Describe the physiological control of systemic vascular resistance (SVR).
This question invited a detailed discussion of the physiological control mechanisms in health, not pathophysiology nor drug-mediated effects. The central and reflex control mechanisms that regulate SVR over time are distinct from the local determinants of SVR. There was often confusion between dependent and independent variables. Cardiac output is generally depended upon SVR, not vice versa, even though SVR can be mathematically calculated from CO and driving pressures. The question asked about systemic vascular resistance and did not require a discussion of individual organs except for a general understanding that local autoregulation versus central neurogenic control predominates in different tissues. Emotional state, temperature, pain and pulmonary reflexes were frequently omitted. Peripheral and central chemoreceptors and low-pressure baroreceptors were relevant to include along with high pressure baroreceptors.
Often, with SAQs like this, the college examiners insist on some sort of definition to be given first, even if it is not explicitly stated in the question stem. This SAQ looked like one of those. Even though the examiners did not specifically ask for it in their comments, this suggested model answer was furnished with such a definition.
- Systemic vascular resistance is defined using Ohm's Law, where R = ΔP/Q
- (R is the resistance, ΔP is the difference in pressure along the circulation, and Q is the blood flow rate)
- The main determinants of resistance are the parameters of the Hagen-Poiseuille equation, which is R = (8 l η) / πr4, where l = length of the vessel, η = viscosity of the blood and r = radius of the vessel
Control mechanisms of systemic vascular resistance consist of systemic and regional mechanisms.
Systemic mechanisms include:
- Arterial baroreflex control (increased BP leads to a decrease in SVR)
- Aortic arch receptors are innervated by the aortic nerve, a branch of the vagus
- Carotid sinus receptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve
- Both synapse within the nucleus tractus solitarius
- Increased arterial wall stretch increases the firing frequency of these receptors
- Activation of these receptors leads to a decrease in sympathetic tone, which decreases both peripheral vascular resistance and the cardiac output
- Autonomic central control
- Sympathetic activity increase associated with pain, emotion, exercise, or other sympathetic stimulus gives rise to peripheral vasoconstriction
- Peripheral and central chemoreceptors (hypoxia leads to increased SVR)
- Pulmonary baroreceptors (hypoxia leads to increased SVR)
- Hormones (eg. vasopressin and angiotensin)
- Temperature (hypothermia leads to increased SVR)
Local/regional mechanisms include:
- Intrinsic myogenic regulation (in response to stretch)
- Metabolic regulation (in response to increased tissue demand)
- Flow- or shear-associated regulation (in response to increased local flow)
- Conducted vasomotor responses (propagating from neighbouring vascular sites)
- Local cooling (which leads to vasoconstriction first, and then to vasodilation again)
- Immunological modulation by inflammatory mediators
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Skimming, Jeffrey W., Sidney Cassin, and Wilmer W. Nichols. "Calculating vascular resistances." Clinical cardiology 20.9 (1997): 805-808.
Joyce, William, et al. "Weighing the evidence for using vascular conductance, not resistance, in comparative cardiovascular physiology." Journal of Experimental Biology 222.6 (2019): jeb197426.
Lautt, W. Wayne. "Resistance or conductance for expression of arterial vascular tone." Microvascular research 37.2 (1989): 230-236.