Acute Heart Failure(s)

Heart failure is not a single entity, and is classified according to the portion of the cardiac cycle that is affected (systolic or diastolic heart failure) and the side of the heart that is involved (right-sided or left-sided heart failure). This chapter describes the different types of heart failure, and focuses on the advanced stages of heart failure that require management in an ICU.

I. Types of Heart Failure

A. Systolic vs. Diastolic Heart Failure

Early descriptions of heart failure attributed most cases to contractile failure during systole (systolic heart failure). However, about 50% of hospital admissions for heart failure are the result of diastolic dysfunction (diastolic heart failure) (1).

1. Pressure-Volume Relationship

The pressure-volume curves in Figure 8.1 will be used to demonstrate the similarities and differences between systolic and diastolic heart failure.

The curves in the top panel of Figure 8.1 (called ventricular function curves) show that heart failure is associated with a decrease in stroke volume and an increase in end-diastolic pressure (EDP). These changes occur in both types of heart failure.
The curves in the lower panel of Figure 8.1 (called ventricular compliance curves) show that the increase
in EDP in systolic heart failure is associated with an increase in end-diastolic volume, while the increase in EDP in diastolic heart failure is associated with a decrease in end-diastolic volume.

The difference in end-diastolic volume (EDV) in systolic and diastolic heart failure is the result of differences in ventricular distensibility or compliance (C), which is defined by the following relationships:

FIGURE 8.1 Pressure-volume curves showing the influence of systolic and diastolic dysfunction on measures of cardiac performance. Upper panel shows ventricular function curves, and lower panel shows diastolic compliance curves. See text for explanation.

The slope of the lower curves in Figure 8.1 is a reflection of ventricular compliance; the decreased slope in diastolic heart failure indicates a decreased compliance. Thus, the functional disorder in diastolic heart failure is a decrease in ventricular distensibility that impairs ventricular filling during diastole.

Figure 8.1 demonstrates that the EDV (not the EDP) is a distinguishing feature that identifies systolic or diastolic heart failure (see Table 8.1). However, the EDV is not easily measured, so the ejection fraction (described next) is used to identify the type of heart failure.

Table 8.1 Measures of LV Performance in Systolic and Diastolic Heart Failure

Measure	Systolic Heart Failure	Diastolic Heart Failure
End-Diastolic Pressure	Increased	Increased
End-Diastolic Volume	Increased	Decreased
Ejection Fraction^†	≤40%	≥50%
^† From Reference 1.

2. Ejection Fraction

The fraction of the end-diastolic volume that is ejected during systole, known as the ejection fraction (EF), is equivalent to the ratio of stroke volume (SV) to end-diastolic volume (EDV):

The EF is directly related to the strength of ventricular contraction, and is used a measure of systolic function.
Transthoracic echocardiography is the most frequently used method of measuring the ejection fraction (1).

CRITERIA: Heart failure with a left ventricular (LV) EF ≤40% is systolic heart failure, and heart failure with an LVEF ≥50% is diastolic heart failure (see Table 8.1) (1). Heart failure with an LVEF of 41–49% is in an intermediate category, but this type of heart failure behaves very much like diastolic failure (1).

3. Terminology

Many cases of heart failure involve some degree of systolic and diastolic dysfunction, so the following terms have been proposed for the different types of heart failure (1):

Heart failure that is predominantly the result of systolic dysfunction is called heart failure with reduced ejection fraction.
Heart failure that is predominantly the result of diastolic dysfunction is called heart failure with preserved ejection fraction.

Because these terms are lengthy, and offer no advantage in identifying the primary problem in ventricular performance, the terms “systolic heart failure” and “diastolic heart failure” are retained in this chapter, and throughout the book.

4. Etiologies

The causes of systolic heart failure are broadly classified as ischemic and dilated cardiomyopathies; the latter term including a heterogeneous group of disorders that includes toxic (e.g., ETOH), metabolic (e.g., thiamine deficiency), and infectious (e.g., HIV) conditions (1).
The most common cause of diastolic heart failure is hypertension with left ventricular hypertrophy, which is responsible for up to 90% of cases (1).

B. Right Heart Failure

Right-sided heart failure is more prevalent than suspected in ICU patients (2,3). Most cases are the result of pulmonary hypertension (e.g., from pulmonary emboli, acute respiratory distress syndrome, or chronic obstructive lung disease) and inferior wall myocardial infarction.

1. Right Ventricular Function

Right heart failure is a contractile (systolic) failure that results in an increase in right ventricular end-diastolic volume (RVEDV).
Despite the increase in RVEDV, the central venous pressure (CVP), which is a measure of right ventricular end-diastolic pressure, is normal in about one-third of cases of right heart failure (2).
The CVP does not rise until the increase in RVEDV is restricted by the pericardium (pericardial constraint). The delayed rise in venous pressure hampers the clinical detection of right heart failure.

2. Echocardiography

Cardiac ultrasound is an invaluable tool for detecting right heart failure in the ICU. Although the transesoph-ageal approach provides better views of the right ventricle, transthoracic echocardiography can provide the following important measurements (see Table 8.2) (3):

The RV:LV area ratio is measured by tracing the area of the two chambers at end-diastole. A ratio >0.6 indicates an enlarged RV chamber.
The right ventricular fractional area change (RVFAC) is the ratio of the change in RV area during systole to the RV area at end-diastole, and is a surrogate measure of the RV ejection fraction. An RVFAC <32% indicates RV systolic dysfunction.

For a more comprehensive description of the ultrasound evaluation of the right ventricle, see References 3 and 4.

Table 8.2 Detecting Right Heart Failure with TTE

Measurement	View	Abnormal Value
RV/LV Area Ratio	Apical Four Chamber	>0.6
RV Fractional Area Change	Apical Four Chamber	<32%
From Reference 3. TTE = Transthoracic Echocardiography.

C. Acute Heart Failure

Most (80–85%) cases of acute heart failure are exacerbations of chronic heart failure, often as a result of noncompliance with medications, uncontrolled hypertension, or rapid atrial fibrillation (5).
About 15–20% of cases are new-onset heart failure, and acute coronary syndromes are the major culprit (5).
Stress-induced cardiomyopathy deserves mention as an emerging cause of acute heart failure. This condition is attributed to catecholamine excess, and typically occurs in postmenopausal women with emotional stress, and in patients with acute neurologic injuries such as subarachnoid hemorrhage and traumatic brain injury (6).
- The clinical presentation includes dyspnea and chest pain, and is often mistaken as an acute coronary syndrome. ECG changes can include ST segment changes and T-wave inversions (6).
- Cardiac ultrasound typically shows apical ballooning or hypokinesis involving the apex of the left ventricle.
- The associated heart failure can be severe, with hemodynamic instability, but the condition resolves in several days to weeks (6).
- Catecholamine drugs (e.g., dobutamine) are NOT advised for hemodynamic support in this condition.

II. Clinical Evaluation

Acute heart failure is a clinical diagnosis based on the patient’s history, the presence of edema (pulmonary and/or peripheral) and evidence of cardiac dysfunction (by ECG and echocardiography). The following tests are also useful.

A. B-Type Natriuretic Peptide

Stretch of the atrial and ventricular walls triggers the release of four natriuretic peptides from cardiac myocytes. These peptides “unload” the ventricles by promoting sodium excretion in the urine (which reduces ventricular preload) and dilating systemic blood vessels (which reduces ventricular afterload).
One of these natriuretic peptides is brain-type or B-type natriuretic peptide (BNP), which is released as a precursor or prohormone (proBNP), which is then cleaved to form BNP (the active hormone) and N-terminal (NT)-proBNP, which is metabolically inactive.
NT-proBNP has a longer half-life than BNP, resulting in plasma levels that are 3–5 times higher than BNP levels.
Clinical Use
- Plasma levels of BNP and NT-proBNP are used to evaluate the presence and severity of heart failure. The predictive value of these peptide levels is shown in Table 8.3 (7,8,9).
- Note that advancing age and renal insufficiency can elevate peptide levels. Other conditions that can elevate peptide levels include critical illness, bacterial sepsis, anemia, obstructive sleep apnea, and severe pneumonia (1).
- Since the conditions other than heart failure that raise peptide levels (including critical illness) are almost universal in ICU patients, the clinical utility of peptide levels in the ICU is questionable.