Chapter Seven
Cardiac Emergencies

The staff of an emergency unit sees a wide spectrum of heart problems, ranging from minor complaints by worried patients to fatal or near-fatal heart attacks. The identification of a sudden change in the state of someone's health as a problem related to the heart is usually made by the patient or a family member on the basis of symptoms such as loss of consciousness, chest pain, shortness of breath, and palpitations. Each of these can be caused by heart disease or by diseases of other organs; furthermore, they may reflect anxiety over a minor complaint.

True cardiac emergencies are usually promptly recognized by medical staff, and appropriate action is taken either in the emergency unit or on transfer to a hospital. The fatal or near-fatal emergencies include

sudden cardiac death

cardiac arrest

syncope

shock

Sudden Cardiac Death

Sudden death is usually defined as unexpected death due to natural causes, with a collapse taking place without warning or preceded by symptoms for no longer than one hour. (The World Health Organization defines sudden death in much broader terms, accepting precollapse symptoms lasting as long as 24 hours; but most

physicians recognize the one-hour limit.) Instantaneous death without warning is very common; symptoms, if any, preceding loss of consciousness almost always involve chest pain or shortness of breath.

The principal causes of sudden cardiac death include ventricular fibrillation, ventricular standstill, acute failure of a ventricle, and catastrophic complication (e.g. cardiac rupture). Autopsy performed after a sudden cardiac death often fails to determine the cause of death, for ventricular fibrillation has no pathologically identifiable features. Only in a minority of cases is a clear-cut explanation of the event available, such as a thrombus in a proximal portion of a principal coronary artery, a large pulmonary embolus, or cardiac rupture. In most cases autopsy reveals general cardiac impairment, such as coronary-artery disease; occasionally the heart may be structurally normal. Coronary-artery disease is by far the commonest cause of sudden cardiac death. Other causes include aortic stenosis and hypertrophic cardiomyopathy.

Sudden cardiac death ranks high among pressing public-health problems. Close to half a million cardiac patients die suddenly each year in the United States. Most sudden cardiac deaths occur in patients with serious heart disease. Yet there is a significant group of patients in the early stages of coronary-artery disease in whom measures aimed at prevention of sudden cardiac death and at early recognition of and resuscitation from ventricular fibrillation can yield good results with a structurally normal heart.

Cardiac Arrest

When the heart suddenly ceases to pump effectively it is said to be in cardiac arrest . This condition is characterized by loss of consciousness resulting from the absence of blood supply to the brain. It is similar to sudden cardiac death, except that rescue efforts initiated within a few minutes of the attack can resuscitate the heart. Delayed resuscitation may reestablish the circulation but often results in "brain death"—irreversible damage to the brain, which is more sensitive to lack of oxygen than any other organ. Loss of consciousness is abrupt, and the pulses disappear. In most cases cardiac arrest is caused by ventricular fibrillation or very rapid ventricular tachycardia.

Survival of cardiac arrest depends on initiating effective treatment as soon as the mechanism of the arrest is clarified. The simplest form of treatment—only occasionally effective but worth trying—is a blow on the chest in the region of the heart, which may terminate ventricular fibrillation or restart a heart in standstill. The definitive treatment of ventricular fibrillation is electric shock to the chest, or defibrillation. If a defibrillator is not immediately available, the circulation of blood can be artificially supported for a short time by periodic chest compression along with mouth-to-mouth breathing. Injection of drugs into the heart is rarely effective.

The success of electric-shock treatment of ventricular fibrillation depends largely on the underlying state of the heart. In most cases ventricular fibrillation develops as an electrical accident in a heart still capable of resuming good function (primary ventricular fibrillation), and its termination is usually successful and complete recovery possible. The long-term prognosis is thus also related to the underlying cardiac status. Ventricular fibrillation frequently develops in a fatally damaged heart (secondary ventricular fibrillation) in which normal rhythm cannot be restored or, if restored, cannot be maintained.

Another mechanism of cardiac arrest is ventricular standstill, or extreme bradycardia (see chap. 6). It occurs in complete heart block or abnormal function of the sinus node. Such patients can be treated with an external electronic pacemaker to restart heart action and maintain it until an intracardiac pacemaker can be inserted.

Syncope

Sudden loss of consciousness (occasionally associated with convulsive seizures) followed by spontaneous resumption of brain function is called syncope. Syncope is related to cardiac arrest and may have the same cause. But syncope, a more benign emergency, not only results from problems of the heart and circulation but also can be caused by malfunction of the brain (it may coincide with epilepsy and other brain-seizure disorders). There are two principal kinds of cardiocirculatory syncope—that caused by arrhythmias and that caused by disturbances of reflex control regulating the circulation.

Arrhythmias may cause syncope when the heart rate becomes

extremely slow or extremely rapid. Bradycardia or standstill may develop in complete heart block or in sinus-node disorders. Tachycardias leading to syncope include very rapid nonsustained ventricular tachycardia (at rates approaching 300 beats a minute) or a paroxysmal form of ventricular flutter or fibrillation.

Malfunction of the reflex mechanism controlling the circulation usually involves abnormal dilation of the blood vessels, which may lower systemic blood pressure and cause abnormal pooling of the blood in peripheral blood vessels. Thus not only is the control of blood pressure impaired, but reduced return of venous blood to the heart affects the quantity of blood pumped into the circulation. Another mechanism involves abnormal stimulation of the vagus nerve, which slows the heartbeat and produces sinus pauses. Among varieties of syncope related to abnormal reflexes are

simple faint, a loss of consciousness triggered by excitement or prolonged standing in the heat

syncope triggered by certain stimuli and representing exaggerated responses to reflex stimulation, such as a cough or the passing of urine

syncope associated with certain heart diseases producing abnormalities of the reflex control of the circulation, such as aortic stenosis, hypertrophic cardiomyopathy, and pulmonary hypertension

syncope due to inhibition of the function of the sinus node by reflexes originating in the arteries of the neck (carotid sinus hypersensitivity)

syncope due to inhibition of the sinus node associated with nausea

Certain types of syncope develop so abruptly that the patient may fall to the ground without warning. Such abruptness is characteristic of syncopes caused by arrhythmias (complete heart block, ventricular tachycardia or fibrillation) or associated with aortic stenosis. Syncopes related to problems of the peripheral circulation tend to develop after some warning, which enables the patient to sit down or brace the fall before losing consciousness.

Persons who are prone to syncope, or who have experienced a syncopal attack in the past, may at times become dizzy or feel faint without losing consciousness. These episodes of incomplete syncope are known as presyncopal attacks.

The prognosis of patients who have suffered one or more syncopal attacks is difficult to establish. The mechanism and cause of syncope are often uncertain, and medical evaluation may show no abnormal findings between attacks. Only occasionally are direct clues to the cause of syncope available, such as when an attack occurs while electronic monitoring is in progress or when a witness to the attack notes an absence of pulse during the attack. Some indirect clues may be helpful in evaluating patients with syncope, such as the presence of less-serious ventricular arrhythmias or atrioventricular conduction disturbances, aortic stenosis, demonstrated hypersensitivity of carotid-sinus reflex, or a tendency to faintness when the patient rapidly stands up. Often the cause of unwitnessed attacks of syncope remains undiscovered.

When findings suggest that ventricular arrhythmia may be the basis of syncopal attacks, electrophysiological testing is commonly performed. Such tests can determine whether stimulation of the heart is capable of initiating a serious arrhythmia, in which case appropriate treatment may prevent further attacks. In the presence of persistent bradycardia or conduction disturbances the placement of a permanent pacemaker is usually indicated.

Shock

When the blood supply to vital organs is severely reduced, a person goes into shock . The most important manifestation of shock is abnormally low arterial pressure, which is usually caused by one or more of the following mechanisms: depressed function of the cardiac pump, faulty regulation of blood pressure, and sudden loss of blood in the body.

Shock, a variety of cardiocirculatory failure, differs in many respects from heart failure, described in chapter 5. In heart failure the arterial pressure is usually maintained at a normal or near-normal level, and blood supply to vital organs is only slightly impaired; its principal deleterious consequences are related to backing up of the blood in the lungs and systemic veins, sometimes called backward heart failure. In shock, or forward failure, the blood pressure is so low that the pumping force is inadequate to maintain the circulation in various organs. There is an obvious similarity between shock and syncope: the former is partial failure

of circulatory adjustment, the latter total. Furthermore, shock represents a prolonged state, whereas syncope is of very short duration. Reduced blood supply to the brain in shock often causes extreme fatigue, restlessness, confusion, and even a semicomatose state. Reduced blood flow to the skin affects temperature control: the skin becomes cool, and a cold perspiration is common. Pallor with bluish tinge (cyanosis) may also be observed.

Shock is a persistent state with a low probability of spontaneous improvement. The prognosis of shock varies widely and depends on its cause and the response to treatment. The most common causes of shock are noncardiac; they include severe infection, serious allergic reaction (anaphylactic shock ), serious hemorrhage, intense pain, and catastrophic events in the gastrointestinal tract, such as perforation of an organ.

The least reversible, and hence most serious, form of shock is cardiogenic shock , produced by a sudden reduction in the pumping efficiency of a cardiac ventricle. The commonest cause of cardiogenic shock is myocardial infarction (due either to the initial injury to the heart muscle or to a later major complication). Cardiogenic shock may also develop as a result of sudden severe overload of the heart, such as rupture of a cardiac valve or massive pulmonary embolism. A state similar to shock but not directly related to malfunction of the cardiac muscle is pericardial tamponade , accumulation of fluid in the sac around the heart that compresses the heart and interferes with its pumping (see chap. 10). Shock may also result from rapid ectopic tachycardia.

The prognosis of cardiogenic shock is always guarded. The mortality rate under drug therapy or insertion of an intraaortic balloon pump remains high. Elimination or amelioration of the cause of cardiogenic shock is occasionally possible by surgical means.

Other Cardiac Emergencies

Patients entering an emergency unit with chest pain, a common event, are preferentially evaluated for possible acute myocardial infarction. A diagnosis of infarction calls for immediate intervention, and the relief of pain may have to take second place to prompt diagnosis. If the cause of the pain is identified as myocardial ischemia (diminished blood supply to the heart muscle), the medical

staff must consider whether the problem is reversible and temporary (angina pectoris) or the heart muscle has sustained permanent damage (myocardial infarction). This question may not be answerable in the emergency unit, in which case it is usually necessary to admit the patient to the hospital for observation and further evaluation.

Other cardiovascular conditions causing sudden onset of severe chest pain include pulmonary embolism, pericarditis, and aortic dissection. Noncardiac conditions associated with chest pain severe enough to bring a patient to an emergency unit include gastrointestinal disease (hiatus hernia, esophageal spasm) and pulmonary disease (pleurisy, pneumonia, pneumothorax). Such pain may also originate in various structures of the chest wall—nerves, muscles, or the junction between the ribs and the sternum.

As explained in this chapter, arrhythmias are responsible for the majority of cases of cardiac arrest or cardiac syncope. However, patients are often sufficiently alarmed about less-serious arrhythmias to seek emergency medical care. A common condition in this category is paroxysmal tachycardia or atrial fibrillation, which may be perceived as severe pounding of the heart, even though it may not produce any abnormality in the cardiac or circulatory function. The emergency unit must decide whether to admit the patient to the hospital or administer drugs and send the patient home. Most supraventricular tachycardias can be promptly terminated by appropriate intervention, and if no underlying heart disease is present, hospitalization is usually unnecessary. Atrial flutter or fibrillation may or may not respond to treatment in the emergency unit. If the ventricular rate is above 150 beats a minute, hospitalization is frequently advisable. Ventricular tachycardia requires prompt intervention and, because of its implications, admission to the hospital.