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.................................................................................. usually occurs in patients with history of HF and previous cardiac dysfunction across the spectrum of LVEF and may include RV dysfunction. Distinct from the acute pulmonary oedema phenotype, it has a more gradual onset, and the main alteration is progressive fluid retention responsible for systemic congestion. Sometimes, congestion is associated with hypoperfusion.426 The objectives of treatment are identification of precipitants, decongestion, and in rare instances, correction of hypoperfusion (Figure 7). 11.2.2 Acute pulmonary oedema Acute pulmonary oedema is related to lung congestion. Clinical criteria for acute pulmonary oedema diagnosis include dyspnoea with orthopnoea, respiratory failure (hypoxaemia-hypercapnia), tachypnoea, >25 breaths/min, and increased work of breathing.448 Three therapies should be commenced, if indicated. First, oxygen, given as continuous positive airway pressure, non-invasive positivepressure-ventilation and/or high-flow nasal cannula, should be started. Second, i.v. diuretics should be administered, and third, i.v. vasodilators may be given if systolic BP (SBP) is high, to reduce LV afterload (Figure 8). In a few cases of advanced HF, acute pulmonary oedema may be associated with low cardiac output and, in this case, inotropes, vasopressors, and/or MCS are indicated to restore organ perfusion. 11.2.3 Isolated right ventricular failure RV failure is associated with increased RV and atrial pressure and systemic congestion. RV failure may also impair LV filling, and ultimately reduce systemic cardiac output, through ventricular interdependence.449 Diuretics are often the first option of therapy for venous congestion. Noradrenaline and/or inotropes are indicated for low cardiac output and haemodynamic instability. Inotropes reducing cardiac filling pressures may be preferred (i.e. levosimendan, phosphodiesterase type III inhibitors). Since inotropic agents may aggravate arterial hypotension, they may be combined with norepinephrine if needed (Figure 9).449 11.2.4 Cardiogenic shock Cardiogenic shock is a syndrome due to primary cardiac dysfunction resulting in an inadequate cardiac output, comprising a lifethreatening state of tissue hypoperfusion, which can result in multiorgan failure and death.450452 Cardiac insult causing severe impairment of cardiac performance may be acute, as a result of the acute loss of myocardial tissue (acute MI, myocarditis) or may be progressive as seen in patients with chronic decompensated HF who may experience a decline in disease stability as a result of the natural progression of advanced HF and/or specific precipitants.426 Diagnosis of cardiogenic shock mandates the presence of clinical signs of hypoperfusion, such as cold sweated extremities, oliguria, mental confusion, dizziness, narrow pulse pressure. In addition, biochemical manifestations of hypoperfusion, elevated serum creatinine, metabolic acidosis and elevated serum lactate are present and reflect tissue hypoxia and alterations of cellular Table 21 Clinical presentations of acute heart failure Acute decompensated heart failure Acute pulmonary oedema Isolated right ventricular failure Cardiogenic shock Main mechanisms LV dysfunction Sodium and water renal retention Increased afterload and/or predominant LV diastolic dysfunction Valvular heart disease RV dysfunction and/or pre-capillary pulmonary hypertension Severe cardiac dysfunction Main cause of symptoms Fluid accumulation, increased intraventricular pressure Fluid redistribution to the lungs and acute respiratory failure Increased central venous pressure and often systemic hypoperfusion Systemic hypoperfusion Onset Gradual (days) Rapid (hours) Gradual or rapid Gradual or rapid Main haemodynamic abnormalities Increased LVEDP and PCWPa Low or normal cardiac output Normal to low SBP Increased LVEDP and PCWPa Normal cardiac output Normal to high SBP Increased RVEDP Low cardiac output Low SBP Increased LVEDP and PCWPa Low cardiac output Low SBP Main clinical presentations1,446 Wet and warm OR Wet and cold Wet and warmb Wet and cold Wet and cold Main treatment Diuretics Inotropic agents/vasopressors (if peripheral hypoperfusion/hypotension) Short-term MCS or RRT if needed Diuretics Vasodilatorsb Diuretics for peripheral congestion Inotropic agents/vasopres- sors (if peripheral hypoperfusion/hypotension) Short-term MCS or RRT if needed Inotropic agents/ vasopressors Short-term MCS RRT LV = left ventricular; LVEDP = left ventricular end-diastolic pressure; MCS = mechanical circulatory support; PCWP = pulmonary capillary wedge pressure; RV = right ventricular; RVEDP = right ventricular end-diastolic pressure; RRT = renal replacement therapy; SBP = systolic blood pressure. aMay be normal with low cardiac output. bWet and cold profile with need of inotropes and/or vasopressors may rarely occur. 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