In a previous blog post, we discussed preload and afterload. You may recall, preload is the amount of ventricular stretch at the end of diastole. Afterload is the pressure the myocardial muscle must overcome to push blood out of the heart during systole. The left ventricle ejects blood through the aortic valve against the high pressure of the systemic circulation, also known as systemic vascular resistance (SVR). The right ventricle ejects blood through the pulmonic valve against the low pressure of the pulmonary circulation, or pulmonary vascular resistance (PVR).

Understanding Systemic Vascular Resistance (SVR)

SVR reflects changes in the arterioles, which can affect emptying of the left ventricle. For example, if the blood vessels tighten or constrict, SVR increases, resulting in diminished ventricular compliance, reduced stroke volume and ultimately a drop in cardiac output. The heart must work harder against an elevated SVR to push the blood forward, increasing myocardial oxygen demand. If blood vessels dilate or relax, SVR decreases, reducing the amount of left ventricular force needed to open the aortic valve. This may result in more efficient pumping action of the left ventricle and an increased cardiac output. Understanding SVR will help the bedside clinician treat a patient’s hemodynamic instability. If the SVR is elevated, a vasodilator such as nitroglycerine or nitroprusside may be used to treat hypertension. Diuretics may be added if preload is high. If the SVR is diminished, a vasoconstrictor such as norepinephrine, dopamine, or vasopressin may be used to treat hypotension. Fluids may be administered if preload is low.

How to Calculate SVR 

SVR is calculated by subtracting the right atrial pressure (RAP) or central venous pressure (CVP) from the mean arterial pressure (MAP), dividing by the cardiac output and multiplying by 80. Normal SVR is 700 to 1,500 dynes/seconds/cm^-5.

Here’s an example:
If a patient's MAP is 68 mm Hg, his CVP is 12 mm Hg, and his cardiac output is 4.3 L/minute, his SVR would be 1,042 dynes/sec/cm^-5.
   

Factors that Increase SVR

Conditions that can increase SVR include (Breitenbach, 2010; Trammel & Sapra, 2023):

• Hypothermia
• Hypovolemia
• Cardiogenic shock
• Stress response
• Syndromes of low cardiac output

Factors that Decrease SVR

Conditions that can decrease SVR include (Breitenbach, 2010; Trammel & Sapra, 2023):

• Anaphylactic and neurogenic shock
• Anemia
• Cirrhosis
• Vasodilation

The accuracy of SVR depends on the direct pressure measurements and indirect cardiac outputs from a pulmonary artery catheter which are subject to error. However, SVR can provide critical information when differentiating various types of shock. Understanding SVR will help the bedside clinician better manage medications and hemodynamic instability.
 
*You may also see systemic vascular resistance index (SVRI); this is calculated by substituting cardiac index (CI) for CO in the equation.

References:
Breitenbach, J. (2010). Putting an end to perfusion confusion. Nursing Made Incredibly Easy!. 5(3), 50-60. https://www.doi.org/10.1097/01.NME.0000393028.13649.14

Fleitman, J. (2023, August 15). Pulmonary artery catheterization: interpretation of hemodynamic values and waveforms in adults. UpToDate. https://www.uptodate.com/contents/pulmonary-artery-catheterization-interpretation-of-hemodynamic-values-and-waveforms-in-adults

Trammel, J.E. & Sapra, A. (2023). Physiology, Systemic Vascular Resistance. Stat Pearls. Treasure Island: FL. https://www.ncbi.nlm.nih.gov/books/NBK556075/

 

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