Cardiovascular Diseases PDF

CARDIOVASCULAR DISEASES ROSELLE JOY C. BALAQUIT, RN CORONARY ARTERY DISEASE Refers to a variety of pathologic conditions causing narrowing or obstruction of coronary arteries, therefore decreasing blood supply to the myocardium Decreased perfusion to myocardial tissue leads to inadequat...

CARDIOVASCULAR DISEASES ROSELLE JOY C. BALAQUIT, RN CORONARY ARTERY DISEASE Refers to a variety of pathologic conditions causing narrowing or obstruction of coronary arteries, therefore decreasing blood supply to the myocardium Decreased perfusion to myocardial tissue leads to inadequate myocardial oxygen supply Results from a central narrowing of large and medium sized coronary arteries due to intimal plaque formation CORONARY ARTERY DISEASE Atherosclerosis (deposits of cholesterol and lipids within the walls of the artery) – is the major causative factor May manifest as angina pectoris or MI Coronary artery narrowing is significant if the lumen diameter of the left main artery is reduced at least 50%, or if any major branch is reduced at least 75% The goal of treatment is to alter atherosclerotic progression Cardiac catheterization provides the most definitive source for diagnosis  ETIOLOGY & RISK FACTORS Age: above 30-50 years old Sex: males and postmenopausal females Race: nonwhites have higher mortality rates Family history of CAD Hypertension DM smoking Obesity Sedentary lifestyle Hyperlipidemia Elevated serum uric acid levels  ETIOLOGY & RISK FACTORS Most important modifiable risk factor Smoking Hypertension DM Cholesterol abnormalities PATHOPHYSIOLOGY RISK FACTORS (non-modifiable/modifiable RF) Non-specific injury to arterial wall Lipids (LDL, VLDL) and platelets form into the vascular intima Attracts monocytes/macrophages into the site Fatty streak (plaque) begins to form in the intima Narrowing of the arterial lumen Reduced coronary artery blood flow Myocardial Ischemia PATHOPHYSIOLOGY When blood flow is reduced and ischemia occurs, ST segment depression, T wave inversion, or both is noted; ST segment returns to normal when the blood flow returns With infarction, cell injury results in ST segment elevation, followed by T wave inversion and an abnormal Q wave Blood lipid levels may be elevated ANGINA PECTORIS It is a transient, paroxysmal chest pain produced by insufficient blood flow Chest pain caused by myocardial ischemia – a condition in which the amount of oxygen getting to the heart muscle is insufficient commonly known as angina – is the sensation of chest pain, pressure, or squeezing, often due to ischemia of the heart muscle from obstruction or spasm of the coronary arteries.  ETIOLOGY & RISK FACTORS Causes include obstruction of coronary blood flow resulting from: Atherosclerosis coronary artery spasm conditions increasing myocardial oxygen consumption  ETIOLOGY & RISK FACTORS CAD Atherosclerosis Hypertension DM Severe anemia Aortic insufficiency smoking Hypercholesterolemia Family history Men are at higher risk than women Increasing age  ETIOLOGY & RISK FACTORS The 4 “e”S (precipitating factors) Exertion – physical exertion Eating – consumption of a heavy meal Extremes of Temperature – very cold or very hot Excitement – strong emotions and sexual activity  TYPES OF ANGINA PECTORIS Stable Angina The typical angina that occurs during exertion and in which the severity does not change Relieved by rest and nitroglycerin Involves episodic pain lasting 5 to 15 minutes Usually has a stable pattern of onset, duration, severity and relieving factors  TYPES OF ANGINA PECTORIS Unstable Angina Also called “pre-infarction angina” Occurs with an unpredictable degree of exertion or emotion and increases in occurrence, duration, and severity over time Occurs with an unpredictable degree of exertion or emotion and increases in occurrence, duration, and severity over time Pain may not be relieved with rest and nitroglycerin Increased risk for MI  TYPES OF ANGINA PECTORIS Unstable Angina An acute coronary syndrome should be treated as a medical emergency There is an increased risk for an MI, severe cardiac dysrhythmia, or cardiac arrest leading to sudden death  TYPES OF ANGINA PECTORIS Prinzmetal Variant Angina Also called Prinzmetal or vasospastic angina Results from coronary artery spasm May occur at rest Attacks may be associated with ST segment elevation noted on the ECG Transmural ischemia with ST segment elevation on ECG when symptomatic but definitive diagnosis is only by coronary angiography PATHOPHYSIOLOGY RISK FACTORS Reduced coronary tissue perfusion Oxygen demands exceeds oxygen supply Diminished myocardial oxygenation Anaerobic metabolism Increased lactic acid production Chest pain  CLINICAL MANIFESTATIONS Pain – most common characteristic symptom Heaviness, tightness, squeezing or burning sensation in the chest Radiates to the jaw, neck, left shoulder and arms Precipitated by activity or exertion Relieved by rest and nitroglycerin  CLINICAL MANIFESTATIONS Dyspnea Pallor Sweating or diaphoresis Palpitations and tachycardia Faintness, dizziness Nausea and vomiting Cold and clammy skin DIAGNOSTIC TESTS ECG – ST segment depression, T wave inversion during chest pain Stress test – abnormal ECG during exercise NURSING MANAGEMENT Monitor and improve client’s cardiopulmonary condition Check VS check client’s arterial blood gas (ABG and oxygen saturation Obtain a 12 lead ECG Provide client teaching and discharge planning Teach the client management of anginal attacks Give instruction on us of nitroglycerin during anginal attacks: Stop all activity Allow tablet to dissolve under the tongue (sublingual) NURSING MANAGEMENT Give instruction on use of nitroglycerin during anginal attacks: If there is no relief with one tablet, take additional tablets at 5 minute intervals, but should be no more than three tablets within a 15 minute period Relax for 15 minutes after taking nitroglycerin to prevent dizziness Headache, dizziness, faintness, tachycardia are a common SE Keep dark bottle tight capped and prevent exposure to air, light and heat Check shelf-life (usually 6 months) and expiration date of tablets Medication causes burning sensation under the tongue Assist client to identify risk factors that can be modified Provide client teaching and discharge planning NURSING MANAGEMENT Ways to minimize precipitating events: Reduce stress and anxiety i.e. relaxation techniques Avoid overexertion Avoid smoking Maintain low-cholesterol, low saturated fat diet, and eat small, frequent meals Avoid extremes of temperature Dress warmly in a cold weather Participate in a regular exercise program Space exercise periods and allow for rest periods NURSING MANAGEMENT Provide other dependent nursing interventions: Administer prescribed medications Nitrates – Nitroglycerin (dilates the coronary arteries to increase blood circulation to myocardial tissue) Platelet aggregation inhibitor – i.e. Aspirin (to prevent thrombus formation) Beta-blockers – i.e. Propanolol (blocking the effect of sympathetic NS reducing BP and HR, thereby reducing cardiac oxygen demand) Calcium channel blocker – i.e. Nifedipine (to dilate coronary artery to reduce vasopasm and decrease the workload of the heart) NURSING MANAGEMENT Promote myocardial perfusion: Instruct client to maintain bed rest Place client in semi to high fowler’s position Administer oxygen at 3 LPM Avoid valsava maneuvers Provide laxatives or high fiber diet to lessen constipation Avoid increase physical activities MEDICAL MANAGEMENT Assist in possible treatment modalities: Percutaneous transluminal coronary angioplasty (PTCA) To compress the plaque against the blood vessel wall thereby increasing the arterial lumen A specially designed balloon-tipped catheter is inserted under fluoroscopoc guidance and advance to the site of coronary artery obstruction Recommended for client with single-vessel coronary artery disease MEDICAL MANAGEMENT Coronary Artery bypass graft (CABG) To improve the blood flow to the myocardial tissue The main purpose is myocardial revascularization The commonly used graft is saphenous vein Recommended if sever narrowing of one or more branches of the coronary artery MYOCARDIAL INFARCTION Occurs when myocardial tissue is abruptly and severely deprived of oxygen Death of myocardial tissue in regions of the heart brought about by inadequate oxygenation caused by sudden and complete blockage Ischemia can lead to necrosis of myocardial tissue if blood flow is not restored Obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infarcted areas appears blue and swollen Characterized by localized formation of necrosis (tissue destruction) with subsequent healing by scar formation and fibrosis  ETIOLOGY CAD Coronary vasospasm Coronary artery occlusion by embolus and thrombus Conditions decreasing perfusion such as hemorrhage and shock Hypertension DM RISK FACTORS Hypercholesterolemia Smoking Hypertension Obesity Stress Sedentary lifestyle Atherosclerotic coronary artery dise PATHOPHYSIOLOGY RISK FACTORS Interrupted coronary artery blood flow Myocardial ischemia Decreased myocardial oxygen supply Cellular hypoxia Anaerobic myocardial metabolism for several hours Pain PATHOPHYSIOLOGY Imbalanced between myocardial oxygen supply and demand Persistent ischemia Depressed cardiac function Trigger autonomic NS response Increased myocardial contractlity (inc. HR) Increased myocardial oxygen demand  CLINICAL MANIFESTATIONS Chest Pain severe, persistent, crushing, prolonged pain radiating to the neck, arm, jaw and back Occurs without cause, primarily early in the morning Not relieved by rest or nitroglycerin Last for 30 minutes or longer  CLINICAL MANIFESTATIONS Nausea and vomiting Diaphoresis, cold and clammy skin Dyspnea Dysrhythmias Elevated temperature Restlessness and anxiety with a feeling of impending doom Initial increase in BP and pulse then followed by a gradual drop DIAGNOSTIC TESTS ECG ST segment elevation dependent on location of myocardial damage T wave inversion and presence of Q wave DIAGNOSTIC TESTS Myocardial enzymes – increased Troponin T and I, CK-MB and LDH Blood tests – elevated wbc count, erythrocyte sedimentation rate (ESR), Elevated serum cholesterol NURSING MANAGEMENT Monitor and improve client’s cardiopulmonary state Monitor ECG Perform complete lung/cardiovascular assessment Monitor urine output and report of less than 30 ml/hour Monitor for complications i.e. dysrhythmias since ventricular tachycardia can happen in the first few hours after MI NURSING MANAGEMENT Minimize client anxiety: Provide information as to procedures and drug therapy Reassure client and provide information as needed NURSING MANAGEMENT Minimize metabolic demands: Provide soft diet Provide a low sodium, low cholesterol and low fat diet NURSING MANAGEMENT Provide oxygen at 2 lpm to relieved dyspnea and prevent arrhythmias: Advise bed rest in semi-fowler’s position Administer medications: Nitrates (dilation of coronary artery), thrombolytics (dissolve clots in the coronary artery), aspirin, ACE inhibitors (prevents formation angiotensin II) and anticoagulants (prevents clot formation) Stool softener and hypolipedemics Analgesics: Morphine sulfate (DOC)  NURSING MANAGEMENT Provide client health teaching: Effects of MI, healing process and treatment regimen Medication regimen including name, purpose, schedule, dosage and side effects Risk factors with necessary life modifications Dietary restrictions: low sodium, low cholesterol, avoidance of caffeine Importance of participation in a progressive activity program Reporting of the following symptoms: increased/persistent chest pain, dyspnea, weakness, fatigue, persistent palpitations and light-headedness Enrolment of a client in a cardiac rehabilitation program NURSING MANAGEMENT After acute episodes: Maintain bed rest for the first 3 days Provide passive range of motion (ROM) exercise Progression of movement: dangling of the feet at the side of the bed, sitting on the bed, then out on a chair for 30 minutes thrice daily, afterwards proceed with ambulation in the room, to the toilet then to the hallway thrice daily Cardiac rehabilitation To extend and improve quality of life For physical conditioning MEDICAL MANAGEMENT Morphine Sulfate Relaxes bronchioles to enhance oxygenation Provides pain and anxiety relief Given IV MEDICAL MANAGEMENT M – morphine O – oxygen N – Nitroglcerine A - Aspirin MEDICAL MANAGEMENT Assist in treatment modalities such as: PTCA CABG  CONGESTIVE HEART FAILURE Inability of the heart to pump the amount of oxygenated blood to meet metabolic requirements of the body Severe circulatory congestion due to decreased myocardial contractility, which results in the heart’s inability to pump sufficient blood to meet the body’s needs Common types: Left sided heart failure Right sided heart failure The right sided- failure is commonly due to left- sided failure CLASSIFICATION OF HEART FAILURE Class 1 Ordinary physical activity does not cause chest pain and fatigue No pulmonary congestion No limitation in activities of daily living (ADL) Class 2 Slight limitation in ADLs No symptom at rest (+) symptom with activity CLASSIFICATION OF HEART FAILURE Class 3 Marked limitation in ADLs Comfortable at rest but symptoms present in less than ordinary activity Class 4 Symptoms are present at rest ETIOLOGY Decreased myocardial contractility due to cardiac diseases: CAD MI Valvular heart disease Hypertensive heart disease Dysrhythmias Pericardial tamponade Pericarditis LEFT SIDED HEART FAILURE Left ventricular damage usually due to MI, hypertension, ischemic heart disease, aortic valve disease or mitral stenosis Left ventricular damage causes blood to back up through the left atrium and into the pulmonary veins Increased pressure causes transudation into the interstitial tissues of the lungs with resultant pulmonary congestion LEFT SIDED HEART FAILURE The congestion occurs primarily in the lungs leading to the symptoms referable to the pulmonary systems Blood flow from the left ventricle is diminished, causing decreased flow to the brain, kidneys and other tissues PATHOPHYSIOLOGY Left ventricular failure----pump failure---- back up of blood into the pulmonary veins--- -increased pulmonary capillary pressure---- pulmonary congestion Left ventricular failure----decreased cardiac output----decreased perfusion to the brain, kidney and other tissues----oliguria, dizziness  CLINICAL MANIFESTATIONS Respiratory system Dyspnea on exertion Paroxysmal nocturnal dyspnea (PND) Orthopnea Adventitious breath sound: pulmonary crackles/rales, possible bronchial wheezing Cough with pinkish, frothy to blood tinged sputum  CLINICAL MANIFESTATIONS Cardiovascular system Peripheral and central cyanosis with pallor of the skin Tachycardia with S3 heart sound, PMI displaced laterally Decreased peripheral pulses and capillary refill longer than 3 seconds  CLINICAL MANIFESTATIONS Other manifestations Cool extremities Muscle weakness, malaise, easy fatigability Insomnia Signs of cerebral anoxia DIAGNOSTIC TEST Chest X-Ray – cardiac hypertrophy (cardiomegaly), vascular congestion of the lung fields 2D Echocardiography – increased size of the chamber ECG – identify cardiac hypertrophy ABG – decreased partial oxygen pressure (PaO2), increased partial carbon dioxide pressure (PaCO2) DIAGNOSTIC TEST Pulse oximeter – decreased SaO2 Pulmonary Artery Pressure (PAP) and Pulmonary Capillary Wedge Pressure (PCWP) – increased depends on the degree of heart failure RIGHT SIDED HEART FAILURE Weakened right ventricle is unable to pump blood into the pulmonary system Systemic venous congestion occurs as pressure builds up Caused by: left sided heart failure Right ventricular infarction Atherosclerotic heart disease COPD Pulmonic stenosis Pulmonary embolism PATHOPHYSIOLOGY Right ventricular failure---blood pooling in the venous circulation---increased hydrostatic pressure----peripheral edema Right ventricular failure----blood pooling--- venous congestion in the kidney, liver and GIT  CLINICAL MANIFESTATIONS Systemic manifestations: Distended neck vein (jugular venous distension) Bounding pulses, pulsus alternans Peripheral dependent pitting edema, Ascites, Hepatomegaly Oliguria Weight gain Cool extremities Anorexia, nausea Body weakness DIAGNOSTIC TESTS Chest x-ray – cardiomegaly ECG – cardiac hypertrophy 2D Echocardiography – hypokinetic heart, increased size of cardiac chambers ABG – decreased partial pressure of oxygen (PaO2) SaO2 – decreased oxygen saturation by pulse oximeter Liver enzymes – increased  NURSING MANAGEMENT Monitor and improve client’s cardiac pulmonary state Assess the respiratory status – assess breath sounds for presence of adventitious breath sounds Provide adequate ventilation when CHF progresses to pulmonary edema – administer oxygen therapy, maintain in semi to high fowler’s position to improve chest expansion Monitor ABG Weight client daily and monitor for fluid retention NURSING MANAGEMENT Increase cardiac output: Monitor VS ECG and hemodynamic monitoring Administer digitalis as ordered and monitor its effects Administer vasodilators as ordered NURSING MANAGEMENT Provide physical and emotional rest: Maintain quiet, relaxed environment Maintain bed rest with limited activity to provide adequate rest periods to prevent fatigue Organize nursing care around rest periods Assess level of anxiety NURSING MANAGEMENT Prevent complications of immobility: Assist the client in active/assistive ROM or perform passive ROM Apply anti-embolic stockings to prevent deep vein thrombosis as ordered NURSING MANAGEMENT Reduce/Eliminate edema: Obtain daily weights and report if the client gains 3 pounds or more per day (a sign of fluid retention) Maintain accurate intake and output (I & O) recording Assess for peripheral edema Measure abdominal girths daily Monitor electrolyte levels Administer diuretics as ordered NURSING MANAGEMENT Provide dependent nursing interventions: Determination and elimination/control of underlying cause Sodium-restricted diet to decrease fluid retention and cardiac workload Drug therapy such as cardiac cardioglycoside, diuretics, vasodilators and anti-lipidemics NURSING MANAGEMENT Provide client teaching and planning: Monitoring of self daily for signs and symptoms of CHF – pedal edema, weight gain of 1-2 lbs in a 2 day period, dyspnea, loss of appetite, cough Medication regimen – name, purpose, dosage, frequency and side effects Prescribed dietary meal planning – low/restricted sodium, small frequent meals Avoidance of fatigue and planning rest periods MEDICAL MANAGEMENT Drug used to treat CHF: Vasodilators Act to directly relax vascular muscle tone causing a decrease in blood pressure with pooling of blood in the veins Decrease preload and afterload Example – Calcium channel blocker, nitrates MEDICAL MANAGEMENT Drug used to treat CHF: ACE inhibitor Agents that block the conversion of angiotensin I to angiotensin II decreasing vasoconstriction and blood volume Decrease afterload E.g Captopril MEDICAL MANAGEMENT Drug used to treat CHF: Diuretics Used to decrease the blood volume causing a decrease in venous return and blood pressure Decrease preload and afterload Example – Furosemide (Lasix) MEDICAL MANAGEMENT Drug used to treat CHF: Beta Stimulators Stimulates the beta receptors in the sympathetic nervous system, thereby increasing the myocardial contraction (positive inotropic effect) E.g. Digoxin (lanoxin)