5. Identify arrhythmias. a. Etiology: ischemic conditions of the myocardium, electrolyte imbalance, acidosis or alkalosis, hypoxemia, hypotension, emotional stress, drugs, alcohol, caffeine.
b. Ventricular arrhythmias: originate from an ectopic focus in the ventricles (outside the normal conduction system).
• Significant in adversely affecting cardiac output.
• Premature ventricular contractions (PVCs): a premature beat arising from the ventricle; occurs occasionally in the majority of the normal population. On ECG: no P wave; a bizarre and wide QRS that is premature, followed by a long compensatory pause. Serious PVCs: >6 per minute, paired or in sequential runs, multifocal, very early PVC (R on T phenomena). • Ventricular tachycardia (VT): a run of four or more PVCs occurring sequentially; very rapid rate (150–200 bpm); may occur paroxysmally (abrupt onset); usually the result of an ischemic ventricle. On ECG: wide, bizarre QRS waves, no P waves. Seriously compromised cardiac output. ○ NSVT (non-sustained ventricular tachycardia): a run of four or more consecutive beats in duration, terminating spontaneously in less than 30 seconds. ○ VT (sustained ventricular tachycardia): VT >30 seconds in duration and/or requiring termination due to hemodynamic compromise in less than 30 seconds. • Ventricular fibrillation (VF): a pulseless, emergency situation requiring emergency medical treatment: cardiopulmonary resuscitation (CPR), defibrillation, medications. Characterized by chaotic activity of ventricle originating from multiple foci; unable to determine rate. On ECG: bizarre, erratic activity without QRS complexes. No effective cardiac output; clinical death within 4–6 minutes.
c. Atrial arrhythmias: rapid and repetitive firing of one or more ectopic foci in the atria (outside the sinus node).
• Atrial fibrillation: On ECG, P waves are abnormal (variable in shape) or absent and rhythm is irregular. Rate is up to 180 bpm. • Atrial flutter: On ECG, repeated P waves prior to QRS, often is repetitive pattern (resemble teeth on a saw). Usually regular and rate is 250–250 bpm. • Cardiac output is usually maintained if rate is controlled; may precipitate ventricular failure in an abnormal heart.
d. Atrioventricular blocks: abnormal delays or failure to conduct through normal conducting system. • First-, second-, or third- (complete) degree atrioventricular blocks; bundle branch blocks. • If ventricular rate is slowed, cardiac output decreased. • Third degree, complete heart block is life threatening: requires medications (atropine), surgical implantation of pacemaker.
6. Metabolic and drug influences on the ECG. a. Potassium levels. • Hyperkalemia: widens QRS, flattens P wave, T wave becomes peaked. • Hypokalemia: flattens T wave (or inverts), produces a U wave.
b. Calcium levels. • Hypercalcemia: widens QRS, shortens QT interval. • Hypocalcemia: prolongs QT interval. c. Hypothermia: elevates ST segment; slows rhythm. d. Digitalis: depresses ST segment, flattens T wave (or inverts), QT shortens. e. Quinidine: QT lengthens, T wave flattens (or inverts), QRS lengthens. f. Beta blockers (e.g., propranolol [Inderal]): decreases heart rate, blunts heart rate response to exercise. g. Nitrates (nitroglycerin): increases heart rate. h. Antiarrhythmic agents: may prolong QRS and QT intervals.
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