Current concepts in the management of heart failure.

OBJECTIVE: To review current concepts in the management of patients with heart failure. DATA SOURCES: A review of articles reported on acute and chronic heart failure. SUMMARY OF REVIEW: Heart failure has been defined as that state which occurs when the heart fails to maintain the needs of the body despite a satisfactory venous return. While it has been divided functionally into high-output failure and low-output failure, it is often used to describe patients with left ventricular low-output failure and is divided into systolic or diastolic heart failure, depending on left ventricular ejection fraction. The clinical features are due largely to venous congestion and reduction in cardiac output with symptoms of fatigue, orthopnoea, paroxysmal nocturnal dyspnoea and peripheral oedema being common complaints. Plasma natriuretic peptide levels are elevated in patients with symptomless left ventricular failure and have been useful in diagnosing heart failure in patients admitted with acute dyspnea. Treatment of heart failure is aimed at correcting both the underlying disorder as well as the precipitating cause (e.g. ischaemia, valvular heart disease, anaemia, thyrotoxicosis, etc), as well as reducing cardiac work, enhancing myocardial contractility and treating the complications (e.g. reducing salt and water retention, and neurohumoral activation). Angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor antagonists, beta-blockers and spironolactone have all been associated with a reduction in mortality in patients with chronic heart failure. While digoxin and diuretics are used to reduce the number of episodes of pulmonary oedema, they have not been associated with a significant reduction in mortality. Surgery (e.g. transplantation, mechanical assist devices) has a definite place in young patients with chronic dilated cardiomyopathy with severe heart failure although other therapeutic agents (e.g. growth hormone, thyroxine and antioxidants) are yet to be shown to be of benefit. CONCLUSIONS: Heart failure is a common condition caused by many disorders leading to left ventricular dysfunction. Management of the underlying disorder (e.g. ischaemia, valvular disease, hypertension) maintenance of sinus rhythm, as well as reducing excessive neurohumoral activation (ACE inhibitors, angiotensin receptor antagonists, beta-blockers, spironolactone) can reduce mortality and improve morbidity in patients with chronic heart failure.

Cardiac arrhythmias: diagnosis and management. The tachycardias.

OBJECTIVE: To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts on tachycardias and bradycardias. SUMMARY OF REVIEW: Normal cardiac rhythm originates from impulses generated within the sinus node. These impulses are conducted to the atrioventricular node where they are delayed before they are distributed to the ventricular myocardium via the His-Purkinje system. Abnormalities in cardiac rhythm are caused by disorders of impulse generation, conduction or a combination of the two and may be life threatening due to a reduction in cardiac output or myocardial oxygenation. Cardiac arrhythmias are commonly classified as tachycardias (supraventricular or ventricular) or bradycardias. The differentiation between supraventricular and ventricular tachycardias usually requires an assessment of atrial and ventricular rhythms and their relationship to each other. In the critically ill patient the commonest tachycardia is sinus tachycardia and treatment generally consist of management of the underlying disorder. Other supraventricular tachycardias (SVTs) include, atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia (PSVT) all of which may require cardioversion, although to maintain sinus rhythm, antiarrhythmic therapy is often needed. Adenosine is useful in management and treatment many SVTs although its use in PSVT with Wolff-Parkinson-White syndrome is hazardous. Multifocal atrial tachycardia is a characteristic supraventricular tachycardia found in the critical ill patient. While it usually responds to intravenous magnesium sulphate, its management also requires removal of various precipitating factors. Ventricular tachycardia (VT) and ventricular fibrillation (VF) require urgent cardioversion and defibrillation respectively. Torsade de pointes should be differentiated from these ventricular arrhythmias as antiarrhythmic therapy may be contraindicated. CONCLUSIONS: Supraventricular and ventricular tachycardias in the critically ill patient often have underlying disorders that precipitate their development (e.g. hypokalaemia, hypomagnesaemia, anti-arrhythmic proarrhythmia, myocardial ischaemia, etc). While antiarrhythmic therapy and cardioversion or defibrillation may be required to achieve sinus rhythm, correction of the associated abnormalities is also required.

Cardiac arrhythmias: diagnosis and management. The bradycardias.

OBJECTIVE: To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts on tachycardias and bradycardias. SUMMARY OF REVIEW: Bradycardias are caused by a failure of the sinus node to generate normal impulses or due to a defect in cardiac conduction that in turn causes a delay or failure of impulse propagation. During sleep, the heart rate may decrease to 30 beats per minute (bpm) with episodes of sinoatrial block, junctional rhythms and first and second degree atrioventricular block that occur often enough (particularly in trained athletes) to be considered normal variants. However, treatment is required if symptoms of dizziness, confusion, fatigue Stokes-Adams attacks or heart failure occur. Sinus node dysfunction or 'sick sinus syndrome' is usually caused by intrinsic nodal disease and may present with episodes of tachycardia and bradycardia (tachycardia-bradycardia syndrome). Treatment usually requires a permanent pacemaker. Atrioventricular (AV) conduction disturbances are characterised by a delay or failure of the atrial impulse to be conducted through the AV conducting system. If the escape rhythm is unstable the patient also requires a pacemaker. In the critically ill patient tachycardias are more often encountered than bradycardias. However, the intensivist should be familiar and skilled in the management of complete heart block and asystole, correcting the underlying defect (drug toxicity, hyperkalaemia, etc), while using catecholamines, atropine aminophylline and a temporary pacemaker for initial resuscitation. CONCLUSIONS: Bradycardias are uncommon in the critically ill patient and often are caused by an underlying disorder (e.g. hyperkalaemia, calcium channel blocker toxicity, beta adrenergic receptor blocker toxicity, etc). However, post cardiac bypass and acute myocardial infarction may cause cardiac conduction defects that may require urgent resuscitation with a temporary pacemaker.

Neurologic complications of critical illness: part I. Altered states of consciousness and metabolic encephalopathies.

OBJECTIVE: To review the metabolic encephalopathies and neuromuscular abnormalities commonly found in the critically ill patient in a two-part presentation. DATA SOURCES: A review of articles reported from 1980 to 2002 and identified through a MEDLINE search on metabolic encephalopathy, polyneuropathy and myopathy in critical illness. SUMMARY OF REVIEW: An alteration in the conscious state can be caused by space occupying lesions or infections of the central nervous system. However, in the critically ill patient a metabolic encephalopathy is often the cause of an acute confusional state or a reduced state of consciousness. There is no specific treatment for the metabolic encephalopathies as they commonly resolve when the underlying disorders (e.g. sepsis, renal failure, hepatic failure, electrolyte disturbance) are corrected. Management may also require judicious pharmacological and/or physical restraint in the case of the acute confusional states and ensuring an adequate airway, ventilation and circulation in the case of a reduced state of consciousness, while the underlying disorder is corrected and the encephalopathy resolves. CONCLUSIONS: In the critically ill patient a metabolic encephalopathy is commonly the cause of confusion, disorientation, agitation, drowsiness or coma. Sedative agents and tranquilisers may be required as well as management of the airway, ventilation and circulation while the underlying disorder is corrected to allow the encephalopathy to resolve.

Neurologic complications of critical illness: part II. Polyneuropathies and myopathies.

OBJECTIVE: To review the metabolic encephalopathies and neuromuscular abnormalities commonly found in the critically ill patient in a two-part presentation. DATA SOURCES: A review of articles reported from 1980 to 2002 and identified through a MEDLINE search on metabolic encephalopathy, polyneuropathy and myopathy in critical illness. SUMMARY OF REVIEW: Severe weaknes in the critically ill patient may have many causes, although Guillain-Barré syndrome, critical illness polyneuropathy and critical illness myopathy are the motor disorders commonly found in the critically ill patient. Guillain-Barré syndrome is characterised by an acute ascending weakness 1-3 weeks after a gastrointestinal or upper respiratory tract infection. Intravenous immune globulin (or plasmapheresis) should be initiated as soon as possible to shorten the duration of ventilation, time to walk unaided and halt the progression of the disease. Critical illness polyneuropathy and critical illness myopathy often coexist in the critically ill patient and are probably caused by a small number of activated leucocytes that infiltrate skeletal muscle and produce pro and anti-inflammatory cytokines. Axonal degeneration of both motor and sensory fibres with preservation of the myelin sheath cause the neuropathy, and muscle fibre necrosis and atrophy causes the myopathy. Apart from treatment of the underlying cause (e.g sepsis), there is no specific treatment, although a 44% reduction in the incidence of critical illness polyneuropathy has been described in mechanically ventilated critically ill patients who received intensive insulin therapy to maintain the blood glucose level between 4.4-6.1 mmol/L. Recovery usually occurs over weeks to months depending on the severity of the disease. CONCLUSIONS: An acute motor weaknesses in the critically ill patient may be caused by Guillain-Barré syndrome, critical illness polyneuropathy or critical illness myopathy. Patients with severe Guillain-Barré syndrome should be managed in an intensive care unit and given intravenous immune globulin. Treatment of critical illness polyneuropathy or myopathy requires largely management of the underlying disorder.

Clinical toxicology: part I. Diagnosis and management of common drug overdosage.

OBJECTIVE: To review the diagnosis and management of drug overdosage in a two-part presentation. DATA SOURCES: A review of articles reported on drug overdose and poisoning. SUMMARY OF REVIEW: A patient who has taken an overdose of a common drug often presents with an alteration in neurological, cardiovascular and respiratory functions. The differential diagnosis includes, central nervous system injury and metabolic encephalopathies (e.g. hepatic failure, hyponatraemia, hypocapnia, hypoglycaemia). In general, measures to prevent absorption (e.g. emesis, gastric lavage) or increase excretion (e.g. diuresis, catharsis) of the drug, have not been shown consistently to reduce mortality associated with drug toxicity. However, in selected instances adsorbents (activated charcoal, Fuller's earth), gastric lavage and haemodialysis or continuous renal replacement therapy are useful in the management of drug overdosage and specific antidotes can be recommended for individual poisons. Nevertheless, as the major hazards of an overdose are aspiration, hypoventilation, hypoxia, hypotension and cardiac arrhythmias, the most important aspects in the management of a poisoned patient is the maintenance of the patient's airway, ventilation and circulation, while the drug is excreted. The diagnosis and management of common drug overdoses (e.g sedative, hypnotic, psychoactive, neuroleptic, anticonvulsant, sympathomimetic, analgesic and cardiac drugs) as well as the alcohols are discussed in the first part of this presentation on clinical toxicology. CONCLUSIONS: In the critically ill overdosed patient, while activated charcoal, continuous renal replacement therapy and specific antidotes may be of benefit in selected cases, maintenance of the patient's airway, ventilation and circulation still remain the most important aspects of management.

Clinical toxicology: part II. Diagnosis and management of uncommon poisonings.

OBJECTIVE: To review the diagnosis and management of drug overdose and poisonings in a two-part presentation. DATA SOURCES: A review of articles reported on drug overdose and poisonings. SUMMARY OF REVIEW: In patients who attempt suicide it is usual for the overdose to be a therapeutic agent, although in the severely mentally disturbed patient the agent may be an unusual poison. As with any overdose, the most important aspects in the management is the maintenance of the patient's airway, ventilation and circulation, while the toxin is metabolised and excreted. Adsorbents, gastric lavage and haemodialysis or continuous renal replacement therapy and specific antidotes may be beneficial in individual cases. The diagnosis and management of uncommon poisonings, including pesticides and herbicides (e.g. organophosphates, carbamates, paraquat, chlorophenoxy herbicides), carbon monoxide, cyanide, strychnine, halogenated hydrocarbons, elemental poisons (e.g. iron, arsenic, lead, mercury, selenium, barium, thallium, lithium, sodium, rubidium, cesium), alkaloids (e.g. mushroom, aconite, conium) and cantharidin poisoning along with the miscellaneous poisonings of quinine, chloroquine, isoniazid, thyroxine, cytotoxic agents (e.g. azothioprine, 6-mercaptopurine, colchicine, methotrexate) are discussed in the second part of this presentation on clinical toxicology. CONCLUSIONS: In the critically ill patient who has taken an overdose of a non therapeutic agent, while activated charcoal, continuous renal replacement therapy and specific antidotes may be of benefit, maintenance of the patient's airway, ventilation and circulation still remain the most important aspects of management.

The essentials of calcium, magnesium and phosphate metabolism: part I. Physiology.

OBJECTIVE: To review the components of calcium, phosphate and magnesium metabolism that are relevant to the critically ill patient in a two-part presentation. DATA SOURCES: A review of articles reported on calcium, phosphate and magnesium disorders in the critically ill patient. SUMMARY OF REVIEW: Calcium, phosphate and magnesium have important intracellular and extracellular functions with their metabolism often linked through common hormonal signals. A predominant portion of total body calcium is unionised within bone and serves an important structural function. Intracellular and extracellular ionised calcium changes are often linked and have important secretory and excitatory roles. The extracellular ionised calcium is carefully regulated by parathyroid hormone and vitamin D, whereas calcitonin is secreted largely in response to hypercalcaemia. Phosphorous is needed for bone structure although it also has an important role in cell wall structure, energy storage as ATP, oxygen transport and acid-base balance. Ionised calcium, in as far as it controls PTH secretion, indirectly controls urinary phosphate excretion. When plasma phosphate increases, tubular reabsorption also increases up to a maximum (TmPO4), thereafter phosphate is excreted. The minimum oral requirement for phosphate is about 20 mmol/day. Magnesium is a predominantly intracellular ion that acts as a metallo-coenzyme in more than 300 phosphate transfer reactions and thus has a critical role in the transfer, storage and utilisation of energy within the body. Extracellular magnesium concentrations are largely controlled by the kidneys with the renal tubular maximum reabsorption (TmMg) controlling the plasma magnesium concentration. CONCLUSIONS: In the critically ill patient calcium, magnesium and phosphate metabolism, are often disturbed with an alteration in intake, increased liberation from bone and damaged tissue and reduced excretion (e.g. during renal failure), causing alterations in extracellular concentrations and subsequent disordered organ function.