Cardiac Catheterization and Hemodynamic Assessment

Cardiac Catheterization and Hemodynamic Assessment

Punag Divanji

Joseph Yang


Since the late 1960s, the use of the Swan-Ganz balloon-tipped catheter for the measurement of intracardiac hemodynamics has been a cornerstone in the diagnosis and management of acute myocardial infarction and cardiogenic shock.1,2 Standard right heart catheterization involves the percutaneous placement of an introducer sheath—commonly into the internal jugular, subclavian, brachial, or femoral veins—with subsequent use of a balloon-tipped catheter for pressure waveform recording, blood co-oximetry measurement, and assessment of thermodilution cardiac output.


When performed in the cardiac catheterization laboratory with fluoroscopy, right heart catheterization can be performed from a variety of venous access points, including the brachial, internal jugular, subclavian, and femoral veins. With the development of smaller caliber (5 and 6 French) catheters and hydrophilic slender sheaths, the brachial vein has become more commonly used (Table 40.2). An antecubital 20-gauge peripheral IV can be placed and then exchanged over a wire in the cardiac catheterization laboratory for a 5- or 6-French sheath. This access point is most comfortable for the patient and virtually eliminates the risk of pneumothorax that can be associated with internal jugular or subclavian access.4 Bedrest is also not required for brachial venous access as compared with femoral venous access. In cases where fluoroscopic guidance is not available (such as at the bedside in the intensive care unit), the right internal jugular vein or the left subclavian vein is the preferred access point, with ultrasound-guided access and hemodynamic waveform-guided advancement.5


The basics of right heart catheterization consist of percutaneous venous access using sterile technique to place an introducer sheath into a central vein with ultrasound guidance. Pressure measurements and blood oximetry can then be obtained using a variety of catheter shapes such as the Multipurpose, Gensini, and Goodale-Lubin. However, the most commonly used catheter remains the balloon-tipped Swan-Ganz catheter, which can also be used to measure both intracardiac filling pressures and cardiac output.2


Patients may present with a wide spectrum of lesions that alter normal cardiac hemodynamics, resulting in symptoms of dyspnea or heart failure. Right heart catheterization allows for the measurement of valuable clinical data to solve difficult diagnostic challenges in the patient with structural heart disease. Careful consideration of the intracardiac pressures and oxygen saturations can allow the clinician to diagnose the cause of symptoms and determine therapeutic options. There are a variety of indications for right heart catheterization, primarily in patients with heart failure, dyspnea, valvular heart disease, or suspected pulmonary hypertension (Table 40.1).

From a number of access sites, the Swan-Ganz pulmonary arterial catheter is advanced through the great veins (superior or inferior vena cava), to the right atrium (RA), the right ventricle (RV), and the pulmonary artery (PA). Importantly, these balloon-tipped, end-hole catheters can be advanced into the smaller pulmonary arterioles, ostensibly occluding inflow and allowing for measurement of the PA occlusion wedge pressure (PAWP). A plethora of data can be attained during this process, including venous and intracardiac pressures, oxygen saturation by chamber, cardiac output, and vascular resistance (by calculation). Additionally, these data can be used to calculate more advanced markers of cardiac function, including pulmonary artery pressure index (PAPi), stroke volume index (SVi), and cardiac power output (CPO) (Table 40.3).6

Hemodynamic Assessment

Right heart catheterization allows for the measurement of venous, intracardiac, and PA pressures, which can be used to determine filling pressures, resistance, and transvalvular gradients. To ensure the validity of the data prior to its clinical use, it is imperative to ensure both accuracy and precision of pressure measurements during catheterization. Thus, it is important to correctly set up the transducer system in every case. Typically, the pressure transducer is mounted on the procedure table (or patient bed, if performed outside of the catheterization laboratory) at the mid-chest level. Transducers are connected to the procedural catheter using plastic tubing filled with sterile saline. The catheter, tubing, and transducer are flushed to eliminate any bubbles, which lead to pressure waveform overdamping. After flushing, the transducer is calibrated at the mid-chest level. This process involves opening the transducer to air and allowing the system to “zero” to atmospheric pressure. Thus, measurements must be taken with a high-fidelity pressure transduction system per institutional standards, with fluid-filled tubing and optimal pressure damping to allow for appropriate interpretation of the tracings. Overdamping, often caused by air bubbles, thrombi, loose connections, or kinked catheters, can lead to underestimation of the systolic pressure, loss of the dicrotic notch, and distorted waveforms. On the other hand, underdamping, caused by excess tubing, excess components, or a defective transducer can lead to a falsely elevated systolic peak pressure, underestimated diastolic pressure, and significant waveform artifact.7

Accurate measurements should be taken at end expiration because the negative intrathoracic pressure produced during inspiration will lower intracardiac pressures. Of note, in intubated patients receiving mechanical ventilation with positive end-expiratory pressure, measurements are either taken at end inspiration, or an expiratory hold maneuver is performed with the ventilator to account for the impact of positive pressure. Venous and atrial pressure measurements are taken as a mean over several cardiac cycles, whereas ventricular pressure measurements are described as systolic and end-diastolic values. Arterial pressure measurements (ie, PA, aorta, peripheral arteries), are composed of systolic, diastolic, and mean values. Under fluoroscopic guidance, the flow-directed PA catheter can be advanced through the vena cava, into the RA, RV, PA, and PA wedge positions, with pressure and oxygen measurements taken in each position sequentially, either during forward advancement or during pullback. This information is then integrated with a comprehensive understanding of normal values to elucidate the clinical and hemodynamic picture.

Intracardiac Pressures

Right Atrium. The RA pressure tracing (Figure 40.1) consists of distinct components, with positive deflections described as “waves,” and negative deflections described as “descents,” with a normal mean RA pressure range of 2 to 6 mm Hg. The “a-wave” represents an increase in RA pressure caused by atrial contraction in late diastole, directly after the P-wave on the electrocardiogram (ECG). This is followed by the “c-wave,” which represents the displacement of the closed tricuspid valve into the RA during the isovolumic contraction phase of early systole, typically occurring at the end of the QRS complex. As ventricular systole continues, the RA relaxes and the tricuspid annulus is pulled down toward the RV apex, resulting in a drop in atrial pressure known as the “x-descent.” Corresponding to the end of the T-wave on ECG, the hemodynamic “v-wave” represents a back-pressure reflection from atrial filling against the closed tricuspid valve during ventricular systole. Finally, the “y-descent,” a pressure decrease caused by the tricuspid valve opening in early diastole, occurs before the P-wave on the ECG. These components combine to form the atrial pressure tracing, and the cause of clinical various presentations can be identified via aberrations in the normal waveform (Table 40.3).

Right Ventricle. Crossing the competent tricuspid valve allows measurement of the RV pressure, which is described by its peak systolic pressure (12-24 mm Hg) and end-diastolic pressure (2-6 mm Hg) (Figure 40.1). However, the pressure tracing can be subdivided into four distinct phases: systole is composed of (1) isovolumetric contraction, from tricuspid valve closure to pulmonic valve opening, and (2) ejection, from pulmonic valve opening to its closure; diastole is composed of (3) isovolumetric relaxation, from pulmonic valve closure to tricuspid valve opening, and (4) filling, from tricuspid valve opening to its closure.

Clinically, elevations in RV systolic pressure occur most commonly in the setting of pulmonary hypertension, but can also be owing to left ventricular (LV) pressure overload, pulmonic valve stenosis, RV outflow tract (RVOT) obstruction, or hemodynamically significant left-to-right shunting. Conversely, reductions in RV systolic pressure can be caused by cardiogenic shock, hypovolemia, or cardiac tamponade.

Similarly, elevations in RV end-diastolic pressure occur most commonly in the setting of volume overload of any cause, such as congestive heart failure, but can also be caused by decreased chamber compliance, ventricular hypertrophy, tricuspid regurgitation, pericardial constriction, or cardiac tamponade. Low RV end-diastolic pressure is primarily caused by hypovolemia but can also occur in the setting of tricuspid valve stenosis.

Pulmonary Artery. Beyond the pulmonic valve and into the main PA, the PA tracing is described by its peak systolic pressure (12-24 mm Hg), diastolic pressure (6-12 mm Hg), and mean pressure (10-22 mm Hg) (Figure 40.1). Similar in appearance to the aortic tracing, albeit with lower pressures, a dicrotic notch is seen in the PA, representing closure of the pulmonic valve.

An elevated PA systolic or diastolic pressure can occur in the setting of pulmonary hypertension (of any cause), mitral stenosis, mitral regurgitation, volume overload, left-to-right
shunting, and pulmonary embolism (PE). A reduced PA systolic or diastolic pressure can occur in the setting of hypovolemia or any lesion restricting PA inflow (tricuspid valve stenosis, pulmonic valve stenosis, RVOT obstruction, tricuspid atresia, Ebstein anomaly). An isolated reduction in PA diastolic pressure (and therefore a wide PA pulse pressure) can occur because of pulmonic valve regurgitation, whereas a reduced PA pulse pressure occurs in the setting of cardiogenic shock, RV infarct, PE, or cardiac tamponade.

Pulmonary Artery Wedge Pressure. The PAWP estimates left atrial (LA) pressure and is used as a measure of left-sided intracardiac filling pressure. In the absence of mitral valve disease or cardiac disease, mean PAWP is similar to mean LV end-diastolic pressure. However, these pressures may be disparate in patients with aortic valvular disease, systemic arterial hypertension, and coronary artery disease, in whom LV end-diastolic pressure exceeds mean PAWP because of LV noncompliance and a prominent a wave. Hence, in patients with mitral valve disease or cardiac disease, mean PAWP cannot be used reliably to assess LV end-diastolic pressure.

To obtain a wedge pressure, the inflated, balloon-tipped catheter is advanced into a branch PA with the intent of blocking PA inflow. This allows the end hole of the catheter to indirectly measure the LA pressure. Therefore, the PAWP tracing is similar to the left atrial pressure tracing, consisting of the same a-c-x-v-y waveform (Table 40.4). Similar to the RA, the PAWP “a-wave” represents atrial systole, the “c-wave” represents the displacement of the closed mitral valve into the LA, and the “x-descent” represents LA relaxation. The “v-wave,” which is intimately related to atrial compliance, represents atrial filling occurring during ventricular systole. Finally, the “y-descent” is caused by mitral valve opening in early diastole. Importantly, the PAWP tracing is often less distinct than the RA waveform and delayed compared with the ECG, as the pressure is transmitted through the pulmonary vascular system before being measured by the catheter.

With a normal mean of 6 to 12 mm Hg at end expiration, the PAWP is 0 to 6 mm Hg less than the PA diastolic pressure under normal conditions (ie, no increased pulmonary vascular resistance [PVR]). An appropriate “wedge” position should be confirmed by measuring greater than 95% oxygen saturation of blood drawn through the catheter end hole while in the wedge position. If the oxygen saturation is lower than 95%, the balloon is likely “underwedged,” leading to what is essentially a damped PA measurement. Conversely, the catheter can also be “overwedged,” leading to a damped PAWP waveform (nearly flat) and an estimated PAWP pressure that is higher than the PA diastolic pressure. Thus, in cases where the mean PAWP exceeds the PA diastolic pressure, “overdamping” should be considered.

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Cardiac Catheterization and Hemodynamic Assessment
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