A 62-year-old man with a history of nonischemic cardiomyopathy presents with worsening shortness of breath, orthopnea, lower extremity edema, and weight gain. He is diagnosed with acute on chronic systolic heart failure. Attempts at diuresis with furosemide 80 mg IV twice daily are unsuccessful and his renal function worsens. Right heart catheterization reveals elevated filling pressures and low cardiac output. He is started on inotropes and continuous furosemide infusion with improvement in his symptoms and renal function.
Right heart catheterization (RHC) can be used for a variety of clinical indications in critically ill patients; use in decompensated heart failure (HF) is among the most common.
Allows direct measurement of right atrial (RA), right ventricular (RV), and pulmonary artery (PA) pressures.1
Can also estimate left atrial (LA) pressure by measuring the pulmonary capillary wedge pressure (PCWP).
Cardiac output can be estimated using automated thermodilution techniques or calculated using the Fick method.
Samples of mixed venous blood can be used to quantify oxygen consumption.
Value of RHC use in HF remains controversial.2
Unnecessary in most patients who present with acute decompensated HF, but can provide valuable information in select patients.
Randomized ESCAPE trial showed no benefit (or increased risk) of using RHC in mortality or days alive out of the hospital.3
ESCAPE did not enroll all consecutive patients because many physicians would not enroll and risk a 50% chance of not having pulmonary artery catheter.
Based on ESCAPE trial, routine RHC in HF is not recommended. However, it can be useful in a subset of advanced HF patients.
The 2013 ACC/AHA HF guidelines suggest RHC be performed in patients with respiratory distress or impaired systemic perfusion when clinical assessment is inadequate.
Filling pressure of the right heart reflecting venous return to the RA during ventricular systole and RV end-diastolic pressure.
Waveform normally has 3 distinct positive waves and 2 negative descents (Figure 24-1).
a wave reflects pressure increase at atrial contraction.
x descent reflects fall in pressure during atrial relaxation.
c wave (generally small) reflects pressure increase due to bulging of tricuspid valve into the RA during ventricular isovolumetric contraction.
v wave is increased atrial pressure from passive blood return to the atria while the tricuspid valve remains closed.
y descent reflects fall in atrial pressure as the tricuspid valve opens and blood rushes from the atrium to the ventricle.
a wave is usually slightly larger than the v wave.
Normal RA pressure is 3 to 7 mm Hg (Table 24-1).
Characteristic RA pressure waveforms:
Tricuspid regurgitation can result in tall v waves due to blood regurgitated into the RA during systole (Figure 24-2).
Atrial fibrillation results in loss of normal a waves due to lack of organized atrial activity.
Atrioventricular (AV) dissociation (seen in complete heart block, ventricular tachycardia, or ventricular pacing) may result in large “cannon” a waves due to contraction of the atrium against a close tricuspid valve.
Figure 24-1
Normal hemodynamic recordings during RHC. From left to right: right atrium (RA), right ventricle (RV), pulmonary artery (PA), and pulmonary capillary wedge pressures (PCWP) are shown. Note in the arterial tracings, a and v waves can be seen immediately following the P and T waves of the electrocardiogram, respectively. (Reproduced with permission from Kasper DL, Fauci AS, Hauser D, et al. Harrison’s Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill Education; 2015. Figure 272-1.)
Usually measured at maximal systolic pressure, minimal early diastolic pressure, and end-diastolic pressure (Figure 24-1).
Ventricular systole is characterized by rapid upstroke and downstroke.
Ventricular diastole consists of an early rapid filling phase, slow filling phase, and atrial systolic phase.
End-diastolic pressure is expressed as the pressure immediately before the onset of ventricular contraction and after atrial contraction.
Normal systolic RV pressure is 20 to 30 mm Hg and normal diastolic pressure is 3 to 7 mm Hg (Table 24-1).
Elevated RV pressure is seen in pulmonary hypertension (HTN), pulmonic stenosis, and pulmonary embolism.
Systolic pressure gradient between the RV and PA is seen in pulmonic stenosis.
Waveform includes systolic pressure, diastolic pressure, and dicrotic notch, which represents closure of the pulmonic valve (Figure 24-1).
Normal systolic PA pressure is 20 to 30 mm Hg and normal diastolic pressure is 8 to 12 mm Hg (Table 24-1).
Elevations of PA pressure are seen with decompensated left HF or a range of conditions in which pulmonary vascular resistance is elevated.
Obtained by gently inflating a balloon at the distal end of the catheter obstructing blood flow and creating a static column of blood between the catheter tip and left atrium.
Assuming no obstruction to flow between the PA and left ventricle, the PCWP estimates the left ventricular end-diastolic pressure (LVEDP) (ie, the left heart “filling pressure”).4,5
Normal PCWP is 8 to 12 mm Hg (Table 24-1).
Waveform is similar to that seen in the RA (Figure 24-1).
a wave reflects pressure increase at atrial contraction.
x descent reflects fall in pressure during atrial relaxation.
c wave (often not seen) reflects pressure increase due to bulging of the mitral valve into the LA during ventricular isovolumetric contraction.
v wave is increased atrial pressure from passive blood return to the atria while the mitral valve remains closed.
y descent reflects fall in atrial pressure as the mitral valve opens and blood rushes from the atrium to the ventricle.
v wave is usually slightly larger than the a wave.
PCWP may be lower than the LVEDP in conditions with decreased LV compliance (diastolic dysfunction, positive pressure ventilation, myocardial ischemia, or cardiac tamponade)6 or other situations associated with premature closure of the mitral valve such as aortic stenosis.
PCWP may be greater than the LVEDP when there is hypoxia or pulmonary disease due to constriction of small pulmonary veins.
PCWP should be recorded at end expiration (which can differ considerably from mean PCWP).
PCWP should be measured at the a wave to avoid large v waves confounding the interpretation.
PCWP position should be confirmed by fluoroscopy, waveform inspection, and confirming that oxygen saturation from blood drawn distal to the balloon is consistent with systemic arterial saturations.
Characteristic PCWP waveforms:
Conditions of increased resistance to LV filling, such as mitral stenosis, left-sided volume overload, or decreased LV compliance, can result in elevations of the a wave.
Mitral regurgitation may lead to tall v waves.
The height of the v wave does not accurately reflect the degree of mitral regurgitation and elevated v waves are neither sensitive nor specific for the diagnosis of mitral regurgitation.7-10
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