Cardiovascular - Summary Saunders Comprehensive Review for the Nclex-Rn Examination PDF

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Everything you need to know about cardiovascular nursing (excluding pharmacology) based on lecture notes and Saunders Comprehensive Review for the NCLEX-RN Examination. ...

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Cardiovascular

Diagnostic Tests CK-MB (creatinine kinase, myocardial muscle)

Troponin

Myoglobin

Cardiac Markers - an elevation in value indicates myocardial damage - an elevation occurs within hours and peaks at 18 hours following an acute ischemic attack Normal value male: 2-6ng/mL Normal value female: 2 to 5ng/mL Values are low, any rise can indicate myocardial cell damage - troponin I: rises within 3 hours and persists for up to 7-10 days (this one is especially related to myocardial injury) … less than 0.3ng/mL - troponin T less than 0.2ng/mL - serum levels of troponin T and I increase 4-6 hours after the onset of the MI, peak at 10-24 hours, and return to baseline after 10-14 days - myoglonin is an oxygen-binding protein found in cardiac and skeletal muscle - the level rises within 2 hours after cell death, with a rapid decline in the level after 7 hours - may not be cardiac specific

Complete Blood Count (CBC) Red Blood Cell Count - decreases in rheumatic heart disease and infective endocarditis - increases in conditions characterized by inadequate tissue oxygenation White Blood Cell Count - increases in infectious and inflammatory diseases of the heart - increases after an MI because large numbers of WBCs are needed to dispose of the necrotic tissue resulting from the infarction Hemocysteine - elevated levels may increase the risk of cardiovascular disease - normal value: 0.54 to 1.9 mg/L

Highly Sensitive C-Reactive Protein - detects an inflammatory process (e.g. atherothrombosis) - less than 1mg/dL is considered low risk - greater than 3mg/dL Blood Coagulation Factors - an increase can occur during and after an MI, which places the patient at greater risk for thrombophlebitis and formation of clots in the coronary arteries Serum Lipids - the lipid profile measures serum cholesterol, triglyceride, and lipoprotein levels - lipid profile is used to assess the risk of developing coronary artery disease - lipoprotein-a or Lp(a) increases atherosclerotic plaques and increases clots…. Normal value should be less than 30mg/dl Electrolytes * electrolyte and mineral imbalances can cause cardiac electrical instability that can result in life-threatening dysrhythmias Potassium Hypokalemia - causes increased cardiac electrical instability, ventricular dysrhythmias, and increased risk of digoxin toxicity - ECG shows flattening and inversion of the T wave, the appearance of a U wave, and ST depression

Sodium

Calcium

Phosphorus

Magnesium

Hyperkalemia - causes asystole and ventricular dysrhythmias - ECG shows tall, peaked T waves, widened QRS, or flat P waves - the serum sodium level decreases with the use of diuretics - the serum sodium level decreases in heart failure, indicating water excess Hypocalcaemia - can cause ventricular dysrhythmias, prolonged ST and QT intervals, and cardiac arrest Hypercalcemia - can cause atrioventricular block, tachycardia or bradycardia, digitalis hypersensitivity, cardiac arrest - should be interpreted with calcium levels because the kidneys retain or excrete one electrolyte in an inverse relationship to the other - low level can cause ventricular tachycardia and fibrillation

- ECG will show tall T waves and depressed ST segments (low level) - high level can cause muscle weakness, hypotension, and bradycardia Blood Urea Nitrogen - BUN is elevated in heart disorders that adversely affect renal circulation, such as heart failure and cardiogenic shock - range: B-type Natriuretic peptide (BNP) - BNP is released in response to atrial and ventricular stretch; it serves as a marker for heart failure - should be less than 100pg/mL… the higher the level, the more severe the heart failure

Diagnostic Procedures Chest X-Ray - done to determine anatomical changes such as size, silhouette, and position of the heart Holter Monitoring - noninvasive test where the client wears a monitor and an electrocardiographic tracing is recorded over 24 or more hours while the client performs their activities of daily living - the monitor identifies dysrhythmias and evaluates the effectiveness of anti-dysrhythmic or pacemaker therapy Echocardiography - non-invasive procedure that evaluates structural and functional changes in the heart - used to detect vulvar abnormalities, congenital heart defects, cardiac function Exercise Electrocardiography Testing (stress test) - studies the heart during activity and detects and evaluates coronary artery disease - treadmill testing is the most common - if the client is unable to tolerate exercise, an IV infusion of dipyridamole or dobutamine hydrochloride is given to dilate the coronary arteries and stimulate the effects of exercise (NPO for 3-6 hours before) Cardiac Catheterization - an invasive test involving the insertion of a catheter into the heart and surrounding vessels - obtains information about the structure and performance of the heart chambers and valves and the coronary circulation  Pre-procedure interventions: - obtain informed consent

- assess for allergies to seafood, iodine, or radiopaque dyes… if allergic, pre-medicate with antihistamines and corticosteroids to prevent a reaction - withhold solid foods for 6 to 8 hours and liquids for 4 hours to prevent vomiting and aspiration - document height and weight (determines how much dye is needed) - document baseline vitals, especially peripheral pulses - inform patient that they may feel a fluttery feeling as the catheter passes through the heart - shave and cleanse the insertion site  Post-procedure interventions: - asses vitals and cardiac rhythms every 30 minutes for at least 2 hours - assess peripheral pulses - monitor chest pain - notify HCP if patient complains of numbness and tingling, cool pale or cyanotic extremities, or loss of peripheral pulses… emergency; could be a clot formation - maintain strict bed rest for 6 to 12 hours

NOTE: Metformin must be held for 24 hours before any procedure involving iodine dye because of the risk of lactic acidosis and the medication is not returned until prescribed by the HCP

Cardiac Dysrhythmias Management of Dysrhythmias 1. Vagal Maneuvers Carotid sinus massage - turn head away from the side - massage over 1 carotid artery for a few seconds to determine whether a change in cardiac rhythm occurs - the client must be on a cardiac monitor (ECG) and get a rhythm strip before, during, and after the procedure Valsalva Maneuver - HCP instructs the client to bear down or induces a gag reflex to stimulate a vagal response - monitor HR, rhythm, and BP - rhythm strip before, during, and after - provide an emesis basin if the gag reflex is stimulated - have a defibrillator and resuscitative equipment available 2. Cardioversion - cardioversion is a synchronized countershock to convert an undesirable rhythm to a desirable one

- lower amount of energy used than defibrillation - can be used for stable tachydysrhythmias resistant to medical therapies or an emergent procedure for hemodynamically unstable ventricular or supraventricular tachydysrhythmias Pre-procedure: - if it is elective, ensure that informed consent is obtained - administer sedation as prescribed - if elective, hold digoxin for 48 hours - if elective for atrial fibrillation or flutter, the client should receive anticoagulant therapy for 4 to 6 week pre-procedure During procedure: - ensure skin is clean and dry in the area where the electrode pads/hands-off pads will be placed - stop oxygen during procedure to avoid fire hazard - ensure that no one is touching the bed or client when delivering the countershock Post-procedure: - priority assessment includes ability of the client to maintain the airway and breathing - resume oxygen administration - assess vitals and level of consciousness - monitor cardiac rhythm - monitor for indications of successful response, such as conversion to a normal sinus rhythm, strong peripheral pulses, adequate BP, and adequate urine output 3. Defibrillation - used for pulseless ventricular tachycardia or fibrillation - the defibrillator is charged to 360 joules for 1 countershock, then CPR is resumed immediately and continued for about 2 minutes - reassess the rhythm after 2 minutes, and if VF or VT continues, the defibrillator is charged to give a second shock NOTE: it is very important to ensure that oxygen is shut off before defibrillating and that no one is touching the bed or the client Until the defibrillator is attached and charged, the client is resuscitated with CPR. Once the defibrillator has been attached:  check the ECG to ensure the proper rhythm is there (ventricular fibrillation or pulseless ventricular tachycardia)  leads are checked for loose connections  nitroglycerin patch is removed from patient  patient does NOT have to be intubated Evaluation of successful defibrillation – patient is rousable, has a sinus rhythm, and a blood pressure within acceptable ranges

Pacemakers Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the client’s intrinsic pacemaker fails to provide a perfusing rhythm Synchronous (demand): senses the client’s rhythm and paces only if the client’s intrinsic rate falls below the set pacemaker rate Asynchronous (fixed): paces at a pre-set rate regardless of the client’s intrinsic rhythm and is used when the client is asystolic or profoundly bradycardic Temporary Non-invasive transcutaneous pacing: used as a temporary emergency measure in the profoundly asystolic or bradycardic paitent - large electrode pads are placed on the chest and back and connected to an external pulse generator - wash skin with soap and water beforehand (no need to shave) - place the posterior electrode between the spine and left scapula behind the heart - place the anterior electrode between V2 and V5 over the heart - do not place over breast tissue, but below it - do not take pulse or BP on the left side... will not be accurate Invasive transvenous pacing - pacing lead wire is placed through the antecubital, femoral, jugular, or subclavian vein into the right atrium or right ventricle so that it is in direct contact with the endocardium - restrict patient movement to prevent lead wire displacement - monitor insertion site NOTE: vital signs are monitored and cardiac monitoring is done continuously for the client with a pacemaker

Permanent - pulse generator is internal and surgically implanted in a subcutaneous pocket below the clavicle - may be powered by a lithium battery with an average lifespan of 10 years or nuclear powered with an average lifespan of 20 years - pacemaker function can be checked in the HCP office by a pacemaker interrogator or programmer from home, using a special telephone transmitter device Client Teaching  Signs of battery failure and when to notify the HCP  Report any fever, redness, swelling, or drainage from the insertion site  Report signs of dizziness, weakness, fatigue, swelling of the ankles and legs, chest pain, or shortness of breath  Keep a pacemaker identification card in the wallet and wear a MedicAlert bracelet  Instruct patient how to take pulse, to take the pulse daily, and to maintain a diary of daily pulse rates  Wear loose-fitting clothing over the pulse generator site  Inform airport security  Most electrical appliances can be used without any interference, however, do not operate electrical appliances directly over the site  Avoid contact sports  Avoid transmitter towers and anti-theft devices in stores  If any unusual feeling occurs when near any electrical devices, move 5 to 10 feet away and check the pulse  Use cellphones on side opposite the pacemaker

Coronary Artery Disease (CAD) The 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 - death It develops over time; many years. When symptomatic, the disease process is usually well advanced; symptoms occur when the coronary artery is occluded to the point that inadequate blood supply to the muscle occurs, causing ischemia. Goal of treatment: alter the atherosclerotic progression.

Risk Factors Unmodifiable:  age  gender (men > women until 60yr)  ethnicity (African American > Caucasian)  genetic predisposition  family history of heart disease Modifiable:  increased serum lipids  hypertension  cigarette smoking  obesity  physical inactivity  diabetes mellitus  stressful lifestyle  psychosocial state  homocysteine level  metabolic syndrome Clinical Manifestations – 3 Major 1. Chronic Stable Angina 2. Acute Coronary Syndrome - unstable angina - MI 3. Sudden cardiac death Assessment  possibly normal findings during asymptomatic periods  chest pain  palpitations  dyspnea  syncope  cough or hemoptysis  excessive fatigue Interventions  assist the client to identify modifiable risk factors and to set goals to reduce the impact of risk factors  assists to identify barriers to compliance  instruct about low-calorie, low-sodium, low-cholesterol, low-fat diet with increased fiber  stress the importance that dietary changes are not temporary and must be maintained for life  provide community resources regarding exercise, smoking cessation, and stress reduction

 encourage weight loss  drug therapy – lipid-lowering medications (questran, socor, Lipitor, pravachol) Medications  nitrates – dilate the coronary arteries and decrease preload and afterload  calcium channel blockers – dilate coronary arteries and reduce vasospasm  cholesterol lowering drugs – reduce the development of atherosclerotic plaque  beta blockers – reduce BP in those who are hypertensive  lipid lowering drugs Diagnostic Studies Electrocardiography - when blood flow is reduced and ischemia occurs: ST depression, T wave inversion, or both is noted… ST segment returns to normal when the blood flow returns Cardiac Catheterization - shows the presence of atherosclerotic lesions Blood Lipid Levels - may be elevated - cholesterol-lowering medications may be prescribed to reduce the development of atherosclerotic plaques

Angina Clinical syndrome characterized by paroxysms of pain or a feeling of pressure in the anterior chest caused by myocardial ischemia as a result of inadequate myocardial blood and oxygen supply. - imbalance between oxygen supply and demand - causes include obstruction of coronary blood blow resulting from atherosclerosis, coronary artery spasm, or conditions increasing myocardial oxygen supply Types 1. Stable angina – aka exertional angina - occurs with activities that involve exertion or emotional stress - relieved with rest or nitroglycerin - usually has a stable pattern of onset, duration, severity, and relieving factors 2. Unstable angina – aka preinfarction angina - occurs with an unpredictable degree of exertion or emotion and increases in occurrence, duration, and severity over time - pain may not be relieved with nitroglycerin 3. Variant angina – aka Prinzmetal’s or vasospatic angina - results from coronary artery spam

- may occur at rest - attacks may be associated with ST elevation 4. Intractable angina - chronic, incapacitating angina unresponsive to treatment 5. Preinfarction angina - associated with acute coronary insufficiency - lasts longer than 15 minutes - symptoms of worsening cardiac ischemia - characterized by chest pain that occurs days to weeks before an MI Precipitating Factors  physical activity  temperature extremes  strong emotions  consumption of heavy meal  cigarette smoking  sexual activity  stimulants  circadian rhythm patterns Assessment  pain - usually described as mild or moderate - substernal, crushing, squeezing - may radiate to the shoulders, arms, jaw, neck, or back - pain intensity is unaffected by inspiration and expiration - pain usually lasts less than 5 minutes, but can last up to 15 to 20 - pain is relieved by nitroglycerin  dyspnea  pallor  sweating  palpitations and tachycardia  dizziness and syncope  hypertension  digestive disturbances (indigestion) Interventions IMMEDIATE:  assess pain and institute pain relief measures  administer oxygen by nasal cannula  assess vitals and provide continuous cardiac monitoring and nitroglycerin to dilate the coronary arteries  ensure that bed rest is maintained and that patient is in semi-Fowlers

 stay with the patient  obtain a 12-lead ECG Following acute episode:  assist the client to identify angina-precipitating events  instruct to stop activity and rest if chest pain occurs and to take nitroglycerin… call 911 if nitro does not relieve the pain (can take aspirin too)  assist the client to identify modifiable risk factors and to set goals to reduce the impact of risk factors  provide community resources regarding exercise, smoking cessation, and stress reduction  encourage weight loss

Diagnostic Studies Electrocardiography - readings are normal during rest – ST depression or T wave inversion during acute episode Stress Testing - chest pain or changes in the ECG or vital signs during testing may indicate ischemia Cardiac enzymes and troponin - findings are normal in angina Cardiac Catheterization - provides a definitive diagnosis by providing information about the patency of the coronary arteries Medications  antiplatelets (ASA) – reduces risk of MI  b-adrenergic blockers (Lopressor)  nitrates (nitrostat, isordil)

 calcium channel blockers (Cardizem)  ACE Inhibitors (Capoten)  analgesics

Myocardial Infarction (MI) MI occurs as a result of sustained ischemia, causing irreversible cellular death. Infarction does not occur instantly but evolves over several hours. Obvious physical changes do not occur in the heart until 6 hours after, when the infarcted area becomes blue and swollen. After 48h, the infarction turns grey with yellow streaks. By 8-10 days, granulation tissue forms. Causes  thrombus  occlusion  coronary artery spasm  hypoxemia Risk Factors  atherosclerosis  CAD  high cholesterol  smoking  hypertension  obesity  physical inactivity

 impaired glucose tolerance  stress Symptoms  severe, immobilizing chest pain not relieved by rest, position change, or nitrates  pain may occur while active, at rest, or sleeping; most common in early am  heaviness, pressure, tightness, burning, constricting, or crushing  substernal, retrosternal, or epigastric locations  radiation to neck, jaw, arms, or back  occasionally fever  pain lasts 30 minutes or longer  nausea and vomiting  diaphoresis  dyspnea  dysrhythmias  feelings of fear/anxiety/impending doom  pallor, cyanosis, grey/ashen, coolness of extremities OR…. Patient can be asymptomatic, have atypical discomfort, or diabetic clients may not feel severe pain because cardiac neuropathy Diagnostic Studies Troponin: level rises within 3 hours and remains elevated for up to 7-10 days Total CK: rises within 6 hours after the onset of chest pain and peaks within 18 hours after death of cardiac tissue CK-MB: peak elevation occurs 18 hours after the onset of chest pain and returns to normal 48-72h later WBC: elevated wbc count appears on the second day following the MI and lasts up to 1 week ECG: shows either ST elevation, T wave inversion, or non-ST elevation with an abnormal Q wave - hours to days afterward, the ST and T wave changes will return to normal, but Q wave changes are usually permanent

Interventions – ACUTE 1. obtain a description of chest discomfort 2. Administer O2 and institute pain relief measures (morphine and nitroglycerin) 3. Assess vitals and cardiovascular status and maintain cardiac monitoring 4. Assess respiratory rate and breath sounds for signs of HF 5. Ensure bed rest and place in semi-Fowler’s 6. Establish IV access 7. Obtain 12-lead ECG 8. Monitor laboratory values 9. Monitor for cardiac dysrhythmias (particularly tachycardia and PVCs) 10. Administer thrombolytic therapy (within first 6 hours) and monitor for bleeding 1...