When the procedure is performed in the cardiac catheterization lab, there is a performing physician, a nurse that can administer medications and a monitoring technologist for recording the data that is obtained. The performing physician usually is assisted by a cardiovascular technologist.[15]

After obtaining informed consent, the patient is brought to the cardiac catheterization lab. The patient is placed in the supine position on the table, and the access sites are cleaned and draped in a sterile fashion. For providing a sterile access site, chlorhexidine is used. The operating physician and the assistant will require sterile gowns, gloves, head caps, and facial protection. The needles, access sheaths, catheters are flushed to avoid introducing air into the systemic circulation.[14]

A local anesthetic is administered subcutaneously at the access site. Venous access is obtained with or without ultrasound guidance. Access can be obtained using a standard 18-gauge needle or a smaller 21-gauge needle in the femoral and jugular sites. In the case of the antecubital vein, use of the 21-gauge needle may reduce the chances of injury to nearby arterial structures. Ultrasound guidance requires a sterile ultrasound probe sleeve so as to avoid contaminating the rest of the sterile field. Once venous access is obtained, an appropriately sized sheath is placed in the vein and secured. The pulmonary artery catheter is advanced through the sheath into the vein. The balloon is inflated after the catheter is advanced to roughly 15 cm so to avoid inflating it within the access sheath. Balloon inflation will then make advancing the catheter to the right atrium much easier. If the catheter advances easily, use of wire cannulation is not necessary. The catheter will reach the right atrium from the internal jugular vein when it is advanced to roughly 20 cm. From the femoral venous access site, it will reach the right atrium when it is advanced to roughly 45 cm. Nonetheless, the catheter movement can also be observed using fluoroscopy. 

When the catheter reaches the right atrium, a pulsatile right atrial waveform will be observed. Prior to recording pressures, a reference is established by zeroing the system. Zeroing involves opening the air-fluid transducer to air so that it equilibrates with atmospheric pressure. When this is being performed, the air-fluid transducer must be at the level of the heart. Roughly this is done by holding the air-fluid transducer at the level of the fourth intercostal space, at an imaginary plane between the anterior and the posterior chest walls. If it is lower than the heart level, the observed pressures may be falsely high. If the transducer is higher than heart level, then the observed pressures may be falsely low.

Once the right atrial pressure waveform is obtained, the catheter is manipulated to turn towards the right ventricle, and right ventricular pressure is obtained. Following this, the catheter is usually advanced to wedge position to measure the pulmonary capillary wedge pressure. Once this is done, the balloon can be deflated and brought back a few cms into the pulmonary artery where pulmonary artery pressure can be recorded. It is important to know that all pressures should be measured ideally at end-expiration. The pulmonary artery blood sample is withdrawn using the distal yellow port, and mixed venous oxygen saturation is obtained. Arterial saturations have to be obtained separately so as to determine the cardiac output using the Fick method. Thermodilution can be performed by injecting cold saline into the proximal blue port into the right atrium where it mixes with blood, and the temperature difference is detected by a thermistor. Thermodilution is repeated a minimum of three times to obtain an average cardiac output and cardiac index. The pulmonary artery catheter can be manipulated and placed in the superior or inferior vena cava for withdrawing blood samples and estimating oxygen saturations. The same can be done in the right ventricle or the right atrium.[11][12]

Possible complications include ventricular arrhythmias, right bundle branch block that are usually transient and resolve once the catheter is removed or the catheter tip position is adjusted. Very rarely complete heart block in the setting of prior left bundle branch block can occur that may require temporary pacemaker placement.

Air embolism can occur if there was air in the catheters or the fluid-filled pressure transducers. The patient can manifest with sudden onset of chest pain, dyspnea, hypotension, tachycardia. If this is suspected, the patient should be placed in the Trendelenburg position, and high flow oxygen must be administered. This helps in the reduction of the nitrogen in blood and promotes reabsorption of the injected air. In some situations, hyperbaric oxygen therapy is required.

The rate of pulmonary artery perforation is 0.03%, which can occur in the setting of prolonged balloon inflation and distal placement of the catheter into the pulmonary arteries for wedge pressure measurement, particularly in the setting of prior pulmonary hypertension and systemic anticoagulation. This can manifest as sudden dyspnea and cardiogenic shock. Fluoroscopy can help identify if the tip of the catheter is very distal in the pulmonary artery branches. If this occurs, the catheter should be left in place with the balloon inflated so as to minimize pulmonary hemorrhage. The patient should be emergently intubated with a double-lumen endotracheal tube and placed in the lateral decubitus position with the affected side down so as to protect the unaffected side from the ongoing hemorrhage. Emergent surgery or embolization should be considered.

For indwelling pulmonary artery catheters, the potential complications include access site infection, pulmonary infarction, right-sided chamber or pulmonary artery perforation, arrhythmias, thrombosis of the accessed vein.[14]

There are various pressure measurement and hemodynamic parameters that can be obtained when performing a right heart catheterization. The common parameters that are evaluated and the hemodynamic profiles of commonly encountered scenarios are described in the following sections.

Normal mean right atrial pressure is between 1 to 5 mm Hg. Normal right ventricular systolic and diastolic pressures are 15 to 30 mm Hg and 1 to 7 mm Hg, respectively. Normal pulmonary artery systolic and diastolic pressures are 15 to 30 mm Hg and 4 to 12 mm Hg, respectively. Mean pulmonary artery pressure is usually around 15 mm Hg. Normal pulmonary capillary wedge pressure is 4 to 12 mm Hg. [14]

The measured pressures can be used to calculate cardiac output, cardiac index, pulmonary vascular resistance, systemic vascular resistance, stroke work index, right ventricle stroke work, pulmonary artery pulsatility index (PAPi), the Gorlin equation to calculate mitral and aortic valve areas and the Hakki equation to calculate aortic valve area.[12][16]

Right Atrial or Pulmonary Capillary Wedge Pressure Waveforms

The right atrial pressure waveform consists of three positive upstrokes and two descents. The first positive upstroke is the “a” wave that correlates with atrial systole. This is followed by the “x” descent that signifies atrial relaxation. The next wave is the “c” wave that indicates tricuspid valve closure. The next wave is a positive upstroke “v” wave that represents passive atrial filling during right ventricular contraction. The “v” wave is followed by the ‘y” descent that represents atrial emptying after the tricuspid valve opens in ventricular diastole. The pulmonary capillary wedge waveform is similar to the right atrial pressure waveform and consists of three positive upstrokes and two downstrokes.[14]

In the setting of atrial fibrillation, there is a loss of the “a” wave due to the loss of the atrial contribution to the waveform. Tall “a” waves can occur due to an increase in atrial pressure that can occur in tricuspid or mitral stenosis. Cannon “a” waves are very large “a” waves that are caused by any condition that can cause atrioventricular dissociation such as complete heart block, ventricular tachycardia, AV nodal reentrant tachycardia. Large “v” waves occur due to increased ventricular volume during right ventricular contraction like tricuspid or mitral regurgitation, right or left ventricular failure, severe non-compliance of right or left ventricle, ventricular septal defect. Also, mitral stenosis, post-operative or rheumatic changes of the atrium can produce large atrial “v” waves.[17] A very rapid “y” descent is due to rapid diastolic filling of the ventricle that can occur in constrictive pericarditis. Similarly, a rapid “x” descent occurs in constrictive pericarditis.[18]The “y” descent is absent in cardiac tamponade as there is an equalization of diastolic pressures, and the ventricular diastolic pressure does not fall enough to allow for complete diastolic filling.[12]

Right Ventricle Systolic and Diastolic Pressures

Right ventricular and pulmonary artery systolic pressures are elevated in pulmonary embolism, pulmonary hypertension.[19][20]

There is an increase in and equalization of end-diastolic pressures, pulmonary capillary wedge pressures in constrictive pericarditis, restrictive cardiomyopathy, and cardiac tamponade. However, in constrictive pericarditis, there is ventricular interdependence that is best identified by simultaneous right and left heart catheterization. Interdependence results in discordance of right and left ventricular pressures, which are evidenced by a reduction in the right ventricle systolic pressure tracing when there is an increase in the left ventricle pressure tracing and vice versa with respiration. In restrictive cardiomyopathy, there is no interdependence, and therefore there is a concordance of right and left ventricular pressures on simultaneous measurement. Concordance is evidenced by concordant right ventricle and left ventricle systolic pressure tracings with respiration. This is mathematically calculated as the systolic area index, which is defined as the ratio of the right ventricle to the left ventricle area in inspiration versus expiration. A systolic area index greater than 1.1 has a sensitivity of greater than 95% in identifying constrictive pericarditis. Even though there have been various parameters that have been developed in the past to distinguish between constrictive pericarditis and restrictive cardiomyopathy, the systolic area index appears to have the best predictive accuracy. While the clinical presentation of constrictive pericarditis and restrictive cardiomyopathy is mostly chronic, cardiac tamponade physiology is frequently acute.[18][21] 

Cardiac Output

Cardiac output by right heart catheterization is generally calculated by using the indirect Fick principle and the thermodilution technique. The Fick principle was created by Adolf Fick in 1870, who observed that by determining the amount of oxygen carried in the systemic and pulmonary circulation, the blood volume required to carry that amount of oxygen could then be deduced. For this method, the hemoglobin levels, central arterial, and venous oxygen saturation, maximum oxygen consumption values are required. The maximum oxygen consumption is assumed to be 250 ml/minute, or 125 ml/min/method involves direct measurement of oxygen consumption using exhaled air. This is cumbersome and requires specialized equipment. Therefore indirect Fick method that uses the assumed maximum oxygen consumption value is widely used. However, it has been shown that cardiac output derived by the indirect Fick method varies from the direct Fick method by roughly 25% in up to 25% of individuals. These differences appear to be marked in individuals with a body mass index greater than 40 kg/m.[22][23][24] 

For thermodilution, 10 cc of saline is injected using the proximal blue port of the pulmonary artery catheter. This mixes with the right atrial blood and causes a slight drop in temperature, which is then detected by the thermistor at the tip of the catheter. However, there are pitfalls to the thermodilution technique. The Thermodilution technique is not considered accurate when cardiac output is low. The area under the curve is small in this scenario, and anything that causes the area under the curve to become smaller can underestimate cardiac output. Similarly, in severe tricuspid or pulmonic valve regurgitation, there is a recirculation of blood and can falsely underestimate cardiac output. In the setting of intracardiac shunts, it can do the opposite and falsely overestimate cardiac output. It is important to know the pitfalls associated with these measurements and that Fick and thermodilution techniques can produce variable results within the same patient.[12][24]

Cardiac Index

Cardiac index is calculated by indexing the cardiac output for body surface area. Normal cardiac output can be variable based on body mass and size. But a normal cardiac index is greater than 2.5 liters per minute per meter squared. Cardiogenic shock is defined as an index lesser than 2.2 liters per minute per meter squared with a pulmonary capillary wedge pressure greater than 15 mm Hg.[25][26] 

Cardiac Power Index

Cardiac power output is calculated in Watts and is obtained by dividing the product of mean arterial pressure and cardiac output in liters per minute by 451. Cardiac power index is cardiac power output that is indexed to body surface area. Cardiac power output lesser than 0.6 Watts has a very strong correlation with in-hospital mortality in patients with shock. In the setting of cardiogenic shock, cardiac power output has a greater correlation with adverse outcomes compared with cardiac index, ejection fraction, pulmonary artery systolic pressure, and mean arterial pressure.[27]

Systemic and Pulmonary Vascular Resistance

Systemic vascular resistance is calculated by the equation,

[(Mean arterial pressure – right atrial pressure) x 80 / cardiac output]

It is measured in Wood units or dynes per second per cm squared. The normal range is 700 to 1600 dynes per second per cm or 10 to 20 Wood units.

Similarly, pulmonary vascular resistance is calculated by the equation,

[(Mean pulmonary artery pressure – pulmonary capillary wedge pressure) x 80/ cardiac output]

It is measured in Wood units or dynes per second per cm squared. The normal range is 20 to 120 dynes per second per cm or less than 2 Wood units.[12]

Pulmonary Artery Pulsatility IndexPulmonary artery pulsatility index or PAPi is the ratio between pulmonary artery pressure and right atrial pressure. It is calculated as [(Systolic pulmonary artery pressure – diastolic pulmonary artery pressure)/right atrial pressure]. 

PAPi of less than 0.9 has very high sensitivity and specificity in predicting right ventricular failure and in-hospital mortality in acute inferior wall myocardial infarction.[16]

PAPi less than 1.85 is also used to predict if patients will experience right ventricle failure and thereby require right ventricular hemodynamic device support after placement of left ventricular assist devices.[28][29]  It is also used to predict adverse outcomes in patients with chronic right heart failure.[30]

Cardiac catheterization remains the gold standard for diagnosing pulmonary hypertension, assessing disease severity, and determining prognosis and response to therapy. By directly measuring pressures, cardiac output, right heart catheterization allows for the determination of multiple prognostic markers such as right atrial pressure, cardiac output, cardiac power output, cardiac index, mean pulmonary artery pressure, pulmonary artery pulsatility index, right atrial: pulmonary capillary wedge ratio, etc.

Right heart catheterization appears to be generally performed in patients with cardiac and pulmonary disorders. These patients receive multi-disciplinary care from their primary care physicians, pulmonary physicians, and cardiologists. There must be recognition of conditions that could be appropriately diagnosed or can be excluded by right heart catheterization. In addition, the optimal performance of these procedures relies on the entire team performing the procedure, including the nurse, the cardiovascular technologists, to ensure safety against potential risks and complications of the procedure. Identifying potential issues with the fluid-filled transducer system and recognition of abnormal waveforms due to technical issues are critical to performing the right heart catheterization. The Society for Cardiovascular Angiography and Interventions has developed best practice guidelines for cardiac catheterization procedures, which help adhere to national and international standards.