Cardiac Output Measurement Techniques (Invasive)
PREREQUISITE NURSING KNOWLEDGE
• Understanding of normal anatomy and physiology of the cardiovascular system and pulmonary system is necessary.
• Understanding of basic dysrhythmia recognition and treatment of life-threatening dysrhythmias is needed.
• Pathophysiologic changes associated with structural heart disease (e.g., ventricular dysfunction from myocardial infarction, diastolic or systolic changes and valve dysfunction) should be understood.
• Understanding of the principles of aseptic technique is necessary.
• Understanding of the pulmonary artery (PA) catheter (see Fig. 73-1), lumens and ports, and the location of the PA catheter in the heart and PA (see Fig. 73-2) is needed.
• Multiple pressure transducer systems (see Procedure 76) should be understood.
• Competence in the use and clinical application of hemodynamic waveforms and values obtained with a PA catheter is necessary. Hemodynamic waveform interpretation of right atrial pressure (RAP) or central venous pressure (CVP), pulmonary artery pressure (PAP), and pulmonary artery occlusion pressure (PAOP) or pulmonary artery wedge pressure (PAWP) provides confirmation of proper catheter placement.
• Knowledge of vasoactive and inotropic medications and their effects on cardiac function, ventricular function, coronary vessels, and vascular smooth muscles is needed.
• Cardiac output (CO) is defined as the amount of blood ejected by the left ventricle per minute and is the product of stroke volume (SV) and heart rate (HR). It is measured in liters per minute.
• Normal CO is 4 to 8 L/min. The four physiologic factors that affect CO are preload, afterload, contractility, and heart rate.
• Stroke volume is the amount of blood volume ejected from either ventricle during one beat. Left ventricular stroke volume is the difference between left ventricular end-diastolic volume and left ventricular end-systolic volume. Left ventricular stroke volume is normally 60 to 100 mL/beat. Major factors that influence stroke volume are preload, afterload, and contractility.
• Right heart preload refers to the amount of blood in the right ventricle (RV) at the end of diastole and is measured by the RAP or CVP. Elevations in left heart filling pressures may be accompanied by parallel changes in RAP, especially in patients with left systolic ventricular dysfunction. Other factors that affect RAP are venous return, intravascular volume, vascular capacity, and pulmonary pressure. Right heart preload is increased in right heart failure, right ventricular infarction, pericardial tamponade, tension pneumothorax, tricuspid regurgitation, and fluid overload. Right heart preload is decreased in hypovolemic states.
• Left heart preload refers to the amount of blood in the left ventricle (LV) at the end of diastole and is measured by the PAOP or PAWP. When LV preload or end-diastolic volume increases, the muscle fibers are stretched. The increased tension or force of contraction that accompanies an increase in diastolic filling is called the Frank-Starling law. The Frank-Starling law allows the heart to adjust its pumping ability to accommodate various levels of venous return. Note: In patients with advanced chronic LV dysfunction and remodeled hearts (spherical or globular-shaped LV instead of the normal elliptical-shaped LV), the Frank-Starling law does not apply. In these patients, muscle fibers of the heart are already maximally lengthened; as a result, the heart cannot respond significantly to increased filling or stretch with increased force of contraction.
• Afterload refers to the force the ventricular myocardial fibers must overcome to shorten or contract. It is the force that resists contraction. The amount of force the LV must overcome influences the amount of blood ejected into the systemic circulation. Afterload is influenced by peripheral vascular resistance (the force opposing blood flow within the vessels), systolic blood pressure, systolic stress, and systolic impedance. Peripheral resistance is affected by the length and radius of the blood vessel, arterial blood pressure, and venous constriction or dilation. The systolic force of the heart is increased in conditions that cause vasoconstriction (increased afterload), including aortic stenosis, hypertension, or hyperviscosity of blood (e.g., polycythemia). The systolic force of the heart is decreased in conditions that cause vasodilation or decrease the viscosity of blood (e.g., anemia). Right ventricular afterload is measured as pulmonary vascular resistance. Left ventricular afterload is measured as systemic vascular resistance.
• Contractility is defined as the ability of the myocardium to contract and eject blood into the pulmonary or systemic vasculature. Contractility is increased by sympathetic neural stimulation, the release of calcium, and norepinephrine and decreased by parasympathetic neural stimulation, acidosis, and hyperkalemia. Contractility and HR can be influenced by neural, humoral, and pharmacologic factors.
• In addition to stroke volume, CO is affected by heart rate. Normally, nerves of the parasympathetic and sympathetic nervous system regulate heart rate through specialized cardiac electrical cells. Heart rate and rhythm are influenced by neural, humoral, and pharmacologic factors. Decreased HR can be the result of increased parasympathetic neural stimulation, decreased sympathetic neural stimulation, or decreased body temperature. Increased HR can be triggered by exercise, catecholamine release, or hypotension. At HRs greater than 180 beats/min, there may be inadequate time for diastolic filling, resulting in decreased CO. Because multiple factors regulate cardiac performance and impact CO, these factors must be assessed (Fig. 67-1).
• Cardiac index adjusts the CO to an individual’s body size (square meter of body surface area). It is a more precise measurement of cardiac performance than CO.
• Refer to Table 67-1 for normal hemodynamic values and calculations.
Table 67-1
| Parameters | Calculations | Normal Value |
| Body surface area (BSA) | Weight (kg) × height (cm) × 0.007184 | Varies with size (range = 0.58 to 2.9 m2) |
| CO | HR × SV | 4-8 L/min |
| Stroke volume (SV) | CO × 1000 ÷ HR | 60-100 mL/beat |
| Stroke volume index (SVI) | SV ÷ BSA | 30-65 mL/beat/m2 |
| Cardiac index (CI) | CO ÷ BSA | 2.5-4.5 L/min/m2 |
| Heart rate (HR) | 60-100 beats/min | |
| Preload | ||
| Central venous pressure (CVP) or RAP | 2-6 mm Hg | |
| Left atrial pressure (LAP) | 4-12 mm Hg | |
| Pulmonary artery diastolic pressure (PADP) | 5-15 mm Hg | |
| PAOP | 4-12 mm Hg | |
| RVEDP | 0-8 mm Hg | |
| LVEDP | 4-10 mm Hg | |
| Afterload | ||
| Systemic vascular resistance (SVR) | MAP − CVP/RAP × 80 ÷ CO | 900-1400 dynes/s/cm−5 |
| SVR index (SVRI) | MAP − CVP/RAP × 80 ÷ CI | 2000-2400 dynes/s/cm−5/m2 |
| Pulmonary vascular resistance (PVR) | PAMP − PAOP × 80 ÷ CO | 100-250 dynes/s/cm−5 |
| PVR index (PVRI) | PAMP − PAOP × 80 ÷ CI | 255-315 dynes/s/cm−5/m2 |
| Systolic blood pressure | 100-130 mm Hg | |
| Contractility | ||
| Ejection fraction (EF): | ||
| Left | LVEDV × 100 ÷ SV | 60%-75% |
| Right | RVEDV × 100 ÷ SV | 45%-50% |
| Stroke work index: | ||
| Left | SVI (MAP − PAOP) × 0.0136 | 50-62 g-m/m2/beat |
| Right | SVI (MAP − CVP) × 0.0136 | 5-10 g-m/m2/beat |
| Pressures: | ||
| MAP | DBP + ⅓ (SBP − DBP) | 70-105 mm Hg |
| PAMP | PADP + ⅓ (PASP − PADP) | 9-16 mm Hg |
Adapted from Tuggle D: Optimizing hemodynamics: strategies for fluid and medication titration in shock. In Carlson K, editor: AACN advanced critical care nursing, St Louis, 2009, Saunders, 1106; and Ahrens T: Hemodynamic monitoring, Crit Care Nurs Clin N Am 11:19-31, 1999.
• At the bedside, cardiac output measurements are obtained through a PA catheter via the intermittent bolus thermodilution CO method (TDCO) or the continuous CO (CCO) method.
• The TDCO method proceeds as follows:
An injectate (5% dextrose in water) of a known volume (10 mL) and temperature (room or cold temperature) is injected into the right atrium (RA) through the proximal port of the PA catheter. This injectate exits in the RA, where it mixes with blood and flows through the right ventricle to the PA. A thermistor located at the tip of the PA catheter senses the change in blood temperature as the blood passes the tip of the catheter in the PA. The CO is calculated as the difference in temperatures on a time versus temperature curve.
• CO can be calculated from PA catheters with two types of thermistors:
A single thermistor has one inline temperature sensor near the tip of the catheter that lies in the PA when in proper position.
A dual thermistor has two inline temperature sensors, one in the right atrium/superior caval vein (immediately above the injectate port opening) and one near the tip of the catheter (same position as single thermistor). Because a temperature sensor is located in the right atrium, there is no need to enter a “correction factor” or “computation constant” into the computer to account for the loss in thermal indicator (heat) from the hub of the RA injectate port to the RA. Investigators found that the second thermistor improved accuracy when compared with Fick CO measurements and also improved precision or repeatability of CO measurements in both cold and room temperature.4,24 In one study, cold injectate had excellent precision with the standard single-thermistor PA catheter. Researchers concluded that the dual-thermistor PA catheter provided the greatest benefit in decreasing measurement variability when room temperature injections were used to measure CO.4
• The change in temperature over time is plotted as a curve and displayed on the bedside monitor screen. CO is mathematically calculated from the area under the curve and is displayed digitally and graphically on the monitor screen (Fig. 67-2). The area under the curve is inversely proportional to the rate of blood flow. Thus, a high CO is associated with a small area under the curve, whereas a low CO is associated with a large area under the curve (Fig. 67-3, A).
Figure 67-2 A, Examining cardiac output curves to establish reliability of values. B, Normal cardiac output curve with rapid upstroke and smooth progressive decrease in temperature sensing. (B: From Ahrens T: Hemodynamic monitoring, Crit Care Nurs Clin North Am 11[1]:28, 1999.)
• The thermistor near the distal tip of the catheter detects the temperature change and sends a signal to the CO computer and bedside monitor. The computer calculates the CO with the modified Stewart Hamilton equation, and the CO number is displayed on the monitor screen. The average result of three to five measurements is used to determine CO.
• Accuracy of TDCO is dependent on adequate mixing of blood and injectate, forward blood flow, steady baseline temperature in the PA, and appropriate procedural technique.3,16,19 In addition, loss of thermal indicator (heat), respiratory artifact, and hemodynamic instability can cause variability from one injection to another.19,29
• Commercially available closed system delivery sets (CO-Set, Edwards Lifesciences, LLC, Irvine, CA) can be used with both cold and room temperature injectate (Figs. 67-4 and 67-5).
Figure 67-4 Closed injectate delivery system. Cold temperature injectate. (From Edwards Lifesciences, LLC, Irvine, CA.)
Figure 67-5 Closed injectate delivery system. Room temperature injectate. (From Edwards Lifesciences, LLC, Irvine, CA.)
• The CCO method proceeds as follows:
CO can be obtained with a heat-exchange CO catheter. This catheter has a membrane that allows for heat to exchange with blood in the right atrium. Continuous measurement of CO can be performed without the need for injected fluid.
The PA catheter with CCO capability contains a 10-cm thermal filament located close to the injection port (15 to 25 cm from the tip of the catheter, near the proximal lumen port). When a PA catheter is properly placed, the thermal filament section of the catheter is located in the right ventricle. This filament emits a pulsed low heat energy signal in a 30- to 60-second pseudorandom binary (on/off) sequence,2 which allows blood to be heated and the heat signal adequately processed over time as blood passes through the ventricle. A bedside computer constructs thermodilution curves detected from the pseudorandom heat impulses and measures CO automatically. The computer screen displays digital readings updated every 30 to 60 seconds, reflecting the average CO of the preceding 3 to 6 minutes. The CCO eliminates the need for fluid boluses, reduces contamination risk, and provides a continuous CO trend.1,2,29
Because the CCO computer constantly displays and frequently updates the CO, treatment decisions can be expedited. Derived hemodynamic calculations (e.g., cardiac index and systemic vascular resistance) can be obtained with greater frequency, thereby providing up-to-time information in assessment of response to therapies that affect hemodynamics.1
• CCO has been compared with TDCO, transesophageal Doppler scan technique, and aortic transpulmonary technique to determine its precision. Study results all show small bias, limits of agreement, and 95% confidence limits, reflecting that CCO provides accurate measurement of CO and is a reliable method.1,2,6,21,29,36,48
• Adequate mixing of blood and indicator (heat) is necessary for accurate CCO measurements. Conditions that prevent appropriate mixing or directional flow of the indicator or blood include intracardiac shunts or tricuspid regurgitation.
• The CCO method is based on the same physiologic principle as the TDCO method (indicator-dilution technique). The TDCO method uses a bolus of injectate as the indicator for measurement of CO. The CCO method uses heat signals produced by the thermal filament as the indicator. The CCO computer provides a time-averaged rather than instantaneous CO reading. CCO values are influenced by the same principles as TDCO.
• The heated thermal filament has a temperature limit to a maximum of 44°C (111.2° F). When calibrated by the manufacturer, CCO computers produce reliable calculations within a temperature range of 30°C to 40°C (86° F to 104° F) or 31° C to 43° C (87.8° F to 109.4° F). An error message appears if the temperature in the PA is out of range.
• Infusions through proximal lumens should be limited to maintenance of patency of the lumen. Concomitant infusions through the proximal lumen can theoretically affect CCO measurements by altering the pulmonary artery temperature. Studies have shown that such infusions can cause variations in TDCO measurements.18,45 To date, no published data describing the effect of concurrent central line infusions on the accuracy of CCO measurements are available, but large infusions of fluid are discouraged.8,15
• Because bolus injections are not needed with the CCO method, the prevalence of user error is theoretically reduced.14
• The CCO catheter can be used to obtain both CCO and TDCO measurements.
• The CCO does not reflect acute changes in CO values because the updated value on the monitor display is an average of 3 to 6 minutes of data. A delay of approximately 10 or more minutes to detect a change of 1 L/min in CO may occur. When monitoring a patient with an unstable condition that is being aggressively treated with medication or other therapies, one should be aware of the delay in data displayed.
EQUIPMENT
PATIENT AND FAMILY EDUCATION
• Explain the procedure for CO and the reason for its measurement. Include expectations related to sensations during the procedure (the patient should not experience pain or discomfort). 
Rationale: Explanation decreases patient and family anxiety. Preparatory information of sensations decreases patient fear of the impending procedure.
• Explain the monitoring equipment involved, the frequency of measurements, and the goals of therapy. 
Rationale: Explanation encourages the patient and family to ask questions and voice specific concerns about the procedure.
• Explain any potential variations in temperature the patient may or may not experience if a cold injectate is used. 
Rationale: This explanation acknowledges the varying physical responses to the injectate and the possible perception of cold solution and may decrease anxiety associated with the procedure.
PATIENT ASSESSMENT AND PREPARATION
Patient Assessment
• Assess the patient’s history of medication therapy, including medication allergies, recent bolus therapies, and current medication regime. 
Rationale: Medications can influence CO measurements.
• Assess the patient’s medical history for the presence of coronary artery disease, valvular heart disease, and left or right ventricular dysfunction. 
Rationale: Medical history provides baseline information regarding cardiovascular performance.
• Assess current intracardiac pressures and PAP, RAP, and PAOP waveforms. 
Rationale: This assessment ensures the PA catheter is positioned properly with a free-floating thermistor sensor and provides useful information about the presence and severity of mitral and tricuspid valve regurgitation.
• Assess the patient’s vital signs, fluid balance, heart and lung sounds, skin color, temperature, mentation, peripheral pulses, cardiac rate and rhythm, and hemodynamic values. In patients with advanced systolic heart failure, assess for pulsus alternans (alternating strong and weak pulses). 
Rationale: Clinical information provides data regarding blood flow and tissue perfusion. Abnormalities can influence the variability of CO measurements.
Patient Preparation
• Verify correct patient with two identifiers. 
Rationale: Prior to performing a procedure, the nurse should ensure the correct identification of the patient for the intended intervention.
• Ensure that the patient and family understand preprocedural teaching. Answer questions as they arise, and reinforce information as needed. 
Rationale: Understanding of previously taught information is evaluated and reinforced.
• Assist the patient to the supine position. 
Rationale: CO measurements are most accurate in the supine position.
References
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