Nursing Care of Clients with Altered Tissue Perfusion PDF

MODULE 3: Nursing Care of Clients with Altered Tissue Perfusion Lesson 1 - Understanding Cardiovascular System Lesson 2 - Nursing Care of Clients with Altered Tissue Perfusion Acute Ischem...

MODULE 3: Nursing Care of Clients with Altered Tissue Perfusion Lesson 1 - Understanding Cardiovascular System Lesson 2 - Nursing Care of Clients with Altered Tissue Perfusion Acute Ischemic Heart Disease/ Coronary Artery Disease/Acute Coronary Syndrome Heart Failure Cardiogenic Shock Hypertensive Crisis Cardiomyopathy Arrhythmias (Assessment and Management) SHELDY M. PERALTA, RN, MAN  111 MODULE 3: CARE OF CLIENTS WITH ALTERED TISSUE PERFUSION INTRODUCTION Nurses constitute the largest category of healthcare personnel in nearly every country of the global community. They are the key professionals who need to be included in the process of setting a worldwide agenda for holistic patient care. As you begin the study of critical care nursing, you may be excited, uncertain, and even somewhat anxious. The field of critical care nursing often seems a little unfamiliar or mysterious, making it hard to imagine what the experience will be like or what nurses do in this area. This module presents essential information about how to safely and competently care for critically ill patients with altered tissue perfusion and their families. It recognizes the learners’ needs to assimilate foundational knowledge before attempting to master more complex critical care nursing concepts. LEARNING OUTCOMES After studying the module, you should be able to: 1. Demonstrate safe, appropriate and holistic care utilizing the nursing process. 2. Identify health needs of clients by demonstrating proper and effective health assessment and management to care for higher acuity patients and provide evidence-based interventions. 3. Observe bioethical principles, core values, and standards of nursing care. 4. Identify own learning needs. MODULE ORGANIZER There are three lessons in the module. Read each lesson carefully then answer the exercises/activities to find out how much you have benefited from it. Work on these exercises carefully and submit your output to your tutor or to the CCHAMS office. Submit your outputs to your tutor at the CCHAMS office. You may also wish to send an electronic copy of your outputs your instructor’s email or to our NUPC 119 Google classroom using your official DMMMSU email. Aside from the main content, there are supplementary materials included in this module to strengthen your learning represented by the following icons: Books or Journals Video Links Website Pages Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  112 This icon introduces some important ideas to remember. Read carefully and store them in your memory. ? At the end of the lesson/module you will find this icon. It signifies a module test to determine how well you achieved in the objectives of the module. Read carefully the questions and they must have to be answered to reinforce your learning. If you cannot answer the question satisfactorily, go back to the text. Answers to the test are to be submitted to the faculty concerned. In case you encounter difficulty, discuss this with your tutor during the face-to-face meeting. If not contact your tutor at the CCHAMS office. Good luck and happy reading!!! Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  113 Lesson 1 & Understanding Cardiovascular System Cardiovascular System The cardiovascular system consists of the heart and the blood vessels. This complex system functions to: carry life-sustaining oxygen and nutrients in the blood to all cells of the body remove metabolic waste products from the cells move hormones from one part of the body to another. HEART The heart is about the size of a closed fist. It lies beneath the sternum in the mediastinum (the cavity between the lungs), between the second and sixth ribs. The right border of the heart aligns with the right border of the sternum. The left border aligns with the midclavicular line. The exact position of the heart varies slightly in each patient. Let us have a quick review on the internal structures of the heart. Figure 1. Internal structure of the heart The heart has four chambers: right atrium, left atrium, right ventricle and left ventricle. The right and left atria serve as reservoirs for blood. The right atrium receives deoxygenated blood returning from the body. The left atrium receives oxygenated blood from the lungs. Contraction of the atria forces blood into the ventricles below. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  114 The right and left ventricles are the pumping chambers of the heart. The ventricles— which have thicker walls and are larger than the atria—are composed of highly developed muscles. The myocardium is composed of muscle tissue that contracts with each heartbeat. The right ventricle receives blood from the right atrium and pumps it through the pulmonary arteries to the lungs, where it picks up oxygen and drops off carbon dioxide. The left ventricle receives oxygenated blood from the left atrium and pumps it through the aorta and then out to the rest of the body. The inter- ventricular septum separates the ventricles and helps them to pump. Cardiovascular Assessment A. Health history – introduce yourself and explain what happens during the health history taking. a. Ask for details about the client’s chief complaint (chest pain, cough, shortness of breath, weakness/fatigue, irregular heart beat/palpitations, headache, dizziness, leg pain or cramps, swelling of the extremities, unexplained weight change) b. Ask the client for details about his family history and past medical history (health habits, drugs he/she is taking, previous surgeries, ADLs, environmental or occupational considerations, stressors and coping mechanisms). B. Pain – if the client is experiencing chest pain, ask him/her to rate the pain on a scale of 0 to 10, in which 0 indicates no pain and 10 indicates the worst chest pain imaginable. Let the client describe his condition in his own words. Ask him to describe the location, radiation, intensity, and duration of pain and any precipitating, exacerbating, or relieving factors to obtain an accurate description of chest pain. C. Physical examination – before you begin the physical examination, wash your hands thoroughly. Obtain a stethoscope with a bell and a diaphragm, an appropriate- sized blood pressure cuff, and a penlight. Perform an assessment of the client’s heart health in this order: a. inspection some abnormal findings you may note: cyanosis, pallor, or cool or cold skin, may indicate poor cardiac output and tissue perfusion. Flushed skin if the client has fever. Absence of body hair on arms or legs may indicate diminished arterial blood flow to those areas. Swelling or edema, may indicate heart failure b. Palpation note skin temperature, turgor and texture c. percussion locate the cardiac borders – begin percussing at the anterior axillary line and continue toward the sternum along the fifth intercostal space. The sound changes from resonance to dullness over the left border of the heart, normally at the midclavicular line. The right border of the heart is usually aligned with the sternum and can’t be percussed. d. Auscultation – cardiac auscultation requires a methodological approach and lots of patience. S1, 2, 3, 4, and more – systole is the period of ventricular contraction. As pressure in the ventricles increases, the mitral and tricuspid valves snap closed. The closure produces the first heart sound, S1; at the end of ventricular contraction, the aortic Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  115 and pulmonic valves snap shut. This produces the second heart sound, S2; always identify S1 and S2, and then listen for adventitious sounds, such as third and fourth heart sounds, S3 S4. Thank you Also listen for murmurs (vibrating, blowing, or rumbling sounds) and rubs (harsh, scratchy, scraping or squeaking sounds). Diagnostic tests Advances in diagnostic testing allow for earlier and easier diagnosis and treatment of cardiovascular disorders. 1. 12-lead electrocardiogram – measures the heart’s electrical activity and records it as waveforms. It’s one of the most valuable and commonly used diagnostic tools. 2. Cardiac marker studies – analysis of cardiac markers (proteins) aids diagnosis of acute MI. 3. Echocardiography – is used to examine the size, shape, and motion of cardiac structures. It’s done using a transducer placed at an acoustic window (an area where bone and lung tissue are absent) on the client’s chest. The transducer directs sound waves toward cardiac structures, which reflect these waves. 4. Cardiac catheterization – involves passing a catheter into the right, left, or both sides of the heart. 5. Hemodynamic monitoring – is used to assess cardiac function and determine the effectiveness of therapy (refer to module 1). 6. Cardiac output monitoring – the amount of blood ejected by the heart in one minute – is monitored to evaluate cardiac function. The normal range for cardiac output is 4-8 L/minute. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  116 Lesson 2 & Common Cardiovascular Disorders COMMON CARDIOVASCULAR DISORDERS you encounter in the Critical Care Unit 1. ACUTE CORONARY SYNDROME (ACS) formerly known as ACUTE ISCHEMIC HEART DISEASE also called as CORONARY ARTERY DISEASE Patients with acute coronary syndromes have some degree of coronary artery occlusion. The degree of occlusion defines whether the acute coronary syndrome is: unstable angina non–ST-segment elevated MI (NSTEMI) ST segment elevated MI (STEMI). The development of any acute coronary syndrome begins with a rupture or erosion of plaque—an unstable and lipid-rich substance. The rupture results in platelet adhesions, fibrin clot formation, and activation of thrombin. Figure 2. “Figure A is an overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B is a cross-section of the coronary artery with plaque buildup and a blood clot resulting from plaque rupture.” by National Heart Lung and Blood Institute (NIH). Causes: Patients with certain risk factors appear to face a greater likelihood of developing an acute coronary syndrome. These factors include: family history of heart disease obesity smoking high-fat, high-carbohydrate diet sedentary lifestyle menopause Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  117 stress diabetes hypertension hyperlipoproteinemia. An acute coronary syndrome most commonly results when a thrombus progresses and occludes blood flow. (An early thrombus doesn’t necessarily block blood flow.) The effect is an imbalance in myocardial oxygen supply and demand. The degree and duration of blockage dictate the type of infarct that occurs: If the patient has unstable angina, a thrombus partially occludes a coronary vessel. This thrombus is full of platelets. The partially occluded vessel may have distal microthrombi that cause necrosis in some myocytes. If smaller vessels infarct, the patient is at higher risk for MI, which may progress to NSTEMI. Usually, only the innermost layer of the heart is damaged. STEMI results when reduced blood flow through one of the coronary arteries causes myocardial ischemia, injury, and necrosis. The damage extends through all myocardial layers. What to look for: A patient with angina typically experiences: burning squeezing crushing tightness in the substernal or precordial chest that may radiate to the left arm, neck, jaw, or shoulder blade. Angina most frequently follows physical exertion but may also follow emotional excitement, exposure to cold, or a large meal. Angina is commonly relieved by nitroglycerin and rest. It’s less severe and shorter-lived than the pain of acute MI. Four Forms of ANGINA 1. Stable – predictable pain, in frequency and duration, which can be relieved with nitrates and rest 2. Unstable – increased pain, which is easily induced 3. Prinzmetal’s or a variant – pain from unpredictable coronary artery spasm 4. Microvascular – angina-like chest pain due to impairment of vasodilator reserve in a patient with normal coronary arteries A patient with MI experiences severe, persistent chest pain that isn’t relieved by rest or nitroglycerin. He may describe pain as crushing or squeezing. The pain is usually substernal, but may radiate to the left arm, jaw, neck, or shoulder blades. Other signs and symptoms of MI include: a feeling of impending doom fatigue nausea and vomiting shortness of breath cool extremities perspiration anxiety Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  118 hypotension or hypertension palpable precordial pulse muffled heart sounds. Diagnostic Tests These tests are used to diagnose CAD: ECG during an anginal episode shows ischemia. Serial 12-lead ECGs may be normal or inconclusive during the first few hours after an MI. Abnormalities include serial ST-segment depression in NSTEMI and ST-segment elevation and Q waves, representing scarring and necrosis, in STEMI. (See Locating myocardial damage Table) Coronary angiography reveals coronary artery stenosis or obstruction and collateral circulation and shows the condition of the arteries beyond the narrowing. Myocardial perfusion imaging with thallium-201 during treadmill exercise discloses ischemic areas of the myocardium, visualized as “cold spots.” With MI, serial serum cardiac marker measurements show elevated CK, especially the CK-MB isoenzyme (the cardiac muscle fraction of CK), troponin T and I, myoglobin, and ischemia modified albumin. C-reactive protein (CRP) levels help measure cardiac risk. Patients with chest pain and a higher CRP level have an increased risk of CAD. The PLAC test is a new test that also helps identify patients at a higher risk for CAD. With STEMI, echocardiography shows ventricular wall dyskinesia. Locating Myocardial damage After you’ve noted characteristic lead changes of an acute myocardial infarction, use this chart to identify the areas of damage. Match the lead changes in the second column with the affected wall in the first column and the artery involved in the third column. Column four shows reciprocal lead changes. Wall affected Leads Artery involved Reciprocal changes Anterior V2 to V4 Left coronary artery, II, III, aVf left anterior descending (LAD) artery Anterolateral I, aVL, V3 to V6 LAD artery, II, III, aVF circumflex artery Anteroseptal V1 to V4 LAD artery None Inferior II, III, aVF Right coronary I, aVL (diaphragmatic) artery Lateral I, aVL, V5, V6 Circumflex artery, branch of left II, III, aVF coronary artery Posterior V8, V9 Right coronary artery, circumflex V1 to V4 artery Right ventricular V4R, V5R, V6R Right coronary None artery Treatment For patients with angina, the goal of treatment is to reduce myocardial oxygen demand or increase oxygen supply. These treatments are used to manage angina: Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  119 Nitrates reduce myocardial oxygen consumption. Beta-adrenergic blockers may be administered to reduce the workload and oxygen demands of the heart. If angina is caused by coronary artery spasm, calcium channel blockers may be given. Antiplatelet drugs minimize platelet aggregation and the danger of coronary occlusion. Antilipemic drugs can reduce elevated serum cholesterol or triglyceride levels. Obstructive lesions may necessitate CABG or PTCA. Other alternatives include laser angioplasty, minimally invasive surgery, atherectomy, or stent placement. MI Relief The goals of treatment for MI are to relieve pain, stabilize heart rhythm, revascularize the coronary artery, preserve myocardial tissue, and reduce cardiac workload. Here are some guidelines for treatment: Thrombolytic therapy should be started within 6 hours of the onset of symptoms (unless contraindications exist). Thrombolytic therapy involves administration of streptokinase (Streptase), alteplase (Activase), or reteplase (Retavase). PTCA or stent placement are options for opening blocked or narrowed arteries. Oxygen is administered to increase oxygenation of the blood. Nitroglycerin is administered sublingually to relieve chest pain, unless systolic blood pressure is less than 90 mm Hg or heart rate is less than 50 or greater than 100 beats/minute. Heart ache Morphine is administered as analgesia because pain stimulates the sympathetic nervous system, leading to an increase in heart rate and vasoconstriction. Aspirin and anti-platelet drugs are administered to inhibit plate- let aggregation. I.V. heparin is given to patients who have received tissue plasminogen activator to increase the chances of patency in the affected coronary artery. Lidocaine, transcutaneous pacing patches (or a transvenous pacemaker), defibrillation, or epinephrine may be used if arrhythmias are present. Physical activity is limited for the first 12 hours to reduce cardiac workload, thereby limiting the area of necrosis. I.V. nitroglycerin is administered for 24 to 48 hours in patients without hypotension, bradycardia, or excessive tachycardia, to reduce afterload and preload and relieve chest pain. Glycoprotein IIb/IIIa inhibitors (such as abciximab [ReoPro]) are administered to patients with continued unstable angina or acute chest pain, or following invasive cardiac procedures, to reduce platelet aggregation. I.V. beta-adrenergic blocker is administered early to patients with evolving acute MI; it’s followed by oral therapy to reduce heart rate and contractibility and reduce myocardial oxygen requirements. ACE inhibitors are administered to those with evolving MI with ST-segment elevation or left bundle-branch block, to reduce after- load and preload and prevent remodeling. Laser angioplasty, atherectomy, or stent placement may be initiated. Lipid-lowering drugs are administered to patients with elevated LDL and cholesterol levels. Nursing interventions During anginal episodes, monitor blood pressure and heart rate. Take an ECG before administering nitroglycerin or other nitrates. Record duration of pain, amount of medication required to relieve it, and accompanying symptoms. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  120 On admission to the coronary care unit, monitor and record the patient’s ECG, blood pressure, temperature, and heart and breath sounds. Also, assess and record the severity, location, type, and duration of pain. Obtain a 12-lead ECG and assess heart rate and blood pressure when the patient experiences acute chest pain. Monitor the patient’s hemodynamic status closely. Be alert for indicators suggesting decreased cardiac output, such as decreased blood pressure, increased heart rate, increased PAP, increased PAWP, decreased cardiac output measurements, and decreased right atrial pressure. Assess urine output hourly. Monitor the patient’s oxygen saturation levels and notify the practitioner if oxygen saturation falls below 90%. Check the patient’s blood pressure after giving nitroglycerin, especially the first dose. During episodes of chest pain, monitor ECG, blood pressure, and PA catheter readings (if applicable) to determine changes. Frequently monitor ECG rhythm strips to detect heart rate changes and arrhythmias. Obtain serial measurements of cardiac enzyme levels as ordered. Watch for crackles, cough, tachypnea, and edema, which may indicate impending left-sided heart failure. Carefully monitor daily weight, intake and output, respiratory rate, serum enzyme levels, ECG waveforms, and blood pressure. Auscultate for S3 or S4 gal- lops. Prepare the patient for reperfusion therapy as indicated. Administer and titrate medications as ordered. Avoid giving I.M. injections; I.V. administration provides more rapid symptom relief. Organize patient care and activities to allow rest periods. If the patient is immobilized, turn him often and use intermittent com- pression devices. Gradually increase the patient’s activity level as tolerated. Provide a clear-liquid diet until nausea subsides. Anticipate a possible order for a low- cholesterol, low-sodium diet without caffeine. Provide a stool softener to prevent straining during defecation. 2. HEART FAILURE Heart failure occurs when the heart can’t pump enough blood to meet the metabolic needs of the body. Heart failure results in intravascular and interstitial volume overload and poor tissue perfusion. An individual with heart failure experiences reduced exercise tolerance, a reduced quality of life, and a shortened life span. Figure 3. (A) Normal and (B) Heart failure (Cordial infarction caused by the rupture of plaque during coronary artery disease). Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  121 Causes The most common cause of heart failure is CAD, but it also occurs in infants, children, and adults with congenital and acquired heart defects. Heart Failure may be classified into four general categories: 1. left-sided heart failure 2. right-sided heart failure 3. systolic dysfunction 4. diastolic dysfunction Left-sided Heart Failure Left-sided heart failure is a result of ineffective left ventricular contractile function. As the pumping ability of the left ventricle fails, cardiac output drops. Blood is no longer effectively pumped out into the body; it backs up into the left atrium and then into the lungs, causing pulmonary congestion, dyspnea, and activity intolerance. If the condition persists, pulmonary edema and right-sided heart failure may result. Common causes include: left ventricular infarction hypertension aortic and mitral valve stenosis. Right-sided Heart Failure Right-sided heart failure results from ineffective right ventricular contractile function. When blood isn’t pumped effectively through the right ventricle to the lungs, blood backs up into the right atrium and into the peripheral circulation. The patient gains weight and develops peripheral edema and engorgement of the kidney and other organs. Right-sided heart failure may be due to an acute right ventricular infarction or a pulmonary embolus. However, the most common cause is profound backward flow due to left- sided heart failure. Other causes of right-sided heart failure include: arrhythmias volume overload mitral and pulmonic valve stenosis cardiomyopathy. Systolic Dysfunction Systolic dysfunction occurs when the left ventricle can’t pump enough blood out to the systemic circulation during systole and the ejection fraction falls. Consequently, blood backs up into the pulmonary circulation and pressure increases in the pulmonary venous system. Cardiac output decreases; weakness, fatigue, and shortness of breath may occur. Causes of systolic dysfunction include: MI dilated cardiomyopathy arrhythmias aortic valve insufficiency acute rheumatic fever. Diastolic Dysfunction Diastolic dysfunction occurs when the ability of the left ventricle to relax and fill during diastole is reduced and the stroke volume falls. Therefore, higher volumes are needed in the Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  122 ventricles to maintain cardiac output. Consequently, pulmonary congestion and peripheral edema develop. Diastolic dysfunction may occur as a result of left ventricular hypertrophy, hypertension, cardiomyopathy, MI, or cardiac tamponade. This type of heart failure is less common than that due to systolic dysfunction, and treatment isn’t as clear. Compensatory mechanisms All types of heart failure eventually lead to reduced cardiac output, which triggers compensatory mechanisms that improve cardiac output at the expense of increased ventricular work. The compensatory mechanisms include: increased sympathetic activity activation of the renin-angiotensin-aldosterone system ventricular dilation ventricular hypertrophy. Increased Sympathetic Activity Increased sympathetic activity—a response to decreased cardiac output and blood pressure—enhances peripheral vascular resistance, contractility, heart rate, and venous return. Signs of increased sympathetic activity, such as cool extremities and clamminess, may indicate impending heart failure. Renin-Angiotensin-Aldosterone System Increased sympathetic activity also restricts blood flow to the kidneys, causing them to secrete renin which, in turn, converts angiotensinogen to angiotensin I, which then becomes angiotensin II—a potent vasoconstrictor. Angiotensin causes the adrenal cortex to release aldosterone, leading to sodium and water retention and an increase in circulating blood volume. This renal mechanism is helpful; however, if it persists unchecked, it can aggravate heart failure as the heart struggles to pump against the increased volume. Ventricular Dilation In ventricular dilation, an increase in end-diastolic ventricular volume (preload) causes increased stroke work and stroke volume during contraction. This stretches cardiac muscle fibers so that the ventricle can accept the increased volume. Eventually, the muscle becomes stretched beyond optimum limits and contractility declines. Ventricular Hypertrophy In ventricular hypertrophy, an increase in ventricular muscle mass allows the heart to pump against increased resistance to the out- flow of blood, improving cardiac output. However, this increased muscle mass also increases the myocardial oxygen requirements. An increase in the ventricular diastolic pressure necessary to fill the enlarged ventricle may compromise diastolic coronary blood flow, limiting the oxygen supply to the ventricle and causing ischemia and impaired muscle contractility. Counterregulatory substances In heart failure, counterregulatory substances—prostaglandins, atrial natriuretic factor, and BNP—are produced in an attempt to reduce the negative effects of volume overload and vasoconstriction caused by the compensatory mechanisms. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  123 The kidneys release the prostaglandins prostacyclin and prostaglandin E2, which are potent vasodilators. These vasodilators also act to reduce volume overload produced by the renin-angiotensin-aldosterone system by inhibiting sodium and water reabsorption by the kidneys. Counteracting hormones Atrial natriuretic factor is a hormone that’s secreted mainly by the atria in response to stimulation of the stretch receptors in the atria caused by excess fluid volume. This hormone works to counteract the negative effects of sympathetic nervous system stimulation and the renin-angiotensin-aldosterone system by producing vasodilation and diuresis. B-type natriuretic peptide (BNP) is another hormone that’s secreted by the ventricle in response to increased ventricular pressures. BNP works in the same manner as atrial natriuretic factor to help counteract the sympathetic nervous system and the renin- angiotensin- aldosterone system. What to look for Learn to recognize the signs and symptoms of both right- and left-sided heart failure to ensure that your patient receives attention promptly. Left-Sided Heart Failure Look for these early and later signs of disease. Early signs and symptoms of left-sided heart failure include: dyspnea orthopnea paroxysmal nocturnal dyspnea fatigue nonproductive cough. Later clinical manifestations of left-sided heart failure may include: crackles on auscultation hemoptysis displacement of the PMI toward the left anterior axillary line tachycardia S3 heart sound S4 heart sound cool, cyanotic skin confusion. Right-Sided Heart Failure Look for these clinical manifestations of right-sided heart failure: neck vein distention hepatojugular reflux and hepatomegaly right upper quadrant pain anorexia and nausea nocturia weight gain pitting edema ascites or anasarca S3 heart sound. Diagnostic Tests These tests are used to diagnose heart failure: Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  124 Chest X-ray shows increased pulmonary vascular markings, interstitial edema, or pleural effusion and cardiomegaly. ECG may indicate hypertrophy, ischemic changes, or infarction, and may also reveal tachycardia. Laboratory testing may reveal abnormal liver function, elevated BUN and creatinine levels, and elevated BNP levels ABG analysis may reveal hypoxemia from impaired gas exchange and respiratory alkalosis because the patient blows off more carbon dioxide as respiratory rate increases in compensation. Echocardiography may reveal left ventricular hypertrophy, dilation, and abnormal contractility. Pulmonary artery monitoring typically demonstrates elevated PAP and PAWP, left ventricular end-diastolic pressure and de- creased CO/CI in left-sided heart failure, and elevated right atrial pressure or CVP in right-sided heart failure. Radionuclide ventriculography may reveal an ejection fraction less than 40%; in diastolic dysfunction, the ejection fraction may be normal. Treatment The goal of therapy is to improve pump function. Correction of heart failure may involve: treatment of the underlying cause, if it’s known diuretics to reduce fluid volume overload, venous return, and preload ACE inhibitors for patients with left ventricle dysfunction to reduce production of angiotensin II, resulting in preload and after- load reduction beta-adrenergic blockers in patients with mild to moderate heart failure caused by left ventricular systolic dysfunction to pre- vent remodeling digoxin for patients with heart failure due to left ventricular systolic dysfunction to increase myocardial contractility, improve cardiac output, reduce the volume of the ventricle, and decrease ventricular stretch diuretics, nitrates, morphine, and oxygen to treat pulmonary edema administration of synthetic BNP medications, such as neseritide (Natrecor), to help increase contractility lifestyle modifications to reduce symptoms of heart failure, such as weight loss if obese; limited sodium (to 2 g per day) and alcohol intake; reduced fat intake; smoking cessation; stress reduction; and development of an exercise program CABG surgery or angioplasty for patients with heart failure due to CAD heart transplantation in patients receiving aggressive medical treatment but still experiencing limitations or repeated hospitalizations other surgery or invasive procedures, such as cardiomyoplasty, insertion of an IABP, partial left ventriculectomy, use of a mechanical ventricular assist device, and implantation of an ICD or a biventricular pacemaker. Nursing Interventions Place the patient in Fowler’s position to maximize chest expansion and give supplemental oxygen, as ordered, to ease his breathing. Monitor oxygen saturation levels and ABGs as indicated. If respiratory status deteriorates, anticipate the need for ET intubation and mechanical ventilation. Institute continuous cardiac monitoring, and notify the practitioner of changes in rhythm and rate. If the patient develops tachycardia, administer beta-adrenergic blockers as ordered; if Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  125 atrial fibrillation is present, administer anticoagulants or antiplatelet agents as ordered to prevent thrombus formation. If the patient develops a new arrhythmia, obtain a 12-lead ECG immediately. Monitor hemodynamic status, including cardiac output, cardiac index, and pulmonary and systemic vascular pressures closely, at least hourly, noting trends. If available, institute continuous cardiac output monitoring. Administer medications as ordered. Check apical heart rate before administering digoxin. Assess respiratory status frequently, at least every 1 to 2 hours. Auscultate lungs for abnormal breath sounds, such as crackles, wheezes, and rhonchi. Encourage coughing and deep breathing. Obtain daily weights and observe for peripheral edema. Assess hourly urine output. Also, monitor fluid intake, including I.V. fluids. Frequently monitor BUN and serum creatinine, liver function studies, and serum potassium, sodium, chloride, magnesium, and BNP levels daily. Organize all activities to provide maximum rest periods. Assess for signs of activity intolerance, such as increased shortness of breath, chest pain, increased arrhythmias, heart rate greater than 120 beats per minute, and ST-segment changes, and have the patient stop activity. To prevent deep vein thrombosis caused by vascular congestion, assist the patient with ROM exercises. Enforce bed rest and apply antiembolism stockings or intermittent compression devices. Prepare the patient for surgical intervention or insertion of IABP or ICD if indicated. 3. CARDIOGENIC SHOCK Cardiogenic shock is a condition of diminished cardiac output that severely impairs tissue perfusion. It’s sometimes called pump failure. Cardiogenic shock is a serious complication in nearly 15% of all patients hospitalized with acute MI. It typically affects patients whose area of infarction involves 40% or more of left ventricular muscle mass; in such patients, mortality may exceed 85%. Causes Cardiogenic shock can result from any condition that causes significant left ventricular dysfunction with reduced cardiac output, such as: MI (most common) myocardial ischemia papillary muscle dysfunction cardiomyopathy chronic or acute heart failure acidosis. Other causes include myocarditis and depression of myocardial contractility after cardiac arrest and prolonged cardiac surgery. Mechanical abnormalities of the ventricle, such as acute mitral or aortic insufficiency or an acutely acquired ventricular septal defect or ventricular aneurysm, may also result in cardiogenic shock. Regardless of the cause, here’s what happens: Left ventricular dysfunction initiates a series of compensatory mechanisms that attempt to increase cardiac output and, in turn, maintain vital organ function. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  126 As cardiac output falls, baroreceptors in the aorta and carotid arteries initiate responses in the sympathetic nervous system. These responses, in turn, increase heart rate, left ventricular filling pressure, and afterload to enhance venous return to the heart. These compensatory responses initially stabilize the patient but later cause the patient to deteriorate as the oxygen demands of the already compromised heart increase. The events involved in cardiogenic shock comprise a vicious cycle of low cardiac output, sympathetic compensation, myocar- dial ischemia, and even lower cardiac output. What to look for Cardiogenic shock produces signs of poor tissue perfusion, such as: cold, pale, clammy skin drop in systolic blood pressure to 30 mm Hg below baseline or a sustained reading below 90 mm Hg that isn’t attributable to medication tachycardia rapid respirations oliguria (urine output less than 20 mL per hour) anxiety confusion narrowing pulse pressure crackles heard in lungs neck vein distention S3, faint heart sounds, and possibly a holosystolic murmur. Diagnostic Tests Pulmonary artery pressure monitoring reveals increased CVP, PAP, PAWP, and SVR, reflecting an increase in left ventricular end-diastolic pressure (preload) and heightened resistance to left ventricular emptying (afterload) caused by ineffective pumping and increased peripheral vascular resistance. Thermodilution catheterization reveals a reduced cardiac index. Invasive arterial pressure monitoring shows systolic arterial pressure less than 90 mm Hg caused by impaired ventricular ejection. ABG analysis may show metabolic and respiratory acidosis and hypoxia. ECG demonstrates possible evidence of acute MI, ischemia, or ventricular aneurysm and arrhythmias. Echocardiography is used to determine left ventricular function and reveals valvular abnormalities. Serum enzyme measurements display elevated levels of CK, aspartate aminotransferase, and alanine aminotransferase, which indicate MI or ischemia and suggest heart failure or shock. CKMB (an isoenzyme of CK that occurs in cardiac tissue) and troponin isoenzyme levels may confirm acute MI. Brain natriuretic peptide (BNP) levels are elevated, indicating ventricular overload. Cardiac catheterization and echocardiography may reveal other conditions that can lead to pump dysfunction and failure, such as cardiac tamponade, papillary muscle infarct or rupture, ventricular septal rupture, pulmonary emboli, venous pooling (associated with venodilators and continuous or intermittent positive- pressure breathing), hypovolemia, and acute heart failure. Treatment The goal of treatment is to enhance cardiovascular status by increasing cardiac output, improving myocardial perfusion, and decreasing cardiac workload. Treatment consists of administering a combination of cardiovascular drugs and mechanical-assist techniques. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  127 Treatment begins with these measures: maintaining a patent airway; preparing for intubation and mechanical ventilation if the patient develops respiratory distress supplemental oxygen to increase oxygenation continuous cardiac monitoring to detect changes in heart rate and rhythm; administration of antiarrhythmics, as necessary initiating and maintaining at least two I.V. lines with large-gauge needles for fluid and drug administration I.V. fluids, crystalloids, colloids, or blood products, as necessary, to maintain intravascular volume. Cardiovascular drugs Drug therapy may include I.V. dopamine, phenylephrine, or nor- epinephrine to increase blood pressure and blood flow to kidneys. Inamrinone or dobutamine—inotropic agents that increase myocardial contractility and cardiac output—are commonly used. A vasodilator, nitroglycerin or nitroprusside, may be used with a vasopressor to further improve cardiac output by decreasing afterload (SVR) and reducing left ventricular end-diastolic pressure (preload). However, the patient’s blood pressure must be adequate to support nitroprusside therapy and must be monitored closely. Diuretics also may be used to reduce preload (PAWP) in patients with fluid volume overload. Antiarrhythmics may also be used to prevent or control arrhythmias that may reduce cardiac output. Mechanical Assistance Treatment may also include mechanical assistance by IABP to improve coronary artery perfusion and decrease cardiac workload. The IABP is inserted through the femoral artery into the descending thoracic aorta. The balloon inflates during diastole to increase coronary artery perfusion pressure and deflates before systole (before the aortic valve opens) to reduce resistance to ejection (afterload) and therefore reduce cardiac workload. Improved ventricular ejection significantly improves cardiac output. Subsequent vasodilation in the peripheral vessels leads to lower preload volume and reduced workload of the left ventricle. This is because of decreasing systemic vascular resistance. When drug therapy and IABP insertion fail, a VAD may be inserted to assist the pumping action of the heart. When all other medical and surgical therapies fail, heart transplantation may be considered. More measures Additional treatment measures for cardiogenic shock may include: thrombolytic therapy or coronary artery revascularization to restore coronary artery blood flow, if cardiogenic shock is due to acute MI emergency surgery to repair papillary muscle rupture or ventricular septal defect, if either is the cause of cardiogenic shock. Nursing Interventions Begin I.V. infusions of normal saline solution using a large-bore (14G to 18G) catheter, which allows easier administration of later blood transfusions. Administer oxygen by face mask or artificial airway to ensure adequate oxygenation of tissues. Adjust the oxygen flow rate to a higher or lower level, as ABG measurements indicate. Many Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  128 patients need 100% oxygen, and some require 5 to 15 cm H2O of positive end-expiratory or continuous positive airway pressure ventilation. Monitor and record blood pressure, pulse, respiratory rate, and peripheral pulses every 1 to 5 minutes until the patient stabilizes. Monitor cardiac rhythm continuously. Systolic blood pressure less than 80 mm Hg usually results in inadequate coronary artery blood flow, cardiac ischemia, arrhythmias, and further complications of low cardiac output. Using a PA catheter, closely monitor CVP, PAP, PAWP, SVR and cardiac output. High CVP and PAWP readings indicate heart failure, increased systemic vascular resistance, decreased cardiac output, and decreased cardiac index and should be reported immediately. Determine how much fluid to give by checking blood pressure, urine output, CVP, or PAWP. Whenever the fluid infusion rate is increased, watch for signs of fluid overload, such as an increase in PAWP. If the patient is hypovolemic, preload may need to be increased, typically accomplished with I.V. fluids. However, I.V. fluids must be given cautiously, being increased gradually while hemodynamic parameters are closely monitored. In this situation, diuretics aren’t given. Insert an indwelling urinary catheter to measure hourly urine output. If output is less than 30 mL per hour in adults, increase the fluid infusion rate but watch for signs of fluid overload such as an increase in PAWP. Notify the practitioner if urine output doesn’t improve. Administer a diuretic, such as furosemide, as ordered, to decrease preload and improve stroke volume and cardiac output. Monitor ABG values, CBC, and electrolyte levels. Expect to administer sodium bicarbonate by I.V. push if the patient is acidotic. Administer electrolyte replacement therapy as ordered. During therapy, assess skin color and temperature and note any changes. Cold, clammy skin may be a sign of continuing peripheral vascular constriction, indicating progressive shock. If your patient is on the IABP, move him as little as possible. Never flex the patient’s “ballooned” leg at the hip because this may displace or fracture the catheter. Never place the patient in a sitting position for any reason (including chest X-rays) while the balloon is inflated; the balloon will tear through the aorta and result in immediate death. During use of the IABP, assess pedal pulses and skin temperature and color to ensure adequate peripheral circulation. Check the dressing over the insertion site frequently for bleeding, and change it according to facility protocol. Also check the site for hematoma or signs of infection, and culture any drainage. If the patient becomes hemodynamically stable, gradually reduce the frequency of balloon inflation to wean him from the IABP. When weaning the patient from the IABP, watch for ECG changes, chest pain, and other signs of recurring cardiac ischemia as well as for shock. Prepare the patient for possible emergency cardiac catheterization to determine eligibility for PTCA or CABG to reperfuse (re- store blood flow to) areas with reversible injury patterns. To ease emotional stress, plan care measures to allow frequent rest periods and provide as much privacy as possible. Allow family members to visit and comfort the patient as much as possible. 4. HYPERTENSIVE CRISIS A hypertensive emergency, commonly called hypertensive crisis, refers to the abrupt, acute, and marked increase in blood pressure from the patient’s baseline that ultimately leads to acute and rapidly progressing end-organ damage. Typically, the patient’s diastolic blood pressure is greater than 120 mm Hg, and his MAP is greater than 150 mm Hg. The increased blood pressure value, although important, is probably less important than how rapidly the blood pressure increases. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  129 Causes Most patients who develop hypertensive crisis have long histories of chronic, poorly controlled, or untreated primary hypertension. Conditions that cause secondary hypertension, such as pheochromocytoma, Cushing’s syndrome, or autonomic dysreflexia, may also be responsible. Arterial blood pressure is a product of total peripheral resistance and cardiac output: Cardiac output is increased by conditions that increase heart rate or stroke volume, or both. Peripheral resistance is increased by factors that increase blood viscosity or reduce the lumen size of vessels, especially the arterioles. Hypertension may result from a disturbance in one of the body’s intrinsic mechanisms, including: renin-angiotensin system autoregulation sympathetic nervous system antidiuretic hormone. The renin-angiotensin system increases blood pressure in these ways: Sodium depletion, reduced blood pressure, and dehydration stimulate renin release. Renin reacts with angiotensinogen, a liver enzyme, and converts it to angiotensin I, which increases preload and afterload. Angiotensin I converts to angiotensin II in the lungs; angiotensin II is a potent vasoconstrictor that targets the arterioles. Circulating angiotensin II increases preload and afterload by stimulating the adrenal cortex to secrete aldosterone. This in- creases blood volume by conserving sodium and water. In autoregulation, several intrinsic mechanisms together change an artery’s diameter to maintain tissue and organ perfusion despite fluctuations in systemic blood pressure. These mechanisms include stress relaxation and capillary fluid shifts: In stress relaxation, blood vessels gradually dilate when blood pressure increases, reducing peripheral resistance. In capillary fluid shift, plasma moves between vessels and extra- vascular spaces to maintain intravascular volume. Sympathetic nervous system mechanisms control blood pressure. When blood pressure decreases, baroreceptors in the aortic arch and carotid sinuses decrease their inhibition of the medulla’s vasomotor center. Consequent increases in sympathetic stimulation of the heart by norepinephrine increases cardiac output by: strengthening the contractile force raising the heart rate augmenting peripheral resistance by vasoconstriction. Stress can also stimulate the sympathetic nervous system to increase cardiac output and peripheral vascular resistance. The release of antidiuretic hormone can regulate hypotension by increasing reabsorption of water by the kidney. In reabsorption, blood plasma volume increases, thus raising blood pressure. In hypertensive crisis, one or more of these regulating mechanisms is disrupted. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  130 Hypertensive crisis can result in hypertensive encephalopathy because of cerebral vasodilation from an inability to maintain autoregulation. Blood flow increases, causing an increase in pressure and subsequent cerebral edema. This increase in pressure damages the intimal and medial lining of the arterioles. What to look for Your assessment of a patient in hypertensive crisis almost always reveals a history of hypertension that’s poorly controlled or hasn’t been treated. Signs and symptoms may include: severe, throbbing headache vomiting irritability confusion blurred vision or diplopia dyspnea on exertion, orthopnea, or paroxysmal nocturnal dyspnea angina possible left ventricular heave palpated at the mitral valve area S4 heart sound acute retinopathy with retinal exudates. Check the head If the patient has hypertensive encephalopathy, you may note: decreased LOC disorientation seizures focal neurologic deficits, such as hemiparesis, and unilateral sensory deficits papilledema temporary vision loss. Kidney-related consequences If the hypertensive emergency has affected the kidneys, you may note reduced urine output as well as elevated BUN and creatinine levels. Diagnostic Tests Blood pressure measurement confirms the diagnosis of hyper- tensive emergency. Blood pressure measurement, obtained several times at an interval of at least 2 minutes, reveals an elevated diastolic pressure greater than 120 mm Hg. If there’s renal involvement, BUN may be greater than 20 mg/dL and serum creatinine level may be greater than 1.3 mg/dL. ECG may reveal ischemic changes or left ventricular hypertrophy. Echocardiography may reveal increased wall thickness with or without an increase in left ventricular size. Chest X-ray may reveal enlargement of the cardiac silhouette with left ventricular dilation, or pulmonary congestion and pleural effusions with heart failure. Urinalysis results may be normal unless there’s renal impairment; then specific gravity is low (less than 1.010); hematuria, casts, and proteinuria may also be found. If the patient’s condition is due to a disease condition, such as pheochromocytoma, a 24-hour urine test reveals increases in vanillylmandelic acid and urinary catecholamines. Renal ultrasound may reveal renal artery stenosis. CT or MRI of the brain may show cerebral edema or hemorrhage. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  131 Treatment Treatment is focused immediately on reducing the patient’s blood pressure with I.V. antihypertensive therapy. However, care must be taken not to reduce the patient’s blood pressure too rapidly because the patient’s autoregulatory control is impaired. The current recommendation is to reduce the blood pressure by no more than 25% of the MAP over the first 2 hours. Further reductions should occur over the next several days. Sodium nitroprusside given as an I.V. infusion and titrated ac- cording to the patient’s response is the drug of choice. It has a rapid onset of action and its effects cease within 1 to 5 minutes of stopping the drug. Thus, if the patient’s blood pressure drops too low, stopping the drug almost immediately allows the blood pressure to increase. Other agents that may be used include labetalol, nitroglycerin (the drug of choice for treating hypertensive emergency when myocardial ischemia, acute MI, or pulmonary edema is present), and hydralazine (specifically indicated for treating hypertension in pregnant women with preeclampsia). Lifestyle changes may include weight reduction, smoking cessation, exercise, and dietary changes After the acute episode is controlled, maintenance pharmacotherapy to control blood pressure plays a key role. Nursing Interventions Immediately obtain the patient’s blood pressure. If not already in place, institute continuous cardiac and arterial pressure monitoring to assess blood pressure directly; determine the patient’s MAP. Assess ABGs. Monitor the patient’s oxygen saturation level using pulse oximetry; if you’re monitoring the patient hemodynamically, assess mixed venous oxygen saturation. Administer supplemental oxygen, as ordered, based on the findings. Administer I.V. antihypertensive therapy as ordered; if using nitroprusside, wrap the container in foil to protect it from the light and titrate the dose based on specified target ranges for systolic and diastolic pressures. Immediately stop the drug if the patient’s blood pressure drops below the target range. Monitor blood pressure every 1 to 5 minutes while titrating drug therapy, then every 15 minutes to 1 hour as the patient’s condition stabilizes. Continuously monitor ECGs and institute treatment as indicated if arrhythmias occur. Auscultate the patient’s heart, noting signs of heart failure, such as S3 or S4 heart sounds. Assess the patient’s neurologic status every hour initially and then every 4 hours as the patient’s condition stabilizes. Monitor urine output every hour and notify the practitioner if output is less than 0.5 ml/kg/hour. Evaluate BUN and serum creatinine levels for changes and monitor daily weights. Obtain serum thiocyanate levels after 48 hours of therapy and then regularly thereafter while the patient is receiving nitroprusside. Administer other antihypertensives as ordered. As the patient’s condition stabilizes, expect to begin oral antihypertensive therapy while gradually weaning I.V. drugs to prevent hypotension. If the patient is experiencing fluid overload, administer diuretics as ordered. Assess the patient’s vision and report changes, such as increased blurred vision, diplopia, or loss of vision. Administer analgesics as ordered for headache; keep your patient’s environment quiet, with low lighting. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  132 5. CARDIOMYOPATHY Cardiomyopathy generally refers to disease of the heart muscle fibers. It takes three main forms: Dilated Hypertrophic Restrictive (extremely rare) Cardiomyopathy is the second most common direct cause of sudden death; CAD is first. Because dilated cardiomyopathy usually isn’t diagnosed until its advanced stages, the prognosis is generally poor. Figure 4. Types of Cardiomyopathy Causes Most patients with cardiomyopathy have idiopathic, or primary, disease, but some cases are secondary to identifiable causes. Hypertrophic cardiomyopathy is almost always inherited as a non- sex-linked autosomal dominant trait. Males and blacks are at greatest risk for cardiomyopathy; other risk factors include hypertension, pregnancy, viral infections, and alcohol use. The disease course in cardiomyopathy depends on the special type, as outlined here. Dilated Cardiomyopathy Dilated cardiomyopathy primarily affects systolic function. It results from extensively damaged myocardial muscle fibers. Consequently, contractility in the left ventricle decreases. As systolic function declines, stroke volume, ejection fraction, and cardiac output decrease. As end-diastolic volumes increase, pulmonary congestion may occur. The elevated Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  133 end-diastolic volume is a compensatory response to preserve stroke volume despite a reduced ejection fraction. The sympathetic nervous system is also stimulated to increase heart rate and contractility. The kidneys are stimulated to retain sodium and water to maintain cardiac output, and vasoconstriction occurs as the renin-angiotensin system is stimulated. When these compensatory mechanisms can no longer maintain cardiac output, the heart begins to fail. Left ventricular dilation occurs as venous return and systemic vascular resistance increase. The stretching of the left ventricle eventually leads to mitral insufficiency. Subsequently, the atria also dilate, as more work is required to pump blood into the full ventricles. Cardiomegaly is a consequence of dilation of the atria and ventricles. Blood pooling in the ventricles increases the risk of emboli. Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy primarily affects diastolic function. The features of hypertrophic cardiomyopathy include: asymmetrical left ventricular hypertrophy hypertrophy of the intraventricular septum rapid, forceful contractions of the left ventricle impaired relaxation obstruction of left ventricular outflow. The hypertrophied ventricle becomes stiff, noncompliant, and unable to relax during ventricular filling. Consequently, ventricular filling is reduced and left ventricular filling pressure rises, causing increases in left atrial and pulmonary venous pressures and leading to venous congestion and dyspnea. The increase in venous pressures and venous congestion leads to tachycardia, which causes a decrease in left ventricular filling time. Reduced ventricular filling during diastole and obstruction to ventricular outflow lead to low cardiac output. If papillary muscles become hypertrophied and don’t close completely during contraction, mitral insufficiency occurs. Moreover, intramural coronary arteries are abnormally small and may not be sufficient to supply the hypertrophied muscle with enough blood and oxygen to meet the increased needs of the hyperdynamic muscle. Restrictive Cardiomyopathy Restrictive cardiomyopathy is characterized by stiffness of the ventricle caused by left ventricular hypertrophy and endocardial fibrosis and thickening. The ability of the ventricle to relax and fill during diastole is reduced. Furthermore, the rigid myocardium fails to contract completely during systole. As a result, cardiac output decreases. What to look for Generally, for patients with dilated or restrictive cardiomyopathy, the onset is insidious. As the disease progresses, exacerbations and hospitalizations are frequent regardless of the type of cardiomyopathy. Dilated Cardiomyopathy For a patient with dilated cardiomyopathy, signs and symptoms may be overlooked until left-sided heart failure occurs. Be sure to evaluate the patient’s current condition and then compare it with that over the past 6 to 12 months. Signs and symptoms of dilated cardiomyopathy may include: shortness of breath, orthopnea, dyspnea on exertion, fatigue Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  134 peripheral edema, hepatomegaly, jugular vein distention tachycardia, palpitations pansystolic murmur associated with mitral and tricuspid insufficiency S3 and S4 gallop rhythms irregular pulse if atrial fibrillation exists crackles in lungs. Hypertrophic cardiomyopathy Signs and symptoms vary widely among patients with hypertrophic cardiomyopathy. The presenting symptom is commonly syncope or sudden cardiac death. Other possible signs and symptoms include: angina dyspnea and orthopnea fatigue systolic ejection murmur along the left sternal border and apex ventricular arrhythmias irregular pulse with atrial fibrillation, palpitations S4 and possible S3 gallop rhythms, split S2 heart sound. Restrictive Cardiomyopathy A patient with restrictive cardiomyopathy presents with signs of heart failure and other signs and symptoms, including: fatigue and weakness dyspnea orthopnea chest pain hepatomegaly peripheral edema S3 or S4 gallop rhythms systolic murmurs heart blocks. Diagnostic Tests These tests are used to diagnose cardiomyopathy: Dilated Cardiomyopathy Chest X-ray shows an enlarged heart and pulmonary edema. An ECG will show biventricular enlargement and, commonly, atrial fibrillation. Echocardiogram will show decreased ventricular movement and ejection fraction. It will also demonstrate an increase in atrial and ventricular chamber size and abdomen wall motion. It may also demonstrate mitral valve insufficiency. Hemodynamic monitoring will show an increased PAWP and PAP and a decreased CO/CI. In late stages, the CVP may also be elevated. Hypertrophic cardiomyopathy Chest X-ray shows an enlarged heart with pronounced left atrial dilation. Pulmonary congestion may also be seen. An ECG will show left atrial enlargement and left ventricular hypertrophy. ST and T-wave changes may be seen. Atrial fibrillation and ventricular arrhythmias, such as ventricular tachycardia and ventricular fibrillation are also common. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  135 An echocardiogram will show an enlarged left atrium and hypertrophy of the intraventricular septum. Left ventricular outflow narrowing, if present, can also be seen. Abnormal wall motion may also be present. Cardiac catheterization with heart biopsy can provide definitive diagnosis. Restricted Cardiomyopathy Chest X-ray shows an enlarged heart and pulmonary edema. An ECG will demonstrate low QRS complex voltage. AV heart blocks are commonly seen. Echocardiogram will show atrial enlargement. The walls of the ventricles will be thickened but the interior chamber size will be decreased. Hemodynamic monitoring will show increased PAP and PAWP. Left and right end-diastolic pressures will also be elevated. Treatments There’s no known cure for cardiomyopathy. Treatment is individualized based on the type of cardiomyopathy and the patient’s condition. Dilated Cardiomyopathy For a patient with dilated cardiomyopathy, treatment may involve: management of the underlying cause, if it’s known ACE inhibitors, and angiotensin II receptor blockers (ARBs), to reduce afterload through vasodilation and increase cardiac output diuretics, taken with ACE inhibitors, to reduce fluid retention digoxin, for patients not responding to ACE inhibitor and di- uretic therapy, to improve myocardial contractility hydralazine and isosorbide dinitrate, in combination, to produce vasodilation beta-adrenergic blockers for patients with mild or moderate heart failure antiarrhythmics, such as amiodarone, used cautiously to control arrhythmias cardioversion to convert atrial fibrillation to sinus rhythm pacemaker insertion to correct arrhythmias anticoagulants to reduce the risk of emboli revascularization, such as CABG surgery, if dilated cardiomyopathy is due to ischemia valvular repair or replacement, if dilated cardiomyopathy is due to valve dysfunction lifestyle modifications such as smoking cessation; low-fat, low- sodium diet; physical activity; and abstinence from alcohol heart transplantation in patients resistant to medical therapy inotropes, such as dobutamine, to improve myocardial contractility and improve heart failure. Hypertrophic Cardiomyopathy For a patient with hypertrophic cardiomyopathy, treatment may involve: beta-adrenergic blockers to slow the heart rate, reduce myocardial oxygen demands, and increase ventricular filling by relaxing the obstructing muscle, thereby increasing cardiac output antiarrhythmic drugs, such as amiodarone, to reduce arrhythmias cardioversion to treat atrial fibrillation anticoagulation to reduce the risk for systemic embolism with atrial fibrillation verapamil and diltiazem to reduce ventricular stiffness and elevated diastolic pressures ablation of the AV node and implantation of a dual-chamber pacemaker Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  136 (controversial), in patients with obstructive hypertrophic cardiomyopathy and ventricular tachycardias, to reduce the outflow gradient by altering the pattern of ventricular contraction ICD to correct ventricular arrhythmias ventricular myotomy or myectomy (resection of the hypertrophied septum) to ease outflow tract obstruction and relieve symptoms mitral valve replacement to correct mitral insufficiency heart transplantation for intractable symptoms. Restrictive Cardiomyopathy For a patient with restrictive cardiomyopathy, treatment may involve: management of the underlying cause such as administering deferoxamine to bind iron in restrictive cardiomyopathy due to hemochromatosis digoxin, diuretics, and a restricted sodium diet to ease the symptoms of heart failure, although no therapy exists for patients with restricted ventricular filling oral vasodilators to control intractable heart failure. Nursing Interventions Administer drugs, as ordered, to promote adequate heart function. Assess hemodynamic status every 2 hours or more frequently, if necessary. Monitor intake and output closely and obtain daily weights; institute fluid restrictions as ordered. Institute continuous cardiac monitoring to evaluate for arrhythmias. Assess the patient for possible adverse drug reactions, such as orthostatic hypotension associated with use of vasodilators, diuretics, or ACE inhibitors. Urge the patient to change positions slowly. Be aware that patients with hypertrophic cardiomyopathy should not receive medication that may decrease preload (diuretics, nitrates) or dopamine or digoxin because the increase in myocardial contractility may worsen the outflow obstruction. Auscultate heart and lung sounds, being alert for S3 and S4 heart sounds or murmurs, or crackles, rhonchi, and wheezes indicative of heart failure. Monitor vital signs for changes, especially a heart rate greater than 100 beats/minute, respiratory rate greater than 20 breaths per minute, and a systolic blood pressure less than 90 mm Hg, all of which suggest heart failure. Assist the patient with ADLs to decrease oxygen demand. Administer supplemental oxygen as ordered. Assess for changes in LOC, such as restlessness or decreased responsiveness, indicating diminished cerebral perfusion. If the patient has a PA catheter in place, evaluate mixed venous oxygen saturation levels; if not, monitor oxygen saturation levels using pulse oximetry. Organize care to promote periods of rest for the patient. Prepare the patient, as indicated, for insertion of pacemaker, ICD, IABP, or cardiac transplantation. 6. CARDIAC ARRYTHMIAS In cardiac arrhythmia, abnormal electrical conduction or automaticity changes heart rate and rhythm. Cardiac arrhythmias vary in severity, from those that are mild, asymptomatic, and require no treatment (such as sinus arrhythmia, in which heart rate increases and decreases with respiration) to catastrophic ventricular fibrillation, which requires immediate resuscitation. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  137 Cardiac arrhythmias are generally classified according to their origin (ventricular or supraventricular). Their effect on cardiac out- put and blood pressure, partially influenced by the site of origin, determines their clinical significance. Lethal arrhythmias, such as ventricular tachycardia and ventricular fibrillation, are a major cause of sudden cardiac death. Causes Common causes of cardiac arrhythmias include: congenital defects myocardial ischemia or infarction organic heart disease drug toxicity degeneration of the conductive tissue connective tissue disorders electrolyte imbalances cellular hypoxia hypertrophy of the heart muscle acid-base imbalances emotional stress. Cardiac arrhythmias may result from: enhanced or depressed automaticity altered conduction pathways abnormal electrical conduction. What to look for When a patient presents with a history of symptoms suggestive of cardiac arrhythmias, or has been treated for a cardiac arrhythmia, be alert for: reports of precipitating factors, such as exercise, smoking, sleep, emotional stress, exposure to heat or cold, caffeine intake, position changes, or recent illnesses attempts to alleviate the symptoms, such as coughing, rest, medications, or deep breathing reports of sensing the heart’s rhythm, such as palpitations, irregular beating, skipped beats, or rapid or slow heart rate. Physical examination findings vary depending on the arrhythmia and the degree of hemodynamic compromise. Circulatory failure along with an absence of pulse and respirations is found with asystole, ventricular fibrillation, and sometimes with ventricular tachycardia. Additional findings may include: pallor cold and clammy extremities reduced urine output dyspnea hypotension weakness chest pains dizziness syncope anxiety fatigue auscultation of S3. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  138 Diagnostic Tests A 12-lead ECG is the standard test for identifying cardiac arrhythmias. A 15-lead ECG (in which additional leads are applied to the right side of the chest) or an 18-lead ECG (in which additional leads are also added to the posterior scapular area) may be done to provide more definitive information about the patient’s right ventricle and posterior wall of the left ventricle. (See Understanding cardiac arrhythmias, page 30-33.) Laboratory testing may reveal electrolyte abnormalities, hypoxemia or acid-base abnormalities (with ABG analysis), or drug toxicities as the cause of arrhythmias. Exercise testing may reveal exercise-induced arrhythmias. Electrophysiologic testing may be used to identify the mechanism of an arrhythmia and location of accessory pathways and to assess the effectiveness of antiarrhythmic drugs. Treatments The goals of treatment are to return pacer function to the sinus node, increase or decrease ventricular rate to normal, regain AV synchrony, and maintain normal sinus rhythm. Treatments to correct abnormal rhythms include therapy with: antiarrhythmic drugs electrical conversion with defibrillation and cardioversion Valsalva’s maneuver temporary or permanent placement of a pacemaker to maintain heart rate implantable cardioverter-defibrillator (ICD) if indicated surgical removal or cryotherapy of an irritable ectopic focus to prevent recurring arrhythmias management of the underlying disorder such as correction of hypoxia. Nursing Interventions Care for the patient experiencing a cardiac arrhythmia as follows: Evaluate the patient’s ECG regularly for arrhythmia and assess hemodynamic parameters as indicated. Document arrhythmias and notify the practitioner immediately. When life-threatening arrhythmias develop, rapidly assess the patient’s LOC, pulse and respiratory rates, and hemodynamic parameters. Monitor his ECG continuously. Be prepared to initiate CPR if indicated. Administer oxygen to help improve myocardial oxygen supply. Administer analgesics, as appropriate, and help the patient de- crease anxiety. Assess the patient for predisposing factors, such as fluid and electrolyte imbalance, and signs of drug toxicity, especially with digoxin. Administer medications as ordered, monitor for adverse effects, and monitor vital signs, hemodynamic parameters (as appropriate), and appropriate laboratory studies. Prepare to assist with or perform cardioversion or defibrillation if indicated. If you suspect drug toxicity, report it to the practitioner immediately and withhold the next dose. If a temporary pacemaker needs to be inserted, make sure that a fresh battery is installed to avoid temporary pacemaker mal- function and carefully secure the external catheter wires and the pacemaker box. After pacemaker insertion, monitor the patient’s pulse rate regularly and watch for signs of pacemaker failure and decreased cardiac output. Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  139 Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  140 Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  141 Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  142 You can visit the following link for supplemental learning on ECG Reading. Skillstat.com END OF MODULE 3 Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA  143 4 MODULE SUMMARY In this module, you were able to have some review about the cardiovascular system. Common cardiovascular problems seen in the critical area, its assessment and management were also discussed. Additional treatment modalities were also discussed for further understanding about the nursing care of clients with altered tissue perfusion function. Congratulations! You may now proceed to module 4 after taking the graded quiz. ? SUMMATIVE TEST 1. Graded quiz, covering the three lessons, will be administered thru correspondence. FEEDBACK After using this module I perceived that this module is __________________________________________________________________________ __________________________________________________________________________ __________________________________________________________________________ __________________________________________________ I would recommend that ______________________________________________ __________________________________________________________________________ __________________________________________________________________________ __________________________________________________________________________ __________________________________________________ Module 3: Care of Clients with Altered Tissue Perfusion SMPERALTA