Chapter 20 Acute heart failure

The pattern of heart failure seen in the community, outpatients clinics and specialist cardiac wards is dominated by the acute coronary syndromes and chronic heart failure, predominantly caused by ischaemic heart disease and hypertension.^1,² Heart failure is the commonest cause of hospital admission in people over 65 years of age and it has been estimated that in North America and Europe over 15 million patients have heart failure and 1.5 million new cases are diagnosed each year.³ Patients present with chest pain, shortness of breath, fatigue and oedema and will usually have single-organ failure. Management focuses on reducing cardiac work to relieve symptoms and prevent further myocardial damage.^4,⁵

Patients either admitted with or who develop acute heart failure on the intensive care unit (ICU) frequently have overt or occult underlying coronary artery disease, but will usually have significant other organ dysfunction. Management in this setting focuses on both improving global and regional oxygen delivery and maintaining perfusion pressure, often with the use of drugs that stimulate rather than rest the myocardium.⁶^–⁸ The resolution of this apparent paradox requires that for each patient management should attempt to achieve the frequently difficult balance between the best interests of the myocardium and the circulatory requirements of the other vital organs. The critical care physician should target the minimum necessary oxygen delivery and arterial pressure to maintain other organ function at maximum cardiac efficiency (e.g. ensuring adequate fluid resuscitation before starting beta-agonists) so that cardiac work and the risk of myocardial ischaemia and necrosis from exuberant beta-agonist use are minimised and the cardiologist should consider the wider circulation and other organ requirements when instituting strategies to protect the myocardium.

DIAGNOSIS OF ACUTE HEART FAILURE

The diagnosis of acute heart failure in critically ill patients can be more difficult than is commonly recognised. Although the underlying pathology in most patients with acute heart failure on intensive care will be coronary artery disease, other diagnoses must be considered (Table 20.1).

Table 20.1 Causes of acute heart failure on the intensive care unit

Coronary artery disease

Infection – systemic sepsis,⁹ myocarditis

Mechanical – endocarditis, pulmonary emboli, valve problems, septal defects, tamponade, high intrathoracic pressure with inadequate preload

Drugs – beta-blockers, calcium antagonists, cytotoxic therapy

Hypoxaemia

Metabolic – acidaemia, thiamine deficiency, hypocalcaemia, hypophosphataemia

Myocardial contusion – blunt thoracic trauma

Myocardial infiltration – tumour, sarcoidosis, amyloidosis

Vasculitis – rare

It is also important to reassess critically the patient referred with a diagnosis of acute heart failure to decide whether this is indeed the primary problem. The history, examination and initial investigations with routine blood tests, electrocardiogram (ECG) and chest X-ray may be compatible with this diagnosis but many such patients are elderly with multiple comorbidities and deciding whether the patient is suffering from a primary myocardial pathology as opposed to a pulmonary problem or indeed systemic sepsis ⁹ can be difficult. Equally, patients believed to have a primary respiratory problem may fail to wean from ventilatory support because of a failure to realise that they have left ventricular failure with a high left atrial pressure and incipient pulmonary oedema, causing a reduction in pulmonary compliance, an increased work of breathing and respiratory distress when ventilatory support is withdrawn.

Further investigations that can help to confirm or refute an initial diagnosis of acute heart failure are echocardiography and the measurement of recently available biomarkers such as troponin and brain natriuretic peptide.

ECHOCARDIOGRAPHY (SEE CHAPTER 23)

Echocardiography is an extremely valuable investigation in the management of the critically ill patient with acute heart failure ¹⁰ and the modern critical care physician should at least be able to perform a basic examination. It will frequently establish the underlying cardiac pathology and can be used to monitor the response to treatment. It will:

1 identify pericardial effusions and determine whether ventricular filling is impaired (tamponade) and whether drainage is indicated. However, ultimately tamponade is a clinical diagnosis based on the full haemodynamic picture in the context of pericardial fluid demonstrated on the echocardiogram. Many of the diagnostic features related to alterations with respiration are affected by positive-pressure ventilation and drainage may be appropriate even if such classic echocardiographic criteria are not present. Even small effusions may cause tamponade since it is the rate of accumulation of fluid rather than the amount of fluid that determines the degree of cardiac compromise

2 identify obstruction to cardiac filling from other intrathoracic space-occupying lesions that increase intrathoracic pressure, particularly in ventilated patients (pleural effusion, alveolar gas trapping in asthma)

3 assess adequacy of volume preload of left ventricle, particularly in the context of raised preload pressures and monitor response to fluid challenge

4 identify primary valvular heart disease (critical aortic stenosis, acute mitral regurgitation from papillary muscle rupture, acute endocarditis) when urgent surgery is indicated and distinguish this from functional valvular regurgitation due to primary ventricular disease for which surgery could be lethal

5 identify septal defects, regional wall motion abnormalities and aneurysmal dilatation from recent or previous myocardial infarction

6 identify the presence of intracardiac thrombus or clot

7 identify increased end-systolic and diastolic dimensions, indicating ventricular contractile failure. However the use of ejection fraction as an index of ventricular dysfunction can be misleading, especially in patients on inotropic drugs

8 identify diastolic dysfunction when high-pressure preload measurements fail to reflect true volume preload and extra fluid volume may be indicated

9 identify pulmonary hypertension associated with tricuspid regurgitation when an estimate of pulmonary artery (PA) pressure can be made

The images obtained with transthoracic echocardiography (TTE) may be poor in ventilated patients but the experienced operator can achieve considerable improvement using microbubble contrast techniques.¹¹

Transoesophageal echo (TOE) gives excellent views of the aorta (dissections), the atria and left heart valves and is indicated if transthoracic views are very difficult to obtain or if better resolution is required. Right heart structures and the left ventricle are less well imaged.

MEASUREMENT OF TROPONIN AND BRAIN NATRIURETIC PEPTIDE

Myocardial injury and the development of acute heart failure are common but frequently unrecognised complications of critical illness occurring not only in patients with an overt acute coronary syndrome but also in other conditions such as sepsis and major pulmonary embolism (PE).¹² Relying on blood tests alone to establish a diagnosis or to plan management is inadvisable but, when interpreted in conjunction with the wider clinical picture, brain-type natriuretic peptide (BNP) and cardiac troponin are two tests that are becoming routinely available and appear to be sensitive markers of myocardial stress and necrosis and to have significant prognostic significance.

BRAIN-TYPE NATRIURETIC PEPTIDE

BNP was first isolated from porcine brain but the major source is the ventricular myocardium. The main stimulus for synthesis and release is myocardial wall stress. As a triage tool in the emergency department it is able to discriminate patients with heart failure from those with pulmonary or other non-cardiac causes for acute dyspnoea and has been shown to reduce rates of ICU admission, length of hospital stay and cost.¹³ Several studies have demonstrated that, below a cut-off of 100 pg/ml, BNP has a sensitivity of almost 90% and a specificity approaching 80% as a test for excluding heart failure.¹⁴ It is now included in both the European and UK National Institute for Clinical Excellence guidelines for the management of heart failure^15,¹⁶ and BNP has also been shown to be a marker of myocardial dysfunction and prognosis in severe sepsis.¹⁷

CARDIAC TROPONIN I AND T (cTnI, cTnT)

Troponin is part of the thin filament of the myocyte contractile apparatus and has three subunits: (1) I, which binds actin to inhibit actin-myosin contraction; (2) T, which binds tropomyosin to facilitate contraction; and (3) C, which binds calcium ions. The cardiac isoforms cTnI and cTnT are specific to the heart and can be measured in the blood after myocyte necrosis with 50% release by 4 hours, peaking at 12–24 hours and remaining elevated for up to 10 days. It is far more sensitive than the traditional cardiac enzyme tests such as creatine kinase and indeed it has substantially changed the diagnosis and management of acute myocardial infarction, as reflected in the new guidelines issued by the European Society of Cardiology ¹⁵ and American College of Cardiologists. Troponin may be released in conditions other than acute coronary ischaemia¹⁸ such as sepsis and after chemotherapy and in the absence of evidence of myocardial necrosis as in acute heart failure or major PE, where it is believed that the acute ventricular dilatation causes increased membrane permeability. Raised troponin levels are also associated with increased morbidity and mortality in surgical ICU patients.¹⁹

In combination with BNP, cTnI is valuable in screening for massive PE: in massive and submassive PE both are raised and further investigation with computed tomography pulmonary angiogram (CTPA) is indicated but in minor PE both will be negative.

Raised levels of either of these markers, but particularly BNP indicating early myocardial stress, may have an important role in alerting the clinician to impending myocardial failure and the need to review the use of drugs that stimulate the myocardium and to consider the introduction of a beta-blocker, particularly in the context of tachycardia.

It should be remembered that, for critically ill patients with acute heart failure not resulting from primary myocardial infarction, if the precipitating cause is successfully treated without significant myocardial necrosis occurring, the acute heart failure will resolve, cardiac function will return to its premorbid state and the prognosis will be improved.

The remainder of this chapter addresses the assessment and principles of management of ventricular function in patients admitted to the ICU with acute heart failure. This inevitably involves reference to circulatory failure and the state of the peripheral circulation but the more detailed aspects of oxygen delivery and control of the regional and microcirculation are considered elsewhere ²⁰ (see Chapters 11 and 12), as are the acute coronary syndromes² (see Chapter 16) and chronic heart failure.¹

CIRCULATORY FAILURE OR ‘SHOCK’

The principal function of the heart is the generation of the energy necessary to perfuse the lungs with venous blood and to propel the oxygenated arterial blood through the systemic circulation at a rate and pressure that ensure that the fluctuating metabolic requirements of the various organs are met at rest and during exercise. This should be performed at maximum efficiency so that the work performed is not at the cost of unnecessarily high myocardial energy expenditure and the risk of myocardial ischaemia is minimised.

Failure to maintain an adequate oxygen supply to the tissues with the consequent development of anaerobic cellular metabolism defines circulatory failure or ‘shock’, a term that benefits from brevity but little else since it implies neither cause nor prognosis, but its use is now widespread and inescapable. Table 20.2 classifies circulatory ‘shock’.

Table 20.2 Major categories of circulatory failure or ‘shock’

Cardiogenic	Myocardial infarction, myocarditis, vasculitis, valve dysfunction (e.g. critical aortic stenosis, mitral regurgitation, acute endocarditis), post cardiac bypass surgery, drug overdose (β-blockers, calcium antagonists)
Hypovolaemic	Haemorrhage, burns, gastrointestinal fluid loss
Obstructive	Pulmonary embolus, cardiac tamponade, tension pneumothorax
Anaphylactic	Drugs, blood transfusion, insect sting
Septic	Bacterial infection, non-infective inflammatory conditions, e.g. pancreatitis, burns, trauma
Neurogenic	Intracranial haemorrhage, brainstem compression, spinal cord injury

In considering these causes of circulatory failure, several points require emphasis:

1 Acute heart failure resulting in cardiogenic shock is not a pathological diagnosis but a collective term that embraces all causes of myocardial failure. Treatment must focus on the underlying diagnosis.

2 Patients admitted to ICU may have acute heart failure either as the primary reason for admission, e.g. severe myocardial infarction, or develop it as part of multipleorgan failure triggered by an extracardiac cause, frequently the delayed or ineffective treatment of severe sepsis.

3 Pre-existing cardiac disease, usually ischaemic heart disease, is an important factor in determining the physiological response to critical illness. Several studies investigating the effect of manipulating oxygen delivery have demonstrated the poor prognosis associated with the inability of the heart to achieve a hyperdynamic response to critical illness either spontaneously or with volume loading and inotropic support.^7,^8,²¹ Preoperative assessment with exercise testing is probably appropriate for all patients undergoing major surgery as a means of identifying those with poor physiological reserve so that the true risk of surgery can be identified and perioperative management planned accordingly.

4 Although hypotension is often considered to be the cardinal sign of circulatory failure, other global features (persistent tachycardia, confusion, tachypnoea, impaired peripheral perfusion, progressive metabolic acidaemia) occur earlier since the body has powerful homeostatic mechanisms that maintain pressure at the expense of flow.

5 The heart must provide its own blood supply and, if coronary blood flow does not match myocardial oxygen requirements, coronary ischaemia develops and cardiac and global circulatory failure may ensue.²²

6 The primary problem in hypovolaemic, cardiogenic and obstructive shock is a progressive decline in cardiac output (CO) and global oxygen delivery, which, if not corrected, leads to secondary failure of the peripheral circulation and progressive organ dysfunction. In septic, anaphylactic and neurogenic shock, however, the primary problem is the loss of control of the peripheral circulation resulting in systemic hypotension and disordered distribution of blood flow, although CO and global oxygen delivery are usually increased.²³

7 Although a primary cause for the circulatory failure may be identified, other causes may contribute to the evolution of the final pathology. For example, in septic shock the initial and major derangement is peripheral: it is characterised by microcirculatory chaos triggered by cytokine release, white-cell activation, disruption of the coagulation cascade resulting in microthrombi that occlude the microvasculature and endothelial disruption resulting in interstitial oedema. This same process occurs in the coronary microvasculature impairing myocyte function.²⁴ There is also widespread loss of fluid from the intravascular to the extravascular space, resulting in hypovolaemia. The primary peripheral circulatory failure may therefore be compounded by both cardiogenic and hypovolaemic shock.

8 ‘Early’ and ‘late’ shock are terms that reflect the association between the duration and severity of the circulatory derangement and prognosis. Early intervention in circulatory shock has a major impact on survival.²⁵ If treatment is delayed until organ failure is established, the underlying pathological processes are frequently irreversible.

9 Although not a true ‘mixed’ venous sample, the oxygen saturation of blood taken from an internal jugular (S_ijO₂) or subclavian cannula has been shown to be valuable in assessing whether global oxygen delivery (DO₂) is adequate for global tissue oxygen consumption. A value < 70% should prompt consideration of whether a fluid challenge or other strategy to increase DO₂ is indicated. A value > 70% is not necessarily reassuring in patients with established hyperdynamic shock as this may reflect an inability of the tissues to extract and utilise oxygen.

ASSESSMENT OF VENTRICULAR FUNCTION

Making the considerable assumption that the circulation can be analysed as a constant-flow, fixed-compliance system, six key measurements traditionally define ventricular performance:

• Right and left atrial pressures (RAP, LAP or ventricular preload)

• Mean systemic and pulmonary arterial pressures (MAP, PAP or ventricular afterload)

• Heart rate (HR)

• CO (Q_t)

Table 20.3 illustrates typical values in normal subjects and in the common causes of circulatory failure with calculation of the associated vascular resistances and oxygen delivery. The values quoted are merely examples that indicate the pattern of circulatory derangement produced by these pathologies: pre-existing cardiopulmonary disease and the severity of the condition will affect the precise figures obtained in individual cases and the response to vasoactive therapy.

Table 20.3 Measurements in a normal 75-kg adult and in various conditions causing circulatory ‘shock’