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.
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
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.
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).
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
|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
|PVR = (MPAP − PAWP)/CO
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
|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).
‡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
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:
where 0.0136 is a conversion factor for changing pressure to work.
Ventricular stroke work is a measure of myocardial work per contraction. It is the product of the stroke volume index (SVI) times the pressure across the vascular bed. Normal left ventricular stroke work index (LVSWI) and right ventricular stroke work index (RVSWI) values are as follows:
End-diastolic ventricular size can be assessed by the end-diastolic volume (EDV), defined as the amount of blood in the ventricle at the end of filling (diastole). The most common indirect method of measuring the end-diastolic ventricular size is the measurement of the end-diastolic pressure (EDP). Further discussion of the EDV and EDP relationship is found in the Ventricular Function Curves section.
Normal EF is 65% to 70%. The EF declines as cardiac function deteriorates. When the EF falls to the 30% range, a patient’s exercise tolerance is severely limited because of the heart’s inability to maintain an adequate CO.
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.
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.
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.
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 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.
Atrial contraction contributes approximately 30% of the subsequent SV and total CO by loading the ventricle at the end of diastole. When a patient develops atrial fibrillation, atrioventricular dissociation, or third-degree heart block or is being paced by a ventricular pacemaker, this so-called “atrial kick” is lost and CO may fall.
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.
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.
Increased intrapleural pressure, as occurs during the Valsalva maneuver, decreases venous returns and thereby may decrease CO. Increased intrapleural pressure also occurs with loss of spontaneous breathing, disruption of the chest wall, collection of fluid or air in the pleural space, or positive-pressure ventilation.
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.
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:
When the ventricle is distended from too much volume and pressure, tension in the muscle increases, and more oxygen and energy are required for contraction. Thus, afterload increases. Similarly, as intrathoracic pressure becomes more negative, the vacuum-like effect favors the opening and filling of the ventricle but increases resistance to ventricular emptying.
Positive intrathoracic pressure favors compression of the ventricle, decreases the pressure gradient across the ventricular wall, and decreases resistance to ventricular emptying but opposes right ventricular filling. Positive-pressure ventilation with PEEP may compress the heart during inspiration, reducing diastolic filling but at the same time enhancing systolic emptying. This combination may be beneficial for many patients in congestive heart failure.
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.