The two major classes of symptoms in HF are those due to volume overload (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, gastrointestinal symptoms) and those due to a reduction in CO (fatigue and weakness). The most common are dyspnea and fatigue. Dyspnea (at exertion or at rest) is related to complex physiological mechanisms involving both pulmonary venous congestion and a buildup of lactic acid by working muscle increasing the ventilatory response to exercise. On the other hand, low cardiac output state often results in fatigue and weakness due to reduced skeletal muscle perfusion or atrophy. Elevated systemic venous pressures like those occurring in volume overload or right ventricular dysfunction states are responsible for abdominal discomfort (liver congestion and abdominal ascites), anorexia, and peripheral edema. Common physical findings are summarized in Table 7.2. The most common clinical findings are dyspnea (approximately 90 %), rales, and peripheral edema (65 %).

On the basis of typical clinical and hemodynamic characteristics, AHF patients may present with one of several distinct clinical profiles considering that some overlap between groups may exist [8]. The main clinical profiles and relative features are summarized in Table 7.3.

Another classification scheme has been previously proposed (Forrester classification) and is based on the severity of disease at presentation rather than on the cause of HF [12, 13]. It is a simple strategy to classify patients into specific hemodynamic profiles that may be helpful to guide the initial management strategy. Accordingly, a patient presenting with AHFS may be classified into one of the four specific hemodynamic profiles based on the absence or presence of signs of congestion (wet or dry) and the adequacy of peripheral perfusion (warm or cold): warm and dry, warm and wet, cold and dry, and cold and wet.

Traditionally, the diagnosis of HF is a clinical diagnosis combining characteristic symptoms with physical findings, and still today no single tests can absolutely establish its presence or absence. Unfortunately, signs and symptoms of HF often overlap with those of other common medical conditions (especially with chronic lung disease), and those more specific are also less common (like orthopnea and paroxysmal nocturnal dyspnea) or less reproducible (third heart sound and jugular venous distension) so that several ancillary tests, also contributing to determine mechanisms underlying the AHF, are usually needed to support the clinical diagnosis of AHF.

A chest radiography should be performed initially because it may aid in diagnosis of HF as well as in ruling out other differential diagnoses (e.g., pneumonia). Findings suggestive of HF include cardiomegaly (cardiac-to-thoracic width ratio above 50 %), upper zone vascular redistribution (cephalization), interstitial edema with Kerley B-lines, alveolar edema, and pleural effusions. Radiographic evidence of signs of pulmonary congestion in a patient with dyspnea makes the diagnosis of heart failure more likely; however, the absence of radiographic pulmonary congestion does not exclude diagnosis of AHF. Patients with chronic heart failure, despite AHF symptoms and elevated PCWP, may have few radiographic signs because of enhanced lymphatic drainage. Electrocardiography (ECG) is not useful for diagnosis but offers possible clues to identify both specific treatable precipitating factors of AHF (acute myocardial ischemia and arrhythmias) and also possible etiology of HF (e.g., Q wave in ischemic cardiomyopathy).

Laboratory tests (blood chemistry and hematological tests) are useful to guide initial therapy, to detect reversible cause of HF (e.g., hypocalcemia, thyroid dysfunction) and comorbidities (anemia), and to obtain prognostic information. Serial monitoring of myocardial necrosis biomarkers (troponin) is recommended initially for diagnostic (exclude acute coronary syndrome) and prognostic purpose. Troponin elevation in acute HF does not necessarily indicate the presence of an acute coronary syndrome. A significant number of patients with AHFS have increased levels of troponin as a result of myocardial injury during AHF episode resulting from ischemic injury and myocyte apoptosis. Such troponin elevation is associated, however, with poor long-term prognosis.

Measurement of natriuretic peptide (NP) levels is helpful especially when the diagnosis is in question. Natriuretic peptides (BNP and NT-proBNP) are a family of hormones released in increased amounts from myocytes (especially ventricular) secondary to myocardial stretch and elevated end-diastolic filling pressure as occurs in AHFS. Increased NP levels are indicators of both the presence and severity of illness. Accordingly, European guidelines recommend measurement of NP levels both to exclude alternative causes of dyspnea and to obtain prognostic information. Patient presenting with acute onset or worsening of symptoms suggestive of HF with a plasma BNP level <100 pg/ml or NT-proBNP <300 pg/ml is unlikely to have AHFS. For patients presenting in nonacute way (slow onset of symptoms), a lower exclusion NP cutoff point should be used to avoid “false-negative” diagnosis (35 pg/ml for BNP and 125 pg/ml for NT-proBNP). Results of NP tests should be always interpreted in the context of all available clinical data and should not be used in isolation to diagnose HF. A variety of conditions associated with myocardial stretch even in the absence of AHF can still be associated with NP elevation (e.g., atrial fibrillation, pulmonary hypertension, and pulmonary embolism). In addition, NP levels are falsely increased in renal failure and tend to be lower in obese patients.

An initial bedside transthoracic echocardiography is recommended both to support the diagnosis of AHFS and to determine its etiology through an assessment of cardiac anatomy and function (left and right ventricular systolic function and wall motion, diastolic function, valvular function, and pulmonary artery pressure). The TD-derived E/Ea parameter is being used to noninvasively estimate LV filling pressures. In addition, especially for those with hypotensive AHFS, echocardiographic assessment of inferior vena cava (IVC) diameter and its respiratory variation aid to determine the patient volume status.

The main goal of short-term therapy (hours to days) for AHFS has been to achieve the lowest left ventricular filling pressure possible without decreasing cardiac output (especially renal perfusion), increasing heart rate, or further activating neurohormones because these factors have been associated with a worse prognosis [2]. The physician’s challenge is that many of the current medications that improve hemodynamics and symptoms may have potential deleterious effect on such variables [8].

Currently, the use of available pharmacological agents for the acute management of AHFS is largely empirical. None of the employed agents would meet today’s standards for approval based on evidence for clinical efficacy and safety. However matter, no major clinical practice guidelines include any therapeutic class I, level-of-evidence A recommendations for the pharmacological treatment of AHFS [1].

Evaluation and management of AHFS include three main phases: the initial or early phase (stabilization phase), the in-hospital phase, and the discharge phase. The main goals of each phase are summarized in Table 7.4.

After treatment of life-threatening conditions, improving hemodynamics and correlated symptoms are the key goals in early management. This requires a basic understanding of pathophysiologic mechanisms underlying an episode of acute HF and how potential overt precipitants adversely affect the cardiovascular system. These conditions and all HF precipitants should be targeted and treated for optimal results. Aligning treatment decision to initial patient clinical profile can yield to treat specific subgroups of patients with more tolerable therapies.

Taking the above consideration in mind, according to recommendations from ESC 2012 Guidelines [1], early management of acute pulmonary edema/congestion includes an initial intravenous bolus of loop diuretics at time of presentation (usually furosemide 40 mg i.v. or 2.5 time the total outpatient oral loop diuretic dose) and eventually an i.v. vasodilator if SBP >110 mmHg (class of recommendation II, level B) or an i.v. inotropic agent if SBP <85 mmHg (class of recommendation II, level of evidence C) as adjunctive therapy. Of note, in the American Guidelines (AHA 2013) on heart failure, no specific cutoff values exclude the use of a vasodilator, but its use is advocated generally in the absence of symptomatic hypotension. Subsequently, patients should be reevaluated (within 1 h) for adequate response. Response to treatment includes reduction in dyspnea and adequate diuresis (>100 ml/h urine production in first 2 h), accompanied by an increase in oxygen saturation and usually reduction in respiratory rate and heart rate. In the absence of adequate response, all clinical-laboratory parameters should be reassessed (ECG, echocardiogram with hemodynamic measures, and principle laboratory tests) and several options considered. The most common cause of inadequate response is, however, poor response to the diuretic regimen utilized. Strategies to enhance diuretic efficacy will be discussed below in this chapter. AHF patients unresponsive to diuretic pharmacological therapy may be eventually considered for transient venovenous ultrafiltration (UF) that allows mechanical extracorporeal removal of plasma water. In patients with persistent hypotension (low CO) despite initial vasoactive therapy, other conditions like acute ischemic mechanical complications, severe valve dysfunction (particularly aortic stenosis), or alternative diagnoses (e.g., pulmonary embolism) requiring primary intervention rather than palliation of consequences should be reconsidered. Pulmonary artery catheterization may be sometimes useful in such unresponsive patients especially to ensure that hypotension is not due to inadequate LV filling pressure enabling more tailored vasoactive therapy (both inotropes and vasopressors). Finally, in unresponsive patients with persistent hypotension or cardiogenic shock with a rapid deterioration, a short-term mechanical circulatory support (including intra-aortic balloon pump and ECMO) may be considered as a “bridge to decision therapy.”

Approximately 80 % of patients are hospitalized with worsening of HF. For those with new-onset HF who stabilize after initial management, a chronic HF should be considered, and they should be treated according to recommendation of current guidelines. Initiation or implementation of evidence-based pharmacological therapies for chronic heart failure such as beta- blockers, ACE inhibitors, aldosterone-blocking agents, ARB, and electrical device should occur soon during this phase after stabilization. This topic will be extensively addressed in the chapter on chronic heart failure. For the acute setting, it is important to underline that the outpatient oral HF medications should be always carefully reviewed at admission. Generally, HF therapy should be continued at same doses during an AHFS episode unless the patient has hypotension or contraindications (such as hyperkalemia and severe renal failure for ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists) that may require dose reduction or complete withholding. Several reports have shown that continuation of HF medical therapy with ACE inhibitors (or angiotensin receptor antagonists) and with beta- blockers for most patients is usually well tolerated and results in better outcomes [14, 15].