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).1
The right ventricle ejects blood through the pulmonic valve against the low pressure of the pulmonary circulation, or pulmonary vascular resistance (PVR).1
Let’s dig a little deeper into these concepts.
Systemic vascular resistance (SVR)*
Systemic vascular resistance (SVR) reflects changes in the arterioles2
, 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.1
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.2
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, vasopressin or neosynephrine may be used to treat hypotension. Fluids may be administered if preload is low.
SVR is calculated by subtracting the right atrial pressure (RAP) or central venous pressure (CVP) from the mean arterial pressure (MAP)
, divided by the cardiac output and multiplied by 80. Normal SVR is 700 to 1,500 dynes/seconds/cm-5
Here’s an example:
If a patient's MAP is 68 mmHg, his CVP is 12 mmHg, and his cardiac output is 4.3 L/minute, his SVR would be 1,042 dynes/sec/cm-5
Conditions that can increase SVR include1,2:
Conditions that can decrease SVR include1,2:
- Cardiogenic shock
- Stress response
- Syndromes of low cardiac output
- Anaphylactic and neurogenic shock
Pulmonary vascular resistance (PVR)*
Pulmonary vascular resistance (PVR) is similar to SVR except it refers to the arteries that supply blood to the lungs. If the pressure in the pulmonary vasculature is high, the right ventricle must work harder to move the blood forward past the pulmonic valve. Over time, this may cause dilation of the right ventricle, and require additional volume to meet the preload needs of the left ventricle.1
PVR can be calculated by subtracting the left atrial pressure from the mean pulmonary artery pressure (PAP), divided by the cardiac output (CO) and multiplied by 80. To obtain the left atrial pressure, a pulmonary artery catheter (PAC) is needed to perform a pulmonary artery occlusion pressure (PAOP), also known as pulmonary artery wedge pressure (PAWP). Normal PVR is 100 – 200 dynes/sec/cm-5
Here’s an example:
If a patient's mean PAP is 16 mmHg, his PAOP is 6 mmHg, and his cardiac output is 4.1 L/minute, his PVR would be 195 dynes/sec/cm-5
Factors that increase PVR include1:
Factors that decrease PVR include1:
- Vasoconstricting drugs
- Hypercapnia (high partial pressure of arterial carbon dioxide [PaCO2])
- Vasodilating drugs
- Hypocapnia (low PaCO2)
- Strenuous exercise
The accuracy of SVR and PVR 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 and PVR is useful when diagnosing the severity of pulmonary hypertension.3
Understanding these parameters will help the bedside clinician better manage medications and hemodynamic instability.
*You may also see systemic vascular resistance index (SVRI) or pulmonary vascular resistance index (PVRI) reported; these measurements are calculated by substituting cardiac index (CI) for CO in the equations.
Myrna B. Schnur, RN, MSN
1. Breitenbach, J. (2010). Putting an end to perfusion confusion. Nursing Made Incredibly Easy!. 5(3): 50 60
2. Gowda, C. (2008). Don’t be puzzled by cardiovascular concepts. Nursing Made Incredibly Easy!. 6(4): 27-30.
3. Silvestry, F. (2015). Pulmonary artery catheterization: interpretation of hemodynamic values and waveforms in adults. Uptodate. Retrieved on April, 17, 2017 from https://www.uptodate.com/contents/pulmonary-artery-catheterization-interpretation-of-hemodynamic-values-and-waveforms-in-adults