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poem > Circulation Part 3: Cardiac Arrest/Peri-Arrest Arrhythmias > Flashcards

Circulation Part 3: Cardiac Arrest/Peri-Arrest Arrhythmias Flashcards

1
Q

Name the two shockable rhythms in cardiac arrest.

A

Pulseless ventricular tachycardia (VT) / Ventricular fibrillation

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2
Q

Name the two non-shockable rhythms in cardiac arrest.

A

Pulseless electrical activity (PEA) / Asystole

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3
Q

List the 8 reversible causes of cardiac arrest.

A
  • Hypoxia
  • Hypovolaemia
  • Hypo/hyperkalaemia
  • Hypothermia
  • Thrombo-embolism (cardiac/pulmonary)
  • Toxins
  • Tamponade (cardiac)
  • Tension pneumothorax
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4
Q

Diagnose and manage in hospital cardiac arrest in an adult (outline the adult life support algorithm).

A

First, diagnose a cardiac arrest:

  • Try to get a patient response (unresponsive –> AVPU)
  • Open the patient’s airway
  • Check for normal breathing (beware agonal breathing)
  • Check circulation (carotid or femoral) –> if no pulse, this is an arrest
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5
Q

Outline the following arrhythmia:

Ventricular fibrillation

A
  • Shockable
  • No CO
  • Bizarre, irregular waveform
  • No recognisable QRS complex
  • Uncoordinated electrical activity
  • Exclude movement/interference as a cause
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6
Q

Outline the following arrhythmia:

Ventricular tachycardia

A
  • Shockable
  • No CO
  • QRS usually wide (usually constant QRS morphology)
  • More organised electrical activity than ventricular fibrillation
  • BUT, high risk of deteriorating to ventricular fibrillation
  • ONLY defibrillate if pulseless
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7
Q

Outline the following arrhythmia:

Polymorphic ventricular tachycardia

A
  • Shockable
  • a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration.
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8
Q

Outline the following arrhythmia:

Torsades de Pointes

A

a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation; it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line e.g. hypokalaemi

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9
Q

Identify the following arrhythmia:

A

Monomorphic VT

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10
Q

Identify the following arrhythmia:

A

Polymorphic VT

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11
Q

Identify the following arrhythmia:

A

Torsades de Pointes (polymorphic VT)

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12
Q

Identify the following arrhythmia:

A

Ventricular fibrillation

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13
Q

When you have identified a ventricular tachycardia on ECG; what is an important distinction to make?

A
  • Ventricular tachycardias can be with a pulse or without a pulse; your team should confirm this during ABCDE assessment. This changes management.
  • VT/VF with a pulse = tachycardia algorithm
  • VT/VF without a pulse = cardiac arrest algorithm
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14
Q

Outline the following arrhythmia:

Pulseless electrical activity (PEA)

A
  • Non-shockable
  • Clinical features of a cardiac arrest
  • 2 minute cycles CPR + 1mg IV Adrenaline 1:10,000, 3-5min
  • refers to a clinical diagnosis of cardiac arrest in which a heart rhythm is observed on the ECG that should be producing a pulse, but is pulseless (i.e. an ECG usually associated with a CO)
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15
Q

Outline the following arrhythmia:

Asystole

A
  • Non-shockable
  • refers to a clinical diagnosis of cardiac arrest in which a heart rhythm is observed on the ECG that should be producing a pulse, but is pulseless.
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16
Q

Identify the following arrhythmia:

A

Pulseless electrical activity (PEA)

NB/can look like normal ECG without a pulse

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17
Q

Identify the following arrhythmia:

A
  • Asystole
  • Note the P-waves still intact
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18
Q

Outline adequate chest compression.

A
  • 30:2
  • Compression at centre of chest
  • 5-6 cm depth
  • 2 per second (100-120/min)
  • Maintain high quality compressions with minimal interruptions
  • Commence continuous compressions once the airway is secured (iGel + Ambu-bag - 10-12 ventilations a minute)
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19
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of hypoxia.

A
  • Ensure a patent airway
  • Give high flow supplemental O2 (LMA/iGel + ambu bag with room air augmented up to 100%)
  • Avoid hyperventilation (16-20 resps/min is normal)
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20
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of hypovolaemia.

A
  • Actively look for a PEA arrest
  • Look for covert bleeding
  • Control the haemorrhage
  • IV fluids
  • IV blood and blood products
  • Transexamic acid (if trauma cardiac arrest)
  • Left-side positioning if patient pregnant
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21
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of hypo-/hyperkalaemia and metabolic disorders.

A
  1. Hyperkalaemia = calcium chloride/insulin + dextrose/salbutamol
  2. Hypokalaemia/hypomagnesaemia = U&E + electrolyte supplementation
  3. Hypoglycaemia = glucose/glucagon
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22
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of hypothermia.

A
  • Rare if inpatient
  • Use low reading thermometre (rectal/oesophageal)
  • Use active rewarming techniques
  • Consider cardiopulmonary bypass
  • If <30 degrees Celsius = 3 shocks/no drugs, then delay further shocks until >=28-30 degrees Celsius
  • If 30-35 degrees Celsus = shocks as usual, double time interval between doses of drugs
  • If >35 degrees Celsius = ALS algorithm as usual
23
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of thrombosis - coronary/pulmonary.

A
  • PCA and PCI may be feasible
  • Automated mechanical chest compression device or extracorpeal CPR
  • If high clinical suspicion of PE, consider fibrinolytic therapy
  • If fibrinolytic therapy given, continue CPR for 60-90 minutes before discontinuing resuscitation
24
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of tension pneumothorax.

A
  • Emergency needle decompression
  • Chest tube thoracostomy
  • Prevents CV compromse (mediastinal shift)
25
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of cardiac tamponade.

A
  • Difficult to diagnose without echo
  • Consider penetrating chest trauma/after cardiac surgery/recent MI/or a concurrent uraemia
  • Treat with needle pericardiocentesis or resuscitative thoracotomy
26
Q

Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of toxicity.

A
  • Usually PEA arrest
  • ABCDE
  • Avoid mouth-to-mouth
  • Activated charcoal - absorbs certain drugs (within 1 hour intact/protected airway)
  • Antidotes:

TCA overdose = bicarbonate

CCBs/Beta-blockers = glucagon/calcium

Cocaine = benzodiazepines

27
Q

Identify and describe the management of bradycardia (Resus Council Bradycardia 2021 Guidelines)

A
28
Q

What is a bradycardia?

A
  • HR <60 bpm
  • Can be physiological or a peri-arrest arrhythmia
  • May be regular, irregular, narrow complex, and broad complex
29
Q

List some adverse signs in symptomatic bradycardia.

A
  • Syncope
  • Breathless
  • Chest pain
  • Dizziness

THINK SHOCK!

30
Q

List the physiological causes of bradycardia.

A
  • Athletes
  • Young
  • Sleeping
31
Q

List some of the intrinsic pathological causes of bradycardia.

A
  • Intrinsic damage to AV conduction system
  • Degenerative changes/ischaemia/structural disease
32
Q

List some of the extrinsic pathological causes of bradycardia.

A
  • Drugs
  • Vagal stimulation
  • Hypothyroidism
  • Hypothermia
  • Increased ICP (Cushing’s reflex = hypertension/bradycardia/apnoea)
33
Q

Outline first degree heart block (AV block).

A

Rhythm: regular

P wave: every P wave is present and followed by a QRS complex

PR interval: prolonged >0.2 seconds (5 small squares)

QRS complex: normal morphology and duration (<0.12 seconds

Usually incidental finding and patient asymptomatic

Atheletes/drugs/fibrosis/structural heart disease/IHD

34
Q

Outline second degree heart block Mobitz type 1 (Wenckebach phenomenon).

A

Rhythm: irregular

P wave: every P wave is present, but not all are followed by a QRS complex

PR interval: progressively lengthens before a QRS complex is dropped

QRS complex: normal morphology and duration (<0.12 seconds), but are occasionally dropped

Athletes/inferior MI

35
Q

Outline Mobitz type 2.

A

Rhythm: irregular (may be regularly irregular in 3:1 or 4:1 block)

P wave: present but there are more P waves than QRS complexes

PR interval: consistent normal PR interval duration with intermittently dropped QRS complexes

QRS complex: normal (<0.12 seconds) or broad (>0.12 seconds)

The QRS complex will be broad if the conduction failure is located distal to the bundle of His

Features: palpitations/pre-syncope/syncope

Requires cardiac monitoring

Permanent transvenous pacemaker if no reversible cause identified (risk of complete AV block)

36
Q

Outline third degree (complete) AV block.

A

Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction. Atria and ventricles therefore act independently.

Cardiac function is maintained by a junctional or ventricular pacemaker.

Rhythm: variable

P wave: present but not associated with QRS complexes

PR interval: absent (as there is atrioventricular dissociation)

QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) depending on the site of the escape rhythm (above or below bifurcation of Bundle of His). BROAD COMPLEX = RISK OF ASYSTOLE!

37
Q

What is the mechanism of action of atropine in the management of peri-arrest bradycardia?

A
  • Muscarininc acetylcholine receptor antagonist.
  • Blocks vagus nerve input to atrioventricular node and SA node.
38
Q

What is the appropriate dose of atropine in peri-arrest bradycardia scenarios?

A
  • 500 mcg IV
  • Repeat to a maximum dose of 3 mg (6 doses)
39
Q

When is cardiac pacing employed in peri-arrest bradycardias?

A
  • More reliable method of treating bradycardias
  • Used in the presence of adverse signs or when drugs have failed
40
Q

List the 2 methods of non-invasive pacing?

A
  • Percussion
  • Transcutaneous
41
Q

Outline percussion pacing

A
  • Side of closed fist
  • Lower edge of sternum
  • 50-70/min
  • May have to move fist to contact position to achieve capture
  • Palpable pulse indicates a mechanical capture
  • Monitor the ECG to see if this creates a QRS complex
  • Useful when waiting for a defibrillator/pacing device
42
Q

Outline transcutaneous pacing (use of electricity).

A
  • Painful - consider sedation and analgesia
  • ECG monitoring electrodes and pads
  • Pacing rate is 60-90/min
  • QRS and T-waves indicate electrical capture
  • A palpable pulse indicates a mechanical response
43
Q

List the 2 methods of invasive pacing.

A
  • Temporary transvenous
  • Permanent implanttable pacemaker

*require expert help for insertion

44
Q

Identify and explain the management of tachycardia (Resus Council Tachycardia Algorithm 2021).

A
45
Q

Why is it important to avoid tachyarrhythmias?

A
  • They reduce ventricular filling time and reduce the diastolic filling period of the cardiac cycle
  • They reduce coronary artery filling time (fill during diastole)
  • Increase myocardial O2 requirements
  • May precipitate MI
46
Q

Outline the main causes of a sinus tachycardia (do not require tachycardia algorithm - treate the case).

A
  1. Sympathetic activity (fear/anxiety/hypozaemia/hypercapnia)
  2. Increased metabolic rate (fever/hyperthyroidism/pregnancy)
  3. Compensatory (anaemia/hypovolaemia/PE/reduced SVR i.e. sepsis or anaphylaxis)
47
Q

What does ‘synchronised’ mean in relation to the defibrillator delivering shocks?

A
  • Delivers shock on the P-wave when the ventricle is depolarised
48
Q

What is a stable, regular narrow complex tachycardia otherwise known as?

A

Supraventricular tachycardia

49
Q

Outline atrial flutter.

A
  • Normally the electrical signal passes through the atria once, simulating a contraction then disappears through the AV node into the ventricles. Atrial flutter is caused by a “re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway. The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm. The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction. It gives a “sawtooth appearance” on ECG with P wave after P wave.
  • Rate control with beta-blocker or rhythm control with cardioversion
  • May require radiofrequency ablation of re-entry circuit
  • Anti-coagulation based on CHA2DS2VASc score
50
Q

Outline supraventricular tachycardias.

A

Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles. Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

AVNRT = re-entry back through AV node

AVRT = accessory pathway (WPW)

Atrial tachycardia = originates in atria other than SA node

51
Q

Outline the use of adenosine in tachyarrhythmias.

A
  • Adenosine transiently slows the conduction through the AV node.
  • It can interrupt the re-entry pathways through the AV node/accessory pathways.
  • Restores sinus rhythm in patients with paraoxysmal SVT, including PSVT associated with WPW.
  • Brief period of aystole/bradycardia - “impending feeling of doom”
  • Fast IV bolus in wide bore cannula (grey) - 6/12/12 mg if no improvement between doses
52
Q

Outline Wolff-Parkinson White Syndrome.

A

Wolff-Parkinson White Syndrome is caused by an extra electrical pathway connecting the atria and ventricles.

Extra pathway = Bundle of Kent.

The definitive treatment for Wolff-Parkinson White syndrome is radiofrequency ablation of the accessory pathway.

ECG Changes:

Short PR interval (< 0.12 seconds)

Wide QRS complex (> 0.12 seconds)

“Delta wave” which is a slurred upstroke on the QRS complex

53
Q

Outline the causes of QT prolongation (relevant to broad complex irregular tachyarrhythmias e.g. polymorphic VT/Torsades de Pointes

A
  1. Long QT Syndrome (inherited)
  2. Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
  3. Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
54
Q
A

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