VOLUME 20 : NUMBER 2 : April 1997
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Improved understanding of the pathophysiology of cardiac arrest, together with a critical review of previously accepted treatment, has led to changes in management. However, conventional management algorithms tend to be complex and confusing. Rigid adherence to these can cause problems in the emergency situation.Advanced cardiac life support can be divided into `core' interventions required in almost all cases. These are `blind' defibrillation, endotracheal intubation, hyperventilation, intravenous fluid loading and giving (high dose) adrenaline. Further interventions depend on which of asystole, ventricular fibrillation or electromechanical dissociation is present.
Key words: resuscitation, defibrillation, emergencies, life support.
Aust Prescr 1997;20:41-5
The prognosis for cardiac arrest remains very poor. However, there is proven benefit for early DC (direct current) counter shock in ventricular fibrillation and for cardiopulmonary resuscitation by laypersons (`bystander CPR') if this is rapidly followed by advanced cardiac life support.
Treatment protocols for cardiac arrest, based on current concepts and research, are a guide to management (Fig.1). Doctors should be prepared to exercise their own clinical judgment.
Basic cardiac life support
Basic cardiac life support aims to restore a circulation of oxygenated blood before professional help arrives. It comprises the basic skills of cardiopulmonary resuscitation (CPR) and combines closed chest compression with artificial ventilation of the lungs.
1. Diagnose cardiac arrest by checking the patient's response to sound and touch, absent respirations and impalpable carotid or femoral pulses.
2. If the arrest is witnessed, consider giving one or two precordial thumps.
3. Assess and clear the airway with the patient on their side. Then position the patient on their back. To prevent obstruction of the upper airway by the tongue, lift the jaw forwards and tilt the head backwards.
4. Occlude the patient's nose and give two breaths into the mouth, or, in small children, into the mouth and nose together. Each breath should last about 1.5 seconds. Do not exhale too vigorously to avoid inflating the stomach. Observe the chest wall rising and falling with each expired air ventilation.
5. Perform external chest compressions:
i. Locate the middle of the sternum by finding the point half-way between the suprasternal notch and the xiphisternum. Compress the chest at or just below this position.
ii. Perform chest compressions at a rate of 80-100 per minute in adults and at least 100 per minute in children and babies.
iii. With each compression, depress the chest wall to a depth of approximately 4-5 cm in adults, 3-4 cm in children and 2-3 cm in babies.
6. The single resuscitator performs 15 chest compressions followed by two exhaled air ventilations. With two operators, cycles comprise 5 chest compressions followed by a pause, during which the lungs are inflated once. These sequences are continued until help arrives.
Simultaneous chest compression and ventilation is no longer advocated.
Devices such as resuscitation bags and masks and oropharyngeal airways may improve the efficiency, hygiene and aesthetics of CPR.
Advanced cardiac life support
Basic life support maintains viability for only a few minutes. For successful resuscitation, additional advanced cardiac life support is usually required and comprises electrical defibrillation, endotracheal intubation and intravenous drugs and fluids. The principles of management are similar in adults and children. Guidelines on paediatric advanced life support were published in 1996.1
Unless there is immediate return of spontaneous cardiac output, certain `core' interventions are necessary in all cardiac arrests. Additional interventions depend on the specific circumstances of each arrest.
The `core' interventions in the advanced management of all cardiac arrests are:
Early `blind' electrical defibrillation
Direct current (DC) cardioversion improves outcomes when cardiac arrest is due to ventricular fibrillation (VF). It should be performed as soon as the diagnosis of VF is confirmed. In cardiac arrest where the rhythm is in doubt, two or three DC shocks (200, 200 then 360 joules) should be tried `blind'. The interval between each shock should be less than one minute with a check of rhythm being made after each shock.
Endotracheal intubation and ventilation of the lungs
Although not mandatory, endotracheal intubation is the most efficient means of providing artificial ventilation and a cuffed tube may protect the airway from aspiration of gastric contents. It may also be used as a conduit for giving certain drugs, in particular, adrenaline and lignocaine.
In order to correct respiratory acidosis, the lungs should be moderately hyperventilated at a rate of 12-15 ventilations per minute.
An intravenous line should be established at the antecubital fossa (not at the hand or wrist) and 1000 mL of normal saline infused rapidly. Central venous cannulation is not mandatory, but may be required if other venous access cannot be gained. Volume loading is necessary to maintain an adequate venous return to the heart because, during cardiac arrest, there is pooling of blood in venous capacitance vessels and `third space' fluid losses from the vascular compartment. Colloid solutions such as polygeline (Haemaccel) are not usually required. Dextrose solutions are contraindicated as they do not adequately expand the circulation and glucose may be toxic to hypoxic brain cells.
In adults, current recommendations are for intravenous adrenaline 1 mg (10-15 microgram/kg) to be given immediately and repeated every 3-5 minutes. However, both the American Heart Association and the European Resuscitation Council recognise the theoretical advantages of adrenaline in higher doses (i.e. 100 microgram/kg) if the initial lower dose fails. In adults, this represents 5-10 mg every 5 minutes.
It does not matter whether 1:1000 or 1:10 000 strengths of adrenaline are used if it is injected into an intravenous fluid infusion. The currently available ampoules of either concentration contain 1 mg of adrenaline.
Rationale for high dose adrenaline
CPR produces only 10-15% of normal cardiac output and during cardiac arrest there is also loss of vasomotor tone and venous pooling of blood. As there is no hope of restoring a spontaneous cardiac output unless the myocardium itself is oxygenated, the highest priority in cardiac arrest is to maximise the available blood flow through the coronary arteries. The alpha adrenergic activity of high-dose adrenaline produces peripheral vasoconstriction and thereby redistributes the available circulatory output centrally, increases coronary artery perfusion pressure and promotes coronary blood flow. Adrenaline does not convert asystole to VF, nor does it `coarsen' so-called `fine' VF.
Note: Adrenaline should be withheld if VF becomes intractable despite treatment. It must also be ceased as soon as spontaneous cardiac output is achieved as adrenergically-induced vasoconstriction now represents a high after load which is detrimental to a sick heart. Fortunately, the half-life of adrenaline is very short and its residual effects quickly wear off.
Although high-dose adrenaline contributes to improved initial survival from cardiac arrest, there is as yet no evidence that increased numbers of cardiac arrest victims actually leave hospital or that hypoxic neurological damage is reduced.
Routes of drug administration
All drugs should be given via the intravenous line with normal saline running. There is no role for intracardiac administration. If there is delay in gaining intravenous access, some drugs, including adrenaline, lignocaine and atropine, may be administered via the endotracheal tube at twice the intravenous dose (however, this is empiric and the bioavailability of drugs given endotracheally is unknown). In young children, the intraosseous route can be used for both fluid and drug delivery and is comparable to intravenous administration.
Management of specific dysrhythmias
The core procedures are continued throughout the management of the arrest. According to circumstances, additional specific interventions are also utilised.
This is the commonest rhythm in cardiac arrest. VF can be triggered by acute ischaemia, electrolyte disturbance, hypothermia, hypoxia or electric shock. The ECG shows irregular electrical activity with no discrete P waves or QRS complexes.
DC counter shock in ventricular fibrillation
Defibrillation is the only acceptable first-line specific therapy in VF and is the cornerstone of treatment.
Current flow through the heart is optimised by correctly positioning the paddles and reducing transdermal electrical resistance. Usually one paddle is located at the cardiac apex and the other to the right of the upper sternum. However, the operator should visualise a mental picture of the passage of current flow through the heart and should modify the paddle positions accordingly. Firm pressure should be applied to the paddles which should be in good electrical contact with the skin using either conducting gel or special conducting pads. Shocks should initially be at 200 joules, but if the first two or three have been unsuccessful, all subsequent shocks should be at 360-400 joules. For children, use 3-4 joules per kilogram.
Defibrillation is not benign, but as it is the most important therapeutic modality in VF, it should be used repeatedly according to the doctor's judgement.
Drugs in ventricular fibrillation
Drugs are secondary to electrical defibrillation and have limited efficacy. All drugs should be given as boluses, with lignocaine being tried first. Other drugs may be considered subsequently. There should be cycles of at least a further 3 DC shocks and continued CPR for one minute (approximately 10 sequences of 5:1 compression-ventilation) before each new drug is given.
Lignocaine. There is little (if any) evidence that lignocaine terminates VF and theoretically it may adversely raise the threshold for successful electrical defibrillation. The major effective use for lignocaine is to suppress ectopic ventricular activity once spontaneous circulation has returned. The initial dose is 1.5 mg/kg followed by an infusion of 2-8 mg/minute.
Other antiarrhythmic agents. In refractory VF which is not responding, other antiarrhythmic drugs may be tried, usually amiodarone (5 mg/kg) or sotalol (1.5 mg/kg). Both these drugs have beta blocking and class III antiarrhythmic activity, but their efficacy in intractable VF remains speculative. Procainamide (class Ia) is occasionally tried (50 mg increments at 5 minute intervals up to 20 mg/kg).
Magnesium sulphate (5-20 mmol intravenously) may be useful in polymorphic ventricular tachycardia (torsades de pointes), especially when this is secondary to drug toxicity such as tricyclic antidepressants. It may be tried in VF, but there is no evidence of efficacy.
Potassium chloride (5-20 mmol intravenously) raises the threshold for membrane depolarisation. Many cardiac patients are chronically potassium-depleted due to diuretic therapy and this may predispose them to fibrillation. Potassium chloride probably has little effect in intractable VF.
Asystole or agonal bradycardia
Asystole carries a very grim prognosis. If the ECG shows a flat line, quickly check the connections and settings of the ECG monitor to exclude the possibility of instrument malfunction. It is worthwhile switching through the various leads on the monitor as a low amplitude VF in one lead may be misinterpreted as asystole.
Treatment of asystole is maintenance of CPR and repeated adrenaline. There are few specific therapies.
Atropine (1-2 mg) is often given, but probably has little or no effect in cardiac arrest. The dose is not repeated.
Transvenous cardiac pacing may be tried if a temporary pacing wire is immediately available. External transcutaneous pacing is ineffective in asystole.
Adenosine antagonism is a theoretical pharmacological approach. Myocardial accumulation of adenosine has been postulated as contributing to persistent asystole. Aminophylline (250 mg intravenous bolus) is an adenosine antagonist and has been reported to result in spontaneous cardiac output in some patients in asystole not responding to standard therapy. Such claims remain unproven.
Electro-mechanical dissociation (pulseless electrical activity)
Electro-mechanical dissociation is the presence of an electrical rhythm without mechanical cardiac output and may imply that there is little viable or functional myocardium. It may also be associated with profound hypovolaemia, drug toxicity, electrolyte imbalance or mechanical obstruction to cardiac output such as pulmonary embolism, cardiac tamponade or tension pneumothorax.
Along with ongoing CPR and repeated high-dose adrenaline, treatment is obviously directed at correcting any reversible underlying cause. Calcium is not used except in specific circumstances.
Other interventions in cardiac arrest
Bicarbonate is inappropriate in at least the first 20 minutes of cardiac arrest except in situations such as septicaemia where a profound metabolic acidosis may already exist. The acid-base disturbance during the early stages of cardiac arrest is respiratory in type due to a combination of ventilatory arrest and decreased pulmonary blood flow. Metabolic acidosis takes about 20 minutes to develop and may even be advantageous as myocardial high-energy phosphate stores are conserved in an acidotic environment.
The treatment of the respiratory acidosis of early cardiac arrest is CPR with hyperventilation. Giving bicarbonate theoretically makes the situation worse as it is buffered to carbonic acid which dissociates into carbon dioxide and water, increasing the already elevated PaCO2. Carbon dioxide freely enters cells and induces a paradoxical intracellular acidosis. If bicarbonate is subsequently given, a small dose should be used (0.5-1.0 mmol/kg).
Arterial blood gases
Arterial blood gas analysis provides no useful information during cardiac arrest. Blood sampled from a peripheral artery during circulatory stasis does not reflect the acid-base status of myocardial cells. Additionally, in the rapidly changing circumstances of cardiac arrest, the results when received no longer reflect the current situation.
Isoprenaline is absolutely contraindicated in all cardiac arrests irrespective of cause (other than torsades de pointes). Its unopposed beta adrenergic activity not only increases myocardial oxygen demand but also reduces peripheral vascular resistance, lowers coronary perfusion pressure and reduces coronary arterial blood flow. Isoprenaline may be used to accelerate a bradyarrhythmia, but only in the presence of a cardiac output.
Calcium gluconate and calcium chloride
Although calcium is essential physiologically for electro-mechanical coupling, it is erroneous to believe that pharmacological doses can promote myocardial activity in asystole or electro-mechanical dissociation. During cardiac arrest, hypoxic membrane dysfunction allows a net flux of calcium ions into cells, disrupting cellular architecture and accelerating cell death.
Calcium is only indicated in cardiac arrest in the presence of hypocalcaemia, calcium channel blocker toxicity or hyperkalaemia.
The decision to stop treatment
After 10 minutes without a spontaneous output, the chances of a patient surviving long term are very slim. Even in survivors, the probability of profound hypoxic neurological deficit is very high. Cardiac arrest with no return of spontaneous circulation for greater than 20 minutes is usually hopeless and, at this stage, withdrawal of treatment should be considered. Even if cardiac output is eventually restored, virtually none of these patients ever leave hospital. An exception to this general principle is made in the case of a profoundly hypothermic patient - especially in an immersion incident involving a child. In such cases, there have been reports of successful outcomes after protracted resuscitation lasting over an hour. Thus the aphorism: `never dead until warm and dead'. Some clinicians also claim that patients in cardiac arrest secondary to overdose with some drugs such as tricyclic antidepressants should undergo prolonged resuscitative attempts as the occasional successful outcome has been reported.
Cardiac arrest still has a very poor prognosis, although recent advances based on scientific rather than anecdotal principles have increased the possibility of at least short-term survival. The issues of long-term survival and quality of life are unresolved.
1. Advanced Life Support Committee of the Australian Resuscitation Council. Paediatric advanced life support. The Australian Resuscitation Council Guidelines. Med J Aust 1996;165:199-206.
Advanced Life Support Committee. Policy statement. Advanced cardiac life support. Melbourne: Australian Resuscitation Council, 1993.
American Heart Association, Emergency Cardiac Care Committee and Subcommittees. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Part III. Adult advanced cardiac life support. JAMA 1992;268:2199-241.
Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, et al. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multi center High-Dose Epinephrine Study Group. New Engl J Med 1992;327:1051-5.
Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J. A randomized clinical trial of high-dose epinephrine and norepinephrine vs. standard-dose epinephrine in prehospital cardiac arrest. JAMA
Lindner KH, Koster R. Vasopressor drugs during cardiopulmonary resuscitation. A statement for the Advanced Life Support Working Party of the European Resuscitation Council. Resuscitation 1992;24:147-53.
Paradis NA, Martin GB, Rivers EP, Goetting MG, Appleton TJ, Feingold M, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA 1990;263:1106-13.
Viskin S, Belhassen B, Roth A, Reicher M, Averbuch M, Sheps D, et al. Aminophylline for bradyasystolic cardiac arrest refractory to atropine and epinephrine. Ann Intern Med 1993;118:279-81.
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