Cardiac Output Measurement

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Cardiac Output Measurement

Ruben D. Restrepo

Cardiac output monitoring provides essential information regarding the adequacy of perfusion and helps guide the management of patients at increased risk for developing cardiac complications. Adequacy of perfusion is the most important factor in the assessment of the cardiovascular system’s ability to meet the body’s metabolic demands. Early detection of key circulatory function derangements allows the clinician to begin proactive therapeutic interventions. This is important because most patients do not succumb to their disease but to vital organ failure.

The aim of this chapter is to describe the physiologic principles used to measure cardiac output and the most common techniques used to assess it. Chapter 15 describes the specific vascular pressure parameters used in the intensive care unit (ICU) to monitor patients with circulatory issues.

Cardiac Output

The amount of blood pumped out of the left ventricle in a minute is known as cardiac output (CO). It is the product of heart rate (HR) and stroke volume (SV), which is the volume of blood ejected by the ventricle by a single heartbeat (Box 16-1). Normal SV for adults is 60 to 130 mL/beat and is roughly equal for both the left and right ventricles. The average CO for men and women of all ages is approximately 5 L/minute at rest (reference range is 4 to 8 L/minute); however, the normal CO for an individual varies with age, sex (10% higher in men), body size, blood viscosity (hematocrit), and the tissue demand for oxygen.1

Box 16-1   Cardiac Output: An Overview

Cardiac Output (CO)

The normal heart is capable of pumping approximately 10 to 13 L/minute and twice that amount when stimulated by the sympathetic nervous system. A well-trained athlete’s heart enlarges sometimes as much as 50% and is capable of pumping up to 35 L/minute.1 Under normal conditions, the heart plays a passive role in CO and pumps whatever amount of blood is returned to it. When the diseased or damaged heart can no longer pump the amount of blood returned to it, it is said to be failing.

Venous Return

The volume of blood returning to the right atrium is known as the venous return. The resting blood flow through an organ is determined by the metabolic needs of the organ. As the organ’s demand for oxygen increases, perfusion to the organ increases. The muscles, liver, and kidneys receive the greatest amount of blood flow in the resting state because of their high metabolic needs. When the metabolic activity of the tissues increases (as during exercise) or when the availability of oxygen to the tissues decreases (as occurs at high altitudes or with carbon monoxide or cyanide poisoning), vasodilation allows more blood to flow to the tissues.

The concentration of oxygen, carbon dioxide (CO2), hydrogen ions, electrolytes, and other humoral substances regulate capillary blood flow. The presence of low oxygen concentration and increased levels of hydrogen ions and CO2 at the tissue level causes vasodilation and increases blood flow to the affected area.

In addition to providing tissue regulatory control of CO, the venous system acts as a reservoir of blood. Normally about two thirds of the total blood volume resides in the venous system. When blood volume to vital organs decreases, the veins and the spleen constrict and redistribute volume to maintain venous return and cardiac pressures. In fact, 20% to 25% of the total blood volume can be lost without altering circulatory function and pressures.2 In cases of severely reduced CO such as heart failure, the central nervous system (CNS) elicits a sympathetic stimulation that increases vasoconstriction. As the heart fails, this compensatory mechanism reduces blood flow to the liver, kidneys, and other body areas to maintain perfusion to the most vital organs (heart and brain).

Measures of Cardiac Output and Pump Function

Cardiac Index

Because CO, like most other hemodynamic measurements, varies with body size, cardiac index (CI) is often used to describe flow output. CI is obtained by dividing CO by body surface area (BSA) and is reported as liters per minute per square meter (L/minute/m2). BSA is calculated using the patient’s weight and height and the DuBois nomogram (Fig. 16-1). The advantage of using an index is that values are standardized and comparisons can be made among patients of different heights and weights.

A commonly cited resting CI reference range for patients of all ages is 2.5 to 4.0 L/minute/m2, with the average for adults being about 3.0 L/minute/m2 (Table 16-1). The CI is highest at 10 years of age and decreases with age to approximately 2.4 L/minute/m2 at age 80 years.2

TABLE 16-1

Hemodynamic Variables, Example Reference Ranges, and Formulas3,4

Variable Example Reference Range Formula
Cardiac output (CO) 4-8 L/min CO = direct measurement
Cardiac index (CI) 2.5-4.0 L/min/m2 CI = CO/BSA
Stroke volume (SV) 60-130 mL/beat SV = CO/HR or EDV − ESV
Stroke volume index (SVI) 30-50 mL/m2 SVI = CI/HR or SV/BSA
Ejection fraction (EF) 65%-75% EF = SV/EDV or direct measurement
End-diastolic volume (EDV) 120-180 mL/beat EDV = direct measurement
End-systolic volume (ESV) 50-60 mL ESV = direct measurement
Rate-pressure product (RPP) <12,000 mm Hg RPP = systolic BP × HR
Coronary perfusion pressure (CPP) 60-80 mm Hg CPP = diastolic BP − PAWP
Left cardiac work index (LCWI) 3.4-4.2 kg/min/m2 LCWI = CI × MAP × 0.0136
Right cardiac work index (RCWI) 0.4-0.66 kg/min/m2 RCWI = CI × MPAP × 0.0136
Left ventricular stroke work index (LVSWI) 50-60 g/min/m2/beat LVSWI = SI × MAP × 0.0136
Right ventricular stroke work index (RVSWI) 7.9-9.7 g/min/ m2/beat RVSWI = SI × MPAP × 0.0136
Pulmonary vascular resistance (PVR) <2 units
110-250 dynes-sec/cm5
PVR = (MPAP − PAWP)/CO × 80§
Pulmonary vascular resistance index (PVRI) 225-315 dynes-sec/cm5/m2 PVRI = (MPAP − PAWP)/CI × 80§
Systemic vascular resistance (SVR) 15-20 units
900-1400 dynes-sec/cm5
SVR = (MAP − CVP)/CO × 80
Systemic vascular resistance index (SVRI) 1970-2400 dynes-sec/cm5/m2 SVRI = (MAP − CVP)/CI × 80§

BP, blood pressure; BSA, body surface area; CVP, central venous pressure (mm Hg); HR, heart rate; MAP, mean arterial pressure (mm Hg); MPAP, mean pulmonary artery pressure (mm Hg); PAWP, pulmonary artery occlusion pressure (mm Hg).

Commonly cited references ranges for adults. Sources vary somewhat in the ranges reported.

Conversion factor to convert L/mm Hg to kg/min/m2; 0.0144 is used by some sources.4

Conversion factor to convert mL/mm Hg to g/min/m2; 0.144 is used by some sources.4 An alternative version of the formula includes subtraction of the filling pressures: LVSWI = SV × (MAP − PAWP) × 0.0136; RVSWI = SV × (MPAP − CVP) × 0.0136.2,3

§Conversion factors of 79.92 and 79.96 may also be used.3,4

Cardiac Work

Cardiac work is a measure of the energy the heart uses to eject blood against the aortic or pulmonary pressures (resistance). It increases as the end-diastolic ventricular size increases and correlates well with the oxygen requirements of the heart. Although the left and right ventricles eject the same volume of blood, the left ventricle must eject against the mean aortic pressure (MAP), which is about six times greater than the mean pulmonary artery pressure (MPAP). Therefore, the work performed by the left ventricle is much greater than that performed by the right ventricle. This is evident in comparing the cardiac work index for each ventricle (LCWI and RCWI). This index measures the work per minute per square meter for each ventricle and is calculated using the following formulas:

< ?xml:namespace prefix = "mml" />LCWI=CI×MAP×0.0136=3.44.2kg/min/m2




where 0.0136 is a conversion factor for changing pressure to work.

Determinants of Pump Function

The performance ability of the heart (CO) is determined by both HR and SV. SV is determined by three factors: preload, afterload, and contractility (Fig. 16-2).

Heart Rate

HR normally does not play a large role in control of CO in the adult except when it is outside the normal range or when a dysrhythmia is present.

Bradycardia is an HR less than 60 beats/minute in an adult; however, low HR does not drop CO if the heart can compensate with increased SV. A well-trained athlete may have a resting pulse rate below 50 beats/minute but still maintain normal blood pressure. However, if a patient has a damaged heart that cannot alter SV to compensate for bradycardia, CO will fall.

Tachycardia (adult HR >100 beats/minute) is the body’s way of maintaining CO when compensatory mechanisms to increase SV are inadequate. In the resting patient, CO may begin to decline at rates of 120 to 130 beats/minute. Because diastole is shortened by increased rates, the time for ventricular filling is decreased. In addition, maintaining the higher rate requires an increased oxygen consumption that the patient with coronary artery disease may not be able to provide. In subjects with a healthy heart who undergo exercise and sympathoadrenal stimulation, the CO does not decline until the HR reaches about 180 beats/minute. Premature heartbeats (premature ventricular contractions and premature atrial contractions) also alter the time for ventricular filling and may decrease CO.


Preload is the stretch on the ventricular muscle fibers before contraction. Preload is created by the EDV. In 1914, Starling found that up to a critical limit, the force of a muscle contraction was directly related to the initial length of the muscle before contraction. His theory is known as Starling’s law of the heart. Simply stated, the greater the stretch on the resting ventricle, the greater the strength of contraction within physiologic limits. When the physiologic limits are exceeded, greater stretching of the muscles does not result in an increased force of contraction.

Ventricular Function Curves

Figure 16-3 shows ventricular function curves (often called Starling curves) for the right and left ventricles. The horizontal axis represents the volume (preload), and the vertical axis is a measure of the heart’s output: CO, CI, SV, stroke index, or ventricular SWI. Increasing the volume increases output. However, when the pump becomes overstretched, it can no longer eject all of its blood efficiently and CO begins to fall.

Continuously measured EDV is the ideal but time-consuming way to assess preload. Most critical care units only measure ventricular volumes on a periodic basis using echocardiography or radionuclide imaging. Therefore, atrial pressures, which can be measured continuously, are used to reflect EDV. During diastole, the atrioventricular valves (tricuspid and mitral) are open. If there is no narrowing or dysfunction of the valves, the pressures in the atrium and ventricle should be the same at end-diastole. The filling pressure for the right heart is right atrial pressure, commonly measured as the central venous pressure (CVP). The filling pressure for the left heart is left atrial pressure, commonly measured as pulmonary artery wedge pressure (PAWP). How these pressures are measured is discussed in Chapter 15. Because a nonlinear relationship exists between the EDV and EDP, filling pressure does not always reflect ventricular volume in the critically ill patient when ventricular compliance is altered. An example in which EDP does not accurately reflect EDV is in patients with increased ventricle chamber stiffness (e.g., myocardial infarction). In these cases, EDP may remain constant as EDV decreases.

Ventricular Compliance

It is important to understand that pressure is the result of the volume, space, and compliance of the chamber the volume is entering. Forcing 100 mL of water into a small, rigid chamber takes more pressure than filling a compliant balloon with 100 mL of water. Figure 16-4 shows how ventricular pressure is affected by changes in volume and ventricular compliance (distensibility). When compliance is reduced, a much higher pressure is generated for a given volume. Pressure also increases more rapidly as the ventricle fills; thus, the ends of the curves rise more abruptly as the ventricle becomes full and tension is developed in the ventricular walls.

Factors that decrease ventricular compliance and therefore cause the pressure to increase out of proportion to the volume include the following:

Factors that increase ventricular compliance include the following:

Factors that Affect Venous Return, Preload, and Cardiac Output

The three main factors affecting the amount of blood returned to the heart are the following:

Circulating Blood Volume

Circulating blood volume is obviously altered by bleeding but is also decreased by loss of other body fluids. Excessive urine output (as occurs with diuretics), wound drainage, diarrhea, perspiration, and gastric secretions can result in a large decrease in blood volume (hypovolemia). Fluid can also shift into the interstitial space. Sepsis, burns, and shock may result in tremendous amounts of fluid being moved into this so-called “third space.” On the other hand, fluids ingested or given intravenously increase the circulating blood volume. Administration of colloids (large-molecular-weight solutions) pulls water from the interstitial space to “dilute out” the large molecules, resulting in an increase in blood volume. Use of continuous bland aerosols or even heated humidification to overcome a patient’s humidity deficit can also cause a net fluid gain, especially in small children.

Distribution of the Blood Volume

Distribution of the blood volume is altered not only by third spacing but also by changes in body position, venous tone, intrathoracic pressure, and, rarely, obstruction of the large veins returning to the heart. As the body changes position, blood tends to move to dependent areas. Standing decreases venous return; conversely, raising the legs of a patient who is lying down increases venous return.

Venous tone also alters the distribution of blood in the body. Venous tone may increase (vasoconstriction) as a compensatory mechanism and shift more blood to the vital organs (heart, lungs, and brain). Vasodilation therapy relaxes vascular tone and may decrease venous return.

Raised intrathoracic pressure decreases venous return. Tension pneumothorax, the Valsalva maneuver, breath holding in children, prolonged bouts of coughing, and positive-pressure ventilation increase intrathoracic pressure and thereby decrease venous return.

Clinical Applications of Ventricular Function Curves

Preload is the major determinant of contractility, but ideal filling pressures vary greatly with cardiac compliance and the patient’s condition. Ventricular function curves may be constructed to find a patient’s ideal filling pressure at a given time and provide information about ventricular compliance. Most commonly, they are used when large amounts of fluid are administered; however, they may also be used to monitor CO response to changes in filling pressure resulting from volume unloading (diuresis) and administration of intravenous cardiopulmonary drugs such as inotropes and vasodilators.

To construct a ventricular function curve, CI, CO, SV, or another measure of heart output is plotted on the vertical axis. Filling pressure (usually pulmonary artery diastolic or PAWP) is plotted on the horizontal axis. A baseline CO measurement is obtained, and the point corresponding to the CO reading and simultaneous pressure reading is plotted (Fig. 16-5A). A fluid challenge is administered, and another set of output and pressure measurements is obtained. Pressure is again plotted against output. As the plotting continues, a Starling (or ventricular function) curve is created. When satisfactory CO is achieved or when CO begins to decline as the filling pressure increases, the fluid challenge is stopped. The pressure that corresponds to the highest CO reading obtained is used to indicate optimal preload. Volume can then be administered as needed to maintain this optimal pressure. It is important to remember that the venous system will begin to “relax” and expand as the volume status is corrected, so it is necessary to follow the patient carefully and reassess the need for additional volume.

FIGURE 16-5 Ventricular function curves constructed to determine optimal filling pressure using pulmonary artery wedge pressure (PAWP, mm Hg) as the filling pressure measurement and cardiac output (CO, L/min) as the heart output measurement. A, Fluid challenge curve for a patient with low output (CO 2.4 L/min) and low filling pressure (PAWP 4 mm Hg) treated with four intravenous (IV) fluid challenges. Administrations of the first three fluid challenges (a-c) were followed by increases in filling pressure and output (↑ PAWP to 8, ↑ CO to 3.3). After the fourth challenge (d), filling pressure continued to increase, but output began to fall (e) (↑ PAWP to 16, ↓ CO to 3.5), suggesting volume overload. The fluid challenge was stopped. Subsequent measurements confirmed that output increased as the filling pressure dropped back toward normal (f) (↓ PAWP to 12, ↑ CO to 4.1). An optimal filling pressure near 12 mm Hg using PAWP was suggested. B, Diuresis curve for a heart failure patient with low cardiac output (2.2 L/min) and high filling pressure (PAWP 23 mm Hg) treated with two doses of IV furosemide. Diuresis after the first dose of furosemide decreased the filling pressure with a corresponding improvement in heart output (b) (↓ PAWP to 19, ↑ CO to 3.3). A second dose of furosemide was given to further unload the ventricle and improve pulmonary congestion. Filling pressure decreased toward the normal range and output improved (c-d) (↓ PAWP to 14, ↑ CO to 3.9). However, continuing diuresis caused the filling pressure and the output to drop (e) (↓ PAWP to 11, ↓ CO to 3.0). A fluid challenge was given to increase filling pressure and output improved (f) (↑ PAWP to 14, ↑ CO to 3.9). An optimal filling pressure near 14 mm Hg using PAWP was suggested.

Effects of Mechanical Ventilation on Preload and Venous Return

Normal Spontaneous Breathing

During normal spontaneous inspiration, contraction of the diaphragm and enlargement of the thoracic cage reduce the intrapleural pressure to approximately −6 cm H2O. The drop in intrapleural pressure increases the negative gradient between the intrathoracic and extrathoracic vessels. This higher gradient favors the movement of blood into the chest and heart, thus increasing venous return. Because the negative inspiratory pressure is also transferred to the heart, more blood is pulled in the right atrium, which augments preload.

During spontaneous expiration, the reverse occurs. Recoil of the thoracic cage causes the intrathoracic pressure to rise, augmenting CO and creating the slight rise in arterial blood pressure that is normally seen with expiration. Thus, spontaneous inspiration functions as a circulatory assist pump for the heart. During labored breathing, as often seen in the patient having a severe asthma attack, these pressure swings are exaggerated and may result in a paradoxical pulse, which is a drop in blood pressure of more than 10 mm Hg during inspiration.

Positive-Pressure Ventilation and Compliance

The effect of positive-pressure ventilation on venous return depends on how much of the airway pressure is transferred to the pleural space. When lung and thorax compliances are equal, only about half of the change in airway pressure is transmitted to the pleural space. If the lung compliance decreases, as occurs with certain types of respiratory failure, less positive pressure is transmitted to the pleural space; thus, these patients can tolerate positive-pressure ventilation better and may experience little effect on cardiovascular function.

When chest wall compliance decreases, as commonly seen with abdominal distention or after thoracic or abdominal surgery, more airway pressure is transmitted to the pleural space. If chest wall compliance is decreased while lung compliance is increased (e.g., chronic obstructive pulmonary disease), even more of the elevated airway pressure is transmitted to the pleural space. These patients are more likely to develop problems of both decreased venous return and increased pulmonary vascular resistance during positive-pressure ventilation, with the potential result being a reduction in CO.


Positive expiratory pressures, including auto-PEEP (intrinsic PEEP), exaggerate the inspiratory effects of positive-pressure ventilation and maintain increased intrapleural pressure throughout expiration, thus having an even greater potential for decreasing venous return. It has been shown that venous return is affected most by continuous mechanical ventilation (CMV) with PEEP. However, if intravascular volume is maintained or increased to offset the ventilator-induced reduction in venous return, CO may not be affected when positive airway pressure is used. The effect of mechanical ventilation on vascular pressure measurements is discussed in Chapter 15.


Afterload, the resistance or sum of the external factors that oppose ventricular ejection, has the following two components:

Ventricular Wall Stress

Ventricular wall stress is directly related to the tension on the wall of the ventricle (ventricular pressure × radius) and inversely related to the wall thickness. Cardiac factors that decrease ventricular emptying include the following:

Peripheral Resistance

The peripheral component of afterload is determined by the following:

Increased Vascular Resistance

The radius of the vessels is the greatest determinant of peripheral resistance to blood flow. In the presence of vasoconstriction, the heart must exert more energy to eject the blood. As afterload increases, the myocardial oxygen demands on the heart also increase. When the heart is receiving an inadequate supply of oxygen (as occurs with coronary artery disease), it is not able to produce the amount of energy needed to eject efficiently against the afterload, and failure worsens. A downward cycle of cardiac failure ensues if afterload is not decreased; inadequate CO causes vasoconstriction, which causes increased work for the heart, resulting in less CO and more vasoconstriction, and so on. The cycle is broken by maximizing cardiac oxygenation and performance and decreasing the afterload, either by vasodilator therapy or with a cardiac assist device such as an intra-aortic balloon pump.

Afterload also increases as the viscosity of the blood increases. This is an important consideration in some patients with chronic pulmonary disease because the concentration of red blood cells often rises above normal in order to increase their oxygen-carrying capacity (see Chapter 7). When hematocrit levels exceed 60%, CO often decreases. Conversely, one of the causes of high CO (hyperdynamic state) is anemia (low hematocrit).

Blood flow is also dependent on a pressure gradient. When the backpressure in the venous system increases, as occurs when the right heart is not able to pump blood efficiently, the pressure gradient across the capillary beds decreases. Blood flow from the arteries through the capillaries to the venous system slows. This damming effect causes the afterload to increase, which can lead to left heart failure.

Decreased Vascular Resistance
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