289
From: Contemporary Cardiology: Heart Disease Diagnosis and Therapy:
A Practical Approach, Second Edition
Edited by: M. Gabriel Khan © Humana Press Inc., Totowa, NJ
7 Cardiac Arrest
CONTENTS
DEFINITION AND CAUSES
CARDIOPULMONARY RESUSCITATION
MANAGEMENT OF VF
DRUG THERAPY OF CARDIAC ARREST
BRADYARRHYRHMIAS: ASYSTOLE OR EMD BIBLIOGRAPHY
DEFINITION AND CAUSES
Sudden cardiac death is defined as a sudden natural death caused by cardiac disease that is associated with the following:
• An abrupt loss of consciousness within 1 hour of onset of acute symptoms.
• Known or unknown pre-existing heart disease.
• Unexpected time and mode of death.
Hinkle and Thaler classified cardiac death as follows:
• Class I: An arrhythmic death if circulatory failure follows the disappearance of the pulse.
In these situations, the nature of the terminal illness is an acute cardiac event in more than 98% of victims, and ventricular fibrillation (VF) or asystole has been observed to be the terminal event in approximately 83% and 17% of patients, respectively.
• Each day in the United States, approximately 1000 sudden deaths occur, and it is esti- mated that about 30% result from asystolic cardiac arrest.
• Class II: Circulatory failure death if the disappearance of the pulse is preceded by circu- latory failure. This scenario is common in patients with terminal illnesses and usually is associated with a terminal bradyarrhythmia; asystole and VF have been observed in 67 and 33% of these patients, respectively.
Cardiac arrest is defined as the abrupt cessation of cardiac pump function that results in death, which may be averted if prompt intervention is instituted. A number of cardiac disorders cause lethal tachyarrhythmias or failure of formation or transmission of the cardiac impulse that results in cardiac arrest, but the mechanisms that initiate these fatal arrhythmias are mostly unknown and are diverse.
• VF or pulseless ventricular tachycardia (VT): in at least 80%; VF is defined as a pulseless, chaotic, disorganized rhythm with an undulating irregular pattern that varies in size and shape and a ventricular waveform greater than 150 minutes.
• Asystole: 10%.
• Electromechanical dissociation (EMD): 5%.
• Myocardial rupture, cardiac tamponade, acute disruption of a major blood vessel, and acute mechanical obstruction to blood flow that includes the pulmonary embolism.
The American College of Cardiology/American Heart Association (AHA) advise that there are only two cardiac arrest rhythms:
• VF/pulseless VT.
• Non-VF/VT: asystole and pulseless electrical activity (PEA).
Always assume VF or pulseless VT because patients who can be saved from cardiac arrest usually have these cardiac arrest rhythms. The single most effective intervention that can save victims of sudden cardiac arrest is the earliest delivery of defibrillation and widespread distribution of automatic external defibrillators will assist to accomplish early defibrillation programs.
Approximately 75% of all cases of cardiac arrest involve an unstable atheromatous plaque with overlying thrombus, causing occlusion or distal embolization of a major coronary artery. Cardiac arrest in coronary disease may occur with little or no warning (plaque emboli), during the acute phase of myocardial infarction (occlusion) or, later, caused by an arrhythmia circuit that may respond to trigger factors (catecholamines, ischemia, hypokalemia, critically timed ventricular premature beats) to precipitate VF.
A history of ischemic heart disease (IHD) is present in up to 50% of patients; in a significant number of these patients, atheromatous coronary disease is silent until the time of the event.
Most sudden cardiac deaths are the result of coronary atherosclerosis. In these individu- als, VF usually occurs either because of a new acute ischemic event or because of myo- cardial scarring and/or hypertrophy, which predisposes the myocardium to re-entrant tachycardia that triggers VF. In a study by Davies, of 168 consecutive cases of sudden coronary death within 6 hours of symptoms, the proportion of deaths owing to IHD at time intervals of less than 1 hour and less than 6 hours did not differ. In this study, 73.3%
showed thrombosis on an unstable plaque (Fig. 7.1.). No acute change in the coronary artery was observed in 19%. Adopting this principle, it is determined that cardiac sudden death is associated with no acute coronary lesion in approximately 20% of individuals who succumb to unexpected cardiac arrest.
Other underlying diseases or disturbances that may result in cardiac arrest include:
• Aortic stenosis.
• Hypertrophic cardiomyopathy.
• Dilated cardiomyopathy.
• Complete heart block or sinoatrial disease.
• Wolff-Parkingson-White syndrome in patients with very short refractory period of the bypass tract.
• Torsades de pointes in patients taking antiarrhythmic drugs or in those with prolonged QT syndromes (congenital or acquired).
• Structural abnormalities, such as pulmonary embolism or aortic dissection.
Rarely, a sudden cardiac death resulting from electrical dysfunction occurs without discernible cardiac pathology (primary electrical disease). Current information strongly indicates that coronary artery spasm, latent pre-excitation, and prolonged QT syndromes do not play a role in patients with idiopathic VF. Physical and mental stress appears to be implicated in fewer than 33% of cases of idiopathic VF.
Pathogenesis of the syndrome of sudden death during sleep in young apparently healthy southeast Asian males is undetermined and appears to be unrelated to idiopathic VF in
“normal” hearts. Wellens et al. suggest that because of the rarity of sudden arrhythmic death and the unexplained mechanisms in the absence of heart disease, a worldwide registry of these patients should be maintained.
Fig. 7.1. The ABCs of cardiopulmonary resuscitation. (A) The airway is opened using the heat tilt/
chin lift technique. (B) Breathing: the victim’s nostrils are pinched closed and the rescuer breathes twice into the victim’s mouth. (C) Circulation: if no pulse is present, external chest compression is instituted at 90–100/minute. Two rescuers: five compressions to one ventilation. One or two rescuers: 15 compressions to 2 ventilations. Modified from Khan M. Gabriel. Cardiac Drug Therapy. Sixth Edition. London: WB Saunders, 2003, with permission from Elsevier.
to the patient via emergency vehicles was devised and put into practice by Pantridge and Geddes in Belfast as long ago as 1966 (and was quickly accepted in the US), the concept has only gradually gained acceptance in a number of countries. The AHA state-of-the- art review, Improving Survival from Cardiac Arrest: The Chain of Survival Concept is a timely one:
• Early access.
• Early cardiopulmonary resuscitation (CPR).
• Early defibrillation.
• Early advanced care.
Because prompt defibrillation is the single-most effective lifesaving intervention for most victims of cardiac arrest, the Advanced Cardiac Life Support Subcommittee and the Emergency Cardiac Care Committee of the AHA have approved the widespread distri- bution of automated external defibrillators, which are now required items in all ambu- lances or emergency vehicles engaged in the transit of cardiac patients. It is a logical approach to have these lifesaving devices in housing complexes, stadiums, and at all large public gatherings, shopping centers, and so on. The AHA has endorsed the position that all first-responding hospital and nonhospital personnel (e.g., doctors, nurses, medical technicians, paramedics, firefighters, volunteer emergency personnel, and several other categories in the population) be trained in the use of and be permitted to operate a defibrillator. Zipes indicates that the time to defibrillation and/or pacing may be short- ened by developing external devices that incorporate the automatic approaches to ar- rhythmia recognition and therapy available in the multiprogrammable, implantable pacemaker-cardioverter-defibrillator. These devices should become as accessible as fire extinguishers. A similar call for the widespread distribution of defibrillators was made by Dr. Pantridge and the late Dr. Grace in the early 1970s.
CARDIOPULMONARY RESUSCITATION
Unless immediate defibrillation is possible (e.g., in the cardiac care unit), early CPR is essential. Late CPR and/or late advance support must be avoided. Although in Seattle up to 20% of prehospital VF patients survive, in other areas of the United States, fewer than 10% of all cardiac arrest patients in or out of the hospital survive and, unfortunately, up to 50% of these patients have been observed to have a neurological deficit. Thus, unless the arrest is witnessed and CPR can be instituted within 4 minutes or with a defibrillator available within 8 minutes, caution is necessary. In the elderly or in patients with noncardiac underlying disease, such as stroke, terminal renal failure, cancer, or other chronic disease, the final arrhythmia is not unexpected and does not constitute true cardiac arrest. When appropriate in these situations, families and patients should be aware of the possibilities in advance.
CPR Technique
Basic life support (BLS) algorithm directs the rescuers to start the 6 basic steps of the international BLS algorithm:
1. Check responsiveness. Rapidly establish that the patient is unconscious and unresponsive.
2. Open the airway. Use the head tilt/chin lift maneuver to open the airway (seeFig. 7.1.).
3. Determine breathlessness. Promptly verify that the patient is not breathing; take a deep breath, seal your lips around the mouth.
4. Give two full breaths, 1–1.5 seconds/breath, and allow the chest to deflate fully between each breath.
5. Assess circulation. Determine that the pulses are absent in the large arteries.
6. Start chest compression if no circulation detected:
• One or two rescuers: 15 compressions to two ventilations.
• The compression rate should be about 90 to 100/minute.
• At the end of compressions two full breaths are given.
• When the airway is secured with a cuffed endotracheal tube, use five compressions to one ventilation.
MANAGEMENT OF VF
Immediate defibrillation within 2–4 minutes of witnessed cardiac arrest is the most important single therapy that may rescue patients in cardiac arrest, without producing tragic iatrogenic brain damage from attempting full CPR and the unavoidable hesitations that occur in many settings of cardiac arrest:
• Turn the monitor power on.
• Apply conductive medium to defibrillator paddles and evaluate rhythm with the “quick look” paddles.
• If VF is present, turn defibrillator power on. Be certain that the defibrillator is not in synchronous mode.
• Select energy and charge the defibrillator.
• Defibrillate using 200 J (Table 7.1.). While recharging of the defibrillator or administra- tion of intravenous (IV) bolus drugs, CPR must be continued. Immediate de-fibrillation for the patient with VF is the key to success; intubation, establishment of IV lines, and administration of medications should commence only if the first series of direct current shocks fails to restore a spontaneous circulation.
If a defibrillator is immediately available and defibrillation is achieved within 4 min- utes of a cardiac arrest, long-term survival rates of 20–30% are possible. However, without prompt defibrillation, the survival rate ranges from 1 to 5% and is not acceptable.
Eisenberg and Mengert have listed common errors that occur during CPR:
• Defibrillation errors: synchronized mode accidentally selected before defibrillation is attempted, thus no shock is delivered.
• The operator believes that lead I, II, or III is being displayed when, in fact, the selection is set to paddles and asystole is falsely displayed.
• Considerable chest hair should be shaved off where the paddles are to be placed, and smeared gel across the chest should be toweled off.
Paramedic systems have been shown to achieve defibrillation in an average of 12 minutes, which is considered to be late defibrillation, resulting in about a 10% survival rate. Several countries and many communities in the United States have approved the use of semiautomated defibrillators by emergency medical technicians trained as first respond- ers, after completion of a 40-hour training program. It is feasible to train ambulance per- sonnel, firefighters, police officers, emergency volunteers, security guards, airline crews, designated attendants at stadiums, and so on.
The operation of semiautomatic devices does not demand complex learning skills in rhythm analysis, and operation of the device can be mastered within hours. A single control activates the defibrillator to quickly analyze the cardiac rhythm, indicates that a shock is required, and, on command, charges and delivers the shock.
In four communities in the United States, survival rates for patients in VF increased from an average of 4–18% with the use of emergency defibrillators by medical technicians.
DRUG THERAPY FOR CARDIAC ARREST Epinephrine
Epinephrine and other cardiac arrest drugs and their dosages are listed in Table 7.2.
Salutary effects of epinephrine are:
• Increased myocardial contractility.
• Elevated perfusion pressure.
• Possible conversion of EMD to electromechanical coupling.
• Improved chances for defibrillation.
• Improved blood flow to the heart and brain when sinus rhythm is restored.
Epinephrine is an α- and β-adrenergic agonist and is the drug of first choice, admin- istered as an initial 1-mg IV bolus after the third shock fails to defibrillate. Intracardiac epinephrine is not recommended, except when IV or intratracheal routes are not possible.
A high dose of epinephrine is necessary to maintain adequate diastolic blood pressure to produce adequate coronary and cerebral perfusion. The drug produces peripheral arteriolar constriction and an increase in systemic vascular resistance, thus increasing aortic and coronary diastolic perfusion pressure. Also, coronary artery dilatation occurs.
Management of VF or Pulseless VT
Apply quick look paddles or press analyzea: VF confirmed switch to DF
Nonsynchronized Immediate
1st shock 200 J Check pulse, rhythm VF: CPR; recharge DF
2nd shock 300 J VF persists: recharge DF
3rd shock 360 J CPR
1 mg epinephrine IV bolus Repeat every 3–5 minutes
40 U vasopressin IV, single dose, 1 time only IV line, intubate
4th shock 360 J VF: CPR, for 1 minute (allow drug action) 100 mg lidocaine IV
5th shock 360 J VF
1 mg epinephrineb IV VF persists, assess pH
6th shock 360 J VF: CPR
50 mg lidocaine IV allow 2 min 7th shock 360 J VF: arrest > 10 min pH < 7.1
50 mEq NaHCO3 IV bolus
8th shock 360 J VF: CPR
aSemiautomated external defibrillator.
bRepeat every 5 minutes.
Table 7.2. Cardiac Arrest Drugs DrugDosageSuppliedComment Epinephrine1 mg IV bolus10 mL (1 mg in 1:10,000 dilution)Do not give with NaHCO3 in same IV repeated q 3–5 min 10 mL tracheobronchial (1:10,000) Sodium bicarbonate1 mEq IV bolus (mmol)/kg,50 mL of 8.4% = 50.0 mEq (mmol)Used for hyperkalemic arrest usually 50 mEq (mmol) initially;Recommended for trial after 7th shock, 1 amp = 44 mEq then 0.5 initialpH < 7.1, or 10 min in asystole dose q 10–15 min Atropine1 mg In asystole q10 mL = 1 mg 2-5 min (max of 3 mg)5 mL = 0.5 mg 0.5 mg bradycardia(UK, 1-mL amp = 0.6 mg or 1 mg) q 5 min–2 mg Lidocaine75–100 mg IV bolus50 mg in 5 mL (l%) (lignocaine)simultaneous infusion100 mg in 10 mL (1%) 2–3 mg/min 100 mg in 5 mL (2%) Propranolol for VFUSA: 1 mg overUseful in recurrent VF if lidocaine 2–5 min (q 2–5 min to max 5 mg)fails; also for VF following electrocution UK: 1 mg over 2 min (q 2 min to max 5 mg) Metoprolol5 mg IV over 5 min Calcium chloride2.5–5 mL 10%,10 mL 10%CaCl2Not recommended in cardiac arrest, (5–7 mg/kg 250–500 mg) IV bolusexcept with hyperkalemia or postverapamil Do not give with NaHCO3 Modified from Khan M. Gabriel. Cardiac drug therapy. Sixth Edition. London: WB Saunders, 2003, with permission from Elsevier.
• Fine VF is made coarse and more susceptible to removal by electrical counter-shock.
• VF that fails to respond to countershock may respond after epinephrine.
• Asystole and pulseless idioventricular rhythms.
• EMD.
Vasopressin
Vasopressin has recently been shown to be effective for both VF and asystole. Vaso- pressin is recommended by the ACC/AHA only for VF/pulseless VT. The recommended dosage of vasopressin is a single 40-U IV dose, one time only. There is no evidence to support the value of repeat vasopressin doses. If there is no response 5–10 minutes after a single dose of vasopressin, it is advisable to resume epinephrine.
The guidelines indicate that there is no evidence to support its use in asystole or pulseless electrical activity.
Most importantly, Wenzel et al. showed the success of vasopressin alone and vaso- pressin followed by epinephrine in refractory asystolic cardiac arrest; this represents a major breakthrough and guidelines will change. In this randomized study, out-of-hospital cardiac arrest patients were assigned to receive two injections of either vasopressin 40 IU or 1 mg of epinephrine followed by additional treatment epinephrine if needed. 589 patients received avasopressin; 597 received epinephrine. The effects of vasopressin were similar to those of epinephrine in the management of VF and PEA.
Vasopressin was however, superior, to epinephrine in patients with asystole. The authors concluded that vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest.
Lidocaine (Lignocaine)
Lidocaine is given, after a fourth shock fails to defibrillate, as a 100-mg IV bolus, followed, after about 1 minute of CPR, by a 360-J shock. If defibrillation is successful, give a 50-mg bolus of lidocaine and an infusion at 2–3 mg/minute immediately. The lower dose is used for the elderly or those with heart failure (seeFigs. 1.10. and 1.11.).
An additional bolus is given 10 minutes later to maintain therapeutic lidocaine levels.
Lidocaine is preferred to bretylium because trials have not shown bretylium to be superior and lidocaine does not produce severe hypotension, which is often seen with bretylium.
Sodium Bicarbonate
This agent is no longer recommended for routine use during cardiac arrest of brief duration except in patients with preexisting hyperkalemia. However, after about 10 minutes of CPR and if a seventh shock fails to result in defibrillation, an IV bolus of sodium bicarbonate (50 mEq) is advisable. The drug should not be used simultaneously with calcium chloride or epinephrine.
Calcium Chloride
Calcium chloride is no longer recommended. The drug may be useful if asystole is caused by verapamil or in the management of hyperkalemia causing arrest. The drug is, however, of no value in EMD.
DOSAGE
Give 2.5–5 mL 10% calcium chloride or (UK), calcium gluconate IV bolus; 10 mL of a 10% solution.
Amiodarone
The role of bretylium has dwindled appropriately with the availability of amiodarone, and manufacturing has been halted because of lack of supplies. Amiodarone is useful in the management of cardiac arrest. Amiodarone is superior to bretylium and is advisable if it is necessary to continue resuscitative measures (see Chapter 6 for discussion on amiodarone).
For VF/pulseless VT, give 300 mg IV push and for recurrence 150–500 mg bolus over 5–10 minutes, followed by 10 mg/kg/24 hours (0.5 mg/mL) continuous infusion; maxi- mum 2.2 g over 24 hours.
Magnesium Sulfate
One to 2 g IV in polymorphic VT (TdP) may expedite ventricular defibrillation and is advisable for suspected hypomagnesemia.
BRADYARRHYTHMIAS: ASYSTOLE OR EMD
Severe symptomatic bradycardia is usually treated with 0.5–0.6 mg atropine repeated every 2 minutes to a maximum of 2.4 mg. When atropine is used to treat asystole before pacing, a dose of 1 mg is given immediately, followed by an additional 1 mg after 2 minutes. In severe bradycardia or atrioventricular block without a QRS complex, atro- pine is worth a trial. No harm can ensue, as if VF is precipitated by atropine; defibrillation may produce a stable rhythm to allow coronary perfusion before pacing. Be aware that VF may masquerade as asystole. Thus, rotate the monitoring electrodes and check the monitor to ensure that VF is not present. Give epinephrine with the hope that fibrillation may ensue and then countershock.
Asystole in a heart that was beating forcefully minutes before the occurrence of asys- tole may complicate anterior infarction, and pacing may be lifesaving. Asystole in the atonic heart (agonal) and EMD are usually caused by irreversible myocardial damage and prognosis is very poor.
Management of EMD
• Commence CPR.
• IV line.
• Epinephrine (1-mg IV bolus).
• Intubate.
• Assess for cardiac rupture and tamponade.
Search for Extracardiac Causes of EMD
• Inadequate ventilation, including intubation of right main stem bronchus and tension pneumothorax.
• Poor perfusion: hypovolemia (jugular venous pressure [JVP] decreased), give fluid chal- lenge. If the JVP is markedly elevated, suspect cardiac tamponade or massive pulmonary embolism.
• Severe acidosis or hyperkalemia.
CPR should be continued with the hope that one of these factors may be correctable.
Mobitz Type 2 block and complete heart block must be managed with ventricular pacing.
If there is asystole or severe bradycardia unresponsive to atropine continue CPR, give 1 mg epinephrine IV or endotracheal. If there is no response, consider pacing. For severe hypotension with mild bradycardia, dopamine is advisable (see Infusion Pump Chart, Table 3.6.).
LA, Eliastam M, Kerber, RE, et al. Report of the American Heart Association Task Force on the future of cardiopulmonary resuscitation. Circulation 1992;85:2346.
Cummins RO, Ornato JP, Thies WH, et al. Improving survival from sudden cardiac arrest: the “Chain of Survival” concept. Circulation 1991;83:1832.
Davies MJ. Anatomic features in victims of sudden coronary death. Circulation 1992;85 (suppl l):l–19.
Dimarco JP. Management of sudden cardiac death survivors: role of surgical and catheter ablation. Circu- lation 1992;5(Suppl I):1–125.
Echt DS, Cato EL, Coxe DR. pH-Dependent effects of lidocaine on defibrillation energy requirements in dogs. Circulation 1989;80:1003.
Forgoros RN, Elson JJ, Bonnet CA. Long-term outcome of survivors of cardiac arrest whose therapy is guided by electrophysiologic testing. J Am Coll Cardiol 1992;19:780.
Gray WA, Capone RJ, Most AS. Unsuccessful emergency medical resuscitation—are continued efforts in the emergency department justified? N Eng J Med 1991;325:1393.
Hinkle LE, Thaler JH. Clinical classification of cardiac deaths. Circulation 1982;65:457.
Hurwitz JL, Josephson ME. Sudden cardiac death in patients with chronic coronary heart disease. Circulation 1992;85(Suppl I):1-143.
Kerber RE. Statement on early defibrillation. From The Emergency Cardiac Care Committee, American Heart Association. Circulation 1991;83:2233.
Lars W, Kramer-Johansen J, Myklebust H, et al. Quality of cardiopulmonary resuscitation during out-of- hospital cardiac arrest. JAMA 2005;293:299–304.
Lazzam C, McCans JL. Predictors of survival of in-hospital cardiac arrest. Can J Cardiol 1991;7:113.
Pantridge JF, Geddes JS. Cardiac arrest after myocardial infarction. Lancet 1966;1:807.
Pantridge JF, Geddes JS. A mobile intensive-care unit in the management of myocardial infarction. Lancet 1967;2:271.
The Public Access Defibrillation Trial Investigators. Public-access defibrillation and survival after out-of- hospital cardiac arrest. N Engl J Med 2004;351:637–646.
Ruskin JN. Role of invasive electrophysiological testing in the evaluation and treatment of patients at high risk for sudden cardiac death. Circulation 1992;85(Suppl I):1–152.
Sanders AB, Ewy GA. Cardiopulmonary resuscitation in the real world: when will the guidelines get the message? JAMA 2005;293:363–365.
Schwartz PJ, La Rovere MT, Vanoli E. Autonomic nervous system and sudden cardiac death. Experimental basis and clinical observations for post-myocardial infarction risk stratification. Circulation 1992;85(Suppl I):1–77.
Siscovick DS, Raghunathan TE, Psaty BM, et al. Diuretic therapy for hypertension and the risk of primary cardiac arrest. N Engl J Med 1994;330:1852.
Viskin S, Belhassen B. Idiopathic ventricular fibrillation. Am Heart J 1990;120:661.
Weaver WD. Resuscitation outside the hospital—what’s lacking? N Eng J Med 1991;325:1437.
Wellens HJJ, Lemery R, Smeets JL, et al. Sudden arrhythmic death without overt heart disease. Circulation 1991;85(Suppl I):1–92.
Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH. European Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation Study Group. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004;350:105–113.
Zipes DP. Sudden cardiac death. Future approaches. Circulation 1992;85(Suppl I):1–160.
