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Summary Cardiology notes state exam
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concise notes for internal state exam
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Cardiac ArrythmiasDefinition: disturbance of the electrical rhythm of the heart.
• Often as a result of structural heart disease
• Also due to abnormal conduction or depolarisation in otherwise healthy heart.
• General rule:
o Heart rate >100bpm = tachycardia
o Heart rate <60bpm = bradycardia
Pathogenesis of cardiac arrythmias:
• Pathology of the conduction system of the heart
o Usually the cardiac cycle initiated by electical discharge from SA node, atria and
ventricles then activate sequentially.
o Sinus node is a pacemaker and the intrinsic rate is controlled by ANS
o Vagal activity decreases the HR and sympathetic increases it
3 main mechanisms of tachycardia:
• Increased automaticity
• Re-entry
• Triggered activity
Increased automaticity:
• tachycardia due to spontaneous depolarisation of an ectopic focus in the atria, AV junction
or ventricles, often in response to catecholamines.
o Single depolarisation à atrial, junctional or ventricular premature ectopic beats
o Repeated depolarisation à atrial, junctional or ventricular tachycardia.
Re-Entry:
• Tachycardia is initiated by ectopic beat, and is sustained by a re-entry circuit, this is the most
common cause of tachyarrhythmias.
Triggered Activity:
• Causes ventricular arrythmias in patients with underlying coronary artery disease, it is a form
of secondary depolarisation arising from an incompletely repolarised cell membrane. They
can be Supraventricular (sinus, atrial or junctional) or ventricular in origin.
Supraventricular Rhythms à narrow QRS complexes (ventricles are still depolarised in their normal
sequence via the AV node)
• Sometimes supraventricular tachycardia can mimic ventricular tachycardia and present as a
broad complex tachycardia due to a co-existing bundle branch block or presence of an
additional accessory pathway.
Ventricular Rhythms à broad, bizarre, QRS complexes because the ventricles are activated in an
abnormal sequence.
Bradycardia
• Due to reduced automatacity of the SA node
• Due to abnormalities of conduction through the AV node
,If the heart rate becomes excessively slow, a part of the conduction system more distally will take
the role of the pacemaker – this is known as an escape rhythm and may arise in the AV node or his
bundle (junctional), or ventricles (idioventricular).
Clinical Features of Arrythmias:
• May are asymptomatic
• Sustained tachycardias à rapid palpitation, dizziness, chest discomfort, breathlessness.
Extreme tachycardias à syncope
• Bradycardias à dizziness, fatigue, syncope
• Extreme brady or tachycardias can precipitate cardiac arrest or death.
Investigations
• 12 lead ECG is always the first choice of diagnostic method, and is diagnostic in many cases
• If resting ECG is normal, an ambulatory ECG may be done for intermittent types
Specific Types of Arrythmias:
Sinus Arrythmia
• Cyclical alteration of heart rate during respiration, increase during inspiration and decrease
during expiration usually occurs.
• It is a normal phenomenon and is more pronounced in children, absence of the variation in
rate with breathing may be a sign of diabetic neuropathy, autonomic problems in patients
with peripheral nerve diseases or increased sympathetic drive. No treatment is needed.
Sinus Bradycardia
• Occurs in healthy people at rest, common in athletes
• Pathological causes include: myocardial infarction, sick sinus syndrome, hypothermia,
hypothyroidism, cholestatic jaundice and increased intracranial pressure.
Sinus Tachycardia
• Usually due to an increase in sympathetic activity during exercise, emotion and pregnancy.
Healthy young adults can produce a HR up to 200bpm during exercise, sinus tachycardia
doesn’t need treatment, but if it is severe and persistent, may be associated with underlying
heart disease. Pathological causes include: thyrotoxicosis, anemia, heart failure,
pheochromocytoma.
Sick Sinus Syndrome
• Most commonly occurs in older people, caused by fibrosis and degeneration of the SA node,
and is characterized by a wide variety of arrythmias including: sinus bradycardia, sinus
arrest, paroxysmal atrial fibrillation, paroxysmal atrial tachycardia, and AV block.
• Typical presentation is with palpitation, dizzy spells, syncope or SA block and sinus arrest. A
permanent pacemaker is the treatment of choice and atrial pacing may prevent episodes or
atrial fibrillation, it only affects the symptoms and not the underlying disease.
Atrial Ectopic Beats
• Usually cause no symptoms but can give the sensation of a missed heart beat or abnormally
strong beats. On ECG this is seen as a premature but otherwise normal QRS complex, if
visible, the preceeding P wave has different morphology because the atria are activated
from an abnormal site. These usually have no consequence, but if they occur often enough
they can lead to onset of atrial fibrillation.
Atrial tachycardia
• As a manifestation of increased atrial automaticity, sinoatrial disease or digoxin toxicity. It à
narrow complex tachycardia with abnormal P wave sometimes associated with AV block.
• If atrial rate is rapid, it may respond to beta blockers (reduce automaticity) or to class 2 or 3
antiarrythmic drugs.
,Atrial Flutter
• Characterized by a large, macro re-entry circuit, usually in the RA encircling the tricuspid
annulus.
• Atrial rate is approximately 300/min and is usually associated with a 2:1, 3:1 or 4:1 AV block
with corresponding HR of 150, 100 or 75bpm
• ECG shows saw tooth flutter waves
• Atrial flutter should always be expected when there is a narrow complex tachycardia of
150/min
• Management is with beta blocks, or digoxin or verapamil. As they help to control the
ventricular rate.
• It may sometimes be more preferable to restore sinus rhythm via direct current
cardioversion, following this, beta blockers or amiodarone can be used to prevent reccurent
episodes of atrial flutter.
• Catheter ablation is highly effective offering a 90% chance of complete cure.
Atrial Fibrillation
• Most common sustained cardiac arrythmia, increased prevalence with increasing age
• Associated with significant mortality and morbidity due to its association with systemic
embolism and stroke.
• AF is a complex arrythmia characterized by: abnormal automatic firing and the presence of
multiple interacting re-entry circuits that loop around the atria.
• Episodes of AF are initiated by rapid bursts of ectopic beats arising from conducting tissue in
the pulmonary veins or from diseased atrial tissue.
• The episodes are sustained by multiple re-entrant conduction within the atria or due to
continuous ectopic firing.
• Re-enrty occurs more often in enlarged atria, or atria with slow conduction.
• During AF the atria beat rapidly but in an uncoordinated and ineffective manner. The atria
are activated irregularly at a rate determined by conduction through the AV node à
irregularly irregular pulse.
• ECG shows normal but irregular QRS complexes, there are no P waves but the baseline may
show irregular fibrillation waves.
Atrial fibrillation is classified:
• Paroxysmal – these are intermittent episodes of fibrillation that self terminate within 7 days,
unfortunately becomes permanent in many cases.
• Persistant – prolonged episodes that can be terminated with electrical or pharmacological
cardioversion
• Permanent – permanent and sustained fibrillation.
Atrial fibrillation often becomes sustained and permanent due to the process of electrical
remodelling which are changes that are undergone in the heart triggered by the onset of atrial
fibrillation. This leads to atrial fibrosis and dilation which predisposes to chronic disease.
Causes of atrial fibrillation include:
• Coronary heart disease
• Valvular heart disease especially rheumatic mitral valve disease
• Hypertension
• Sinoatrial disease
• Hyperthyroidism
• Alcoholism
, • Cardiomyopathies
• Congenital heart disease
• Chest infection, pulmonary embolism
• Pericardial disease
• Idiopathic isolated (lone atrial fibrillation)
The typical presentation of atrial fibrillation is with palpitation, breathlessness, and fatigue. It can
also aggrevate cardiac failure due to loss of atrial function and heart rate control.
Management
• Depends on whether the AF is transient of persistant and whether there is a clear
precipitating factor. Usually the precipitating factor and underlying cause is treated first and
the AF will resolve as a result of this.
• In cases where the AF does not resolve, the main objectives are to control heart rate, restore
sinus rhythm and prevent thromboembolic events.
Management of Paroxysmal Atrial Fibrillation:
• Beta blockers used as a first line treatment if symptoms are troubling – they reduce the
ectopic firing which usually initiates the arrythmia.
• They are very useful for patients with AF and coronary artery disease, hypertension and
cardiac failure.
• Digoxin and verapamil are not useful for AF but can be used to control the rate by slowing
down AV node conduction.
• Catheter ablation is considered where anti-arrythmic drugs fail and prevents ectopic firing
within the atria subsequently preventing re entry.
• Ablation is able to prevent AF in 75% of patients with prior drug resistant episodes.
Management of Persistent Atrial Fibrillation:
• There are two options:
o Attempt to restore and maintain sinus rhythm
o Accept the fibrillation and try to control the ventricular rate
• Both options require concurrent thromboembolic prophylaxis.
Rhythm Control
• Attempt to restore the rhythm is particularly important in patients with troublesome
symptoms or if there is a modifiable or treatable underlying cause. This can be achieved by
cardioversion either using DC or pharmacological agents.
• Immediate cardioversion can be used if the AF has been present for less than 48 hours in
stable patients with no structural heart disease. In this case IV flecainide 2mg/kg for 30 mins
(max dose 150mg) can be used for pharmacological cardioversion and usually restores
rhythm in 75% of patients within 8 hours.
• In patients with structural or ischemic heart disease, amiodarone can be used instead
through a central venous catheter.
• Cardioversion should be delayed if the AF has been present for more than 48 hours of if
there is dount about its duration, and oral anticoagulation should be done for 4 weeks
before attempting cardioversion.
Rate Control
• If the rhythm cannot be controlled, then treatment is directed at controlling the heart rate
• Beta blockers, digoxin, verapamil and diltiazem are used here as they reduce the ventricular
rate by slowing AV conduction. Beta blockers are particularly useful in patients with
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