Anaesthesia, 1976, Volume 31, pages 758-763
Thoughts on immediate care Anaesthetists are being increasingly called upon to give immediate treatment for various life-threatening conditions in casualty departments and elsewhere. Thisfeature of short papers by invited experts is designed to describe the proper management of patients who require immediate care before the opinion of specialists in a particular field can be obtained.
Immediate care of cardiac emergencies D. A. C H A M B E R L A I N A N D J. H . WILLIAMS
Cardiac emergencies can conveniently be divided into those due to abnormalities of heart rhythm, and those which follow from a defect in the mechanics of cardiac contraction. Serious haemodynamic disturbances may follow from either or both types of disorder, but rhythm abnormalities can usually be treated much more successfully than pump failure occurring alone. The emphasis in this article on emergency treatment is therefore directed principally to those rhythm disorders which cause or threaten a critical reduction in cardiac output. The following is intended to provide only guidelines for immediate care. It assumes no special knowledge of cardiology or electrocardiography. The circumstances of cardiac resuscitation are almost infinitely variable and recommendations must not be regarded as inflexible. Arrhythmias Ventricularfibrillation
Ventricular fibrillation (VF) is due principally but not exclusively to anoxic injury to the myocardium. Only exceptionally can an underlying cause be corrected as the essential first measure (e.g. faulty oxygen supply during anaesthesia; reversible airway obstruction; catheter occlusion of the ostium of a coronary artery during angiography ; ‘micro-shock’ through an intra-cardiac catheter or electrode). In most cases defibrillation should be attempted as soon as possible. This is especially true for VF of very recent onset. Immediate ventricular defibrillation (1) Mechanical defibrillation may be successful within the initial 20-30 seconds; e.g. a cough if the patient is still conscious, otherwise a thump over the precordium. (2) Usually a DC shock will be necessary. Try 200 J first, 400 J only if this is unsuccessful. D. A. Chamberlain, MD, FRCP, Consultant Physician, and J. H. Williams, FFARCS, Consultant Anaesthetist, Royal Sussex County Hospital, Brighton, Sussex.
758
Immediate care of cardiac emergencies
759
(3) Do not delay the first attempt at defibrillation in order to intubate the patient unless airway obstruction was the primary cause of the rhythm disturbance. (4) Do not delay the first attempt at defibrillation in order to provide external cardiac massage (ECM). Most cases of V F in high dependency areas are best managed without ECM. ( 5 ) In cases of definite circulatory arrest do not delay defibrillation if monitoring oscilloscope or electrocardiograph are not immediately available to confirm cardiac rhythm. An inappropriate DC shock is unlikely to cause further harm, even to patients with sudden severe hypovolaemia. (6) Remember the sooner the heart is defibrillated, the greater the chance of eventual recovery. Ventricular dejibrillation after delay
The emphasis is somewhat different for patients who have had VF for more than 2-3 minutes, whether or not ECM has been administered. They will be acidotic and almost certainly seriously anoxic. A prolonged attempt at resuscitation will usually be necessary. An immediate DC shock is still recommended in most circumstances but may not restore co-ordinated rhythm. Asystole is the most frequent immediate sequel. (1) Maintain ECM continually, except when DC shocks are being administered. (2) Intubate as soon as possible if the patient is apnoeic or breathing inadequately. (3) Give sodium bicarbonate intravenously for acidosis. Formula: 1 mEq per kg body weight initially followed by one-tenth of this dose per minute of subsequent arrest. (4) For defibrillation use full charge of 400 J initially, preferably with paddles front and back of chest to achieve maximum current density in the heart. Transient asystole is to be expected : do not use stimulant drugs for a minute or so because co-ordinated rhythm may supervene or VF recur. Even after return to co-ordinated rhythm continue ECM until an effective heartbeat has been restored, i.e. until a spontaneous peripheral pulse is palpable. After return of an adequate pulse, give two injections of intravenous lignocaine 100 mg within 15 minutes and set up an infusion at 3 mg/minute. (5) Use other drugs as sparingly as possible, but adrenaline 10 ml 1 : 10,000 intravenously might render$ne VF more susceptible to defibrillation. Use calcium chloride 10 ml 10% solution intravenously followed by adrenaline if necessary for refractory asystole resulting from defibrillation. If drugs are given peripherally into an arm vein then remember to elevate the limb and ‘milk’ downwards. Asystole
This carries a much worse prognosis than does VF. It may occur transiently after defibrillation as mentioned above, but it is also seen as a terminal event in a dying heart. Asystole may call for vigorous attempts at resuscitation in two other circumstances: first, when it occurs as a result of bilateral bundle branch block, usually after myocardial infarction or with idiopathic conducting system disease; secondly, as a complication of metabolic disorder (e.g. hyperkalaemia) or drug therapy. In both these circumstances it is usually intermittent at first, and ECM should be used as
760
D. A . Chamberlain and J. H . Williams
necessary until pacing and definitive therapy for any underlying disease can be established, Occasionally light mechanical stimuli will ‘trigger’ QRS complexes. An effective rhythm may then result from light taps over the sternum delivered at a rate of about one per second. An intravenous infusion of isoprenaline 1-4 pglminute may help to maintain spontaneous rhythm (larger doses of isoprenaline or adrenaline may be used initially during the phase of asystole) but in general drugs should be used sparingly and with caution, to avoid the dangers of cardiac depression or recurrent arrhythmias. However, 10 ml of 10% calcium chloride intravenously with large doses of intravenous adrenaline or isoprenaline may be used if a brief period of ECM is not followed by spontaneous beats. Intracardiac injections should be given only as a last resort. Supraventricular and ventricular tachycardias
The precise nature of a rhythm rapid enough to require emergency treatment will usually be difficult to determine; even supraventricular tachycardia (SVT) is likely to show wide QRS complexes under these circumstances. Fortunately some general guidelines for treatment are applicable for both types of tachycardia arising in most circumstances. Treatment of tachycardias
(1) Try carotid massage if possible (unless vascular reflexes are blocked by anaesthesia, etc.). Caution : this may be dangerous in digitalis-induced arrhythmias. It is ineffective for ventricular tachycardias (VT), and so even transient response is of diagnostic value. (2) Give lignocaine 100 mg intravenously. It is usually ineffective but harmless in SVT. (3) Give practolol* 5 mg or propranolol 1 mg intravenously over several minutes. These doses may be repeated three or four times if necessary. Note. The tachycardia may revert 5-10 minutes after the completion of the injection of practolol or propranolol, so do not hasten to repeat doses or give further depressant drugs. Caution:p-adrenoreceptor antagonists are dangerous in the presence of serious myocardial dysfunction. (4) Zf digitalis-induced, try lignocaine 100 mg intravenously or phenytoin 50-200 mg intravenously as drugs of choice. Practolol is a third option if myocardial function is not severely impaired. DC shock is contra-indicated but may be used in lifethreatening situations (see below). (5) For refractory cases, or in any patient with severe haemodynamic disturbances, use DC shock. Caution: if the arrhythmia might be digitalis-induced, but a DC shock is still felt to be mandatory, start with 25 J and progress to 50, 100, 200, 300 and 400 J. The appearance of multiple ventricular extrasystoles after any shock is an indication for lignocaine cover. (6) Other drugs to consider for refractory cases: di-isopyramide 150 mg or bretylium tosylate 350 mg intravenously over 10-20 minutes :procainamide 100 mg intravenously every 5 minutes to a maximum of eight doses. But try to avoid excessive suppressant drugs, especially with a damaged myocardium. (7) SVT and VT which recur frequently despite optimal drug therapy may often be managed by pacing techniques.
* Still available in hospitals for intravenous use.
Immediate care of cardiac emergencies
761
(8) Atrial flutter is a special case. It responds poorly to drugs but well to DC shocks, usually at low energies, e.g. 50 J. Some cases respond only transiently: give digitalis to control the ventricular response though this may not always be successful. Flutter can also be controlled by pacing techniques.
A trial fibr illation This is an emergency in two situations: (A) if an uncontrolled ventricular response causes severe haemodynamic disturbances due to impaired myocardial function or valve lesion; (B) when it occurs prior to or during anaesthesia in a high-risk patient. Prophylaxis. Susceptible patients, if identified, should usually be digitalised before anaesthesia: digoxin 14-1-5 mg in divided doses over 24 hours, orally if possible, otherwise intravenously over several hours. Treatment of atrial fibrillation (1) Urgent drug therapy for established AF: digoxin 1.5 mg or for faster action ouabain 1.0 mg intravenously, preferably over a t least 2 hours but rapidly in lifethreatening situations. Note. Even after full intravenous doses rate may slow only over some hours. Persisting rapid rate may not, therefore, indicate under-digitalisation. Check that patient is not already digitalised ! (2) Always consider the use of a synchronised DC shock especially for rapid rates and when the patient’s haemodynamic state is unsatisfactory. Remember that a persisting rapid rate after myocardial infarction will cause extension of muscle necrosis. It is not harmful to start intravenous digitalisation before DC shock is given. Note. In very urgent situations unsynchronised shock is permissible if a synchronised machine is not available. The risk of inducing VF is small, and if it should occur it can be dealt with expeditiously.
Bradycardias and blocks
Detailed consideration of the differential diagnosis of sinus bradycardia, sino-atrial block, AV nodal block, and bilateral bundle branch block is outside the scope of this article. However, general methods for dealing with critically slow heart rates can be listed. Treatment of bradycardias and blocks (1) Intravenous atropine may be effective in all the bradyarrhythmias except those arising as a result of bilateral bundle branch block. Increased vagal tone may occasionally protect the ischaemic heart from predisposition to ventricular arrhythmias, so that atropine may have a deleterious effect by neutralising this protection. In other respects atropine is a very safe agent. The initial dose should be restricted to 0.3 mg after myocardial infarction to avoid the risk of undesirable tachycardias, which increase myocardial damage. (2) An isoprenaline infusion may speed all types of bradyarrhythmias. Dose rates are 1-4 pglminute. In life-threatening situations very much larger doses may be used
762
D. A . Chamberlain and J. H. Williams
initially. Always use the smallest effective dose because of the oxygen-wasting potential and arrhythmogenic action of catecholamines. (3) Patients with extreme bradycardia resulting from bilateral bundle branch block may not respond to any drugs. ECM should be used until pervenous pacing can be initiated. These extreme bradycardias are managed in the same way as asystole (see above). Acute left heart failure This dramatic emergency occurs either as a result of obstruction at the mitral or aortic valve, or because of impairment of left ventricular function. The event may be precipitated by a tachyarrhythmia (e.g. AF) in susceptible subjects.
Treatment (1) Correct any rhythm abnormality as quickly as possible.
(2) Intravenous morphine remains the drug of choice. It reduces venous return and therefore right ventricular output, also reducing the work of the left heart by lowering peripheral resistance. Its central actions relieve patients’ distress. (3) Diuretics (frusemide 40-80 mg intravenously) should always be given, especially because they reduce the risk of subsequent attacks. Digitalis and glucagon are of some value. Cuffs around the thighs inflated to just below diastolic blood pressure will further reduce venous return to the right heart. Cardiogenic shock The prognosis is very poor if cardiogenic shock persists after adequate treatment of pain, and correction of rhythm disturbances and pH. Very rarely after myocardial infarction, hypotension and critical reduction in cardiac output are associated with reduced filling pressure in the right and left heart rather than with failure; the patient’s condition will improve with volume expanders. Pulmonary artery pressure should be monitored under these circumstances for inappropriate infusion may cause pulmonary oedema. Little effective treatment is available for the common form of cardiogenic shock associated with high filling pressure. Intravenous catecholamines are not of proven value, but some authorities recommend salbutamol infusion at 10-50 pglminute. Only a few centres can utilise intra-aortic balloon pumping, and its late results are not impressive. Cyanotic attacks with congenital heart disease Some patients with right-to-left shunts may have periods of increased cyanosis induced by such factors as effort, emotion, blood loss, or anaesthesia. The intracardiac defect permits some desaturated blood to shunt away from the pulmonary artery (which will have restricted access because of a stenotic outflow tract or restricted egress due to a hypertensive pulmonary bed) and into the aorta. Constriction of a hypertrophied infundibulum by sympathetic tone or reduction in peripheral resistance for any reason will increase flow of desaturated blood into the aorta. A vicious circle can become
Immediate care of cardiac emergencies
763
established, because a marked decrease in systemic saturation may further reduce peripheral resistance. Cyanotic attacks of this type can be fatal, so that it is essential to avoid even the moderate hypotension often associated with routine induction of anaesthesia. Immediate first-aid treatment of cyanotic attacks calls for appropriate measures to increase systemic blood pressure, usually by the administration of a pressor agent of the methoxamine type. Cardiac tamponade Cardiac tamponade occurs most commonly as a result of rupture of the ventricular wall after myocardial infarction. Circulatory arrest in the presence of continued electrical activity of the heart implies an untreatable catastrophe. Tamponade should always be considered as a cause of unexplained deterioration after cardiac surgery and recent chest trauma (even wihout external evidence of chest injury) and, if confirmed, calls for urgent surgical exploration. Tamponade from other causes should be treated by aspiration. A long needle is inserted high in the angle between the xiphisternal cartilage and adjoining rib, and after penetration deep to the sternum, is guided as sharply upwards as possible to enter the pericardial sac anteriorly and near the mid-line. Summary The emergency treatment of serious disorders of cardiac rhythm, left heart failure, cardiogenic shock, and cyanotic attacks is discussed. The article is intended for medical practitioners without special cardiological experience.
Thoughts on immediate care Anaesthetists are being increasingly called upon to give immediate treatment for various life-threatening conditions in casualty departments and elsewhere. Thisfeature of short papers by invited experts is designed to describe the proper management of patients who require immediate care before the opinion of specialists in a particular field can be obtained.
Immediate care of cardiac emergencies D. A. C H A M B E R L A I N A N D J. H . WILLIAMS
Cardiac emergencies can conveniently be divided into those due to abnormalities of heart rhythm, and those which follow from a defect in the mechanics of cardiac contraction. Serious haemodynamic disturbances may follow from either or both types of disorder, but rhythm abnormalities can usually be treated much more successfully than pump failure occurring alone. The emphasis in this article on emergency treatment is therefore directed principally to those rhythm disorders which cause or threaten a critical reduction in cardiac output. The following is intended to provide only guidelines for immediate care. It assumes no special knowledge of cardiology or electrocardiography. The circumstances of cardiac resuscitation are almost infinitely variable and recommendations must not be regarded as inflexible. Arrhythmias Ventricularfibrillation
Ventricular fibrillation (VF) is due principally but not exclusively to anoxic injury to the myocardium. Only exceptionally can an underlying cause be corrected as the essential first measure (e.g. faulty oxygen supply during anaesthesia; reversible airway obstruction; catheter occlusion of the ostium of a coronary artery during angiography ; ‘micro-shock’ through an intra-cardiac catheter or electrode). In most cases defibrillation should be attempted as soon as possible. This is especially true for VF of very recent onset. Immediate ventricular defibrillation (1) Mechanical defibrillation may be successful within the initial 20-30 seconds; e.g. a cough if the patient is still conscious, otherwise a thump over the precordium. (2) Usually a DC shock will be necessary. Try 200 J first, 400 J only if this is unsuccessful. D. A. Chamberlain, MD, FRCP, Consultant Physician, and J. H. Williams, FFARCS, Consultant Anaesthetist, Royal Sussex County Hospital, Brighton, Sussex.
758
Immediate care of cardiac emergencies
759
(3) Do not delay the first attempt at defibrillation in order to intubate the patient unless airway obstruction was the primary cause of the rhythm disturbance. (4) Do not delay the first attempt at defibrillation in order to provide external cardiac massage (ECM). Most cases of V F in high dependency areas are best managed without ECM. ( 5 ) In cases of definite circulatory arrest do not delay defibrillation if monitoring oscilloscope or electrocardiograph are not immediately available to confirm cardiac rhythm. An inappropriate DC shock is unlikely to cause further harm, even to patients with sudden severe hypovolaemia. (6) Remember the sooner the heart is defibrillated, the greater the chance of eventual recovery. Ventricular dejibrillation after delay
The emphasis is somewhat different for patients who have had VF for more than 2-3 minutes, whether or not ECM has been administered. They will be acidotic and almost certainly seriously anoxic. A prolonged attempt at resuscitation will usually be necessary. An immediate DC shock is still recommended in most circumstances but may not restore co-ordinated rhythm. Asystole is the most frequent immediate sequel. (1) Maintain ECM continually, except when DC shocks are being administered. (2) Intubate as soon as possible if the patient is apnoeic or breathing inadequately. (3) Give sodium bicarbonate intravenously for acidosis. Formula: 1 mEq per kg body weight initially followed by one-tenth of this dose per minute of subsequent arrest. (4) For defibrillation use full charge of 400 J initially, preferably with paddles front and back of chest to achieve maximum current density in the heart. Transient asystole is to be expected : do not use stimulant drugs for a minute or so because co-ordinated rhythm may supervene or VF recur. Even after return to co-ordinated rhythm continue ECM until an effective heartbeat has been restored, i.e. until a spontaneous peripheral pulse is palpable. After return of an adequate pulse, give two injections of intravenous lignocaine 100 mg within 15 minutes and set up an infusion at 3 mg/minute. (5) Use other drugs as sparingly as possible, but adrenaline 10 ml 1 : 10,000 intravenously might render$ne VF more susceptible to defibrillation. Use calcium chloride 10 ml 10% solution intravenously followed by adrenaline if necessary for refractory asystole resulting from defibrillation. If drugs are given peripherally into an arm vein then remember to elevate the limb and ‘milk’ downwards. Asystole
This carries a much worse prognosis than does VF. It may occur transiently after defibrillation as mentioned above, but it is also seen as a terminal event in a dying heart. Asystole may call for vigorous attempts at resuscitation in two other circumstances: first, when it occurs as a result of bilateral bundle branch block, usually after myocardial infarction or with idiopathic conducting system disease; secondly, as a complication of metabolic disorder (e.g. hyperkalaemia) or drug therapy. In both these circumstances it is usually intermittent at first, and ECM should be used as
760
D. A . Chamberlain and J. H . Williams
necessary until pacing and definitive therapy for any underlying disease can be established, Occasionally light mechanical stimuli will ‘trigger’ QRS complexes. An effective rhythm may then result from light taps over the sternum delivered at a rate of about one per second. An intravenous infusion of isoprenaline 1-4 pglminute may help to maintain spontaneous rhythm (larger doses of isoprenaline or adrenaline may be used initially during the phase of asystole) but in general drugs should be used sparingly and with caution, to avoid the dangers of cardiac depression or recurrent arrhythmias. However, 10 ml of 10% calcium chloride intravenously with large doses of intravenous adrenaline or isoprenaline may be used if a brief period of ECM is not followed by spontaneous beats. Intracardiac injections should be given only as a last resort. Supraventricular and ventricular tachycardias
The precise nature of a rhythm rapid enough to require emergency treatment will usually be difficult to determine; even supraventricular tachycardia (SVT) is likely to show wide QRS complexes under these circumstances. Fortunately some general guidelines for treatment are applicable for both types of tachycardia arising in most circumstances. Treatment of tachycardias
(1) Try carotid massage if possible (unless vascular reflexes are blocked by anaesthesia, etc.). Caution : this may be dangerous in digitalis-induced arrhythmias. It is ineffective for ventricular tachycardias (VT), and so even transient response is of diagnostic value. (2) Give lignocaine 100 mg intravenously. It is usually ineffective but harmless in SVT. (3) Give practolol* 5 mg or propranolol 1 mg intravenously over several minutes. These doses may be repeated three or four times if necessary. Note. The tachycardia may revert 5-10 minutes after the completion of the injection of practolol or propranolol, so do not hasten to repeat doses or give further depressant drugs. Caution:p-adrenoreceptor antagonists are dangerous in the presence of serious myocardial dysfunction. (4) Zf digitalis-induced, try lignocaine 100 mg intravenously or phenytoin 50-200 mg intravenously as drugs of choice. Practolol is a third option if myocardial function is not severely impaired. DC shock is contra-indicated but may be used in lifethreatening situations (see below). (5) For refractory cases, or in any patient with severe haemodynamic disturbances, use DC shock. Caution: if the arrhythmia might be digitalis-induced, but a DC shock is still felt to be mandatory, start with 25 J and progress to 50, 100, 200, 300 and 400 J. The appearance of multiple ventricular extrasystoles after any shock is an indication for lignocaine cover. (6) Other drugs to consider for refractory cases: di-isopyramide 150 mg or bretylium tosylate 350 mg intravenously over 10-20 minutes :procainamide 100 mg intravenously every 5 minutes to a maximum of eight doses. But try to avoid excessive suppressant drugs, especially with a damaged myocardium. (7) SVT and VT which recur frequently despite optimal drug therapy may often be managed by pacing techniques.
* Still available in hospitals for intravenous use.
Immediate care of cardiac emergencies
761
(8) Atrial flutter is a special case. It responds poorly to drugs but well to DC shocks, usually at low energies, e.g. 50 J. Some cases respond only transiently: give digitalis to control the ventricular response though this may not always be successful. Flutter can also be controlled by pacing techniques.
A trial fibr illation This is an emergency in two situations: (A) if an uncontrolled ventricular response causes severe haemodynamic disturbances due to impaired myocardial function or valve lesion; (B) when it occurs prior to or during anaesthesia in a high-risk patient. Prophylaxis. Susceptible patients, if identified, should usually be digitalised before anaesthesia: digoxin 14-1-5 mg in divided doses over 24 hours, orally if possible, otherwise intravenously over several hours. Treatment of atrial fibrillation (1) Urgent drug therapy for established AF: digoxin 1.5 mg or for faster action ouabain 1.0 mg intravenously, preferably over a t least 2 hours but rapidly in lifethreatening situations. Note. Even after full intravenous doses rate may slow only over some hours. Persisting rapid rate may not, therefore, indicate under-digitalisation. Check that patient is not already digitalised ! (2) Always consider the use of a synchronised DC shock especially for rapid rates and when the patient’s haemodynamic state is unsatisfactory. Remember that a persisting rapid rate after myocardial infarction will cause extension of muscle necrosis. It is not harmful to start intravenous digitalisation before DC shock is given. Note. In very urgent situations unsynchronised shock is permissible if a synchronised machine is not available. The risk of inducing VF is small, and if it should occur it can be dealt with expeditiously.
Bradycardias and blocks
Detailed consideration of the differential diagnosis of sinus bradycardia, sino-atrial block, AV nodal block, and bilateral bundle branch block is outside the scope of this article. However, general methods for dealing with critically slow heart rates can be listed. Treatment of bradycardias and blocks (1) Intravenous atropine may be effective in all the bradyarrhythmias except those arising as a result of bilateral bundle branch block. Increased vagal tone may occasionally protect the ischaemic heart from predisposition to ventricular arrhythmias, so that atropine may have a deleterious effect by neutralising this protection. In other respects atropine is a very safe agent. The initial dose should be restricted to 0.3 mg after myocardial infarction to avoid the risk of undesirable tachycardias, which increase myocardial damage. (2) An isoprenaline infusion may speed all types of bradyarrhythmias. Dose rates are 1-4 pglminute. In life-threatening situations very much larger doses may be used
762
D. A . Chamberlain and J. H. Williams
initially. Always use the smallest effective dose because of the oxygen-wasting potential and arrhythmogenic action of catecholamines. (3) Patients with extreme bradycardia resulting from bilateral bundle branch block may not respond to any drugs. ECM should be used until pervenous pacing can be initiated. These extreme bradycardias are managed in the same way as asystole (see above). Acute left heart failure This dramatic emergency occurs either as a result of obstruction at the mitral or aortic valve, or because of impairment of left ventricular function. The event may be precipitated by a tachyarrhythmia (e.g. AF) in susceptible subjects.
Treatment (1) Correct any rhythm abnormality as quickly as possible.
(2) Intravenous morphine remains the drug of choice. It reduces venous return and therefore right ventricular output, also reducing the work of the left heart by lowering peripheral resistance. Its central actions relieve patients’ distress. (3) Diuretics (frusemide 40-80 mg intravenously) should always be given, especially because they reduce the risk of subsequent attacks. Digitalis and glucagon are of some value. Cuffs around the thighs inflated to just below diastolic blood pressure will further reduce venous return to the right heart. Cardiogenic shock The prognosis is very poor if cardiogenic shock persists after adequate treatment of pain, and correction of rhythm disturbances and pH. Very rarely after myocardial infarction, hypotension and critical reduction in cardiac output are associated with reduced filling pressure in the right and left heart rather than with failure; the patient’s condition will improve with volume expanders. Pulmonary artery pressure should be monitored under these circumstances for inappropriate infusion may cause pulmonary oedema. Little effective treatment is available for the common form of cardiogenic shock associated with high filling pressure. Intravenous catecholamines are not of proven value, but some authorities recommend salbutamol infusion at 10-50 pglminute. Only a few centres can utilise intra-aortic balloon pumping, and its late results are not impressive. Cyanotic attacks with congenital heart disease Some patients with right-to-left shunts may have periods of increased cyanosis induced by such factors as effort, emotion, blood loss, or anaesthesia. The intracardiac defect permits some desaturated blood to shunt away from the pulmonary artery (which will have restricted access because of a stenotic outflow tract or restricted egress due to a hypertensive pulmonary bed) and into the aorta. Constriction of a hypertrophied infundibulum by sympathetic tone or reduction in peripheral resistance for any reason will increase flow of desaturated blood into the aorta. A vicious circle can become
Immediate care of cardiac emergencies
763
established, because a marked decrease in systemic saturation may further reduce peripheral resistance. Cyanotic attacks of this type can be fatal, so that it is essential to avoid even the moderate hypotension often associated with routine induction of anaesthesia. Immediate first-aid treatment of cyanotic attacks calls for appropriate measures to increase systemic blood pressure, usually by the administration of a pressor agent of the methoxamine type. Cardiac tamponade Cardiac tamponade occurs most commonly as a result of rupture of the ventricular wall after myocardial infarction. Circulatory arrest in the presence of continued electrical activity of the heart implies an untreatable catastrophe. Tamponade should always be considered as a cause of unexplained deterioration after cardiac surgery and recent chest trauma (even wihout external evidence of chest injury) and, if confirmed, calls for urgent surgical exploration. Tamponade from other causes should be treated by aspiration. A long needle is inserted high in the angle between the xiphisternal cartilage and adjoining rib, and after penetration deep to the sternum, is guided as sharply upwards as possible to enter the pericardial sac anteriorly and near the mid-line. Summary The emergency treatment of serious disorders of cardiac rhythm, left heart failure, cardiogenic shock, and cyanotic attacks is discussed. The article is intended for medical practitioners without special cardiological experience.
