# Emergency medical responder (EMR)/Critical interventions/Asystole

Asystole, also commonly known as "flatline" is the absence of all activity in the myocardium, be it electrical or mechanical.
As soon as an absence of a rhythm has been confirmed, CPR and intubation can be started (if not already) to maintain perfusion. The use of epinephrine (adrenaline in the UK) and atropine, to stimulate the heart is the current standard of care, as specified by ACLS guidelines.
As in many forms of cardiac arrest, prognosis is decidedly poor. Asystole remains one of the most important signs in pronouncing death.
Possible reversible underlying causes, to be considered in treatment include the Hs and Ts.
* Hypovolemia
* Hypoxia
* Hydrogen ions (Acidosis)
* Hypothermia
* Hyperkalemia or Hypokalemia
* Hypoglycemia
* Tablets or Toxins (Drug overdose)
* Cardiac Tamponade
* Tension pneumothorax
* Thrombosis (Myocardial Infarction)
* Thrombosis (Pulmonary embolism)
* Trauma (Hypovolemia from blood loss)

## Mechanism

Asystole can also be primary or secondary. Primary asystole occurs when the heart's electrical conduction system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (ie, sclerosis) of the sinoatrial (SA) node or atrioventricular (AV) conducting system. Primary asystole usually is preceded by a bradydysrhythmia due to sinus node block-arrest, complete heart block, or both.
Reflex bradyasystole/asystole can result from ocular surgery, retrobulbar block, eye trauma, direct pressure on the globe, maxillofacial surgery, hypersensitive carotid sinus syndrome, or glossopharyngeal neuralgia. Episodes of asystole and bradycardia have been documented as manifestations of left temporal lobe complex partial seizures. These patients experienced either dizziness or syncope. No sudden deaths were reported, but the possibility exists if asystole were to persist. The longest interval was 26 seconds.
Secondary asystole occurs when factors outside of the heart's electrical conduction system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia with metabolic acidosis. Asystole or bradyasystole follows untreated VF and commonly occurs after unsuccessful attempts at defibrillation. This forebodes a dismal outcome.

## Treatment

Immediate diagnosis of asystole requires the recognition of a full cardiac arrest and a confirmed flat-line rhythm in 2 perpendicular leads. Lightheadedness or syncope may precede asystole when it follows a bradyasystolic rhythm.
If the rhythm is truly asystole and has been present for more than several seconds, the patient will be unconscious and unresponsive. A few agonal (final gasping) breaths may be noted, but detectable heart sounds and palpable peripheral pulses are absent.
The only 3 drugs recommended or acceptable by the American Heart Association (AHA) for adults in asystole are epinephrine, vasopressin, and atropine. In spite of full vagolytic doses of atropine (0.03 mg/kg) and high-dose epinephrine (0.20 mg/kg), or the use of vasopressin 40 units (U), few patients survive to leave the hospital neurologically intact. Atropine is no longer recommended in young children and infants in asystole but can be considered in adults with slow pulseless electrical activity (PEA) rhythms.
Epinephrine is used to increase coronary and cerebral blood flow during CPR. May enhance automaticity during asystole. Can be used for bradycardia in adult and pediatric patients.
In asystole, the heart will not respond to defibrillation because it is already depolarized. However, some emergency physicians advocate a trial of defibrillation in case the rhythm is actually fine ventricular fibrillation, although little evidence exists to support the practice.