Circulation Part 3: Cardiac Arrest/Peri-Arrest Arrhythmias Flashcards
(54 cards)
1
Q
Name the two shockable rhythms in cardiac arrest.
A
Pulseless ventricular tachycardia (VT) / Ventricular fibrillation
2
Q
Name the two non-shockable rhythms in cardiac arrest.
A
Pulseless electrical activity (PEA) / Asystole
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
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
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
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
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.
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
9
Q
Identify the following arrhythmia:
A
Monomorphic VT
10
Q
Identify the following arrhythmia:
A
Polymorphic VT
11
Q
Identify the following arrhythmia:
A
Torsades de Pointes (polymorphic VT)
12
Q
Identify the following arrhythmia:
A
Ventricular fibrillation
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
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)
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.
16
Q
Identify the following arrhythmia:
A
Pulseless electrical activity (PEA)
NB/can look like normal ECG without a pulse
17
Q
Identify the following arrhythmia:
A
- Asystole
- Note the P-waves still intact
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)
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)
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
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
- Hyperkalaemia = calcium chloride/insulin + dextrose/salbutamol
- Hypokalaemia/hypomagnesaemia = U&E + electrolyte supplementation
- Hypoglycaemia = glucose/glucagon
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
Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of cardiac tamponade.
- 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
Whilst responding to a cardiac arrest you should be thinking about reversible causes. Outline the management of toxicity.
- 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
Identify and describe the management of bradycardia (Resus Council Bradycardia 2021 Guidelines)
28
What is a bradycardia?
- HR \<60 bpm
- Can be physiological or a peri-arrest arrhythmia
- May be regular, irregular, narrow complex, and broad complex
29
List some adverse signs in symptomatic bradycardia.
* Syncope
* Breathless
* Chest pain
* Dizziness
THINK SHOCK!
30
List the physiological causes of bradycardia.
- Athletes
- Young
- Sleeping
31
List some of the intrinsic pathological causes of bradycardia.
- Intrinsic damage to AV conduction system
- Degenerative changes/ischaemia/structural disease
32
List some of the extrinsic pathological causes of bradycardia.
- Drugs
- Vagal stimulation
- Hypothyroidism
- Hypothermia
- Increased ICP (Cushing's reflex = hypertension/bradycardia/apnoea)
33
Outline first degree heart block (AV block).
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
Outline second degree heart block Mobitz type 1 (Wenckebach phenomenon).
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
Outline Mobitz type 2.
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
Outline third degree (complete) AV block.
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
What is the mechanism of action of atropine in the management of peri-arrest bradycardia?
- Muscarininc acetylcholine receptor antagonist.
- Blocks vagus nerve input to atrioventricular node and SA node.
38
What is the appropriate dose of atropine in peri-arrest bradycardia scenarios?
- 500 mcg IV
- Repeat to a maximum dose of 3 mg (6 doses)
39
When is cardiac pacing employed in peri-arrest bradycardias?
- More reliable method of treating bradycardias
- Used in the presence of adverse signs or when drugs have failed
40
List the 2 methods of non-invasive pacing?
- Percussion
- Transcutaneous
41
Outline percussion pacing
- 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
Outline transcutaneous pacing (use of electricity).
- 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
List the 2 methods of invasive pacing.
- Temporary transvenous
- Permanent implanttable pacemaker
\*require expert help for insertion
44
Identify and explain the management of tachycardia (Resus Council Tachycardia Algorithm 2021).
45
Why is it important to avoid tachyarrhythmias?
- 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
Outline the main causes of a sinus tachycardia (do not require tachycardia algorithm - treate the case).
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
What does 'synchronised' mean in relation to the defibrillator delivering shocks?
- Delivers shock on the P-wave when the ventricle is depolarised
48
What is a stable, regular narrow complex tachycardia otherwise known as?
Supraventricular tachycardia
49
Outline atrial flutter.
- 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
Outline supraventricular tachycardias.
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
Outline the use of adenosine in tachyarrhythmias.
- 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
Outline Wolff-Parkinson White Syndrome.
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
Outline the causes of QT prolongation (relevant to broad complex irregular tachyarrhythmias e.g. polymorphic VT/Torsades de Pointes
1. Long QT Syndrome (inherited)
2. Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
3. Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
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