pulmonary circulation Flashcards
pulmonary vs systemic
Wall thickness:lumen ratio is smaller in pulmonary arteries (thinner muscles) so more compliant as pressure is lower, and stops uneccessary increase in blood pressure (prevents pulmonary hypertension)
Lungs close to heart, so localised, so don’t need a high pressure circuit
Right ventricle much thinner wall to generate a reduced force
Systemic Circulation: 4.5L; Pulmonary Circulation: 0.5L - most of each volume exists in veins
10% volume at 15% of the pressure with 10% of the gradient (artery to veins)
Much lower resistance to increase flow
3 functions of pulmonary circulation
Gas exchange: pulmonary transit time = 0.75s, with CO2 leaving and O2 entering (or CO/anaesthetics/etc.)
Metabolism of vasoactive substance: endothelial cells express ACE to convert AGTI to AGTII (vasoconstrictor) and break down bradykinin (vasodilator) allowing for vasoconstriction
Blood filtration: emboli (e.g. Air bubbles/ruptured fatty plaques/venous thrombosis) are caught in the pulmonary vessels, filtering out before reaches systemic arteries (can break down) - if large will be local perfusion obstruction
3 pulmonary shunts
Pulmonary shunts: circumstances leading to the bypassing of the respiratory exchange surfaces
Bronchial circulation: blood from left side of the heart supplies the parenchyma but drains back to pulmonary veins to re-enter left side of heart
Foetal circulation: in utero blood bypasses non-ventilated lungs as beneficial using the foramen ovale (RA to LA) and the ductus arteriosus (Pulmonary arteries to aortic arch)
Congenital defects: atrial septal defect (/patent foramen ovale) or ventricular septal defects lead to blood mixing across the septa
pulmonary vascular resistance
Increasing cardiac output: pulmonary circulation is low resistance, high capacity circuit (at resting Q = 5L/min) - increased Q should increase MAP and pulmonary oedema and reduce function BUT arteries distend due to greater compliance and perfusion to hypoperfused beds (towards the apex) increases, leading to negligible MAP change and minimal fluid leakage
Effect of increasing ventilation: inspiration compresses alveolar vessels (compressible as no cartilage so alveolar size increases compresses) and expiration extra-alveolar vessels (thorax decreases in volume to pinch outside) - when really full or empty then resistance increases
Hypoxaemia evaluation:
when is it beneficial or detrimental
Hypoxaemia evaluation:
Beneficial: during foetal development to increase resistance in pulmonary circuit, and hence increase flow through shunts (first breath increases alveolar PO2 and dilates pulmonary vessels
COPD: reduced alveolar ventilation and air trapping means all lung vessels constrict leading to pulmonary hypertension, right ventricular hypertropy and CHF
what is Pulmonary fluid balance:
depends on interstitial/capillary hydrostatic and oncotic pressures
depends on the starling equation
3 causes of pulmonary oedema
Mitral valve stenosis: plasma hydrostatic pressure increases because pressures back up through pulmonary circulation, increasing pressure; causes net accumulation of fluid that exceeds lymphatic capacity leading to oedema and SOB on exertion
Liver failure: liver synthesises plasma proteins, so reduced plasma oncotic force means reduced return to vessels and oedema development
Metastatic breast cancer: normal fluid accumulation but compromised lymph clearance will lead to the development of oedema
what happens in hypoxaemia?
Hypoxaemia: systemically causes vasodilation but in pulmonary circulation causes vasoconstriction (O2 sensitive K+ channels close, decreasing the efflux of ions and increasing membrane potential until depolarisation and VSMC contraction) - stops blood flow through unventilated alveoli to match ventilation and perfusion
how does infection cause oedema?
In infection, proteins and leukocytes will accumulate in the interstitium which draws more water out of the blood.
describe pulmonary circulation
short
low pressure
low resistance
more compliant circuit
define vascular recruitment
when during increased cardiac output, the more of the top of the lungs is perfused
greater number of capillary beds are perfused
vessels distend more to accommodate extra flow