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Cardiology > Cardiac arrhythmias > Flashcards

Cardiac arrhythmias Flashcards

1
Q

Causes of sinus tachycardia?

A

Anxiety, fever, pain,

hypovolaemia, catecholamines, thyrotoxicosis, CHF, myocardial disease, anaemia, shock

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2
Q

Causes of bradycardia?

A

Vagal stimulation, raised ICP, hypothyroidism, hypothermia, hypoxia, hyperkalaemia, drugs eg B-blockers

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3
Q

What is a sinus pause and causes?

A

Sinus node pacemaker momentarily ceases activity (Sinus arrest is longer, and escape beats are present from other pacemakers)

  • Increased vagal tone, hypoxia, sick sinus syndrome, digitalis toxicity
  • less than 2 seconds is normal
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4
Q

What rhythms originate in the atrium?

A
  1. Premature atrial contraction- benign
  2. Wandering atrial pacemaker- benign
  3. Ectopic (autonomic) atrial tachycardia-
    - —risk of cardiomyopathy, needs ablation therapy
  4. Multifocal atrial tachycardia
    - – 3 or more distinct p waves
  5. Atrial flutter
  6. Atrial fibrillatio
  7. Supraventricular tachycardia
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5
Q

What is the difference on ECG between sinus and atrial rhythms?

A
  1. Abnormal p waves. Axis or number of P waves per QRS
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6
Q

What is the important feature in atrial flutter?

A

Ventricular rate determines cardiac output. If too high can lead to heart failure.
Other complications- thromboembolic events, syncope, chest pain

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7
Q

What are the options for treating atrial flutter acutely?

A
  1. Adenosine to block AV conduction (doesn’t stop flutter)
  2. Synchronized DC cardioversion
  3. Transoesophageal atrial overdrive pacing
  4. Amiodarone and procainamide
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8
Q

What are the principles of managing Atrial flutter and fibrillation?

A
  1. Acute conversion
  2. Decrease risk of thromboembolism (TOE/Warfarin)
  3. Rate control- Ca blockers or propanolol
  4. Prevent recurrence: Antiarrhythmic drugs being careful of anticholinergic effects of class 1A
  5. Radiofrequency ablation in refractory cases
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9
Q

What are the two mechanisms of SVT?

A
  1. Re-entry (majority)

2. Automaticity. Eg atrial ectopic tachycardia, and junctional ET

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10
Q

What characterizes rhythms starting in the AV node?

A
  1. P wave is absent or inverted and follows the QRS
  2. QRS is usually normal

Only the lower NH part of the AV node has pacemaker ability. The upper and middle delay the conduction

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11
Q

What are the types of AV node rhythms?

A
  1. Junctional/Nodal premature beats. Normal QRS (-) P wave
  2. Junctional/ Nodal escape beats- When SA impulse fails
  3. Junctional/Nodal rhythm- No/inverted Ps, 40-60 beats
  4. Accelerated Nodal rhythm- No/inverted Ps, 60-120
  5. Junctional ectopic tachycardia- Post op/congenital. Loss of AV synchrony and impaired cardiac function. 35% mortality

(Consider Digitalis toxicity)

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12
Q

What are the types of rhythms originating in the ventricle?

A
  1. PVC
  2. Accelerated ventricular rhythm- benign
  3. Ventricular Tachycardia
  4. Ventricular fibrillation
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13
Q

How to distinguish ventricular rhythms on ECG

A
  1. Bizarre and wide QRS complexes
  2. T waves point in opposite directions to QRS
  3. QRS randomly related to P waves, if visible
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14
Q

When should you care about PVCs?

A
  1. Associated with underlying heart disease
  2. History of syncope or FHx or sudden death
  3. Precipitated or exacerbated by activity
  4. Multiform (differing foci), esp couplets
  5. Runs of PVCs with symptoms
  6. Incessant/frequent episodes of paroxysmal VT (myocardial tumour)
    * 3 or more successive PVCs called VT
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15
Q

What are the causes of VT (and VF)?

A
  1. Structural heart disease (TOF, AS, hypertrophy/dilation, MVP)
  2. Post-operative CHDs
  3. Myocarditis, CMPs, Chagas, myocardial tumours, ischaemia
  4. Pulmonary hypertension
  5. Arrhythmogenic RV dysplasia/Brugada and LQTS
  6. Metabolic- Hypoxia, acidosis, hyper/hypokalaemia, low Mg
  7. Mechanical irritation from catheter
  8. Pharmacological: Dig, coke, OPP, class 1A, 1C, and 3 antiarrhythms
  9. Drugs that prolong QT
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16
Q

What are the complications of VT?

A
  1. Sudden death (arrhythmogenic RV dysplasia, hypertrophic and dilated CMP, genetic electrical heart diseases)
  2. Decreased cardiac output and deterioration into VF
  3. Tachycardia-mediated cardiomyopathy
  4. Polymorphic VTs worse than monomorphic
  5. Structurally abnormal hearts more at risk
  6. Exercise induced VTs (as opposed to suppressed) more significant
17
Q

How is VT treated acutely?

A
  1. Synchronized DC cardioversion if haemodynamically unstable
  2. Lignocaine bolus
  3. Amiodarone
  4. MgSO4 for torsades de pointes
  5. Adenosine trial in structurally normal hearts
18
Q

What are the types of congenital long QT sydrome?

A
  1. Jervell and Lange- Nielson. AR, + deafness, syncope and death.
  2. Roman- Ward syndrome; AD, no deafness
  3. Sporadic RWS
  4. Anderson-Tawil and Timothy syndromes
19
Q

What are some causes of acquired QT prolongation?

A
  1. Drugs
  2. Electrolyte abnormalities
  3. Bradycardia: AV block, SSS
  4. Myocardial dysfunction: Anthracyclin, CHF, myocarditis
  5. Endocrineopathies: High PTH, low T4, pheochromocytoma
  6. Neurological: Encephalitis, head trauma, SAH, CVA
  7. Nutritional: Alchololism, anorexia nervosa, starvation
20
Q

Why is prolonged QT bad?

A

Prolonged recovery from electrical excitation increases risk of dispersion of refractoriness with some parts not responding to the next depolarisation. Consequently, the wave of excitation follows a pathway around a focal point leading to circus re-entry and VT.

21
Q

What drugs should be avoided in WPW SVT and why?

A

Digoxin and Verapamil, may increase rate of anterograde conduction of the impulse through the accessory pathway

22
Q

What clinical features are present in LQTS?

A
    • FHx in 60%
  2. Present with syncope, sz, cardiac arrest, presyncope, palpitations
  3. Usually during exertion (symptoms related to Ventricular arrhythmia)
  4. Syncope in context of intense adrenergic arousal, emotion, exercise
    - - Swimming especially and abrupt loud noises.
23
Q

ECG features in LQTS?

Which are risk factors for sudden death?

A
  1. Prolonged QTc: usually >0.46 sec
  2. Abnormal T-wave morphology (bifid, diphasic, notched)
  3. Bradycardia (20%), second degree AV block, multiform PVCs, monomorphic or polymorphic VTs are risk factors for sudden death
24
Q

What is the preferred lead to measure QTc?

A

Lead II as q wave is usually present (V1, 3, 5 also good with better T wave definition)

25
Q

How is QT measured in prolonged QRS duration?

A

JT interval, normal JT is 0.32-0.34

26
Q

What is the diagnostic strategy for LQTS?

A
  1. History of presyncope, syncope, seizure, palpitation and FHx
  2. Exclude causes of acquired LQTS
  3. Examine ECG for QTc and T wave morphology. (and family)
  4. LQTS score calculated. (Schwartz)
  5. > 4 = LQTS,
27
Q

What are some general measures for managing LQTS

A
  1. Avoid prescribing meds that can prolong QT
  2. Educate parents on these drugs. qtdrugs.org
  3. Avoid catecholamines and sympathomimetics –> Torsades
  4. No competitive sports, and no swimming
  5. Remove alarm clocks and bedside phones.
  6. Educate against non-compliance
  7. Beta blockers
  8. Cardiac pacemaker
  9. ICD
28
Q

Features of Brugada?

A

Mutation in sodium channel
Ventricular tachyarrhythmias during sleep
Autosomal dominant, in south east asian men
Mean age of death 40yrs
ECG: concave ST elevation and J point elevation with a negative T wave in right precordial leads and RBBB
Fever precipitates syncope
Don’t respond to beta blockers
ICD

29
Q

What is the difference between Mobitz I & II 2nd degree AV block?

A

A. 1 PR progressively prolonged until one QRS dropped, 2 AV conduction is normal or completely blocked
B. 1 is at level of AV node, 2 is below
C. 1 rarely progresses to heart block, 2 does (Stokes- Adams attack)
Same causes. Healthy or myocarditis, CMP, infarction, CHD, surgery, digitalis

30
Q

What is the definition and significance of high grade AV block?

A

When 2 or more P waves are not conducted
Usually at bundle of His +/- AV nodal block.
May progress to CHB

31
Q

What are the causes of CHB?

A
  1. Congenital: In abscence of CHD, 60-90 % due to neonatal lupus eythematosus. Maternal Abs cross placenta. CHD 25-33%
  2. Acquired: Cardiac surgery, severe myocarditis, lyme carditis, ARF, mumps, diphtheria, CMPs, tumours, infarction and drugs.
32
Q

What is required for sinus rhythm on ECG?

A
  1. P wave preceding each QRS

2. P axis between 0 and + 90 degrees.

Cardiology (13 decks)

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