hyperlipidemia MAJOR RISK FACTORS OF CHD HYPERLIPIDEMIA HYPERTENSION CIGARETTE SMOKING MAJOR BODY LIPIDS CHOLESTEROL TRIGLYCERIDES

Transported by LIPOPROTEINS

LIPOPROTEINS Fasting (9-12 h) profile q 5 yrs - - 20 yrs old and > Lipoproteins LDL : <70 mg/dL (AHA, 2004) Total cholesterol :<200 mg/dL HDL : > 60 mg/dL Triglycerides : <150 mg/dL

LDL CHOL means.. less than 100 mg/dL is optimal 100 to 129 mg/dL or less is near-optimal between 130 and 159 is borderline high 160 mg/dL or more is high 190 mg/dL or more is very high

HYPERLIPIDEMIA GENETIC METABOLIC ABNORMALITIES DUE TO OVERPRODUCTION OR UNDERPRODUCTION OF SPECIFIC LIPOPROTEINS OR ENZYMES

PRIMARY or SECONDARY PRIMARY METABOLIC/ GENETIC

SECONDARY VERY COMMON; MULTIFACTORIAL Chronic diseases e.g. dm, hypothyroidism, nephrotic syndrome, liver disease Obesity, dietary

Pregnancy, alcoholism, beta-blockers and diuretics

consequences Atherosclerotic plaques in blood vessels Narrowing, ischemia, and possible, thrombotic formation Cardiovascular, cerebrovascular, and peripheral vascular disease

medications HMG-CoA REDUCTASE INHIBITORS (STATINS) Simvastatin (Zocor), fluvastatin (Lescol), Atorvastatin (Lipitor), Rosuvastatin (Crestor) BILE ACID SEQUESTRANTS = cholestyramine (Questran) FIBRIC ACIDS Gemfibrozil (Lopid) CHOLESTEROL ABSORPTION INHIBITORS Ezetimide (Zetia) -

PER SERVING meat or fish: palm of your hand fresh fruit: fist cooked vegetables, rice, or pasta: cupped hand

CARDIAC OUTPUT PROF. CECILIA GEONANGA-BERCILES, RN, MAN MARCH 2011 DETERMINANTS STROKE VOLUME HEART RATE

STROKE VOLUME FACTORS REGULATING SV Starlings law ..degree of stretch of the cardiac muscle before contraction; det by blood volume in the vent at the end of diastole/diastolic filling Contractility .. Preload ..the filling of the vent at the end of diastole; volume coming into vent increased in hypervolemia, cardiac regurgitation

Afterload the pressure in the aorta/resistance that the vent must overcome to pump blood into sys circ Increased in hypertension. Vasoconstriction

INCREASED AFTERLOAD increases cardiac workload

CELL CHARACTERISTICS AUTOMATICITY

EXCITABILITY CONDUCTIVITY REFRACTORINESS the inability of the cell to respond to incoming stimuli IMPULSE GENERATION RESTING STATE : cell is ready to receive an impulse DEPOLARIZATION REPOLARIZATION

DEPOLARIZATION electrical activation of myocardial cell caused by the influx of Na into the cell & exit of K, initiating muscle contraction Process by w/c cardiac muscle cells change from a more negatively charged to a more positively charged intracellular state

REPOLARIZATION Return of the cell to the resting phase, caused by K reentry & exit of Na Process by w/c cardiac muscle cells return to a more negatively charge intracellular condition, their resting state

CONDUCTION PATHWAYS P-WAVE: SA node impulse, initiating atrial depolarization PR INTERVAL: delay of imp at the AV node & bundle of His to promote vent filling QRS COMPLEX T WAVE U wave

DISORDERS OF THE CARDIAC PUMP ASHD/CAD/ACS NONMODIFIABLE RISK FACTORS FAMILY hx : 1st deg relative at 55 or younger (MEN); 65 yr or younger (WOMEN) INCREASING AGE : >45 (MEN); >55 (WOMEN GENDER RACE

MODIFIABLE RISK FACTORS HYPERLIPIDEMIA, HYPERCHOLESTEROLEMIA CIGARETTE SMOKING, TOBACCO USE HYPERTENSION

DIABETES MELLITUS Metabolic syndrome, obesity, physical inactivity

CIGARETTE SMOKING EFFECTS INHALATION >s blood CO level; Hb combines more readily with CO, decreasing amt of available O2; DECREASES HEARTS ABILITY TO PUMP NICOTINIC ACID triggers CATECHOLAMINES : HR, BP rise; vasoconstriction Adversely affects vascular endothelium, inc platelet adhesion

ANGINA PECTORIS: TYPES CHRONIC STABLE/EXERTIONAL UNSTABLE /PREINFARCTION **occurs with an unpredictable deg of emotion, exertion; NOT relieve with NTG/rest PAIN> 15 min PRINZMETAL ANGINA/VARIANT *coronary artery spasm; may occur at rest diagnostics s/s ECG Cardiac enzymes and troponin tests Stress test cardiac catheterization

treatment Primary goal: to relieve pain and prevent future attacks Meds: vasodilators, beta-adrenergic blockers, calcium-channel blockers, antiplatelet aggregators Surgical PTCA, INTRACORONARY STENTS, CARDIAC REVASCULARIZATION

TREATMENT Restricted activity Supplemental oxygen Control of modifiable risk factors

MYOCARDIAL INFARCTION RISK FACTORS : ASHD, SUDDEN INCREASE IN EXERCISE, none Without precipitating factors Most common : REM sleep

Left coronary artery: 3 branches Left main coronary 1)left anterior desc a (anterior wall of the heart);2) circumflex artery (encircles the lateral left wall)

Right coronary right side of the heart to the inferior wall; post descending a (posterior wall of the heart)

DEGREES OF MYOCARDIAL DAMAGE ZONE OF NECROSIS - complete O2 deprivation, irreversible damage ZONE OF INJURY - surrounds the necrosis, inflamed, but still viable if adequate O2 can be restored ZONE OF ISCHEMIA surrounds area of injury, viable

MANIFESTATIONS CHEST PAIN Diffuse, steady substernal pain Crushing, squeezing Not relieved by rest , NTG Radiating > 15 MINS Anxiety and fear

SILENT MI / ATYPICAL epigastric/ abdominal distress, dull aching tingling sensations, SOB, extreme fatigue Elderly hypotension, low body temp, stroke like symptoms, dizziness; DYSPNEA; RADIATES TO BOTH ARMS

FEMALE HEART ATTACK shortness of breath (57.9%) weakness (54.8%) unusual fatigue (42.9%) Nausea Dizziness Lower chest discomfort Upper abdominal pressure/ discomfort that may feel like indigestion Back pain

SPECIFIC CARDIAC MARKERS TROPONIN I rises within 3 h and persists for up to 7 days; Normal : <0.5ng/ml TROPONIN T rises within 3 h and persists for up to 14 days : Normal : <0.2 ng/mL MYOGLOBIN rises within 1 h after cell death; peaks in 4 6 h , returns to normal with 24 36 h (NORMAL: <70mg/ml)

Cardiac markers CREATINE KINASE/ CK -MB rises within 4 6 h and peaks 18-24 h after attack returns to normal 48h; (normal: 0-7 U/L)

LDH rises in 24 h; peaks in 48 72 h total)

returns to normal 5-10days; normal 70-200 IU/L (LDH1-14-26% of

MYOCARDIAL HEALING FIRST 24 H inflammation occurs, leukocyte invasion, and cardiac enzymes are released from damaged cells 4 10 DAYS necrotic zone is well defined 10 14 days formation of scar tissue foundation begins DANGER OF DEATH FROM AN MI IS GREATEST DURING THE FIRST TWO HOURS

MANAGEMENT OXYGEN THERAPY: nasal cannula PAIN CONTROL: MORPHINE SULFATE, VASODILATOR, BENZODIAZEPINES THROMBOLYTIC AGENTS ANTIARRHYTHMICS SURGERY

ABSOLUTE CONTRAINDICATIONS OF THROMBOLYTICS Active bleeding Known bleeding disorder Hx of hemorrhagic stroke Hx of intracranial vessel malformation Recent major surgery or trauma Uncontrolled hypertension pregnancy

NURSING DIAGNOSES PAIN related to an imbalance in oxygen supply and demand DECREASED CARDIAC OUTPUT related to decreased cardiac contractility and dysrhythmias ANXIETY related to chest pain, fear of death, threatening environment, invasive therapy, and uncertain prognosis INEFFECTIVE TISSUE PERFUSION (MYOCARDIAL) R/2 coronary restenosis, extension of reinfarction INEFFECTIve COPING r/2 threats to self-esteem, disruption of rest-sleep pattern, lack of significant support system, and loss of control

NURSING INTERVENTIONS OBJECTIVES REDUCE PAIN ALLEVIATE ANXIETY MAINTAIN HEMODYNAMIC STABILITY INCREASE ACTIVITY TOLERANCE

PREVENT BLEEDING MAINTAIN TISSUE PERFUSION STRENGTHEN COPING ABILITIES

PAIN REDUCTION Semi-Fowlers position O2 by nasal cannula Admin NTG and morphine,/thrombolytic as ordered Monitor BP Attach ECG electrodes for continuous cardiac monitor/monitor rate and rhythm

IMPROVING CARDIAC OUTPUT Adm IVF, vasopressors as ordered Monitor closely s/s left vent failure, hourly urine output, mental status, hemodynamics Interpret ECG strip at least every 4 h; adm antiarrhythmics as ordered

ANXIETY RELIEF EXPLAIN equipment, procedures, frequent assessment, visiting hours, need for rest Monitor s/s of anxiety esp autonomic s/s Adm anxiolytics as ordered Offer back massage Maintain continuity or care consistency on routine and staff

CARDIOMYOPATHY SUBACUTE/CHRONIC DISORDER of the MYOCARDIUM TYPES dilated, hypertrophic, restrictive affect the functional or structural ability of the heart Primary or secondary Dilated, hypertrophic (obstructive and nonobstructive), restrictive

classification Primary Secondary..ischemia, viral infections, alcohol/drug abuse, pregnancy

Dilated cardiomyopathy Fibrosis of myo- and endocardium > > dilated chambers Mural wall thrombus MOST COMMON FORM

DILATED .S/S

Fatigue, weakness, left side HF, dysrrhythmias/heart block, systemic/pulmonary emboli, S3 and S4 Moderate to severe cardiomegaly

Dilated.treatment Symptomatic tx of HF Vasodilators anti-arrhythmics Surgery : heart transplant

HYPERTROPHIC CARDIOMYOPATHY TYPES: non-obstructed and obstructed Nonobstructed wall hypertrophy, septum hypertrophy, relatively small size chamber Obstructed same ..obstructed ventricular outflow b/c of hypertrophied septum and mitral valve incompetence

Hypertrophic.s/s NONOB- dyspnea, angina, fatigue, syncope, palpitations, mild cardiomegaly, S4, vent dysrrhythmias, sudden death (common), heart failure OBS same + mitral regurgitation murmur, atrial fibrillation

RESTRICTIVE Mimics constrictive pericarditis, fibrosed walls (cannot expand), chambers narrowed, emboli (common) Dyspnea, cougn, rt sided HF, mild to moderate cardiomegaly, S3, S4, heart block, emboli **PRIMARY S/S exercise intolerance LEAST COMMON

TREATMENT : PALLIATIVE LIFESTYLE changes and shortened life span Vasodilators, antiarrhythmics, beta-blockers Exercise restrictions DIGITALIS, NITRATES, and other vasodilators CONTRAINDICATED IN THE OBSTRUCTED CARDIOMYOPATHY

BRONCHIAL ASTHMA : PATHOPHYSIOLOGY (Summarized from PORTH'S PATHOPHYSIOLOGY) TWO-DEFINED PHASES :e.g. BRONCHIAL ASTHMA **INITIAL/EARLY RESPONSE: VASODILATATION, VASCULAR LEAKAGE, SMOOTH MUSCLE CONTRACTION **SECONDARY/LATE RESPONSE: more intense infiltration of tissues with eosinophils, acute & chronic inflammatory cells--> epithelial cell damage

INITIAL/EARLY RESPONSE PHASE... **5-30 minutes--> subsides within 1h

**mediated by mast cell degranulation & release of preformed mediators i.e. histamine, acetylcholine, proteolytic enzymes (chymase, trypsin) that leads to KININ GENERATION **HISTAMINE: POTENT VASODILATOR, >s capillary & venule permeability; smooth muscle contraction, bronchial constriction

EARLY.... **ACETYLCHOLINE : bronchial smooth muscle contraction; small BV dilatation **KININS : vasodilatation & smooth muscle contraction

LATE-PHASE/ SECONDARY **SETS IN 2 to 8 hr later---> several days **RESULTS FROM ACTION OF LIPID MEDIATORS & CYTOKINES **LIPID MEDIATORS : derived from mast cell membrane PHOSPHOLIPIDS, w/c are broken down--> ARACHIDONIC ACID (parent compound from which leukotrienes & PG are synthesized)---> effects are similar to histamine & acetylcholine tho---????

Late....... MAST CELLS also produce CYTOKINES & CHEMOTACTIC FACTORS prompt INFLUX of EOSINOPHILS & WBC to the site of allergen contact--> INFLAMMATION