arrythmias

Question 1

What are the features of left bundle branch block?

Answer 1

LBBB is: - almost always pathological - wide QRS (indicating prolonged ventricular depolarisation) - M pattern in V5

Question 2

Name some causes of LBBB?

Answer 2

1) IHD 2) LVH 3) Aortic valve disease 4) Cardiomyopathy 5) Myocarditis

Question 3

What is the characteristic ECG abnormality in right bundle branch block?

Answer 3

RSR pattern in V1 MaRRoW - majority of the QRS complex lies above the isoelectric line in lead 1 and below the line in lead 6

Question 4

Name some causes of RBBB?

Answer 4

1) Normal variant 2) RVH/ RV strain (e.g. PE) 3) IHD 4) Congenital heard disease (e.g. ASD) 5) Myocarditis

Question 5

What are the features of right ventricular hypertrophy on ECG?

Answer 5

1) Right axis deviation 2) Positive right wave in V1 Causes of RVH are: - Mitral valve disease - Pulmonary hypertension - Pulmonary stenosis - PE - Fallot’s tetralogy - Cor pulmonale

Question 6

What are the causes of low voltage complexes on ECG?

Answer 6

1) Dextrocardia 2) Pericardial effusion 3) COPD 4) Hypothyroidism 5) Cardiomyopathy

Question 7

Name some causes of a short PR interval?

Answer 7

1) WPW syndrome 2) Lown-Ganong-Lavine syndrome 3) P wave followed by ventricular ectopics

Question 8

What conditions are associated with a long PR interval

Answer 8

1) IHD 2) Digoxin toxicity 3) Hypokalaemia 4) Rheumatic fever 5) Lyme disease 6) Myotonic dystrophy

Question 9

What is the prolonged QT syndrome?

Answer 9

The QT interval is increased and this is associated with delayed repolarisation of the ventricles. It is associated with syncope and ventricular tachycardia and death (especially from polymorphic VT).

Question 10

What causes prolonged QT syndrome?

Answer 10

) Familial (90%) - Romano- Ward syndrome (autosomal dominant, no deafness) - Jervell-Lang-Neilson syndrome (autosomal recessive; includes deafness; caused by abnormal potassium channel) 2) IHD 3) Metabolic - HYPOcalcaemia - HYPOkalaemia -HYPOmagnesaemia 4) Drugs - erythromycin - amiodarone - terfenadine (non sedating antihistamine)

Question 11

What causes ST depression?

Answer 11

Myocardial ischaemia (including posterior MI) Digoxin therapy LVH with strain

Question 12

What causes ST elevation?

Answer 12

Pericarditis Hyperkalaemia Coronary artery spasm (variant/ Prinzmetals angina) Left ventricular aneurysm MI

Question 13

What are the causes of pulseless electrical activity (PEA)?

Answer 13

4Hs and 4Ts - Hypo-or Hyperkalaemia - Hypothermia - Hypovolaemia - Hypoxia - Cardiac Tamponade - Tension pneumothorax - Pulmonary thromboembolus - Drug/ Toxin overdose Others include aortic dissection and MI.

Question 14

What are the two main types of arrhythmia?

Answer 14

Bradycardia - the heart rate is slow (100bpm). Tachycardias are more likely to be symptomatic if they are fast and sustained. They are divided into supraventricular (SVT), which arise from the atrium or atrioventricular junction, and ventricular tachycardias which arise from the ventricles

Question 15

What are the general principles of arrhythmia management?

Answer 15

Patients with adverse symptoms and signs (low cardiac output with cold clammy extremities, hypotension, impaired consciousness, or severe pulmonary oedema) require urgent treatment for their arrhythmia. Oxygen is given to all patients, IV access is established and serum electrolyte abnormalities are corrected.

Question 16

What are the causes of sinus bradycardia?

Answer 16

Athleticism Drugs - e.g. beta blockers, digoxin, verapamil MI (especially inferior) Increased vagal tone - e.g. vomiting Hypothyroidism Hypothermia Sinus node disease Raised intracranial pressure

Question 17

How is symptomatic bradycardia treated?

Answer 17

Patients with persistent symptomatic bradycardia are treated with a permanent cardiac pacemaker. First line treatment in the acute setting with adverse signs is atropine (500 micro grams i.v. repeated to a maximum of 3mg but contra indicated in myasthenia gravis and paralytic ileus). Temporary pacing is an alternative.

Question 18

What is sick sinus syndrome? What are the ECG features?

Answer 18

Bradycardia is caused by intermittent failure of sinus node depolarisation (sinus arrest) or failure of the sinus impulse to propagate through the perinodal tissue to the atria (sinoatrial block). The slow heart rate predisposes to ectopic pacemaker activity and tachyarrhythmias are common (tachy-brady syndrome). The ECG shows severe sinus bradycardia or intermittent long pauses between consecutive P waves (>2s, dropped p wave). Permanent pacemaker insertion is indicated in symptomatic patients. Thromboembolism is common in sinus node dysfunction and patients are anticoagulated unless there is a contraindication.

Question 19

What is heart block?

Answer 19

common causes of heart block are coronary artery disease, cardiomyopathy, and particularly in the elderly, fibrosis of the conduction tissue. Block in either the AV node or His bundle results in atrioventricular block, whereas block lower in the conduction system produces right or left bundle branch block.

Question 20

What are the features of first degree heart block?

Answer 20

n first degree there is prolonged PR interval (>0.22s). No change in heart rate occurs and treatment is unnecessary. It is caused by delayed atrioventricular conduction.

Question 21

What are the features of second degree heart block?

Answer 21

) Mobitz type I (Wenckebach block phenomenon) - successive increasing PR interval until a P wave is not conducted (i.e. absent QRS complex after a P wave) - PR interval returns to normal and cycle repeats itself ii) Mobitz type II - unpredictable failure to conduct p waves - often progresses to complete heart block - usually requires a permanent pacemaker

Question 22

What is complete heart block

Answer 22

There is no association between atrial and ventricular activity; P waves and QRS complexes occur independently of one another. Ventricular contractions are maintained by a spontaneous escape rhythm originating from a site below the block: 1) His bundle - which gives rise to a narrow complex QRS at a rate of 50-60bpm and is relatively stable. Recent onset block due to transient causes, e.g. ischaemia, may respond to i.v. atropine without the need for pacing. Chronic narrow complex AV block usually requires permanent pacing 2) His-Purkinje system (i.e. distally) - gives rise to a broad QRS complex, is slow, unreliable and often associated wit dizziness and blackouts (Stokes-Adams attack). Permanent pacemaker insertion is indicated

Question 23

What are supraventricular tacchycardias?

Answer 23

sinus tachycardia - atrioventricular junctional tachycardias - atrial tachyarrhythmias (atrial fibrillation, atrial flutter, atrial ectopics) (Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT)

Question 24

What causes sinus tachycardia?

Answer 24

exercise and excitement. It also occurs in fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, and drugs (e.g. catecholamines, and atropine). Treatment is aimed at correcting the underlying cause. If necessary beta blockers may be used to slow the sinus rate, e.g. hyperthyroidism.

Question 25

What are atrioventricular junctional tachycardias?

Answer 25

In these cases, tachycardia arises as a result of re-entry circuits in which there are two separate pathways for impulse conduction. They are usually referred to as paroxysmal SVTs and are often seen in young patients with no evidence of structural heart disease. The two forms are: i) atrioventricular nodal re-entry tacchycardia (AVNRT) ii) atrioventricular reciprocating tachycardia (AVRT)

Question 26

What are the features of AVNRT?

Answer 26

AVNRT is the commonest type of SVT. It is due to the presence of a ring of conducting pathway in the atrioventricular node of which the “limbs” have different conduction times and refractory periods. This allows a re-entry circuit and an impulse to produce a circus movement tachycardia

Question 27

What causes atrioventricular reciprocating tachycardia (AVRT)?

Answer 27

AVRT is due to the presence of an accessory pathway that connects the atria and ventricles and is capable of anterograde or retrograde conduction, or in some cases both. Wolff-Parkinson-White syndrome is the best known type of AVRT in which there is an accessory pathway (bundle of Kent) between atria and ventricles.

Question 28

What are the symptoms of paroxysmal SVT?

Answer 28

rapid regular palpitations usually with abrupt onset and sudden termination. Other symptoms are dizziness, dyspnoea, central chest pain and syncope. Exertion, coffee, tea or alcohol may aggravate the arrhythmia.

Question 29

How should acute paroxysmal SVT be treated?

Answer 29

Unstable patient - emergency electrical cardioversion is required in patients whose arrhythmia is accompanied by adverse symptoms and signs Haemodynamically stable: - increase vagal stimulation of the sinus node by the Valsalva manouvre (ask the patient to blow into a 20mL syringe with enough force to push back the plunger) or right carotid sinus massage (contraindicated in the presence of carotid bruit) - i.v. adenosine 6mg –> 12 mg –> 12 mg; contraindicated in asthmatics, verapamil is the preferred choice

Question 30

What is the long term management of patients with paroxysmal SVT?

Answer 30

Radiofrequency ablation of the accessory pathway via a cardiac catheter is successful in about 95% of cases. Flecainide, verapamil, sotalol and amiodarone are the drugs most commonly used.

Question 31

What are the different types of AF?

Answer 31

first detected episode (irrespective of whether it is symptomatic or self-terminating) - recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days -in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate.

Question 32

What are the signs and symptoms of AF?

Answer 32

Symptoms: - palpitations -dyspnoea - chest pains Signs: - irregularly irregular pulse

Question 33

How should AF in a haemodynamically unstable patient be managed?

Answer 33

When AF is caused by an acute precipitating event, such as alcohol toxicity, chest infection or hyperthyroidism, the underlying cause should be treated. If the patient is unstable, give immediate heparinization and attempted cardioversion with a synchronized DC shock. If cardioversion fails or AF recurs, intravenous amiodarone is given before a further attempt at cardioversion. A second dose of amiodarone can be given.

Question 34

What are the options for long term management of stable patients in AF?

Answer 34

NICE advocate using a rate control strategy except in a number of specific situations such as coexistent heart failure, first onset AF or where there is an obvious reversible cause.

Question 35

How are patients rate controlled in AF?

Answer 35

A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line to control the rate in AF. If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following: a beta blocker diltiazem digoxin (preferred choice if patient also has heart failure)

Question 36

What patients should be rhythm controlled in AF?

Answer 36

Rhythm control is generally appropriate in younger patients (i.e. < 65 years of age), patients who are highly symptomatic, patients who also have congestive heart failure, and individuals with recent onset AF (< 48 h). Conversion to sinus rhythm is achieved by electrical DC cardioversion and then administration of β-blockers to sup- press the arrhythmia. Other agents used depend on the presence (use amiodarone) or absence (sotalol, ecainide, propafenone) of under- lying heart disease.

Question 37

How should patients with AF be assessed for anticoagulation?

Answer 37

Clinicians use risk stratifying tools such as the CHA2DS2-VASc score to determine the most appropriate anticoagulation strategy. Score of 0 = no treatment needed Score of 1 = Males: Consider anticoagulation Females: No treatment (this is because their score of 1 is only reached due to their gender) Score of 2 or more = offer anticoagulation (either warfarin or NOAC)

Question 38

What are the NICE recommendations for managing patients with AF who develop a stroke?

Answer 38

Following a stroke or TIA warfarin should be given as the anticoagulant of choice. Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities. In acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

Question 39

What is atrial flutter?

Answer 39

Atrial flutter is associated with AF. The atrial rate is typically 300 beats/min and the AVN usually conducts every second flutter beat, giving a ventricular rate of 150 beats/ min. The ECG characteristically shows a “sawtooth” appearance (flutter, “F” waves) which are most clearly seen when AV conduction is transiently impaired by carotid sinus massage or drugs.

Question 40

How is atrial flutter managed?

Answer 40

Management is similar to that of atrial fibrillation although medication may be less effective. Atrial flutter is more sensitive to cardioversion however so lower energy levels may be used. Radiofrequency ablation of the tricuspid valve isthmus is curative for most patients.

Question 41

What are the causes of ventricular tachyarythmias?

Answer 41

MI or chronic IHD Myocarditis Cardiomyopathy Hyper or hypokalaemia Left ventricular aneurysm Prolonged QT interval Rhythm types include ventricular extrasystoles, VT, VF and long QT syndrome.

Question 42

What is sustained ventricular tachycardia?

Answer 42

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are usually associated with underlying heart disease. The ECG in sustained VT (>30s) shows a rapid ventricular rhythm with broad abnormal QRS complexes. Supraventricular tachycardia with bundle branch block also produces a broad complex tachycardia which can usually be differentiated from VT on ECG criteria. However, the majority of broad complex tachycardias are VT and if in doubt treat as such. Urgent DC cardioversion is necessary if the patient is haemodynamically compromised.

Question 43

What drug should not be used in VT?

Answer 43

Verapimil

Question 44

What is non sustained VT?

Answer 44

This is defined as VT >5 consecutive beats but lasting <30s. It is common in patients with heart disease (and a few individuals with normal hearts). The treatments indicated are beta blockers in symptomatic patients or an ICD in patients with poor left ventricular function (EF <30%) in whom it improves survival.

Question 45

What is ventricular fibrillation?

Answer 45

This is a very rapid and irregular ventricular activation with no mechanical effect and hence no cardiac output. The patient is pulseless and becomes rapidly unconscious and respiration ceases (cardiac arrest). Treatment is with immediate defibrillation. Survivors of VF are, in the absence of identifiable reversible cause (e.g. during the first few days post MI, severe metabolic disturbance) at high risk of sudden death and treatment is with an ICD.

Question 46

What are the non shockable rhythms?

Answer 46

PEA (pulseless electrical activity) and asystole