Acute Decompensated Heart Failure

Abstract

Heart failure is a common condition associated with significant morbidity and mortality. Acute decompensated heart failure (ADHF) is the leading cause of hospitalization among elderly patients in the USA. The hemodynamic categorization of patients with ADHF is based on the intracardiac filling pressures and the adequacy of cardiac output. Much of the information required to assess these patients can be derived from the clinical examination. Noninvasive hemodynamic assessment with Doppler echocardiography is helpful in the management of heart failure patients and may provide important information at the time of acute decompensation. Right heart catheterization with placement of a pulmonary artery catheter is generally reserved for patients in whom hemodynamics remain uncertain despite optimal clinical and noninvasive evaluation. The primary goal of treatment is to relieve congestion rather than increasing cardiac output.

Epidemiology of Acute Decompensated Heart Failure (ADHF)

Heart failure is estimated to affect 2% of the adult population. There are over one million hospitalizations for ADHF in the USA per year, and, among the Medicare population, it is the leading discharge diagnosis [1, 2]. About 25% of these patients present as de novo heart failure, and 75% present as an exacerbation of chronic heart failure. When not due to an arryhthmia or primary valvular disease, heart failure may arise in those with either reduced (≤40%), preserved (≥50%), or mid-range (40–50%) left ventricular ejection fraction [3, 4]. The inpatient mortality ranges from 3% to 25% depending on associated comorbidites and clinical characteristics [5]. The readmission rate at 30 days is a staggering 20–25% [6].

Hemodynamics of Decompensated Heart Failure

The hemodynamic perturbations in the syndrome of decompensated heart failure are characterized by elevated intracardiac filling pressures, normal or reduced cardiac output, and abnormalities in the systemic and pulmonary vascular resistance (PVR). Although there are syndromes in which the cardiac output is abnormally elevated, these will not be discussed in this chapter.

Intracardiac Filling Pressures

When volume overload (increased preload) and increased afterload occur, there is an elevation of left ventricular end-diastolic pressure from baseline (which may already be elevated). This leads to a rise in left atrial pressure and thus pulmonary capillary wedge pressure (PCWP). The elevation in the PCWP leads to passive pulmonary hypertension (pulmonary venous hypertension, WHO Group 2). Either volume overload or pulmonary hypertension (or both) leads to elevation of the right atrial pressure (RAP). The extent of pulmonary hypertension depends on the degree and chronicity of elevation of the PCWP and the degree of superimposed pulmonary vasoconstriction and vascular remodeling (see section “Vascular Resistance”).

In patients with ADHF, PCWP is usually >22 mmHg and right atrial pressure >10 mmHg; such a patient is typically classified as “wet.” In the average ADHF patient, a RAP >10 mmHg correlates to a PCWP >22 mmHg about 80% of the time [7,8,9,10]. In these “concordant” cases, PCWP is usually about 2–2.5 times RAP. About 20% of the time, there is “discordance” in this relationship; one example is in patients with disproportionate RV failure in whom RAP is significantly elevated with a normal or only mildly elevated PCWP. The other example is when RAP is normal with a significantly elevated PCWP as one may see in acute left-sided heart failure without volume overload or a very noncompliant LV with high resting filling pressure despite euvolemia. These are important hemodynamic concepts to understand as they may affect management.

Cardiac Output

Cardiac output is a product of stroke volume and heart rate (see Chap. 4). Stroke volume is determined by preload (filling pressure), myocardial contractility, and afterload (mainly systemic vascular resistance). In patients with ADHF, a decrease in cardiac output is more likely due to low stroke volume but occasionally can be due to an inappropriately low heart rate. It is important to note that in the majority of cases of ADHF, the cardiac output remains normal. Low cardiac output, as measured by Fick or thermodilution (we more often use the Fick method at our institution), occurs in a minority of patients who have advanced heart failure or excessively low filling pressures due to overdiuresis. Arbitrarily, a cardiac index (cardiac output/body surface area) of <2.2 is considered low, and such a patient is typically classified as “cold” while a patient with a cardiac index >2.2 is classified as “warm [11].” A patient with a low cardiac index may be compensated and have no signs or symptoms of low perfusion at rest; thus, it is important to consider the overall clinical picture in addition to the calculated cardiac index when deciding treatment options and prognosis.

When evaluating a patient with ADHF, it is useful to categorize the patient according to the estimation or measurement of left-sided filling pressures and cardiac output. The classification scheme shown in Fig. 19.1 is a simple and efficient way to clinically categorize patients and help guide appropriate treatment strategies.

Fig. 19.1

Hemodynamic profiles in patients with left-sided heart failure

Vascular Resistance

Systemic vascular resistance (SVR) is measured as the difference between mean arterial pressure and right atrial pressure divided by cardiac output. Classically, in ADHF, SVR is high as a result of an increased level of vasoconstricting neurohormones such as norepinephrine , angiotension II, and endothelin. However, in the contemporary era in which treatment with agents that block the renin angiotensin aldosterone system (ACE inhibitors/angiotensin receptor blockers/angiotensin receptor blocker + neprilysin inhibitors) and beta blockers is common, the SVR can be normal or sometimes even low. Patients with right-sided heart failure and renal insufficiency are more likely to have normal or low SVR. Knowing the blood pressure and/or the SVR is important with respect to determining treatment options.

Pulmonary vascular resistance (PVR) is measured as the difference between mean pulmonary artery pressure and PCWP (left atrial pressure surrogate) divided by cardiac output. It is important to note that in some patients, in addition to passive pulmonary hypertension due to elevated left atrial pressure, there is an additional component of pulmonary arterial vasoconstriction, raising pulmonary vascular resistance and thus further raising pulmonary artery pressure (pulmonary arterial hypertension). Long-standing elevation of PCWP can also lead to pulmonary vascular remodeling. This component of pulmonary vascular resistance cannot be reversed by acutely lowering PCWP or with the use of pulmonary vasodilators. Reversal of pulmonary vascular remodeling can be accomplished by long-term consistent lowering of left atrial pressure (e.g., correction of mitral stenosis, left ventricular assist device placement). Patients with an elevated PVR that cannot be reversed have a worse prognosis.

Hemodynamic Evaluation of Decompensated Heart Failure

There are many ways to evaluate hemodynamics in heart failure. The initial and most practical strategy is starting with the clinical history and the physical examination (H&P). Further important hemodynamic information can be gleaned from echocardiography. The most invasive and accurate way to assess hemodynamics is with right heart catheterization using a pulmonary artery catheter, which is reserved for special situations.

Clinical Assessment

The H&P, together with a chest X-ray and basic labs, provides the majority of the hemodynamic information needed to treat patients with acute decompensated heart failure (ADHF). The shortcomings of an H&P are important to acknowledge however, and some of these will be highlighted as we discuss each of the clinical cases at the end of the chapter.

Clinical Estimation of Filling Pressures

Using the H&P, experienced clinicians can estimate, with reasonable accuracy, the intracardiac filling pressures [12, 13]. Some of the important signs and symptoms of elevated filling pressures are outlined in Table 19.1. Symptoms of elevated right atrial pressure, depending on the degree and chronicity, include abdominal bloating and discomfort, early satiety, and RUQ pain that can mimic an abdominal etiology. Signs of elevated right atrial pressure include lower extremity edema, hepatomegaly, and, in advanced right heart failure, ascites. However, the most reliable sign of elevated right atrial pressure is elevation of the jugular venous pressure (JVP), and depending on the skill of the examiner, the right atrial pressure can be reliably assessed at the bedside in most heart failure patients. Indeed, patients with elevation of right atrial pressure may have no edema or ascites, and the only sign may be elevated jugular venous pressure. It is in these patients that congestion is often missed and the patient is incorrectly assumed to be euvolemic.

Table 19.1 Symptoms and signs of elevated intracardiac filling pressures

Elevation of left atrial pressure/PCWP pressure leads to symptoms of exertional/resting dyspnea, dry cough (worse in the recumbent position), orthopnea, and paroxysmal nocturnal dyspnea. In fact, orthopnea and particularly paroxysmal nocturnal dyspnea are the most specific symptoms of elevated PCWP. The physical exam finding that is most specific for an elevated PCWP (in the absence of mitral stenosis) is an S3 gallop; however, it is not a sensitive finding as most patients with an elevated PCWP do not have an S3 gallop. One of the best clues that a heart failure patient has an elevated PCWP is elevation in the jugular venous pressure. This is because elevated right atrial pressure is predictive of an elevated PCWP in most chronic heart failure patients (see section “Intracardiac Filling Pressures”).

Clinical Estimation of Cardiac Output

Estimating cardiac output is more difficult at the bedside [12], but there are several clues to low cardiac output (see Table 19.2). General fatigue, impaired mentation, cool extremities, low urine output, and increased lactate level are useful clues. An objective measure is to calculate the “proportional pulse pressure” which is the systolic blood pressure minus the diastolic blood pressure divided by the systolic blood pressure. A proportional pulse pressure <25% suggests a cardiac index of <2.2 [11].

Table 19.2 Signs and symptoms of low cardiac output

Echocardiography

The echocardiogram is an important tool in the assessment of heart failure. In patients presenting with a new diagnosis, it is essential in establishing the mechanism of heart failure (preserved versus reduced ejection fraction or valvular etiology; see Chap. 6). Performing a baseline echocardiogram is given a Class I (should be performed) recommendation in patients with a new diagnosis of heart failure according to the ACC/AHA guidelines [14]. For patients with an acute exacerbation of chronic heart failure, it is not always necessary to obtain an echocardiogram. This is particularly true when there is an obvious precipitant for the change in clinical status. When the patient is critically ill or the symptomatic decline is precipitous, the echocardiogram can exclude new structural abnormalities. This is given a IIa (reasonable to perform) recommendation by the ACC/AHA guidelines [14] and has been shown to provide reliable estimates of invasive hemodynamics in this setting [15].

Echo Assessment of Filling Pressures

The measured size of the inferior vena cava (IVC) and its changes with respiration is traditionally used to estimate right atrial pressure [16]. Using this method, there is an assumption that there is continuity between central veins and the right atrium, the same assumption used in interpreting the jugular venous pressure as a reflection of right atrial pressure. Patients with an IVC measuring ≤2.2 cm in diameter that collapses by 50% or more with a sniff are designated as having a low RA pressure (assigned a value of 3 mmHg for the purposes of calculations). Patients with a distended IVC that does not collapse with sniff are designated as having a high RA pressure (15 mmHg). Patients with intermediate findings are assigned an RA pressure of 8 mmHg [16]. An example of this technique is given in Case 3.

Echocardiographic estimation of left ventricular end-diastolic pressures is a continued area of active investigation. The ratio of early diastolic inflow velocity across the mitral valve (E) to the early peak velocity of the mitral valve annulus (E′) has been shown to have a reasonably good correlation with LVEDP [17, 18]. This technique is used in a semiquantitative fashion. An E:E′ ratio of <8 suggests a normal LVEDP. An E:E′ ratio of >15 suggests an LVEDP of greater than 15 [17]. The E:E′ ratio was shown to be less predictive among patients with advanced heart failure admitted to the ICU [19]. Research is underway to find more consistent and precise echocardiographic predictors of LVEDP.

Echo Estimation of Pulmonary Pressures

The most well-accepted means of estimating pulmonary pressures with echocardiography is to calculate the pressure gradient across the tricuspid valve using the peak velocity of the tricuspid regurgitation jet [16]. Using a simplified Bernoulli equation, the pressure gradient between the right ventricle and the right atrium can be estimated as P = 4v ². This is also discussed in detail in Chap. 6, and an example will be reviewed in Case 3.

Echo Assessment of Cardiac Output

Stroke volume (and therefore cardiac output) can be estimated by echocardiography, although it requires several important assumptions be made [20]. The technique for making this estimation is as follows (see also Chap. 6).

The Doppler profile of flow through the LV outflow tract is a graph of velocity vs. time. Taking the integral of this curve gives a unit of distance. When this distance is multiplied by the surface area of the left ventricular outflow tract (LVOT), the resulting number (a volume) is the stroke volume. The LVOT area can be estimated by using 2D echo measurements of its diameter in long axis and then assuming that it is a circle. Although this method is not frequently employed, it should yield a reasonably accurate estimate of stroke volume and therefore of cardiac output (when multiplied by heart rate).

Right Heart Catheterization

Right heart catheterization remains the gold standard for measuring many of the hemodynamic parameters important in the management of heart failure. As noninvasive methodology has improved, however, there are now fewer situations in which this information is necessary [14]. Additionally, a large randomized study showed no benefit to the routine use of a pulmonary artery catheter to manage patients with ADHF in terms of the combined endpoint of mortality and days outside of hospital at 6 months [21].

Right heart catheterization should be considered in a patient who is refractory to initial therapy, whose volume status and cardiac filling pressures are unclear, who has clinically significant hypotension (typically SBP <80 mmHg) or worsening renal function during therapy, or who is being considered for cardiac transplant and needs assessment of the degree and reversibility of pulmonary hypertension and PVR [14, 22]. This latter issue will be discussed further in Case 3.

In each of Cases 1–3, pressures in the right atrium (RA) and pulmonary artery (PA) as well as PCWP as derived from right-heart catheterization are displayed. RA pressure and PCWP are commonly used clinically as descriptors of right and left ventricular “preload” respectively (see Chapter 1). The PA pressure is reported as systolic PA pressure/diastolic PA pressure (mean PA pressure). The cardiac index, as estimated using the Fick principle (see Chap. 4), is also shown. The cardiac index is calculated by dividing the cardiac output by the patient’s body surface area. This factor in the size of the patient which is clearly important as normal cardiac output varies with size.

Implantable Hemodynamic Monitoring

There has been recent interest in the use of implantable hemodynamic monitoring systems in the management of heart failure. The CardioMEMS HF system (St. Jude Medical), approved by the FDA in 2016, is a small device implanted in a branch of the pulmonary artery allowing for continuous monitoring of PA pressure. A large randomized clinical trial using this device in patients with chronic NYHA III heart failure demonstrated a reduction in heart failure hospitalizations [23].

General Principles of Management

The majority of patients who present with ADHF are congested and have elevated filling pressures. The central goal of therapy is to decongest the patient and optimize filling pressures to normal or near normal levels. This is most effectively achieved with the use of an intravenous loop diuretic. In instances of diuretic resistance, combining a loop diuretic with a thiazide, amiloride, and/or spironolactone can be highly effective. If this approach is not successful, as can be the case in advanced renal dysfunction, ultrafiltration may be considered [24, 25].

To further optimize hemodynamics, vasodilators which reduce filling pressures can be used in conjunction with diuretics. Vasodilators, in addition to lowering filling pressures, improve cardiac output by reducing afterload, decreasing functional mitral regurgitation (and thereby increasing forward cardiac output), and reducing wall stress [26,27,28]. The patients who benefit the most from vasodilators are those with elevated blood pressure and high SVR. It is important to note, however, that a patient with “normal” blood pressure may still have an elevated SVR and benefit from vasodilator therapy. Both “wet and warm” and “wet and cold” patients may be treated with vasodilators.

Intravenous vasodilators used in heart failure are nitroprusside, nitroglycerin, and nesiritide. The vasodilator of choice at our own institution is nitroprusside, which should be administered in an ICU setting with hemodynamic monitoring using a right heart catheter and, in most instances, a blood pressure cuff (as opposed to an arterial line). This is well tolerated and the incidence of cyanide or thiocyanate toxicity is extremely rare to nonexistent [29, 30]. A mean arterial pressure of approximately 65 mmHg is targeted, but this depends on the patient and may need to be higher if renovascular or coronary artery disease is present or suspected, or if the patient is chronically hypertensive with an altered renal autoregulatory threshold. Excessive or overexuberant vasodilation with decrease in blood pressure beyond the renal autoregulatory threshold often leads to decreased renal perfusion, worsening renal function, and should be avoided. Once patients have clinically and hemodynamically improved on intravenous vasodilators, they may be transitioned to an oral vasodilator regimen of either ACE inhibitors, the combination of hydralazine and isosorbide dinitrate, or a combination of all three agents [31].

Intotropic therapy (milrinone or dobutamine) should be reserved for low output states associated with hypotension and end-organ hypoperfusion [32]. The typical patient has advanced systolic dysfunction, a low proportional pulse pressure, cool extremities, and worsening renal function despite adequate filling pressure (need to rule out hypovolemia) and is unresponsive to or intolerant of intravenous vasodilators. These patients constitute no more than 5% of the total ADHF population. Inotropes can also be used as palliative therapy for end-stage heart failure or as a bridge to transplantation.

It is important to note that inotropes increase myocardial oxygen consumption by increasing heart rate and myocardial contractility and can precipitate atrial and ventricular arrhythmias as well as myocardial ischemia. In contrast to dobutamine, milrinone has a long half-life (2.5 h) and is renally excreted, and the dose should be adjusted for renal function. Also, given that milrinone is a more powerful vasodilator, hypotension is more common with this agent and therefore should be used with caution or even avoided when the systolic blood pressure is <90 mmHg. In the setting of background beta blocker therapy, dobutamine will be ineffective unless used in high doses, and milrinone is favored [33, 34]. In rare circumstances, vasopressors are used (dopamine, norepinephrine, vasopressin), when the patient is vasodilated with a low SVR and profound hypotension.

In patients who are managed on a telemetry floor without invasive monitoring, the goal of therapy is to normalize intravascular volume as reflected by relief of edema and normalization of the jugular venous pressure (<8 cmH₂O). When this is achieved, most patients will no longer have orthopnea or dyspnea. Signs of overdiuresis consist of orthostatic decrease in blood pressure and worsening renal function. A common clinical error is incorrectly assuming euvolemia has been achieved when edema has resolved yet unrecognized elevation of the jugular venous pressure persists. By the same token, one may have normalized the jugular venous pressure and achieved intravascular euvolemia but may still have residual edema due to low albumin, venous insufficiency, or drug side effect (e.g., calcium channel blockers) and wrongly assumed to be intravascularly volume overloaded.

In patients managed with hemodynamic monitoring with a right heart catheter, vasodilator therapy (both intravenous and oral) and diuretics are “tailored” to certain hemodynamic goals. Typically a PCWP of ≤16 mmHg, an RA pressure of ≤8 mmHg, and an SVR of about 1000–1200 dyn are targeted. A common misconception that patients with dilated dysfunctional ventricles require higher filling pressures to maintain cardiac output based on the Starling curve has been dispelled by data showing that most of these patients can maintain and even improve cardiac output with normal or near normal PCWP [30, 35]. As far as RA pressure goals, patients with primarily RV failure may require a higher RA pressure than 8 mmHg to maintain cardiac output and renal perfusion. It has been shown that patients with very elevated RA pressure can have worsening renal function on the basis of renal venous congestion. By lowering RA pressure with diuretics and vasodilators, the kidney is “decongested” or decompressed and renal function often improves [36,37,38] (see Fig. 19.2).

Fig. 19.2

Renal venous congestion: increased right atrial pressure leading to elevated pressure in the IVC and thus the renal vein (especially when coupled with low mean arterial pressure) can lead to worsening renal function by “congesting the kidney.” Decreasing right atrial pressure and thus the renal venous pressure can lead to improved renal function

The goal of cardiac index is usually >2.2, but one has to acknowledge that using the Fick equation, oxygen consumption is estimated and not measured and that up to a 20% variation in cardiac output can be seen [39]. Thus, targeting a specific number per se is simplistic, and the entire clinical picture needs to be considered (e.g., a patient with a cardiac index of 1.8 who with normal PCWP feels well may not need further intervention). Although cardiac output frequently improves, the cardiac output is not the primary target of therapy, rather the reduction of the filling pressures [40]. The general principles of management for the different presentations of heart failure are shown in Fig. 19.3.

Fig. 19.3

Treatment paradigm in patients with left-sided heart failure

Clinical Presentations of Acute Heart Failure

Case 1

A 46-year-old male with a history of diabetes and hypertension presents with sudden onset of retrosternal chest pain. He is brought by emergency medical services to the hospital where he is found to have an elevated jugular venous pressure, bilateral rales, and edematous and well-perfused extremities. His electrocardiogram reveals ST segment elevation in the inferior leads (ECG leads II, III, and aVF). He is transferred to the cardiac catheterization laboratory but becomes dyspneic and hypoxic lying flat on the table. On examination, his HR is 90 bpm and BP measures 130/90 mmHg. His oxygen saturation is 93% on a high-flow oxygen mask.

A left heart catheterization is performed. The right coronary artery is found to be completely occluded, and the patient undergoes successful angioplasty and stenting to the vessel with good results. A pulmonary artery catheter is placed yielding the following hemodynamics:

RA	PA	PCWP	Cardiac index
12	38/25 (30)	24	3.2

A sample from his left heart catheterization is shown in Fig. 19.4. The LVEDP is elevated and correlates closely with the PCWP obtained with right heart catheterization. An echocardiogram is performed which demonstrates severe akinesis of the inferior wall from base to apex. The overall left ventricular systolic function is described as mildly decreased. Right ventricular function is reported as normal.

Fig. 19.4

Case 1: left ventricular pressure tracing

Case 1: Hemodynamic Assessment

This is an example of so-called “warm and wet” heart failure (based clinically on his JVP, lower extremity edema and warm extremities, and hemodynamically on an elevated PCWP with a cardiac index in the normal range). Occlusion of the right coronary artery led to systolic and diastolic dysfunction of the left ventricle. This resulted in elevation of the left-sided filling pressures with pulmonary edema.

The orthopnea and hypoxia suggested an acute rise in PCWP. The relationship between PCWP and clinical signs of pulmonary congestion has been well characterized in patients with acute myocardial infarction. The onset of pulmonary congestion generally occurs at a PCWP between 18 and 20, and acute pulmonary edema generally correlates with a PCWP of greater than 30 [41]. These data have been challenged, however [42], and were collected prior to the use of reperfusion techniques such as fibrinolysis and primary percutaneous coronary intervention.

In this case, the importance of echocardiography was to confirm that the main problem was a left ventricular wall motion abnormality and not acute mitral regurgitation, which can be a mechanical complication of inferior myocardial infarction. Suspicion was low for this patient as such cases generally present with cardiogenic shock. However, a high index of suspicion is important. Another known complication of inferior myocardial infarction can be right ventricular infarction. This occurs in some patients when there is proximal occlusion of the right coronary artery but would generally be manifested by an elevated JVP and hypotension without pulmonary congestion. The right heart catheterization provided accurate measurement of cardiac output which has important prognostic implications [43].

In this case, the underlying cause of left ventricular dysfunction is acute coronary occlusion. This is best treated by promptly opening the culprit vessel (here with emergent PCI) in efforts to improve contractility by restoring flow to the compromised ischemic myocardium. Diuretic therapy was also provided to facilitate reduction of volume overload and clearance of pulmonary edema. This is generally considered to be a mainstay of the treatment of decompensated heart failure with increased RA pressure and PCWP. The patient was treated with intravenous furosemide with excellent response. After several days, he no longer required supplemental oxygen, and clinical and radiographic evidence of pulmonary congestion had improved.

Case 2

A 19-year-old G₁P₁ female presents to the emergency department with profound fatigue and right upper quadrant discomfort. Two weeks prior, she gave birth to a healthy baby boy via an uncomplicated vaginal delivery. Since the delivery, she has noticed gradual progression of tiredness to the point where she is no longer able to carry out basic activities of daily living and is short of breath at rest. There is no orthopnea or leg swelling but occasional paroxysmal nocturnal dyspnea. She complains of a dull aching discomfort in the right upper quadrant of her abdomen.

On examination, she is tachycardic with a HR of 120 bpm and BP of 106/88 mmHg. Her extremities are warm. The JVP is elevated to 8 cm above the sternal angle at 60°. The chest is clear to auscultation. In addition to loud first and second heart sounds, a prominent S3 is heard. There is right upper quadrant abdominal tenderness with no rebound tenderness or guarding. A chest X-ray is performed and shows an enlarged cardiac silhouette. An ECG shows sinus tachycardia with low voltages and a nonspecific ST abnormality. Labs are notable for elevated liver enzymes.

Echocardiography shows severe left ventricular dysfunction with an LVEF of 10%, moderate mitral regurgitation, and moderate right ventricular dysfunction. She is given a presumptive diagnosis of a peripartum cardiomyopathy. She is admitted to a heart failure intensive care unit and a pulmonary artery catheterization is performed. Samples from the tracings are seen in Fig. 19.5. Note the somewhat exaggerated waveforms on the section of the tracing labeled pulmonary artery, a commonly encountered artifact.

Fig. 19.5

Case 2 sample hemodynamic tracings : Pressures were recorded with the catheter positioned in the right atrium (RA), right ventricle (RV), and pulmonary artery (PA) as well as with pulmonary capillary “wedging” (PCWP). The following pressures were noted: RA mean pressure of 10 mmHg (normal, 0–8 mmHg); RV, pressure of 46/10 mmHg (normal 15–30/0–8 mmHg); PA, pressure of 46/30 mmHg (normal 15–30/4–12 mmHg); and PCWP, mean pressure of 32 mmHg (normal 1–10 mmHg)

Her reported hemodynamics are as follows:

RA	PA	PCWP	Cardiac index
10	46/30 (35)	32	2.0

Case 2: Hemodynamic Assessment

This is a case of a patient with so-called “cold and wet” heart failure. The cardiac index is reduced, and both the RA pressure and the PCWP are increased. When accompanied by findings of impaired end-organ function, this state would be termed cardiogenic shock (see Chap. 14). For this patient, there is no clinical evidence of a low perfusion state, such as hypotension, decreased level of consciousness, cool extremities, or renal failure.

The right upper quadrant pain and elevated liver enzymes reflect passive congestion of the liver. The physical examination disclosed an elevated JVP which corresponds to the elevated RA pressure. Note that there were no rales on chest examination and only minimal pulmonary edema on chest X-ray. These findings may have led the clinician to suspect that PCWP was not elevated. Unfortunately, such findings of elevated PCWP are frequently not present among chronic heart failure patients when the time-course of the decompensation is gradual. In such cases, pulmonary lymphatic drainage is enhanced and sufficient to prevent the accumulation of interstitial edema in the lungs. The finding of an S3 should definitely steer the clinician in the right direction, however. The low cardiac output was not recognized at the bedside due to the lack of cool extremities, altered mentation, and low urine output underscoring the insensitivity of these findings [12, 44]. However, if one calculates the proportional pulse pressure in this patient (106–88/106), a value of 17% is obtained suggesting a low cardiac index of <2.2 (see section “Clinical Estimation of Cardiac Output”) [11].

The presence of a significant resting sinus tachycardia is ominous however. It suggests that the patient is compensating for a reduced stroke volume by increasing heart rate to maintain cardiac output.

The echocardiogram was crucial in confirming that severe biventricular dysfunction was the cause of the heart failure syndrome. The right heart catheterization was performed because of a concern that the patient was potentially unstable and needed invasive monitoring. In this case, the right heart catheterization also shows mild elevation in pulmonary artery pressure. The calculated pulmonary vascular resistance (see Chap. 12 for more details) is normal at 1.0 Wood unit:

$$ {\displaystyle \begin{array}{l}\mathrm{PVR}=\frac{\left(\mathrm{Mean}\ \mathrm{PA}\ \mathrm{pressure}-\mathrm{PCWP}\right)}{\mathrm{Cardiac}\ \mathrm{output}}\\ {}\mathrm{PVR}=\frac{35-32}{3\ast }=1\end{array}} $$

∗Cardiac index of 2.0 corresponded to cardiac output of 3 L/min because of body surface area of 1.5 m².

This suggests that the patient’s pulmonary hypertension is passive and there is no element of pulmonary vasoconstriction or pulmonary vascular remodeling.

The patient was treated with diuretic therapy, ACE inhibitors, and digoxin and observed carefully in an ICU setting. Beta blockers should not be initiated in such a patient until they become euvolemic and hemodynamically stable. She was discharged from the hospital 7 days later. Over the next 6 months, the patient was followed closely as an outpatient and had dramatic improvement in symptoms and complete resolution of LV dysfunction. She was advised to avoid pregnancy in the future due to the high risk of recurrent heart failure.

Case 3

A 58-year-old male is referred to a specialized heart failure clinic for evaluation. He has been followed for several years for a non-ischemic dilated cardiomyopathy with severe limitation of his exercise tolerance. His physician sends him for evaluation for the possible need for heart transplantation due to end-stage heart failure. When questioned, he reports that over the past 3 weeks, he has had worsened symptoms of weight gain and leg swelling. These symptoms began after he had started taking a nonsteroidal anti-inflammatory drug for arthritis. On examination, his HR is 90 bpm and his BP measures 98/70 mmHg. He is grossly edematous with pitting edema of both legs as well as scrotal edema. His JVP is elevated with prominent v waves. Auscultation of the chest reveals normal breath sounds with no rales or wheeze. On examination of the precordium, there is a loud pulmonic component of the second heart sound and an S3 gallop.

Echocardiography shows severe left ventricular dysfunction with an LVEF of 10% and moderate mitral regurgitation. Severe right ventricular dysfunction is also noted. The estimated RVSP by echocardiography is 88 mmHg (see Fig. 19.6).

Fig. 19.6

Case 3: estimation of pulmonary artery systolic pressure by echocardiography. Peak velocity of the tricuspid regurgitation jet is 4.27 m/s (a) – this suggests a gradient from the RV to the RA of ∼73 mmHg. [RV to RA gradient = 4v ² = 4 × (4.27)² = 72.9 mmHg. The IVC is dilated (b) with a diameter of 2.8 cm and less than 50% variation with respiration – these findings suggest an RA pressure of 15 mmHg. Estimated peak pulmonary artery pressure is 88 mmHg (assuming no pulmonary valve stenosis) (73 +  15 = 88)

The patient is admitted to the hospital, and a right heart catheterization is performed with the following results:

RA	PA	PCWP	Cardiac index
19	88/44 (59)	39	1.5

Case 3: Hemodynamic Assessment

This is another case of so-called “cold and wet” heart failure with reduced cardiac output and elevated right- and left-sided filling pressures. Note again that the patient was not hypoxic and auscultation of the chest did not reveal rales despite a very high PCWP. In contrast to the previous case, the pulmonary hypertension is severe with pulmonary artery pressures approaching the systemic pressures. The loud pulmonic component of S2 is consistent with these high pressures, although it is not a sensitive finding.

The calculated pulmonary vascular resistance is very high (see calculations below) suggesting that there is a pulmonary arterial component to the pulmonary hypertension that would not be immediately reversed if the PCWP was lowered.

$$ {\displaystyle \begin{array}{l}\mathrm{PVR}=\frac{\left(\mathrm{Mean}\ \mathrm{PA}\ \mathrm{pressure}-\mathrm{PCWP}\right)}{\mathrm{Cardiac}\ \mathrm{output}}\\ {}\mathrm{PVR}=\frac{59-39}{2.5}=8\kern0.5em \mathrm{Wood}\ \mathrm{units}\end{array}} $$

Note how closely the PA pressure was estimated by the transthoracic echocardiogram. Studying the parasternal short-axis images from the echocardiogram also gives us some idea of the relative left- and right-sided intracardiac pressures (Fig. 19.7). The flattened configuration of the interventricular septum during both systole and diastole suggests that the pressure in the right ventricle (and hence the pulmonary artery) is very high during both systole and diastole.

Fig. 19.7

Case 3: parasternal short-axis echo images showing pronounced flattening of the interventricular septum during diastole (a) which is still present during systole (b). This produces a “D-shaped appearance” of the left ventricle as emphasized in the cartoon above. Severe left ventricular dysfunction is suggested by the minimal change in area of the left ventricular cavity

The patient was treated with inotropic therapy using milrinone, as well as a continuous infusion of furosemide. He was felt to have advanced heart failure, but his high pulmonary vascular resistance precluded heart transplantation because of the risk that the transplanted heart would develop acute right ventricular failure. He underwent placement of a left ventricular assist device which functions as an additional mechanical pump that reroutes blood from the left ventricle into the aorta. With this intervention, he had a dramatic improvement in symptoms and exercise tolerance as well as a marked reduction in PCWP and pulmonary artery pressure.

Pearls of Assessment

• The history and physical examination provide the majority of the hemodynamic information required to manage acute decompensated heart failure.

• No single symptom or sign is perfectly sensitive or specific for the diagnosis of acute decompensated heart failure.

• The most reliable sign of elevated right atrial pressure is elevation of the jugular venous pressure.

• Paroxysmal nocturnal dyspnea is a specific symptom for elevated PCWP.

• Transthoracic echocardiography is an important means of establishing the mechanism of newly diagnosed heart failure and of excluding new structural problems as the trigger for heart failure exacerbation.

• Echocardiography is not needed in routine heart failure exacerbations when a cause for decompensation is clear.

• Need for right heart catheterization is being obviated by noninvasive means of estimating hemodynamic parameters in most situations.

• Right heart catheterization in acute decompensated heart failure is indicated when volume status and cardiac filling pressures are unclear and clinically significant hypotension or worsening renal function during therapy occurs and for the evaluation of pulmonary vascular resistance.

Review Questions

• 1. A patient with known chronic systolic heart failure is admitted with acute decompensated heart failure. The patient has orthopnea and paroxysmal nocturnal dyspnea. On exam, the jugular venous pressure (JVP) is elevated and estimated to be 10 cm above the sternal angle while the patient is seated upright. Auscultation reveals an S3 gallop. Which of the following suggests an elevated pulmonary capillary wedge pressure (PCWP)?

• A. Orthopnea

• B. S3 gallop

• C. Elevated JVP

• D. All of the above

Answer D

Orthopnea and paroxysmal nocturnal dyspnea are the most specific symptoms for elevated PCWP . Although an S3 gallop is not sensitive, it is the most specific sign of left ventricular filling pressure. Elevated jugular venous pressure, although directly estimates right atrial pressure, is a surrogate for elevated PCWP in the vast majority of cases.

• 2. A patient admitted with decompensated heart failure undergoes right heart catheterization. The right atrial pressure is 5 mmHg, the pulmonary capillary wedge pressure is 10 mmHg, and the cardiac output is 4.0 L/min with cardiac index 1.9 L/min/m².

This is an example of:

• A. Warm and wet heart failure

• B. Warm and dry heart failure

• C. Cold and wet heart failure

• D. Cold and dry heart failure

Answer D

The cardiac output of 4 L/min is close to normal. However, this patient has a large body surface area, and his calculated cardiac index is low. The PCWP and RA pressure are both in the normal range.

• 3. A 72-year-old male presents to the emergency department with a 2-week history of progressive shortness of breath with orthopnea and paroxysmal nocturnal dyspnea. On exam, he has peripheral edema and an elevated JVP at 12 cm above the sternal angle while seated upright. A prominent third heart sound is heard. The patient has inspiratory rales to the mid lung zones bilaterally. A chest X-ray confirms the presence of pulmonary congestion with vascular redistribution, Kerley B lines, and small bilateral pleural effusions.

The most appropriate next study to assess this patient’s etiology of heart failure and hemodynamics is:

• A. 2D echocardiogram with Doppler

• B. Right heart catheterization

• C. Computed tomography with IV contrast

• D. Magnetic resonance imaging

Answer A

Echocardiography is a noninvasive, readily available and relatively inexpensive tool for evaluation of left ventricular function, valvular disease, and hemodynamics. It is recommended as a first-line investigation for patients with a new diagnosis of heart failure.

• 4. The following are all appropriate indications for use of a pulmonary arterial catheter in heart failure except:

• A. Distinction of pulmonary edema related to heart failure from other causes of hypoxia in a critically ill patient in the intensive care unit

• B. Assessment of a patient in shock when intracardiac filling pressures cannot be adequately estimated by noninvasive means

• C. Monitoring of response to beta blocker therapy on routine annual follow-up

• D. Measurement of pulmonary pressures and calculation of pulmonary vascular resistance prior to planned heart transplantation

Answer C

For reasons discussed in the section on hemodynamic assessment, the use of pulmonary artery catheters in heart failure should be limited to certain scenarios such as those outlined in answers A, B, and D.

• 5. A patient admitted with decompensated heart failure undergoes right heart catheterization. The right atrial pressure is 10 mmHg, and the pulmonary arterial pressures are 59/32 mmHg with a mean of 40 mmHg. The pulmonary capillary wedge pressure is 34 mmHg, and the cardiac output is 4.0 L/min.

The pulmonary pressure in this case could be described as:

• A. Normal – no evidence of pulmonary hypertension

• B. Elevated on the basis of pulmonary venous hypertension

• C. Elevated on the basis of pulmonary arterial hypertension

• D. Representing a mixture of pulmonary venous and pulmonary arterial hypertension

Answer B

A pulmonary pressure in this range is clearly abnormal. Determining the extent to which these pressures are elevated due to elevated left-sided pressures alone hinges on the calculation of the pulmonary vascular resistance. The pulmonary vascular resistance calculates out to be 1.5 Wood units, which is within the normal range. This suggests that if the LVEDP could be brought down to normal (with diuresis for example), the pulmonary pressures would become normal. This is the definition of pulmonary venous hypertension.