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Cardiovascular > Cardiac arrhythmias > Flashcards

Cardiac arrhythmias Flashcards

1
Q

What symptoms may arrhythmias cause?

A

sudden death, syncope, heart failure, chest pain, dizziness, palpitations or no symptoms at all

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2
Q

How is the rate of sinus node discharge modulated?

A

The autonomic nervous system

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3
Q

What is sinus arrhythmia?

A

Fluctuations of autonomic tone result in phasic changes of the sinus discharge rate. During inspiration, parasympathetic tone falls and the heart rate quickens; on expiration, the heart rate falls. This variation is normal, particularly in children and young adults. Typically, sinus arrhythmia results in predictable irregularities of the pulse.

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4
Q

What is sinus bradycardia?

A

A sinus rate of <60 b.p.m. during the day or <50 b.p.m. at night is known as sinus bradycardia. It is usually asymptomatic unless the rate is very slow. Sinus bradycardia is normal in athletes owing to increased vagal tone.

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5
Q

What are the common extrinsic causes of sinus bradycardia?

A
  • hypothermia, hypothyroidism, cholestatic jaundice and raised intracranial pressure
  • drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs
  • neurally mediated syndromes
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6
Q

What are the common intrinsic causes of sinus bradycardia?

A
  • acute ischaemia and infarction of the sinus node (as a complication of acute myocardial infarction)
  • chronic degenerative changes, such as fibrosis of the atrium and sinus node (sick sinus syndrome)
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7
Q

What causes sick sinus syndrome (sinoatrial disease)?

A

It is usually caused by idiopathic fibrosis of the sinus node. Other causes of fibrosis, such as ischaemic heart disease, cardiomyopathy or myocarditis, can also cause the syndrome.

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8
Q

What are neutrally mediated syndromes in reference to arrhythmias?

A

Neurally mediated syndromes are due to a reflex (called Bezold–Jarisch) that may result in both bradycardia (sinus bradycardia, sinus arrest and AV block) and reflex peripheral vasodilatation. These syndromes usually present as syncope or pre-syncope (dizzy spells).

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9
Q

What is carotid sinus syndrome?

A

It occurs in the elderly and mainly leads to bradycardia. Syncope occurs

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10
Q

What is neurocardiogenic (vasovagal) syncope (syndrome)?

A

It usually presents in young adults but may present for the first time in elderly patients. It results from a variety of situations (physical and emotional) that affect the autonomic nervous system. The efferent output may be predominantly bradycardic, predominantly vasodilatory or mixed.

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11
Q

What is postural orthostatic tachycardia syndrome?

A

It is a sudden and significant increase in heart rate associated with normal or mildly reduced blood pressure and produced by standing. The underlying mechanism is a failure of the peripheral vasculature to constrict appropriately in response to orthostatic stress, which is compensated by an excessive increase in heart rate.

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12
Q

How is sinus bradycardia managed?

A

The management of sinus bradycardia is first to identify and then, if possible, to remove any extrinsic causes. Temporary pacing may be employed in patients with reversible causes until a normal sinus rate is restored, and in patients with chronic degenerative conditions until a permanent pacemaker is implanted.

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13
Q

How is chronic symptomatic sick sinus syndrome managed?

A

Chronic symptomatic sick sinus syndrome requires permanent pacing (DDD), with additional antiarrhythmic drugs (or ablation therapy) to manage any tachycardic element. Thromboembolism is common in tachy–brady syndrome and patients should be anti­coagulated unless there is a contraindication.

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14
Q

A patient presents with carotid sinus hypersensitivity, where the symptoms are reproduced by a cardiac massage and life-threatening causes of syncope have been excluded. What will be beneficial for them?

A

Pacemaker implantation

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15
Q

What are the treatment options in vasovagal attacks?

A
  • avoidance, if possible, of situations known to cause syncope in a particular patient, and sitting/lying down and applying counter-pressure manœuvres (pushing the palms together or crossing the legs) if an attack threatens
  • Increased salt intake, compression of the lower legs with hose, and drugs such as beta-blockers, alpha-agonists (e.g. midodrine) or myocardial negative inotropes (e.g. disopyramide) may be helpful.
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16
Q

What is helpful for patients with “malignant” neorocariogenic syncope (syncope associated with injuries and demonstrated asystole)?

A

Permanent pacemaker therapy. These patients benefit from dual-chamber pacemakers with a feature called ‘rate drop response’, which, once activated, paces the heart at a fast rate for a set period of time in order to prevent syncope.

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17
Q

What is first-degree heart block?

A

This is a simple prolongation of the PR interval to >0.22 s. Every atrial depolarization is followed by conduction to the ventricles but with delay

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18
Q

What is second-degree heart block?

A

This occurs when some P waves conduct and others do not. There are several forms:
• Mobitz I block (Wenckebach block phenomenon) is progressive PR interval prolongation until a P wave fails to conduct. The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave.
• Mobitz II block occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation. Usually, the QRS complex is wide (>0.12 s).
• 2 : 1 or 3 : 1 (advanced) block occurs when every second or third P wave conducts to the ventricles. This form of second-degree block is neither Mobitz I nor II.

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19
Q

What is a Wenckebach AV block generally due to?

A

A block in the AV node

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20
Q

What is a Mobitz II block generally due to?

A

A block at an infra-nodal level, such as the His bundle

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21
Q

True or false? Acute myocardial infarction may produce first-degree heart block?

A

False: It may produce second-degree heart block

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22
Q

In anterior myocardial infarction, what second-degree heart block associated with?

A

A high risk of progression to complete heart block (temporary pacing followed by permanent pacemaker implantation is usually indicated)

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23
Q

What is third degree (complete) AV block?

A

Complete heart block occurs when all atrial activity fails to conduct to the ventricles. In patients with complete heart block, the aetiology needs to be established. In this situation, life is maintained by a spontaneous escape rhythm.

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24
Q

What should one look for when assessing a patient with complete heart block?

A

Are there signs of haemodynamic compromise?

  • chest pain
  • breathlessness
  • poor urine output
  • impaired consciousness (AVPU: Alert, responds to Voice, responds to Pain, Unresponsive), often governed by the blood pressure:
  • hypertensive: compensating … for now
  • hypotensive: needs urgent intervention

Is there a reversible cause?

  • beta-blocker, a calcium-channel blocker, digoxin overdose
  • disturbed acid-base and electrolyte imbalance.

If the patient is currently stable, what is the escape rhythm like?

  • narrow-complex and relatively normal in rate
  • broad- complex and very slow.
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25
Q

What can be done to support a patient with third-degree AV block?

A

Supportive adjuncts during this time can be a reversal of toxins/drugs, support with vasopressors (e.g. adrenaline (epinephrine)), attempts to speed the sinus rate with isoprenaline and temporary pacing, either transcutaneously or transvenously.

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26
Q

What are the reversible causes of complete heart block?

A

· Drugs
· Autoimmune or infectious conditions if treated promptly without permanent myocardial fibrosis
· Acute myocardial infarction
· Immediate post-cardiac surgery

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27
Q

What are the non-reversible causes of heart block?

A 
· Ischaemic cardiomyopathy (consider implantable cardioverter-defibrillator and biventricular device)
· Structural heart disease
· Progressive neurological conditions
· Iatrogenic causes
· Biventricular device
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28
Q

What are the congenital causes of complete heart block?

A
  • Autoimmune (e.g. maternal SLE)

* Structural heart disease (e.g. transposition of great vessels)

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29
Q

What are the idiopathic causes of complete heart block?

A
  • Lev’s disease (progressive fibrosis of distal His–Purkinje system in elderly patients)
  • Lenegre’s disease (proximal His–Purkinje fibrosis in younger patients)
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30
Q

What are the causes of ischaemic heart disease that can cause complete heart block?

A
  • Acute myocardial infarct

* Ischaemic cardiomyopathy

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31
Q

What are the non-ischaemic heart disease causes of complete heart block?

A
  • Calcific aortic stenosis
  • Idiopathic dilated cardiomyopathy
  • Infiltrations (e.g. amyloidosis, sarcoidosis, neoplasia)
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32
Q

What types of cardiac surgery can cause complete heart block?

A

Following aortic valve replacement, CABG, VSD repair

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33
Q

What are the iatrogenic causes of complete heart block?

A

Radiofrequency AV node ablation and pacemaker implantation

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34
Q

Give examples of drugs that can cause complete heart block

A

Digoxin, beta-blockers, non-dihydropyridine calcium-channel blockers, amiodarone

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35
Q

What infections can cause complete heart block?

A
  • Endocarditis
  • Lyme disease
  • Chagas’ disease
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36
Q

Give examples of autoimmune conditions that can cause complete heart block

A

SLE, rheumatoid arthritis

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37
Q

Give an example of a neuromuscular disease that can cause complete heart block

A

Duchenne muscular dystrophy

38
Q

Where would the block lie in a narrow-complex escape rhythm?

A

It implies that it originates in the His bundle and therefore that the region of the block lies more proximally in the AV node.

39
Q

What is the treatment of narrow-complex escape rhythm?

A

Treatment depends on the aetiology. Recent-onset, narrow-complex AV block that has transient causes may respond to intravenous atropine, but temporary pacing facilities should be available for the management of these patients. Chronic narrow-complex AV block requires permanent pacing (dual-chamber) if it is symptomatic or associated with heart disease. Pacing is also advocated for isolated, congenital AV block, even if asymptomatic.

40
Q

Where would the block lie in a broad-complex escape rhythm?

A

It implies that the escape rhythm originates below the His bundle and therefore that the region of the block lies more distally in the His–Purkinje system.

41
Q

What is the aetiology of broad-complex escape rhythm?

A

In the elderly, it is usually caused by degenerative fibrosis and calcification of the distal conduction system (Lev’s disease). In younger individuals, a proximal progressive cardiac conduction disease due to the inflammatory process is known as Lenegre’s disease. Sodium channel abnormalities have been identified in both syndromes. Broad-complex AV block may also be caused by ischaemic heart disease, myocarditis or cardiomyopathy.

42
Q

What is the management of broad-complex escape rhythm?

A

Permanent pacemaker implantation is indicated, as pacing considerably reduces the mortality. Because ventricular arrhythmias are not uncommon, an implantable cardioverter-defibrillator (ICD) may be indicated in those with severe left ventricular dysfunction (>0.30 s duration).

43
Q

What is a bundle branch conduction delay?

A

This produces slight widening of the QRS complex (up to 0.11 s). It is known as an incomplete bundle branch block.

44
Q

What is a complete block of a bundle branch?

A

This is associated with a wider QRS complex (≥0.12 s). The shape of the QRS depends on whether the right or the left bundle is blocked

45
Q

What does a right bundle branch block look like on ECG?

A

It produces late activation of the right ventricle. This is seen as deep S waves in leads I and V6, and as a tall late R wave in lead V1 (late activation moving towards right-sided leads and away from left-sided leads).

46
Q

What does a left bundle branch block look like on ECG?

A

produces the opposite of the right: a deep S wave in lead V1 and a tall late R wave in leads I and V6. Because left bundle branch conduction is normally responsible for the initial ventricular activation, left bundle branch block also produces abnormal Q waves.

47
Q

What is a hemiblock?

A

Delay or block in the divisions of the left bundle branch produces a swing in the direction of depolarization (electrical axis) of the heart. When the anterior division is blocked (left anterior hemiblock), the left ventricle is activated from inferior to superior.

48
Q

What would hemiblock look like on an ECG?

A

It produces a superior and leftward movement of the axis (left axis deviation). Delay or block in the postero-inferior division swings the QRS axis inferiorly to the right (right axis deviation).

49
Q

What is a bifascicular block?

A

It is a combination of a block of any two of the following: the right bundle branch, the left antero-superior division and the left postero-inferior division. Block of the remaining fascicle will result in complete AV block.

50
Q

What are the clinical features of bundle branch blocks?

A
  • Usually asymptomatic
  • Right bundle: wide but physiological splitting of the second heart sound
  • Left bundle: may cause reverse splitting of the second sound
  • Patients with intraventricular conduction disturbances may complain of syncope
51
Q

What is the aetiology of right bundle branch blocks?

A
  • occurs as an isolated congenital anomaly or is associated with cardiac or pulmonary conditions
  • can be a normal finding in about 5% of individuals
  • Commonly associated conditions: congenital cardiac disorders, such atrial and ventricular septal defects, pulmonary stenosis and Fallot’s tetralogy, pulmonary embolism, pulmonary hypertension, myocardial infarction, fibrosis of conduction tissue and Chagas’ disease
52
Q

What is the aetiology of a combination of both right bundle branch and left bundle branch block?

A

Seen in patients with ostium primum atrial septal defects, but more often signifies diffuse conduction tissue disease affecting the right bundle and the left anterior fascicle

53
Q

What is the aetiology of complete left bundle branch block?

A

Complete left bundle branch block is often associated with extensive left ventricular disease. The most common causes include aortic stenosis, hypertension, myocardial infarction and severe coronary disease, and are similar to those of complete heart block.

54
Q

Where do supraventricular tachycardias arise from?

A

The atrium or the atrioventricular junction

55
Q

What is the most common cause of palpitations in patients with normal hearts?

A

Atrioventricular nodal re-entrant tachycardia (AVNRT)

56
Q

What is the most common tachycardia in patients over 65?

A

Atrial fibrillation

57
Q

What should be suspected in any patient with regular SVT at 150 BPM?

A

Atrial flutter

58
Q

What sort of patients present with atrial tachycardia?

A

Usually occurs in patients with structural heart disease or following extensive ablation within atria

59
Q

What is inappropriate sinus tachycardia and who might have it?

A

Inappropriate sinus tachycardia is a persistent increase in resting heart rate unrelated to, or out of proportion with, the level of physical or emotional stress. It is found predominantly in young women and is not uncommon in health professionals

60
Q

What are the acute causes of sinus tachycardia?

A
  • Exercise
  • Emotion
  • Pain
  • Fever
  • Infection
  • Acute heart failure
  • Acute pulmonary embolism
  • Hypovolaemia
61
Q

What are the chronic causes of sinus tachycardia?

A
  • Pregnancy
  • Anaemia
  • Hyperthyroidism
  • Catecholamine excess
62
Q

How is sinus tachycardia managed?

A

The underlying cause should be found and treated, rather than treating the compensatory physiological response. If necessary, beta-blockers may be used to slow the sinus rate, in hyperthyroidism, for example; ivabradine, an IF (pacemaker current) blocker, may be useful when beta-blockade cannot be tolerated.

63
Q

What induces an atrioventricular nodal re-entrant tachycardia attack?

A

Clinically, the tachycardia often strikes suddenly without obvious provocation, but exertion, emotional stress, coffee, tea and alcohol may aggravate or induce the arrhythmia

64
Q

How does an atrioventricular nodal re-entrant tachycardia attack stop?

A

An attack may stop spontaneously or may continue indefinitely until medical intervention

65
Q

What is the leading symptom of most supraventricular tachycardia?

A

Rapid regular palpitations, usually with an abrupt onset and a sudden termination, which can occur spontaneously or be precipitated by simple movements. A common feature is termination by Valsalva manœuvres. In younger individuals with no structural heart disease, the rapid heart rate can be the main pathological finding

66
Q

Other than rapid regular palpitations, what symptoms can occur in supraventricular tachycardia?

A
  • Anxiety
  • Dizziness
  • Dyspnoea
  • Neck pulsation
  • Central chest pain
  • Weakness
  • Polyuria may occur (especially during AVNRT and atrial fibrillation)
  • Prominent jugular venous pulsations may be observed during atrioventricular nodal re-entrant tachycardia attack (AVNRT)
  • Syncope
67
Q

Why may polyuria occur in supraventricular tachycardia?

A

because of the release of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia

68
Q

Why may prominent jugular venous pulsations be observed in atrioventricular nodal re-entrant tachycardia attack?

A

due to atrial contractions against closed AV valves

69
Q

If a patient presents with supraventricular tachycardia and haemodynamic instability, what is required?

A

Emergency cardioversion

70
Q

If a patient presents with supraventricular tachycardia and is haemodynamically stable, what should be done?

A

vagal manœuvres, including right carotid massage, the Valsalva manœuvre and facial immersion in cold water, can be successfully employed

71
Q

What is the Valsalva manoever?

A

Abrupt voluntary increase in intra-abdominal and intrathoracic pressure by straining.

72
Q

If the physical manoeuvres for supraventricular tachycardia do not work, what should be done?

A

intravenous adenosine (initially 6 mg by i.v. push, followed by 12 mg if needed) should be tried

73
Q

What are the side effects of adenosine?

A
  • bronchospasm
  • flushing
  • chest pain
  • heaviness of the limbs
  • sense of impending doom
74
Q

When is adenosine contraindicated?

A

In patients with a history of asthma

75
Q

What is an alternative to adenosine?

A

verapamil 5–10 mg i.v. over 5–10 min, i.v. diltiazem, or beta-blockers (esmolol, propranolol, metoprolol)

76
Q

When must verapamil not be given?

A

after beta-blockers or if the tachycardia presents with broad (>0.12 s) QRS complexes

77
Q

What pharmacological treatments are there for long term management of supraventricular tachycardia?

A

Verapamil, diltiazem and beta-blockers have proven efficacy in 60–80% of patients. Sodium-channel blockers (flecainide and propafenone), potassium repolarization current blockers (sotalol, dofetilide, azimilide) and the multichannel blocker amiodarone may also prevent the occurrence of tachycardia

78
Q

What non-pharmacological treatments are there for long term management of supraventricular tachycardia?

A

Catheter ablation

79
Q

What are atrial tachyarrhythmias?

A

atrial fibrillation, atrial flutter, atrial tachycardia and atrial ectopic beats, all arise from the atrial myocardium. They share similar aetiologies, of which the most commonly encountered in clinical practice are increasing age, myocardial infarction, hypertension, obesity, diabetes mellitus, hypertrophic cardiomyopathy, heart failure, valvular heart disease, myocarditis, pericarditis, cardiothoracic surgery, electrolyte imbalance, alcohol use, obstructive airway disease, chest infections and hyperthyroidism.

80
Q

What are the cardiac causes of artial tachyarrythmias?

A
  • Hypertension
  • Congestive ehart failure
  • Cornory ehart disease (and myocardial infarction)
  • Valvular heart disease
  • Cardiomyopathy (dilated, hypertrophic)
  • Myocarditis and pericarditis
  • Wolff-Parkinson-White syndrome
  • Sick sinus syndrome
  • Cardiac tunours
  • Cardiac surgery
  • Famillial tachyarrythmia (e.g. lone atrial fibrillation)
  • Genetic presdisposition
81
Q

What are the non-cardiac causes of atrial tachyarrythmias?

A
  • Thyrotoxicosis
  • Phaeochromocytoma
  • Acute and chronic pulmonary disease (pneumonia, chronic obstructive disease)
  • Pulmonary vascular disease (puolmonary embolism)
  • Electrolyte disturbances (hypokalaemia)
  • Increased sympathertic tone (exercise, adrenegically mediated arrythmia)
  • Increased parasympathetic tone (vagally induced and postprandial arrythmia)
  • Alcohol misuse (“holiday heart” and long term use of caffeine, smoking, recreational drug use e.g. cannabis)
  • Myotonic dystrophy type 1
  • Chagas’ disease
82
Q

What can cause atrial fibrillation?

A

Any condition resulting in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium may cause atrial fibrillation

83
Q

What are the clinical features of atrial fibrillation?

A

Symptoms attributable to atrial fibrillation are highly variable. In some patients (about 30%), it is an incidental finding, while others attend hospital as an emergency with rapid palpitations, dyspnoea and/or chest pain following the onset of atrial fibrillation. Most patients with on-going atrial fibrillation experience some deterioration of exercise capacity or wellbeing, but this may be appreciated only once sinus rhythm is restored. When caused by rheumatic mitral stenosis, the onset of atrial fibrillation results in considerable worsening of cardiac failure.

84
Q

What are the clinical classifications of atrial fibrillation?

A
  • first detected – irrespective of duration or severity of symptoms
  • paroxysmal – stops spontaneously within 7 days
  • persistent – continuous >7 days
  • longstanding persistent – continuous >1 year
  • permanent – continuous, with a joint decision between the patient and the physician to cease further attempts to regain sinus rhythm.
85
Q

What are the stratagies for the acute management of atrial fibrillation?

A
  • Ventricular rate control. This is achieved by drugs that block the AV node
  • Cardioversion. This is achieved electrically by DC shock, or medically by intravenous infusion of an antiarrhythmic drug such as flecainide, propafenone, vernakalant or amiodarone. Cardioversion can also be achieved by giving an oral agent (flecainide or propafenone) previously tested in hospital and found to be safe in a particular patient (‘pill-in-pocket’ approach)
86
Q

What does the choice of stratagies for the acute management of atrial fibrillation depend on?

A
  • how well the arrhythmia is tolerated (is cardioversion urgent?)
  • whether anticoagulation is required before considering elective cardioversion
  • whether spontaneous cardioversion is likely (previous history? reversible cause?).
87
Q

What are the stratagies for the long-term management of atrial fibrillation?

A
  • ‘rate control’ (AV nodal slowing agents plus oral anticoagulation)
  • ‘rhythm control’ (antiarrhythmic drugs plus DC cardioversion plus oral anticoagulation).
88
Q

What sort of atrial fibrillation patient should have rythm control?

A

younger, symptomatic and physically active patients

89
Q

What sort of atrial fibrillation patient should have rate control?

A
  • have the permanent form of the arrhythmia associated with symptoms that can be further improved by slowing heart rate, or are older than 65 years with recurrent atrial tachyarrhythmias (‘accepted’ atrial fibrillation)
  • have persistent tachyarrhythmias and have failed cardioversion(s) and serial prophylactic antiarrhythmic drug therapy, and in whom the risk/benefit ratio from using specific antiarrhythmic agents is shifted towards increased risk.
90
Q

How is rate control usually achieved?

A

with a combination of digoxin, beta-blockers or non-dihydropyridine calcium-channel blockers (verapamil or diltiazem)

91
Q

When is anticoagulation indicated?

A

In patients with atrial fibrillation related to rheumatic mitral stenosis or in the presence of a mechanical prosthetic heart valve

Cardiovascular (2 decks)

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