E

Fig. 19. Right heart blood pressure waveforms. As the pulmonary artery catheter is floated into the distal pulmonary artery, the morphology of the pressure waves changes as it goes through the chambers of the heart. CVP, central venous pressure; PA, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; RV, right ventricle pressure.

Fig. 19. Right heart blood pressure waveforms. As the pulmonary artery catheter is floated into the distal pulmonary artery, the morphology of the pressure waves changes as it goes through the chambers of the heart. CVP, central venous pressure; PA, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; RV, right ventricle pressure.

capillary wedge pressures (Fig. 18 [see JPEG 7 on the Companion CD]).

One of the advantages of the pulmonary artery catheter is that blood pressure information associated with the left heart may also be obtained via the pulmonary capillary wedge pressure. Under conditions of normal pulmonary physiology and left ventricular function and compliance, the pulmonary capil lary wedge pressure is proportional to the left ventricular end-diastolic pressure, which is proportional to left ventricular end-diastolic volume. Left ventricular preload is best estimated by left ventricular end-diastolic volume:

cvp ~ pad ~ pcwp ~ lap ~ lvedp ~lvedv where CVP is the central venous pressure, PAD is the pulmonary artery diastolic pressure, PCWP is the pulmonary capillary wedge pressure, LAP is the left atrial pressure, LVEDP is the left ventricular end-diastolic pressure, and LVEDV is the left ventricular end-diastolic volume.

Typically, after establishing central venous access, a pulmonary artery catheter is "floated" into the pulmonary artery with the catheter balloon inflated (see MPEG of pulmonary artery catheter on the Visible Heart® CD). The location of the pulmonary artery catheter balloon is monitored by analysis of the waveform as the catheter is floated from the vena cava to the right atrium, to the right ventricle, and ultimately into the pulmonary artery (Fig. 19). Once the catheter is in the pulmonary artery, it is advanced further until the balloon wedges into a distal arterial branch of the pulmonary artery (Fig. 20). The mean pressure and waveform are the pulmonary capillary wedge pressure. Under normal physiological conditions, this pressure correlates well with the left atrial pressure. However, the pulmonary artery catheter balloon should not be kept inflated for long durations or kept in wedged position because of the possibility of this causing pulmonary artery rupture.

Whenever the catheter is advanced, the balloon (see JPEG 8 on the Companion CD) should be inflated, and when it is pulled

Fig. 20. Floating a pulmonary artery catheter through chambers of a heart until the balloon wedges in the distal pulmonary artery. 1, Tip (balloon) of PA catheter in the right atrium.; 2, tip of PA catheter in the right ventricle; 3, tip of PA catheter in pulmonary artery; 4, tip of PA catheter wedged in the distal pulmonary artery. Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. Diagram courtesy of Sock Lake Group LLC, Roseville, MN.

Fig. 20. Floating a pulmonary artery catheter through chambers of a heart until the balloon wedges in the distal pulmonary artery. 1, Tip (balloon) of PA catheter in the right atrium.; 2, tip of PA catheter in the right ventricle; 3, tip of PA catheter in pulmonary artery; 4, tip of PA catheter wedged in the distal pulmonary artery. Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. Diagram courtesy of Sock Lake Group LLC, Roseville, MN.

back (or removed), the balloon should be deflated. The balloon on most pulmonary artery catheters holds a specific volume of air (1.5 mL). Exceeding this volume may result in balloon rupture or catastrophic pulmonary artery rupture. Most currently available catheter systems come with a balloon inflation syringe that minimizes the risk of such an error.

As with all pressure transducers, the pulmonary artery catheter pressure transducer must be accurately calibrated and zeroed prior to obtaining pressure readings. The pressure transducer should be zeroed at the level midway between the anterior and posterior chest at the level of the sternum; this is usually near the level of the right atrium. The pulmonary artery pressure should be obtained at end expiration (either spontaneous or mechanical ventilations).

Proper positioning of the pulmonary artery catheter in the lung region is important in obtaining accurate pressure measurements. Because a greater portion of blood flow goes to the right lung (~ 55%), the balloon of the pulmonary artery catheter most often floats to the right pulmonary artery. West et al. (9) categorized three lung zones (I, II, III) based on the correlation among pulmonary arterial pressure, alveolar pressure, and venous pressure. Proper placement of the pulmonary artery catheter requires the catheter tip to be in zone III. This is the area in the lung where blood flow is uninterrupted and therefore capable of transmitting the most accurate blood pressure; it is also the zone least affected by airway pressures.

For the pulmonary capillary wedge pressure to correlate best with left atrial pressures, the distal tip of the catheter should be in a patent vascular bed. If the catheter tip is in the area of lung where alveolar pressure is greater than perfusion pressure, the pulmonary capillary wedge pressure will reflect the alveolar pressure and not left atrial pressure. Controlled mechanical ventilation utilizing positive end-expiratory pressure decreases the size of West zone III and may affect correlation of pulmonary capillary wedge pressure and left atrial pressure (4). Other clinical settings in which pulmonary capillary wedge pressure may not accurately reflect left atrial pressure include those for patients with pulmonary vascular disease, mitral valve disease, chronic obstructive pulmonary disease, and those administered positive end-expiratory pressure (10).

It is possible to convert zone III into zone II, and even zone I, with major increases in pulmonary alveolar pressure, such as positive-pressure ventilation and positive end-expiratory pressure (11). Again, conditions such as positive-pressure ventilation, obstructive and restrictive lung disease, and cardiac diseases (i.e., valvular and altered ventricular compliance, tachycardia, and pneumonectomy) are situations for which pulmonary capillary wedge pressures do not accurately correlate with left ventricular end-diastolic pressures (12,13) and hence left ventricular end-diastolic volumes.

The pulmonary capillary wedge pressure waveform is similar to the central venous pressure waveform and occurs at a similar time-point within the cardiac cycle. Myocardial changes (i.e., myocardial ischemia) that commonly occur in compliance and valvular disease will affect the waveform. Large v waves occur with mitral regurgitation, myocardial ischemia, papillary muscle dysfunction, and infarction (Fig. 17). Large v waves may look similar to the pulmonary artery waveform. To prevent errors in interpreting pulmonary capillary wedge pressure and pulmonary artery pressure, the waveform must be viewed and correlated with the ECG tracing. The v wave will always occur after the QRS complex and peak systemic arterial waveform and will not have a dicrotic notch. The pulmonary artery waveform has a dicrotic notch. A large a wave typically occurs in patients with mitral stenosis or left ventricular hypertrophy.

Pulmonary artery catheters may be contraindicated in patients with known abnormal anatomy of the right heart, such as tricus-pid and pulmonic valve stenosis or masses in the right heart. Such catheters may also be contraindicated in patients with left bundle branch block of the myocardial conduction system; floating the pulmonary artery catheter through the right heart may cause right bundle branch block and increase the risk of developing complete heart block. The existence of cardiac pacer leads is not a contraindication, but may make placement of a pulmonary artery catheter more difficult (see MPEG of pulmonary artery catheter and pacer wires on the Visible Heart CD).

Care also must be taken when removing such a catheter. Reported complications associated with pulmonary artery catheters include cardiac arrhythmias, heart block, pulmonary artery rupture, infection, and/or pulmonary infarction (14). During cardiac surgery such as lung and heart transplant, it is possible to have the pulmonary artery catheter inadvertently sutured in the surgical field. Note that any resistance to catheter removal must alert the clinician to the above possibility.

11. CARDIAC OUTPUT/CARDIAC INDEX MONITORING

Determining cardiac output is now considered vital when managing a critically ill patient, particularly those with severe cardiac disease, pulmonary disease, or multiorgan failure. Cardiac output is the total blood flow pumped by the heart, measured in liters per minute (L/min); in an average adult, cardiac output is approx 5-6 L/min. Cardiac output is often equated with global ventricular systolic function. Any increase in demand for oxygen delivery is usually accomplished with an increase in cardiac output. Furthermore, increasing cardiac output is an important factor in oxygen delivery. Cardiac output is dependent on heart rate and stroke volume. In a normal heart, stroke volume is dependent on preload, afterload, and contractility. Myocardial wall motion abnormalities and valvular dysfunction will also affect stroke volume.

Starling's law describes the relationship between cardiac output and left ventricular end-diastolic volume (Fig. 3). As preload is increased, the cardiac output increases in direct proportion to the left ventricular end-diastolic volume until an excessive preload is reached. At this point, increases in left ventricular end-diastolic volume do not result in increased cardiac output and may actually decrease it.

Because of variations in body size and weight, cardiac output is frequently expressed as a cardiac index. Cardiac index is equal to cardiac output divided by body surface area and has a normal range of 2.5-4.3 L/min/m2:

where CO is cardiac output, HR is heart rate, SV is stroke volume, CI is cardiac index, and BSA is body surface area.

The equation for cardiac output can be derived by rearranging the oxygen extraction equation. Oxygen extraction is the product of cardiac output and the difference between arterio-venous oxygen content:

where VO2 is oxygen extraction, CO is cardiac output, CaO2 is arterial oxygen content, and CvO2 = venous oxygen content.

Rearranging the oxygen extraction equation allows calculation of cardiac output:

A limitation of the Fick method is that frequent blood samples from the arterial and venous circulation are required. Expiratory gas must also be analyzed to measure oxygen consumption.

Cardiac output can also be measured by utilizing an indicator (dye) dilution technique or a thermodilution technique. In the indicator dilution technique, a nontoxic dye (e.g., methylene blue or indocyanine green) is injected into the right heart. The dye mixes with blood and goes out the pulmonary artery to the systemic circulation. A circulating arterial blood sample with diluted indicator dye is collected and measured using spectrophotometric analysis. Repeat cardiac output measure

Fig 21. Cardiac output monitoring. Cardiac output is inversely proportional to the area under the thermodilution curve.

ments utilizing the indicator dilution technique are limited because of increasing concentrations of dye with each subsequent measurement.

The thermodilution method to measure cardiac output is a modification of the indicator dilution technique initially described by Fegler (15) in 1954. Thermodilution techniques are not affected by recirculation, as are the indicator dilution techniques. Typically, the distal tips of the pulmonary artery catheters contain thermistors that detect temperatures of the blood. The more proximal portion of the pulmonary artery catheter contains an opening that allows for injection of fluid such as normal saline or D5W (dextrose 5% in water). The injected solution may be at an ambient temperature or iced. An iced solution increases the temperature differential and therefore the signal-to-noise ratio (16); thus, it is considered better than an injectate at room temperature.

A computer program within the monitoring system commonly calculates the cardiac output utilizing the thermodilution cardiac output equation. The components of the equation include the following: specific heat of blood, specific gravity of blood and injectate, volume of injectate, and area of blood temperature curve. A modified Stewart-Hamilton equation (17) can also be used to calculate cardiac output:

CO = V(Tb - T) X K x K2//ATb(i)di where CO is cardiac output in liters per minute, V is volume of injectate (mL), Tb is initial blood temperature (°C), Ti is initial injectate temperature, K1 is density factor, K2 is a computation constant, and ¡ATb(t)dt is the integral of blood temperature change over time.

Cardiac output is inversely proportional to the area under the curve (Fig. 21).

Nevertheless, an accurate calculation of cardiac output requires both proper position of the pulmonary artery catheter and a consistent volume of injectate. Situations such as tricuspid and pulmonic value regurgitation and intracardiac shunts will cause recirculation of blood and thus result in false elevation of cardiac output. The errors of intermittent bolus thermodilution techniques include volume and temperature of injectate, technique of injection, and timing of injection with the respiratory cycle (18). Cardiac output measurements are also affected by clinical conditions such as tricuspid insufficiency, intracardiac shunts, or atrial fibrillation (10).

The accuracy of the system depends on the measurement of temperature differences from the injection port to the distal measurement thermistor. In the thermodilution technique, the volume of injectate must be constant (10 mL). Smaller amounts of cold solution reaching the thermistor will result in a higher cardiac output. Such detected differences may be caused by actual increased cardiac output, small amounts of injectate, warm indicator or injectate, a clot on the thermistor, or a wedged catheter. A calculated small cardiac output will result when the blood reaching the thermistor is too cold; this may occur if there is too large an amount of injectate, if the solution is too cold, if there is an actual decrease in cardiac output, or if the patient has an intracardiac shunt.

Continuous cardiac output monitoring has been made possible with advanced pulmonary artery catheters (see JPEG 9 on the Companion CD). Typically, continuous cardiac output monitors utilize a thermal coil positioned in the right ventricle; this coil intermittently heats the blood. Once the continuous cardiac output catheter and system reach a steady state with the surroundings, the thermal coil intermittently heats blood. The temperature change of the surrounding blood is detected by a thermistor located at the distal tip of the pulmonary artery catheter. The recorded blood temperature varies inversely with cardiac output.

A major limitation of the continuous cardiac output method is its slow response time to acute changes in cardiac output (18,19). Although the response time may be slow, it is still faster in detecting cardiac output changes than the traditional intermittent thermodilution technique. In general, continuous cardiac output monitoring is considered more accurate than the intermittent thermodilution technique (20,21).

Noninvasive methods to measure cardiac output include Doppler modalities, transpulmonary dilution technique (22,23), gas rebreathing technology (23,24), and bioimpedance (23,25, 26) technique. Briefly, the noninvasive Doppler method to measure cardiac output is an esophageal Doppler monitor. An esophageal Doppler probe is placed, and an ultrasound beam is directed at the descending aorta. By knowing the cross-sectional area of the aorta and blood velocity, the stroke volume is calculated (23).

The transpulmonary dilution method for measuring cardiac output requires injections of an indicator (lithium or thermodilution) in the venous circulation (central or peripheral) and subsequent assessment of the indicator level of the systemic arterial circulation; a typical example is the lithium chloride solution technique (27-29). Lithium chloride indicator is injected through a central or peripheral vein, and the plasma concentration of this indicator is measured via a lithium-specific electrode connected to the arterial line (30). A concentration-time curve is generated, and cardiac output is calculated from the area under the curve associated with the lithium ion concentrations (31).

The thoracic bioimpedance method measures cardiac output by detecting the change in flow of electricity with alteration in blood flow (23). For thoracic bioimpedance, a low-amplitude and high-frequency current is transmitted and then sensed by sets of electrodes placed on both sides of the thorax and neck. The cardiac alterations in impedance (resistance to current flow) are analyzed and calculated as the blood volume changes for each heartbeat (stroke volume). The thoracic bioimpedance method of measuring cardiac output may be useful in clinical situations such as major trauma (32,33) and cardiac disease (34).

Gas technology utilizing the measurement of carbon dioxide (23,35) applies the Fick principle of oxygen consumption and cardiac output, but substitutes carbon dioxide production for oxygen consumption. By determining the change in CO2 production and end-tidal CO2, modification of the Fick equation can be applied to calculate cardiac output (36):

CO = AVCO2/AEtCO2

where CO is cardiac output, AVCO2 is change in CO2 production, and AEtCO2 is end-tidal CO2.

It should be noted that the accuracy of the carbon dioxide rebreathing method to measure cardiac output is, at present, inconclusive (36-39).

Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

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