Flashcards in CAM201: SPecific Circulations Deck (12)
What determines/affects coronary blood flow?
Coronary blood flow pressure is driven by aortic root diastolic pressure. This is because blood flow through the myocardium is prevented/restricted during systole because contraction of the myocardial compresses the coronary vessel, preventing flow. Thus, blood flow can only occur during Diastole.
As the coronary arteries originate at the aortic root, their flow is driven by aortic root diastolic pressure.
What pathologies can disturb coronary blood flow, and why?
Aortic regurgitation: Regurgitation of blood back into the LV during diastole increases LV diastolic blood pressure, thus inhibiting coronary blood flow (increased myocardial pressure compresses coronary vessels, inhibiting flow). Additionally, due to the regurgitation, the aortic root diastolic pressure is low, so there is a reduced driving force behind the coronary artery circulation.
Aortic stenosis BP can look something like 130/40. High systolic because regurgitation back into LV during diastole elicits a high EDV, thus increased systolic pressure because so much blood is being ejected. But, because of regurgitation, the pressure drops away quickly, resulting in low diastolic pressure
Other mechanisms: Pulmonary Embolism. Reduced flow through pulmonary cirulcation, reduced pulmonary vvenous return, thus reduced EDV in LV, reduced stroke volume, thus reduced aortic root diastolic pressure = reduced driving force behind coronary circulation
What normal physiology could decrease coronary blood flow?
Increased HR. With increased HR, diastole is reduced. Thus, when HR gets quite high, there is less opportunity for coronary blood flow to occur. This is dangers, especially because the myocardium will need more O2 during exercise because t is contracting so fast and with more force (SNS effect)
Via this mechanism, it is possible for myocardial ischaemia to occur with normal coronary vessels, if HR is high enough >~200bpm
**This is also affected by atrial fibrilation*
What is autoregulation of blood flow?
It is well understood that SNS and PSNS activity (ANS) plays a large role in the regulation of BP and blood flow.
Many specific circulations, however, engage in local autoregulation of flow, depending on specific demands.
Auto-regulation can only occur if there is adequate perfusion. There is a range of adequate perfusion within which autoregulation can occur.
Autoregulation is when blood flow within a specific circulation is regulated by local mediators, rather than by the ANS. Mediators such as O2, CO2, and metabolic byproducts can lead to vasoconstriction or vasodilation to restrict, increase, or direct blood flow.
Autoregulation in the coronary circulation:
As long as there is adequate perfusion, the coronary circulation engages in auto-regulation.
In the coronary circulation, the most important determinant in flow (if perfusion is adequate) is myocardial O2 consumption. Local myocardial consumption results in increased CO2 and other metabolite production.
The endothelial cells of coronary blood vessels are very sensitive to these metabolites, in particular ADENOSINE. Adenosine causes local vasodilation to increase flow and thus O2 delivery to the myocardium
As long as perfusion is adequate, SNS and PSNS controls do not play as big a role as auto-regulation.
Describe Autoregulation in Cerebral Blood FLow
As long as perfusion is adequate, cerebral blood flow is mainly controlled by auto-regulation.
Autoregulatory mechanisms in cerebral circulation are mainly in tune to O2 and CO2. Decreased O2 leads to a steep increase in flow (vasodilation), and increases in CO2 elicit and even more powerful response (vasodilation).
There are also myogenic auto-regulatory mechanisms in play in the cerebral circulation. I.e. vessels dilate or constrict in response to levels of local vessel wall stretch.
In general, ANS activity has quite a minimal effect on cerebral circulation.
(A maximum SNS stimulation will elicit only a 25% increase in cerebral vascular resistance, compared to reaping a maximum of 500% increase elsewhere in the body)
How do cerebral hydrostatic pressures differ from elsewhere in the body, and what are the implications of this?
The amount of blood flow through a vessel is affected by the intra-vessel pressures and the surrounding interstitial pressures. If interstitial pressures exceed vessel pressure, there is reduced flow, and vice versa.
In the cerebral circulation, rather than Interstitial pressure being a major player, it is the Intra-crainial pressure (ICP) - which is exerted by virtue of the face that the brain is contained within a solid encasement (the skull).
Thus, swelling of the brain can completely cut off cerebral circulation - because of the skull, there is no way to alleviate the pressure, without breaching the skull.
**Brain death can be determined by the absence of blood flow to/from the brain. When the brain dies, it swells, completely compressing the vasculature. Thus there will be no blood return from the brain.
What mechanisms control flow in skeletal muscle flow?
Skeletal muscle plays an important role in regulating systemic blood pressure at rest, because so much of the body's capillary beds are found in skeletal muscle.
At rest, blood flow to skeletal muscle is mainly controlled by SNS and PSNS via the baroreflex.
During exercise, however, autoregulation mainly takes over.
In skeletal muscle capillary beds, autoregulation is affected by the metabolites produced by skeletal muscle undergoing increased activity and thus increased cellular metabolism.
Metabilites released result in local vasodilation and increased flow:
CO2, Lactic Acid, Adenosine, Prostaglandins, Bradykinin
What factors contribute to the pulmonary circulation being a low pressure system?
1) Pulmonary circulation is short (length of a tube is proportional to the amount of pressure within), thus it is lower pressure
2) The vessels are very compliant: the arteries, veins, etc. all have much thinner and more distensible walls that arteries and veins elsewhere in he body. Even the capillaries are more distensible than systemic capillaries.
3) In Pulmonary circulation, resistance is evenly shared throughout the arteries, capillaries and veins. By comparison, in the systemic circulation, 70% of resistance occurs in the arterioles.
4) The RV does not generate a lot of force - the pressure is generally so low that there is even low/no perfusion to the apices of the lungs
Why can pulmonary circulation handle a wide range of blood volumes without significant increase in pressure?
Recruitment and Distension of capillaries.
Recruitment: unused/un-needed capillaries tend to close up. When blood volume increases, previously un-perfused capillaries can be 'recruited' to share the load.
Distension: the vessels are so compliant, thus they can each accommodate more blood.They are also, on average, much thinner than the vessels of systemic circulation.
Pulmonary capillary recruitment and compliance mean that volume changes of even 70-200mls reap very minimal pressure changes
How does pulmonary capillary blood flow change throughout the breathing cycle.
During inspiration, intra-alveolar (within the septae between alveoli) capillaries tend to become compressed due to increased pressure from alveoli filling with air.
Extra-alveolar capillaries are contained in the surrounding parenchyma, yet are tethered to the airways and passages. Thus, when the airways expand, they are actually opened up more, as the whole lung expands, and they are tethered to the surrounding connective tissues.
Thus, intra-alveolar capillary flow is greatest upon expiration, and extra-alveolar capillary flow is greatest upon inspiration