Management of pt with CVD

Chapter 28

Coronary Artery Disease

Includes Coronary atherosclerosis, acute coronary syndrome, and MI.  Coronary Atherosclerosis Accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls. Block and narrow coronary vessels which reduce blood flood to the myocardium. Repeated inflammatory response to injury of the artery wall and subsequent alteration in the structural and biochemical properties of the arterial wall. Patho- fatty streaks of lipids that are deposited in the intima of aterial wall. Can begin in childhood. Develop over many years. Results in inflammatory response which begins injury to the vascular endothelium. Iniated by smoking, HTN, and other factors. If plaque ruptures thrombus may obstruct blood flow leading to acute coronary syndrome which may lead to MI.

Clinical manifestations of CAD

Produces symptoms and complications according to the location and degree of narrowing of the arterial lumen, thrombus formation, and obstruction of blood flow to the myocardium. Inadequate blood supply deprives cardiac muscle cells of oxygen needed for survival. Causes ischemia. Angina pectoris refers to chest pain that is brought about by myocardial ischemia. Caused by significant coronary atherosclerosis. Ischemia caused from decreased blood flow will in turn cause scar tissue formation leading to myocardial dysfx. Most common manifestation of MI is angina pectoris. SOB and women showing signs of dyspnea, nausea, and weakness Some experience prodromal symptoms ie angina hrs to days before acute episode

Risk factors for CAD

Elevated LDL CAD, diabetes, PAD, abdominal aortic aneurysm, or corotid artery disease Age, systolic BP, smoking hx, total cholesterol, HDL, and metabolic syndrome

Diagnosis for metabolic syndrome

Insulin resistance(fasting plasma glucose greater than 100 or abnormal glucose tolerance test) Central obesity Dyslipidemia (triglycerides greater than 150, HDL less than 50 in women, 40 in men) BP greater than 130/85 Proinflammatory state (increase level of CRP) Prothrombotic state

Prevention of CAD
Cholesterol abnormalities, tobacco use, HTN, and diabetes management Control cholesterol abnormalties- 20 year of age or older should have fasting lipid profile performed at least once every 5 years and more often if abnormal results. Patients with acute MI, PCI, or CABG require assess of LDL within few months because LDL may be low immediately after subsequently lipids should be monitored every 6 weeks until desired level achieved and then every 4-6 months. Fasting lipid profile less than 100. Total cholesterol less than 200. HDL greater than 60. Triglyceride less than 160.  Dietary recommends cessation of smoking, increased physical activity, and weight loss. Diet that promotes veggies and fish and restricts red meat. Soluble fibers found in fresh fruit, cereal, grains, veggies, and legumes recommended. Restrict sugar intake.  Physical activity help manage elevated triglycerides. Focus on weight reduction and increased physical activity. Moderate exercise 30 min day (brisk walking increase HDL and decrease triglycerides). Pt should stop any activity with chest pain, SOB, dizziness, light headedness, or nausea occur.  Medications used if diet alone doed not normalize. Lipid lowering med used. Meds reduce CAD mortality. See Table 28-2 on page 761

Prevention of CAD
 Managing hypertension- risk of cardiovascular disease increases as BP increases and those with BP higher than 120/80 prehypertensive and at risk. Long standing elevated BP result in increased stiffness of vessel walls, leading to vessel injury and resulting inflammatory response within the intima. Inflammatory mediators then lead to the release of growth promoting factors that cause vessel hypertrophy and hyperrespnsiveness. Result in acceleration and aggravation of atherosclerosis. HTN also increase work of L ventricle, which has to pump harder to eject blood into the arteries. Cause enlarge and thicken and lead to HF. Control diabetes- hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered RBC fx which lead to thrombus formation. Impair endothelial cell dependent vasodilation and smooth muscle fx, promoting development of atherosclerosis. Tx with insulin and metformin and other interventions that lower plasma glucose levels can lead to improved endothelial fx and pt outcomes

Angina pectoris
Patho- usually caused by atherosclerotic disease. Obstruction of at least one major coronary artery.  Clinical syndrome characterized by episodes/paroxysms of pain/pressure in the anterior chest.  Insufficient coronary blood flow with decreased O2 supply when increase myocardial demand for O2 in response to physical exertion/emotional stress

Types of Angina
1. Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin 2. Unstable angina: symptoms increase in frequency and severity; may not be relieved with rest or nitroglycerin 3. Intractable or refractory angina: severe incapacitating chest pain 4. Variant angina: pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm 5. Silent ischemia: objective evidence of ischemia with no report of pain

Factors associated with anginal pain

Physical exertion Exposure to cold- vasoconstriction and elevated BP Eating heavy meals- alter blood flow to area Stress or any emotion provoking situationreleases catecholamines which increase BP, HR, and myocardial workload

Clinical Manifestations
Pain- felt deep in chest behind sternum; poorly localized and may radiate to neck, jaws, shoulders, and inner aspects of upper arms, usually L arm Tightness or heavy choking/strangling Diabetic neuropathy dulls perception of pain Weakness/numbness in arms, wrists/hands, SOB, pallor, diaphoresis, dizziness, lightheadedness, and N/V Unstable characterized by attacks that increase in frequency and severity and not relieved with rest and nitro Presenting symptom in elderly is dyspnea, meds to manage used cautiously bc associated with increase adverse reactions

Assessment and diagnostic

12 lead ECG CRP and cardiac biomakers Exercise or pharmacologic stress test cardiac cath or coronary angiography

Medical management w meds

1. Nitroglycerin- reduce myocardial O2 consumption to decrease ischemia and relieve pain. Dilated veins and arteries. Lowers BP and decrease afterload. Sublingual tab or spray, oral cap, topical agent, IV. Sublingual alleviate pain within 3 min. Not given if systolic BP less than 90. Oral or topical within 24 hr after symptom free. Beta-blocker- metoprolol and atenolol reduce myocardial O2 consumption by blocking beta-adrenergic sympathetic stimulation to heart. Reduces HR, slow conduction of impulses, decreases BP, and reduce myocardial contractility to balance myocardial O2 needs and amount of O2 available. Control chest pain and delays onset ischemia during wk/exercise. Reduce incidence of recurrent angina, infarction, and cardiac mortality. Titrate til resting HR of 50-60bpm. Cardiac side effects and contraindications- hypotension, bradycardia, advanced atrioventricular block, and acute HF. With IV- ECG, BP, and HR monitored closely. Side effects include decreased libido, and masking of symptoms of hypoglycemia. Don t stop abruptly Monitor blood glucose closely with diabetes and monitor S/S of hypoglycemia

2.

o o o o

Medical management w meds

3. Calcium channel blockers- decrease sinoatrial node automaticity and atrioventricular node conduciton resulting in slower HR and decrease in the strength of myocardial contraction. Decrease workload of heart. Relax blood vessels causing decrease BP and increase coronary artery perfusion. Increase myocardial O2 supply by dilating smooth muscle wall of coronary arterioles. Decrease myocardial O2 demands by reducing systemic arterial pressure and workload of L ventricle. o Amlodipine and diltiazem commonly used with pt who can t take beta blockers, with side effects to beta blockers or nitro, or who still have pain despite using beta blockers or nitro. Used to prevent and tx vasospasm. o Nifedipine avoided or used in caution in people with HF bc decrease myocardial contractility. o Amlodipine and felodipine choice for pt with HF. o Hypotension may occur after IV administration. o Other side effects include atrioventricular block, bradycardia, constipation, and gastric distress.

Medical management w meds

4. Antiplatelet and anticoagualants- prevent platelet aggregation and thrombosis. o Aspirin- prevent platelet aggregation and reduce incidence of MI and death of pt with CAD. 160-325mg dose given with angina and then 81325mg daily. o Clopidogrel- (Plavix) given in addition to aspirin for pt at risk for MI o Heparin- IV prevent formation of new blood clots. Those hospitalized may be given a bolus and started on continuous infusion. Monitor PTT value. LMWH tx unstable angina or non ST segment elevation MIs. Beneficial during PCIs and ST segment elevation MIs. Monitored for S/S of external and internal bleeding, such as low BP, increased HR, and decreased serum H&H. BLEEDING PRECAUTIONS! Decrease in platelet count or evidence of thrombosis may indicate heparin induced thrombocytopenia, antibody mediated reaction to heparin that may result in thromosis. Those who received heparin within the past 3 months and receiving unfractioned heparin fro 5-15 days are at high risk for HIT.

Medical management meds/O2

5. Glycoprotein IIb/IIIa- for unstable angina and as adjunct therapy for PCI. Prevent platelet aggregation by blocking the GP IIb/IIIa receptors on plateles, preventing adhesion of fibrinogen and other factors that crosslink platelets to each other and thus form platelet clots. Bleeding major side effect. 6. O2 administration- given with onset of chest pain to increase amount of O2 delivered to myocardium and decrease pain. Keep O2 level above 93%. Administer 2L

Collaborative problems
1. 2. 3. 4. ACS and/or MI Dysrhythmias and cardiac arrest HF Cardiogenic shock

Nursing interventions for angina

1. Tx angina- stop activities and sit or rest in semi fowler s to reduce O2 requirement or ischemic myocardium. Note that change may indicate worsening of disease. Assess vitals and observe for respiratory distress. 12 lead ECG to scrutinize for ST segment and T wave changes. Give Nitroglycerin sublingually. Repeated up to 3 doses. Assess BP, HR, and ST segment with each dose. O2 therapy if RR increased or O2 sat level decreased. Usually 2L given. Reduce anxiety Prevent Pain- minimal activity by alternating with rest periods. Promote home and community based care- teach self care. Pt needs to know that any pain unrelieved within 15 min by usual methods including nitro should seek immediate emergency care. Continuing care by home care nurse.

o o 2. 3. 4.

Acute coronary syndrome and MI

Patho- In unstable angina, there s reduced blood flow in coronary artery due to rupture of atherosclerotic plaque where artery isn t completely occluded. With MI, area of myocardium is permanently destroyed bc plaque rupture and subsequent thrombus formation result in complete occlusion of the artery. Vasospasm of coronary aretery, decrease O2 supply, and increased O2 demand are other causes of MI. Area of infarction develops over min to hrs. As cells are deprived of O2, ischemia develops, cellular injury occurs, and lack of O2 results in infarction or death of cells. ID MI: type(NSTEMI, STEMI), location of injury to ventricular wall, and point in time within process of infarction(acute, evolving, or old). ECG identify type and location of MI, and other ECG indicators such as Q wave and pt hx id timing. ACS is emergent situation characterized by acute onset of myocardial ischemia that result in myocardial death if definitive interventions not prompt. ACS include unstable angina, non ST segment elevation MI, and ST segment elevation MI.

Clinical manifestation of ACS/MI

Sudden chest pain and continues even with rest or medication. Prodromal symptoms or previous diagnosis of CAD SOB, indigestion, nausea, and anxiety Cool, pale, and moist skin Increased HR and RR Stimulation of sympathetic nervous system

Assess and diagnostic findings

1. 2. o o o o Patient hx ECG- rule out or diagnose MI Monitor location, evolution, and resolution of MI Classic ECG changes are T wave inversion, ST segment elevation, and development of abnormal Q wave. First ECG signs of acute MI occur as result of myocardial ischemia and injury. Myocardial injury cause T wave to become enlarged and symmetric. As area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing T wave to invert. The ischemic region may remain depolarized while adjacent areas of the myocardium return to the resting state. Myocardial injury also caused ST segment changes. Injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing ST segment to rise at lease 1 mm above isoelectric line when measured .06-.08 sev after end of the QRS(Jpoint). This elevation in the ST segment in 2 contiguous leads is a key diagnostic indicator for MI. Appearance of abnormal Q waves in another indicator of MI. Q waves develop within 1-3 days bc there is no depolarization current conduction from necrotic tissue. New and significant Q wave is .04 sec or longer and 25% of R wave depth. An acute MI may also cause a significant decrease in height of the R wave. An abnormal Q wave may be present without ST segment and T wave changes, which indicates an old, not acute MI

Assess and diagnostic findings

o Unstable angina: coronary ischemia, but ECG and cardiac biomarkers show no evidence of MI o STEMI: ECG evidence of acute MI with characteristic changes in 2 contiguous leads on 12 lead ECG. Significant damage to myocardium. o NSTEMI: elevated cardiac biomarkers but no definite ECG evidence of acute MI o During recovery, ST segment oftern first WCG indicator to return to normal(1-6 wks). T wave becomes large and symmetric for 24 hrs, and inverts within 1-3 days for 1-2 wks. Q wave alternations usually permanent. Old STEMI indicated by abnormal Q wave or decreased ht of the R wave without ST segment and T wave changes. 3. Echocardiogram- evaluate ventricular fx. Diagnose MI and detect hypokinetic and akinetic wall motion as well as determine ejection fraction.

Assess and diagnostic findings

4. Laboratory tests- cardiac enzymes and biomarkers are used to diagnose acute MI. Cardiac biomarker (myoglobin and troponin) analyzed rapidly. Based of release of cellular contents into circulation when myocardial cells die. Creatine Kinase and its Isoenzymes- CK-MM (skeletal muscle), CKMB (heart muscle), and CK-BB (brain tissue) CK-MB is cardiac specific isoenzyme found mainly in cardiac cells and increases only with damage to cells. Elevated CK-MB assessed by mass assay is indicator of acute MI (begins to increase within few hr and peaks within 24 hrs of MI). If area reperfused, peaks earlier. Myoglobin- heme protein transport O2. Found in cardiac and skeletal muscle. Starts to increase within 1-3 hrs and peaks within 12 hrs after onset of symptoms. Increase not very specific in indicating acute cardiac event. Negative results rule out acute MI

Assess and diagnostic findings

o Troponin- protein found in myocardium. Regulates myocardial contractile process. 3 isomers of troponin: C,I, and T. Troponin I and T specific for cardiac muscle and recognized as reliable and critical markers of myocardial injury. Increased level can be detected within a few hours during acute MI. Remains elevated for a long time, as long as 3 wks, and can be used to detect recent myocardial damage.

Medical management of ACS/MI

o Goal is to minimize myocardial damage, preserve myocardial fx, and prevent complications. o Reperfuse area with emergency use of thrombolytic meds or by PCI. o Minimize damage by reducing myocardial O2 demand and increase O2 supply w meds, O2 administration, and bed rest. o Resolution of pain and ECG changes indicate demand in equilibrium as well as reperfusion. o Visualization of blood flow through open vessel in cath lab

Pharmacologic therapy
o Aspirin, nitro, morphine, IV beta-blocker o Should continue beta-blocker thru hospitalization and after D/C bc long term therapy with beta blockers can decrease incidence of future cardiac events. o Unfractionated heparin or LMWH prescribed with platelet inhibiting agents to prevent clot formation. o NSAIDS D/C

Pharmacologic therapy
1. 2. Analgesics- morphine by IV bolus to reduce pain and anxiety. Reduces preload and afterload which decrease workload of heart and relax bronchioles to enhance O2. Monitor BP (will decrease), and RR (slows). Angiotensin-Converting enzyme inhibitors- (ACE-I) prevent conversion of angiotensin I to angiotensin II. BP decreases and kidneys excrete Na and fluid, decreasing O2 demand on heart. Decreases mortality rate and prevents remodeling of myocardial cells that associated with onset of HF. Ensure pt not hypotensive, hyponatremic, hypovolemic, or hyperkalemic before giving. Monitor BP, UO, serum Na, K, and CREA. Thrombolytics- tx acute MI. Given IV. Dissolve thrombus in coronary artery and minimize size of infarction as well as preserving ventricular fx. First line therapy. Dissolve ALL clots, not just ones in coronary arteries. Don t use if pt formed protective clot such as after major sx or hemorrhagic stroke. Pt at risk for bleeding. Given as early as possible, usually within 30 of presentation of ER. Alteplase and reteplase- Alteplase is tissue plasminogen activator that activates plasminogen present on blood clot. IV bolus given and followed with infusion. Aspirin and Heparin/LMWH used with t-PA to prevent another clot from forming at site of lesion. Reteplase administered in 2 bolus doses, followed by heparin infusion.

3.

Emergent Percutaneous Coronary Intervention

o STEMI may be taken directly to cardiac cath for immediate PCI. o Open occluded coronary artery and promote reperfusion to area deprived of O2. o Tx atherosclerotic lesion. o Perform asap less than 60 from admit

Cardiac Rehabilitation
o Continuing care program for pt with CAD that targets risk reduction by means of education, individual/group support, and physical activity. o Limit the effects and progression of atherosclerosis, return pt to work and pre-illness lifestyle, enhance psychosocial and vocational status of pt, and prevent another cardiac event. o Cardiac efficiency is achieved when work and activities of daily living can be performed at a lower HR and BP- reducing cardiac workload. o Observe pt for chest pain, dyspnea, weakness, fatigue, and palpations as well as instruct to stop exercise if these occur. o Monitored for increase in HR above target HR, increase BP of more than 20, decrease in systolic BP, onset or worsening of dysrhythmias, or ST segment changes o Pt who are able to walk 3-4 miles can usually resume sexual activities.

Phases of cardiac rehab

o Phase I begins with the diagnosis of atherosclerosis, which may occur when pt admitted to hospital for ACS. Low level activities and initial education for pt and family improve pt outcomes Teach S/S of need for 911, meds, rest-activity balance, and follow up appointments. o Phase II is after pt D/C. Attends sessions 3 times a week for 4-6 wks up to 6 months. Supervised ECG monitoring, exercise training individualized based on results of exercise stress test. o Phase III is long term outpatient program that focuses on maintaining cardiovascular stability and long term conditioning. Pt self directed.

Assess of pt with ACS

1. 2. 3. 4. 5. 6. 7. o Chest pain/discomfort SOB/dyspnea Palpations Unusual fatigue or faintness Diaphoresis Complete physical assessment Monitor IV sites (when stable change to saline lock) Each symptom evaluated in regard to time, duration, and factors that precipitate symptom and relieve it and in comparison with previous symptoms

Collaborative problems of ACS

1. 2. 3. 4. 5. Acute pulmonary edema HF Cardiogenic shock Dysrhythmias and cardiac arrest Pericardial effusion and cardiac tamponade

Nursing interventions
1. 2. 3. 4. Balancing myocardial O2 supply with demand top priority O2 along with meds to assist with relief of symptoms. O2 raises the circulation of O2to reduce pain associated with low levels of myocardial O2. Usually 2-4L nasal cannula Vitals assessed frequently as long as pt experiencing pain and/or other S/S of acute ischemia. Physical rest in bed with backrest elevated help decrease chest discomfort and dyspnea. Elevation helps tidal volume bc reduce pressure from abdominal contents on diaphragm and better lung expansion, drainage of upper lung lobes inprove, and venous return to heart(preload) decreases, reducing work of the heart. Improve respiratory fx- monitor fluid volume status to prevent overloading heart and lungs and encourage pt to breathe deeply and change positions frequently. Monitor RR and pulse ox. Adequate tissue perfusion- bed or chair rest during initial phase of tx helps reduce myocardial O2 consumption. Check skin temp and peripheral pulses frequently Reduce anxiety- decreased sympathetic stimulation decreases the workload of the heart which relieves pain and other S/S ischemia.

5. 6. 7.

Nursing interventions cont

8. Monitoring and managing complications- for changes in cardiac rate and rhythm, heart sounds, BP, chest pain, respiratory status, UO, skin color, and temp, sensorium, ECG changes, and lab values. 9. Promote home and community based carefacilitate pt involvement in cardiac rehab. Home care nurse for assistance if necessary.

Percutaneous coronary interventions

o Types of procedures 1. Percutaneous transluminal coronary angioplasty (PTCA)- balloon tipped cath used to open blocked coronary vessels and resolve ischemia. Used on pt with angina and as intervention for ACS. Used to open blocked CABGs. Improve blood flow within coronary artery by compressing and cracking atheroma. Hollow cath called sheaths inserted (at femoral artery/vein) providing conduit for other cath. Caths threaded thru femoral artery, up thru aorta, and into coronary arteries. Angiography performed using contrast to id location and extent of blockage. Balloon tipped dilation cath passed thru sheath and positioned over lesion. When cath positioned, balloon inflated with high pressure for several sec and then deflated. Pressure compresses and cracks off atheroma. Improvement of blood flow and residual stenosis of less than 20% Increase in artery s lumen and no arterial trauma. Pt may complain of chest pain and ECG display ST segment changesbc blood supply of coronary artery decrease as balloon inflated. Intracoronary stents positioned in intima of vessel to maintain patency after balloon withdrawn.

Percutaneous coronary interventions

2. Coronary Artery stent- release mediators which leads to vasoconstriction, clotting, and scar tissue formation. Stent is metal mesh that provides structural support to the vessel at risk of acute closure. It is positioned over the balloon. Balloon inflated and mesh expands/presses against the vessel wall, holding artery open. Some stents coated w med such as sirolimus or paclitaxel which minimize formation of thrombi or scar tissue within stent. Antiplatelet meds (aspirin and clopidogrel) given. Clopidogrel cont for a month following placement of bare metal stent and for a year following drug eluting stents. 3. Atherectomy- removal of atheroma from coronary artery by cut, shave, or grind. Directional coronary atherectomy and transluminal

Percutaneous coronary interventions 4. Brachytherapy- reduces recurrence of obstruction, preventing vessel restenosis by inhibiting smooth cell proliferation. Gama and beta radiation by placing radioisotope close to lesion. Drug eluting stents are used more commonly to prevent restenosis, bc they more effective and less expensive than bradytherapy.

Complications of PCI
During PCI 1. 2. 3. 4. Dissection Perforation Abrupt closure Vasospasm of coronary artery 5. Acute MI 6. Acute dysrhythmia 7. Cardiac arrest After PCI 1. Abrupt closure of coronary artery 2. Bleeding at site of insert 3. Retroperitoneal bleeding 4. Hematoma 5. Arterial occlusion 6. Acute renal failure

Postprocedure care
o Those with no complications go home next day o Emergent stay in CCU a few days o Monitored for signs of bleeding since given heparin or thrombin inhibitor during PCI, some are given GP IIb/IIIa for several hours after. o Femoral sheath removed with hemostasis achieved. Use vascular closure device or device that sutures vessel. o Remain flat in bed and keep affected leg straight until sheaths are removed an then for a few hours afterward to maintain hemostasis o Analgesics and sedations as directed o Sheath removal and application of pressure on the vessel insertion site may cause HR to slow and BP to decrease. IV bolus of atropine given to treat. o Those with unstable lesions and high risk for abrupt vessel close are restarted on heparin after sheath removal. (may get GP IIa/IIIb inhibitor) o On day after incision, site inspected and bandage removed. Monitor site for bleeding or develop of hard mass indicative of hematoma.

Coronary Artery Revascularizaion

o CABG sx procedure in which blood vessel grafted to occluded coronary artery so blood can flow beyond occlusion. Also called bypass graft o Major indications for CABG: 1. Alleviation of angina that can t be controlled w med or PCI 2. Tx of L main coronary artery stenosis or multivessel CAD 3. Prevention and tx of MI, dysrhythmias, or HF 4. Tx for complications from unsuccessful PCI

Coronary Artery Revascularizaion

o Recommendation for CABG determined by number of diseased coronary vessels, degree of L ventricular dysfx, presence of other health problems, pt symptoms, and previous tx. o CABG may be preferred tx for high risk pt such as those with severe triple vessel CAD, ventricular dysfx, and diabetes. o To be considered for CABG, coronary to be bypassed must be 70% occluded. Artery must also be patent beyond the area of blockage or the flow thru bypass will be impeded. o Greater saphenous vein used followed by lesser saphenous vein. Cephalic and basilic veins also used. Grafted to ascending aorta and coronary artery distal to lesion. o Common adverse effect of vein removal is edema in extremity from which vein taken. o R and L internal mammary arteries and radial and gastroepiploic arteries used occasionally.

Traditional coronary artery bypass graft

o CABG performed under general anesthesia. o Median sternotomy and connects pt to cardiopulmonary bypass machine. Blood vessel from another part of pt body grafted distal to coronary artery lesion, bypass obstruction. o CPB disconnected , chest tubes and epicardial pacing wires placed, then incision closed. Pt admitted to CCU.

Cardiopulmonary bypass
o Machine circulated and O2 blood for body while bypassing heart and lungs. Maintains perfusion to body organs and tissues and allows surgeon to complete anastomoses in motionless, bloodless field. o CPB accompanied by putting cannula in R atrium, vena cava, or femoral vein to withdraw blood from body. Cannula connected to tubing filled with isotonic crystalloid solution. Venous blood removed fro body by cannula filtered, O2, cooled/warmed by machine, and returned to body. Cannula used to return O2 blood usually inserted in ascending aorta, or inserted in femoral artery. Heart is stopped by injection of K rich cardioplegia solution into coronary arteries. Pt given heparin to prevent clots. Protamine sulfate administered to reverse heparin. o During procedure, hypothermia maintained (82.4-89.6). Blood cooled during CPB and returned to body. Lowers basal metabolic rate, decreasing O2 demand. Crystalloid solution given to prevent blood from being viscous. After sx blood warmed and put back in body. o UO, ABG, electrolytes, and coagulation monitored.

Alternative CABG
o OPCAB involves standard median sternotomy incision without CPB. Beta adrenergic blocker may be used to slow HR. My use myocardial stabilization device to hold the site still for anastomosis of bypass graft into coronary artery while heart continues to beat. o OPCAB decrease incidence of stroke and neurological complications, renal failure, and postoperative complications. o Pt with multiple bypass grafts to arteries on dorsum of heart may not be candidate of technique.

Complications of CABG
1. 2. 3. o hemorrhage Dysrhythmias MI CABG isn t a cure for CAD, and angina, exercise intolerance, or other symptoms experienced before CABG may recur. o Medications required sx may need to be continued. o Lifestyle modifications recommended.

Nursing interventions
o Preoperative management 1. Assessment for baseline for postoperative comparison 2. Evaluate pt understanding of sx procedure, informed consent, and adherence to tx protocol 3. Preoperative testing- chest x-ray, ECG, lab tests, coagulation studies, and blood typing and cross matching 4. Assess pt for disorders that could complicate or affect postoperative course, such as diabetes, HTN, and preexisting disabilities 5. Monitor blood glucose to avoid complications with sx. 6. Reduce fear and anxiety- allow pt time to express fears. Administer anxiolytic agents such as ativan and valium. 7. Monitor and manage complications- nitro and O2 for angina 8. Provide teaching about meds(anticoagulants, antihypertensives, and diabetic). Shower with antiseptic solution. Most pt remain intubated and on mechanical ventilaion for 2-24 hours after sx. Answer questions and teach about deep breathing/cough, incentive spirometer and foot exercises. Also about early ambulation and frequency

Nursing interventions
o Intraoperative management 1. Comfort and safety 2. Chest tubes inserted to evacuate air and drainage from mediastinum and thorax. Temporary epicardial pacemaker electrodes may be implanted on surface of R atrium and R ventricle. Epicardial electrodes can be connected to an external pacemaker if pt persistent bradycardia perioperatively. 3. Possible intraoperative complications include low CO, dysrhythmias, hemorrhage, MI, stroke, embolization, and organ failure from shock, embolus, or adverse drug reactions.

Nursing interventions
o Postoperative nursing management 1. Achieve and maintain hemodynamic stability and recovery from general anesthesia. 2. Pt transferred to PACU; sx team and anesthesia report off 3. Once cardiac and respiratory status stable, pt transferred to sx progressive unit with telemetry. 4. Monitor cardiopulmonary status, pain management, wound care, progressive activity, and nutrition. 5. Educate about meds and risk factor modifications. 6. Hourly assessment of all systems for at least 8 hrs afterwards. Neurological status: LOC, pupil size and reaction to light, reflexes, facial symmetry, movement of extremities, and hand grip strength.

Nursing interventions
Cardiac status: HR and rhythm, heart sounds, pacemaker status, ABG, CVP, and in selected pt, hemodynamic parameters: pulmonary artery pressure, pulmonary artery wedge pressure, CO, and index, systemic and pulmonary vascular resistance, mixed venous O2 saturation. Respiratory status: chest movement, breath sounds, ventricular settings, RR, peak inspiratory pressure, SaO2. percutaneous O2 saturation, end tidal CO2, pleural chest tube drainage, ABGs Peripheral vascular status: peripheral pulses, color of skin, nail beds, mucosa, lips, and earlobes, skin temp, edema, condition of dressings and invasive lines. Renal fx: UO, urinary specific gravity and osmolality Fluid and electrolyte status: Intake, output from drainage tubes, CO parameters, and electrolyte imbalance Pain: nature, type, location, and duration; apprehension; response to analgesics Check equipment and tubes to ensure fx properly: endotracheal tube, ventilator, end tidal CO2 monitor, SpO2 monitor,pulmonary arter cath, SvO2 monitor, arterial and IV lines, IV infusion devices and tubing, cardiac monitor, pacemaker, chest tubes, and urinary drainage system. Monitor characteristic signs of delirium Coping of family

Nursing interventions
7. 8. Monitor for complications Decreased CO- preload alterations occur when little blood volume returns to heart and results in hypovolemia, persistent bleeding, or cardiac tamponade. Excessive postoperative bleed can lead to decreased intravascular volume, hypotension, and low CO. Bleeding problems are common after cardiac sx bc of the effects of CPB, trauma from sx, and anticoagulation. Preload can also be altered if too much volume returns to the heart, causing fluid overload. Afterload alterations occur when arteries are constricted as result of postoperative HTN or hypothermia, increasing workload of the heart. HR alterations from bradycardia, tachycardia, and dysrhythmias can lead to decreased CO, and contractility can be altered in cardiac failure, MI, electrolyte imbalances, and hypoxia.

Nursing interventions
Fluid volume and electrolyte imbalance- monitor weight, I and O, hemodynamic parameters, hematocrit levels, distention of neck veins, edema, liver size, breath sounds, and electrolyte levels Dangerously high or dangerously low levels of K, Mg, Na, and Ca are extremely important to monitor. Elevated glucose common postoperatively. IV insulin may be give to pt with or without diabetes achieve glycemic control necessary to promote wound healing and recovery. 10. Impaired gas exchange- endotracheal tube with ventilator assistance may be used for 24 hrs or more.Stable pt may be extubated as early as 2-4 hrs after sx. Assess for signs of impaired gas exchange: restlessness, anxiety, cyanosis of mucous membranes and peripheral tissues, tachycardia, and fighting the ventilator. Breath sounds assessed often to detect pulmonary congestion and monitor lung expansion. ABG, SpO2, and end tidal CO2 are assessed for decreased O2 and increased carbon dioxide. After extubation, turning, coughing, deep breathing, and early ambulation to prevent atelectasis and pneumonia. 9.

Nursing interventions
11. Impaired cerebral circulation- observe the S/S of hypoxia: restlessness, confusion, dyspnea, hypotension, and cyanosis. Neurologic status for LOC, response to verbal commands and painful stimuli, pupil size and reaction to light, facial symmetry, movement of extremities, hand grip strength, presence of pedal and popliteal pulses, and temp and color of extremities. Hypoperfusion or microemboli may produce central nervous system injury after cardiac sx. 12. Restoring CO- measure BP, HR, CVP, arterial pressure, and pulmonary artery pressures Renal fx related to cardiac fx, BP and CO drive glomerular filtration. UO measured. UO of less than 30mL/hr indicate decrease in CO or inadequate fluid volume Body tissues depend of CO for O2 blood for body and organ systems. Observe for cyanosis or duskiness as possible sign reduced CO. Distention of neck veins when head of bed elevated 30 degrees or more may signal R sided HF. If CO decreased, skin cool, moist, and cyanotic. Dysrhythmias may develop w decreased perfusion to/irritation of myocardium from sx. (a-fib, bradycardia, tachycardia, and ectopic beats.

Nursing interventions
13. Promote adequate gas exchange- assess patency of endotracheal tube. Suctioning necessary when crackles or coughing present. 100% O2 delivered to pt from ventilator or by manual resuscitation bag before and after suction to minimize risk of hypoxia that can result from suctioning procedure. ABG determinations compared with baseline data. Body position is changed every 1-2 hrs. Provides optimal pulmonary ventilation and perfusion by allowing the lungs to expand more fully. Before being extubated, pt should have cough and gag reflex and stable VS, lift head off bed or have firm hand grasp, adequate vital capacity, negative inspiratory force, and minute volume appropriate for body size, and have acceptable ABG while breathing warm humidified O2 without assistance of ventilator. Encourage deep breathing an coughing at least every 1-2 hrs to clear secretions, open alveolar sacs, and promote effective ventilation. Maintain fluid and electrolyte balance Minimize sensory perception imbalance- clinical manifestations of delirium include restlessness, agitation, visual and auditory hallucinations, and paranoia. Appears after 2-5 day stay in intensive care. Causes include anxiety, sleep deprivation, increased sensory input, meds, and physiologic problems such as hypoxemia and metabolic imbalance. Relieve pain- in the peri incisional area or throughout chest, shoulder, and back. Record nature, type, location, and duration of pain. PCA pump used. Pt comfort improves after removal of chest tubes. Pain causes tension which releases catelcholamines resulting in constriction of arterioles and increase HR. Increase afterload and decreased CO. Opioids usedand help sleep as well as reduce metabolic rare and O2 demand. Adverse effects of opioids include respiratory depression, hypotension, constipation, ileus, or urinary retention. ( Narcan antagonist)

14. 15.

16.

Nursing interventions
17. Maintain adequate tissue perfusion- check peripheral pulses to assess for arterial obstruction. Thromboembolic events can occur from vascular injury, dislodgement of clot from damaged valve, loosening of mural thrombi, or coagulation problems. Air embolism result from CPB or central venous cannulation. Embolic sites are the lungs, coronary arteries, mesentery, spleen, extremities, kidneys, and brain. Observe for onset of chest pain and respiratory distress from pulmonary embolus or MI, abdominal or back pain from mesentric emboli, pain, cessation of pulses, blanching, numbness, or coldness in extremity, one sided weakness and pupillary changes, as in stroke Prevent venous stasis(causes deep vein thrombosis/pulmonary embolism)- apply suquential pneumatic compression wraps or anti embolism stockings, discourage crossing legs, avoid elevating knees on bed, omit pillows in popliteal space, and begin passive exercises followed by active exercises to promote circulation and prevent venous stasis. Trauma to blood cells during CPB can cause hemolysis of RBCs, which then occlude renal glomeruli. Use of vasopressor agents to increase BP may constrict renal arterioles and reduce blood flow to kidneys. Monitor blood urea nitrogen, CREA, glomerular filtration rate, and electrolyte levels. Maintain normal body temp- warm gradually. After sx, at risk for developing elevated body temp as result of tissue inflammation or infection. Inflammatory response to to sx includes release of cytokines that cause fever. Increase in metabolic reate increases tissue O2 demand and icrease cardiac workload. Give antipyretics.

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Common sites of postoperative infection include lungs, urinary tract, incisions, and intravascular cath. Use aseptic tech to change dressings and when providing endotracheal tube and cath care. Deep breath and cough Postpericardiotomy syndrome characterized by fever, pericardial pain, pleural pain, dyspnea, pericardial effusion, pericardial friction rub, and arthralgia. May occur days to weeks after sx. Antiinflammatory improve symptoms. 19. Promote home and community careSpecific instructions provided about incision care, S/S infection, diet, activity progression and exercise, deep breathing, incentive spirometry, smoking cessation, weight and temp monitor, med regimen, follow up visits, and rehabilitation.