# Cardiac Catheterization Hemodynamics

## Pressure Waveform Analysis

### Normal Hemodynamic Values

| Chamber/Location | Normal Pressure (mmHg) | Key Abnormality Thresholds |
|---|---|---|
| Right Atrium (mean) | 2-8 | Elevated in RV failure, tamponade, constriction |
| Right Ventricle (systolic/diastolic) | 25/0-5 | Systolic > 35 suggests pulmonary hypertension |
| Pulmonary Artery (systolic/diastolic/mean) | 25/10/15 | Mean > 20 defines pulmonary hypertension |
| PCWP (mean) | 6-12 | > 15 suggests left heart disease; > 18 defines elevated filling |
| Left Ventricle (systolic/end-diastolic) | 120/0-12 | LVEDP > 15 in HF; > 25 in decompensated HF |
| Aorta (systolic/diastolic) | 120/80 | Gradient across aortic valve in AS |
| Cardiac Index (L/min/m^2) | 2.5-4.0 | < 2.2 low output state; < 1.8 cardiogenic shock |
| SVR (dynes-sec-cm^-5) | 800-1200 | Elevated in cardiogenic shock; low in sepsis |
| PVR (Wood units) | < 1.5 WU | > 2 WU defines pre-capillary PH; > 5 WU contraindication to transplant |

### Right Atrial Pressure

The right atrial pressure waveform, with a normal mean of 2 to 8 mmHg, contains several discrete components that provide critical diagnostic information. The a wave reflects atrial contraction, the c wave represents tricuspid valve closure and isovolumic right ventricular contraction, and the v wave corresponds to atrial filling during ventricular systole. The x descent reflects atrial relaxation, while the y descent represents passive atrial emptying after the tricuspid valve opens.

Abnormalities in these waveform components carry specific diagnostic significance. Giant a waves occur in conditions where the atrium contracts against increased resistance, including tricuspid stenosis, pulmonic stenosis, pulmonary hypertension, and right ventricular failure. Cannon a waves result from atrial contraction against a closed tricuspid valve, as seen in atrioventricular dissociation during complete heart block or ventricular tachycardia, and in junctional rhythm. Prominent v waves are the hallmark of tricuspid regurgitation, where the v wave replaces the x descent to create a fused cv wave. The Kussmaul sign, characterized by right atrial pressure that fails to decrease or paradoxically increases with inspiration, is observed in constrictive pericarditis, restrictive cardiomyopathy, right ventricular infarction, and massive pulmonary embolism. In atrial fibrillation, the organized a waves are absent and replaced by an irregularly irregular fibrillatory baseline.

### Right Ventricular Pressure

Normal right ventricular pressure measures 25/0-5 mmHg for systolic and end-diastolic pressures, respectively. Elevated right ventricular systolic pressure indicates pulmonary hypertension, pulmonic stenosis, or right ventricular failure. Elevation of right ventricular end-diastolic pressure occurs in right ventricular failure, constrictive pericarditis, restrictive cardiomyopathy, right ventricular infarction, and cardiac tamponade. The dip-and-plateau pattern, also known as the square root sign, is characterized by a rapid rise in right ventricular end-diastolic pressure to a plateau during early diastole and is a characteristic hemodynamic finding of both constriction and restriction. A gradient between peak right ventricular systolic pressure and pulmonary artery systolic pressure indicates pulmonic stenosis.

### Pulmonary Artery Pressure

Normal pulmonary artery pressure measures 25/10 mmHg with a mean of 15 mmHg. A mean pulmonary artery pressure exceeding 20 mmHg defines pulmonary hypertension by the updated hemodynamic threshold. In the absence of pulmonary vascular disease, the pulmonary artery diastolic pressure approximates the mean pulmonary capillary wedge pressure. A gradient between pulmonary artery diastolic pressure and pulmonary capillary wedge pressure exceeding 5 mmHg suggests elevated pulmonary vascular resistance with a pre-capillary component. The pulmonary artery waveform is characterized by a systolic upstroke, a dicrotic notch corresponding to pulmonic valve closure, and a diastolic decline.

### Pulmonary Capillary Wedge Pressure (PCWP)

The pulmonary capillary wedge pressure, normally measuring 6 to 12 mmHg in mean, reflects left atrial hemodynamics through waveform components analogous to those of the right atrium, including a and v waves, though temporally delayed due to transmission through the pulmonary vasculature. Elevation of the wedge pressure occurs in left heart failure of both systolic and diastolic etiology, mitral stenosis, mitral regurgitation, constrictive pericarditis, and cardiac tamponade. Giant v waves in the wedge tracing are classically associated with acute severe mitral regurgitation, where the v wave may exceed 40 to 60 mmHg, though it is important to recognize that v wave height alone is not entirely specific, as a large, compliant left atrium may dampen v waves even in the presence of chronic severe mitral regurgitation.

Confirming a true wedge position is essential for accurate hemodynamic assessment. The oxygen saturation obtained from blood aspirated at the wedge position should be 95% or greater, reflecting pulmonary venous blood. Fluoroscopy should confirm the catheter tip in a distal pulmonary artery branch, and the mean wedge pressure must be less than or equal to the mean pulmonary artery pressure. Common pitfalls include overwedging, where the catheter is impacted in a small branch producing falsely elevated pressures, underwedging, where the catheter is not fully advanced and reflects pulmonary artery pressure, and failure to achieve a zone 3 position, where the gravity-dependent lung zone ensures that arterial pressure exceeds venous pressure exceeds alveolar pressure.

### Left Ventricular Pressure

Normal left ventricular pressure measures 120/0-12 mmHg for systolic and end-diastolic values. The left ventricular end-diastolic pressure reflects ventricular compliance and filling pressure, and is elevated in heart failure with reduced and preserved ejection fraction, aortic stenosis, hypertensive heart disease, acute myocardial infarction, and constrictive pericarditis. The Brockenbrough-Braunwald-Morrow sign is a pathognomonic hemodynamic finding in hypertrophic cardiomyopathy. Following a premature ventricular contraction, post-extrasystolic potentiation causes the subsequent beat to generate increased left ventricular pressure, but the aortic pulse pressure paradoxically decreases due to worsened left ventricular outflow tract obstruction from the increased contractility. This is in contrast to aortic stenosis, where the post-premature ventricular contraction beat shows increased left ventricular and aortic pressure without dynamic obstruction. The diastolic waveform of the left ventricle comprises the a wave from atrial contraction, a rapid filling phase, diastasis, and a pre-systolic rise, with restrictive physiology manifesting as a rapid rise to a plateau producing the characteristic square root sign.

### Aortic Pressure

Normal aortic pressure of 120/80 mmHg features a dicrotic notch corresponding to aortic valve closure. Several aortic waveform abnormalities carry important diagnostic significance. Pulsus paradoxus, defined as a systolic blood pressure drop exceeding 10 mmHg during inspiration, suggests cardiac tamponade, severe asthma or chronic obstructive pulmonary disease, constrictive pericarditis, or massive pulmonary embolism. Pulsus parvus et tardus, characterized by a slow upstroke, delayed peak, and diminished amplitude, is characteristic of severe aortic stenosis. Bisferiens pulse, with two systolic peaks, is observed in combined aortic stenosis and regurgitation or hypertrophic cardiomyopathy with obstruction. Pulsus alternans, with alternating strong and weak beats, indicates severe left ventricular dysfunction.

<image>
A comprehensive hemodynamic waveform reference diagram showing simultaneous pressure tracings. Display six stacked panels on a common time axis (with ECG rhythm strip at the top for timing reference). Panel 1: Right atrial pressure (0-20 mmHg scale) with clearly labeled a, c, v waves and x, y descents, showing normal tracing in blue and an abnormal tracing with giant v waves (tricuspid regurgitation) overlaid in red dashed line. Panel 2: Right ventricular pressure (0-40 mmHg scale) showing normal systolic and diastolic pressures, with a dip-and-plateau pattern overlaid in red dashed line (labeled "square root sign - constriction/restriction"). Panel 3: Pulmonary artery pressure (0-40 mmHg scale) with systolic peak, dicrotic notch labeled, and diastolic runoff. Panel 4: PCWP (0-30 mmHg scale) with a and v waves labeled; giant v wave pattern overlaid in red dashed (labeled "severe MR"). Panel 5: LV pressure (0-150 mmHg scale) with LVEDP marked at the end-diastolic point. Panel 6: Aortic pressure (0-150 mmHg scale) with dicrotic notch, showing normal tracing and pulsus paradoxus variation with respiratory cycle overlaid. Each panel labeled with the chamber name, normal values, and scale. Use blue for normal tracings, red for pathological overlays.
</image>

## Hemodynamic Calculations

### Cardiac Output

Cardiac output measurement in the catheterization laboratory employs two principal methods. The Fick method calculates cardiac output as oxygen consumption divided by the arteriovenous oxygen content difference multiplied by 10. Oxygen consumption can be directly measured or assumed at 125 mL/min/m squared multiplied by body surface area. Arterial oxygen content is calculated as 1.36 times hemoglobin concentration times arterial oxygen saturation, while mixed venous oxygen content uses the same formula with the mixed venous saturation obtained from the pulmonary artery. When assumed oxygen consumption values are used rather than directly measured values, an error of approximately 25% may be introduced, making direct measurement preferable for critical clinical decisions such as transplant evaluation and mechanical circulatory support candidacy.

Thermodilution provides an alternative method, involving injection of a known volume of cold saline into the right atrial port of the pulmonary artery catheter. The temperature change measured by the thermistor at the pulmonary artery tip is used to calculate cardiac output through the Stewart-Hamilton equation. Important pitfalls include tricuspid regurgitation, which causes early recirculation and underestimates cardiac output, reduced accuracy in low cardiac output states, and invalidation of the measurement in the presence of intracardiac shunts. Cardiac index, calculated as cardiac output divided by body surface area, normally ranges from 2.5 to 4.0 L/min/m squared. A cardiac index below 2.2 indicates a low output state, while values below 1.8 define cardiogenic shock.

### Valve Area Calculations

#### Gorlin Equation (Aortic Valve)

The Gorlin equation for aortic valve area is calculated as cardiac output divided by 44.3 times the systolic ejection period times heart rate times the square root of the mean gradient. The systolic ejection period is measured in seconds per beat from left ventricular and aortic pressure tracings. The simplified Hakki formula provides a rapid bedside estimate by dividing cardiac output by the square root of the peak-to-peak gradient. In low-flow states, the gradient may underestimate stenosis severity because it is flow-dependent; dobutamine administration to increase cardiac output helps differentiate true-severe from pseudo-severe aortic stenosis.

#### Gorlin Equation (Mitral Valve)

The Gorlin equation for mitral valve area is calculated as cardiac output divided by 37.7 times the diastolic filling period times heart rate times the square root of the mean gradient. The diastolic filling period is measured in seconds per beat. Simultaneous left atrial or pulmonary capillary wedge pressure and left ventricular pressure recordings are required, with the mean transmitral gradient calculated from the area between the wedge and left ventricular diastolic waveforms. When pulmonary capillary wedge pressure is used as a surrogate for direct left atrial pressure, a time delay is introduced that may affect the accuracy of gradient calculation.

### Vascular Resistance

Systemic vascular resistance is calculated as the difference between mean arterial pressure and right atrial pressure, multiplied by 80, and divided by cardiac output, with normal values of 800 to 1200 dynes-sec-cm to the negative fifth power. Pulmonary vascular resistance is calculated as the difference between mean pulmonary artery pressure and pulmonary capillary wedge pressure, multiplied by 80, and divided by cardiac output, with normal values below 120 dynes-sec-cm to the negative fifth power or less than 1.5 Wood units. Pulmonary vascular resistance expressed in Wood units is calculated by dividing the transpulmonary gradient by cardiac output, with pre-capillary pulmonary hypertension defined by a pulmonary vascular resistance exceeding 2 Wood units.

### Shunt Calculations

The ratio of pulmonary blood flow to systemic blood flow provides a quantitative assessment of intracardiac shunting. This ratio is calculated as systemic arterial saturation minus mixed venous saturation divided by pulmonary venous saturation minus pulmonary artery saturation. A ratio exceeding 1.5 indicates a significant left-to-right shunt, with values exceeding 2.0 generally requiring intervention. A ratio below 1.0 indicates a right-to-left shunt, consistent with Eisenmenger physiology when chronic. The oxygen saturation step-up during an oximetric run identifies the level of the shunt by sampling saturations in the superior vena cava, inferior vena cava, right atrium, right ventricle, and pulmonary artery. A significant step-up suggesting a shunt at a given level is defined as 7% or greater at the atrial level, 5% or greater at the ventricular level, and 5% or greater at the pulmonary artery level.

<image>
A diagram illustrating the oximetric shunt run for detection of intracardiac shunts. Show a schematic of the heart with the catheter path from IVC through RA, RV, PA, and into the pulmonary capillary wedge position. At each chamber location, show a blood sample being drawn with the corresponding normal oxygen saturation values: IVC (75-80%), SVC (70-75%), RA (high 70s%, calculated mixed venous: [3 x SVC + IVC] / 4), RV (75%), PA (75%), PCWP/PV (98%). Alongside the normal values, show an abnormal case with ASD: SVC 72%, IVC 78%, RA 88% (step-up of 12%, highlighted in red with arrow), RV 88%, PA 87%, PV 98%. Calculate Qp/Qs using the formula shown: (98 - 74) / (98 - 88) = 2.4 (significant L-to-R shunt). Below, include a table showing significant oxygen saturation step-ups by level: atrial >= 7%, ventricular >= 5%, great vessel >= 5%. Use color gradient from blue (deoxygenated) to red (oxygenated) for the blood samples.
</image>

## Specific Hemodynamic Patterns

### Cardiac Tamponade

The hemodynamic hallmark of cardiac tamponade is equalization of diastolic pressures, with right atrial pressure, right ventricular end-diastolic pressure, pulmonary artery diastolic pressure, and pulmonary capillary wedge pressure converging to within 5 mmHg of one another. The waveform demonstrates a blunted y descent, reflecting impaired ventricular filling, while the x descent remains prominent, reflecting preserved atrial relaxation during ventricular systole. Pulsus paradoxus exceeding 10 mmHg is present, representing the inspiratory decline in systolic blood pressure. The underlying mechanism involves enhanced ventricular interdependence within the rigid pericardial sac, where inspiratory increases in right-sided filling come at the expense of left-sided filling. Echocardiographic correlates include right atrial diastolic collapse lasting more than one-third of the cardiac cycle and right ventricular early diastolic collapse.

### Constrictive Pericarditis

The hemodynamic signature of constrictive pericarditis includes the dip-and-plateau pattern in both right and left ventricular diastolic pressures, representing rapid early diastolic filling followed by abrupt cessation when cardiac volume reaches the constraint imposed by the thickened pericardium. The most reliable hemodynamic differentiator from restrictive cardiomyopathy is the discordant ventricular pressure change with respiration: during inspiration, left ventricular systolic pressure decreases while right ventricular systolic pressure increases, reflecting enhanced ventricular interdependence within the rigid pericardial shell. A prominent y descent is characteristic, corresponding to the rapid early diastolic filling before pericardial constraint halts further filling, creating the "dip" portion of the waveform. The Kussmaul sign, manifested as a paradoxical rise in right atrial pressure with inspiration or failure of the normal inspiratory decline, is present in approximately 50% of cases.

Near-equalization of diastolic pressures occurs, similar to tamponade, but with the distinguishing feature that the right ventricular end-diastolic pressure approximates one-third of the right ventricular systolic pressure, the so-called one-third rule. In contrast to constriction, restrictive cardiomyopathy demonstrates respiratory pressure concordance, where both left and right ventricular pressures move in the same direction with respiration. Dynamic respiratory changes in pulmonary capillary wedge pressure exceeding 3 to 5 mmHg further favor the diagnosis of constriction.

### Severe Aortic Stenosis

The hemodynamic assessment of severe aortic stenosis reveals a systolic pressure gradient between the left ventricle and the aorta, which can be measured directly by pullback of the catheter slowly withdrawn from the left ventricle to the aorta across the valve. The aortic waveform characteristically demonstrates pulsus parvus et tardus. Elevation of the left ventricular end-diastolic pressure indicates ventricular decompensation. In the low-gradient pattern with low cardiac output, the mean gradient may be less than 40 mmHg despite a valve area below 1.0 cm squared, necessitating a dobutamine challenge to differentiate true-severe from pseudo-severe stenosis.

### Acute Mitral Regurgitation

Acute mitral regurgitation produces giant v waves in the pulmonary capillary wedge tracing, which may exceed 60 mmHg. However, the height of the v wave depends critically on left atrial compliance. In chronic mitral regurgitation with a dilated, compliant left atrium, v waves may be only modestly elevated despite severe regurgitation. It is also important to recognize that tall v waves can occur with ventricular septal defects, where the left-to-right shunt increases pulmonary venous return to the left atrium. Differentiation relies on the oximetric run: in ventricular septal defect, an oxygen saturation step-up is present in the right ventricle and pulmonary artery, whereas no step-up is observed in mitral regurgitation.

### Hypertrophic Obstructive Cardiomyopathy

The hemodynamic assessment of hypertrophic obstructive cardiomyopathy reveals a left ventricular outflow tract gradient on catheter pullback, with pressure decreasing as the catheter crosses from the left ventricular body to the outflow tract and aorta. The gradient increases with Valsalva maneuver and following premature ventricular contractions. The Brockenbrough sign is pathognomonic for dynamic left ventricular outflow tract obstruction: the post-premature ventricular contraction beat demonstrates an increased left ventricular-aortic gradient accompanied by a paradoxical decrease in aortic pulse pressure. The aortic waveform displays a distinctive spike-and-dome configuration, with an initial rapid upstroke before the obstruction develops, a mid-systolic dip at the onset of systolic anterior motion and obstruction, and a late systolic recovery.

### Cardiogenic Shock

The hemodynamic assessment of cardiogenic shock reveals a low cardiac index below 2.2 L/min/m squared, elevated pulmonary capillary wedge pressure above 18 mmHg, elevated systemic vascular resistance, and systolic blood pressure below 90 mmHg. Hemodynamic profiling guides management across four distinct categories. The wet-cold profile, characterized by elevated wedge pressure and low cardiac index, represents the most common shock presentation and is managed with diuretics, inotropes or vasopressors, and mechanical circulatory support. The wet-warm profile, with elevated wedge pressure but normal or elevated cardiac index, suggests a distributive component such as sepsis and is managed with diuretics and vasodilators. The dry-cold profile, featuring low wedge pressure and low cardiac index, should prompt a volume challenge and evaluation for right ventricular failure or hypovolemia. The dry-warm profile, with normal wedge pressure and cardiac index, indicates adequate perfusion and filling and does not represent a shock state.

## Right Heart Catheterization: Technical Considerations

### PA Catheter Placement

The standard 7 French Swan-Ganz catheter is inserted via the internal jugular or femoral vein. Advancement proceeds with the balloon inflated, passing through the right atrium into the right ventricle, where an abrupt increase in systolic pressure is observed, then into the pulmonary artery, where an increase in diastolic pressure and the appearance of a dicrotic notch are noted, and finally into the pulmonary capillary wedge position, identified by a damped waveform with a and v waves and a drop in mean pressure. Confirmation of wedge position requires a pulmonary venous oxygen saturation of 95% or greater, fluoroscopic evidence of the catheter tip in a distal pulmonary artery branch, a mean wedge pressure less than or equal to the mean pulmonary artery pressure, and appropriate waveform morphology.

### Complications

Arrhythmias are the most common complication of right heart catheterization, with premature ventricular complexes and nonsustained ventricular tachycardia frequently occurring during passage through the right ventricle, though these are usually self-limited. Sustained ventricular tachycardia is rare. Pulmonary artery perforation is an uncommon but potentially fatal complication, with risk factors including pulmonary hypertension, anticoagulation, and overinflation of the balloon in a distal pulmonary artery position. Catheter knotting occurs more commonly with excess catheter length and is prevented by fluoroscopic guidance. Pulmonary artery catheter-associated thrombus is mitigated by heparin bonding of the catheter surface, and infection risk increases with catheter duration exceeding 72 hours.

<image>
A clinical hemodynamic assessment diagram for cardiogenic shock showing the four hemodynamic profiles in a 2x2 grid. The x-axis represents cardiac index (CI, L/min/m^2) with a dividing line at 2.2 (low on left, normal/high on right). The y-axis represents PCWP (mmHg) with a dividing line at 18 (low on bottom, high on top). Top-left quadrant (Wet-Cold, red): "CI < 2.2, PCWP > 18; Most common shock profile; Treatment: inotropes, vasopressors, MCS; Consider: dobutamine, milrinone, Impella, ECMO." Top-right quadrant (Wet-Warm, yellow): "CI >= 2.2, PCWP > 18; Treatment: IV diuretics, vasodilators; Consider: distributive process, sepsis." Bottom-left quadrant (Dry-Cold, blue): "CI < 2.2, PCWP < 18; Treatment: volume resuscitation; Evaluate: RV failure, hypovolemia." Bottom-right quadrant (Dry-Warm, green): "CI >= 2.2, PCWP < 18; Adequate perfusion and filling; Not in shock." Include SVR ranges and clinical examples in each quadrant. Center of grid: small PA catheter icon with arrow showing measurement direction.
</image>

## Key Clinical Pearls

- Always confirm true wedge position: PVO2 >= 95%, mean PCWP <= mean PAP, and appropriate waveform -- false wedge readings lead to incorrect clinical decisions
- The "giant v wave = MR" dogma is an oversimplification -- v wave height depends on LA compliance (acute MR with non-compliant LA produces tall v waves; chronic MR with enlarged compliant LA may have minimal v waves); large v waves can also be seen in VSD
- In suspected constriction vs. restriction, look for discordant ventricular pressures with respiration -- this single finding (LV falls while RV rises during inspiration) is the most reliable hemodynamic differentiator
- The Brockenbrough sign (increased LV-aortic gradient with decreased aortic pulse pressure post-PVC) is pathognomonic for dynamic LVOT obstruction and distinguishes HCM from fixed aortic stenosis
- Fick cardiac output using assumed VO2 can be inaccurate by 25% -- in critical clinical decisions (transplant evaluation, MCS candidacy), directly measured VO2 should be used
- Fluid challenge during RHC (rapid 500 mL saline) can unmask occult left heart disease in patients with borderline PCWP (12-15 mmHg) -- this is particularly valuable in the HFpEF diagnostic workup

## References

- Kern MJ, et al. Hemodynamic Rounds: Interpretation of Cardiac Pathophysiology from Pressure Waveform Analysis. 4th ed. Wiley-Liss. 2018.
- Nishimura RA, Carabello BA. Hemodynamics in the Cardiac Catheterization Laboratory of the 21st Century. Circulation. 2012;125:2138-2150.
- Halpern SD, Taichman DB. Misclassification of Pulmonary Hypertension Due to Reliance on Pulmonary Capillary Wedge Pressure Rather Than Left Ventricular End-Diastolic Pressure. Chest. 2009;136:37-43.
- Thadani U, et al. Hemodynamic Assessment in the Contemporary Cardiac Catheterization Laboratory. Circ Cardiovasc Interv. 2020;13:e009265.