Cardiac output or the volume of blood pumped by the heart, delivers oxygen and nutrients to the body to meet metabolic demands. As physiologic demands increase, cardiac output must also increase. Cardiac output is determined by two factors: heart rate and stroke volume. Heart rate multiplied by stroke volume produces cardiac output, expressed in liters per minute (L/min) (see Chapter 1, Figure 1-7).

Heart rate is regulated by both the parasympathetic and sympathetic nervous systems. As metabolic demands increase, heart rate should also increase to provide adequate cardiac output. Careful consideration should be paid to this rising heart rate, as excessively rapid heart rates are associated with decreased diastolic filling time, which contributes to cardiac ischemia, decreased contractility, and reduced cardiac output.

Stroke volume is the amount of blood pumped from the ventricle with each cardiac contraction, usually measured in milliliters (mL). It is calculated in the cardiac catheterization laboratory by subtracting the end-systolic volume from the end-diastolic volume within the ventricle (see Chapter 1, Figure 1-8). Stroke volume is determined by three factors: preload, afterload, and contractility. When using the PAC it is calculated by dividing the cardiac output by the heart rate.

Preload is a measure of force, but conceptually, it relates to the end-diastolic volume of the ventricle. The stretch of the cardiac muscle fibers at the end of diastole is directly related to ventricular compliance. For example, a heart with a thick ventricular wall and decreased compliance will require increased preload, or volume, compared with a heart of normal size with normal compliance. Decreased preload in an injured heart greatly decreases stroke volume, ultimately decreasing cardiac output. Measurement of pressure in the right atrium (RAP) is used as a proxy for preload volume in the right heart, and PAOP is used to estimate preload volume in the left heart.

Afterload is the tension against which the ventricular muscle fibers must eject during systole. Afterload is affected by ventricular size, ventricular wall thickness, and blood pressure. A quantitative assessment of afterload can be calculated using hemodynamic pressure and flow data obtained from the PAC. The calculations for pulmonary vascular resistance (PVR), and systemic vascular resistance (SVR) are listed in Box 5-2.

PVR represents the afterload on the right ventricle. When pressures in the pulmonary vasculature rise, as is seen with volume overload or left heart failure, PVR increases, which results in an increased afterload for the right ventricle. Any increase in PVR increases the workload of the right ventricle.

SVR represents the afterload on the left ventricle. Increased afterload may be seen with conditions that cause vasoconstriction, for example, systemic hypertension or hypothermia induced vasoconstriction. Afterload reduction can be accomplished with peripheral vasodilators such as nitroprusside or nitroglycerin. Decreased afterload is seen in conditions that cause vasodilation, for example, hyperthermia and sepsis-induced vasodilation. Afterload or SVR may be increased by using vasopressors such as phenylephrine or norepinephrine. Although increasing SVR may improve blood pressure initially, the increased afterload may ultimately decrease cardiac output if there is a fall in the ejected stoke volume in a poorly contractile heart. The physiologic effects of vasopressors, vasodilators, and inotrope medications are discussed in detail in Chapter 9.

Contractility is the ability of the heart muscle to forcibly contract and, thus, to eject blood. Independent of preload and afterload, many forces may affect contractility. Sympathetic activity and circulating catecholamines may increase contractility. In addition, various medication infusions such as epinephrine, dobutamine, and milrinone are used to improve contractility. Contractility may decrease with acidosis, electrolyte abnormalities, hypoxia, ischemia, or medications that slow the heart rate such as beta-blockers. Sepsis may decrease cardiac output and contractility because of the effects of circulating cytokines. Myocardial infarction also decreases contractility due to lack of myocardial blood flow and poor oxygenation to the area of damaged heart muscle.

The PAC is used to assess volume status, for regulating fluid management, monitoring cardiac output, and titration of vasoactive and inotropic medications. Pulmonary artery catheterization is necessary for the diagnosis of pulmonary hypertension. These catheters are often used in patients undergoing major cardiac or vascular surgery and refractory shock states. The decision to use a PAC should be based on a clinical need. It is important to understand that the catheter is a diagnostic tool and not a therapeutic intervention.

In a 2012 review on the role of the PAC, Jean-Louis Vincent suggested the following indications for use in critically ill patients:

For patients with acute heart failure, the American College of Cardiology (ACC) and the American Heart Association (AHA) have published guidelines for PAC use.¹³ See Table 5-2.

A major benefit of using a PAC is its ability to guide therapy when the patient’s clinical trajectory does not follow an expected pattern, as described in the case study at the end of this chapter. The PAC monitors intracardiac pressures from the right heart, the pulmonary vasculature, and end-diastolic pressures in the left heart (Figure 5-1). The PAC also provides real-time data on volume status, cardiac output, and venous oxygen saturation. In addition, PVR and SVR may be calculated, along with other calculated data to give estimates of left-sided heart function (see Box 5-2). The immediate availability of information is useful in providing ongoing assessment of a patient’s clinical picture to assist a clinician with therapeutic interventions.

Insertion of a Pulmonary Artery Catheter

Intravenous access is obtained by placement of an introducer into a central vein. The PAC is inserted through the introducer. To promote ease of insertion, the preferred site is the right internal jugular (IJ) vein, but other options include the left IJ vein the subclavian vein or the femoral vein. The PAC comes packaged with a natural preformed curve that facilitates placement of the catheter. Given the curve of the catheter, the right IJ vein provides the easiest and most direct access to the right heart. The second best access point is the left subclavian vein. Femoral vein sites are the most challenging and may require placement via fluoroscopy. Black marks on the catheter, at 10 centimeter (cm) intervals, assist with placement.

Once the access for the introducer has been obtained, the PAC is inserted under continued sterile conditions. The balloon at the catheter tip must be tested first by using the syringe provided in the packaging. This syringe has a maximum volume of 1.5 mL and is the only syringe that should be used on the catheter to prevent over inflation of the balloon. The balloon is first inflated and then deflated to ensure integrity. The proximal (RA) and distal (PA) ports are then connected to a transducer setup, and the lines are thoroughly flushed with saline. Finally, if an extra port is available, the line is flushed with saline and a screw cap should be placed on the extra port to exclude all air. A sleeve for the PA catheter must be placed prior to insertion. Once the catheter is inserted into the introducer, the tip is advanced to the right atrium (approximately 15 cm) and a right atrial waveform should be visualized on the monitor (Figure 5-6). At this point, the balloon is inflated. The catheter is then carefully advanced to the right ventricle (see Figure 5-7) and then into the pulmonary artery (see Figure 5-8). The catheter is advanced, or “floated,” using the balloon on the catheter tip, until the tip of the catheter wedges into a small pulmonary blood vessel (see Figure 5-9). Once the catheter is in the wedge position, the PAOP pressure should be noted, and then the air in the balloon is released. Once the balloon is deflated, the PAOP waveform should return back to the PA waveform, with corresponding PA digital pressure values (see Figure 5-7) on the monitor. At this time, the black mark at the insertion site of the PAC should be documented (in cm) to note the distance of the catheter from the insertion site into the heart. If any difficulty arises during the process of advancing the catheter, the balloon should be deflated, and the catheter withdrawn back into the RA to re-attempt insertion. During insertion, the bedside nurse assists the physician or the advanced practice provider with the setup and flushing of the catheter. The nurse will also assist in monitoring the catheter waveforms and electrocardiography (ECG) reading during insertion. Portable anteroposterior chest radiography is performed to confirm placement (Figure 5-10). Once the catheter is correctly placed, waveform analysis may begin.