of the CV

CAD • Refers to the variety of pathologic conditions that cause narrowing of the coronary arteries • Atherosclerosis. obesity. smoking. hyperlipidemia. DM. HPN.Deposits of cholesterol and lipids within the walls of the artery • Risk Factors: Family history. sedentary/stressful lifestyle .

stressful/sedentary lifestyle Anti hyperlipidemics Lifestyle mods Endothelial Injury Inflammation Thromboxane Permeability Release of Adhesion Molecules Macrophage adhere to Endothelium ASA Foam Cells Fatty Streaks Vasoconstriction Platelet Aggregation PTCA. smoking. endartherectomy Release of enzymes and toxic O2 Radicals Oxidation Serotonin.Family history.HPN Hyperlipidemia. DM. Endothelin Vessel obstruction Necrosis of vessel tissue Smooth muscle cells develop Endothelial Dysfunction Fibrous Plaque . Hyperlipidemia. obesity.

niacin Hmg CoA blockers Enter circulation and periphery Liver proceeds fats Into HDL.LDL .Metabolism of Fats Dietary Fats Stomach Small Intestines Bile acid sequestrants Gall bladder releases bile Fat emulsification Bile acids recycled to liver Micelles absorbed into intestines Fibrates Chylomicrons absorbed into lymphatics Gemfibrozil.

then drop in BP. LDH • ECG Changes: pathologic Q wave. dyspnea. N&V. CPK.restlessness • Laboratory findings: Elevated WBC. cool and clammy skin. ST segment elevation.initial increase. AST. inverted T wave .Myocadial Infarction • Death of myocardial cells from inadequate oxygenation • Signs and symptoms: Pain. elevated temperature.

V5-V6 LCX Posterior V1-V2 RCA LADA . Avf RCA Lateral I. III.Types of MI TYPE Artery Occluded Anterior Location of ST/Q wave changes V1-V4 Inferior II. Avl.

Types of MI TYPE Layer affected Subendocardial Inner layer Subepicardial Inner and middle layer Transmural All layers .

ASHD. Laxatives.CABG.ASA Thrombolytocs Myocardial Ischemia CKMB. gender.CAD. DM. age. Lifestyle Mod O2 Supply ≠ O2 Demand Leukocytosis. Stress. thrombosis/embolism PTCA. Fatty Acids Diaphoresis HR After Load Cool. NTG.ESR Cellular Hypoxia Cellular Necrosis Anaerobic Metabolism H Ions Antiarrythmics Morphine Cell membrane permeability K.Mg Lactic Acid LDH Flipping Chest Pain Sympathetic Response N & V Glucose.Ca. Clammy Skin Contractility Cardiotonics BP Disatolic Filling CO . CBR. T O2. TROP I. HPN.

hepatomegaly. • valvular insuffucienscy • Cardiomegaly • SOB. muscle and CNS • Assessment findings • Major (Jone’s Criteria) • Carditis • Aschoff nodules.Rheumatic Heart Disease • Inflammatory disorder that involves the heart. edema • Polyarthritis • Sunbcutaneus nodules • Chorea/ Sydenham’s chorea/St. joints. Vitus’ dance • Erythema marginatum .

WBC. ASO titer .• Minor • History of GAS infection • Fever • Elevated ESR.

NSAIDS) CNS Binds to receptors within…. pain arthralgia Decrease stimulation Safety precautions Joints Polyarthritis Subcutaneus nodules . heat. elevated WBC.GAS infection (Beta hemolytic Streptococcus) Fever. Heart Positioning ASA Chorea Swelling.ESR Inflammatory response Penicillin/ Erythromycin Activation of T cells by streptococcal antigens Anti-inflammatory ents ( steroids.

Heart Pericarditis Endocardial Inflammation Friction rub Chest pain Inflammation of valve leaflets Erosion of leaflet contact Valve replacement. thrombolytics Murmur Clumping of vegetation With platelets & fibrin Penetrates myocardium Scarring/shortening Fibrin deposits Develop with area of necrosis Decreased elasticity Mitral/ Tricuspid regurgitation Bed rest CHF Aschoff nodules .

Arrythmias • Disruption in the normal events of cardiac cycle which may/ may not lead to decreased cardiac output (to which the manifestations are attributed). .

Shock. cellular hypoxia Exercise. strong emotions. identify effective coping strategies Decreased CO Decreased arterial pressure Sympathetic stimulation Hyperthyroidism Increased Cathecolamines Ca channel blockers Increased HR >100BPM Pathophysiology of Sinus Tachycardia . respiratory distress. pain. Bed rest Carotid massage. anxiety O2. anemia.

hypothermia Late hypoxia Sleep. digoxin. MI. Bed rest Symphatomimetics pacers Decreased automaticity Decreased ATP Increased vagal stimulation HR <60BPM Pathophysiology of Sinus Bradycardia . valsalva maneuver vomiting O2.Hyperkalemia.

Electrolyte imbalance Anterior MI Hypoxia Correct imbalance 2nd deg AVblock O2. Bed rest Shortening of the phases of cardiac cycle Circus reentry & Increased automaticity Increased cell permeability Impulses not conducted to the ventricles Digoxin. class Ia. II antiarrythmics. Ca channel Blockers. sychronized cardiovertion Atrial rate 200-400BPM Pathophysiology of Atrial Fibrillation/Flutter .

correct electrolyte levels. hypoxia myocardial ischemia drug intoxication (cocaine.Electrolyte imbalance. acidosis. TCA) Decreased oxygen demand. Class Ib. amphetamines. II antiarrythmics Disruption of electrolyte shifts During depolarization and repolarization Synchronized cardioversion Irritability Ectopic beat/ PVC’s Pathophysiology of Premature Ventricular Contraction .