Systemic Vascular Resistance (SVR): Formula, Normal Range & Meaning

Systemic vascular resistance is the afterload the left ventricle pumps against — and reading it is how clinicians tell one kind of shock from another. This guide covers the formula, the normal range, and exactly what a high or low SVR is telling you.

What is systemic vascular resistance?

Systemic vascular resistance (SVR) is the resistance the heart must overcome to push blood through the systemic circulation. It represents the afterload on the left ventricle and is set mainly by the tone of the small arteries and arterioles — constrict them and resistance rises, dilate them and it falls.

Think of it with an Ohm's-law analogy: just as voltage equals current times resistance, the pressure drop across the circulation equals blood flow times vascular resistance. Rearranged, resistance is the pressure gradient divided by flow — which is exactly how SVR is calculated.

Systemic vascular resistance formula

SVR is derived from the pressure gradient across the systemic circulation divided by cardiac output:

SVR = (MAP − CVP) ÷ cardiac output × 80

• MAP — mean arterial pressure (mmHg). Work it out with our MAP calculator.
• CVP — central venous (right atrial) pressure (mmHg).
• Cardiac output — in L/min, measured by thermodilution or the Fick method.
• × 80 — a constant that converts the result to the standard units of dynes·s·cm⁻⁵.

Indexed to body size, the systemic vascular resistance index (SVRI) = SVR × body surface area. Run the numbers instantly with our SVR & PVR calculator.

Normal systemic vascular resistance range

Measure	Normal range
SVR	800–1200 dynes·s·cm⁻⁵
SVR index (SVRI)	1970–2390 dynes·s·cm⁻⁵·m²

Some references cite a slightly wider SVR band (about 700–1600 dynes·s·cm⁻⁵). Values below the range mean the vessels are dilated; values above mean they are constricted.

What does a high SVR mean?

A high SVR means the arterioles are constricted, raising the afterload the left ventricle must work against. Common causes:

• Hypovolemic and cardiogenic shock — the body clamps down peripherally to defend blood pressure.
• Vasopressor drugs — norepinephrine, phenylephrine, vasopressin.
• Essential hypertension and high circulating catecholamines.
• Hypothermia.

A persistently high SVR increases myocardial oxygen demand and, in a failing heart, can drag cardiac output down — which is why afterload reduction is a treatment strategy in heart failure.

What does a low SVR mean?

A low SVR means the vessels are dilated, so blood pressure can fall even when cardiac output is normal or high. This is the hallmark of distributive shock. Causes include:

• Septic shock — the classic "warm" shock: low SVR with a high or normal cardiac output.
• Anaphylaxis and neurogenic shock.
• Vasodilator drugs — nitroprusside, nitrates, calcium channel blockers, and many anesthetics.
• Liver failure.

Recognising a low SVR is what points the team toward vasopressors and a search for a source of sepsis. See how it fits the wider picture in our shock hemodynamics guide.

SVR vs PVR (pulmonary vascular resistance)

The systemic circuit has a high-pressure, high-resistance counterpart on the right side: the pulmonary circuit. Pulmonary vascular resistance (PVR) = (mean PA pressure − PCWP) ÷ cardiac output × 80, and it is normally far lower than SVR.

	SVR	PVR
Circuit	Systemic (left heart)	Pulmonary (right heart)
Pressure gradient	MAP − CVP	mean PAP − PCWP
Normal	800–1200	< 250 dynes·s·cm⁻⁵

How is SVR measured?

SVR is calculated, not measured directly. You need three inputs: a mean arterial pressure (from an arterial line), a central venous pressure, and a cardiac output. The last two typically come from a pulmonary-artery (Swan-Ganz) catheter using thermodilution, or cardiac output can be derived by the Fick principle. This makes SVR a bedside/cath-lab number that the invasive cardiovascular team helps generate.

Why SVR matters clinically

• Shock differentiation — low SVR points to distributive shock; high SVR fits hypovolemic or cardiogenic shock.
• Titrating drugs — vasopressors raise SVR; vasodilators lower it.
• Heart-failure management — reducing afterload can improve forward output.

These relationships are heavily tested on the RCIS exam. Reinforce them with our hemodynamics practice questions.

Key takeaways

• SVR is the afterload the left ventricle pumps against, set by arteriolar tone.
• SVR = (MAP − CVP) ÷ cardiac output × 80; normal is 800–1200 dynes·s·cm⁻⁵.
• Low SVR = distributive (e.g. septic) shock; high SVR = hypovolemic or cardiogenic shock.
• PVR is the pulmonary counterpart and is normally much lower.
• SVR is calculated from MAP, CVP, and cardiac output.

Frequently asked questions

What is systemic vascular resistance?

The resistance the heart must overcome to pump blood through the systemic circulation — effectively the afterload on the left ventricle, set mainly by the tone of the small arteries and arterioles.

What is the systemic vascular resistance formula?

SVR = (mean arterial pressure − central venous pressure) ÷ cardiac output × 80, giving units of dynes·s·cm⁻⁵.

What is a normal SVR?

About 800–1200 dynes·s·cm⁻⁵ (some references cite up to ~1600). The indexed value, SVRI, is roughly 1970–2390 dynes·s·cm⁻⁵·m².

What causes a low SVR?

Distributive shock — sepsis, anaphylaxis, and neurogenic shock — as well as vasodilator drugs and liver failure. Blood pressure can be low despite a normal or high cardiac output.

What causes a high SVR?

Compensatory vasoconstriction in hypovolemic or cardiogenic shock, vasopressor drugs, hypertension, high catecholamines, and hypothermia.

What is the difference between SVR and SVRI?

SVR is systemic vascular resistance; SVRI is SVR multiplied by body surface area, which adjusts the value for patient size.

How is SVR measured?

It is calculated, not measured directly, using mean arterial pressure, central venous pressure, and cardiac output — the last two usually from a pulmonary-artery catheter.

What is the difference between SVR and PVR?

SVR is the resistance of the systemic circulation (left heart); PVR is the resistance of the pulmonary circulation (right heart) and is normally far lower, under about 250 dynes·s·cm⁻⁵.