Welcome to ICU Primary PrepCast. Hi, I'm Maddy. Hi, I'm Swapnil.
And today we are going to discuss another primary snippet. So Maddy, this primary snippet is about systemic vascular resistance. Can you please describe the physiological control of SVR? Sure. So SVR is the change in pressure divided by the blood flow and blood flow is volume over time.
We know from the Hagen-Cussell law that resistance is eight times the length of the vessel times the viscosity of blood divided by pi multiplied by the radius of a vessel to the power of four. So we know that the radius of the vessel is the most significant determinant of systemic vascular resistance. The vascular system has components that are in series and components that are in parallel.
And these all comprise systemic vascular resistance. The components in series, we know that the total resistance is a sum of all the individual resistance. And for the ones in series, the smaller arteries and the arterioles make up the bulk of this total resistance, so about 70% of total resistance. The large arteries need a significant decrease in their radius to have an effect on total resistance, as they normally contribute only around 1% of the total resistance.
So that's why the major determinant is the small arteries and arterioles resistance. For those vascular systems that are in parallel, the total resistance equals the inverse of the sum of the inverse of the individual resistance. So therefore, we know that parallel arrangement of vessels reduce the resistance to blood flow.
So these are things like capillaries, which have low resistance, and even though they have a very small diameter, they make up only a very small amount of the total vascular resistance. Therefore, the primary way that... the SPR is controlled is via changing the radius of the arterioles. So then if we think about it in this way, we know that the factors that control the radius of the arterioles can be thought of in terms of the things that can systemically control it and those that control the arterial radius locally.
So in terms of systemic factors, these are things like peripheral and central chemoreceptors, arterial baroreflex, autonomic central control. and hormonal control and temperature. So peripheral and central chemoreceptors respond to a variety of things such as hypoxia, hypercapnia and acidosis.
This all increases sympathetic activity which increases systemic vascular resistance. Then there's the arterial baroreflex. So this can be through high pressure baroreceptors which respond to changes in the wall stretch which increases action potentials, increases the activity.
stimulation in the autonomic nervous system and inhibits the baseline sympathetic vasomotor outflow, which decreases SBR. Then there's low pressure baroreceptors, such as those in pulmonary arteries and large veins, which are primarily activated in response to volume. So if there's an increase in volume, there's an increase in wall stretch, which activates the vasomotor center, increases the heart rate and also increases atrial natural peptide release.
and decreases renin and aldosterone, which causes vasodilatation. Then there's autonomic central control, which the arterial barrier reflex and chemoreceptors are also a part of. But we know that in the body, there's a baseline of a sympathetic tone acting on alpha receptors to cause vasoconstriction, and that different vascular beds have a different amount or intensity of response to the changes in sympathetic neural activity. So places like the muscle arterioles.
black neck system, renal and skin, they're very, very sensitive to changes in sympathetic activation. This is in comparison to cerebral or coronary arteries. So therefore these non-essential vascular bands can be vasoconstricted to preserve flow to the vital organs like the heart and the brain. Anything that increases this sympathetic activation will activate the renal, the renin angiotestin outer sterone system and activate the adrenal medulla to release catecholamide. And this causes an increase in systemic vascular resistance.
Whereas if there's a reduction of the sympathetic activation, the opposite will occur. Then there's hormonal control. So things like antidiuretic hormone, which is triggered by an increase in osmolarity, decreased volume or increased angiotensin 2 will cause increased ADH and increased water resorption in the kidneys.
And it also increases vascular resistance by the RELON receptor. Then the renin-angioautosterone. System, as we've mentioned before, so any decrease in renal perfusion pressure will increase renin. And this eventually increases sympathetic activity, aldosterone release and ADH, which also releases NORAD and adrenaline, which increases SBR. And then catecholamines, which have a similar effect to the sympathetic nerve activation, but these effects are longer lasting.
So things like exercise, hypoglycemia or pain increases the release of adrenaline and noradrenaline from the adrenal medulla and causes vasoconstriction. And finally, temperature. So any increase in temperature causes vasodilatation to decrease SBR. In terms of local control, there's myogenic control, metabolic control, or flow control.
So myogenic control, if there's any increase of pressure in a vessel, the smooth muscle is stretched, which causes increased depolarization, increased intracellular calcium, and vasoconstriction. And the myogenic control varies in terms of sensitivity depending on the organ. So for example, in the brain, where it's really important to control blood flow, it's very responsive.
Metabolic control is where... basically demand is met by supply. So if there's any increase in the metabolic demand of tissue, this will relieve certain substances such as lactate, ATP, potassium, which causes dilatation of arterioles and increased supply.
And then flow control. So any local vasodilatation in any distal arterioles increases the flow in the local proximal arteriole, which increases the sheer stress and causes more vasodilatory substances. and then causes more vasodilatation in the proximal arteriole.
So there's a different variety of both systemic and local control factors that control overall systemic vascular resistance. But the key is to know that it's mainly dependent on the radius of the small arteries and arterioles in the body. Thanks, Maddy.
So that's a very comprehensive answer on SVR and physiological factors controlling SVR. We'll be back with another primary snippet in a week's time. Till then, goodbye and have a nice time. Thanks for listening. See you next time.