Clinical meaning
Vascular resistance is the opposition to blood flow within the circulatory system, determined by vessel radius, vessel length, and blood viscosity as described by Poiseuille's law: Resistance = (8 × viscosity × length) / (π × radius⁴). The radius is the most powerful determinant because resistance is inversely proportional to the fourth power of the radius -- halving vessel radius increases resistance 16-fold. Systemic vascular resistance (SVR) represents total peripheral resistance to left ventricular ejection and is calculated as SVR = (MAP - CVP) / CO × 80 dynes·sec/cm⁵ (normal: 800-1200 dynes·sec/cm⁵). Pulmonary vascular resistance (PVR) represents resistance to right ventricular ejection: PVR = (mPAP - PCWP) / CO × 80 dynes·sec/cm⁵ (normal: 100-250 dynes·sec/cm⁵). Mean arterial pressure (MAP) is determined by the equation MAP = CO × SVR, meaning blood pressure depends on both cardiac output and vascular resistance. In clinical practice, SVR is modulated by the sympathetic nervous system (alpha-1 adrenergic vasoconstriction), the renin-angiotensin-aldosterone system (angiotensin II vasoconstriction), endothelial-derived factors (nitric oxide vasodilation, endothelin vasoconstriction), and circulating hormones (vasopressin, catecholamines). In shock states, SVR patterns are diagnostic: distributive shock (septic, anaphylactic, neurogenic) shows low SVR with vasodilation; cardiogenic and hypovolemic shock show high SVR from compensatory vasoconstriction. The NP applies these principles to select appropriate vasoactive medications: vasopressors (norepinephrine, vasopressin, phenylephrine) increase SVR to treat vasodilatory hypotension; vasodilators (nitroprusside, nitroglycerin, nicardipine) decrease SVR to treat hypertensive emergencies or reduce afterload in heart failure; inotropes (dobutamine, milrinone) increase cardiac contractility and output independent of resistance manipulation.