Pulmonary Vascular Physiology Flashcards
Pulmonary circulation
From right ventricle
Receives 100% of cardiac output (4.5-8 L/min)
Low pressure system
Bronchial circulation
2% of left ventricular output
Red cell transit time of pulmonary circulation
5 seconds
Number of capillaries and alveoli in pulmonary circulation
280 billion capillaries
300 million alveoli
Surface area for gas exchange 50-100 m^2
Pulmonary artery vessel walls
Thin
Minor muscularisation
No need for redistribution in normal state
Systemic artery vessel walls
Thick as high pressure system
Significant muscularisation
Need for redistribution
Pulmonary circulation right atrial pressure
5 mmHg
Pulmonary circulation right ventricular pressure
25/0 mmHg
Pulmonary circulation pulmonary arterial pressure
25/8
Systemic circulation left atrial pressure
5 mmHg
Systemic circulation left ventricular pressure
120/0 mmHg
Systemic circulation aortic pressure
120/80 mmHg
Ohm’s law
Voltage = current x resistance
Pressure across circuit = cardiac output x resistance
Mean pulmonary arterial pressure - pulmonary arterial wedge pressure left atrial pressure =
mPAP - PAWP =
Cardiac output x pulmonary vascular resistance
Pulmonary arterial wedge pressure
Pressure of left atrium
Pouiseuille’s law
Resistance = (8 x length x viscosity)/ (3.14… x r^4)
Why does on exercise CO increase significantly but mPAP remains stable/increases slightly
Reduced pulmonary vascular resistance
Recruitment of closed vessels to perfuse a larger amount of capillary bed
distention (expand radius of vessels)
in response to increased pulmonary artery pressure
Potential Causes of increased viscosity of blood
Erythrocytosis (over-production of RBCs)
Type I respiratory failure
pO2 < 8 kPa
pCO2 < 6 kPa
Type II respiratory failure
pO2 < 8 kPa
pCO2 > 6 KPa
Failure to ventilate alveoli
Causes of hypoxaemia (low oxygen)
Hypo ventilation
Diffusion impairment
Shunting
V/Q mismatch
Causes of Hypoventilation
Type II respiratory failure
Muscular weakness
Obesity
Loss of respiratory drive
Gaseous Diffusion impairment
Pulmonary oedema
Blood Diffusion impairment
Anaemia
Membrane Diffusion impairment
Interstitial fibrosis- layering of connective tissue (increases thickness of membrane)
Emphysema- destruction of alveolar bed
Perfusion- zone 1 (top of lung)
Alveolar pressure > arterial pressure> venous pressure
At resting state- minimal perfusion of lungs
High V/Q ratio
Perfusion zone 2 (middle of lungs)
Arterial pressure > alveolar pressure > venous pressure
Flow during systole
Why does perfusion of lung increase down lung
Change in pressures and gravity
Perfusion zone 3 (bottom of lung)
Arterial pressure > venous pressure > alveolar pressure
Low V/Q ratio
Flow always
How does ventilation change down the lung from apex to base
Increases
How does V/Q (ventilation/blood flow relationship) change throughout lung
At bottom of lung, blood flow greater than ventilation (low V/Q)- wasted perfusion
At top of lung, ventilation greater than blood flow (High V/Q)- wasted ventilation
Average V/Q
0.8
Complete shunt
Lobar collapse
V/Q = 0
Decreased V/Q
Narrowing of bronchioles (shunting)
Decreases V/Q
Pneumonia
COPD
Pulmonary shunts
Complete Lobar Collapse
ArterioVenous Malformation (AVM)
Intracardiac shunts
eg VSD - R-L Shunt (Eisenmenger’s Syndrome)
Physiological shunts
Bronchial arteries
Eisenmenger’s syndrome
Intracardiac shunt due to hole in interventricular septum
Shunt reverses because of high right ventricle pressure
High pulmonary artery pressure- which damages them causing narrowing. Increases pressure
Symptoms: cyanosis., clubbing, erythrocytosis
Hypoxic pulmonary vasoconstriction
Blood is redistributed away from area of lung which are poorly ventilated - not perfusing not ventilated lungs
Local action of hypoxia on pulmonary artery wall
Weak response as little muscle
Aims to maintain V/Q matching
-Local hypoxia (eg peanut)
-Generalised hypoxia (eg altitude)
Dead space ventilation v V/Q mismatch
Reduction in perfusion
Causes: peripheral pulmonary embolism
Increase V/Q as ventilation maintaining by Q decreases
Alveolar dead space ventilation
Central pulmonary embolism
V/Q = infinity as ventilation continues but no blood perfusion
Diseases of the Pulmonary Circulation
Pulmonary Embolism
Pulmonary Hypertension
Pulmonary AVMs
Pulmonary embolism
Begins with clot in veins in legs which breaks off and travels to lungs
Central = ischaemia
Peripheral = infarction
Lung infarction: ‘minor’ PE- sharp pleuritic pain and peripheral arteries
Central ‘major’ PE- shock, central chest pain, hypoxia, risk of immediate mortality, affects ability of right ventricle to pump blood
Virchow’s triad
Thrombosis (clots in blood) = circulatory stasis (eg laying in bed, reduced blood flow) + endothelial injury + hypercoaguable state
Ventilation/perfusion scan
Shows ventilation and perfusion of lungs
Pulmonary Arterial Hypertension
Increased Pulmonary Vascular Resistance
Eg uncontrolled proliferation of vessel of wall —> decreases lumen of vessel —> increases after load —> increased size of RV and decreased LV
Pulmonary Arteriovenous Malformation
Shunt between artery and vein so large amount of blood is going through the lungs without passing capillaries and alveoli
Causes low oxygen, capillaries normally filter blood eg small clots
How is CO2 transported in circulation
23% bound to Hb
Dissolved in plasma
As HCO3 -
Hb is fully saturated……. Of the way through capillary bed
25%
LA and RA pressure
5 mmHg
RV pressure
25/0 mmHg
LV pressure
120/0 mmHg
Aorta pressure
120/80 mmHg
Pulmonary artery pressure
25/8 mmHg
Mean pulmonary arterial pressure - left arterial pressure=
CO x pulmonary vascular resistance
Pulmonary arterial hypertension
Increased pulmonary vascular resistance due to decreased lumen size
Which pressure gradient best describes the pressure that drives pulmonary blood flow in an upright lung base
Arterial pressure is greater than venous pressure
