BY MRUNMAYI JOGLEKAR NAMRATA KAUL CARDIAC ARRHYTHMIAS BY MRUNMAYI JOGLEKAR NAMRATA KAUL

Heart Physiology

Heart Physiology P - atria depol. QRS - ventricle depol. Closed system Pressure driven Supply nutrients/O2 Remove metabolites P - atria depol. QRS - ventricle depol. PR - conduction A-V T - ventricle repol. QT - duration ventricle repolarization

Heart Physiology Pressure driven Closed system Pressure driven Supply nutrients/Oxygen Remove metabolites

Heart’s Electrical System The heart’s rhythm is coordinated by its own electrical system. With each heartbeat, the electrical impulse begins at the sinus (or sinoatrial, SA) node, also called the heart’s natural pacemaker. The SA node is a cluster of specialized cells,located in the right atrium. The SA node produces the electrical impulses. The impulse then reaches the atrioventricular (AV) node, which acts as an electrical bridge allowing impulses to travel from the atria to the ventricles. From the AV node, the impulse travels through a pathway of fibers called the HIS-Purkinje system. The SA node fires another impulse and the cycle begins again.

DEFINATION & OCCURRENCE OF CARDIAC ARRHYTHMIAS

DEFINATION of Arrhythmias : Definitions: - normal sinus rhythm (60-90bpm), SA node pacemaker - arrhythmia; any abnormality of firing rate, regularity or site of origin of cardiac impulse or disturbance of conduction that alters the normal sequence of activity of atria and ventricles Occurrence: - 80% of patients with acute myocardial infarctions - 50% of anaesthetized patients - about 25% of patients on digitalis

MECHANISM OF CARDIAC ARRHYTHMIAS

Mechanisms of arrhythmias : 1. Abnormal impulse generation (abnormal automaticity) a. automaticity of normally automatic cells (SA, AV, His) b. generation of impulses in normally non-automatic cells - development of phase 4 depolarization in normally non-automatic cells - ‘triggered activity’ due to afterdepolarizations - early afterdepolarization - delayed afterdepolarization 2. Abnormal impulse conduction (more common mechanism) a. AV block – ventricle free to start own pacemaker rhythm b. Re-entry: re-excitation around a conducting loop, which produces tachycardia - unidirectional conduction block - establishment of new loop of excitation - conduction time that outlasts refractory period

CLASSIFICATION OF CARDIAC ARRHYTHMIAS

Classification of arrhythmia : 1. Characteristics: a. flutter – very rapid but regular contractions b. tachycardia – increased rate c. bradycardia – decreased rate d. fibrillation – disorganized contractile activity 2. Sites involved: a. ventricular b. atrial c. sinus d. AV node e. Supraventricular (atrial myocardium or AV node)

Ventricular Arrythmias *Premature ventricular contractions (PVCs) *Ventricular tachycardia (V-tach) *Ventricular fibrillation (V-fib)

Ventricular tachycardia Characterized by rapid ventricular rates generally around 100 to 200 beats per minute This arrhythmia often results from triggered activity in the context of other electrophysiological abnormalities, especially a prolonged QT interval .

Premature Ventricular Contractions These are early, extra beats beginning in the lower chambers of the heart (ventricles). PVCs are common,most of the time they cause no symptoms and require no treatment. In some people, they can be related to stress, too much caffeine or nicotine, or exercise. Sometimes, PVCs can be caused by heart disease or an electrolyte imbalance.

Ventricular Fibrillation The ventricles are the large lower chamber of the heart. They are responsible for moving blood to the organs and tissues of the body. In ventricular fibrillation, the heart’s ventricles contract in a rapid and chaotic manner. As a result, little or no blood is pumped from the heart. Unless medical help is provided immediately, ventricular fibrillation will lead to cardiovascular collapse and sudden death.

Ventricular fibrillation is an immediately life-threatening arrhythmia in which the heart's electrical activity and associated contraction become disordered and ineffective. It is characterized by rapid, irregular activation of the ventricles and thereby prevents an effective mechanical contraction. Blood pressure instantaneously drops to zero, leading to death within minutes due to lack of cardiac output unless successful electrical defibrillation is performed; spontaneous conversion to sinus rhythm is rare. During ventricular fibrillation, the ECG has no distinctive QRS complexes but instead consists of an undulating baseline of variable amplitude. Although the sinus node continues to function properly, P waves cannot be discerned in the VF waveform. Ventricular tachycardia in many cases can degenerate to ventricular fibrillation.

Causes of ventricular fibrillation Inadequate blood flow to the heart due to coronary artery disease (CAD) Scar tissue within the heart due to previous injury to heart, such as a heart attack (myocardial infarction) Congestive heart failure (CHF) Infection of the heart muscle ( myocarditis ) Shock Electrical shock Drowning Dangerously low body temperature ( hypothermia ) Electrolyte imbalance (eg, very low levels of potassium or magnesium in the blood) Drugs that affect the electrical currents of the heart (eg, sodium or potassium channel blockers) Low atmospheric oxygen

Diagnosis Ventricular fibrillation is suspected when a person collapses suddenly and has no detectable pulse or heartbeat. The diagnosis is confirmed by electrocardiography (ECG) . ECG records the heart’s activity by measuring electrical currents through the heart muscle.

Supraventricular Arrythmias Arrhythmias that begin above the ventricles, such as in the upper chambers or atria.

Types Of Supra-ventricular arrythmias Atrial tachycardia - a rapid heart rhythm or arrhythmia that originates in the atria. Atrial fibrillation - a very common irregular rhythm. Atrial flutter - an atrial arrhythmia due to one or more rapid circuits in the atrium. Atrial flutter is usually more organized and regular than atrial fibrillation Premature atrial contractions (PACs) - early, extra beats that originate in the upper chambers of the heart (atria). Paroxysmal supraventricular tachycardia (PSVT) - a rapid but regular rhythm that comes from the atria. PSVT begins and ends suddenly. Accessory pathway tachycardia (such as Wolff-Parkinson-White syndrome) - a fast heart rhythm due to an extra abnormal electrical pathway or connection between the atria and ventricles. AV nodal re-entrant tachycardia (AVNRT) - a fast heart rate due to having more than one pathway through the atrioventricular (AV) node.

Atrial flutter Re-entrant supraventricular arrhythmia characterized by a rapid "sawtooth" appearance of the ECG owing to the presence of multiple P waves between QRS complexes. Atrial rates typically fall between 250 and 350 beats per minute Treatment options for atrial flutter include direct electrical cardioversion and catheter ablation

Atrial fibrillation Complex arrhythmia characterized by an extremely rapid atrial rate (350 to 600 beats per minute). AF can be treated by direct cardioversion but more frequently is treated with antiarrhythmic and/or anti-coagulation drug therapy

1st Degree Heart Block First-degree AV block, or PR prolongation, is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds The impulse conducting from atria to ventricles through the AV node is delayed and travels slower than normal

2nd Degree Heart Block Also called as ‘Woldemar Mobitz’. This occurs when 1 or more atrial impulses fail to conduct to ventricles. Hence, a complete but intermittent inhibition of pacing impulse. ECG w/f—2/3 P waves/QRS

3rd Degree Heart Block Complete block of S.A node impulse, accessory pacemakers conduct to ventricles. Hence, total and continuous impulse blockage Occurs anywhere in conduction system ECG w/f- wide QRS.

Causes The most common causes of first-degree heart block are: An AV nodal disease, Myocarditis Acute myocardial infarction (especially acute inferior MI) Electrolyte disturbances and medication. Drugs like calcium channel blockers, beta-blockers, cardiac glycosides, and anything that increases cholinergic activity such as cholinesterase inhibitors.