Cardiac arrest Flashcards

1
Q

What is cardiac arrest?

A

Acute cessation of cardiac function leading to circulatory failure.

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2
Q

What is the aetiology of cardiac arrest? (x8)

A
  • Classical reversible causes of cardiac arrest are the four Hs and four Ts:
  • Hypoxia, Hypothermia, Hypovolaemia, Hypo- or hyperkalaemia
  • Tamponade, Tension pneumothorax, Thromboembolism, Toxins and other metabolic disorders such as drugs, therapeutic agents and sepsis
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3
Q

What is the pathophysiology of cardiac arrest? (x4 +1 point)

A
  • Characterised by four different types of cardiac arrythmias:
  • Ventricular fibrillation
  • Pulseless VT (includes Torsades de pointes and often related to hypomagnesaemia)
  • Pulseless electrical activity: organised electrical depolarisation of the myocardium without appropriate myocardial contraction, leading to inadequate circulation. The mechanism for this is loss of contractile force despite normal electrical stimulation
  • Asystole
  • ISCHAEMIA: mechanism for arrythmia is usually re-entrant circuit generated by surviving myofibrils within areas of fibrosis
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4
Q

What are the most common types of cardiac arrest?

A

VT and VF, most commonly with IHD aetiology.

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5
Q

Which cardiac arrest types are shockable?

A

Pulseless VT and VF

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6
Q

What is the definition of VT?

A

More than 3 successive ventricular extrasystoles (broad QRS complexes >120ms) at a rate of over 120/min.

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7
Q

What is the definition of VF?

A

Irregular, rapid ventricular activation with no CO.

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8
Q

What are the signs and symptoms of cardiac arrest?

A

Unconscious, not breathing, absent peripheral and central pulses. Often preceded by chest pain or dyspnoea

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9
Q

What are the risk factors for cardiac arrest?

A

IHD, hypertrophic cardiomyopathy, long QT syndrome, acute medical/surgical emergency, illicit substances such as cocaine and opioids, Brugada syndrome.

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10
Q

What is Brugada syndrome?

A

Autosomal dominant condition that affects depolarising sodium channels, associated with pseudo-right bundle branch block pattern and ST-segment elevations in leads V1 through V3.

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11
Q

What are the investigations for cardiac arrest? (x3)

A
  • Cardiac monitoring as rhythm dictates management
  • ABG, U&Es, FBC, cardiac biomarkers (troponin, CK, BNP), toxicology screen for aetiology
  • Electrocardiography for aetiology (valvular disorders, tamponade, cardiomyopathy)
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12
Q

How is cardiac arrest managed: BLS?

A
  1. If the arrest is witnessed, precordial thump with ulnar aspect of hand (see photo)
  2. A: clear and maintain airway with head tilt, jaw thrust and chin lift if C-spine consideration
  3. B: look, listen AND feel. If not breathing, give two effective breaths immediately
  4. C: assess carotid pulse for 10 seconds. If absent, give 100 compressions/min. Continue cycles of 30 compressions for every two breaths
  5. Proceed to ALS
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13
Q

How is cardiac arrest managed: ALS? (x3 and x3 +1)

A
  1. Attach cardiac monitor and defibrillator
  2. Assess the rhythm:
  3. (A) If shockable, defibrillate once with 150-360 J for biphasic defibrillators or 360 J for monophasic defibrillators. Then resume CPR for 2 mins (cycles of 30 compressions for every two breaths), reassess, then continue to defibrillate/CPR. Administer 1mg IV adrenaline after second defibrillation and again every 3-5 mins. If shockable rhythm persists after third shock, administer amiodarone (anti-arrythmic) 300mg IV bolus (or lidocaine)
  4. (B) If PEA or asystole, CPR for 2 mins (cycles of 30 compressions for every two breaths), reassess, then continue CPR. Administer 1mg IV adrenaline every 3-5 mins, and 3mg IV atropine (once only) if asystole/PEA with rate less than 60/min
  5. During asystole, secure airway (endotracheal intubation and high-flow oxygen). Once airway is secure, give continuous compressions and breaths.
  6. Consider 2g IV magnesium over 5-10 mins as a single dose in patients with cardiac arrest due to Torsades des pointes
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14
Q

What are the complications of cardiac arrest? (x6)

A
  • Death
  • Rib fractures
  • Irreversible hypoxic brain damage
  • Ischaemic liver injury (‘shock liver’)
  • Renal tubular necrosis
  • Recurrence of cardiac arrest
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