Cardiac functions Automaticity – ability to initiate electrical stimulus independently Excitability – ability to respond to electrical stimulation Conductivity – ability

to transmit electrical stimulus from the cell in the heart Contractility – ability to stretch as a single unit and recoil Rhythmicity – ability to repeat the cycle with regularity Myocardial blood supply • the LEFT CORONARY ARTERY branches out into the LEFT ANTERIOR DESCENDING (LAD) ARTERY and the CIRCUMFLEX ARTERY o LAD artery supplies the anterior wall of the ventricle, the anterior ventricular septum, and the bundle branches o The circumflex artery provides blood to the lateral and posterior portions of the left ventricle • The RIGHT CORONARY ARTERY (RCA) fills the groove between the atria and ventricles and gives rise to the RIGHT MARGINAL ARTERY ending as the POSTERIOR DESCENDING ARTERY o The RCA sends blood to the sinus and atrioventricular nodes to the right atrium o The posterior descending artery supplies the posterior and inferior wall of the left ventricle and the posterior portion of the right ventricle • Coronary arteries receive blood primarily during ventricular relaxation (diastole) • Blood is pumped out to the systemic circulation during contraction of the ventricles (systole) Electrical Conduction • the heart contains specialized muscle fibers that generate and conduct their own electrical impulses spontaneously • the SINOATRIAL (SA) NODE< INTERNODAL TRACTS, ATRIVENTRICULAR (AV) NODE, BUNDLE OF HIS, RIGHT and LEFT BUNDLE BRANCHES, and PURKINJE FIBERS make up the system that conducts electrical impulses and coordinates chamber contractions • impulses follow a RIGHT-TO-LEFT, TOP-TO-BOTTOM path • a normal electrical impulse is initiated at the SA NOPDE, the heart’s intrinsic pacemaker Cardiac Function CO – total amount of blood ejected per minute SV – amount of blood ejected with each beat

Coronary artery disease • narrowing / obstruction in the coronary circulation resulting to ↓↓ tissue perfusion atherosclerosis • accumulation of lipid-containing plaque in the coronary arteries • leads to ↓↓perfusion to myocardial tissue thus inadequate myocardial O2 supply • can cause angina, dysrhythmias, myocardial infarction, heart failure and death RISK FACTORS • family Hx of coronary heart disease • increasing age • gender • race • high blood cholesterol * high blood cholesterol * cigarette smoking/tobacco use * HPN * diabetes mellitus * physical inactivity * obesity

- symptoms occur when the coronary artery is occluded to the point that inadequate blood supply to the muscle occurs, causing ischemia - coronary artery narrowing is significant if the lumen diameter of the LCA is reduced at least 50%, or if any major branch is reduced at least 75% - the goal of the treatment is to alter the atherosclerotic progression lipid/atheroma formation or accumulation in arterial wall ↓↓ immune system activation ↓↓ inflammatory response ↓↓ chemotaxis (macrophages, lymphocytes) engulf fat deposits and then die ↓↓ proliferation of smooth muscle forming fibrous cap over dead fatty core ↓↓ atheroma / plaque formation ↓↓ narrowing of the artery ↓↓ obstruction ↓↓ (rupture of the atheroma) ↓↓ (thrombus formation) ↓↓ (Myocardial Infarction)

CLINICAL MANIFESTATION a. b. c. d. e. f. g. chest pain palpitation dyspnea/ SOB syncope nausea excessive fatigue cough or hemoptysis

PREVENTION A. controlling cholesterol abnormalities LDL > 160mg/dl (with no risk) >130 mg/dl (with 2 or more risk factors) > 100mg/dl (with CAD) HDL normal value > 40 mg/dl Ideal value > 60mg/dl TGA >200mg/dl (abnormally high) B. diet modification Soluble dietary fibers Fresh fruits Cereal gains Vegetables Legumes C. physical activity Regular, moderate activity = 30min, 3-4x per week Activity adjusted to an intensity that does not preclude their ability to talk Hot and humid weather, exercise is best early in the morning/ indoors Stop activity when: +chest pain Unusual SOB +dizziness Lightheadedness Nausea D. medications Control cholesterol levels 1. HMG-CoA Lovastatin, Atorvastatin, Pravastatin, Simvastatin 2. Nicotinic Acid 3. Fibrinic Acid/ fibrates Clofibrate, Fenofibrate 4. Bile acid sequestrants/resins Cholestyramine E. manage/ prevention of other risk factors

Therapeutic Regimen 1. Percutaneous Transluminal Coronary Angioplasty (PTCA) Coronary arteries are dilated with balloon-tipped catheter 2. Coronary stents Insertion of meshwork in the narrowed artery 3. Coronary Artery Bypass Graft (CABG) Occluded coronary arteries are bypassed with the client’s own blood vessel 4. Heart transplant Angina pectoris • chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply • caused by imbalance between O2 supply and demand • goal of treatment: to provide relief of an acute attack correct the imbalance between myocardial oxygen supply and demand, prevent the progression of the disease and further attacks to reduce the risk of MI • pathophysiology obstruction of the coronary blood flow risk factors – atherosclerosis, coronary artery spasm, ↑↑ myocardial O2 demand ↓↓ ↓↓ blood perfusion ↓↓ O2 supply/ ↑↑O2 demand ↓↓ Ischemia ↓↓ pain **precipitating factors: physical exertion, exposure to cold, eating a heavy meal, stress/emotion – provoking situation Patterns of Angina

1. stable angina/ exertional angina

- occurs with activities that involve exertional or emotional stress, and is relieved with rest or nitroglycerin - has stable pattern on onset, duration, severity, and relieving factors 2. unstable / preinfarction/ crescendo angina - occurs with unpredictable degree of exertion or emotion and increases in occurrence, duration and severity over time - pain may not be relieved with nitroglycerine 3. variant / prinzmetal/ Vasospastic angina - results from coronary artery spasm and may occur at rest - attacks may be associated with ST segment elevation on ECG 4. intractable angina - chronic, incapacitating that is unresponsive to interventions 5. silent ischemia - objective evidence of ischemia ( ECG changes with stress test) but patient reports no symptoms ASSESSMENT 1. pain a. can develop slowly or quietly b. usually describes as mild or moderate pain c. substernal, crushing, squeezing pain d. may radiate to he shoulders, arms, jaw, neckm back e. usually lasts less than 5 minutes but may last up to 15-21 minutes f. relieved by nitroglycerine or rest 2. dyspnea 3. pallor 4. sweating 5. palpitations and tachycardia (apprehension; feeling of impending death) 6. dizziness and faintness 7. hypertension 8. digestive disturbances DIAGNOSTIC STUDIES 1. ECG: ST depression or elevation/ T wave inversion 2. stress test: chest pain or changes in ECG 3. cardiac catherization: provides definitive diagnosis by providing information about the patency of coronary arteries pre-procedure: obtain consent assess for allergies to seafoods, iodine and radiopaque dyes withhold meals before the procedure

document baseline VS have the client void administer sedatives as ordered mark distal pulses inform the client that a warm or flushing feeling sensation may be felt as the contrast medium is injected; fluttery feeling as the catheter passes through the heart post-procedure monitor VS and cardiac rhythm for dysrhythmias assess for chest pain monitor peripheral pulses, color, warmth and sensation distal to the insertion sites monitor for bleeding and hematoma extremity is extended for 4-6 hours post procedure strict bed rest for 6-12 hours encourage fluids monitor for signs of hypersensitivity MEDICAL MANAGEMENT Goal: decrease O2 demand and increase O2 supply 1. pharmacologic Therapy a. Nitrates: Nitroglycerine MOA: dilates coronary artery Decrease preload and afterload Routes: sublingual, topical (patch), IV S/e: headache, hypotension b. Beta-blockers: propranolol, metoprolol, atenolol MOA: block B-adrenergic sympathetic stimulation ↓↓HR, BP , myocardial contractility = ↓↓↓ O2 demand C/I : hypotension, bradycardia, AV block, HF Asthma/ COPD c. Ca- channel blockers: amlodipine, verapamil, diltiazem MOA: ↓ conduction --- ↓↓ HR and muscle contraction = ↓↓↓ O2 demand Relax blood vessels--↓↓BP, coronary vasodilation = ↓↓O2 demand d. antiplatelet ad anticoagulant MOA: Prevents platelet aggregation and formation of new blood clots aspirin  heparin (monitor for APTT: therapeutic level = 1.5 to 2x normal) S/e: bleeding!!!!!!!!!!!

2. O2 therapy NURSING INTERVENTION A. treating angina Stop all activities – rest in semi-fowler’s to decrease O2 requirement Assess the pain Measure VS, obtain 12-lead ECG Administer NTG O2 therapy at 2-3L/min B. reduce anxiety Provide information about illness, diagnostic procedures, treatment and methods to prevent progression C. Preventing pain Identify level of activity and plan for rest periods D. Provide Home and community based care Lifestyle changes Myocardial infarction • occurs when myocardial tissue is abruptly and severely deprived of oxygen • ischemia can lead to necrosis of myocardial tissue if blood flow is not restored • infarction evolves over several hours • obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infracted area appears blue and swollen total blockage of coronary artery ↓↓ ischemia ↓↓ necrosis ↓↓ neutrophils invade the infracted area ↓↓ granulation of tissue, scar development ↓↓ permanently changes due to scar formation - changes in the size and shape of the entire myocardium Location of MI
1. Left anterior descending (LAD) artery – anterior MI or septal MI or both

2. circumflex artery – posterior wall MI or lateral wall MI 3. right coronary artery (RCA) – inferior wall MI Risk Factors 1. atherosclerosis 2. CAD 3. smoking 4. hypertension 5. obesity 6. physical inactivity 7. impaired glucose tolerance 8. stress Diagnostic studies 1. ECG a. Ischemia = ST segment depression, T wave inversion b. Infarction = ST segment elevation, followed by T wave inversion Hypocalcemia – U wave, depressed ST segment, short T wave Hyperkalemia – prolonged QRScomplex, elevated STsegment, peaked T wave MI – ST segment elevation, inverted T wave, pathologic Q wave
2. Laboratory tests: Cardiac enzymes increase when myocardial cells die

Enzyme CPK-MB Myoglobin Troponin I LDH

Onset 3-6 h 1-3h 3-4h 12h

Peak 12-18h 4-12h 4-24h 18h

Return to normal 18h 12h 1-3wk 10-14days

3. cardiac catheterization - provides the most definitive source of diagnosis - shows the presence of atherosclerotic lesions R sided heart catheterization: medial cubital or brachial vein L sided heart catheterization: brachial or femoral artery Medical management Goal: to minimize myocardial damage To preserve myocardial function To prevent complications 1. Emergent Percutaneous Transluminal Coronary Angoplasty To open occluded coronary artery and promote reperfusion 2. Pharmacologic Therapy a. Thrombolytics: dissolve and lyse thrombi

Indications: chest pain > 20min unrelieved by NTG ST segment elevation in at least 2 lead systems < 24 hour from onset of pain Nursing considerations: Minimize skin puncture Treat major bleeding by discontinuing thrombolytic therapy and anticoagulants, apply pressure and notify physician immediately treat minor bleeding by applying direct pressure is accessible and appropriate Examples: urokinase streptokinase tissue plasminogen activator b. analgesics: Morphine sulfate : decreases pain and anxiety : promotes blood vessel dilatation, decreasing preload and heart Workload : relaxes bronchioles, increasing oxygenation Nsg consideration: Monitor BP, RR, and ECG c. Angiotensin-Converting Enzyme (ACE) inhibitor : prevent Heart failure Nsg consideration: WOF s/e of the medication (coughing) Examples: captopril, enalapril, remipril, lisonopril d. Nitrates : dilates arteries and veins, decreasing cardiac workload and thus oxygen demand; increases coronary perfusion : decreases vasospasm Examples: NTG S/E : headache, hypotension e. Beta adrenergic blocking agents : decrease myocardial oxygen consumption by blocking beta adrenergic sympathetic response: ↓↓ HR, BP, contractility C/I : patients with asthma and congestive heart failure Examples: propranolol, metoprolol f. Calcium Channel blockers :slows HR and relaxes blood vessel : relieves vasospasm : Diltiazem. Verapamil, Nifedipine, Amlodipine, Felodipine g. Antiplatelets: Aspirin

: prevents platelet aggregation h. anticoagulant: Heparin : prevents formations of new blood clots : amount is based on APTT result 3. O2 administration 4. bed rest Nursing Implementation a. goal: reduce pain, discomfort 1. analgesic: Morphine SO4 2. humidified oxygen 3. position: semi-fowler b. goal: maintain adequate circulation 1. monitor VS and UO, observe for signs of shock 2. monitor ECG for arrhythmia 3. give medications as ordered: Antiarrhythmic drugs: lidocaine Anticoagulants : heparin Thrimbolytic: streptokinase 4. recognize HF: edema, cyanosis, dyspnea, cough, crackles 5. check lab data: serum enzymes, blood gases, electrolytes 6. check CVP: increases with HF c. goal: decrease O2 demand and promote oxygenation 1. oxygen therapy 2. activity: bed rest and increase activity as ordered 3. position: semi-fowler 4. quite and comfortable environment d. goal: maintain fluid and electrolyte, nutritional status 1. IV, CVP, VS, UO 2. lab data (esp electrolytes) within normal limits 3. monitor ECG changes 4. diet: progressive low calorie, low sodium, low fat diet e. goal: health teaching 1. diagnosis and treatment regimen 2. medications: administration, importance, untoward effects 3. control risk factors 4. need for follow-up care for regulation of medications and evaluation of risk factors f. goal: provide emotional support

 Preload – degree of stretch of cardiac muscle fibers at the end of diastole:

Frank-Starling Law – the greater the stretch on the heart, the greater the shortening  Afterload – amount of resistance to ejection of blood from the ventricle Nursing assessment for CARDIOVASCULAR DISORDERS  Genetic disorders: 1. Familial hypercholesterolemia 2. Hypertrophic cardiomyopathy  Chest pain or discomfort – angina pectoris, dysrhythmias, VHD  Shortness of breath or dyspnea- cardiogenic shock, HF, VHD  Peripheral Edema and weight gain – HF  Palpitations  Fatigue – early warning of HF, VHD  Dizziness, syncope or changes in level of consciousness  Chest pain should be taken seriously until cause is determined  Substernal chest pain can result from a number of causes: 1. Pericarditis 2. Pulmonary disorder – pneumonia 3. Esophageal disorders – hiatal hernia, reflux esophagitis 4. Anxiety and panic disorders 5. Musculoskeletal disorders  The severity or duration of chest pain or discomfort does not predict the seriousness of its cause.  Elderly people and patients with diabetes may not experience chest pain as a typical symptom Risk factors Non-Modifiable risk factors  Familial history of coronary artery disease (CAD)  Increasing age  Male gender  Postmenopausal women – have 2-3x the CAD rates of premenopausal women of same age  Race – higher incidence in African American than Caucasians due to greater risk of hypertension Modifiable risk factors LDL < 100 mg/dL; (CAD) < 70mg

HDL > 40 mg/dL TAG <150 mg/dL.  Hyperlipidemia  Hypertension < 140/90; diabetic- < 130/80  Cigarette smoking, exposure to tobacco smoke  Diabetes mellitus FBS < 110 mg/dL HgA1C - <7%  Obesity BMI 18.5-24.9 kg/m2 waist circum male< 40 inches female < 35 inches  Physical inactivity – 30-60 min of moderate intensity activity Physical assessment  General appearance and cognition  Inspection of the skin  Blood pressure  Pulse pressure- 30-40 mmHg  Postural blood pressure changes  Arterial pulses  Jugular venous pulsations  Heart inspection and palpation  Chest percussion  Cardiac auscultations S1- closure of mitral and tricuspid valve S2- closure of aortic and pulmonic valves
 Inspection of the Extremities

1. 2. 3. 4. 5. 6.

Decreased capillary refill time ->3 secs Vascular changes due to decreased arterial circulation Hematoma – due to cardiac procedures Peripheral edema Clubbing of fingers Lower extremity ulcers – arterial or venous insufficiency


1. Tachypnea- rapid, shallow breathing 2. Cheyne-Stokes respirations – rapid respiration alternating with apnea; seen in severe left ventricular failure 3. Hemoptysis – pink frothy sputum indicates pulmonary edema 4. Cough – dry, hacking cough due to pulmonary congestion from HF 5. Crackles – HF and atelectasis 6. Wheezes – caused by interstitial pulmonary edema  ABDOMEN:

1. Hepatojugular reflux – liver engorgement occurs bec of decreased venous return due to RVF  2. Bladder distention – urine output is an important indicator of cardiac function

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