Space: Airways that
do not involve gas exchange

Physiological Dead Space: Anatomical

dead space & the Alveoli that are no
longer working

Coronary Circulation:
Usually thought of as 3 arteries
Left (Main) Coronary Artery
Left Circumflex Artery
Left Anterior Descending Artery

 Right Coronary Artery

AREAS AFFECTED:
Coronary Sinus (returns 5-7% of
blood volume):
Short Trunk receiving blood from
cardiac veins
Empties into the right atrium between
inferior vena cava and AV office
CARDIAC VEINS:
Feeds into the Coronary Sinus
HEART INSPECTION:
Point of Maximal: PMI- 4th and 5th
intercostal space Palpate
Auscultate S1, S2, S3, S4
Sounds: AV, Tricuspid and Bicuspid
valve causes low pitch noise
described as a LOB
The opening of the Pulmonary Aortic
Dob

 S3: Extra Heart Sound hear after an

S2, compatible with Heart failure,
extra sound of heart opening and
closing
S4: Extra Sound hear late in diastolia
instead of following S3, comes before
S1. Sometime failure but not always.
Thrill: paplapable murmur over a
localized obstruction felt on pads of
fingers, can be found on Radial,
Athroscrosis)
Bruit: Hear high pitch of fluid going
through localized obstructions
(Auscultate)
Right MI 25%
Left 80%
MI SIGNS & SYMPTOMS:
Jaw pain

 Chest Pain
Diaphertic
Pale
Dyspnea
60 and above age
Normtensive-Hypertensive