Pulmonary Vascular Physiology Flashcards by Scarlett Enright

Pulmonary circulation

From right ventricle
Receives 100% of cardiac output (4.5-8 L/min)
Low pressure system

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Bronchial circulation

2% of left ventricular output

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Red cell transit time of pulmonary circulation

5 seconds

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Number of capillaries and alveoli in pulmonary circulation

280 billion capillaries
300 million alveoli
Surface area for gas exchange 50-100 m^2

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Pulmonary artery vessel walls

Thin
Minor muscularisation
No need for redistribution in normal state

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Systemic artery vessel walls

Thick as high pressure system
Significant muscularisation
Need for redistribution

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Pulmonary circulation right atrial pressure

5 mmHg

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Pulmonary circulation right ventricular pressure

25/0 mmHg

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Pulmonary circulation pulmonary arterial pressure

25/8

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Systemic circulation left atrial pressure

5 mmHg

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Systemic circulation left ventricular pressure

120/0 mmHg

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Systemic circulation aortic pressure

120/80 mmHg

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Ohm’s law

Voltage = current x resistance
Pressure across circuit = cardiac output x resistance

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Mean pulmonary arterial pressure - pulmonary arterial wedge pressure left atrial pressure =
mPAP - PAWP =

Cardiac output x pulmonary vascular resistance

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Pulmonary arterial wedge pressure

Pressure of left atrium

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Pouiseuille’s law

Resistance = (8 x length x viscosity)/ (3.14… x r^4)

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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

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Potential Causes of increased viscosity of blood

Erythrocytosis (over-production of RBCs)

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Type I respiratory failure

pO2 < 8 kPa
pCO2 < 6 kPa

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Type II respiratory failure

pO2 < 8 kPa
pCO2 > 6 KPa
Failure to ventilate alveoli

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Causes of hypoxaemia (low oxygen)

Hypo ventilation
Diffusion impairment
Shunting
V/Q mismatch

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Causes of Hypoventilation

Type II respiratory failure
Muscular weakness
Obesity
Loss of respiratory drive

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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