BY: MARC ANTHONY LIAO RN

Brief Review Heart Structure

ELECTRICAL HEART CONDUCTION

PHYSIOLOGIC CHANGES OF AGINGLess distensible Less responsive to catecholamines Maximal exercise heart rate declines Decreased rate of diastolic relaxation ( in BP is more pronounced for systolic BP than diastolic BP) Note that hypertension is NOT a normal agerelated process Compensatory mechanism are delayed/insufficient = orthostatic hypotension is common Thickness of LV wall may increase

DIAGNOSTICS1.

ECG (Electrocardiography) graphical recording of the heart s electrical activities; 1st diagnostic test done when cardiovascular disorder is suspected Waves: P wave atrial depolarization (contraction/stimulation) QRS complex ventricular depolarization (changes are irreversible) T wave ventricular repolarization (changes are reversible) PR interval (time for impulse to travel) = 0.12-0.20 s QRS = 0.10s or (100beats per minute. The cause may be Increased Sympathetic Nervous System (SNS) stimulation or decreased Vagal stimulation. Beta-Blockers, Calcium Channel Blockers, Digitalis, or to treat the underlying cause.

SINUS TACHYCARDIA

B. Sinus Bradycardia y The heart has 300-400 beats per minute and there is

no P wave and QRS complex. y The management can be Epinephrine, Beta-Blocker, or Anti-coagulant, Cardioversion

VENTRICULAR DYSRYTHMIASy A. Premature Ventricular Contraction ectopic beat faster from ventricles than the sinus node y B. Ventricular Tachycardia. >100 beats per minute y C. Ventricular Fibrillation. >300-400 beats per minute y Management for Ventricular Dysrhythmia y Lidocaine y Procainamide y Magnesium Sulfate y Bretylium y Cardiopulmonary Resuscitation y Defibrillation

CONDCUTION/ HEART BLOCKy Primary Heart Block. The AV Node is affected.

There is no management. y Secondary Heart Block. It has two types:y Mobitz Type I (Wencheback Phenomenon). AV Node

affectation y Mobitz Type II. Purkinje Fibers are affected

y Management for Heart Block y Atropine y Pacemaker

Antidysrhythmicsy Sodium-Channel Blocker y Procainamide, Dipyridamine, Quinidine. The mode of action is it decreases Sodium flow into the cell. y Tocainide, Phenytoin, Mexilitine, Lidocaine. Mode of action it inhibits ion fluxes and conduction or impulses. y Propafenone. The mode of action is it decreases the influx of Sodium ions, causing excitability. y Beta-Blockers Propranolol, Esmolol, Acebutolol y Indicated for Supraventricular Tachycardia or Atrial Fibrillation y Potassium Channel Blockers Bretylium, Sotalol, Amiodarone, Ibufilide y It is indicated for Tachydysrhythmias. Mode of Action is it decreases

automaticity that initiate electrical impulse conduction and decreases conductivity that transmits electrical impulse. y Calcium Channel blockers y It is indicated for Ventricular Tachycardia and Ventricular Fibrillation. It s mode of action is that it decreases automaticity and AV node conductivity.

CPRy 2010 American Heart Association Guidelines for CPR and y y y y

y y y y

y

Emergency Cardiovascular Care Make sure the scene is safe. Shake the victim s shoulders and shout to see if they respond. COMPRESSIONS Push hard and fast on the center of the chest 30 times, at a rate of at least 100 compressions a minute. Push down at least 2 inches with each compression. If you haven t been trained in CPR, continue to give compressions until an AED arrives or trained help takes over. AIRWAY If you have been trained in CPR, continue CPR by opening the airway with a head tilt chin lift. BREATHING Pinch the victim s nose closed. Take a normal breath a cover the victim s mouth with your mouth, creating an airtight seal. Give two breaths (one second each). Watch for chest rise as you give each breath. Keep giving sets of 30 compressions and two breaths

Cont2. Cardiac Enzymes (Cardiac Markers): y 1st: Myoglobin a. urine = 0 2mg/dL ( within 30mins 2hrs after MI) b. blood =