Pulmonary circulation Flashcards
Pulmonary vs Systemic
Explanation?
Arteries: systemic arteries have more wall for same lumen size then pulmonary arteries
Pulmonary arteries are therefore more compliant which is good to prevent unnecessary increases blood pressure which could potentially become pulmonary hypertension
Reason why differences in arterial thickness is because of differences in distance of circulation (also reflected in ventricular wall thickness)
Systemic vs pulmonary Circuit pressures across circuit
Table with relative pressures:
(slide 6, lecture 17)
LV= either systole or diastole, on or off
Aorta turns it into pulsatile pressure due to vascular compliance
Step down into capillaries until RA
Pulmonary circuit is the same as the systemic circuit but at a lower pressure
Differences in measurements in pulmonary vs systemic circulation: CO Volume MAP MVP Pressure gradient Resistance Velocity Compliance Arterial wall thickness
CO= same
Volume= Pulmonary contains 10% of total volume, most in systemic veins in systemic circuilation, most in pulmonary veins in pulmonary circulation
MAP= much smaller in pulmonary (15% pressure)
MVP= similar
Pressure gradient= lower in pulmonary (10% gradient of systemic)= impacts velocity of blood
Resistance: higher resistance= slower velocity, so need low resistance to ensure blood flow is slow to allow gas exchange to occur (diffusion rates) (R=∆P/V)
Velocity= faster in systemic
Compliance= higher in pulmonary
Arterial wall thickness= thicker in systemic
Functions of pulmonary circulation
- Gas exchange (oxygen delivery, carbon dioxide)
- Metabolism of vasoactive substances
ANG-II= Vasoconstrictor (made in lungs)
Bradykinin= Vasodialator (broken down in lungs) - Filtration of blood (avoids it going to heart/ brain first)
Embolus
‘mass’ within the circulation capable of causing obstruction
Embolism
event’ characterised by obstruction of a major artery
Lungs 3rd function: filtration of blood
Venous thrombosis/ Ruptured fatty plaques/ Air bubbles→ Small embolus/ Large embolus
Small embolus→ Eliminated in pulmonary circulation (chemically broken down (mass)/ slowly diffused out (gas))
Large embolus→ Trapped in pulmonary circulation→ Local perfusion obstructed (pulmonary embolism= occludes blood flow to lungs= effect on systemic pressure+ gas exchange)
3 pulmonary shunts
- Bronchial circulation
- Foetal circulation
- Congenital defect
Bronchial circulation pulmonary shunt
Blood goes through right side of heart, through bronchial circulation, some drains back into pulmonary vein into left side of heart (hits LV twice before RV)
Foetal circulation pulmonary shunt
Lungs aren’t being ventilated so no point sending blood there. Also beneficial not to because of local hypoxic vasoconstriction in that area= vessels are vasoconstricted+ tight= don’t want to put blood into that. Foramen ovale closes in first breath. Ductus arteriosus allows bifocation of pulmonary arteries above pulmonary trunk to connect to the aortic arch.
Congenital defect pulmonary shunt
If foramen ovale doesn’t close, ASD. VSD= mixing of blood across septum. When the heart is contracting on the left hand side, creates higher pressures+ pushes through septal defects into right side= increase atrial + ventricular pressure on right side. Over time, does so much that right side becomes stronger ventricle. Now when ventricles contract shunt goes the other way to left side which is much worse (mixed venous blood from the right side into left side= less O2 in blood) Problem: potential for emboli to bypass the filter+ get into systemic circulation. Depends on severity
Pulmonary vascular resistance
Effect of increasing cardiac output
What should happen
What actually happens
What should happen:
↑ Q= ↑MAP= ↑ fluid leakage (leakage because increase hydrostatic pressure) = ↑ pulmonary oedema= ↓pulmonary function
What actually happens:
↑ Q= ↑ pulmonary artery distension (pulmonary vessels= more compliant= more willing to stretch) + ↑ perfusion of hypoperfused beds (most hypoperfused beds are at the base of the lung so if pressure goes up it opens up more vessels above)= Negligible change in MAP= Minimal fluid leakage= No onset of pulmonary oedema= No detriment to pulmonary function
Allows CO to increase significantly without allowing fluid accumulation+ compromising on lung function.
Pulmonary vascular resistance
Effect of increasing ventilation
Graph of Resistance+ lung volume at set points (slide 15, lecture 17)+ explanation
Inspiration compresses alveolar vessels, and expiration compresses extra-alveolar vessels
Lungs live inside pleura but vessels don’t completely= alveoli apply pressure alveolar vessels during inspiration
FRC (Functional residual capacity)= mechanical equilibrium of lungs+ chest, this is when resistance is lowest but resistance increases much more when you get to TLC (total Lung Capacity) and RV (Residual Volume).
At RV, creating positive intrathoracic pressure= allows to air to be forced out= vessels close to alveoli distend but compresses extra-alveolar vessels (associated with mechanical structyures of lungs)
At TLC, pulls vessels apart at mechanical parts= reduced pressure+ resistance= allows more blood to flow into chest but compresses alveolar vessels
This is why lungs don’t want to be at RV/ TLC
Vascular resistance proportional to lung volume
Pulmonary vascular resistance
effect of hypoxaemia
Reason for response?
Systemic vascular response to hypoxia is vasodilation
Pulmonary response to hypoxia is vasoconstriction:
Hypoxia→ Closure of O2 sensitive K+ channels→ decrease K+ efflux→ Increase membrane potential→ Membrane depolarisation+ opening of VGCCs→ Vascular smooth muscle constriction
Reason: to achieve Ventilation/ Perfusion matching, if there is inadequate ventilation to a certain part of the lung, there is no point sending blood there, trying to match ventilation+ perfusion (not perfect)
Mechanism not particularly important, just know that K is moving (affects membrane potential), not Ca
Works well when there is a part of the lung that is not working properly, but if you are breathing low O2 air/ have COPD, problematic because it becomes a widespread vasoconstriction across lungs= RV working much harder= becomes stronger (concentric hypertrophy)= impacts end diastolic volume= impacts stroke volume
Pulmonary vascular resistance
When is the response to effect of hypoxaemia beneficial
During foetal development:
Blood follows the path of least resistance
High-resistance pulmonary circuit means increased flow through shunts
First breath increases alveolar PO2 and dilates pulmonary vessels
