The combination of the aging of the population and improved survival after myocardial infarction has increased the prevalence of heart failure. Most patients with advanced heart failure are admitted to hospital as a result of acute decompensation but some patients with new onset heart failure may present acutely in extremis. Patients with impaired ventricular function who undergo surgery may also present with low output states in the ICU.
The clinical syndrome of heart failure can result from any structural or functional impairment of ventricular filling or ejection of blood. Coronary artery disease remains the most common cause of heart failure. In younger patients (such as the population referred for cardiac transplantation), dilated cardiomyopathy (often of unknown aetiology) is the commonest cause. The true incidence of acute myocarditis in patients with a short history of heart failure is not known because of the difficulty in confirming the diagnosis.
Patients requiring admission to critical care because of severe heart failure usually have one of two clinical syndromes:
2. Cardiogenic shock: defined as tissue hypoperfusion induced by heart failure after correction of preload. It is usually characterised by hypotension (systolic BP <90 mmHg), oliguria (<0.5 ml/kg/hour) and evidence of end-organ dysfunction such as renal, hepatic and cognitive impairment, and elevated blood lactate level.
Bedside assessment may provide clues to the haemodynamic profile of a patient. It is important to distinguish between elevated and non-elevated cardiac filling pressures (‘wet’ or ‘dry’), and adequate or severely impaired tissue perfusion (‘warm’ or ‘cold’) (see Figure 45.1).
Figure 45.1 Assessment of haemodynamic profile using haemodynamic signs and symptoms of patients presenting with heart failure. JVP jugular venous pressure.
Elevated filling pressure can be diagnosed clinically by orthopnoea or by elevated jugular venous pressure. Blood pressure is only a guide to tissue perfusion; proportional pulse pressure (pulse pressure/systolic pressure) less than 25% has been reported to correlate with a cardiac index less than 2.2 l/min/m2 in the population of patients referred for cardiac transplantation.
Patients admitted to the critical care unit are most likely to have elevated filling pressures and inadequate end-organ perfusion (wet and cold). This group is associated with the highest mortality.
Both an acute deterioration and chronic impairment of cardiac function can lead to a progressive decline in renal function. The umbrella term cardiorenal syndrome is used to describe this. The pathophysiology varies depending on specific clinical circumstances; however it involves transrenal perfusion pressure, intrarenal haemodynamics and systemic neurohormonal factors. Alterations in the balance of vasoconstrictor and vasodilator hormones adversely affect renal function, and the combination of increased central venous pressure with low systemic pressure may lead to a severe compromise of net renal perfusion pressure.
In the acute setting, worsening renal function (acute kidney injury) frequently complicates hospital admissions with acute decompensated heart failure. Patients with worsening renal function have a higher mortality and morbidity and increased duration of hospitalisation.
In the more chronic state, renal dysfunction develops in patients who have chronic volume overload, prior renal dysfunction, right ventricular dysfunction and high baseline diuretic requirements. When filling pressures are measured they exceed the optimal levels required to maintain cardiac output. A stable clinical state may be maintained in some patients with high serum urea and creatinine levels but the prognosis is poor. Inotropic infusions may relieve the congestion and improve renal function but the problem often recurs when inotropes are withdrawn.
In addition to a detailed clinical history and physical examination a number of investigations are required:
1. Electrocardiogram to determine rhythm and aetiology of heart failure (e.g. acute coronary syndrome or myocarditis).
2. Chest radiograph for heart size, pulmonary congestion, lung consolidation or pleural effusions.
3. Echocardiography to assess regional and global left and right ventricular function, valve structure and function, pericardial effusion, and mechanical complications of myocardial infarction. The pulmonary artery systolic pressure may also be estimated from the tricuspid regurgitation jet and echocardiography.
4. Blood tests: full blood count, coagulation screen, C-reactive protein, creatinine and electrolytes, glucose and liver function tests in all patients. Troponin and plasma BNP (B-type natriuretic peptide) may also be indicated. For the assessment of a patient presenting with acute dyspnoea a low BNP has a high negative predictive value for heart failure as the aetiology. BNP may be less helpful in the critical care setting.
5. Coronary angiography if revascularisation is indicated.
1. Non-invasive monitoring – temperature, respiratory rate, blood pressure, continuous ECG monitoring and pulse oximetry are required for all patients.
2. Arterial line – essential in unstable patients for continuous arterial blood pressure monitoring and frequent analysis of blood gases.
3. Central venous line – monitoring right sided filling pressure is often essential in patients with advanced heart failure and a central venous line is required for the delivery of fluids and drugs. Estimation of superior vena caval or right atrial oxygen saturation can be a useful marker of oxygen transport. Central venous pressure may be significantly affected by positive end-expiratory pressure ventilation.
Pulmonary artery catheter (PAC) – PAC allows direct measurement of right atrial (RA), right ventricular (RV), pulmonary artery (PA), pulmonary capillary wedge pressure (PCWP) and calculation of pulmonary and systemic vascular resistance. Mixed venous oxygen saturation can also be monitored. This is particularly useful in the presence of severe tricuspid regurgitation when the cardiac output derived by thermodilution may be inaccurate.
In patients with heart failure, right atrial pressure does not correlate well with left sided filling pressure. In many situations, an estimate of left atrial pressure is invaluable. In patients with a high pulmonary vascular resistance (PVR) associated with heart failure, direct measurement of pulmonary pressure is important. In patients requiring inotropic or vasoconstrictor drugs, monitoring of cardiac output and estimation of systemic vascular resistance facilitates therapy based on pathophysiological principles.
Complications associated with the use of a PAC increase with duration of use and it should not be left in situ longer than necessary. In advanced heart failure, therapy tailored to haemodynamic goals as guided by PAC has been shown to result in sustained improvement in symptoms, stroke volume and cardiac output.
Cardiac power output (CPO) describes the relationship between flow and pressure in the circulation and is a powerful predictor of prognosis in cardiogenic shock. It is calculated as the product of simultaneous mean arterial pressure (MAP) and cardiac output corrected for a constant and expressed as watts.
Although PAC is the ‘gold standard’ there are a number of non-invasive cardiac output monitoring devices available that can derive haemodynamic data, but most have not been validated in low cardiac output states.
4. Echocardiography – there is an emerging role for both transthoracic and transoesophageal echocardiography in monitoring haemodynamics in critically ill patients; however, interpretation of data requires specific training and expertise.
The treatment of chronic heart failure has been the subject of several large randomised clinical trials and evidence-based guidelines are available.
Critically ill patients with acute heart failure are a heterogeneous group with respect to aetiology, haemodynamic abnormalities and comorbidities, and are therefore difficult to subject to randomised trials. Treatment strategies should be based on the underlying pathophysiology with the aim of reversing haemodynamic abnormalities. If an underlying treatable cause is identified, clinical condition should be optimised so that definitive treatment can be carried out with the minimum of risk. Immediate therapy should focus on relieving symptoms. Reducing congestion is often the most effective way of achieving this (see Table 45.1).
General management involves a multidisciplinary team due to the complexity of the pathophysiology in the critically ill heart failure patient. In addition to the specific treatments described below, management should include investigation and correction of anaemia, electrolyte abnormalities, thyroid and adrenal function and optimal glucose control. Infection is common; therefore standard infection control measures and evidence-based antimicrobial treatment are essential. Patients should receive appropriate nutrition, mobilisation and physiotherapy. Provision of psychological support and involvement of palliative care teams are also important considerations.
Achieving an adequate level of oxygenation at the cellular level is important to prevent end-organ dysfunction. Treatment should aim to achieve optimal rather than supraphysiological arterial oxygenation, i.e. arterial oxygen saturation above 95%. Respiratory muscle fatigue often results from hypoxaemia and low cardiac output.
Either continuous positive airway pressure (CPAP) or non-invasive ventilation (NIV) can be used to reduce the work of breathing. Both CPAP and NIV result in pulmonary recruitment and an increase in functional residual capacity and a reduction in pulmonary oedema. Clinical trials comparing CPAP with standard therapy have shown a decreased need for endotracheal intubation.
The major goals of medical therapy in the heart failure patient in the ICU are (i) reducing venous congestion (optimising preload), (ii) optimising afterload with vasodilators, in the absence of severe hypotension, and (iii) inotropic support.
The reduction of elevated filling pressures is the most effective way to relieve symptoms of heart failure. Patients with acute decompensation of chronic heart failure are likely to be on diuretic therapy when admitted. Data are lacking on the relative efficacy and tolerability of different diuretics. In the acute setting, a loop diuretic is administered intravenously with dose titration to produce optimal urine output. A large bolus of diuretic may also lead to reflex renal vasoconstriction and a higher risk of ototoxicity. An intravenous infusion of furosemide at 5–10 mg/hour is sufficient in most patients once steps have been taken to increase the cardiac output. Fluid restriction (usually to 1.5 l/day) is an important adjunct to diuretic therapy in severely fluid-overloaded patients. Using a ‘fluid challenge’ in such patients with obvious fluid retention is irrational and has no place in treatment of heart failure patients in the cardiothoracic ICU; inadequate urine output in these patients is usually related to a low cardiac output and treating this often requires inotropic therapy. Once filling pressures have been reduced to normal, the dose of diuretic should be reduced; the dose required to maintain euvolaemia is usually less than that required to achieve it.
The combination of a thiazide (e.g. metolazone or bendroflumethiazide) with a loop diuretic can augment the diuresis achieved in patients with chronic heart failure and is of use in the acute setting. Heart failure patients are often hyponatraemic in the ICU and care needs to be taken not to exacerbate this with combination diuretic therapy. Serum potassium should be monitored as hypokalaemia may predispose to arrhythmias. Combining loop diuretics with a mineralocorticoid receptor antagonist like spironolactone or eplerenone may be effective provided the serum potassium is <5 mmol/l and serum creatinine <200 µmol/l.
In the absence of severe hypotension, vasodilators are indicated in most patients with acute heart failure. Decreasing preload relieves congestion and decreasing afterload is usually beneficial as most patients with heart failure are vasoconstricted (Table 45.2). When administering vasodilators or positive inotropic drugs, the following equation is useful in manipulating the circulation:
MAP − CVP = CO × SVR
where MAP is the mean arterial pressure, CVP is the central venous pressure, CO is the cardiac output and SVR is the systemic vascular resistance.
|Enoximone||0.25–0.75 mg/kg||1.25–7.5 μg/kg/min|
|Milrinone||25–75 μg/kg||0.375–0.75 μg/kg/min|
|Levosimendan||12–24 μg/kg||0.05–0.2 μg/kg/min|