What is the calculation and clinical significance of Systemic Vascular Resistance (SVR)?

Systemic Vascular Resistance: Calculation and Clinical Significance

Formula and Definition

SVR is calculated as (Mean Arterial Pressure - Right Atrial Pressure) divided by Cardiac Output, typically expressed in dynes/sec/cm⁵. 1

• The fundamental relationship is: SVR = (MAP - RAP) / CO 1
• Normal SVR range is 900-1200 dynes/sec/cm⁵ 2
• SVR represents the resistance generated by all systemic vasculature, excluding pulmonary circulation 1
• The major determinant is arteriolar tone, though blood viscosity and vascular capacitance also contribute 1

Clinical Significance and Hemodynamic Relationships

Organ blood flow correlates directly with perfusion pressure and inversely with vascular resistance, making SVR a critical determinant of tissue perfusion. 3

Impact on Cardiac Function

• When ventricular function is healthy, elevated SVR produces hypertension while maintaining cardiac output 3
• With reduced ventricular function, normal blood pressure combined with high SVR indicates reduced cardiac output 3
• Marked elevation in vascular resistance reduces blood flow sufficiently to cause shock 3
• In septic shock, maintaining cardiac index between 3.3-6.0 L/min/m² is associated with best outcomes, compared to >2.0 L/min/m² for non-septic patients 3

Relationship to Blood Pressure and Perfusion

• MAP alone is insufficient to assess tissue perfusion—additional markers including lactate clearance, urine output, mental status, and skin perfusion must be monitored 4
• Maintenance of MAP with norepinephrine improves urine output and creatinine clearance in hyperdynamic sepsis 3
• At low-to-moderate dopamine doses, increased cardiac output occurs with unchanged or decreased SVR 5

Clinical Assessment of SVR Status

High SVR (Vasoconstricted State)

Clinical signs include absent or weak distal pulses, cool extremities, prolonged capillary refill, and narrow pulse pressure with relatively increased diastolic blood pressure. 3, 1

• This pattern indicates the body is vasoconstricting to maintain blood pressure in response to falling stroke volume and contractility 3
• The effective approach is vasodilator therapy with additional volume loading as vascular capacity expands 3, 1
• Vasodilator therapy reduces afterload and increases vascular capacitance, allowing more volume at lower pressures 3
• Nitroprusside is effective for high-afterload left ventricular failure due to potent arterial and venous dilation 1
• Phosphodiesterase inhibitors (milrinone) or α-adrenergic blockers (phenoxybenzamine, phentolamine) reduce SVR in single-ventricle physiology 1

Low SVR (Vasodilated State)

• Norepinephrine is first-line for maintaining MAP in hyperdynamic states with low SVR 1
• Vasopressin at replacement doses effectively offsets potential SVR drops when using inotropes like dobutamine or milrinone 1
• In fluid-refractory vasodilated septic shock, adult data favors norepinephrine as first-line, though children predominantly have low cardiac output rather than high output/low SVR 3

Measurement Techniques

Direct Measurement

• Pulmonary artery catheter provides the most accurate SVR assessment 3, 1
• Pulse index contour cardiac output catheter or femoral artery thermodilution catheter can measure cardiac output for SVR calculation 3
• These invasive techniques are not possible in neonates and smaller infants 3

Non-Invasive Estimation

• Doppler-derived estimated SVR (eSVR) can be calculated as the ratio of systolic blood pressure to left ventricular outflow tract velocity time integral 6
• Elevated eSVR (≥6.9) is associated with increased risk of heart failure, major cardiovascular events, and death 6
• Persistently elevated eSVR during follow-up correlates with the most adverse outcomes 6

Critical Clinical Considerations

Special Populations

In the cardiovascular ICU, SVR must be maintained greater than pulmonary vascular resistance (PVR) to ensure adequate right ventricular coronary perfusion. 1

• When PVR exceeds SVR (systolic pulmonary arterial pressure > systolic systemic arterial pressure), right ventricular ischemia results 1
• Right ventricular coronary perfusion occurs during both systole and diastole, making this relationship critical 1
• Inhaled nitric oxide can acutely decrease PVR and improve cardiac output without affecting SVR 1

Pharmacologic Management Principles

Vasoactive agents must be selected based on their effects on SVR, with continuous monitoring of physiologic parameters essential for correct dosing. 3

• Dobutamine is indicated when low cardiac output exists with adequate or increased SVR 3
• Septic patients demonstrate reduced response to alpha-adrenergic agonists mediated by excess nitric oxide production and receptor alterations 3
• Cardiac beta-adrenergic responsiveness may be reduced by nitric oxide and inflammatory cytokines 3
• Drug pharmacokinetics are altered in critically ill septic children due to impaired liver and kidney perfusion, requiring dose adjustment based on patient response 3

Important Pitfalls

• Blood viscosity must be distinguished from vascular tone when interpreting SVR values—a corrected SVR accounting for viscosity changes provides better assessment of true vascular changes 7
• During hypothermic cardiopulmonary bypass, uncorrected SVR is significantly lower than corrected SVR, underscoring the importance of this correction 7
• Volume status assessment in pulmonary hypertension is notoriously difficult, with non-invasive central venous pressure estimates potentially misleading 1
• The traditional belief that the right ventricle is preload-dependent often leads to inappropriate volume loading in right ventricular dysfunction—the right ventricle prefers euvolemia with CVP 8-12 mmHg 1