SVR
Summary
SVR (Systemic Vascular Resistance) is the resistance offered by the systemic vasculature to blood flow, primarily determined by arteriolar tone. It is a key determinant of blood pressure (BP = CO x SVR) and is used clinically to classify types of shock.
Detail
Systemic Vascular Resistance (SVR) represents the resistance that the left ventricle must overcome to pump blood through the systemic circulation. It is calculated as SVR = (MAP - RAP)/CO x 80 (units: dyn·s·cm⁻⁵). Poiseuille's law shows resistance is most affected by vessel radius (R ∝ 1/r⁴), making arterioles the primary site of SVR regulation via sympathetic tone, local metabolites, and endothelial factors (e.g., nitric oxide, endothelin).
Clinical significance: SVR is central to understanding and classifying shock states: - Hypovolemic/Cardiogenic shock: ↓CO, ↑SVR (compensatory vasoconstriction), ↓PCWP (hypovolemic) or ↑PCWP (cardiogenic) - Septic/Neurogenic/Anaphylactic shock (distributive): ↓SVR, variable/increased CO (early sepsis), warm extremities - Obstructive shock (e.g., tamponade, PE, tension pneumothorax): ↓CO, ↑SVR
Pharmacology: Vasopressors (norepinephrine, phenylephrine, vasopressin) increase SVR via vasoconstriction; vasodilators (nitroprusside, hydralazine, ACE inhibitors) decrease SVR, useful in hypertensive emergencies and heart failure to reduce afterload.
SVR is a major component of afterload, affecting ventricular wall stress and myocardial oxygen demand. In heart failure management, reducing SVR via afterload reduction improves stroke volume per the Frank-Starling and pressure-volume relationships.
Sources
- Guyton and Hall Textbook of Medical Physiology
- First Aid for the USMLE Step 1
- Marino's The ICU Book
- UpToDate: Shock classification and management
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