Peripheral Vascular Resistance

Peripheral vascular resistance (systemic vascular resistance, SVR) is the resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function. When blood vessels constrict (vasoconstriction) this leads to an increase in SVR. When blood vessels dilate (vasodilation), this leads to a decrease in SVR. If referring to resistance within the pulmonary vasculature, this is called pulmonary vascular resistance (PVR)

Vascular resistance is used to maintain organ perfusion. In certain disease states, such as congestive heart failure, there is a hyper-adrenergic response, causing an increase in peripheral vascular resistance. Prolonged increases in blood pressure affect several organs throughout the body. In conditions such as shock, there is a decrease in vascular resistance thus causing decreased organ perfusion which leads to organ malfunction.

The central dictation of peripheral vascular resistance occurs at the level of the arterioles. The arterioles dilate and constrict in response to different neuronal and hormonal signals.

In the human body there is very little change in blood pressure as it travels in the aorta and large arteries, but when the flow reaches the arterioles, there is a large drop in pressure, and the arterioles are the main regulators of SVR. 

Blood pressure mediation is by a balance of the cardiac output and the peripheral vascular resistance. In idiopathic hypertension, most patients will have a near normal cardiac output, but their peripheral resistance is elevated. As mentioned earlier, mediation of this resistance is at the level of the arteriole. As with other tissues in the body, if there is prolonged constriction of the smooth muscle within the arterioles, this will lead to hypertrophy and thickening of the vessel. There are several mechanisms by which the systemic vascular resistance may be altered.

The renin-angiotensin system is mediated by the renal system. Renin is a molecule released in response to under perfusion; renin may also be released via activation of the sympathetic nervous system. Renin converts angiotensinogen into angiotensin I, which subsequently converts into angiotensin II which acts as a vasoconstrictor on blood vessels, thus causing a rise in blood pressure. The autonomic nervous system causes both vasoconstriction and vasodilation. Alpha-1 receptor activation causes vasoconstriction, and beta-2 receptor activation causes vasodilation.[

The endothelium, itself, can modulate blood pressure. The endothelium may release nitrous oxide (vasodilation) or endothelin (vasoconstrictor).

The main concerns of peripheral vascular resistance are when it is at its extremes, called hypertension (too high) and hypotension (too low).

Hypertension (elevated peripheral vascular resistance) can be diagnosed when blood pressure measurements are greater than 140/90 on two separate clinical encounters. The majority of patients with hypertension are said to have essential hypertension, meaning there is no ‘underlying’ cause for the condition, and it is idiopathic. A minority of patients will have secondary hypertension, which is attributable to the underlying pathology. Examples of etiologies of secondary hypertension are renal disease (e.g., renal artery stenosis), endocrine conditions (e.g., Cushing’s disease), and drug-induced (e.g., oral contraceptives). Untreated hypertension can lead to chronic medical conditions consisting of coronary artery disease, renal disease, stroke, aneurysms, aortic dissection, congestive heart failure, peripheral vascular disease, and visual changes (e.g., retinal hemorrhages).

Hypotension is commonly associated with shock to which there are four main types. Hypovolemic shock is due to an excessive loss of blood resulting in a decreased cardiac output and increased SVR, as the body tries to maintain blood pressure. Cardiogenic shock is from a malfunction of the heart which results in decreased cardiac output and increased SVR. Neurogenic shock is from alterations in the autonomic nervous system that also results in decreased cardiac output and a decrease in SVR from a loss of the sympathetic innervation. Distributive shock reduces systemic vascular resistance from anaphylaxis or septic mediators, with an increase in cardiac output.