The functional components of the PAC are outlined in Table 107–1. Direct parameters obtained from the PAC are outlined in Table 107–2.
Table 107–1PAC: functional components. ||Download (.pdf) Table 107–1 PAC: functional components.
|Component ||Function |
|110-cm length ||This length allows passage from the femoral vein to the PA if the neck veins are not accessible |
|Distal PA lumen ||Used to monitor pressure waveforms during PAC insertion and continuous PAP after insertion; PAOP during balloon inflation; true mixed venous blood gas sampling |
|Proximal RA lumen ||CVP/RAP monitoring, fluid bolus for thermodilution CO, infusions |
|Proximal infusion port (VIP) ||Additional infusion port; can perform the functions of the proximal RA lumen port if the RA port becomes occluded |
|Balloon ||Filled via the inflation port during insertion to protect the endocardium from the PAC tip and carry the PAC forward through the right heart; inflated after PAC placement in the PA to determine proper positioning of the PAC; when inflated may provide PAOP |
|Thermistor ||4 cm proximal to the tip; monitors core body temperature; senses temperature change used for thermodilution CO |
Table 107–2PAC: direct measurements. ||Download (.pdf) Table 107–2 PAC: direct measurements.
|Direct Data ||Accuracy ||Comments ||Additional Information |
|CVP/RAP (normal: < 8 mm Hg) ||Accurately reflects central venous pressure which is equal to right atrial pressure; RAP = RVEDP in the absence of TR; both CVP and RAP are inaccurate determinants of intravascular volume or RV preload. ||This parameter should not be used for hemodynamic clinical decision making. ||This parameter does not require a PAC and may be obtained via a central venous catheter. In the PAC the proximal infusion port will be usually located in the SVC, but may also be located within RA or less commonly within the introducer catheter. |
|RV pressures (systolic/diastolic) 15-30/0-8 mm Hg (normal) ||Accurately reflects RV pressures. ||Noted during PAC insertion; RV pressures are not present after the distal tip passes into the pulmonary artery. ||RV systolic pressure is normally equal to the PA systolic pressure; RV diastolic pressure is normally equal to the mean right atrial pressure. |
|Pulmonary artery pressures (systolic/diastolic) 15-30/4-12 mm Hg; mean: ≤ 20 mm Hg (normal) ||Accurately reflects continuous PA pressures; more accurate than PAP estimated by echocardiography. ||Continuously displayed and monitored from the distal port once PAC is in final position in the pulmonary artery. ||The true left ventricular end-diastolic pressure is less than the PAD pressure. |
|PAOP < 12 mm Hg (normal) ||The pressure obtained after the PAC balloon is inflated when the tip of the PAC is in the PA. Highly inaccurate, does not reflect LVEDP, LV preload, or intravascular volume. ||The most inaccurate parameter derived from the PAC. Interpretation errors, physiologic/pathologic limitations. ||The main purpose of balloon inflation should not be to determine a PAOP per se, but to determine that the PAC tip is not located too distally in the PA. |
|Hemodynamic waveforms ||a, c, v waves in RAP tracing; a, v waves in PAOP tracing. ||Waveforms are difficult to visualize with standard ICU monitoring equipment. ||Waves may be absent in pathologic conditions, eg, large v waves absent with atrial enlargement. |
|Core body temperature (CBT) ||Most accurate measure of CBT. ||Measured by a thermistor 4 cm proximal to the PAC tip. ||PAC thermistor readings are altered by rapid fluid infusions and sequential compression/decompression devices leading to errors in CO measurement. |
Thermodilution cardiac output
3-7 L/min (normal)
|Considered the practical “gold standard” for CO measurement; inaccurate in certain situations. ||Right heart thermodilution is an indicator dilution method. Under ideal conditions accuracy is within 10%-20% of true CO. ||Average 3 measurements; do not measure during rapid fluid infusions, SCD inflation, inaccurate in the presence of tricuspid regurgitation. |
|True mixed venous blood gases ||Most accurate representation of global venous blood; central venous blood gases may sample SVC or IVC blood preferentially and do not reflect true mixed venous blood. ||Represent “true” mixed venous blood as the blood is drawn distal to the right ventricle, after the mixing of SVC and IVC blood. ||Svo2 must be interpreted relative to hemoglobin and CO; Pvco2 is a more accurate indicator of flow than Svo2. |
Pressure information derived from the PAC includes CVP, right ventricular (RV) systolic pressure, RV diastolic pressure, PA systolic and PA diastolic pressure and the PAOP (also called the pulmonary capillary wedge pressure [PCWP] or pulmonary artery wedge pressure [PAWP]). CVP measurement does not require a PAC, only a central venous catheter.
Before the PAC was developed, CVP was recommended as a simple measure of intravascular volume and RV filling or preload. Ventricular preload is the ventricular end-diastolic volume. Either absolute CVP or changes in CVP were proposed to differentiate decreased, normal, or increased intravascular volume or RV preload. However, there is no correlation between CVP and blood volume or cardiac preload in critically ill patients or normal volunteers.4,5,6
CVP does not reflect left ventricular end-diastolic pressure (LVEDP) and the major reason the PAC was designed was to provide information about left heart function. The PAC was proposed to provide information about the function of the left ventricle (LV) by occluding a segment of the pulmonary artery via the balloon at the PAC tip, creating a no-flow situation in the vessel, thus the pressure at the PAC tip, the PAOP, would be equal to the pulmonary capillary pressure, pulmonary venous pressure, left atrial pressure, and the LVEDP. In both published research and at the bedside, the PAOP often became equated with LV preload. However, subsequent radionuclide and echocardiography studies have shown that the PAOP does not correlate with LV preload or intravascular volume.7,8 Pressures do not correlate with volume due to alterations in cardiac compliance induced by positive pressure ventilation, positive end-expiratory pressure (PEEP), intra-abdominal pressure, pulmonary vascular disease, cardiac hypertrophy, ischemia, inopressors, and that the heart functions as a suction pump, that is, diastole is active and can create negative pressures within the chambers.9 In fact the PAOP may not even reflect the LVEDP due to pathophysiologic factors (eg, mitral valve disease, pulmonary parenchymal and vascular disease) or that PAOP is a very difficult parameter to measure accurately.8,10 It has also been demonstrated that in stable patients on mechanical ventilation, the PAOP can vary as much as 7 mm Hg in 40% of patients.11
The acronym “PCWP” perhaps best describes its role in hemodynamic monitoring: Parameter that Commonly gives Wrong information about the Patient. The most reliable pressure measurements provided by the PAC are the PA artery systolic and PA diastolic pressures.
PAC CO measurement utilizes the indicator-dilution principle using a thermal load as the indicator, called right heart thermodilution. The thermistor located near the tip of the PAC continuously monitors core body temperature in the PA. There is also an external temperature probe measuring the injectate temperature. To obtain a CO measurement, a thermal load (commonly 10 mL of room temperature fluid [saline or D5W]) is injected rapidly via the proximal (CVP) infusion port and cools the blood as it travels through the right heart, into the PA and as this cooled blood (indicator) passes the thermistor, the temperature change over time is recorded. The monitor displays the curve of temperature over time and the area under the curve is inversely proportional to the rate of blood flow in the pulmonary artery. These data are converted by the monitor into the CO in liters per minute using the Stewart-Hamilton equation:
Where, V1 is the injectate volume, TB is the blood temperature, TI is the injectate temperature, K1 is the injectate density factor, K2 is a computation constant accounting for the catheter dead space and the heat exchange during transit, and ∫ΔTB(t)dt is the area under the time-temperature curve.
A single CO measurement is approximately within 30% of the actual CO. When the average of the 3 closest CO measurements are made, accuracy is within 10% to 20% of the actual CO.12 Average at least 3 similar measurements, for example, within 10% to 15% of the median value discarding those outside this range.13
Right heart thermodilution CO is considered the practical gold standard for CO measurement, but there are conditions that can affect the accuracy of thermodilution CO. These include the following:
Tricuspid regurgitation (TR). Either falsely low (commonly) or falsely high CO as the regurgitant flow causes changes in the temperature curve due to recirculation or loss of indicator. Echocardiography can assess for TR. If there is significant TR another CO method must be used to determine the CO.
Rapid infusion of intravenous (IV) fluids via the introducer port and proximal infusion or VIP port can reduce the thermistor temperature leading to a smaller temperature change and a falsely low CO.
Intermittent SCD. Not in use at the time the PAC was introduced, but very common today, SCD—used to reduce the incidence of deep venous thrombosis (DVT)—increase the flow of relatively colder blood from the lower extremities when they inflate. If thermodilution CO is performed during inflation of the SCD, the thermistor (reading a lower temperature) will sense a smaller temperature change leading to a falsely low CO determination.14
Injectate volume. If less than the expected (eg, 10 mL) injectate volume is injected, a falsely high CO will occur due to a more rapid than expected temperature change.
Respiratory variation can change the temperature of PA blood and alter the CO.
Intracardiac left-to-right shunts, for example, ventricular septal defect (VSD).
The wrong CO computation constant setting in the monitor. The injectate temperature range and the PAC model determine the computation constant.
Thus holding rapid fluid infusion via the introducer, proximal infusion port, and VIP port of the PAC for at least 30 seconds, turning off the inflation of SCD, and timing the start of injection to the same point of the respiratory cycle, for example, end expiration, improves the accuracy of thermodilution CO. Room temperature injectate is used since ice-cooled injectate does not increase the accuracy13 and is more burdensome. However, in the setting of hypothermia (low TB ie, 29°C-30°C) ice-cooled injectate should be used to improve the accuracy by increasing the temperature difference between blood and injectate.
Hemodynamic waveforms from the PAC consist of “a,” “c,”, and “v” waves in the right atrial pressure (RAP) tracing and “a” and “v” waves in the PAOP tracing (Figure 107–5). The “a” wave due to atrial contraction occurs after the P wave of the electrocardiogram (ECG). The “c” wave in the RAP waveform is caused by tricuspid valve closure, the “c” wave caused by mitral valve closure is too small to be reflected across the pulmonary vascular bed, and hence the “c” wave is absent from the PAOP waveform. The “v” wave is caused by filling of the atria against a closed atrioventricular valve during ventricular contraction occurs after the ECG T wave. The downslope after an “a” wave is called the “x” descent and similarly for the “v” wave is called the “y” descent (not labeled in Figure 107–5).
Right atrial pressure tracing demonstrating “a,” “c,” and “v” waves relative to cardiac events on the ECG tracing.15 (Reproduced with permission from Oropello JM, Leibowitz AB, Geffroy V, et al: Hemodynamic Waveform Detection from Pulmonary Artery Catheters in the ICU, J Intensive Care Med 1999;14(1):46-51.)
Large (cannon) “a” waves may be seen with atrioventricular dissociation. Large “v” waves may be seen with TR or mitral valve regurgitation (MR), decreased ventricular compliance or (in the RAP waveform) with a VSD. Enlarged “v” waves may be absent in TR or MR if the right or left atrium is enlarged. An echocardiogram is more specific and sensitive for the detection of TR and MR. In cardiac tamponade early diastolic compression can lead to a prominent “x” descent. In constrictive pericarditis, late diastolic limitation of ventricular expansion can lead to a prominent “y” descent. However in practice, echocardiography is more sensitive and specific for diagnosis if these conditions are suspected.
In reports about hemodynamic waveforms in patients with these and other cardiac disorders, the waveforms are usually obtained in the cardiac catheterization laboratory or coronary care unit setting using equipment that is more sensitive than that used in the general noncoronary intensive care unit (ICU) setting. It is notable that using standard PACs and recording systems in the general ICU setting, no hemodynamic waveform components can be identified in 52% of PAOP tracings and 20% of RAP tracings.15 Increased monitor/recorder sensitivity can enhance the detection of waveform components.
Mixed venous oxygen and carbon dioxide levels provide further information about hemodynamics. The most accurate global venous blood gas, the mixed venous blood gas (MVBG), is obtained by drawing PA blood from the distal port of the PAC. The PA is distal to the mixing of superior vena cava (SVC), inferior vena cava (IVC) blood in the RV. The SVC carries blood returning from the head and upper extremities. Due to the relatively high cerebral metabolic rate of oxygen consumption, SVC oxygen levels are normally lower than in the IVC or mixed venous blood. Depending on tip location, a central line may preferentially sample SVC or IVC blood, thus central venous blood gases may differ from true MVBGs.
The normal mixed venous Po2 (Pvo2) is 40 mm Hg with a mixed venous hemoglobin-oxygen saturation (Svo2) of 75%; it is a mixture of venous return from the SVC and IVC. The normal SVC hemoglobin-oxygen saturation (Ssvco2) is 70% and the normal IVC hemoglobin-oxygen saturation (Sivco2) is 80%. The other important component of the MVBG is the mixed venous carbon dioxide level (Pvco2), which normally is within 5 mm Hg higher than the arterial carbon dioxide level obtained on a simultaneous arterial blood gas (Paco2).
Low or decreased Svo2 levels can result from decreased CO, increased oxygen consumption (vo2), or anemia. A low Svo2 value (eg, 40%) does not necessarily mean that the tissues are not getting enough oxygen or that the CO is decreased or inadequate. For example, if the CO is low and the tissues extract more oxygen per unit of blood flow, the Svo2 will fall, but the tissues may be extracting enough oxygen to meet the metabolic needs. Anemia or increased vo2 (fever, hypermetabolism) can reduce Svo2 despite a normal or increased cardiac output.
High or increased Svo2 levels can result from anatomic systemic left-to-right shunting (arteriovenous [AV] grafts, liver disease) or inability of the cells to utilize oxygen as is commonly seen in sepsis and liver dysfunction as part of the multiple organ failure syndrome—conditions that are the most common in critically ill patients in general medical and surgical ICUs.
Normal Svo2 levels may not indicate that all is well. Normal Svo2 may result from the mixing of venous blood returning from both high and low Svo2 regions, as Svo2 is a global measure.
From the above information, it should be no surprise that Svo2 does not correlate with CO in critically ill patients. Further, looking at Svo2 levels as an indicator of the adequacy of oxygen delivery is similar to looking at the amount of garbage your neighbor throws out to determine if they are getting enough food.
Attempts to increase CO to raise levels of oxygen delivery to arbitrary levels via inotropes or blood transfusions have failed to positively impact patient outcome and may be harmful particularly in older patients.16,17,18
Svo2 levels should be interpreted with regard to hemoglobin level, CO, vo2 and lactate level. Lactate levels correlate more closely with the adequacy of tissue oxygen than Svo2.
Oxygen Content, Delivery, and Consumption
The mixed venous oxygen can be used to calculate oxygen consumption (vo2), which is the difference in AV oxygen content multiplied by the CO. Table 107–3, contains the formulas for oxygen content (CO2), delivery (Do2), and consumption (vo2).
Table 107–3PAC: derived data. ||Download (.pdf) Table 107–3 PAC: derived data.
|Parameter ||Derived From PAC Value ||Formula ||Limitations |
|Stroke volume (SV) ||CO ||CO/HR || |
|Cardiac index (CI) ||CO ||CO/BSA ||CO is more useful in individual patients. CI is used in research, eg, comparing group data; for individual patients the relationship between CO and BSA is nonlinear; BSA is estimated from height and body weight—this adds additional error to any CO error. |
Systemic vascular resistance (SVR)
1100-1500 dynes/s/cm–5 (normal)
|CO, CVP ||MAP - CVP × 80/CO (L/min) ||SVR is not afterload—CVP used in the SVR calculation is not a determinant of LV afterload; a high SVR does not differentiate between intravascular volume depletion, primary LV dysfunction, or low LV due to a high SVR; it is better to note the CO and the arterial BP for analysis and decision making. |
Pulmonary vascular resistance (PVR)
120-450 dynes/s/cm–5 (normal)
|PAP, PAOP, CO ||MPAP - PAOP × 80/CO (L/min) ||Utilizes the least accurate parameter (PAOP) derived from the PAC; it is better to note the CO and the PAP for analysis and decision making. |
Left ventricular stroke work (LVSW)
60-80 g (normal)
|CO, PAOP ||SV × (MAP - PAOP) × 0.0136 ||Utilizes the least accurate parameter (PAOP) derived from the PAC; does not answer the question: is it good to do more work or less work? That depends on the clinical picture. |
|Arterial oxygen content (Cao2) 19-20 mL/dL (normal) ||Not derived from PAC ||Hb (g/dL) × 1.34 × SaO2 + Pao2 × 0.0031 || |
|Mixed venous oxygen content (Cvo2) 15 mL/dL (normal) ||Distal port blood gas ||Hb (g/dL) × 1.34 × Svo2 + Pvo2 × 0.0031 || |
Oxygen delivery (Do2)
900-1100 mL/min (normal)
|CO ||Arterial O2 content × CO (L/min) × 10 ||No clear target parameters affect outcome; some studies demonstrate worse outcomes with intentional increases in oxygen delivery. |
|Oxygen consumption (vo2) 200-250 mL/min (normal) ||Svo2 and CO || |
Arterial mixed venous O2 content × CO × 10
(Normal arterial–mixed venous O2 content difference = 3.5–5.5)
|Consumption normally equals demand, but in critical illness, demand may be higher than consumption, this is usually reflected by increased lactate levels. |
The blood flow to an organ (eg, CO) is equal to the AV difference in the concentration of a substance across the organ multiplied by the release or uptake of that substance by the organ. Using oxygen as the substance and the lung as the organ, CO is equal to the total body oxygen uptake (consumption) as measured by indirect calorimetry divided by the AV oxygen content difference. This is an alternative method to thermodilution indicator-dilution method. The accuracy of Fick-derived CO is limited by considerable inaccuracies in total body oxygen consumption measurement and shunting.
Intracardiac Left-to-Right Shunts
The oxygen levels in the right atrium (RA), RV, and PA are normally similar, for example, Svo2 approximately 75%. An intracardiac left-to-right shunt, for example, VSD, results in step-up in venous oxygen moving from RA to RV to PA from oxygenated LV blood directly ejected into the RV and pulmonary circulation. This can be assessed by sampling blood gases from the distal port of the PAC as it passes each level.
Although Svo2 has garnered the most attention to date, Pvco2 levels correlate more closely with blood flow and CO. A consistent finding is the dissociation between venous and arterial Pco2 (increased P[v-a]co2 gradient) during reductions in blood flow, that is, decreased CO.19,20,21 The normal P[v-a]co2 gradient is less than or equal to 5. The P[v-a]co2 gradient is considered to be increased if it is greater than or equal to 7. Increases in the P[v-a]co2 gradient are inversely proportional to the CO. However, an increased P[v-a]co2 gradient may also be due to an increased metabolic rate. Hypermetabolic rates are usually associated with a fever. An extreme example is malignant hyperthermia which is associated with very high fever and both a hyperdynamic and hypermetabolic state with increased CO and an increased P[v-a]co2 gradient.
Parameters that are derived from PAC data are outlined in Table 107–3. It is important to understand that systemic vascular resistance (SVR) is not equivalent to LV afterload and the pulmonary vascular resistance (PVR) contains an unreliable parameter in its calculation—the PAOP. A more direct approach is to analyze the arterial blood pressures and the pulmonary artery pressure (PAP) in relation to the CO. See Table 107–3 for additional explanation.