Adult Cardiac Arrest

Cessation of effective mechanical cardiac activity with absent circulation, confirmed by unresponsiveness, absent or abnormal breathing and no palpable central pulse. Survival is determined less by drugs than by the quality and continuity of chest compressions and by the interval to defibrillation of a shockable rhythm.

Rhythm categories, which determine everything that follows

Shockable:

• Ventricular fibrillation: chaotic disorganised electrical activity with no coordinated contraction. Usually ischaemic in origin.

• Pulseless ventricular tachycardia: organised broad complex tachycardia without a pulse.

These carry the best prognosis, with survival to discharge of 20 to 40 percent in witnessed arrests with early defibrillation. Survival falls by approximately 7 to 10 percent for every minute defibrillation is delayed, which is why the defibrillator is retrieved at the same moment the team is called rather than afterwards.

Non shockable:

• Pulseless electrical activity: organised electrical activity on the monitor without a palpable pulse. It is a diagnosis that demands a search for a cause rather than a rhythm to be treated in itself.

• Asystole: absent electrical activity. Confirm it is not fine ventricular fibrillation or a disconnected lead by checking gain, leads and connections.

Non shockable rhythms carry survival under 10 percent, and their outcome depends almost entirely on identifying and reversing a cause.

Physiology of chest compressions

Compressions generate a cardiac output of roughly 25 to 33 percent of normal at best. Coronary perfusion pressure, which is the aortic diastolic minus the right atrial diastolic pressure, is the principal determinant of return of spontaneous circulation, and a value above approximately 15 mmHg is required.

This pressure builds progressively over the first several compressions of a cycle and collapses immediately when compressions stop. Every pause therefore costs disproportionately more than its duration suggests, which is the physiological basis for the rule that interruptions must be under 10 seconds.

Excessive ventilation raises intrathoracic pressure, reduces venous return, reduces coronary perfusion and worsens survival. Overventilation is the commonest error made by inexperienced teams and is more harmful than underventilation.

• Unresponsive to voice and to painful stimulus.
• Absent or abnormal breathing. Agonal gasping occurs in up to 40 percent of arrests in the first minutes and is frequently misinterpreted as breathing, which delays the start of compressions. Occasional slow irregular noisy gasps are a sign of arrest, not of life.
• No definite central pulse palpable within 10 seconds. Pulse checking is unreliable even among trained clinicians, and if there is any doubt, start compressions.
• Generalised seizure like movements occur at the onset of arrest from cerebral hypoperfusion and are commonly mistaken for epilepsy, which delays recognition.
• Cyanosis, dilated pupils and pallor are late and unhelpful.

Reversible causes, sought in every arrest and revisited at every rhythm check

• Hypoxia.
• Hypovolaemia, from haemorrhage, sepsis or dehydration.
• Hydrogen ion excess, that is acidosis.
• Hypokalaemia and hyperkalaemia, and hypoglycaemia.
• Hypothermia.
• Tension pneumothorax.
• Tamponade.
• Toxins.
• Thrombosis, pulmonary.
• Thrombosis, coronary.

Hypoglycaemia is explicitly included because it is rapidly identified with a bedside test and rapidly corrected, and it is regularly not checked during arrest.

• The diagnosis is clinical and is made in under 10 seconds. Do not delay compressions for a monitor, a blood pressure or an examination.
• Attach defibrillator pads or paddles as soon as they arrive and determine the rhythm at the next compression pause.
• Attach monitoring leads once compressions are established and set the monitor to lead II.
• Take blood at the time of establishing access for venous blood gas and capillary blood glucose, which together identify hypoxia, acidosis, potassium derangement and hypoglycaemia within minutes.
• Waveform capnography once an advanced airway is in place: it confirms tracheal placement, provides continuous confirmation that the tube has not displaced, gives real time feedback on compression quality with values below 10 mmHg indicating inadequate compressions, and a sudden sustained rise above 35 to 40 mmHg is the earliest indicator of return of spontaneous circulation, appearing before a pulse is palpable. Persistently low end tidal carbon dioxide below 10 mmHg after 20 minutes of high quality resuscitation is a poor prognostic sign, though it must never be the sole basis for stopping.
• Point of care ultrasound during the rhythm check, performed by a designated operator with a subxiphoid or subcostal view acquired in under 10 seconds, identifies tamponade, right ventricular strain suggesting pulmonary embolism, hypovolaemia and cardiac standstill. It must not extend the compression pause.
• Twelve lead electrocardiogram after return of spontaneous circulation.

Recognition and activation

• Confirm unresponsiveness, absent or abnormal breathing and no definite pulse within 10 seconds.
• Activate the resuscitation team and send for the defibrillator simultaneously.
• Where a definite pulse is present with inadequate breathing, open and maintain the airway, give one breath every 6 seconds, recheck the pulse every 2 minutes, and move to post arrest care.

High quality cardiopulmonary resuscitation

This is the intervention that determines survival and it is done badly far more often than it is done well.

• Compress the centre of the chest with two hands, heel of one hand on the lower half of the sternum.
• Rate of 100 to 120 compressions per minute. Faster is not better, since inadequate filling occurs above 120.
• Depth of at least 5 cm and not more than 6 cm in an adult.
• Allow complete chest recoil after each compression. Leaning on the chest between compressions prevents venous return and is a common fault, particularly as rescuers fatigue.
• Minimise interruptions to under 10 seconds. Charge the defibrillator while compressions continue and pause only for the shock delivery itself.
• Change the compressor every 2 minutes, at each rhythm check, since quality deteriorates measurably after 2 minutes even when the rescuer does not feel tired.
• Compression to ventilation ratio of 30 to 2 until an advanced airway is placed. Perform continuous compressions without pausing for ventilation once an advanced airway is in, giving 1 breath every 6 seconds, that is 10 per minute.
• Give just enough volume to produce visible chest rise, and no more.
• Use a bag valve mask with a reservoir at 15 litres per minute of oxygen as soon as available, and give breaths with a bag even before oxygen is connected rather than delaying ventilation.
• Perform continuous compressions until a bag valve mask is available.

Shockable rhythm pathway

• Deliver a shock immediately: 200 J biphasic, or as recommended by the manufacturer, and 360 J monophasic. Use the maximum available energy for all subsequent shocks.
• Resume compressions immediately after the shock without pausing to check a rhythm or pulse, and continue for 2 minutes.
• Establish intravenous or intraosseous access. Intraosseous access in the proximal tibia or proximal humerus is fast, reliable and should be used without hesitation where peripheral access is difficult. Take blood for venous gas and glucose.
• Attach monitor leads.
• At 2 minutes, check the rhythm. If still shockable, shock at maximum energy, resume compressions immediately, and give adrenaline 1 mg intravenously or intraosseously, prepared as 1 mg in 9 mL of normal saline to give 1 mg in 10 mL, followed by a 20 mL saline flush and elevation of the limb. Repeat every 3 to 5 minutes, which corresponds to every second cycle.
• Continue to identify and treat reversible causes.
• At the next rhythm check, if still shockable, shock at maximum energy, resume compressions, and give amiodarone 300 mg intravenously or intraosseously as a bolus with a 20 mL saline flush. A second dose of 150 mg is given after two further cycles if ventricular fibrillation persists.
• Lidocaine 1 to 1.5 mg/kg, then 0.5 to 0.75 mg/kg, is an acceptable alternative where amiodarone is unavailable.
• Consider an advanced airway and capnography.
• Continue the cycle of shock, 2 minutes of compressions, rhythm check, with adrenaline every second cycle.

Non shockable rhythm pathway

• Resume compressions immediately for 2 minutes.
• Establish intravenous or intraosseous access and take blood for venous gas and glucose.
• Give adrenaline 1 mg intravenously or intraosseously as soon as access is available, and repeat every 3 to 5 minutes. In non shockable arrest, adrenaline is given as early as possible, since earlier administration is associated with improved outcome, unlike in shockable arrest where the priority is defibrillation.
• Attach monitor leads.
• Identify and treat reversible causes, which is the entire substance of managing pulseless electrical activity.
• Consider an advanced airway and capnography.
• Recheck the rhythm every 2 minutes and move to the shockable pathway if the rhythm converts.

Specific treatment of reversible causes

• Hypoxia: secure the airway, ventilate with 100 percent oxygen, confirm tube position, exclude obstruction.
• Hypovolaemia: rapid volume with crystalloid, blood for haemorrhage, and control of bleeding. In traumatic arrest the priority is haemorrhage control, bilateral thoracostomies and blood rather than adrenaline and compressions.
• Acidosis: adequate ventilation. Sodium bicarbonate 50 mmol is reserved for hyperkalaemia, tricyclic antidepressant overdose and pre existing severe metabolic acidosis, and is not given routinely.
• Hypokalaemia: potassium 5 mmol intravenously with magnesium sulphate 2 g.
• Hyperkalaemia: calcium chloride 10 mL of 10 percent or calcium gluconate 30 mL of 10 percent intravenously to stabilise the myocardium, then insulin 10 units with 25 g of glucose, and sodium bicarbonate 50 mmol.
• Hypoglycaemia: 50 mL of 50 percent dextrose or equivalent.
• Hypothermia: active rewarming, and recognise that resuscitation should be prolonged, with defibrillation and drugs often withheld below a core temperature of 30 degrees Celsius. No patient is dead until warm and dead.
• Tension pneumothorax: immediate finger thoracostomy in the fifth intercostal space at the anterior axillary line, which is more reliable than needle decompression in arrest, followed by a chest drain.
• Tamponade: pericardiocentesis under ultrasound guidance, or resuscitative thoracotomy in penetrating trauma with signs of life within the preceding 10 to 15 minutes.
• Toxins: specific antidotes, including intravenous lipid emulsion for local anaesthetic toxicity, sodium bicarbonate for tricyclics, high dose insulin euglycaemia for calcium channel blocker overdose, and digoxin specific antibody fragments.
• Pulmonary thrombosis: thrombolysis with alteplase 50 mg intravenously, after which cardiopulmonary resuscitation should continue for 60 to 90 minutes before considering termination.
• Coronary thrombosis: coronary angiography and percutaneous intervention after return of spontaneous circulation, or during resuscitation in centres with the capability.

Airway during arrest

• A bag valve mask with a good seal and an oropharyngeal airway is adequate and is preferred to a difficult intubation attempt that interrupts compressions.
• A supraglottic airway is a reasonable first advanced airway and is placed without stopping compressions.
• Tracheal intubation should be performed only by an operator who can do it without interrupting compressions, and confirmed with waveform capnography.
• Do not hyperventilate.

Recognition of return of spontaneous circulation

A sudden sustained rise in end tidal carbon dioxide, a palpable pulse at the rhythm check, an arterial waveform where invasive monitoring is present, and purposeful movement. Confirm at the rhythm check rather than by interrupting compressions to look.

Termination of resuscitation

There is no single rule.

Consider stopping after a prolonged resuscitation with persistent asystole despite treatment of reversible causes, an unwitnessed arrest with no bystander resuscitation and no return of circulation, and persistently low end tidal carbon dioxide below 10 mmHg after 20 minutes.

Continue far longer in hypothermia, in poisoning, in pregnancy, in the young, in drowning and after thrombolysis for pulmonary embolism.

The decision is a team decision made by the team leader, and it should be verbalised with the opportunity for any member to raise a concern.

Team and human factors

Assign a leader who does not perform tasks, a compressor with a rotation, an airway operator, a drug and access operator, a monitor and timekeeper, and a scribe. Verbalise the plan, state the time to the next rhythm check aloud, and conduct a structured debrief afterwards. Team performance is a measurable determinant of survival and is trainable.

After the arrest

Care of the family, who should where possible be offered the opportunity to be present with a dedicated staff member to support them. Debrief the team. Document accurately with timings.