Arrhythmias.

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Presentation transcript:

Arrhythmias

Rhythms and Arrhythmia SA Node Normal sinus rhythm Sinus Bradycardia Sinus Tachycardia Sick Sinus Syndrome Atria Ectopic beats Fibrillation Flutter Supraventricular tachycardia

Rhythms and Arrhythmia AV Node Reentrant tachycardia 1st 2nd 3rd degree blocks Bundle branch block Ventricles Ectopic beats Tachycardia Preexitation Ischemia

Normal Sinus Rhythm Normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system. EKG Characteristics: Regular narrow-complex rhythm

Sinus Tachycardia Aetiologies Fever Hyperthyroidism Hypovolaemia Anxiety Pheochromocytoma Sepsis Anaemia Exposure to stimulants (nicotine, caffeine) or illicit drugs (amphetamines) Hypotension and shock Pulmonary embolism Acute coronary ischemia and myocardial infarction Heart failure Chronic pulmonary disease Hypoxia http://www.youtube.com/watch?v=zbDtMtJyVtI

Sinus Bradycardia Sinus Bradycardia HR< 60 bpm QRS is narrow and preceded by p wave Can be normal in well-conditioned athletes at rest or children during sleep So when is it not normal? Is not normal if the sinus rhythm can’t increase with exercise

Sinus Bradycardia - aetiologies Normal aging 15-25% following AMI Sick sinus syndrome Hypothyroidism Hypothermia Hypokalemia Situational: micturation, coughing Drugs: beta-blockers, digoxin, calcium channel blockers, amiodarone, lithium http://www.youtube.com/watch?v=Yff9VvNGL5w&feature=related

Sick Sinus Syndrome Aetiology Symptoms Fibrosis Atheroschlerosis of RC artery SLE, collagen vasc diseases Chagas disease - yeay Injury, heart surgery Infiltrative diseases sarcoid amyloid Symptoms Weakness Palpitations Syncope

Disorders of the SA Node Sinus arrest Tachycardia-bradycardia syndrome Alternating brady-tachy causing palpitations SA exit block Normal SA impulse but conduction to atria is impaired

Atrial Ectopic Beats Ectopic P waves look abnormal SA node continues regardless in compensatory delay SA node timing is reset if premature SA firing caused by ectopic – non compensatory

Atrial Fibrillation Constant conduction within the atria, multiple circuits, loss of contractility Can be paroxysmal, persistent or permanent 1 in 5 strokes caused by AF: patients require anticoagulation therapy to prevent clot formation

Atrial Fibrillation Risk Factors Relative Risk History of hypertension 1.6 Heart failure and/or reduced left ventricular function 1.4 Advanced age Diabetes 1.7 Coronary artery disease 1.5

Atrial Flutter Aetiology Pathophysilogy 30% have no underlying cardiovascular disease 30% CAD 30% hypertension Pathophysilogy Single reentrant circuit around the tricuspid valve Distinctive sawtooth ECG

Supraventricular Tachycardias Any tachycardic rhythm originating above the ventricles It usually involves ectopic pacemaker cells or an accessory (reentrant) pathway http://www.youtube.com/watch?v=Y7QdOBYeAS4

Mechanism of Reentry A: slow conduction, short RP B: normal conduction and RP

SA Node Reentrant Tachycardia

AV Node Reentrant Tachycardia Aetiology Formation of “beta” pathway Anxiety Exertion Caffeine, alcohol, drugs Pathophysiology Dual pathways within AV node Alpha: fast, long RP Beta: slow, short RP Signs & Symptoms Palpitation Dizziness, syncope Chest pain, angina (if coexisting CAD)

AV Node Reentrant Tachycardia

First Degree Block If the PR interval is more than 1 small square then this is a 1st degree AV block Not associated with morbidity or mortality but heralds a more severe block if MI occurs Risk factor = age

Second Degree Block A conduction delay within the AV node causing increasingly lengthened PR intervals until the node cannot transmit the signal to the ventricles (the Wenkebach phenominum) Aetiology Structural heart disease Drugs: digoxin, Na, beta and Ca channel blockers, tricyclic antidepressants & lithium at toxic levels Metabolic: hyperkalaemia, hypermagnesaemia, hyperthyroidism, Addison’s Enhanced vagal tone due to pain, athletes at rest A shit load more at http://emedicine.medscape.com/article/161919-overview Mostly intranodal but poor prognosis if infranodal

Second Degree Block Type I Wenckebach: P waves shown by arrows, lengthening PR interval Type II: P waves shown by arrows, unpredictable non-conduction and loss of QRS

Third Degree Heart Block Complete interruption of conduction from the atria Ventricles show escape rhythms Aetiology Infectious: Endocarditis, rheumatic fever Neuromuscular: muscular dystrophy Drugs (see 2nd degree HB) Rheumatic, infiltrative, metabolic, electrolyte ...

Third Degree Heart Block

BBB Normal P waves Normal PR interval Widening of QRS to more than 0.12s because of delayed depolarisation of the ventricle

Ventricular Ectopic BEats Premature beats originating within the myocardium Distinctive tall, wide beats precede the P wave

VT Reentrant arrhythmia as a result of scarring of the myocardium The rhythm can stabilise, revert spontaneously to sinus rhythm or lead to VF and death

Ventricular Preexitation Associated with WPW syndrome Accessory pathway Bundle of Kent allows early ventricular depolarisation forming a blunted Q wave called a delta wave and an abnormal T wave (last 2 beats below)

Myocardial Ischemia Myocardial ischemia caused by narrowing of the coronary arteries results in ST depression Below the depression is shown in the shaded areas

ECG Online Test http://www.andrews.edu/~schriste/HealthTeaching/Practice/Sinus_and_Atrial/si01.html