Describe the 2 circulations in the lungs?
1. Bronchial - part of systemic circulation, arises from aorta, supplies blood to trachea and bronchi. Bronchial venous drainage = mainly pulmonary vein to L atrium and some into bronchial veins. Receives abour 2% of L.ventricular output
2. Pulmonary - from R. ventricle, receives 100% of right heart output
How long does it take blood to pass through lungs?
What is the lungs SA?
What are pulmonary arteries like compared to normal arteries?
How do you calculate pulmonary blood flow?
Thin walled and larger diameter than normal, very distensible and compressible - stretch during systole so they can maintain low systolic pressure.
PBF: pulmonary arterial pressure/pulmonary vascular resistance
(PAP is low - 15mmHg, PVR is much lower than systemic vascular resistance. If PAP increases (>25-30) = pulomary arterial hypertension, life threatening!!)
How is the drop in pressure between pulmonary arteries and veins different in pulmonary capillaries than systemic?
What spinal level is the sympathetic nerve supply to the lungs?
Describe the structure of this nerve supply, incuding what it innervates.
About 4 mmHg in pulmonary compared to around 20mmHg in systemic.
Postganglionic nerves from paravertebral sympathetic ganglia merge with vagal fibres in pulmonary plexus, enter lungs around pulmonary arteries. Sympathetic fibres innervate beta-2 adrenoreceptors on SM of trachea -> terminal bronchioles. Activation = bronchodilation.
NB: little sympathetic vasoconstrictor tone on pulmonary arterioles but sympathetic stim inhibits mast cells = reduces histamine release and inflamm in lungs
Pulmonary vascular resistance varies with lung inflation. Explain how.
Inhale -> alveoli expand and compress capillaries lying between them = increases resistance of these capillaries. Extra-alveolar capillaries are slightly pulled apart due to negative pressure = decreases resistance. They are compressed during expiration.
Result = U shaped curve
What effect does gravity have on pulmonary lung pressure and perfusion?
What are the origional and revised 3 zone models of lung perfusion?
When standing up, pressures lower at apex than base of lungs. The base is well perfused as gravity helps blood circulate there, and apices are poorly perfused.
Origional 3 zones: apices have no blood flow (because alveolar pressure > capillary pressure, so squashes capillaries flat), centre has pulsatile flow (greater in systole), bases have continuous flow.
Modified: NO ZONE 1 b/c capillaries not squashed flat but narrowed. Pulmonary arterial pressure > alveolar pressure in all parts of the lung. (Zone 1 only observed when ventilated with +ve presure or hemorrhage -> alveolar dead space). Zone 2 pulsatile occurs mainly during inspiration when alveolar pressure is less than atm. Flow decreases during expiration when pulmonary alveolar pressure increases and partially blocks capillaries. Zone 3 continuous flow b/c pulm arteriolar and venous pressure always greater than alveolar pressure = best gas exchange.
How do you measure blood flow in upright human lung?
A small zone 4 is often present at lung bases. What is it due to?
Radioactive xenon injected into venous blood and evolves into alveolar gas from pulmonary capillaries. Radiation counters measure amount of xenon passing through each lung zone.
Rise in pulmonary interstitial pressure compressing the capillaries at the base of the lungs.
What is lung compliance? What does the curve look like?
What does the ventilation-perfusion ratio look like at the base and apex?
How would airway or blood flow obstruction affect the V/Q ratio?
Measure of lung stretchability. C=dv/dp (change in vol/change in pressure). S-shape curve, higher in base b/c better ventilated than apices.
Apex: blood = high pO2 and low pCO2, low flow
Base: low pO2 and high pCO2, greter flow
Thus pulm venous blood contains gas levels between apex and base.
Airway obstruction: V/Q LOWER, no GE. Blood flow obstruction: V/Q HIGHER, no GE.
What is the difference between the outcomes of hypoxia in pulmonary and systemic circulation, and why is it important?
Pulmonary: hypoxia -> local vasoconstriction (Euler-Liljestrand response); Systemic: vasodilation (exercising muscles etc.).
Vasoconstriction of capillaries diverts blood away from poorly ventilated regions of lung and toward well ventilated regions.
During exercise, what happens to pulmonary arterial pressure and pulmonary arterial resistance?
PAP doesn't change.
PAR decreases by 3 mechanisms:
1. stretching of thin walls -> reflex vasodilation
2. increase ventilation -> increase alveoli pO2 -> increased relaxation of arteriolar muscle to max
3. arterio-venous shunts open in lungs -> blood directly to pulm veins (but not oxidised!)
1 and 2 = main
What is foetal pulmonary vascular resistance like?
What happens to blood entering the right heart in a foetus?
What happens with the baby's first breath?
V. high b/c generalised hypoxic vasoconstriction. Thus blood flow through lungs low.
Most shunted R -> L via foramen ovale and ductus arteriosus.
Pulmonary vascular resistance decreases, the alveoli of neonate become better oxidised, and pulmonary blood flow becomes equal to cardiac output
What is the a) foramen ovale and b) ductus arteriosus and what happens to them after birth?
What 3 things mean v. little blood enters lungs in the foetus?
a) hole in arterial wall between L and R atria. Closes after birth (but b/c atrial pressures similar, doesnt have to close...)
b) short tube joining aorta and pulmonary artery. Shuts immediately after birth.
1. high vascular resistance 2. foramen ovale 3. ductus arteriosus
Label A and B
A: foramen ovale
B: ductus arteriosus