ADVENTIST UNIVERSITY OF THE PHILIPINES COLLEGE OF MEDICINE (BATCH 2019)

Subject
Topic No.
Lecturer
Transcribe
r

Respiratory Physiology
Title
Dr. Torres
Date
1.

Pulmonary Ventilation
2.

Main functions:
1.
2.
3.
4.

Pulmonary ventilation
Diffusion of O2 and CO2
Transport of O2 and CO2
Respiratory regulation
Normal quiet breathing: right
diaphragm
Inspiration- Respiratory diaphragm
contraction
Expiration- elastic recoil
Heavy breathing: extra force
contraction of abdominal muscles
Muscles that raise the rib cage:
inspiratory muscles
External intercostals bucket handle
Sternocleidomastoid
Serratus anterior
Anterior scalenius
EFFUSION
Muscles that depress the rib cage:
expiratory muscles, internal
intercostals, rectus abdominis
Pressures for movement of air in and
out of the lungs
1. Pleural
2. Alveolar
Going up increase atmospheric pressure

3.

Transpulmonary pressure: difference

between alveolar and pleural pressure
PTB- rupture of alveoli= ATELECTASIS ,
destruction of surfactant
Normal compliance= 200ml/cm of h20
Depends on:
1. elastic forces of the lungs
2. elastic forces by surface tension
surface tension elastic force: 2/3 of the
lungs
**total tska dalwang residual di
namemeasure ng spirometer

SURFACTANT

Measured by spirometer
Total Lung capacity, Force residual capacity
and Residual Volume: cannot be measured

DEAD SPACE AIR

1.
2.
3.

Anatomic dead space

Do not engage in gas exchange (fowlers)
Alveolar dead space
Cannot engage in gas exchange=0
Physiologic dead space
ADS+AlDS= total dead space air (bohrs)
Upper respiratory passages:
a) Trachea
b) Bronchi (L more vertical, R more
horizontal)
c) Bronchioles (Primary, secondary,
tertiary)
20-25 generations before reaching the
alveoli
Bronchioles (great resistance in larger
bronchi)
AUTONOMIC
1. Symphatetic= bronchodilation (beta 2
receptor, adrenergic)
2. Parasympha= bronchoconstriction
Lined by goblet cells and cilia (upward
stroke) protective
Pseudostratified columnar with motile cilia +
goblet cells
Cigarette smoking- paralysis of cilia and
increase mucus secretion

LUNG COMPLIANCE

secreted by type II alveolar cells

(pneumocytes II) DPPC- dipalmitoyl
phosphatidylcholine (type 2 alveolar
cell)
Aka lamellar bodies (in histology)
Type 1- alveolar macrophages
La place: pressure in alveoli inversely
related to radius
smaller alveoli the greater the
collapse pressure
Stabilization of the size of the
alveoli:

Interdependence- alveolo, ducts,

air spaces- share common septal
cells
Fibrous tissue- 50,000 units
surrounded by fibrous septa
Surfactant- reduce the surface
tension

PULMONARY VOLUMES AND CAPACITIES

LUNG COMPLIANCE

January 19, 2016

Most important diagnostic tool

differentiating obstructive from restrictive
lung disease.
restrictive lung disease- decrease FEV1/FVC
obstructive lung diseaseFEV-1 reduced
more than the FVC; marked decrease in
ratio.
distensibility of lungs and chest wall:
transmural pressure: alveolar
pressure- intrapleural pressure
intrapleural pressure negative:
lungs expand/ lung volume
increase
intrapleural pressure positive:
lungs collapse/ lung volume
decrease
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TOPIC TITLE
INCREASED
1.
2.

emphysema
old age (decreased elastic tissue)

DECREASED
1.
2.
3.
4.
5.

GAS EXCHANGE

atelectasis
pulmonary hypertension
pulmonary fibrosis
no surfactant
pulmonary embolism

RESPIRATORY LAWS
1.
2.

3.

LA PLACE
P2T/R (surfactant action)
POISEULLES
R= 8nl/r4
Resistance= 8 x viscosity x
length/ diameter (radius to the
4th power)
BREATHING CYCLE

PULMONARY CIRCULATION

V/Q Ratio (alveolar ventilation/ pulmonary

blood flow)

LUNGS: important blood reservoir= 450 ml

(pulmonary blood volume)
Hydrostatic pressure gradients in the lungs:

Zone 1: top APEX- no blood flow

Commonly attacked by TB
Zone 2: middle- intermittent blood flow
during systole
(arterial pressure greater than the alveolar
pressure)
Less commonly affected by pathologic
diseases
Zone 3: bottom (base)- high continuous
blood flow
(capillary pressure greater than alveolar
pressure)

PULMONARY EDEMA

Accumulation of fluid in the lungs

Common in Left sided congestive heart
failure and mitral valvular disease
Damage to pulmonary capillary membraneinfections or breathing
Noxious substances-leakage of plasma
proteins

Fluid between parietal and visceral fluid

3 ml
Etiologies: *same mechanism in edema
1. Blockage of lymphatic drainage
2. CHF
3. Decreased plasma colloid osmotic
pressure (oncotic)
4. Increased capillary permeabilityinfection or infection

Highest (>1.0) APEX- PO2 highest PCO2

lowest (ventilation)
Lowest (<0.8) BASE- PO2 Lowest PCO2
highest (perfusion)
Airway obstruction= 0, blood
flow normal
Lung diseases= inequalities,
severe hypoxemia/ hypercapnia
Normal ventilation, normal
blood flow
Exchange of O2 and CO2 is optimal
Alveolar PO2= 104 mmHg
More ventilation in the apex, more
perfusion in the base.

RESPIRATORY REGULATIONS

PLEURAL EFFUSION

Respiratory membrane (pulmonary

membrane)- ultimate unit
Respiratory unit:
Terminal bronchiole
Alveolar ducts
Atria
Alveoli
1. Membrane thickness= 0.6 um
2. Membrane surface area= 70
sq.m. (normal adult)
3. Capillary blood volume= 60-140
ml
4. Capillary diameter= 5um

Phrenic nerve- diaphragm

Medullary respiration center: reticular
formation
a. Dorsal group- inspiratory
input: CN 9 and 10
output: phrenic nerve-diaphragm
b. Ventral group- expiratory
Pneumotaxic respiratory center: upper
pons
Inhibits inspiratory volume and rate
Apneustic respiratory center: lower
pons
Stimulates inspiratory gasp (apneusis)
Cerebral cortex: ______
Chemoreceptors: increased rr
Central: MEDULLA- decreased pH,
increased H+, increased PCO2
Peripheral: CAROTID
HERING BREUER REFLEX: prevents
overinflation of the lungs
Parasymphatetic: VAGUS nerve
**Bainbridge reflex- increase heart rate
(Sympha) pressure in lateral common
carotid artery

RECEPTORS FOR BREATHING

1.

Stretch receptors (smooth muscles)

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TOPIC TITLE
Stimulated by the distention of the
lungs
Reflex decrease in breathing
(hering-breuer reflex)
Joint-muscle receptors
Stimulated bu movements during
exercise (proprioceptors)
J receptors (juxtacapillary)
Alveolar walls
At junction of capillary and alveoli
CHF Left-sided
Pulmonary edema- rapid shallow
breathing
Irritant receptors
Airway epithelial cells
Stimulated by dusts, pollen and
allergen

2.
3.

4.

RESPIRATORY RESPONSES DURING EXERCISES

1.
2.
3.
4.
5.
6.
7.
8.

Oxygen consumption- increased

CO2 production- increased
Ventilation rate- increased
Arterial PO2/PCO2*- no change
Arterial pH*- no change (moderate exercise)
-decreased (strenuous exercise)- lactic
acidosis
Venous PCO2- increased
Pulmonary blood flow (CO) - increased
V/Q ratio- uniform/equal (decreased
physiologic dead space)
Right atrium- origin of pulmonary
circulation

ADAPTATION TO HIGH ALTITUDE

1.
2.
3.
4.
5.
6.
7.
8.

10-12,000 ft. above sea level

Alveolar PO2- decreased
Arterial PO2- decreased
Ventilation rate- increased
Arterial pH- increased
HGB concentration- increased
2,3 DPG concentration- increased
Hgb-O2 dissociation curve- shift to the
right
Pulmonary vascular resistanceincreased

OXYGEN THERAPY IN HYPOXIA

Acute mountain sickness

RESPIRATORY INSUFFICIENCY

Tests of pulmonary performance

1. Blood PO2/ PCO2/ pH
2. Maximum expiratory fow (FEV-1):
CRPD- low Lung Volume/ high
Expiratory Force Residual capacity
COPD- high Lung Volume/ low
Expiratory Force Residual capacity
scooped-out

Emphysema
Excess air in alveoli leading to ballooning
effect which when ruptured, air will go to
thoracic cavity
Both obstructive and destructive
Increased airway resistance
Increased pulmonary vascular resistance
Decreased diffusing capacity
Abnormal v/q ratio:
Poor aeration
Wasted ventilation
Pneumonia
Infection and inflammation
Alveoli filled with fluid and blood cells
(consolidation)
Hepatization- end stage
Atelectasis
Lung collapse
Restrictive lung disease
Hyaline membrane disease
Bronchial asthma
Obstructive
Hypersensitivity to allergens
Edema and thick mucus
Spasm of smooth muscles
Air hunger- FRC and RV increased- difficult
expiration
Pulmonary tuberculosis
Macrophage invasion
Walling off fibrous tissue (tubercle)

Atmospheric hypoxia
100% effective
Hypoventilation hypoxia
100% effective
Impaired alveolar membrane diffusion
Increased oxygen diffusion gradient
Oxygen transport deficiency
Anemia
Abnormal hemoglobin
Circulatory deficiency
Physiologic shunt
Less value oxygen therapy
Inadequate tissue oxygen use
Carbon monoxide poisoning
Treated by pure oxygen
Doubtful O2 therapy
Tissue metabolic enzyme system incapable
of utilizing oxygen

HYPERCAPNIA

Excess CO2 in body fluids

Cyanosis
Bluish skin due to deoxygenated
hemoglobin
Polycythemia
Excess hemoglobin leads to cyanosis in
normal

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