Clinical syndrome resulting from a mismatch between the ability to generate cardiac output and metabolic tissue demands (or the ability to meet these demands but only at abnormally elevated cardiac filling pressures). HF may be driven by impairments in stroke volume (SV) (due to impaired systolic function or impaired diastolic filling) or more rarely insufficient heart rate (HR) (significant bradycardia). HF can be univentricular (left ventricle [LV] or right ventricle [RV]) or biventricular. From the perspective of the LV ejection fraction, there are HF syndromes with reduced ejection fraction versus preserved ejection fraction (crudely “systolic” vs “diastolic” HF respectively). HF symptoms may be viewed as secondary to low cardiac output or impaired “forward flow” versus congestion (pulmonary or venous) or “backward fluid build-up”. An additional entity known as high-output HF is distinguished from other forms of HF above by having a high cardiac output but low systemic vascular resistance, resulting in low systemic pressure and activation of the renin-angiotensin-aldosterone axis with resultant salt and water retention (seen in arteriovenous fistulae, cirrhosis, sepsis, anemia, hyperthyroidism, beriberi, etc.).

1. Etiologies and Triggers of Acute HF
1. Be aware of potential triggers that may precipitate HF in patients in the ICU (see Table 18.1).
2. There are multiple mimics of the HF syndrome manifesting with low output and/or congestion, of which ICU clinicians need to be cognizant. These include pericardial effusion and tamponade, pulmonary embolism, pneumothorax, SVC syndrome, and anemia.
2. Signs and Symptoms

Signs and symptoms of HF can be organized conceptually based on the affected ventricle and mechanism of HF (see Table 18.2).

3. HF Classifications
1. A syndrome of low cardiac output (LCOS) is defined as a cardiac index <2.2 L/min/m². This may occur in the absence of hypotension, so should be considered even in normotensive patients and the appropriate clinical context. There is a continuum of LCOS to cardiogenic shock (CS), with the latter including hypotension (with the need for pharmacologic or mechanical circulatory support to maintain normotension and systemic perfusion) coupled with end-organ hypoperfusion and dysfunction.
2. Stevenson Matrix: A clinical assessment of HF, useful for ICU applications, that groups patients into hemodynamic profiles based on perfusion (warm vs cold) and congestion (cold vs dry) axes. These profiles have been shown to predict outcomes, with patients in profiles B and C having higher mortality. These classifications can guide therapy: type B patients have intact perfusion, so their congestion can be treated with fluid removal; type C (cardiogenic shock) and type L patients may require pharmacologic or mechanical circulatory support to augment cardiac output and end-organ perfusion (see Table 18.3).
3. New York Heart Association (NYHA) Class and American Heart Association (AHA)/ACC Stage: These are the primary systems used to classify patients with HF (Table 18.4). The AHA/ACC system describes patients based on the stage of their disease whereas the NYHA classification system categorizes patients clinically based on their degree of symptoms or functional limitation.
4. INTERMACS (Interagency Registry for Mechanically Assisted Circulatory Support): This seven-tiered system is used to further describe and risk-stratify patients with advanced heart failure, specifically NYHA III-IV class patients, and for guiding consideration for mechanical circulatory support candidacy. The higher INTERMACS profiles have been associated with worse outcomes and mortality.
4. Diagnostic Evaluation of HF
1. Signs, symptoms, and examination findings are outlined in Section III.
2. Laboratory markers to evaluate clinical manifestations of heart failure include these.
1. Volume overload: natriuretic peptides (BNP and NT-proBNP), released by cardiac myocytes in response to volume expansion and myocardial wall stress in HF. May be generated in other ICU conditions (eg, pulmonary embolism).
2. Troponin: to evaluate for coronary ischemia precipitating HF, but can also be elevated in a host of ICU comorbidities including myocarditis and myocardial oxygen supply-demand mismatch.
3. End-organ perfusion: include liver function tests (LFTs), lactate, and renal function (using creatinine or Cystatin C).
4. Laboratory markers of advanced heart failure: Hyponatremia (may be seen in HF due to the secretion of arginine vasopressin in the setting of reduced effective arterial circulating volume and renal hypoperfusion) and blood urea nitrogen.
5. Electrolyte monitoring during diuresis: potassium and magnesium levels fluctuate and require replenishment. Hypernatremia may develop during diuresis prompting use of acetazolamide for natriuresis.
6. Central and mixed venous oxygen saturations can help assess cardiac output.
3. Echocardiography is a key method to assess ventricular function, valvular disease, and other structural heart issues (see Chapter 3). Pericardial effusions may also be detected. Thoracic ultrasound is also useful in identifying pleural effusions and B lines reflective of pulmonary edema.
4. Electrocardiogram (EKG) may reflect underlying pathophysiology leading to heart failure. Q waves and ST/T wave changes (reflecting an ischemic process), low voltages (may indicate an infiltrative process), ventricular hypertrophy, or arrhythmias.
5. Chest radiography can show pulmonary edema, pleural effusions, and cardiomegaly.
6. Ischemia evaluation to assess coronary artery disease as etiology if clinically indicated, such as new diagnosis of cardiomyopathy.
7. Many patients in the ICU will have had a CT scan, and this may show coronary calcification, valve calcification, or cardiac chamber enlargement.
8. Other cardiac investigation are sometimes considered including cardiac MRI or endomyocardial biopsy. Cardiac MRI can provide quantitative assessment of biventricular function, valvular disease, shunt hemodynamics, structural heart disease as well as characterizing the myocardium through T2 mapping and late gadolinium enhancement. Endomyocardial biopsy is employed when clinical suspicion is high for particular cardiomyopathy etiologies in which distinct histopathologic findings can aid in the diagnosis.