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2cardiac arrhytmia

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2cardiac arrhytmia

  1. 1. Cardiac arrhythmia  Abnormal cardiac rhythm usually involving a change in rate or regularity.  Synonym: dysrhythmia
  2. 2. Etiology Physiological: -sympathetic or parasympathetic control changes eg. Stress , anxiety, exercise , smoking.  Hypothyroidism, hyperthyroidism, hypoadrenalism, hyperkalemia, hypokalemia and other electrolyte changes.
  3. 3. Pathological:  Valvular heart disease.  Ischemic heart disease.----------MI causing death of pacemaker cells or conducting tissue.  Hypertensive heart diseases.  Congenital heart disease.  Cardiomyopathies.  Carditis.  RV dysplasia.  Drug related.  Pericarditis.  Pulmonary diseases.  Others.
  4. 4. CLINICAL EVALUATION I. PHYSICAL FINDINGS Palpitation. Dizziness. Chest Pain. Abnormal pulse rate , rhythm or amplitude Dyspnea. Anxiety and confusion (from reduced brain perfusion) Fainting (syncope) Skin pallor or cyanosis Reduced blood pressure Weakness Convulsions Decreased urinary output Sudden cardiac death.
  5. 5. II. DIAGNOSTIC TEST RESULTS ECG electrophysiological (EP) testing His bundle study III. LAB FINDINGS: hyperkalemia (>5mEq/L) Hypocalcemia (<4.5mEq/L) hypomagnesemia(<2.5mEq/L)
  6. 6. Mechanism of Arrhythmogensis 1. Disorder of impulse formation. a) Automaticity. b) Triggered Activity. 1) Early after depolarization. 2) Delayed after depolarization. 2. Disorder of impulse conduction. a) b) 3. Block – Reentry. Reflection. Combined disorder.
  7. 7. Nomenclature for describing arrhythmias   Rate tachycardia bradycardia Origin: sinus atrial nodal supraventricular re-entrant ventricular
  8. 8.  Pattern: ectopic Premature contraction paroxysmal flutter fibrillation block torsades electromechanical dissociation
  9. 9. Duration: i) paroxysmal- self terminating episodes upto 7 days ii) persistent -non self terminating more than 7 days iii) permanent - not responding to cardioversion attempts iv) recurrent: returning after once stopped.
  10. 10. Strategies of Antidysrhythmic Agents A. Alter automaticity i. decrease slope of Phase 4 depolarization ii. increase the threshold potential iii. decrease resting (maximum diastolic) potential B. Alter conduction velocity i. mainly via decrease rate of rise of Phase 0 upstroke ii. decrease Phase 4 slope iii. decrease membrane resting potential and responsiveness C. Alter the refractory period i. increase Phase 2 plateau ii. increase Phase 3 repolarization iii. increase action

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