Cardiology: Cardiac Arrest

Cardiac arrest is essentially where the heart stops beating. There will be no contraction of the heart muscle, but there may still be electrical activity in the heart.

Brain damage occurs after 5 minutes of cardiac arrest. When you carry out CPR, you are technically trying to reverse cardiac arrest.

Treatment

In some cases, cardiac arrest may be reversible. The causes of reversible cardiac arrest are the 5H’s and the 4T’s:

H’s	T’s
Hypoxia	Tension pneumothorax
Hypovolaemia	Tamponade (cardiac)
Hypokalaemia	Toxins
Hyperkalaemia	Thrombosis
Hypothermia

Prognosis

Cardiac arrest is a medical emergency, and has extremely poor prognosis.

-          Out of hospital arrest has a survival rate of 2-8%

-          In hospital cardiac arrest has a survival rate of about 15%

Prognosis is particularly dependent on the electrical rhythm of the heart during the arrest.

Defibrillation and cardioversion

When you pass a large current through the heart, you can completely depolarise it. After this time, there will be a period of asystole, hopefully after which normal sinus mechanisms will restore sinus rhythm to the heart.

Defibrillators deliver a high-voltage, short duration DC shock, via two metal pads (coated in conducting gel or jelly) placed on the chest.

These should be placed over the upper right sternal edge and the apex.

You can also deliver a shock right to the heart during open surgery!

Defibrillation vs cardioversion – defibrillation is a general term often used to describe the shock given to the heart, and more specifically it describes an ‘unsynchronised ‘shock. Cardioversion refers to this shock when it is applied at a specific time in the ECG cycle (a ‘synchronised’ shock).

Before attempting to shock the heart, you need to establish what the current rhythm is. Determining the rhythm determines further treatment options. All this will also take place in the context of CPR.

Beware! – if you give a shock at around the peak of the T wave, you can induce unusual and dangerous rhythms such as atrial fibrillation or ventricular tachycardia. Thus the current is usually synchronised with the ECG so that the pulse is given about 0.02s after the peak of the R wave.

In ventricular fibrillation, the timing of the impulse is not important.

Shockable rhythms

Ventricular fibrillation

Pulseless ventricular tachycardia

Non-shockable rhythms

PEA – pulseless electrical activity – this means any electrical activity that appears on an ECG like it should be producing a pulse, but it is not. The most common cause is hypovolaemia.

Asystole – no rhythm present

Cardioversion therapy is often pre-planned, and used to treat significant, although not immediately life-threatening arrhythmias, such as narrow complex tachycardias, atrial fibrillation and atrial flutter.

Sedation or no sedation?

in an emergency situation, the patient is often unconscious as a result of cardiogenic shock, and in such cases, there is no anaesthesia given. In cases where the patient is awake (most commonly elective cardioversion), then the patient may receive sedation to make the treatment more tolerable.

Contraindications and complications

Digoxin – this increases the risk of arrhythmias after cardioversion, and thus in cases of elective cardioversion, the drug is usually withheld for 24 hours before treatment.

Risk of systemic embolus – is increased in patients with long standing atrial arrhythmias who undergo elective cardioversion. Thus, these patients should be given 4 weeks anticoagulant therapy for at least 4 weeks either side of the treatment.

Notes by Tom Leach