Cardiovascular Physiology and Pathophysiology
PhysiologyStructure and Function4 Topics
Lymphatics and Edema Formation
Vascular Control3 Topics
The Cardiac Cycle
Compensation for Circulatory Failure
Determinants of Myocardial Performance7 Topics
Neuro-Control of Heart and Vasculature4 Topics
Electro-Mechanical Association4 Topics
Electrical Side of the Heart4 Topics
Causes of Heart Failure
PathophysiologyDefining Heart Failure
MVO2 and Heart Failure
Cardiac Output and Heart Failure7 Topics
Vascular Tone in Heart Failure
Peripheral Vascular Resistance
Factors affecting peripheral vascular resistance (also called total peripheral resistance or systemic vascular resistance)
Autoregulatory factors (local mechanisms): due to local mechanisms within the tissue.
These intrinsic mechanisms predominate over the extrinsic mechanisms for control of blood flow to critical organs (heart, brain, and working skeletal muscle)
Myogenic response: The form of auto-regulation in circumstances characterized by changes in blood pressure without changes in blood flow. This is well recognized in the brain, heart, and working skeletal muscle. Blood flow is altered in response to perfusion pressure in the absence of a change in metabolic rate. The resultant effect of the change in blood flow on metabolites changes arteriolar resistance to normalize blood flow in spite of an altered perfusion pressure.
Metabolic response: The increase in tissue blood flow in response to increased metabolic rate is called active hyperemia.
- Increased metabolic rate causes increased tissue metabolites (especially CO2, adenosine, lactic acid, and K+) and decreased O2
- Increased metabolism causes local arteriole vasodilation with increased blood flow to the tissue
- As the increased blood flow removes these metabolic products, the stimuli for increased flow is removed so a reduction in blood flow back to resting state occurs
- Another form of metabolic response to tissue perfusion is known as reactive hyperemia, which refers to a temporary increase in blood flow to tissue after a period of restricted flow to this tissue. This occurs due to the accumulation of metabolites as described for active hyperemia.
Extrinsic control factors (nerves/hormones): these mechanisms predominate over the intrinsic mechanism to control blood flow to non-critical organs such as the kidneys, skin, splanchnic, and resting skeletal muscles.
Factors promoting vasoconstriction
- Sympathetic stimulation: Alpha-1 and alpha-2 adrenergic stimulation
- Angiotensin II receptor stimulation
- Endothelin receptor stimulation
- Arginine vasopressin stimulation
Factors promoting vasodilation
- Parasympathetic stimulation (vagal): Muscarinic (M3) receptors cause vasodilation via NO
- Sympathetic stimulation:
- Beta-2 stimulation: causes vasodilation of skeletal muscle arterioles
- Natriuretic peptides
- Endothelium derived relaxin factor