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Hemodynamics in Heart Failure


The first right heart catheterization (RHC) in humans was performed in 1929 by Dr. Werner Forssmann (on himself), who ultimately shared in the 1956 Nobel Prize in Medicine with Andre Cournard and Dickinson Richards for their work in cardiac catheterization. RHC was further refined by the work of Drs. Bradley and Fife, and in 1969 Drs. Scheinman, Abbot, and Rapaport reported their use of a flow-directed right heart catheter. Following their report of a bedside balloon flotation catheter by Drs. Swan and Ganz in the New England Journal of Medicine in 1970, RHC became widespread both in the catheterization laboratory and in intensive care units for critically ill and unstable patients. Despite advances in noninvasive hemodynamic assessment with echocardiography and cardiac magnetic resonance imaging (MRI), RHC and left heart catheterization (LHC) remains the gold standard for hemodynamic assessment in heart disease. Today, the three predominant reasons to obtain invasive hemodynamics in heart failure include:

  • 1.

    To resolve diagnostic uncertainty in patients with cryptic symptoms.

  • 2.

    To assess the suitability for advanced therapies in chronic heart failure.

  • 3.

    To investigate pulmonary hypertension (PH).

The Society for Cardiovascular Angiography and Interventions and the Heart Failure Society of America Clinical Expert Consensus Document on the Use of Invasive Hemodynamics for the Diagnosis and Management of Cardiovascular Disease summarize the recommendations for invasive hemodynamics for specific clinical scenarios in Table 34.1 .

TABLE 34.1
Key Clinical Recommendations for Invasive Hemodynamic Evaluation
Adapted from Sorajja P, Borlaug BA, Dimas VV, et al. SCAI/HFSA clinical expert consensus document on the use of invasive hemodynamics for the diagnosis and management of cardiovascular disease. Catheter Cardiovasc Interv . 2017;89:E233–E247.
Hypertrophic Cardiomyopathy
  • 1.

    For symptomatic patients being considered for septal reduction therapy, invasive hemodynamic assessment with characterization of the dynamic LVOT obstruction should be performed for those in which the noninvasive imaging studies are inconclusive.

  • 2.

    In the cardiac catheterization laboratory, transseptal assessment is preferred for characterization of dynamic LVOT obstruction.

  • 3.

    Dynamic LVOT obstruction at rest and with provocation should be examined.

Valvular heart disease
  • 1.

    An invasive hemodynamic evaluation is recommended to resolve discrepancies between clinical findings and noninvasive imaging data in patients with valvular disease when surgical or catheter-based therapy is being considered.

  • 2.

    Invasive hemodynamic studies of patients with valvular disease should be performed with simultaneous measurement of multiple central cardiac chambers.

  • 3.

    Invasive hemodynamic evaluations are beneficial for patients with valvular regurgitation in certain scenarios, such as eccentric jets with difficult quantitation, prosthetic valves with possible acoustic shadowing, and acute lesions in which color flow Doppler might be limited.

Ventricular Function
  • 1.

    Although diastolic function is most comprehensively assessed by measuring ventricular stiffness and relaxation, the commonly available methods of catheterization with direct measurement of left- and right-sided ventricular filling pressures provide incremental diagnostic data on diastolic function.

  • 2.

    In patients presenting exercise intolerance, in which noninvasive and resting invasive measurements are inconclusive, provocative testing in the cardiac catheterization laboratory should be considered to determine the presence of a cardiac etiology. Cycle ergometry exercise is the most physiologically relevant and sensitive stressor and is preferred over other maneuvers such as saline loading or arm exercise.

Pericardial Disease
  • 1.

    An invasive hemodynamic evaluation should be strongly considered for all patients with suspected constrictive pericarditis due to the frequently complex pathophysiology and the need for high diagnostic specificity when considering surgery.

  • 2.

    Invasive studies for constrictive pericarditis should entail examination of the dynamic respiratory criteria.

  • 3.

    An invasive hemodynamic study is typically not required for the diagnosis of cardiac tamponade.

Pulmonary Hypertension and the Right Ventricle
  • 1.

    Invasive assessment of pulmonary hemodynamics is required for patients with pulmonary hypertension who are being considered for vasodilator therapy and cardiac transplantation.

  • 2.

    Invasive assessment of pulmonary hemodynamics should be considered when there is diagnostic uncertainty regarding pulmonary hypertension based on noninvasive data. This assessment should establish the diagnosis according to WHO classification.

  • 3.

    Invasive assessment of pulmonary hemodynamics should be performed to monitor and assess the effectiveness of pulmonary hypertension therapies.

  • 4.

    Invasive assessment of pulmonary hemodynamics can be used to assess the risk of right ventricular failure with advanced heart failure therapies.

  • 5.

    In the appropriate setting, a properly performed and interpreted exercise hemodynamic assessment can be a highly useful tool to elucidate a cause of dyspnea or mechanism of PH.

Congenital Heart Disease
  • 1.

    Cardiac catheterization should be performed for patients with shunts when there is evidence of elevated pressures, chamber enlargement, or symptoms that are out of proportion to the size of the congenital lesion, and prior to closure of shunts.

  • 2.

    Cardiac catheterization should be performed to assess the hemodynamics of congenital heart disease patients with known or suspected right ventricular failure, especially in palliated single ventricle physiology.

  • 3.

    Cardiac catheterization should be performed to determine the severity of obstructions in series.

Cardiogenic shock and circulatory support devices
  • 1.

    Invasive hemodynamic assessment, with measurement of ventricular filling pressures, cardiac output, and systemic vascular resistance, is recommended for the diagnosis of cardiogenic shock.

  • 2.

    Continuous hemodynamic monitoring with a pulmonary artery catheter is recommended for acute management of patients receiving therapy with mechanical circulatory support.

  • 3.

    Pulmonary artery catheterization is useful to guide withdrawal of mechanical circulatory and pharmacologic support in patients with myocardial recovery from cardiogenic shock.

  • 4.

    In patients without recovery of myocardial and end-organ function, hemodynamic monitoring is useful to assess candidacy for and transition to advanced heart failure therapies, including durable mechanical circulatory support and heart transplantation.

LVOT, Left ventricular outflow tract; PH, pulmonary hypertension; WHO, World Health Organization.

Technical Issues

It is important to recognize that invasive hemodynamics are traditionally measured at rest, in the sedated state, and in a supine position. These limitations should be appreciated when invasive hemodynamics are used to reconcile cryptic symptoms, assess prognosis, or prepare patients for advanced therapies. However, most of our contemporary understanding of heart failure hemodynamics is derived from these resting, supine, and sedated studies. Traditional and novel hemodynamic formulas are illustrated in Fig. 34.1 . Exercise and upright hemodynamics can be obtained in a properly prepared laboratory and are often necessary in certain clinical situations, but are not commonly performed on a routine basis in most clinical catheterization laboratories. The hemodynamic response to various physiologic and/or pharmacologic challenges should also be considered at the time of RHC to maximize the information obtained during this invasive procedure. Finally, it should be appreciated that traditionally obtained hemodynamic measurements lack concomitant measurements of cardiac and/or intravascular volume, so pressure is used as a surrogate for volume.

Fig. 34.1, Hemodynamic formulas and calculations.

Pressure measurements in cardiac catheterization are recorded using fluid-filled catheters connected to strain-gauge pressure transducers using the principle of the Wheatstone bridge. Because of the need for pressure transmission to record a signal, a time delay is inherent and should be accounted for when assessing instantaneous pressure differences (e.g., gradients). Moreover, fluid-filled systems are influenced by various factors, including transducer height, patient position, catheter length, air bubbles, fluid frequency response/damping (e.g., catheter whip artifacts), and open connections.

These issues can be avoided by using micromanometer catheters that use high fidelity pressure sensors at the point of measurement (Millar Instruments, Houston, TX). Such systems can also be combined with special conductance catheters to provide simultaneous volume measurements, but their use is confined to research laboratories. These systems provide more sophisticated measures of ventricular performance such as contractility, diastolic function, and ventricular pressure-volume (PV) relationships.

The impact of respiration on intracardiac pressures should be considered. The dynamic changes in intrathoracic pressures associated with respiration are usually modest (e.g., −1 to 5 mm Hg) but can be quite dramatic (e.g., severe obesity, obstructive pulmonary disease) and will have a significant influence on intracardiac pressures. However, it is common in both clinical practice and investigation that mean pressure measurements rather than respirophasic ranges are reported, which can lead to important misinterpretations. For example, the pulmonary capillary wedge pressure (PCWP) averaged over the duration of the respiratory cycle may underestimate the true end-expiratory left ventricular end-diastolic pressure (LVEDP) and lead to an erroneous diagnosis of World Health Organization (WHO) group 1 rather than group 2 or mixed PH. It is optimal to manually measure end-expiratory pressures since the effects of negative intrathoracic pressures required for ventilation on intracardiac pressures are minimal at end expiration. A breath hold can be useful if done at end expiration as long as a Valsalva maneuver does not ensue.

RHC is generally safe, but its routine use in heart failure management should be tempered by complications associated with any invasive procedure. Serious complications, such as pneumothorax, pulmonary embolism, and pulmonary arterial rupture are rare. In the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) trial, in-hospital adverse events were more common among patients in the RHC group compared with the clinical assessment group (22% vs. 11.5%; P = .04). Adverse events due to the pulmonary artery catheter (PAC) occurred in 4% (n = 9) of the RHC group. The most common complication was access site bleeding. There were no hospital deaths attributed to the PAC. Adverse events included PAC-related infection, catheter knotting, pulmonary infarction and hemorrhage, and ICD shocks. Pulmonary arterial rupture and RBBB (with subsequent complete heart block in the setting of a baseline LBBB) did not occur. Pulmonary artery (PA) rupture is rare in clinical practice, but risk factors include severe PH, anticoagulation, mitral valve disease, and advanced age.

Hemodynamic Waveforms

In clinical practice, it is difficult to measure LV volume throughout the cardiac cycle rendering the use of PV loops for clinical care impractical. The difficulty in obtaining PV loops has resulted in a dependence on pressure versus time rather than pressure versus volume measurements to assess hemodynamic status and ventricular performance.

Each chamber has a distinct waveform and reflects cardiac filling as well as ventricular ejection. Personal inspection of specific cardiac chamber waveforms can often convey important hemodynamic information that is not appreciated by a single measured value.

Right Atrium and Ventricle

The right atrial pressure (RAP) and waveform can provide simple yet important insight into a patient’s overall hemodynamic status. During normal respiration, RAP decreases with inspiration to the same degree as the drop in intrapleural pressure (usually <5 mm Hg) and generally reflects intrapericardial pressure in the absence of pericardial constraint. Lack of an inspiratory fall, or even rise in RAP with inspiration (e.g., Kussmaul sign), is indicative of right ventricle (RV) diastolic dysfunction and often RV overload ( Fig. 34.2 ). Steep y descents are also indicative of RV diastolic dysfunction ( Fig. 34.3 ). The steep y descent results from the rapid inflow required to fill a stiff RV in early diastole, particularly in the presence of an elevated RAP. Similarly, the “dip and plateau” appearance in the RV tracing indicates rapid, early diastolic filling and abrupt cessation of diastolic inflow as the LV and RV reach the point of pericardial restraint. Such findings are commonly found in conditions associated with RV dysfunction, including advanced heart failure with reduced ejection fraction (HFrEF), restrictive cardiomyopathies, heart transplantation, and RV infarction. A prominent v wave is noted in severe tricuspid regurgitation, regardless of chronicity ( Fig. 34.4 ). The central venous pressure may also be approximated by the venous pressure in a peripheral vein with appropriate establishment of the phlebostatic zero reference.

Fig. 34.2, Right atrial pressure waveform.

Fig. 34.3, Right atrial (RA) pressure waveform. Restrictive cardiomyopathy: steep x and y descents. Appearance of the waveform conveys significant right ventricle dysfunction despite the minimal increase in RA pressure of 9 mm Hg.

Fig. 34.4, Right atrial pressure waveform. Severe tricuspid regurgitation: prominent v wave. Waveform appears ventricularized due to the organic disease of tricuspid valve.

The RV is a low-pressure chamber in normal individuals. A small systolic gradient between the RV systolic pressure (RVSP) and PA systolic pressure (PASP) facilitates forward flow in this low-pressure system. The RV waveform can be distinguished from the PA waveform by the rise in pressure during diastole in contrast to the fall in pressure in the PA tracing. The rise in the RVSP over time, dP/dt, can be used to estimate the PA diastolic pressure (ePAD) since pulmonic valve opening will occur at the end of isovolumic contraction or maximum dP/dt ( Fig. 34.5 ). The ePAD will approximate the PCWP (e.g., within 2–3 mm Hg) as long as the pulmonary vascular resistance is normal. This strategy was used for the CHRONICLE device to provide a continuous estimate of the PCWP.

Fig. 34.5, Schematic illustration of computer detection of the QRS complex (ECG Detect) , maximal first derivative of right ventricular pressure (dP/dtmax) and modified preejection interval (mPEI) . Pulmonary artery diastolic pressure (ePAD ) equals right ventricular pressure at maximal first derivative of pressure measured over time (dP/dt) . PAP, pulmonary artery pressure; RV, right ventricle; RVP, right ventricular pressure.

Pulmonary Capillary Wedge

A common concern in RHC is whether a true PCWP has been obtained ( Fig. 34.6 ). Fluoroscopy and a visible change in the waveform is typically used to confirm the PCWP position. Loss of the pulmonary arterial waveform and a change to a “flattened” appearance with attenuated deflections usually signifies the PCWP. A prominent v wave can also be seen with a true PCWP but can be easily confused with the PASP. The v wave of PCWP occurs well after the T wave of the ECG, whereas the peak systolic wave of PASP occurs before or within the T wave. Difficulty in distinguishing between PCWP and PASP is particularly problematic in patients with prominent v waves (e.g., acute severe mitral regurgitation, ventricular septal defects, and severe diastolic dysfunction).

Fig. 34.6, Errors in pulmonary capillary wedge pressure.

Hybrid tracings between PCWP and actual pulmonary artery pressure (PAP) result in an overestimation of PCWP and should be suspected when the PCWP exceeds the PA diastolic pressure ( Fig. 34.7 ). Damping of the hemodynamic waveform should also be considered. Underdamping, which is often referred to as ringing or “whip” artifact, can lead to inaccurate pressure recordings and can be rectified by drawing a small amount of blood or contrast into the catheter to increase the viscosity of the fluid. In patients with severe right ventricular enlargement and dysfunction, caution must be used when it comes to interpreting an elevated PCWP or LVEDP. Right ventricular pressure overload from pulmonary artery hypertension (PAH) can result in elevated LVEDP due to impaired relaxation of the LV secondary to RV enlargement as well as pericardial restraint (see also later discussion). In this setting, LV diastolic dysfunction is a consequence and not independent of the primary abnormality (PAH).

Fig. 34.7, Errors in pulmonary capillary wedge pressure.

If there is still uncertainty about the accuracy of the measured PCWP, it is best confirmed by other means. A common strategy is to use the O 2 saturation from a blood sample obtained from the PCWP position. In the true PCWP position, the O 2 saturation from the PCWP blood sample should have an O 2 saturation comparable to systemic arterial saturation (in the absence of intracardiac shunts). Wedge position can also be confirmed by cautious injection of contrast to document true wedging of the balloon. LVEDP should be directly measured if uncertainty exists as to the accuracy of the PCWP as a surrogate for left ventricular filling. In circumstances where accurate assessment of left atrial pressure (LAP) is critical, consideration should be given to directly measuring LAP across the atrial septum.

The PCWP waveform is similar to that seen in the left atrium with well characterized a and v waves, in addition to x and y descent ( c waves are less apparent in PCWP tracings). PCWP waveforms are also slightly damped and delayed compared to that seen in the LA because of transmission of the pressures through the lung parenchyma. As noted earlier, in the absence of increased pulmonary vascular resistance, PA diastolic pressure is similar to mean PCWP (e.g., within 2–3 mm Hg). If there is PH, the PA end-diastolic pressure will be markedly higher than PCWP. Furthermore, when pulmonary vascular resistance is increased by pulmonary venous hypertension or mitral stenosis, PCWP may overestimate LVEDP. PCWP may also underestimate LVEDP since PCWP is an intrathoracic pressure that is an indirect assessment of LVEDP and is not a direct measurement of LV filling pressure. In one study, PCWP was more than 5 mm Hg lower than LVEDP in about a third of cardiac patients. Therefore when it is critical to have a definitive measure of LV filling pressure, direct measurement of LVEDP is necessary.

The height of the v wave should be reported separately from the mean PCWP, particularly when it exceeds the height of the a wave by greater than 50%. The height of the v wave is determined by left atrial chamber compliance and distending blood volume. Although most commonly associated with acute severe mitral regurgitation (due to the sudden retrograde volume overwhelming the compliance of the left atrium), it is also characteristic of a large volume ventricular septal defect and can be seen in severe left ventricular diastolic dysfunction.

Large v waves augment the mean PCWP and can lead to overestimation in LAPs , as in Fig. 34.8 . In this setting, the mean a wave pressure should be reported, in addition to the mean PCWP and height of the v wave, to reflect the end-diastolic PCWP. Another approach is to use the onset of the QRS, complex to define the end-diastolic PCWP.

Fig. 34.8, Pulmonary artery wedge pressure (PAWP) and time coordinates during diastole.

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