Flashcards in Cardiology - Arrhythmias Deck (52):
What are the features of left bundle branch block?
- almost always pathological
- wide QRS (indicating prolonged ventricular depolarisation)
- M pattern in V5
Name some causes of LBBB?
3) Aortic valve disease
What is the characteristic ECG abnormality in right bundle branch block?
RSR pattern in V1
- majority of the QRS complex lies above the isoelectric line in lead 1 and below the line in lead 6
Name some causes of RBBB?
1) Normal variant
2) RVH/ RV strain (e.g. PE)
4) Congenital heard disease (e.g. ASD)
What are the features of right ventricular hypertrophy on ECG?
1) Right axis deviation
2) Positive right wave in V1
Causes of RVH are:
- Mitral valve disease
- Pulmonary hypertension
- Pulmonary stenosis
- Fallot's tetralogy
- Cor pulmonale
What are the causes of low voltage complexes on ECG?
2) Pericardial effusion
Name some causes of a short PR interval?
1) WPW syndrome
2) Lown-Ganong-Lavine syndrome
3) P wave followed by ventricular ectopics
What conditions are associated with a long PR interval?
2) Digoxin toxicity
4) Rheumatic fever
5) Lyme disease
6) Myotonic dystrophy
What is the prolonged QT syndrome?
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).
What causes prolonged QT syndrome?
1) Familial (90%)
- Romano- Ward syndrome (autosomal dominant, no deafness)
- Jervell-Lang-Neilson syndrome (autosomal recessive; includes deafness; caused by abnormal potassium channel)
- terfenadine (non sedating antihistamine)
What causes ST depression?
Myocardial ischaemia (including posterior MI)
LVH with strain
What causes ST elevation?
Coronary artery spasm (variant/ Prinzmetals angina)
Left ventricular aneurysm
What are the causes of pulseless electrical activity (PEA)?
4Hs and 4Ts
- Hypo-or Hyperkalaemia
- Cardiac Tamponade
- Tension pneumothorax
- Pulmonary thromboembolus
- Drug/ Toxin overdose
Others include aortic dissection and MI.
What are the two main types of arrhythmia?
Bradycardia - the heart rate is slow (<60bpm). Slower heart rates are more likely to cause symptomatic arrhythmias
Tachycardia - the heart rate is fast (>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
What are the general principles of arrhythmia management?
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.
What are sinus rhythms?
The normal cardiac pacemaker is the sinus node, with the rate the sinus node discharges under control by the autonomic nervous system with parasympathetic predominating (causing a slower spontaneous discharge rate).
Fluctuations in autonomic tone result in phasic changes in sinus discharge rate. During inspiration parasympathetic tone falls and the heart rate quickens, and on expiration the heart rate falls. This variation is normal, particularly in children and young adults. Sinus rhythms always have a p wave preceding each QRS complex.
What are the causes of sinus bradycardia?
Drugs - e.g. beta blockers, digoxin, verapamil
MI (especially inferior)
Increased vagal tone - e.g. vomiting
Sinus node disease
Raised intracranial pressure
How is symptomatic bradycardia treated?
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.
What is sick sinus syndrome? What are the ECG features?
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.
What is heart block?
The 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.
What are the features of first degree heart block?
There are three forms of atrioventricular block.
In 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.
What are the features of second degree heart block?
This occurs when some atrial impulses fail to reach the ventricles. There are several forms:
i) 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
What is complete heart block?
Occurs when all atrial activity fails to conduct to the ventricles. 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
What are supraventricular tacchycardias?
These arise from the atrium or the atrioventricular junction. Conduction is via the His-Purkinje system and the QRS shape during tachycardia is usually similar to that seen in the same patient during baseline rhythm.
- 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)
What causes sinus tachycardia?
Sinus tachycardia is a physiological response during 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.
What are atrioventricular junctional tachycardias?
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)
What are the features of AVNRT?
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. On ECG the P waves are either not visible or are seen immediately before or after the QRS complex. The QRS complex is usually of normal shape because the ventricles are activated in the normal way, down the bundle of His.
Occasionally the QRS complex is wide, because of a rate related bundle branch block, and it may be difficult to distinguish from ventricular tachycardia.
What causes atrioventricular reciprocating tachycardia (AVRT)?
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.
The resting ECG in WPW syndrome shows evidence of the pathways existence if the path allows some of the atrial depolarisation to pass quickly to the ventricle before it gets through the AV node. The early depolarisation of part of the ventricle leads to a shortened PR interval and a slurred start to the QRS (delta wave). The QRS is narrow. These patients are also prone to AF and occasionally VF. If the patient is tachycardic then the tachycardia P waves are clearly seen after the narrow QRS complexes.
What are the symptoms of paroxysmal SVT?
The usual history is of 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.
How should acute paroxysmal SVT be treated?
Unstable patient - emergency electrical cardioversion is required in patients whose arrhythmia is accompanied by adverse symptoms and signs
- 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
What is the long term management of patients with paroxysmal SVT?
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.
What is atrial fibrillation (AF)? What is the characteristic ECG change?
Atrial activity is chaotic and mechanically ineffective. The AV node conducts a proportion of the atrial impulses to produce an irregular ventricular response – giving rise to an irregularly irregular pulse. In some patients it is an incidental finding; in others symptoms range from palpitations and fatigue to acute heart failure. AF is associated with a five-fold increased risk of stroke, primarily as a result of embolism of a thrombus that has formed in the atrium. There are no clear P waves on the ECG, only a fine oscillation of the baseline (so-called fibrillation or f waves)
What are the different types of AF?
AF may by classified as either first detected episode, paroxysmal, persistent or permanent.
- 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. Treatment goals are therefore rate control and anticoagulation if appropriate
What are the signs and symptoms of AF?
- chest pains
- irregularly irregular pulse
How should AF in a haemodynamically unstable patient be managed?
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.
What are the options for long term management of stable patients in AF?
There are two main strategies employed in dealing with the arrhythmia element of atrial fibrillation:
1) RATE CONTROL: accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function
2) RHYTHM CONTROL: try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose
For many years the predominant approach was to try and maintain a patient in sinus rhythm. This approach changed in the early 2000's and now the majority of patients are managed with a rate control strategy. 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.
How are patients rate controlled in AF?
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
digoxin (preferred choice if patient also has heart failure)
What patients should be rhythm controlled in AF?
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. Catheter ablation techniques such as pulmonary vein isolation are used in patients who do not respond to antiarrhyth- mic drugs. Patients with infrequent symptomatic paroxysms of AF (< 1/month) which are haemodynamically well tolerated and whom have little underlying heart disease, are treated on an as-needed basis (‘pill in the pocket’) with oral flecainide or propafenone.
How should patients with AF be assessed for anticoagulation?
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)
Clinicians should use the HASBLED score to decide on the risk of anti-coagulation in patients with AF. There are no formal rules on how we act on the HAS-BLED score although a score of >= 3 indicates a 'high risk' of bleeding, defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease >2 g/L, and/or transfusion.
What are the NICE recommendations for managing patients with AF who develop a stroke?
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
What is atrial flutter?
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.
How is atrial flutter managed?
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.
What are atrial ectopic beats?
These are caused by premature discharge of an ectopic atrial focus. On the ECG this produces an early and abnormal P wave, usually followed by a normal QRS complex. Treatment is not usually required unless they cause troublesome palpitations or are responsible for provoking more significant arrhythmias when β-blockers may be effective.
What are the causes of ventricular tachyarythmias?
MI or chronic IHD
Hyper or hypokalaemia
Left ventricular aneurysm
Prolonged QT interval
Rhythm types include ventricular extrasystoles, VT, VF and long QT syndrome.
What are ventricular extrasystoles?
These are asymptomatic or patients complain of extra beats, missed beats, or heavy beats. The ectopic electrical activity is not conducted to the ventricles through the normal conducting tissue and thus the QRS complex on the ECG is widened, with a bizarre configuration. Treatment is with beta blockers if asymptomatic.
What is sustained ventricular tachycardia?
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. If there is no haemodynamic compromise, treatment of VT is usually with i.v. amiodarone or lidocaine (use with caution if underlying left ventricular impairment). Verapamil should NOT be used in VT. If drug therapy fails then an ICD can be inserted. This is a small device implanted behind the rectus abdominis and connected to the heart; it recognizes VT or VF and automatically delivers a defibrillation shock to the heart.
What is non sustained VT?
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.
What is long QT syndrome associated with?
Ventricular repolarization (QT interval) is greatly prolonged. The causes of long QT syndrome include congenital (mutations in sodium and potassium channels), electrolyte disturbances (hypokalaemia, hypocalcaemia, hypomagnesaemia) and a variety of drugs (e.g. TCAs, phenothiazines, and macrolide antibiotics). Symptoms are palpitations and syncope as a result of polymorphic VT (torsade de pointes, rapid irregular sharp QRS complexes that continuously change from an upright to an inverted position on the ECG) that usually terminates spontaneously but may degenerate into VF. Management is with i.v. magnesium sulphate.
What is ventricular fibrillation?
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.
What are the non shockable rhythms?
PEA (pulseless electrical activity) and asystole
How should adrenaline be given during a cardiac arrest?
During a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted, after the third shock and then every 3-5 minutes (during alternate cycles of CPR). In the 2005 guidelines, adrenaline was given just before the third shock. Amiodarone 300 mg is also given after the third shock.