NCM-118-Cardiovascular-Diseases.pdf

Cardiovascular Diseases NCM 118 Prepared by: Dr. Archie Guitche ANATOMY AND PHYSIOLOGY Heart and Heart Wall Layers 1. The heart is located in the left side of the mediastinum. 2. The heart consists of 3 layers. a. The epicardium is the outermost layer of the heart. b....

Cardiovascular Diseases NCM 118 Prepared by: Dr. Archie Guitche ANATOMY AND PHYSIOLOGY Heart and Heart Wall Layers 1. The heart is located in the left side of the mediastinum. 2. The heart consists of 3 layers. a. The epicardium is the outermost layer of the heart. b. The myocardium is the middle layer and is the actual contracting muscle of the heart. c. The endocardium is the innermost layer and lines the inner chambers and heart valves. ANATOMY AND PHYSIOLOGY Pericardial sac 1. Encases and protects the heart from trauma and infection 2. Has 2 layers a. The parietal pericardium is the tough, fibrous outer membrane that attaches anteriorly to the lower half of the sternum, posteriorly to the thoracic vertebrae, and inferiorly to the diaphragm. b. The visceral pericardium is the thin, inner layer that closely adheres to the heart. 3. The pericardial space is between the parietal and visceral layers; it holds 5 to 20 mL of pericardial fluid, lubricates the pericardial surfaces, and cushions the heart. ANATOMY AND PHYSIOLOGY There are 4 heart chambers. 1. The right atrium receives deoxygenated blood from the body via the superior and inferior vena cava. 2. The right ventricle receives blood from the right atrium and pumps it to the lungs via the pulmonary artery. 3. The left atrium receives oxygenated blood from the lungs via 4 pulmonary veins. 4. The left ventricle is the largest and most muscular chamber; it receives oxygenated blood from the lungs via the left atrium and pumps blood into the systemic circulation via the aorta. ANATOMY AND PHYSIOLOGY There are 4 valves in the heart. 1. There are 2 atrioventricular valves, the tricuspid and the mitral, which lie between the atria and ventricles. a. The tricuspid valve is located on the right side of the heart. b. The bicuspid (mitral) valve is located on the left side of the heart. c. The atrioventricular valves close at the beginning of ventricular contraction and prevent blood from flowing back into the atria from the ventricles; these valves open when the ventricles relax. ANATOMY AND PHYSIOLOGY 2. There are 2 semilunar valves, the pulmonic and the aortic. a. The pulmonic semilunar valve lies between the right ventricle and the pulmonary artery. b. The aortic semilunar valve lies between the left ventricle and the aorta. c. The semilunar valves prevent blood from flowing back into the ventricles during relaxation; they open during ventricular contraction and close when the ventricles begin to relax. ANATOMY AND PHYSIOLOGY CONDUCTION SYSTEM OF THE HEART Sinoatrial (SA) node 1. The main pacemaker that initiates each heartbeat 2. It is located at the junction of the superior vena cava and the right atrium. 3. The SA node generates electrical impulses at 60 to 100 times per minute and is controlled by the sympathetic and parasympathetic nervous systems. Atrioventricular (AV) node 1. Located in the lower aspect of the atrial septum 2. Receives electrical impulses from the SA node 3. If the SA node fails, the AV node can initiate and sustain a heart rate of 40 to 60 beats per minute. ANATOMY AND PHYSIOLOGY The bundle of His 1. A continuation of the AV node; located at the interventricular septum 2. It branches into the right bundle branch and the left bundle branch 3. The right and left bundle branches terminate in the Purkinje fibers. Purkinje fibers 1. Purkinje fibers are a diffuse network of conducting strands located beneath the ventricular endocardium. 2.. Purkinje fibers can act as the pacemaker with a rate between 20 and 40 beats per minute when higher pacemakers (such as the SA and AV nodes) fail. ANATOMY AND PHYSIOLOGY Coronary arteries 1. The right main coronary artery supplies the right atrium and ventricle, the inferior portion of the left ventricle, the posterior septal wall, and the SA and AV nodes. 2. The left main coronary artery consists of 2 major branches, the left anterior descending (LAD) and the circumflex arteries. a. The LAD artery supplies blood to the anterior wall of the left ventricle, the anterior ventricular septum, and the apex of the left ventricle. b. The circumflex artery supplies blood to the left atrium and the lateral and posterior surfaces of the left ventricle. ANATOMY AND PHYSIOLOGY HEART SOUNDS A. FIRST HEART SOUND (S1) Comprises mitral (M1) and tricuspid (T1) valve closure BEST heard at the lower left sternal border in younger subjects B. SECOND HEART SOUND (S2) Comprises aortic (A2) and pulmonic (P2) valve closure Individual components BEST heard at the second left interspace with the patient in the SUPINE position DIAGNOSTICS Cardiac markers 1. Troponin a. Troponin is composed of 3 proteins—troponin C, cardiac troponin I, and cardiac troponin T. b. Troponin I especially has a high affinity for myocardial injury; it rises within 3 hours and persists for up to 7 to 10 days. 2. CK-MB (creatine kinase, myocardial muscle) a. An elevation in value indicates myocardial damage. b. An elevation occurs within hours and peaks at 18 hours following an acute ischemic attack. 3. Myoglobin a. Myoglobin is an oxygen-binding protein found in cardiac and skeletal muscle. b. The level rises within 2 hours after cell death, with a rapid decline in the level after 7 hours; however, it is not cardiac specific. DIAGNOSTICS Complete blood count 1. The red blood cell count decreases in rheumatic heart disease and infective endocarditis and increases in conditions characterized by inadequate tissue oxygenation. 2. The white blood cell count increases in infectious and inflammatory diseases of the heart and after MI, because large numbers of white blood cells are needed to dispose of the necrotic tissue resulting from the infarction. 3. An elevated hematocrit level can result from vascular volume depletion. 4. Decreases in hemoglobin and hematocrit levels can indicate anemia. Blood coagulation factors An increase in coagulation factors can occur during and after MI, which places the client at greater risk for thrombophlebitis and formation of clots in the coronary arteries. DIAGNOSTICS Serum lipids 1. The lipid profile measures serum cholesterol, triglyceride, and lipoprotein levels. 2. The lipid profile is used to assess the risk of developing coronary artery disease. 3. Lipoprotein-a or Lp(a), a modified form of low-density lipoprotein (LDL), increases atherosclerotic plaques and increases clots; value should be less than 30 mg/dL (300 mg/L). DIAGNOSTICS Electrolytes 1. Potassium a. Hypokalemia causes increased cardiac electrical instability, ventricular dysrhythmias, and increased risk of digoxin toxicity. b. In hypokalemia, the electrocardiogram (ECG) shows flattening and inversion of the T wave, the appearance of a U wave, and ST depression. c. Hyperkalemia causes asystole and ventricular dysrhythmias. d. In hyperkalemia, the ECG may show tall, peaked T waves, widened QRS complexes, prolonged PR intervals, or flat P waves. 2. Sodium a. The serum sodium level decreases with the use of diuretics. b. The serum sodium level decreases in heart failure, indicating water excess. DIAGNOSTICS Calcium 1. Hypocalcemia can cause ventricular dysrhythmias, prolonged ST and QT intervals, and cardiac arrest. 2. Hypercalcemia can cause a shortened ST segment and widened T wave, atrioventricular block, tachycardia or bradycardia, digitalis hypersensitivity, and cardiac arrest. Phosphorus: Phosphorus levels should be interpreted with calcium levels, because the kidneys retain or excrete one electrolyte in an inverse relationship to the other. DIAGNOSTICS Magnesium 1. A low magnesium level can cause ventricular tachycardia and fibrillation. 2. Electrocardiographic changes that may be observed with hypomagnesemia include tall T waves and depressed ST segments. 3. A high magnesium level can cause muscle weakness, hypotension, and bradycardia. 4. Electrocardiographic changes that may be observed with hypermagnesemia include a prolonged PR interval and widened QRS complex. DIAGNOSTICS Blood urea nitrogen: The blood urea nitrogen level is elevated in heart disorders such as heart failure and cardiogenic shock that reduce renal circulation. Blood glucose: An acute cardiac episode can elevate the blood glucose level. Chest x-ray 1. Description: Radiography of the chest is done to determine anatomical changes such as the size, silhouette, and position of the heart. 2. Interventions a. Prepare the client, explaining the purpose and procedure. b. Remove jewelry. c. Ensure that the client is not pregnant. DIAGNOSTICS Electrocardiography Description: This common noninvasive diagnostic test records the electrical activity of the heart and is useful for detecting cardiac dysrhythmias, location and extent of MI, and cardiac hypertrophy, and for evaluation of the effectiveness of cardiac medications. Interventions a. Determine the client’s ability to lie still; advise the client to lie still, breathe normally, and refrain from talking during the test. b. Reassure the client that an electrical shock will not occur. c. Document any cardiac medications the client is taking. ELECTROCARDIOGRAPHY P wave: Atrial Depolarization QRS Complex: Vent Depolarization T Wave: Vent Repolarization PR Interval: depends on conduction velocity through AV Node QT Interval: Period of Vent Depolarization + Repolarization PR Segment: AV Node Conduction ST Segment: isoelectric; correlates with plateau of Vent AP  6 6 X 9 R waves ELECTROCARDIOGRAPHY ELECTROCARDIOGRAPHY ELECTROCARDIOGRAPHY DIAGNOSTICS Holter monitoring a. A noninvasive test; the client wears a monitor and an electrocardiographic tracing is recorded continuously over a period of 24 hours or more while the client performs her or his activities of daily living. b. The monitor identifies dysrhythmias if they occur and evaluates the effectiveness of antidysrhythmics or pacemaker therapy. Interventions a. Instruct the client to resume normal daily activities and to maintain a diary documenting activities and any symptoms that may develop for correlation with the electrocardiographic tracing. b. Instruct the client using a wired monitor to avoid tub baths, showers, or swimming, because they will interfere with the electrocardiographic recorder device. DIAGNOSTICS Echocardiography a. This noninvasive procedure is based on the principles of ultrasound and evaluates structural and functional changes in the heart. b. Used to detect valvular abnormalities, congenital heart defects, wall motion, ejection fraction, and cardiac function. Interventions Advise the client to lie still, breathe normally, and refrain from talking during the test. DIAGNOSTICS Exercise electrocardiography testing (stress test) a. This noninvasive test studies the heart during activity and detects and evaluates coronary artery disease. b. Treadmill testing is the most commonly used mode of stress testing. c. Instruct the client having a noninvasive test to eat a light meal 1 to 2 hours before the procedure. d. Instruct the client to avoid smoking, alcohol, and caffeine before the procedure. e. Instruct the client to avoid taking a hot bath or shower for at least 1 to 2 hours. 01 HYPERTENSION HYPERTENSION Types of Hypertension A. Essential (primary) HTN has no known cause (idiopathic). B. Secondary HTN develops in response to an identifiable mechanism or another disease. Pathophysiology BP is created by the difference in the pressure of the blood as it leaves the heart and the resistance it meets flowing out to the tissues. Risk Factors Age (arteriosclerosis) Diet and exercise (atherosclerosis) Smoking Obesity Stress HYPERTENSION Nursing Assessment A. BP equal to or greater than 140/90 mm Hg on two separate occasions 1. Obtain BP while client is lying down, sitting, and standing. 2. Compare readings taken lying down, sitting, and standing. A difference of more than 10 mm Hg of either systolic or diastolic indicates postural hypotension. Take pressure in both arms. B. Genetic risk factors (nonmodifiable) 1. Positive family history for HTN 2. Gender (Men have a greater risk for being hypertensive at an earlier age than women.) 3. Age (Risk increases with increasing age.) 4. Ethnicity (African Americans are at greater risk than Whites.) HYPERTENSION C. Lifestyle and habits that increase risk for becoming hypertensive (modifiable) 1. Use of alcohol, tobacco, and caffeine 2. Sedentary lifestyle, obesity 3. Nutrition history of high salt and fat intake 4. Use of oral contraceptives or estrogens 5. Stress D. Associated physical problems 1. Renal failure 2. Impaired renal function 3. Respiratory problems, especially COPD 4. Cardiac problems, especially valvular disorders 5. Dyslipidemia 6. Diabetes HYPERTENSION E. Pharmacologic history 1. Steroids (increase BP) 2. Estrogens (increase BP) F. Assess for headache, edema, nocturia, nosebleeds, and vision changes (may be asymptomatic). G. Assess level of stress and source of stress (related to job, economics, family). H. Assess personality type (i.e., determine whether client exhibits perfectionist behavior). Remember the risk factors for HTN: heredity, race, age, alcohol abuse, increased salt intake, obesity, and use of oral contraceptives. HYPERTENSION HYPERTENSION Nursing Plans and Interventions A. Develop a teaching plan to include 1. Information about disease process a. Risk factors b. Causes c. Long-term complications d. Lifestyle modifications e. Relationship of treatment to prevention of complications 2. Information about treatment plan a. How to take own BP b. Reasons for each medication c. How and when to take each medication d. Necessity of consistency in medication regimen e. Need for ongoing assessment while taking antihypertensives f. Need to monitor serum electrolytes every 90 to 120 days for duration of treatment HYPERTENSION g. Need to monitor renal functioning (BUN and creatinine) every 90 to 120 days for duration of treatment h. Need to monitor BP and pulse rate, usually weekly B. Encourage client to implement nonpharmacologic measures to assist with BP control, such as 1. Stress reduction 2. Weight loss 3. Tobacco cessation 4. Exercise C. Determine medication side effects experienced by client. 1. Impotence 2. Insomnia D. Provide nutrition guidance, including a sample meal plan and how to dine out (low-salt, low-fat, low-cholesterol diet). HYPERTENSION HYPERTENSION PHARMACOLOGIC TREATMENT HYPERTENSION HYPERTENSION HYPERTENSION HYPERTENSION HYPERTENSIVE CRISIS HYPERTENSIVE HYPERTENSIVE URGENCY EMERGENCY BLOOD PRESSURE SBP >180 mmHg SBP >180 mmHg and/or DBP >120 and/or DBP >120 mmHg mmHg TARGET ORGAN None Present DAMAGE MANAGEMENT Reinstitute or Admit to ICU and intensify oral manage based on antihypertensive the presence of drug therapy and compelling arrange close follow-up conditions 02 CORONARY ARTERY DISEASE CORONARY ARTERY DISEASE Coronary artery disease is a narrowing or obstruction of 1 or more coronary arteries as a result of atherosclerosis, which is an accumulation of lipid-containing plaque in the arteries. The disease causes decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply, leading to hypertension, angina, dysrhythmias, MI, heart failure, and death. Collateral circulation, more than 1 artery supplying a muscle with blood, is normally present in the coronary arteries, especially in older persons. CORONARY ARTERY DISEASE Symptoms occur when the coronary artery is occluded to the point that inadequate blood supply to the muscle occurs, causing ischemia. Coronary artery narrowing is significant if the lumen diameter of the 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 the atherosclerotic progression. CORONARY ARTERY DISEASE CORONARY ARTERY DISEASE CORONARY ARTERY DISEASE CORONARY ARTERY DISEASE CORONARY ARTERY DISEASE Diagnostic studies 1. Electrocardiography a. When blood flow is reduced and ischemia occurs, ST-segment depression, T-wave inversion, or both is noted; the ST segment returns to normal when the blood flow returns. b. With infarction, cell injury results in ST-segment elevation, followed by T-wave inversion and an abnormal Q wave. 2. Cardiac catheterization: Cardiac catheterization shows the presence of atherosclerotic lesions. 3. Blood lipid levels a. Blood lipid levels may be elevated. b. Cholesterol-lowering medications may be prescribed to reduce the development of atherosclerotic plaques. CORONARY ARTERY DISEASE Interventions Instruct the client regarding a low-calorie, low sodium, low-cholesterol, and low-fat diet, with an increase in dietary fiber. Stress that dietary changes should be incorporated for the rest of the client’s life; instruct the client regarding prescribed medications. Provide community resources to the client regarding exercise, smoking cessation, and stress reduction as appropriate. CORONARY ARTERY DISEASE Surgical procedures 1. PTCA to compress the plaque against the walls of the artery and dilate the vessel 2. Laser angioplasty to vaporize the plaque 3. Atherectomy to remove the plaque from the artery 4. Vascular stent to prevent the artery from closing and to prevent restenosis 5. Coronary artery bypass grafting past the occluded artery to improve blood flow to the myocardial tissue at risk for ischemia or infarction CORONARY ARTERY DISEASE Medications Nitrates to dilate the coronary arteries and decrease preload and afterload Calcium channel blockers to dilate coronary arteries and reduce vasospasm Cholesterol-lowering medications to reduce the development of atherosclerotic plaques Beta blockers to reduce the BP in individuals who are hypertensive 03 ISCHEMIC HEART DISEASE Ischemic Heart Disease Related entities resulting from myocardial ischemia (imbalance between myocardial supply and demand) Most common cause: atherosclerosis of the coronary arteries (coronary artery disease) Syndromes: o Angina pectoris (literally “chest pain”) o Myocardial infarction (MI) o Chronic IHD with heart failure o Sudden cardiac death (SCD) (under Arrhythmias) ANGINA PECTORIS ANGINA PECTORIS Paroxysms of precordial chest discomfort due to myocardial ischemia that is insufficient to cause myocyte necrosis Stable or Typical Occurs due to exertion (demand problem) (most common form) Prinzmetal Secondary to coronary artery spasm Unstable Prolonged, severe; may happen even at rest (crescendo) Usually caused by plaque disruption and superimposed thrombosis, distal embolization of thrombus, and/or vasospasm (supply problem) ANGINA PECTORIS Common Causes Atherosclerotic heart disease HTN Coronary artery spasm Hypertrophic cardiomyopathy Any activity that increases the heart’s O2 demand; physical exertion, cold temperatures Pathophysiology By reducing the lumen of the coronary arteries, atherosclerosis limits appropriate increases in perfusion when the demand for flow is augmented, as occurs during exertion or excitement. ANGINA PECTORIS Nursing Assessment A. Chest Pain Mild to severe intensity, described as heavy, squeezing, pressing, burning, choking, aching, and feeling of apprehension Substernal, radiating to left arm and/or shoulder, jaw, right shoulder (Levine Sign) Transient or prolonged, with gradual or sudden onset; typically of short duration Often precipitated by exercise, exposure to cold, a heavy meal, mental tension, sexual intercourse Relieved by rest and/or nitroglycerin ANGINA PECTORIS B. Dyspnea, tachycardia, palpitations C. Nausea, vomiting D. Fatigue E. Diaphoresis, pallor, weakness F. Syncope G. Dysrhythmias Diagnostic information 1. ECG: Is generally at client baseline unless taken during anginal attack, when ST-segment depression and T-wave inversion may occur 2. Exercise stress test: Shows ST-segment depression and hypotension 3. Stress echocardiogram: Looks for changes in wall motion (indicated in women) 4. Coronary angiogram: Detects coronary artery spasms 5. Cardiac catheterization: Detects arterial blockage ANGINA PECTORIS Risk factors Nonmodifiable a. Heredity b. Gender: male > female until menopause, then equal risk c. Ethnic background: African Americans d. Age Modifiable a. Hyperlipidemia b. Total serum cholesterol above 300 mg/dL: four times greater risk for developing coronary artery disease (CAD) than those with levels less than 200 mg/dL (desirable level) c. Low-density lipoprotein (LDL), “bad cholesterol”: 60 mg/dL is desirable. In fact, HDL may serve to remove cholesterol from tissues. e. HTN f. Cigarette smoking g. Obesity h. Physical inactivity i. Metabolic syndrome j. Stress k. Substance abuse ANGINA PECTORIS Diagnostics ECG (initial test) Chest x-ray CBC FBS, Lipid profile, Creatinine Urinalysis Echocardiography Ambulatory ECG monitoring Stress test o Useful for patient with intermediate pretest probability for CAD o Stress (ECG vs Echo vs MPI) o Pharmacologic stress test if patient cannot exercise (Dobutamine, Adenosine, Dipyridamole) Coronary Calcium Score Coronary angiography o Definitive test for CAD ANGINA PECTORIS Management Reduce angina o First line: Beta blockers and/or CCB (2014 PHA CAD guidelines) o Second line: Long acting nitrates, Ivabradine, Nicorandil, Trimetazidine It is STRONGLY RECOMMENDED for all patients, whether or not revascularization is being considered, to receive the following medications to improve prognosis, thereby reducing the risk for MI and death: o Aspirin o Clopidogrel (if aspirin intolerant) o Statins irrespective of LDL cholesterol levels o Beta-blockers post MI o ACEi or ARB if with Hypertension or Heart Failure PCI vs. CABG ANGINA PECTORIS Nursing Plans and Interventions A. Monitor medications and instruct client in proper administration. B. Determine factors precipitating pain and assist client and family in adjusting lifestyle to decrease these factors. C. Teach risk factors and identify client’s own risk factors. D. During an attack 1. Provide immediate rest. 2. Take vital signs. 3. Record an ECG. 4. Administer no more than three nitroglycerin tablets, 5 minutes apart 5. Seek emergency treatment if no relief has occurred after taking nitroglycerin. ANGINA PECTORIS E. Physical activity 1. Teach avoidance of isometric activity. 2. Implement an exercise program. 3. Teach that sexual activity may be resumed after exercise is tolerated, usually when able to climb two flights of stairs without exertion. Nitroglycerin can be taken prophylactically before intercourse. F. Provide nutritional information about modifying fats (saturated) and sodium. Antilipemic medications may be prescribed to lower cholesterol levels ANGINA PECTORIS ANGINA PECTORIS ANGINA PECTORIS Medical-Surgical Interventions: 1. Percutaneous transluminal coronary angioplasty (PTCA), also known as percutaneous coronary intervention (PCI). A balloon catheter is repeatedly inflated to split or fracture plaque, and the arterial wall is stretched, enlarging the diameter of the vessel. A rotoblade is used to pulverize plaque. 2. Arthrectomy: A catheter with a collection chamber is used to remove plaque from a coronary artery by shaving, cutting, or grinding. 3. Coronary artery bypass graft (CABG) 4. Coronary laser therapy 5. Coronary artery stent or drug-eluting stents ANGINA PECTORIS MYOCARDIAL INFARCTION MYOCARDIAL INFARCTION Death of cardiac muscle due to prolonged ischemia o Loss of contractility: within 1-2 minutes of onset of severe Ischemia o Irreversible injury: 20-30 minutes, in the setting of severe ischemia (blood flow ≤10% of normal) Earliest detectable feature of myocyte necrosis: sarcolemmal membrane disruption → myocardial proteins in blood o Basis for chemical tests in MI MYOCARDIAL INFARCTION Pathophysiology MYOCARDIAL INFARCTION Risk factors Type 2 Diabetes Mellitus Lifestyle risk factors (smoking, poor diet, poor sleep) Family history of cardiovascular disease Poor fitness Obesity Insulin resistance Diabetic kidney disease Dyslipidemia Hypertension MYOCARDIAL INFARCTION Clinical Presentation Sudden onset chest pain, increasing in intensity, associated with diaphoresis and shortness of breath Chest pain described as heaviness or substernal pressure with radiation to arms and jaw Usually lasting more than 30 minutes (Patients with history of angina usually has chest pain that resolves within minutes. (