Arrhythmia's Flashcards
(73 cards)
1
Q
What is atrial fibrillation?
A
- Characterised by rapid, chaotic and ineffective atrial electrical conduction.
- Irregularly irregular rhythm and no p waves
- Type of SVT, narrow complex tachycardia
(contractions become uncoordinated: instead of 1 big contraction starting in atria, there are many little atrial contractions, heart appears to be quivering)
2
Q
How does atrial fibrillation appear on ECG? Why?
A
no paves, instead there are small sqwiggles b/t irregular QRS waves:
- In AF there are many small area contracting at different times (; no definitive p wave)
- some of these small signals make it down to the ventricles to cause ventricular contraction (QRS complexes are dispursed irregularly)
- The A-wave signifies atrial contraction. As a result of uncoordinated atrial activity, the A-wave will not be seen.
3
Q
Explain the cause for atrial fibrillation:
A
“multiple wavelet theory”: when heart undergoes tissue heterogeneity (changes in heart tissue can be caused by cardiovascular disease, obesity, diabetes, genetics), the different tissues cause mutiple small uncoordinated waves
● There may be no identifiable cause (‘lone AF’)
● Secondary causes lead to an abnormal atrial electrical pathway that results in AF
4
Q
What are some risk factors for Atrial fibrillation?
A
IHD, HF, Hypertension, Mitral Valve Disease, Hyperthyroidism, PE, Pneumonia, Alcohol, High bp, coronary artery disease, obesity, diabetes, genetics
5
Q
What are the different types of atrial fibrillation?
A
- Paroxysmal - intermittent & self-terminate <48hrs (when there are still normal tissues, unchanged)
- Persistent - > 7 days & need to cardiovert (stress on tissue cells start to undergo change)
- Long standing persistent- 12 months (progressive fibrosis)
- Permanent - persistent AF resistant to cardioversion, aim to rate control
6
Q
What is atrial flutter?
A
- Form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.
- (normally once the ventricles contract, they have to wait for a signal from the atria before contracting again, however in atrial flutter a reentrant rhythm enters the atria and causes a signal that can loop back on itself, leading to an endless cycle of atria contracting again and again.)
- Sawtooth pattern. 2:1 ratio of p waves:QRS complexes (ie. 2:1 ratio of atrial impulses being conducted to the ventricles)
7
Q
What presenting symptoms of artial fibrillation?
A
- Often ASYMPTOMATIC
- Palpitations
- Syncope (if low output)
- Fatigue
- Dizziness
- Shortness of breath
- Weakness
- Symptoms of the secondary cause of AF
8
Q
What signs of atrial fibrillation can be found on physical examination?
A
- Tachycardia
- Irregularly irregular pulse
- Variable intensity of first heart sound
- Difference in apical beat and radial pulse (apical is greater than radial)
- signs of LVF
- Check for signs of thyroid disease and valvular disease
9
Q
What investigations are used to diagnose/ monitor atrial fibrillation?
A
- ECG:
- Uneven baseline with absent p waves
- Irregularly irregular intervals between QRS complexes
- If rate >100, ‘fast AF’ - AF with rapid ventricular response - Bloods
- Inflammatory markers (if acute) - may indicate sepsis which can cause AF
- U&Es, Mg2+ and Ca2+ (Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia)
- TFTs [thyroid func] (check for thyrotoxicosis)
- Troponins if chest pain is present
- Cardiac enzymes - CXR: Fast AF can present with heart failure and pulmonary oedema
- Transthoracic Echocardiogram → rule out underlying cardiac structural disease (ie. valvular disease)
- Special tests :
24hr tape or 5 day ECG- useful for paroxysmal AF
10
Q
How is acute atrial fibrillation managed?
A
If Haemodynamically Unstable (BP ≤90/60mmHg) ⇒ emergency DC cardioversion
- Rate Control → 1st line = beta-blocker (propanolol) or rate-limiting CCB (diltiazem or verapamil). 2nd line = digoxin (if patients sedentary or other drugs unsuitable, eg. avoid propanolol in asthmatics)
- Don’t use beta blocker and verapamil together ⇒ can lead to heart block - Rhythm Control (1st line over rate control if clear reversible cause for AF) → DC cardioversion (give LMWH prior) or Amiodarone/Flecainide
- New AF <48hrs ⇒ (Rate or rhythm control- rhythm more favourable if reversible) DC cardioversion or chemical cardioversion (amiodarone or flecainide)
- AF >48hrs ⇒ Rate control & patient should be anticoagulated for 3-4 weeks before electrical cardioversion - Anticoagulation (stroke risk) → DOAC (apixaban). (Don’t need to monitor INR as you do with warfarin, hence DOAC preferred).
chronic: rate control, anticoagulate for 3 weeks before elective cardioversion and then rhythm control (elective cardioversion)
11
Q
What score is used to determine the risk of stroke?
A
CHA2DS2-VASc score to determine the most appropriate anticoagulation strategy (determine risk of stroke)
C: 1 point for congestive cardiac failure.
H: 1 point for hypertension.
A2: 2 points if the patient is aged 75 or over.
D: 1 point if the patient has diabetes mellitus.
S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA).
V: 1 point if the patient has known vascular disease.
A: 1 point if the patient is aged 65-74.
Sc: 1 point if the patient is female.
- 0 = no treatment
- 1 = anticoagulation in males (not in females)- DOAC, if contraindicated offer vit k antagonist
- 2 or more = anticoagulation
*If CHA2DS2-VASc score suggests no need for anticoagulation, do an echocardiogram to exclude valvular heart disease
*If DOACs contraindicated, give warfarin
12
Q
What score is used to assess bleeding risk in patients with AF who are being considered for anticoagulation?
A
ORBIT Score → assesses bleeding risk in patients with AF who are being considered for anticoagulation: HARB
1. Haemoglobin < 130 g/L
2. Age > 74 years old
3. Renal impairment GFR < 60mL
4. Bleeding history
5. Treatment with antiplatelet agents
13
Q
What complications are associated with atrial fibrillation?
A
- THROMBOEMBOLISM
- Embolic stroke risk of 4% per year
- Risk is increased with left atrial enlargement or left ventricular dysfunction
- Worsening of existing heart failure
- Myocardial infarction
- Congestive heart failure
14
Q
Describe the prognosis of atrial fibrillation?
A
Chronic AF in a disease heart does not usually return to sinus rhythm
15
Q
describe the epidemiology of atrial fibrillation?
A
- VERY COMMON in the elderly
- Present in 5% of those > 65 years
16
Q
What are some secondary causes that can lead to atrial fibrillation?
A
- Systemic Causes
o Thyrotoxicosis
o Hypertension
o Pneumonia
o Alcohol
o Hypokalaemia
o Hypomagnesemia - Heart Causes
o Mitral valve disease
o Heart failure
o Ischaemic heart disease, MI (seen in 22%) - Lung Causes
o Bronchial carcinoma
o PE
o Pneumonia - Others: caffeine, alcohol, post-op
- Rare causes: cardiomyopathy, constrictive pericarditis, sick sinus syndrome, lung cancer, atrial myxoma, endocarditis, rheumatic heart disease, haemochromatosis, sarcoid
● Cardiac output drops by 10-20% as ventricles aren’t primed reliably by atria.
● The main risk is embolic stroke.
17
Q
What is atrial flutter?
A
- Form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves. (reentrant signal starts in the R or L atrium causing the atria to contract again and again)
- Sawtooth pattern. 2:1 ratio of p waves:QRS complexes (ie. 2:1 ratio of atrial impulses being conducted to the ventricles).
- Atria contract at HRs roughly 300 bpm
18
Q
What are some presenting symptoms of atrial flutter that can be found in the history ?
A
Often ASYMPTOMATIC
- Palpitations
- Syncope (if low output)
- Fatigue
- Dizziness
- Shortness of breath
- Weakness
19
Q
What signs of atrial flutter can be found on physical examination?
A
- tachycardia
- regular or irregularly regular peripheral pulse (due to variable conduction from the atrioventricular node),
- jugular venous distension, respiratory sounds with crackles in lung fields
- abdominal distention
- lower extremities edema
20
Q
What investigations are used to diagnose atrial flutter?
A
ECG :
o Atrial flutter = narrow complex tachycardia, saw-tooth pattern flutter waves, loss of isoelectric baseline
21
Q
What are some complications that can arise from atrial flutter?
A
- Prolonged tachycardia -> ventricles decompensate -> heart failure
- Atria not contracting effectively -> blood stagnates and forms clots -> embolise to brain -> stroke
22
Q
How is atrial flutter managed?
A
If Haemodynamically Unstable (BP ≤90/60mmHg) ⇒ emergency DC cardioversion
- Rate Control → 1st line = beta-blocker (propanolol) or rate-limiting CCB (diltiazem or verapamil). 2nd line = digoxin (if patients sedentary or other drugs unsuitable, eg. avoid propanolol in asthmatics)
- Don’t use beta blocker and verapamil together ⇒ can lead to heart block - Rhythm Control (1st line over rate control if clear reversible cause for AF) → DC cardioversion (give LMWH prior) or Amiodarone/Flecainide
- New AF <48hrs ⇒ DC cardioversion or chemical cardioversion (amiodarone or flecainide)
- AF >48hrs ⇒ patient should be anticoagulated for 3-4 weeks before electrical cardioversion - Anticoagulation (stroke risk) → DOAC (apixaban). (Don’t need to monitor INR as you do with warfarin, hence DOAC preferred).
23
Q
What is supra ventricular tachycardia?
A
SVT can be used to refer to any tachydysrhythmia arising from above the level of the Bundle of His, usually the atria or AV node. These typically produce a narrow complex tachycardia.
- A regular narrow-complex tachycardia (> 100 bpm) with no p waves and a supraventricular origin.
- Technically, AF and atrial flutter counts as a type of SVT
- However, SVT generally refers to:
● Atrioventricular Nodal Re-entry Tachycardia (AVNRT)
● Atrioventricular Re-entry Tachycardia (AVRT)
24
Q
What are the 2 types of supraventricular tachycardia you can have?
A
- Atrioventricular nodal re-entry tachycardia (AVNRT) → local re-entry circuit within the AV Node
- Atrioventricular re-entry tachycardia (AVRT) → re-entry circuit forms between atria and ventricles due to presence of accessory pathway (bundle of kent)
- Wolf-Parkinson-White Syndrome → delta waves (slurred upstroke in QRS) after SVT termination
25
What presenting symptoms of SVT can be found in the history?
● May have minimal symptoms or may present with syncope
● Symptoms vary depending on rate and duration of SVT
● Palpitations
● Light-headedness
● Polyuria (due to increased atrial pressure causing ANP release)
● Abrupt onset and termination of symptoms
● Other symptoms: fatigue, chest discomfort, dyspnoea, syncope
26
What signs of SVT can be found on physical examinations
1. AVNRT - normal except tachycardia
2. Wolff-Parkinson-White
o Tachycardia
o Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)
27
What are the causes of SVT?
Often physiological (e.g. due to exercise or medication)
AVNRT:
o A localised re-entry circuit forms around the AV node, which conducts to the ventricles faster than normal conduction pathway.
AVRT:
o This occurs when there is normal AV conduction, as well as an accessory pathway present. These form a re-entry circuit between the atria and ventricles.
o An accessory pathway is an abnormal conduction pathway. It can conduct impulses either towards the ventricle (anteretrograde) or away from the ventricle (retrograde) or in both directions.
o A classic example of AVRT is Wolff-Parkinson-White Syndrome, in which the accessory pathway is called Bundle of Kent. WPW Syndrome can lead to AVRT.
28
What are the risk factors for SVT?
o Nicotine
o Alcohol
o Caffeine
o Previous MI
o Digoxin toxicity
29
Summarise the epidemiology of SVT
● VERY COMMON
● 2 x more common in FEMALES
30
What investigations are used to diagnose SVT?
1. ECG
NOTE: acutely, AVRT and AVNRT cannot be differentiated on ECG, as they both appear as narrow complex tachycardia. Only after correcting the tachycardia, you see delta wave in AVRT but no wave in AVNRT:
o AVNRT
⇒ Tachycardia
⇒ Narrow QRS
⇒ P waves may be buried in QRS
⇒ Decreased PR interval
⇒ After SVT terminated, ECG appears normal.
o AVRT
⇒ Narrow complex tachycardia
⇒ Shortened PR interval
⇒ P waves buried in QRS
31
What investigations are used to monitor SVT?
(ECG FOR DIAGNOSIS)
● 24 hr ECG monitoring - will be required in patients with paroxysmal palpitations
● Cardiac Enzymes
o Check for features of MI (especially if there is chest pain)
● Electrolytes - can cause arrhythmia
● TFTs - can cause arrhythmia
● Digoxin Level - for patients on digoxin
● Echocardiogram - check for structural heart disease
32
How is SVT managed?
1. If Haemodynamically UNSTABLE:
o DC cardioversion
2. If Haemodynamically STABLE
o Try VAGAL manoeuvres (e.g. Valsalva, carotid massage)
- Note: Carotid massage could dislodge atherosclerotic plaques, so is only performed in young patients
3. If vagal manoeuvres fail:
o ADENOSINE 6 mg bolus (can increase to 12 mg) - Contraindicated in ASTHMA as it can cause bronchospasm – in asthma, use VERAPAMIL
o Wait 2 minutes – if no change, give 12mg adenosine
o Wait another 2 minutes – if still no change, give 12mg adenosine
o Wait another 2 minutes – if still no change, IV metoprolol/amiodarone/digoxin/synchronised DC cardiovert
4. If unresponsive to chemical cardioversion or tachycardia > 250 bpm or adverse signs (low BP, heart failure, low consciousness)
o Sedate and synchronised DC cardioversion
o Amiodarone
5. Ongoing management of SVT
a. AVNRT
▪ Radiofrequency ablation of slow pathway
▪ Beta-blockers
▪ Alternatives: fleicanide, propafenone, verapamil
b. AVRT
▪ Radiofrequency ablation
c. Sinus Tachycardia
▪ Exclude secondary cause (e.g. hyperthyroidism)
▪ Beta-blocker or rate-limiting CCB
33
Identify possible complications of SVT
● Haemodynamic collapse
● DVT
● Systemic embolism
● Cardiac tamponade
34
Summarise the prognosis for patients with SVT
● Dependent on the presence of underlying structural heart disease
● If structurally normal heart - GOOD PROGNOSIS
● People with pre-excitation have a small risk of sudden death
35
What is Wolff- Parkinson- White syndrome? WPW
● A congenital abnormality which can result in supraventricular tachycardias that use an accessory pathway. It is a pre-excitation syndrome.
● Pre-excitation syndrome: early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway
36
Explain the aetiology/risk factors of WPW syndrome
The accessory pathway (bundle of Kent) is likely to be congenital
Associations:
o Congenital cardiac defects
o Ebstein's anomaly (congenital malformation of the heart characterised by displacement of septal and posterior tricuspid leaflets)
o Mitral valve prolapse
o Cardiomyopathies (e.g. HOCM)
37
Summarise the epidemiology of WPW syndrome
● Relatively COMMON
● Most common of the ventricular pre-excitation syndromes
● Found in ALL AGES
● More common in the YOUNG
● Prevalence decreases with age
38
What presenting symptoms of WPW can be found in the history?
● SVT may occur in early childhood
● Often ASYMPTOMATIC - may be an incidental finding of an ECG
● Symptoms:
o Palpitations
o Light-headedness
o Syncope
39
What signs of WPW can be found on physical examination?
● Paroxysmal SVT may be followed by a period of polyuria, due to atrial dilatation and release of ANP
● Sudden death - if SVT deteriorates into VF
● Clinical features of associated cardiac defects (e.g. mitral valve prolapse, cardiomyopathy)
40
Identify appropriate investigations for WPW syndrome
1. ECG:
● ECG may be normal if the conduction speed of the impulse along the accessory pathway matches the conduction speed down the bundle of His
● Classic ECG findings:
o Short PR interval
o Broad QRS complex
o Slurred upstroke in initial portion of QRS producing a delta wave – this is because ventricles are being excited over a longer period of time.
● Patient may be in SVT (AVRT)
2. Bloods - check for other causes of arrhythmia
3. Echocardiogram - check for structural heart defects
41
What is first degree heart block?
prolonged conduction through the AV node (not really a block, more of a delay)
42
What is 2nd degree heart block?
2nd Degree AV Block:
1. Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle then begins again.
2. Mobitz Type II: intermittent or 2. regular failure of conduction through the AV node (all or nothing). Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)
43
What is third degree heart block?
3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle.
44
What is the cause/ risk factors of heart block?
- MI or ischaemic heart disease (MOST COMMON)
(Complete heart block following MI ⇒ Right Coronary Artery occlusion (supplies AV node) )
- Infection (e.g. rheumatic fever, infective endocarditis)
- Drugs (e.g. digoxin)
- Metabolic (e.g. hyperkalaemia)
- Infiltration of conducting system (e.g. sarcoidosis)
- Degeneration of the conducting system
- Lyme disease (3rd degree)
- Fibrosis and calcification of conduction system
45
What presenting symptoms of heart block can be found in the history?
AV Heart Block
- 1st Degree- asymptomatic
- 2nd Degree- usually asymptomatic
- Mobitz Type II and 3rd Degree- may cause Stokes-Adams Attacks (cardiogenic syncope - syncope caused by cardiac arrhythmia/ventricular asystole)
- May also cause dizziness, palpitations, chest pain and heart failure
46
What is buncle branch block?
- Bifascicular block
- Conduction disturbances below the atrioventricular (AV) node in which the right bundle branch and one of the two fascicles (anterior or posterior) of the left bundle branch are involved
- Left bundle branch block (LBBB) is also a type of fascicular block since it implies both fascicles are affected
47
What is Trifascicular block?
Trifascicular block: 1st degree heart block + LAD/RAD + RBBB/LBBB. Manifests as 3rd degree (complete) block.
48
What signs of heart block can be found on physical examination?
- Often NORMAL
- Complete Heart Block
- Slow large volume pulse
- JVP may show cannon a waves: atria and ventricles contract simultaneously
- Mobitz Type Ii and 3rd Degree Heart Block
- Signs of reduced cardiac output (e.g. hypotension, heart failure)
49
What is the gold standard investigation used to diagnose heart block?
ECG:
1. First Degree- fixed prolonged PR interval (> 0.2 s)
2.
- Mobitz Type I (Wenckebach)- progressively prolonged PR interval = P wave that is NOT followed by a QRS complex. The pattern then begins again. 'e.g. Going, going, gone'. Can be normal variant in athlete.
- Mobitz Type II- intermittently a P wave isNOTfollowed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
3. Complete Heart Block- no relationship between P waves and QRS complexes. If QRS is initiated in the:
- Bundle of His - narrow complex
- More distally - wide complex and slow rate (~ 30 bpm)
50
What investigations, other than ECG are used to monitor a heart black?
1. CXR:
- Cardiac enlargement
- Pulmonary oedema
2. BLOODS:
- TFTs
- Digoxin level
- Cardiac enzymes
- Troponin
3. ECHOCARDIOGRAM:
- Wall motion abnormalities
- Aortic valve disease
- Vegetations
51
How are heart blocks managed?
1. Chronic Block
- Permanent pacemaker is recommended in:
*Complete heart block
*Advanced Mobitz Type II
*Symptomatic Mobitz Type I
2. Acute Block:
- If associated with clinical deterioration use IV atropine
- Consider temporary(external) pacemaker
52
What complications are associated with heart block?
- Asystole
- Cardiac arrest
- Heart failure
- Complications of any pacemaker inserted
53
Describe the prognosis of heart block
Mobitz Type II and 3rd degree block usually indicate serious underlying cardiac disease
54
What is ventricular tachycardia?
A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually >120 bpm.
- One of the shockable rhythms that may be seen in cardiac arrest patients
● MEDICAL EMERGENCY
55
What are the risk factors for VT?
Risk Factors →
- coronary heart disease
- structural heart disease,
o Electrolyte deficiencies (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia)
o Use of stimulant drugs (e.g. caffeine, cocaine)
56
How do you treat pulseless VT?
Pulseless VT: Defibrillate
- Defibrillation - asynchronous delivery of energy, such as the shock is delivered randomly during the cardiac cycle.
- Cardioversion - delivery of energy that is synchronized to the QRS complex.
57
What presenting symptoms of VT can be found in the history?
● Symptoms of ischaemic heart disease or haemodynamic compromise due to poor perfusion
- Chest Pain
- Palpitations
- Dyspnoea
- Syncope
- Depending on degree of haemodynamic instability → Respiratory Distress, Bibasal Crackles, Raised JVP, Hypotension
58
What causes VT?
● Electrical impulses arise from a ventricular ectopic focus – an ectopic focus is an excitable group of cells within the atria/ventricles which cause a premature heart beat outside the normally functioning circulation i.e. abnormal pacemaker sites
59
Summarise the epidemiology of ventricular tachycardia
● Fairly common
● It is one of the shockable rhythms that is seen in cardiac arrest patients
● VT incidence peaks in the middle decades of life
60
Recognise the signs of ventricular tachycardia on physical examination
Signs are dependent on the degree of haemodynamic instability
o Respiratory distress
o Bibasal crackles
o Raised JVP
o Hypotension
o Anxiety
o Agitation
o Lethargy
o Coma
61
Identify appropriate investigations for ventricular tachycardia
1. ECG
o It can sometimes be difficult to distinguish between VT and SVT with aberrant conduction
o If in doubt, treat as a VT
o ECG Features:
● Rate > 100 bpm
● Broad QRS complexes
● AV dissociation
2. Electrolytes - derangement can cause arrhythmias
3. Drug levels - e.g. check for digoxin toxicity
4. Cardiac enzymes - e.g. troponins to check for recent ischaemic event
62
Generate a management plan for ventricular tachycardia
- ABC approach
- CHECK WHETHER THE PATIENT HAS A PULSE OR NOT
1. Pulseless VT - follow advanced life support algorithm
2. Unstable VT - reduced cardiac output
-NOTE: VF and pulseless VT require defibrillation (unsynchronised), but other VTs can be treated with synchronised cardioversion
- DC cardioversion
3. Stable VT- IV amiodarone (if fails, DC cardiovert)
4. Torsades de pointes- IV magnesium sulfate
5. Implantable Cardioverter Defibrillator (ICD)
ICD is considered if:
● Sustained VT causing syncope
● Sustained VT with ejection fraction < 35%
● Previous cardiac arrest due to VT or VF
● MI complicated by non-sustained VT
63
Identify possible complications of ventricular tachycardia
● Congestive cardiac failure
● Cardiogenic shock
● VT may deteriorate into VF
64
Summarise the prognosis of ventricular tachycardia
● GOOD if treated RAPIDLY
● Long-term prognosis depends on the underlying cause
65
What is ventricular fibrillation?
- Irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death
- Ventricular fibres contract randomly causing complete failure of ventricular function, most cases occur in patients with underlying heart disease
● MEDICAL EMERGENCY
66
Explain the aetiology/risk factors of ventricular fibrillation
● The ventricular fibres contract randomly causing complete failure of ventricular function
● Most cases occur in patients with underlying heart disease
● Risk Factors:
o Coronary artery disease – most common
o AF
o Hypoxia
o Ischaemia
o Pre-excitation syndrome
o Cardiomyopathy
o Drugs
o Electrolyte imbalance
67
Summarise the epidemiology of ventricular fibrillation
● The MOST COMMON arrhythmia identified in cardiac arrest patients
● Incidence of VF parallels the incidence of ischaemic heart disease
68
Recognise the presenting symptoms and signs of ventricular fibrillation
1. History of:
o Chest pain
o Fatigue
o Palpitations
2. There may be known pre-existing conditions:
o Coronary artery disease
o Cardiomyopathy
o Valvular heart disease
o Long QT syndrome
o Wolff-Parkinson-White syndrome
o Brugada syndrome
69
Identify appropriate investigations for ventricular fibrillation
1. ECG: chaotic irregular deflections of varying amplitude, no identifiable P waves/QRS complexes/T waves
2. Cardiac enzymes (e.g. troponins) - check for recent ischaemic event
3. Electrolytes - derangement can cause arrhythmias, including VF
4. Drug levels and toxicology screen - anti-arrhythmics can (ironically) cause arrhythmia, as can various recreational drugs (e.g. cocaine)
5. TFTs - hyperthyroidism can cause tachyarrhythmias
6. Coronary angiography - if patient survives VF, to check the integrity of coronary arteries
70
Generate a management plan for ventricular fibrillation
● VF requires urgent defibrillation and cardioversion 🡪 non-synchronised DC shock
● Patients who survive need full assessment of left ventricular function, myocardial perfusion and electrophysiological stability
● Most survivors will need an implantable cardioverter defibrillator (ICD)
● Empirical beta-blockers
● Some patients may be treated with radiofrequency ablation (RFA)
71
Identify possible complications of ventricular fibrillation
● Ischaemic brain injury due to loss of cardiac output
● Myocardial injury
● Post-defibrillation arrhythmias
● Aspiration pneumonia
● Skin burns
● Death
72
Summarise the prognosis for patients with ventricular fibrillation
● Depends on the time between onset of VF and medical intervention
● Early defibrillation is essential (ideally within 4-6 mins)
● Anoxic encephalopathy is a major outcome of VF
73
When is warfarin contraindicated?
Warfarin has several contraindications and clinical considerations for its use. Bleeding tendencies associated with any of the following: Active ulceration or overt bleeding of the gastrointestinal, genitourinary, or respiratory tract. Central nervous system hemorrhage.
