Coronary artery disease

Coronary artery disease
And nursing implications

Etiology & Pathophysiology
Most common form of heart disease Can develop to become: Chronic stable angina Acute coronary syndrome Unstable angina Myocardial infarction Can occur in any artery Prefers coronary arteries

Normal Endothelium & Injury Response
Barrier between the vessel wall and the lumen of the vessel Nonreactive to platelets and leukocytes Nonreactive to coagulation, fibrinolytic, and complement factors Endothelial wall alters as a result of inflammation and injury Injury includes items listed on left of slide

Fatty Streak Earliest lesions
Characterized by lipid-filled smooth muscle cells Can begin as early as age 15 Potentially reversible with lowering LDL cholesterol

Fibrous Plaque Beginning of progressive changes in the arterial wall
Can appear by age 30 and increases with age Lipoproteins transport cholesterol and other lipids into the arterial intima Fatty streak is covered by collagen, forming a fibrous plaque Narrows the artery and a reduces blood flow to the distal tissues

Complicated Lesion Continued inflammation resulting in plaque instability, ulceration, and rupture Platelets accumulate and thrombus forms Increase narrowing or total occlusion of lumen

Collateral Circulation
Factors contributing to the growth and extent of collateral circulation Inherited predisposition to develop new blood vessels Presence of chronic ischemia When occlusion occurs slowly there is an increased chance of adequate collateral circulation and adequate myocardial blood flow With rapid onset CAD or coronary spasm, there is not enough time to establish collateral vessels Diminished arterial flow results in more severe ischemia or infarction Normal open, functioning coronary artery – normally, some arterial connections exist within the coronary circulation Partial coronary artery closure with collateral circulation being established Total coronary artery occlusion with collateral circulation bypassing the occlusion to supply blood to the myocardium Rapid onset CAD occurs in cases like familial hypercholesterolemia

Risk factors for CAD

Nonmodifiable Risk Factors
Age Risk increases with age Gender Incidence is highest in white middle-aged men After age 65, incidence in men and women similar Women tend to manifest CAD 10 years later than men When symptoms develop, women experience symptoms of angina rather than MI – opposite is true in men

Nonmodifiable Risk Factors
Ethnicity White middle-aged men have highest incidence African American women have a higher incidence and death rate compared to white women Native Americans have mortality rates 2x high as other Americans Family history Familial hypercholesterolemia Genetic predisposition Autosomal dominant disorder

Modifiable Risk Factors
Elevated serum lipids Cholesterol >200 mg/dl Triglycerides >150 mg/dl Lipoproteins HDLs - high density high levels desirable low levels associated with risk for CAD LDLs - low density Elevated levels correlate most closely with increased incidence of CAD HDLs increased by: Exercise Moderate alcohol intake Estrogen administration

Elevated blood pressure Hypertension: BP > 140/90 Increases risk of atherosclerosis Tobacco use Nicotine can cause catecholamine release HR, peripheral vasoconstriction, BP Platelet adhesion leading to emboli formation

Physical inactivity People who are active have higher HDLs Exercise increases collateral circulation & lowers BP Obesity BMI > 30 kg/m2 Leads to increased LDLs and triglycerides Associated with hypertension People who are apple-shaped (store fat in abdomen) have higher incidence of CAD

Diabetes & Metabolic syndrome Incidence of CAD 2-4x higher Obesity Hypertension Elevated triglycerides, abnormal serum lipids, elevated fasting blood glucose Insulin resistance

Psychological states Increase risk of CAD Include depression, hopelessness, anxiety, hostility, & anger Stress correlated with CAD Elevated homocysteine level Damage the inner lining of blood vessels Promote plaque build-up Alter the clotting mechanism to make clots more likely to occur

Prevention & Treatment

Health Promotion Hypertension Have regular blood pressure checkups
Take prescribed medications for blood pressure control Reduce salt intake Stop tobacco use; avoid exposure to environmental tobacco (secondhand) smoke Control or reduce weight Perform physical activity regularly

Health Promotion Elevated serum lipids Reduce total fat intake
Reduce animal (saturated) fat intake Take prescribed medications for lipid reduction Adjust total caloric intake to achieve and maintain ideal body weight Engage in regular physical activity Increase amount of complex carbohydrates and vegetable proteins in diet

Health Promotion Tobacco use Enroll in a smoking cessation program
Change daily routines associated with smoking to reduce desire to smoke Substitute other activities for smoking Ask caregivers to support efforts to stop smoking Avoid exposure to environmental tobacco smoke

Health Promotion Physical Inactivity
Develop and maintain at least 30 minutes of moderate physical activity on most days of the week Increase activities to a fitness level

Health Promotion Psychological State
Increase awareness of behaviors that are detrimental to health Alter patterns that are conducive to stress Set realistic goals for self Reassess priorities in light of health needs Learn effective stress management strategies Seek professional help if feeling depressed, angry, or anxious Plan time for adequate rest and sleep

Health Promotion Obesity Change eating patterns and habits
Reduce caloric intake to achieve BMI of <25 Increase physical activity to increase caloric expenditure Avoid fad and crash diets, which are not effective over time Avoid large, heavy meals

Health Promotion Diabetes Follow the recommended diet
Control or reduce weight Take prescribed anti-diabetic medications Monitor blood glucose levels regularly

Nutritional Therapy Reduce or omit red meats, eggs, whole milk
Calorie restrictions Decrease dietary fat/cholesterol Limit saturated fats and cholesterol and emphasize complex carbohydrates Fats – only about 30% of calories Reduce or omit red meats, eggs, whole milk Omega 3 fatty acids

Identify people at risk
Thorough health history Accurate medication list Prescription Over the counter Presence of cardiovascular symptoms Environmental patterns like diet and activity Values and beliefs about health and illness

Cholesterol Lowering Drug Therapy
Drugs that restrict lipoprotein production Statins Inhibit synthesis of cholesterol in the liver Need to monitor liver enzymes Creatine kinase assessed if myopathy suspected Niacin Interferes with the synthesis of LDL and triglycerides Increases HDL Can cause flushing, pruritus, GI complaints, orthostatic hypotension Flushing may be prevented by aspirin or NSAIDs Lopid Lower triglycerides Side effects may include rashes and mild GI disturbances

Cholesterol Lowering Drug Therapy
Drugs that increase lipoprotein removal Bile acid sequestrants (e.g., cholestyramine [Questran]) Increase conversion of cholesterol to bile acids Decrease hepatic cholesterol Side effects include complaints of palatability and upper and lower GI symptoms Drugs that decrease cholesterol absorption Zetia

Antiplatelet Drug Therapy
ASA , Plavix Low dose ASA (81mg) Studies show decrease in first MI’s Can cause GI bleed Use if benefit outweighs risk Plavix has decreased risk of bleed

Clinical Manifestations of CAD

Chronic Stable Angina Temporary myocardial ischemia = Angina (chest pain) Happens when oxygen supply is less than oxygen demand Cardiac Non cardiac Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis

Precipitating Factors of Angina
Physical exertion Temperature extremes Strong emotions Consumption of heavy meal Tobacco use or environmental tobacco smoke Sexual activity Stimulants Circadian rhythm patterns

Chronic Stable Angina Referred pain in left shoulder and arm is from transmission of the pain message to the cardiac nerve roots Pain usually lasts 3 to 5 minutes Pain subsides when precipitating factor relieved Pain at rest is unusual ECG reveals ST-segment depression and/or T-wave inversion

Chronic Stable Angina Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms Constrictive Squeezing Heavy Choking Suffocating sensation

Angina Pain Sites Most of the pain experienced in angina appears substernally, it may also occur in the neck May radiate to: Jaw Shoulders Down the arms Pain between the shoulder blades often is dismissed as not being heart related

Types of Stable Angina Silent Ischemia
Ischemia that occurs in the absence of any subjective symptoms Associated with diabetic neuropathy Confirmed by ECG changes Up to 80% of patients with ischemia are asymptomatic Ischemia with or without pain has same prognosis

Types of Stable Angina Nocturnal angina
Occurs only at night but not necessarily during sleep or in recumbent position Angina decubitus Chest pain that occurs only while lying down Relieved by standing or sitting

Types of Stable Angina Prinzmetal’s Angina
Occurs at rest usually in response to spasm of major coronary artery Seen in patients with a history of migraine headaches and Raynaud’s phenomenon Spasm may occur in the absence of CAD. When spasm occurs Chest pain Marked, transient ST-segment elevation May occur during REM sleep May be relieved by moderate exercise or may disappear spontaneously

Types of Stable Angina Microvascular Angina
May occur in the absence of significant coronary atherosclerosis or coronary spasm Seen especially in women Pain is related to myocardial ischemia associated with abnormalities of the coronary microcirculation.

Acute Coronary Syndrome

Progression of Cardiovascular disease
NSTEMI OR STEMI

Acute Coronary Syndrome
When ischemia is prolonged and is not immediately reversible, acute coronary syndrome (ACS) develops. ACS encompasses Unstable angina (UA) Non–ST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation MI (STEMI)

Deterioration of once stable plague
Progression of CAD Deterioration of once stable plague Rupture Platelet aggregation Thrombus Result Partial occlusion of coronary artery: USA or NSTEMI Total occlusion of coronary artery: STEMI

Unstable Angina Chest pain that is: New in onset Occurs at rest
Has a worsening pattern Chronic stable angina can develop to unstable Significant change in the pattern of pain Increasing frequency Easily provoked by minimal or no exertion Unpredictable and represents a medical emergency UA or USA

Myocardial Infarction
Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis) Necrosis of entire thickness of myocardium takes 4 to 6 hours. Eighty percent to 90% of all acute MIs are secondary to thrombus formation

Infarctions are usually described according to the location of damage Anterior Inferior lateral posterior wall infarction

The degree of altered function depends on the area of the heart involved and the size of the infarct. Contractile function of the heart is disrupted in areas of myocardial necrosis. Most MIs involve the left ventricle (LV).

Clinical Manifestations of ACS
Pain Total occlusion → Anaerobic metabolism and lactic acid accumulation → Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration Described as heaviness, constriction, tightness, burning, pressure, or crushing Common locations: Substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms

Stimulation of sympathetic nervous system results in Release of glycogen Diaphoresis Vasoconstriction of peripheral blood vessels Skin: Ashen, clammy, and/or cool to touch

Cardiovascular Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in cardiac output) Crackles Jugular venous distention Abnormal heart sounds S3 or S4 New murmur

Nausea and vomiting Can result from reflex stimulation of the vomiting center by severe pain Fever Systemic manifestation of the inflammatory process caused by cell death

Diagnostic Studies 12-lead ECG Can rule out or confirm MI
Changes in QRS complex, ST segment, & T wave Not always evident shortly after infarct Serum cardiac markers Released into blood from necrotic heart muscle after MI Troponin CK-MB Myoglobin Serial

ECG Changes

Diagnostic Studies Coronary angiography Cardiac catheterization
Percutaneous coronary intervention (PCI) Stent Balloon angioplasty Stress testing Exercise Drug Persantine Adenocard Echocardiogram

Complications Dysrhythmias Abnormal heart rhythms
Most common complication Present in 80% of MI patients Most common cause of death in the pre-hospital period Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock

Complications Heart failure
A complication that occurs when the pumping power of the heart has diminished Symptoms mild dyspnea restlessness agitation slight tachycardia. pulmonary congestion, crackles jugular vein distention

Complications Cardiogenic shock
Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure Mortality rate is high Signs and symptoms Low BP Confusion pale, clammy skin Decreased urine output Requires aggressive management control of dysrhythmias Intra-aortic balloon pump (IABP) therapy vasoactive drugs

Complications Papillary muscle dysfunction
Causes mitral valve regurgitation Condition aggravates an already compromised LV New systolic murmur at the cardiac apex Confirmed with echocardiogram Requires surgical treatment

Complications Ventricular aneurysm
Results when the infarcted myocardial wall becomes thinned and bulges out during contraction Signs and symptoms Chest pain Ventricular arrhythmias Heart failure Treatment Anticoagulation Surgery

Complications Acute pericarditis
An inflammation of visceral and/or parietal pericardium Occurs 2-3 days after MI May result in cardiac compression, ↓ LV filling and emptying, heart failure Signs and symptoms aggravated by inspiration, coughing, and movement of the upper body Pericardial friction rub may be heard on auscultation Chest pain different from MI pain Treatment includes pain relief with aspirin or corticosteroids

Complications Dressler syndrome May also occur after cardiac surgery
Characterized by pericarditis with effusion and fever that develop 4 to 6 weeks after MI Arthralgia Thought to be caused by an antigen-antibody reaction to the necrotic myocardium Treatment Short-term corticosteroids

Collaborative Care of ACS

Nursing Goals: AMI Maintain cardiac output Treat pain
Assess for complications Increase activity tolerance Relieve anxiety Ongoing and discharge teaching

Emergency management Initial interventions Rapid assessment and diagnosis Administer oxygen therapy 12 lead ECG VS, pulse oximetry Assess lung and heart sounds Establish IV Pain management Administer sublingual nitroglycerin Administer aspirin (chewable) Morphine sulfate (if nitro not effective)

Ongoing interventions Frequent VS and pulse oximetry Bedrest for 12 – 24 hours clear liquid diet NSTEMI ASA, heparin, Lovenox Percutaneous coronary intervention (PCI) – once stabilized STEMI Thrombolytic therapy

Myocardial Revascularization – Emergent PCI Treatment of choice for confirmed STEMI 90 minute door to table time Ambulatory 24 hours after the procedure Variety of procedures Percutaneous transluminal coronary angioplasty (PTCA) Intracoronary stenting Drug-eluting stents

Advantages of PCI Provide alternative to surgical intervention Performed under local anesthetic Patient ambulatory 24 hours after procedure Length of hospital stay decreased 1-3 days vs. 4–6 days after CABG Rapid return to work Return to work 5–7 days vs. 2–8 weeks after CABG

Nursing care post PCI Monitoring for signs of recurrent angina Monitor VS Evaluating groin site for signs of bleeding Monitor for infection Assess CMS of extremity used Assess for hematoma formation Bed rest

Thrombolytic therapy Indications and contraindications History of or current major bleeding problem (hemorrhagic stroke, GI bleed) prevents administration 2nd choice for revascularization Administered at facilities that do not have PCI capabilities May still need PCI after thrombolytics if not fully effective Marker of reperfusion: Return of ST segment to baseline Major complication: Bleeding FFP is used to reverse thrombolytics

Time is muscle; 6-hour window Several thrombolytic agents available, such as: Tissue plasminogen activator (t-PA) Streptokinase Reteplase Heparin and Lovenox

Coronary Artery Bypass Grafting Construction of new conduits Requires Sternotomy Cardiopulmonary bypass Common artery used: Internal mammary artery (IMA) Saphenous vein

Indications for CABG Unstable angina AMI Failure of percutaneous interventions Goals of CABG Increase blood flow to myocardium Relieve symptoms Prolong survival Improve quality of life

Drug Therapy Antiplatelet aggregation therapy
Chewable ASA 160 to 325 mg Nitroglycerin SL Given q 5 minutes 3 doses total IV nitroglycerin Goal: reduce anginal pain and improve coronary blood flow Immediate onset of action Titrated for pain relief Common side effects: HYPOTENSION HEADACHE

Drug Therapy Morphine sulfate
Given if chest pain not relieved with nitro SL Also acts as vasodilator and decreases myocardial oxygen consumption, reduces contractility, and decreased BP and HR Also reduces anxiety and fear β-adrenergic blockers Decrease myocardial oxygen demand by reducing HR, BP, and contractility IV administration in acute phase i.e. metoprolol (Lopressor)

Drug Therapy Angiotensin-converting enzyme (ACE) inhibitors
Prevent ventricular remodeling and prevent or slow progression of HF i.e. captopril (Capoten), enalapril (Vasotec) Antidysrhythmia drugs Dysrhythmias are only treated in life threatening

Drug Therapy Cholesterol-lowering drugs
Must first obtain fasting lipid panel If LDL is elevated, cholesterol-lowering drugs are initiated Stool softeners Promote bowel movement Prevents straining and vagal stimulation from Valsalva maneuver

Nursing Diagnoses Acute Pain Decreased Cardiac Output Anxiety
Activity intolerance Risk for ineffective tissue perfusion

Coronary artery disease

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