CARDIAC ARRHYTHMIAS

is abnormality of cardiac rhythm. such disturbances may cause: - sudden death - syncope - heart failure - dizziness - palpitation - or no symptoms at all! 2 main types of arrhythmias: i. bradycardia ( <60HR) ii. tachycardia ( >100HR) tachycardia is subdivided into: a. supraventricular tachyarrhythmia - arise first from atria (atrial tachyarrhythmia) and from AV junction (junctional tachyarrhythmia) b. ventricular tachyarrhythmia - arise from ventricles - more symptomatic than supraventricular! SINUS RHYTHM describe the normal beating of the heart Sinus rhythm is characterized by a usual rate of anywhere between 60-100 bpm. Every QRS complex is preceded by a P wave but not every P wave must be followed by a QRS as occurs if there is second or third degree AV block. The P wave morphology and axis must be normal and the PR interval will usually be >120 ms or greater. There are typically five distinct waves (identified by the letters P, Q, R, S, and T) in a single beat of the heart in sinus rhythm, and they occur in a specific order, over specific periods of time, with specific relative sizes. While there is a significant range within which variations in rhythm are considered normal, anything that deviates from sinus rhythm by more than a certain amount may be indicative of heart disease. In normal sinus rhythm, electrical impulses from the SA node travel to the AV node with successful contraction of the two atria. The electrical impulses from the AV node successfully contract the ventricles. On the ECG, there are normal PQRST elements with no evidence of arrhythmia, tachycardia, or bradycardia. P-wave: - upright in I and II leads. - Located in front of QRS. Is inverted in aVR Biphasic or negative in V1

SINUS ARRHYTHMIA results from fluctuation of autonomic tone. during inspiration paraS - HR during expiration paraS tone - HR U these situations are normal in children and young adults b4 40 years old! signs of sinus rhythm in ECG ( difference btw R-R distances): - inspiration R-R becomes shorter

- expiration R-R becomes longer SINUS BRADYCARDIA

HR is less than 60 (day time) and less than 50 (at night). it is normal in athletes and elderly! patho causes of sinus bradycardia: - hypothyroidism - hypothermia - cholestatic jaundice - brain traumas ( intracranial pressure) - OD of -blockers, digitalis and after anti-arrhythmic drugs. - Necrosis, fibrosis, degeneration of sinus node due to infarction (MI) or inflammation of myocardium (myocarditis) in ECG, R-R interval are long and equal! SINUS TACHYCARDIA sinus rate >100/min causes: - fever - exercises - emotions - pregnancy - anemia - HF - Thyrotoxicosis - 1 sinus tachycardia (w/o visible cause) in ECG, R-R interval is short!

TACHYARRHYTHMIAS
1. ATRIAL TACHYARRHYTHMIA: 4 types: i. ii. iii. iv. atrial ectopic beats / extrasystole atrial tachycardia atrial flutter atrial fibrillation

general causes of atrial tachyarrhythmias: - arterial HPT - IHD - Rheumatic heart disease - Thyrotoxicosis - Cardiomyopathies - Pneumonia - Carcinoma of bronchial tree - Pericarditis - Pulmoembolism - Acute and chronic alcohol abuse - Congenital atrial-septal defects - Cardiac surgery

[i. atrial ectopic beats] AAR, it X produce any symptoms or pt feels heaviness or irregular heart beat! on ECG appears as early, abnormal P-wave followed by normal QRS complex. treatment is not required OR if it provoke other ATA give -blockers.

[ii. Atrial tachycardia] rare, X common! But is normal in athletes! AAR, HR is ~150/min on ECG, P-waves are abnormally-shaped but still occur in front of QRS complexes!

[iii. Atrial flutter] rhythm disturbances usually associated with organic heart diseases (ie: pericarditis, coronary artery disease, and cardiomyopathy). While atrial flutter can sometimes go unnoticed, its onset is often marked by characteristic sensations of rapid thumping and palpitations. Such sensations usually last for the entire duration of the episode. Atrial flutter may also be accompanied by: - shortness of breath - lightheadedness or dizziness - nausea - and, in some patients, nervousness and feelings of impending doom. U Types of atrial flutter There are two types of atrial flutter: - type I - type II. Most individuals with atrial flutter will manifest only one of these types of atrial flutter. Rarely someone may manifest both types of flutter; however, they can only manifest one type at a time. Type I flutter also known as common atrial flutter or typical atrial flutter. atrial rate - 240 to 350 beats/minute. However, this rate may be slowed by antiarrhythmic agents. Type I flutter has two subtypes, known as: i. counterclockwise atrial flutter ii. clockwise atrial flutter. [Counterclockwise atrial flutter]

 Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen than clockwise atrial flutter. The flutter waves in this rhythm are inverted in II, III, and aVF. [Clockwise atrial flutter] Clockwise atrial flutter is less common than counterclockwise atrial flutter. The flutter waves are upright in II, III, and aVF in this rhythm. Type II flutter Type II flutter is faster than type I flutter, and usually is 340430 beats/minute. Unlike type I flutter, the rhythm of type II flutter cannot be entrained by rapid atrial pacing. atrial rate 280-350/min on ECG regular, saw-tooth-like atrial flutter wave btw QRST complexes. the wave is called F-waves instead of P-waves (normal atrial contraction), flutter of atrium. So theres NO P-waves at all!

HR depends on AV block; HR of ventricles may vary widely! Eg: 3:1 ratio of atrial flutter! [iv. Atrial fibrillation] is VERY common! occurs in 10% of pt over 65 years old. in young adults, maybe seen in: - thyrotoxicosis - mitral stenosis - malignant AHPT - aortic stenosis - aortic regurgitation main cause raised LA pressure. AF is linked to several cardiac causes, but may occur in otherwise normal hearts. Known associations include: Carbon monoxide poisoning High blood pressure Mitral stenosis (e.g. due to rheumatic heart disease or mitral valve prolapse) Mitral regurgitation Heart surgery Coronary artery disease Hypertrophic cardiomyopathy Excessive alcohol consumption ("binge drinking" or "holiday heart syndrome") Hyperthyroidism Hyperstimulation of the vagus nerve, usually by having large meals ("binge eating")

Lung pathology (such as pneumonia, lung cancer, pulmonary embolism, Sarcoidosis) Pericarditis Intense emotional turmoil Congenital heart disease

instead of normal contraction of atria (P-wave), ECG shows: - fine isolation of baseline - f-wave absence of P-waves! - irregular ventricular (QRS) rhythm/contraction. - R-R intervals are all different - R-wave amplitude maybe different - Shape of QRS may also vary alternating QRS complex. In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated electrical discharges produced by larger areas of atrial tissue. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw toothed p-waves on the electrocardiogram. rate of fine isolation, AAR ~450/min. QRS-rhythm if untreated 120-180/min. if treatment become normal, 60-80/min. Atrial fibrillation is often asymptomatic, but may result in symptoms of:

palpitations fainting chest pain heart failure

These symptoms are especially common when atrial fibrillation results in a heart rate which is either too fast or too slow. In addition, the erratic motion of the atria leads to blood stagnation (stasis) which increases the risk of blood clots that may travel from the heart to the brain and other areas. Thus, AF is an important risk factor for stroke, the most feared complication of atrial fibrillation. The symptoms of atrial fibrillation may be treated with medications which slow the heart rate. Several medications as well as electrical cardioversion may be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent atrial fibrillation in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from strokes.

Ecg of atrial fibrillation (top) and sinus rhythm (bottom)

U junctional tachyarrhythmia resembles atrial tachyarrhythmia BUT theres no P-wave infront of QRS-complex!

2. VENTRICULAR TACHYARRHYTHMIAS comprises: i. ii. iii. iv. ventricular extrasystole/ ventricular ectopic beats ventricular tachycardia ventricular fibrillation Torsades de Pointes

[i. ventricular ectopic beats] leads to uncomfortable missed/heavy beats. on ECG, premature beats w/o P-waves has broad duration ( >0.12sec) and bizarre shape of QRS-complex. following premature beats, complete compensatory pause!

[ii. Ventricular tachycardia] Defined as 3 ventricular beats occurring at rate of 120. pt AAR is hypotensive! ECG shows rapid ventricular rhythm with HR, 120-220/min with broad, abnormal QRS-complexes and very fast. separate activity of P-waves maybe seen. atria and ventricles contract independently!

[iii. Ventricular fibrillation] rapid, irregular ventricular activation w/o mechanical effects. pt is pulse-less, becomes rapidly unconscious and respiration. ECG shows shapeless, rapid, isolation w/o organized complexes. AAR, occurs in MI.

[iv. Torsades de Pointes] produces syncope, pre-syncope and may lead to ventricular fibrillation or sudden death. ECG shows rapid, irregular, sharp complexes that continuously change from upright to inverted position. maybe provoked in MI. Common causes for torsades de pointes include: hypomagnesemia hypokalemia malnourished individuals chronic alcoholics drug interactions such as erythromycin taken concomitantly with inhibitors like nitroimidazole Diarrhea dietary supplements various medications, including tricyclic antidepressants and phenothiazines, Factors that are associated with an increased tendency toward torsades de pointes include: Familial long QT syndrome Class IA antiarrhythmics Hypomagnesemia Hypokalemia Hypoxia Acidosis Heart failure Left ventricular hypertrophy Slow heart rate Female gender Treatment: Treatment is directed at withdrawal of the offending agent! infusion of magnesium sulfate antiarrhythmic drugs electrical therapy unsynchronized shock (or defibrillation)

Drugs of Choice for Cardiac Arrhythmias

Arrhythmia (Links point to ECGs) Drug of Choice (Non-drug therapy) Atrial fibrillation/flutter (Cardioversion) Verapamil, diltiazem, or beta-blocker to slow ventricular response Adenosine, verapamil, or diltiazem for termination (RF ablation) No drug therapy for asymptomatic patients (Cardioversion or chest thump is the safest and most effective treatment) Lidocaine for acute treatment (Defibrillation is treatment of choice) Lidocaine to prevent recurrence Torsades de pointes Magnesium sulfate Alternatives (Non-drug therapy) Digoxin to slow ventricular response Class IA, IC drugs for long-term suppression Ibutilide for termination Low dose amiodarone for prevention Dofetilide for prevention (RF ablation) Class II drugs or digoxin for termination (Cardioversion or atrial pacing) Class IA, IC, II, or IV drugs or digoxin for long-term suppression Class II drugs for symptomatic patients Procainamide, bretylium or amiodarone for acute treatment Sotalol, amiodarone, Class IA, IB, II, III can be used for long-term suppression (RF ablation or ICD) Amiodarone, procainamide or bretylium to prevent recurrence (RF ablation or ICD) Lidocaine Phenytoin Avoid cardioversion except for ventricular fibrillation Potassium (if hypokalemic) Remove causative agents Isoproterenol Potassium (if hypokalemic) (Cardiac pacing)

Other supraventricular tachycardias PVCs or non-sustained ventricular tachycardia Sustained ventricular tachycardia Ventricular fibrillation Digitalis-induced ventricular tachyarrhythmia

Digibind for life-threatening toxicity

Adverse Effects of Antiarrhythmic Drugs Most of the antiarrhythmic drugs are associated with severe and sometimes life-threatening adverse effects. A number of recent clinical trials (such as CAST) have demonstrated that many antiarrhythmic drugs increase mortality relative to placebo treatment . The adverse effects of antiarrhythmic drugs can be categorized according to cardiac effects and extra-cardiac effects: o Adverse cardiac effects:

Adverse cardiac effects are often predictable based on antiarrhythmic class . The most common and serious of adverse cardiac effects are proarrhythmias (a new or worsened rhythmic disturbance paradoxically precipitated by antiarrhythmic therapy) which can occur in 5-20% of patients treated with Class I and Class III drugs Adverse extra-cardiac effects: Severe extra-cardiac effects are also common with the antiarrhythmics and tend to be drugspecific.

Class Toxicities of Antiarrhythmic Drugs

Class I Proarrhythmic effects: IA- Torsades de pointes IC- CAST proarrhythmia Negative inotropic effect Infranodal conduction block Class II Sinus bradycardia AV block Depression of LV function (adrenergicdependent) Class III Sinus bradycardia Class IV Sinus bradycardia

Torsades de pointes AV block Negative inotropic effect

Adverse Extra-Cardiac Effects of Selected Antiarrhythmic Drugs

Drug (Class) Adverse Extra-Cardiac Effects and Toxicities Procainamide (IA) Tocainide (IB) Mexiletine (IB) GI disturbances in 30-50% of patients: diarrhea, nausea, vomiting Cinchonism Hypotension (due to alpha-adrenergic blocking activities) Can elevate serum digoxin concentrations, resulting in digitalis toxicity Hypersensitivity reactions: rashes, fever, angioneurotic edema, hepatitis Reversible thrombocytopenia Hypotension (due to ganglionic blocking activity) Long-term use results in a lupus-like syndrome in 15-30% of patients consisting of arthralgia and arthritis (pleuritis, pericarditis, parenchymal pulmonary disease also occur in some patients) GI symptoms in 10% of patients Adverse CNS effects: giddiness, psychosis, depression, hallucinations Hypersensitivity reactions: fever, agranulocytosis (can lead to fatal infections), Raynaud's syndrome, myalgias, skin rashes, digital vasculitis Lowest incidence of toxicity of currently used antiarrhythmic drugs CNS depression: drowsiness, disorientation, slurred speech, respiratory depression, nausea CNS stimulation: tinnitus, muscle twitching, psychosis, seizures Concurrent use of tocainide or mexiletine can cause additive CNS toxicity, including seizures (seizures respond to i.v. diazepam) GI effects: nausea, vomiting CNS effects: dizziness, disorientation, tremor Hematological effects (0.2%) with tocainide: agranulocytosis, bone marrow suppression, thrombocytopenia; can lead to death

Quinidine (IA)

Lidocaine (IB)

 Flecainide (IC) Digitalis (Misc.)

Concurrent use of either of these drugs and quinidine in combination may be effective at lower doses than either drug alone and thereby minimize adverse effects of both drugs CNS effects in 10-15% of patients: dizziness, tremor, agitation, headache, visual disturbances GI upset Although this drug is highly effective in treating many arrhythmias, its large number adverse effects limits its clinical use Adverse effects are common (more than 75% of patients receiving drug) and increase after a year of treatment; some toxicities result in death Half-life of 25-110 days can prolong toxicity Pulmonary toxicity and fibrosis (10-15%, can cause death in 10% of those affected); can be irreversible Constipation in 20% of patients) Hepatic dysfunction; can be irreversible Asymptomatic corneal deposits occur in all patients CNS effects (ataxia, dizziness, depression, nightmares, hallucinations) Hypothyroidism or hyperthyroidism (5% of patients) Cutaneous photosensitivity (25% of patients) and blue-grey discoloration of skin (less than 5% of patients) Peripheral neuropathy Substantial increases in LDL-cholesterol concentrations often seen; phospholipidosis Enhances the effect of warfarin and increases the serum concentrations of digoxin, quinidine, procainamide, flecainide, theophylline and other drugs Many adverse non-cardiac effects (anorexia, nausea, vomiting, diarrhea, abdominal pain, headache, confusion, abnormal vision) Adverse effects may indicate digitalis toxicity Short half-life in blood (less than 10 seconds) minimizes problems Causes hypotension, flushing in 20% of patients Transient dyspnea, chest discomfort (non-myocardial) in more than 10% of patients Metallic taste Headache, hypotension, nausea, paresthesias are less common

Amiodarone (III)

Adenosine (Misc.)

Cinchonism: a syndrome associated with quinidine toxicity characterized by nausea, vomiting, diarrhea and a variety of CNS effects (tinnitus, headache, auditory and visual disturbances, and vertigo)