Help with Hemodynamics!

Hemodynamic measurements are an essential part of cardiovascular physiology that depict the various forces involved in circulating blood throughout the body. This post will define some of the most common hemodynamic values, how the nurse should interpret these values, and various conditions that cause these values to fluctuate. When a patient is in a shock state, the amount of blood being delivered to the tissues (perfusion) is reduced meaning that the amount of oxygen (oxygenation) being delivered to the tissues is also decreased. Tissue perfusion and oxygenation are affected by several hemodynamic parameters including cardiac output/ cardiac index, systemic vascular resistance, central venous pressure, and pulmonary capillary wedge pressure. Let’s discuss each of these individually and then look at how each of these measurements are affected by various types of shock.

Cardiac output

Cardiac output determines the amount of blood reaching the tissues and organs. Cardiac output is measured by multiplying stroke volume times heart rate. Stroke volume is the amount of blood measured in liters that is ejected from the left ventricle PER BEAT; while the heart rate is measured in beats per minute; therefore cardiac output is the amount of blood in liters being pumped out by the heart every minute (L/min). A normal cardiac output is 4-8 L/min. Cardiac index is simply cardiac output that has been adjusted for the patient’s body surface area. A normal cardiac index is 2.5-4 L/min. It is easy to understand that as heart rate fluctuates under the influence of the nervous system, cardiac output will also be affected. Let’s look closer at the influences on stroke volume and exactly how stroke volume influences cardiac output. Stroke volume is determined by three factors: 1. Preload (amount of blood returning to the right side of the heart), 2. afterload (the amount of force the heart must overcome to pump blood out to the body), and 3. contractility (how effectively the heart can squeeze). Here is a practical example: In hypovolemic shock, blood volume is low, therefore, preload, stroke volume, and cardiac output will all be reduced.

SV HR Contractility

Cardiac Output

Systemic Vascular Resistance

Systemic vascular resistance is the amount of resistance within the blood vessels and this measurement also greatly affects perfusion. A normal amount of systemic vascular resistance is 800-1200 dynes/sec/cm. There are several factors that affect the amount of resistance within the blood vessels but the most important of these is blood vessel diameter. Blood vessels with a smaller diameter increase resistance and help propel blood forward, therefore increasing perfusion to tissues and cells. In states of low cardiac output, such as cardiogenic or hypovolemic shock, compensatory mechanisms cause the blood vessels to vasoconstrict therefore increasing systemic vascular resistance. These compensatory mechanisms are the bodies way of trying to increase blood pressure and therefore perfusion to the tissues and cells.

Central Venous Pressure

Central venous pressure (CVP) is an important determinant of the filling pressure (preload) of the right ventricle, which we know contributes to stroke volume. CVP is a direct reflection of the amount of pressure within the right atrium so CVP and Right Atrial Pressure are interchangeable terms. A normal CVP measurement ranges from 2-6 mmHg. Since CVP directly reflects the amount of pressure in the right atrium, it is affected primarily by two components: blood volume and vascular tone. CVP will be decreased in states of hypovolemia and vasodilation. CVP will increase in states of overhydration and vasoconstriction because the increased vascular tone returns more blood volume to the right side of the heart. Disorders that increase pressures within the lungs will also increase CVP measurements because the right side of the heart pumps blood into the pulmonary system. Since CVP is a direct reflection of the amount of pressure on the right side of the heart, if pressure increases within the lungs, CVP increases. For example, pulmonary embolism, pulmonary hypertension, mechanical ventilation with high levels of PEEP, pneumothorax, and pleural effusions all increase CVP readings.

Pulmonary capillary wedge pressure

The final, and possibly most confusing hemodynamic measurement covered in this post in the indirect measurement of pressures within the left atrium, or pulmonary capillary wedge pressure (PCWP). You may also see this referred to as pulmonary artery occlusion pressure (PAOP) so just remember that PCWP and PAOP are interchangeable.

Like cardiac output/index and systemic vascular resistance, the patient must have a pulmonary artery catheter inserted to be able to obtain this measurement. The pulmonary artery catheter is threaded into right atrium, right ventricle, and up through the pulmonary artery where it rests. There is a small balloon at the tip of the catheter to hold it in place with only a small section of catheter left exposed on the other side of the balloon. There is a small port positioned located distal to the balloon which is connected to a pressure transducer. This transducer produces the estimate of left atrial pressure when the balloon is inflated. A normal PCWP is 8-12 mmHg. PCWP readings are extremely helpful for guiding therapy for patients with left ventricular dysfunction such as cardiogenic shock caused by a left ventricular myocardial infarction. Left-sided cardiac dysfunction such as mitral stenosis will also elevate PCWP.