3 What other hemodynamic variables can be measured or calculated from the pulmonary artery catheter? What are their normal values?

Most PA catheters can also measure cardiac output and mixed venous oxygen saturation (SvO₂). Other variables such as heart rate, systemic blood pressure, and body mass index may be needed to derive additional hemodynamic indices such as those in the following list:

SvO2 Cardiac output Cardiac index Stroke volume Stroke index Systemic vascular resistance Pulmonary vascular resistance

4 In what surgical procedures are pulmonary artery catheters most likely to be placed? What medical problems might influence a clinician’s likelihood to insert a pulmonary artery catheter before surgery?

PA catheters are useful in patients undergoing cardiac surgery (valves, coronary arteries, heart and lung transplantation), liver transplantation, and vascular surgery and in high-risk patients having extensive operative procedures with high likelihood of substantial blood loss and fluid shifts. High-risk patients include those with valvular or ischemic heart disease, compromised ventricular function or pulmonary hypertension, or significant deterioration in other organ function (e.g., liver and kidney). In addition, patients who are hemodynamically unstable (e.g., shock or sepsis) or who have extreme ventilatory requirements (e.g., acute lung injury) are often catheterized to guide therapy.

5 Do pulmonary artery catheters improve patient outcomes?

PA catheters entered regular clinical use in the 1970s and still enjoy widespread use (estimated at more than 1.2 million insertions per year). However, only in the past decade have clinicians investigated in a rigorous fashion their clinical efficacy. The strength of evidence demonstrating a benefit has not been substantial overall, and there was some evidence demonstrating that PA catheters were in fact detrimental. At this time well-designed studies do not demonstrate a benefit in all groups. Certainly the issue continues to be examined and debated. Trials are ongoing in many patient subsets such as sepsis, acute lung injury, and congestive heart failure; such well-designed studies will continue to refine our knowledge of the risks and benefits of PA catheters. Finally it isimporant to note that the data obtained from PA catheterization must guide therapies of proven benefit.

6 What complications are associated with pulmonary artery catheterization?

There are the standard risks associated with central line placement, including infection, pneumothorax, hemothorax, carotid or subclavian artery injury, and nerve injury. Concerning the PA catheter itself, patients with complete left bundle-branch block may develop right bundle-branch block as the catheter passes through the right ventricle, resulting in complete heart block. This may be a transient event or require pacing. Other noted arrhythmias include both supraventricular and ventricular tachyarrhythmias and atrial fibrillation. Other complications include knotting, pulmonary hemorrhage and infarction, thromboembolism and air embolism, bacteremia, endocarditis, and sepsis. Air embolism is especially problematic if the patient has a right-to-left intracardiac shunt. To avoid balloon rupture, slowly inflate the balloon using the minimum pressure necessary to acquire the PAOP waveform and allowing the balloon to passively deflate. Finally and not inconsiderably, a complication of PA catheterization is misinterpreting the data.

7 Summarize the usual presentation, major risk factors, and management of pulmonary artery rupture

Pulmonary artery rupture usually manifests as rapid hypotension with hemoptysis. Major risk factors for pulmonary artery rupture include pulmonary hypertension; cardiopulmonary bypass; hypothermia; and aggressive or excessively prolonged balloon inflation, tip migration, and catheter manipulation. Management includes fluid resuscitation, leaving the PA catheter in place, placing a double-lumen endotracheal tube to isolate the affected lung, reversing anticoagulation if any, and preparing the patient for thoracotomy and possible lobectomy or pneumonectomy. Positive end-expiratory pressure (PEEP) has also been found to be useful to control hemorrhage.

Strategies to decrease the risk of pulmonary hemorrhage include not advancing the PA catheter beyond 55 cm and reviewing a chest radiograph after catheter placement—the catheter should not be noted beyond the lateral mediastinal border. Of course, the balloon should only be inflated during measurments of occlusion pressure and then deflated. Some centers withdraw the catheter slightly between occlusion pressure measurments.

8 How might kinking of the pulmonary artery catheter be avoided?

Pay close attention to the depth of catheter insertion. The distance from the access site to the right ventricle (RV) is 35 cm when either the right internal jugular or subclavian veins are accessed and 45 cm if the left internal jugular or subclavian veins are accessed. The PA tracing should be noted within 15 cm of the RV tracing. PA catheters may be difficult to float when pulmonary hypertension, right ventricular distention, or tricuspid regurgitation is present.

KEY POINTS: Pulmonary Artery Catheterization

1. Pulmonary catheterization has not been shown to improve outcome in all patient subsets. Identifying patients that benefit from such treatment continues to be investigated in rigorous scientific fashion.

2. Evaluate the following issues when considering PA catheterization:

The risks of central venous catheterization and PA insertion are many and serious, and the benefits should be identified before these procedures to justify their use.

What are the indications for PA catheter insertion? Consider their use early rather than late and remove them when their usefulness in directing therapy diminishes.

Ensure that the data obtained from the PA catheter are accurate and interpreted correctly.

Based on the data, what are the therapeutic goals and how will they be achieved?

3. To improve accuracy in interpretation, always consider the timing of the waveforms with the ECG cycle.

9 What is the phlebostatic axis?

Reliable and reproducible measurements of intravascular pressures require a fixed reference point. The level of the right heart, located 5 cm below the angle of Lewis (the sternomanubrial angle), is the commonly accepted reference point and is called the phlebostatic axis.

10 Describe the features of the central venous waveform

See Chapter 25, Question 16 (CVP).

11 Describe the features of the right ventricle waveform

The right ventricle waveform has a rapid upstroke to peak systole, a rapid downstroke, and a small terminal rise at the end of diastole. The peak systolic pressure is found after the QRS complex but before the peak of the T wave. End diastole is found near the end of the QRS complex (Figure 26-1).

Figure 26-1 Right ventricle (RV) waveform.

12 Describe the pulmonary artery waveform

Perhaps the most noticeable change as the catheter tip enters the PA is the upstroke in diastolic pressure (Figure 26-2). Other features include a rapid upstroke, a progressive diastolic runoff, and a dicrotic notch secondary to pulmonic valve closure (Figure 26-3). Peak systole is found after the QRS complex but before the peak of the T wave. End diastole is found near the end of the QRS complex.

Figure 26-2 Diastolic pressure increases as the pulmonary artery (PA) catheter tip crosses from the right ventricle to the PA.

Figure 26-3 Pulmonary artery waveform. Peak systole is found after the QRS complex but before the peak of the T wave. End diastole is found near the end of the QRS complex.

13 Review the pulmonary artery occlusion pressure waveform

Like the CVP waveform, the PAOP has three positive waves (a, c, and v). Typically the a wave is most prominent, and the c wave is nonvisible. The a wave occurs with left atrial contraction, the c wave with mitral valve closure, and the v wave with left atrial filling. Note that the v wave occurs after the T wave of the electrocardiogram (ECG). The a wave is averaged to determine the PAOP (Figure 26-4).

Figure 26-4 Typical pulmonary artery occlusion pressure waveform with the c wave not visible.

14 Contrast spontaneous breathing and positive-pressure mechanical ventilation and their effect on pulmonary artery occlusion pressure waveforms

The measurement desired is a transmural pressure (i.e., the difference between the chamber undergoing measurement and pleural pressure). As pleural pressures are not measured in clinical practice, the next best thing is to measure the pressure when intrathoracic pressure is least. Intrathoracic pressures are least at end-expiration while breathing spontaneously (Figure 26-5). PEEP and active expiration confound interpretation of the PAOP.

Figure 26-5 Comparison of pulmonary artery occlusion pressure waveforms during spontaneous and mechanical ventilation.

15 Pulmonary artery catheter pressures are surrogate measures for what important physiologic variables? What assumptions are made about the variables obtained through pulmonary artery catheterization?

Numerous assumptions are made to try to estimate the most important information, left ventricular end-diastolic volume (LVEDV). First, we are using pressures to estimate volume. Second, although we can measure pulmonary artery systolic, diastolic, and occlusion pressures, we are using these measures to estimate left atrial pressure (LAP) and left ventricular end-diastolic pressure (LVEDP). PA diastolic pressure in the healthy heart is a reliable estimate of PAOP, LAP, and LVEDP. However, clearly these relationships fall apart in the presence of cardiac and lung disease. LVEDP is dependent not only on volume but also on ventricular compliance, which can be decreased by ischemia, ventricular hypertrophy and dilation, septal shifts, aortic stenosis, pericardial effusions, use of inotropic agents, and hypertension; in these situations LAP poorly estimates LVEDP. In this instance estimating LVEDP by measuring the a wave of the PAOP is best. LAP may be higher than LVEDP in the presence of mitral regurgitation, as evidenced by a large v wave on the PAOP waveform (Figure 26-6). Increased pulmonary vascular resistance, present in chronic obstructive pulmonary disease, pulmonary embolic disease, acute respiratory failure, hypoxia, and hypercarbia, also decreases the correlation between PA diastolic and occlusion pressures.

Figure 26-6 A large v wave on a pulmonary artery occlusion pressure trace suggests mitral regurgitation. Note that large v waves can be differentiated from a pulmonary artery (PA) waveform based on their timing in relation to the electrocardiogram. PA systole occurs before the T wave while the left atrial v wave occurs after the T wave.

16 In the presence of a large pulmonary artery occlusion pressure v wave, how should pulmonary artery occlusion pressure be estimated?

The best way to estimate PAOP is to average the a wave (Figure 26-7).

Figure 26-7 Average the height of the a wave to estimate pulmonary artery occlusion pressure in the presence of a large v wave.

17 How might catheter position within the lung lead to errors in interpreting left atrial pressure catheter data?

The zones of West, as described in Chapter 2, describe the pressure relationship between pulmonary arterial, pulmonary venous, and alveolar pressure in different anatomic areas of the lung. The zones can change as a patient’s position and intravascular volume status changes. Mechanical ventilation and PEEP also change the zones. Usually a PA catheter will float into zone 3 and in fact must do so to accurately reflect left atrial pressure because only in zone 3 is there a constant fluid column between the pulmonary artery and left atrium. However, it should be noted that, once the catheter is inserted, the patient’s volume and ventilatory status may change remarkably, and the catheter tip may no longer be in a suitable position for correct interpretation (the catheter didn’t wander—the patient’s physiology wandered!).

ACKNOWLEDGMENT

The author gratefully acknowledges Dr. Robert Taylor for contributing the figures used in this chapter.