Ventricular Fibrillation or Pulseless Ventricular Tachycardia

When VF or VT are diagnosed the patient should be defibrillated as quickly as possible using three shocks of 200J, 200J then 360J. Unless the rhythm changes on the ECG trace, there is no point in checking the pulse between shocks as this will delay the next defibrillation attempt. Palpation of a major artery is carried out if the ECG appearances are compatible with an output, or if purposeful movements are made. If these shocks are not successful, CPR should be resumed for one minute while the airway is secured and iv access is achieved. A dose of iv adrenaline (1mg) is injected and consideration is given to any specifically treatable causes of VF such as hypothermia and toxins. After another 10 cycles of CPR, the ECG trace is re-examined. Persistent VF is treated with a further three shocks of 360J as required. These take priority over any continuing attempts at securing the airway or establishing iv access. It is recommended that this sequence is followed for at least 9-12 shocks before consideration is given to the use of antiarrythmic drugs. Adrenaline should be administered every 2-3 minutes during resuscitation.

If there is no cardiac monitor but a defibrillator is available, it is better to treat the rhythm as VF, as this rhythm has the best prognosis.

Asystole or Pulseless Electrical Activity (PEA)

Asystole occurs when there is no detectable electrical activity in the heart and is associated with a very poor prognosis. Pulseless Electrical Activity (or Electro-Mechanical Dissociation - EMD) is present when the ECG shows a rhythm normally associated with an output but with no detectable central pulse. In either case, the defibrillation-based treatment loop is not appropriate.

In asystole or PEA treatment options are more limited. The right-hand loop of the algorithm is followed. The airway is secured and iv access obtained as soon as possible and CPR is continued with doses of adrenaline administered every three minutes. Atropine (3mg) is given once in asystole. The chance of surviving asystole or EMD is improved if a reversible cause can be identified which can be treated. The most likely ones are listed in the algorithm. Acute hypovolaemia is the most commonly treatable cause, and always results from extremely severe haemorrhage (>50% blood volume). These patients usually need immediate surgery to control haemorrhage and rapid fluid replacement. Any change of the ECG consistent with VF should prompt an immediate transfer to the other treatment loop.

Stopping Resuscitation

The decision to stop resuscitation attempts is usually made by the team treating the arrest. It is usually the responsibility of the most experienced doctor present and should involve the whole team. Patients in asystole or PEA, who have no underlying cause diagnosed, and who do not respond to BLS and adrenaline, have a very poor prognosis and in our experience resuscitation attempts are normally stopped after 10 - 15 minutes.

Treatment would normally be continued while the ECG trace indicates the presence of VF. However successful resuscitation becomes unlikely after 12 shocks, and rare after 15 - 20 minutes of attempted resuscitation. The highest survival rates occur in witnessed VF arrests, when BLS has been started immediately and defibrillation is very rapid. Outcome studies from VF carried out in hospitals in the developed world in the 1990's indicated an initial resuscitation success rate of up to 50% but a survival to discharge rate of up to only 20% in this population.

Patients who have severe underlying illnesses or terminal conditions usually have a cardiac arrest as a terminal event and resuscitation in these patients is usually unsuccessful, and often inappropriate. In many hospitals patients in this category may be designated "Not for Resuscitation" after discussion with the relatives and or the patient, and the medical and nursing teams caring for them. The legal position of such decisions, and the methods for making them varies from country to country.

Patients who suffer unwitnessed cardiac arrrests and have delayed BLS / defibrillation as a result have a dismal outlook and resuscitation attempts will be unsuccessful in most cases.

Managing Cardiac Arrests without a Defibrillator.

Clearly without the aid of a defibrillator, cardiac arrest management is more limited and the diagnosis and treatment of the likely underlying problem provides the best chance of survival. Basic life support should be initiated, adrenaline given and resuscitation attempted while any reversible factors (such as hypovolaemia) are diagnosed and treated.

Other Antiarrhythmic Therapy

Although the defibrillator remains the main technique, a number of antiarrhythmic drugs may prove useful. They may be used to treat a persistent, life-threatening arrhythmia, to lower the threshold for successful defibrillation or as prophylaxis against further rhythm disturbances.

Each agent has specific indications but most are negatively inotropic - clearly undesirable in resuscitation. Lignocaine, bretylium, amiodarone and magnesium are the most commonly used agents. There is a lack of human-based evidence for their effectiveness, reflecting the difficulty in performing meaningful clinical studies in resuscitation.

Lignocaine (lidocaine) has antiarrhythmic properties derived from sodium channel blockade, resulting in membrane stabilisation. The pacemaker action of the SA node is suppressed and conduction within the ventricular muscle is inhibited. There is little effect on the atrio-ventricular (AV) node and its myocardial depressant and pro-arrhythmic effects are minimal.

Lignocaine is established for the treatment of ventricular tachycardia. The ability of lignocaine to improve the chances of successful defibrillation of persistent VF is less certain, but it is often tried when repeated unsuccessful attempts at defibrillation have been made. Lignocaine is also used to treat haemodynamically stable VT.

The dose of lignocaine for refractory ventricular fibrillation is 100mg iv and for haemodynamically stable ventricular tachycardia is 1mg/kg iv - repeated once if necessary - and followed by an intravenous infusion of 4mg/min for 30 minutes, 2 mg/min for 2 hours and then 1mg/minute.

Amiodarone produces potassium channel blockade with some inhibition of sodium channel mediated depolarisation, a lengthening of the myocardial action potential and a degree of ß-blockade. This gives it gives it an antifibrillatory action and lowers the defibrillation threshold with a minimal effect on myocardial contractility.

Its routine use during cardiac arrest is yet to be proven and it is generally reserved for the second-line treatment of peri-arrest tachyarrhythmias. Amiodarone is preferably administered centrally and slowly. Usually a 300mg loading dose is given over one hour followed by an infusion of 900mg in 1000ml of 5% glucose over the following 24hrs. In more urgent situations, the first 300mg dose can be given peripherally over 5-15 minutes and followed by a further 300mg over one hour.

Bretylium tosylate stabilises the action potential duration throughout the myocardium. This increases the resistance to VF and lowers the defibrillation threshold. However it is slow to act (15-20minutes) and there is a tendency for it to produce pulseless electrical activity and greater post-arrest hypotension that expected.

Magnesium is a critical factor in myocardial cell stability. A decreased intracellular level promotes myocardial excitability but, even in the absence of a low magnesium level, a bolus of iv magnesium will suppress ventricular ectopic beats. The use of magnesium in cardiac arrest is unproven, but it may be useful when hypokalaemia may have contributed to the arrest and a dose of 10mls of 50% magnesium sulphate may be given if this is the case.

Calcium has a specific indication as emergency protection against the effects of hyperkalaemia or the unusual condition of calcium channel blocker (eg verapamil) overdose. Despite its crucial role in the myocardial action potential and contraction, its administration for any other reason appears to be ineffective, or even detrimental, as high intracellular calcium concentration are damaging to injured myocardial and neuronal cells. However, if the serum potassium level is above 6mmol/L, 10ml of 10% calcium chloride should be given.

Although the individual drugs are chosen largely for their lack of effect on myocardial contractility, administration of several antiarrhythmic agents will result in a cumulative, deleterious effect even if a perfusing rhythm is restored.

If resuscitation is successful, arrythmias remain a likely sequel. The management of subsequent brady-arrythmias and narrow or broad complex tachycardias are beyond the scope of this article.

Cardiac Arrests in Special Circumstances

There are a few circumstances in which the ALS principles need adapting.

Drowning and near-drowning Victims of immersion who are in cardiac arrest on arrival in hospital are a difficult and controversial group to treat. Occasional reports of apparently miraculous recovery after prolonged immersion and resuscitation have been made, particularly in children. These cases have involved rapid, profound cooling in very cold water. Children transferred rapidly to hospital who have suffered a short duration of immersion in cold water should have rectal core temperature measurement and ECG monitoring established immediately. Often asystole is present but occasionally the ECG will show slow sinus rhythm when the patient appears to be dead. If it is thought worth attempting resuscitation:

• Resuscitation should follow standard principles with BLS.
• Early intubation and ventilation with 100% oxygen should be a priority and prolonged BLS may be needed while attempts are made to rewarm the victim to 31⁰C as attempts to defibrillate the hypothermic heart below this temperature are unlikely to be successful.
• Although rewarming the patient can be extremely difficult and sometimes impossible without facilities for cardio-pulmonary bypass, resuscitation should not normally cease until the core temperature has reached 31⁰C or attempts to achieve this have failed.
• Surface warming, heated inspired gases, warm iv fluids and intra-gastric balloons are of limited value, but must be tried. Warmed peritoneal dialysis has been recommended.

The prognosis for victims of drowning discovered in cardiac arrest is very poor. Most will die or be significantly brain damaged. With few signs to indicate the speed of cooling, triage can be difficult. Hyperkalaemia is caused by the pre-hypothermic phase of the cardiac arrest and serum potassium of >10mmol/L measured during resuscitation is incompatible with survival.

Electrocution

The effects of electrocution depend on the conversion of electrical energy into heat energy. The degree of damage depends on:

• Energy delivered
• Tissue resistance to current flow
• Type of current. Alternating current (AC) is more dangerous. It is more likely to reach central tissues and the resulting tetanic muscle contractions prevent the victim from releasing the electrical source.
• Current pathway through the body.

Asystolic arrests are more likely with currents greater than 10 Amps but VT and VF are also common. Rescuers must take great care to avoid receiving an electric shock.

Drug overdose

Deliberate overdose or poisoning should always be considered in an unconscious patient. Cardiac arrhythmias or haemodynamic effects are particularly associated with certain drugs and may require specific treatment or prolonged resuscitation. Cardiac arrhythmias following a tricyclic overdose may respond to an infusion of sodium bicarbonate to maintain the pH within the high normal range and also potassium to keep the serum potassium >4.0mmol. Bupivacaine is able to bind to the myocardium and following a cardiac arrest due to toxicity from this drug, resuscitation should be prolonged (1 hour).

Cardiac Arrests during Anaesthesia

The management of intra-operative cardiac arrests differs from the standard guidelines in that the event is normally witnessed and some form of airway maintenance and intravenous access has already been established. A primary cardiac event may be the cause, but treatment is often needed for an underlying problem such as vagal stimulation, blood loss, hypoxia, bronchospasm, myocardial depression, hypokalaemia, hyperkalaemia etc. The most common cause of cardiac arrests during anaesthesia are hypoxia, vagal stimulation or hypovolaemia. Most can be prevented by careful anaesthesia and close clinical monitoring. Specific treatment should be towards the underlying cause as well as initiating resuscitation procedures. 

(Continued ...)

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