Acute heart failure

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Key Recommendations

Despite advances in technology, diagnosis is primarily clinically based, supported by ancillary tests such as ECG, chest x-ray, B-type natriuretic peptide (BNP), and echocardiogram.[1][2][32] The sensitivity of clinical assessment in identifying left ventricular systolic dysfunction is approximately 81% but the specificity is only 47%. The specificity of this diagnosis is improved to 69% by addition of ECG and to 92% by addition of chest x-ray.[33] Point-of-care lung ultrasound may be used as an alternative to chest x-ray in the emergency setting in conjunction with medical history and physical exam.[34][35]

Other tests (e.g., cardiac catheterization with hemodynamic measurements, computed tomography [CT], and cardiac magnetic resonance [CMR] imaging) can be used when noninvasive tests and echocardiographic images are suboptimal or when an unusual cause of heart failure is suspected, and for diagnosis of specific cardiomyopathies.[1][36]

History and risk factors

A careful history should be taken for causes of acute heart failure, such as myocardial ischemia, uncontrolled hypertension, significant valvular disease (both stenosis and regurgitation, or endocarditis), atrial fibrillation, other arrhythmias, infection, anemia, hyper- or hypothyroidism, pulmonary embolism, and precipitating factors causing exacerbation of chronic heart failure such as dietary indiscretion with excessive salt intake, nonadherence to medication regimen, use of medications with negative inotropic effect (e.g., verapamil, diltiazem) or medications that promote sodium retention, and excessive alcohol or drug intake.[2] A clinical scoring system is sometimes useful for the diagnosis of acute heart failure.[36]

Symptoms

Heart failure presents with dyspnea (including orthopnea or paroxysmal nocturnal dyspnea), cough, decreased exercise tolerance, leg edema, fatigue, and generalized weakness. Sometimes the patient may present with predominant symptoms of the underlying condition, such as chest pain, syncope, palpitations, or viral prodrome.

Signs

Common signs include central cyanosis, tachycardia, elevated jugular venous pressure, displaced apex beat, third heart sound (S3), crepitations or pleural effusion, hepatomegaly, ascites, edema, and cool peripheries. The presence of these signs depends upon the duration, acuity, and the underlying cause of heart failure.[37] Patients with end-stage heart failure may exhibit most of these clinical signs, whereas those in the early phase of the illness may have minimal signs.

Patients with advanced heart failure can be classified clinically into four hemodynamic profiles.[38] These profiles, which are based on hemodynamic principles of presence or absence of elevated filling pressure (wet or dry) and perfusion that is adequate or critically limited (warm or cold), include:[1]

Warm and dry
Warm and wet
Cold and dry
Cold and wet.

Patients with pulmonary edema present with severe respiratory distress with reduced oxygen saturation (usually <90% on room air) and crackles or wheezes on lung exam (“wet”) but may or may not be hemodynamically compromised (“cold” or “warm”). Patients with hemodynamic compromise, systolic BP less than 90 mmHg, or a drop of mean arterial pressure of more than 30 mmHg with a pulse rate over 60 bpm and/or low urine output (<0.5 ml/kg/hour), with or without evidence of organ congestion, are considered to be in cardiogenic shock (“cold”) but may or may not present with concomitant acute pulmonary edema (“wet” or “dry”).

Immediate investigations

An ECG and chest x-ray should be performed immediately in all patients with suspected acute heart failure.[2] ECG findings are commonly related to the underlying pathologies and include presence of Q waves, ST-T changes, left ventricular hypertrophy (LVH), bundle branch block, and atrial fibrillation. ECG abnormality is found in almost all cases of heart failure. If the ECG is completely normal then alternate diagnosis should be considered.[39][Figure caption and citation for the preceding image starts]: ECG showing left ventricular hypertrophy with sinus tachycardiaFrom the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD; used with permission [Citation ends].

Chest x-ray may show cardiac enlargement (cardiothoracic ratio [CTR] >50%); however, there is poor correlation between the CTR and presence of heart failure, as the heart size may be normal in patients with diastolic dysfunction, acute valvular regurgitation as part of infective endocarditis, or acute myocardial infarction. An enlarged CTR may also be seen in the absence of heart failure (e.g., pericardial effusion and LVH).

In most cases, evaluation of the lung fields will show signs of pulmonary congestion, initially in the upper zones, then in the horizontal fissures, followed by pulmonary edema and pleural effusion.[Figure caption and citation for the preceding image starts]: Chest x-ray of acute pulmonary edema showing increased alveolar markings, fluid in the horizontal fissure, and blunting of the costophrenic anglesFrom the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD; used with permission [Citation ends].[Figure caption and citation for the preceding image starts]: Chest x-ray of acute pulmonary edema showing increased alveolar markings and bilateral pleural effusionsFrom the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD; used with permission [Citation ends].

The radiologic findings have to be taken in the context of the clinical picture, as pulmonary infiltrates and congestion, in some cases, may be due to noncardiac causes such as acute respiratory distress syndrome or alveolar hemorrhage.

Chest x-rays rarely may show pericardial calcification, prosthetic valves, or valvular calcification. Such findings may be helpful in identifying the possible underlying etiology for heart failure.

Point-of-care lung ultrasound may be used as an alternative to chest x-ray when the equipment is available and clinicians are proficient in its use, alongside medical history and physical exam.[34][40]

The following blood tests should be requested when patients present with suspected acute heart failure:[2]

Hemoglobin: may identify anemia as a contributing factor.
Thyroid function tests: both hypothyroidism and hyperthyroidism can cause heart failure.
B-type natriuretic peptide (BNP): measurement of serum BNP level in patients with symptoms of heart failure is useful to support or exclude the diagnosis, and is recommended for patients hospitalized with heart failure to establish prognosis.[2] The addition of BNP or N-terminal pro-BNP (NT-proBNP) to clinical assessment significantly enhances the accuracy of diagnosis and effectiveness of acute management.[41][42] BNP is also helpful in differentiating a cardiac from a pulmonary cause of dyspnea.[43] A BNP >500 picograms/mL in a patient with dyspnea points to heart failure as the likely cause, whereas a BNP <100 picograms/mL makes heart failure unlikely. An elevated BNP level is a predictor of in-hospital mortality in patients with acute decompensated heart failure.[44] However, an elevated BNP level should only be taken in the context of the clinical picture as it may be increased in a variety of other conditions, such as atrial fibrillation, pulmonary embolism, or sepsis.[45] In patients presenting with suspected acute heart failure, a finding of BNP <100 picograms/mL, NT-proBNP <300 picograms/mL, and mid-regional pro-atrial natriuretic peptide (MR-proANP) <120 picograms/mL makes the diagnosis of acute heart failure unlikely.[1] Diagnostic accuracy can be improved by combining NT-proBNP assessment with other clinical variables using a validated clinical decision support tool. CODE-HF tool Opens in new window[46]
Cardiac enzymes: >50% of patients with cardiogenic pulmonary edema (but without evidence for myocardial infarction) have elevated troponin T levels.[1][47] Elevated troponin T levels in patients with acute heart failure may reflect subendocardial ischemia due to elevated left ventricular end diastolic pressure. In patients with acute cardiogenic pulmonary edema, a troponin T level ≥0.1 micrograms/L (≥0.1 ng/mL) is a powerful independent predictor and is associated with poor long-term survival.[47] One systematic review and meta-analysis showed a strong association between high sensitive cardiac troponin and the development of incident heart failure.[48]
Other recommended initial baseline blood tests include serum electrolytes, blood urea nitrogen, serum creatinine, glucose, lipid profile, liver function tests (including albumin), and iron studies.[1][2][49]

Echocardiogram is an integral part of the evaluation in a patient with acute heart failure and should be performed as soon as possible to presentation.[2] It is required to assess chamber size, ventricular function (systolic and diastolic), ventricular wall thickness, valvular function, and the pericardium. [Figure caption and citation for the preceding image starts]: Systolic image of dilated left ventricle (arrow); note there is no change from diastolic imageFrom the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD; used with permission [Citation ends].[Figure caption and citation for the preceding image starts]: Diastolic image of dilated left ventricle (arrow)From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD; used with permission [Citation ends].

Subsequent investigations

Left heart cardiac catheterization (coronary angiogram) is needed in cases where significant coronary artery disease is thought to be a contributing factor.[2] Routine use of right heart catheterization and pulmonary artery catheter monitoring is not recommended. However, invasive hemodynamic evaluation or monitoring is helpful if:[2]

Systolic blood pressure (SBP) remains low or symptoms persist despite treatment
Fluid status, perfusion, or systemic or pulmonary vascular resistance is uncertain
Renal function worsens with therapy
Parenteral vasoactive agents are required.

A cardiac CT coronary angiogram is a noninvasive technique to visualize the coronary anatomy in patients with heart failure with low to intermediate pre-test probability of coronary artery disease or those with equivocal noninvasive stress tests, in order to exclude the diagnosis of coronary artery disease.

Endomyocardial biopsy is not recommended for routine evaluation of acute heart failure, but is indicated in patients with rapidly progressive clinical heart failure or worsening ventricular dysfunction that persists despite appropriate medical treatment, where clinical findings suggest acute myocarditis, or where a myocardial infiltrative process (e.g., light chain amyloidosis) or cardiac rejection after heart transplantation is suspected.[2]

Cardiovascular magnetic resonance (CMR) imaging can be used when noninvasive tests and echocardiographic images are suboptimal or when an unusual cause of heart failure is suspected, and for diagnosis of specific cardiomyopathies.[1][2][36]

Single-photon emission CT (SPECT) or positron emission tomography (PET) may be useful in assessing ischemia and myocardial viability. 3,3-diphosphono-1,2-propanodicarboxylic acid (DPD) scintigraphy may be useful for the detection of transthyretin cardiac amyloidosis.[1][2]

Measuring the concentration of certain biomarkers can provide important information about disease severity and helps not only in the detection and diagnosis of heart failure but also in management and prognosis. In addition to natriuretic peptides and troponin, useful biomarkers include soluble suppressor of tumorigenicity 2, interleukin-6, cystatin-C, galectin-3, and procalcitonin.[50]

Central venous catheter insertion: animated demonstration

Ultrasound-guided insertion of a non-tunnelled central venous catheter (CVC) into the right internal jugular vein using the Seldinger insertion technique.

How to perform an ECG: animated demonstration

How to record an ECG. Demonstrates placement of chest and limb electrodes.

Use of this content is subject to our disclaimer