Pathophysiology
Symptoms
Asthma
Hypersensitivity, responds to
environmental triggersAfferent
nerve stimulation
Parasympathetic Immune
Response affecting Airways
REVERSIBLE
Parasympathetic:
Cough (clear mucus)
Vasodilation,
Bronchoconstriction (smooth
muscle hypertrophy in extreme
cases)
BM thickening
Mucosal secretions
Dyspnea
Breath Sounds:
Wheezing,
Tachypnea (as a compensation
for hypoxemia)
Tachycardia (vasodilation due to
low pO2, leads to compensatory
increase in CO due to decreased
TPR)
Pulsus Paradoxus
Chronic Bronchitis
Does not respond to
environmental triggers (except
asthmatic bronchitis)
Comes from acute bronchitis (like
asthma)  Afferent Nerve
Stimulation  Parasympathetic
Immune Response affecting
Airways
Parasympathetic:
Productive Cough
Vasodilation,
Bronchoconstriction (smooth
muscle hypertrophy)
BM thickening
Mucosal secretions
Emphysema
Destruction of
1.) terminal respiratory units
and
2.) alveolar capillary beds
3.) elastic tissue
Protease Inhibitor DeficiencyElastolytic Activity
Dyspnea
Breath Sounds:
Wheezing, Coarse Crackles
Long Slow Breathing
Dyspnea
Breath Sounds:
Wheezing, Crackles, Rales
Tachypnea (as compensatory for
hypoxemia)
Tachycardia (vasodilation due to
low pO2, leads to compensatory
increase in CO due to decreased
TPR)
Polycythemia (due to Chronic
Hypoxemia)
Jugular Vein Distention due to
Pulmonary HPTN (due to Chronic
Hypoxemia)
may lead to Cor Pulmonale
Tachycardia
(vasodilation due to low pO2,
leads to compensatory increase in
CO due to decreased TPR)
Polycythemia (due to Chronic
Hypoxemia)
Jugular Vein Distention due to
Pulmonary HPTN (due to Chronic
Hypoxemia)
May lead to Cor Pulmonale
Cough is rare
V/Q Ratios
Pulmonary Tests
Compliance
Inflammation
Hypoxemia
Hypocapnia
Hypercapnia
High V/Q and Low V/Q:
Because of non-homogenous
airway obstruction, we have overventilated non-obstructed
respiratory units (High V/Q, due
to tachypnea) and we have underventilated obstructed units (low
V/Q).
↓FEV1/FVC
↓Compliance due to
Hyperinflation of Lungs
Yes
Yes
Yes, due to compensatory
increase in respiratory
ratehyperventilation of nonobstructed respiratory units.
Yes, severe asthma attack
Low V/Q only, (no compensatory
tachypnea):
Increase in Physiological Shunting.
High V/Q only, (destruction of
alveolar capillary beds):
Increase in Physiological Dead
Space.
↓FEV1/FVC
↓Compliance due to
Hyperinflation of the Lungs
Yes
Yes, Chronic
No
↓FEV1/FEV
↑Compliance due to Alveolar
Wall Degeneration
No
Yes, Chronic
No, because even though we have
tachypnea, the damage is
homogenous and all units are
obstructed.
Yes
Yes, this attempts to increase RR
IPF (Idiopathic Pulmonary Fibrosis-idiopathic means no one knows etiology)
Type I Epithelial Cell Destruction, replacement by abnormal Type II Proliferating Type Cells
Scarring and Inflammation in Alveolar Units
 ↓in Surfactant
(↓Compliance ↑Lung Recoil via ↑elastic recoil and ↑surface tension)
 Thickening of Alveolar-Capillary Membrane, Loss of Capillary Beds
Symptoms
Idiopathic Symptoms:
Dry Nonproductive Cough
Dyspnea
Tachypnea (due hypoxia, and increased respiratory drive due to stimulation of the C fibers/J receptors in
the alveolar walls)
Inspiratory Crackles (due to fibrosis and loss of normal surfactant)
Digital Clubbing
JVD from Pulmonary HPTN (which is a result of hypoxemia and capillary bed destruction-capillary bed
destruction makes it difficult to flow through those regions) Cor Pulmonale
V/Q Ratios
High V/Q (due to thickening of Alveolar-Capillary Membrane and Loss of Capillary Beds via Scarring and
Inflammation)
Low V/Q (due to ↓compliance)
Pulmonary Tests
FEV1/FVC same (because of proportionate decrease in both FEV1 and FVC)
Compliance
↓
Inflammation
Yes
Hypoxemia
Yes, Chronic
Hypocapnia
Yes, sometimes (mild hypocapnia due to tachypnea)
Hypercapnia
Yes, in the later stages of the disease when the increased work of breathing prevents ventilation
Question: How does hypoxemia occur in the presence of hypocapnia? I thought they both take only 0.25 sec to exchange in the blood.
Pathophysiology
Answer: It is easier to get rid of CO2, because all it is doing is waiting to be eliminated. However, the O2 brought in needs to be used by the
tissues and so full replenishment of O2 in the blood is difficult. Therefore, you can have chronic hypoxemia and also have hypocapnia due to
tachypnea. Tachypnea is a response from the Peripheral Chemoreceptors detecting chronically low pO2 levels, but this hypoxemic tachypnea is
overridden by the hypocapnia that results which stops the tachypnea even before your pO2 levels are increased past 40mm Hg.
Remember: the control pO2 exerts on ventilation is very weak, it basically stops once you get past 40 mmHg. At that point in ventilation, we will
probably already have hypocapnia, which exerts a negative ventilatory control through the central chemoreceptors in the medulla. Reference
the chart in #15.
Pathophysiology
Cardiogenic Pulmonary Edema
Increase in Transmural Pressure, leads to accumulation
of excess fluid in the interstitium.
Jv=(Pc+πi)-(Pi+πc)
Jv=Outward forces-Inward Forces
*Increased Transmural pressure results from
↑Outward forces or ↓Inward forces
Edema fluid has low protein content
Usually whatever flows out of the capillary can be drawn
back due to capillary hydro-osmotic gradient.
Whatever is left can be cleared by lymphatics.
Symptoms
V/Q Ratios
Pulmonary Tests
Mild Dyspnea (due to C fiber activation)
Nonproductive Cough
Compliance falls  Tachypnea and ↑Work of Breathing
Breath Sounds:
Rales, Crackles, Rhonchi
Wheezing may occur
Frothy Sputum (from protein)in the case of a
productive cough
Low V/Q ratios
N/A
Noncardiogenic Pulmonary Edema
Increased Pulmonary Capillary Permeability or Alveolar
Epithelial Permeability, leads to accumulation of fluid in
the interstitium.
Example: ARDS (Acute Respiratory Distress Syndrome)
Destruction of Epithelial Lining (Type I
Pneumocytes), leading to flooding in the alveoli.
This results from:
1.) Inhaled Toxinsepithelial damage
2.) Circulating Toxinsendothelial
damage and eventual epithelial
damage
Fibrosis and Hyperreactivity
 Surfactant ↓ (↓Compliance)  Leads to
Alveolar Edema, Alveolar Hemorrhage,
Atelectasis
Edema fluid has high protein content
Damage to the endothelium leads to leakage of protein
into the interstitium. However, this doesn’t lead to
alveolar flooding because the alveolar epithelium is
completely impermeable to protein, leading to a
powerful osmotic gradient that keeps fluid in the
interstitium. However, in later stages this barrier is
breached and we get alveolar flooding.
Dyspnea
Compliance falls Tachypnea
Low V/Q ratios, High V/Q ratios
N/A
Compliance
Inflammation
Hypoxemia
↓
No
Yes
↓
Yes
Yes
Hypocapnia
Hypercapnia
Can be low due to tachypnea
No, Normal or Low PaCO2 levels
No
Yes, due to increasing dead space ventilation
Stages of Pulmonary Edema:
Stage 1: Eccentric Fluid Accumulation
Stage 2: Crescentic Filling of Alveoli
And Peribronchovascular Intersitium Distention
(When edema is greater than what the lymphatics can remove)
Stage 3: Alveolar Flooding
Pathophysiology
Pulmonary Embolism
Obstruction of Perfusion by a moving clot
(Same Risk Factors as DVT)
↓Surfactant due to hypoperfusion (which interferes with surfactant production in type II cells)
Leads to Alveolar edema, collapse, and atalectasis
Symptoms
Dyspnea
Pleuritic Chest Pain
Hemoptysis
Tachypnea
Increase in Pulmonary Arterial Pressure (due to hypoxemia)
V/Q Ratios
High V/Q ratios (Classic Example of Alveolar Dead Space)
Low V/Q ratios (due to ↓surfactant and ↓compliance)
Angiography, there is a “hole”
↓
No
Yes
Possible
Yes, due to increasing alveolar dead space
Pulmonary Tests
Compliance
Inflammation
Hypoxemia
Hypocapnia
Hypercapnia