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Management of pt with CVD

Chapter 28

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Coronary Artery Disease

Includes Coronary atherosclerosis, acute coronary syndrome, andMI.

Coronary Atherosclerosis

Accumulation of lipid, or fatty substances, and fibrous tissue in the

lining of arterial blood vessel walls. Block and narrow coronaryvessels which reduce blood flood to the myocardium. Repeatedinflammatory response to injury of the artery wall and subsequentalteration in the structural and biochemical properties of thearterial 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 thevascular endothelium. Iniated by smoking, HTN, and other factors.If plaque ruptures thrombus may obstruct blood flow leading toacute coronary syndrome which may lead to MI.

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Clinical manifestations of CAD

Produces symptoms and complications according to the locationand 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 oxygenneeded for survival. Causes ischemia.

Angina pectoris refers to chest pain that is brought about bymyocardial ischemia. Caused by significant coronaryatherosclerosis.

Ischemia caused from decreased blood flow will in turn cause scartissue 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 beforeacute episode

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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

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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

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Prevention of CAD

Cholesterol abnormalities, tobacco use, HTN, and diabetes management

Control cholesterol abnormalties- 20 year of age or older should have fasting lipidprofile 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 monthsbecause LDL may be low immediately after subsequently lipids should bemonitored 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 than60. Triglyceride less than 160.

Dietary recommends cessation of smoking, increased physical activity, and weightloss. Diet that promotes veggies and fish and restricts red meat. Soluble fibersfound in fresh fruit, cereal, grains, veggies, and legumes recommended. Restrictsugar intake.

Physical activity help manage elevated triglycerides. Focus on weight reduction

and increased physical activity. Moderate exercise 30 min day (brisk walkingincrease HDL and decrease triglycerides). Pt should stop any activity with chestpain, SOB, dizziness, light headedness, or nausea occur.

Medications used if diet alone doed not normalize. Lipid lowering med used. Medsreduce CAD mortality. See Table 28-2 on page 761

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Prevention of CAD

Managing hypertension- risk of cardiovascular disease increases as BP increasesand those with BP higher than 120/80 prehypertensive and at risk.

Long standing elevated BP result in increased stiffness of vessel walls, leading tovessel injury and resulting inflammatory response within the intima.

Inflammatory mediators then lead to the release of growth promoting factors thatcause vessel hypertrophy and hyperrespnsiveness. Result in acceleration andaggravation of atherosclerosis.

HTN also increase work of L ventricle, which has to pump harder to eject bloodinto the arteries. Cause enlarge and thicken and lead to HF.

Control diabetes- hyperglycemia fosters dyslipidemia, increased plateletaggregation, and altered RBC fx which lead to thrombus formation.

Impair endothelial cell dependent vasodilation and smooth muscle fx, promotingdevelopment of atherosclerosis. Tx with insulin and metformin and otherinterventions that lower plasma glucose levels can lead to improved endothelial fxand pt outcomes

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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 forO2 in response to physical exertion/emotional

stress

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Types of Angina

1. Stable angina: predictable and consistent pain that occurson exertion and is relieved by rest and/or nitroglycerin

2. Unstable angina: symptoms increase in frequency andseverity; may not be relieved with rest or nitroglycerin

3. Intractable or refractory angina: severe incapacitatingchest pain

4. Variant angina: pain at rest with reversible ST-segmentelevation; thought to be caused by coronary arteryvasospasm

5. Silent ischemia: objective evidence of ischemia with noreport of pain

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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 situation-

releases catecholamines which increase BP,HR, and myocardial workload

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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

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Assessment and diagnostic

12 lead ECG

CRP and cardiac biomakers

Exercise or pharmacologic stress test

cardiac cath or coronary angiography

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Medical management w meds1. Nitroglycerin- reduce myocardial O2 consumption to decrease ischemia

and relieve pain. Dilated veins and arteries. Lowers BP and decreaseafterload. Sublingual tab or spray, oral cap, topical agent, IV. Sublingualalleviate pain within 3 min. Not given if systolic BP less than 90. Oral ortopical within 24 hr after symptom free.

2. Beta-blocker- metoprolol and atenolol reduce myocardial O2 consumptionby blocking beta-adrenergic sympathetic stimulation to heart. Reduces HR,

slow conduction of impulses, decreases BP, and reduce myocardialcontractility to balance myocardial O2 needs and amount of O2 available.Control chest pain and delays onset ischemia during wk/exercise. Reduceincidence of recurrent angina, infarction, and cardiac mortality. Titrate tilresting HR of 50-60bpm.

o Cardiac side effects and contraindications- hypotension, bradycardia,advanced atrioventricular block, and acute HF.

o With IV- ECG, BP, and HR monitored closely. Side effects include decreasedlibido, and masking of symptoms of hypoglycemia.

o Dont stop abruptly

o Monitor blood glucose closely with diabetes and monitor S/S ofhypoglycemia

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Medical management w meds

3. Calcium channel blockers- decrease sinoatrial node automaticity andatrioventricular node conduciton resulting in slower HR and decrease inthe strength of myocardial contraction. Decrease workload of heart.Relax blood vessels causing decrease BP and increase coronary arteryperfusion. Increase myocardial O2 supply by dilating smooth musclewall of coronary arterioles. Decrease myocardial O2 demands byreducing systemic arterial pressure and workload of L ventricle.

o Amlodipine and diltiazem commonly used with pt who cant take betablockers, with side effects to beta blockers or nitro, or who still havepain despite using beta blockers or nitro. Used to prevent and txvasospasm.

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.

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Medical management w meds

4. Antiplatelet and anticoagualants- prevent platelet aggregation andthrombosis.

o Aspirin- prevent platelet aggregation and reduce incidence of MI anddeath of pt with CAD. 160-325mg dose given with angina and then 81-325mg daily.

o Clopidogrel- (Plavix) given in addition to aspirin for pt at risk for MIo 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. Beneficialduring PCIs and ST segment elevation MIs. Monitored for S/S of externaland internal bleeding, such as low BP, increased HR, and decreased serumH&H. BLEEDING PRECAUTIONS!

Decrease in platelet count or evidence of thrombosis may indicate heparininduced thrombocytopenia, antibody mediated reaction to heparin thatmay result in thromosis.

Those who received heparin within the past 3 months and receivingunfractioned heparin fro 5-15 days are at high risk for HIT.

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Medical management meds/O2

5. Glycoprotein IIb/IIIa- for unstable angina and asadjunct therapy for PCI. Prevent plateletaggregation by blocking the GP IIb/IIIa receptors

on plateles, preventing adhesion of fibrinogenand other factors that crosslink platelets to eachother and thus form platelet clots. Bleedingmajor side effect.

6. O2 administration- given with onset of chest painto increase amount of O2 delivered tomyocardium and decrease pain. Keep O2 levelabove 93%. Administer 2L

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Collaborative problems

1. ACS and/or MI

2. Dysrhythmias and cardiac arrest

3. HF4. Cardiogenic shock

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Nursing interventions for angina

1. Tx angina- stop activities and sit or rest in semi fowlers to reduceO2 requirement or ischemic myocardium. Note that change mayindicate worsening of disease. Assess vitals and observe forrespiratory distress. 12 lead ECG to scrutinize for ST segment andT wave changes.

o Give Nitroglycerin sublingually. Repeated up to 3 doses. AssessBP, HR, and ST segment with each dose.

o O2 therapy if RR increased or O2 sat level decreased. Usually 2Lgiven.

2. Reduce anxiety

3. Prevent Pain- minimal activity by alternating with rest periods.4. Promote home and community based care- teach self care. Pt

needs to know that any pain unrelieved within 15 min by usualmethods including nitro should seek immediate emergency care.Continuing care by home care nurse.

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Acute coronary syndrome and MI

Patho- In unstable angina, theres reduced blood flow in coronary arterydue to rupture of atherosclerotic plaque where artery isnt completelyoccluded. With MI, area of myocardium is permanently destroyed bcplaque rupture and subsequent thrombus formation result in completeocclusion of the artery. Vasospasm of coronary aretery, decrease O2supply, and increased O2 demand are other causes of MI. Area ofinfarction develops over min to hrs. As cells are deprived of O2, ischemiadevelops, cellular injury occurs, and lack of O2 results in infarction ordeath of cells.

ID MI: type(NSTEMI, STEMI), location of injury to ventricular wall, andpoint 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 notprompt. ACS include unstable angina, non ST segment elevation MI, andST segment elevation MI.

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Clinical manifestation of ACS/MI

Sudden chest pain and continues even with

rest or medication.

Prodromal symptoms or previous diagnosis ofCAD

SOB, indigestion, nausea, and anxiety

Cool, pale, and moist skin Increased HR and RR

Stimulation of sympathetic nervous system

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Assess and diagnostic findings1. Patient hx2. ECG- rule out or diagnose MI

o Monitor location, evolution, and resolution of MI

o Classic ECG changes are T wave inversion, ST segment elevation, and development ofabnormal Q wave.

o First ECG signs of acute MI occur as result of myocardial ischemia and injury.

o Myocardial injury cause T wave to become enlarged and symmetric. As area of injury

becomes ischemic, myocardial repolarization is altered and delayed, causing T waveto invert. The ischemic region may remain depolarized while adjacent areas of themyocardium return to the resting state. Myocardial injury also caused ST segmentchanges. Injured myocardial cells depolarize normally but repolarize more rapidlythan normal cells, causing ST segment to rise at lease 1 mm above isoelectric linewhen measured .06-.08 sev after end of the QRS(Jpoint). This elevation in the STsegment in 2 contiguous leads is a key diagnostic indicator for MI.

o Appearance of abnormal Q waves in another indicator of MI. Q waves develop within1-3 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 MImay also cause a significant decrease in height of the R wave.

o An abnormal Q wave may be present without ST segment and T wave changes,which indicates an old, not acute MI

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Assess and diagnostic findings

o Unstable angina: coronary ischemia, but ECG and cardiacbiomarkers show no evidence of MI

o STEMI: ECG evidence of acute MI with characteristic changes in 2contiguous leads on 12 lead ECG. Significant damage tomyocardium.

o NSTEMI: elevated cardiac biomarkers but no definite ECG evidenceof acute MI

o During recovery, ST segment oftern first WCG indicator to return tonormal(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 usuallypermanent. Old STEMI indicated by abnormal Q wave or decreasedht of the R wave without ST segment and T wave changes.

3. Echocardiogram- evaluate ventricular fx. Diagnose MI and detecthypokinetic and akinetic wall motion as well as determine ejectionfraction.

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Assess and diagnostic findings

4. Laboratory tests- cardiac enzymes and biomarkers are used todiagnose acute MI. Cardiac biomarker (myoglobin and troponin)analyzed rapidly. Based of release of cellular contents intocirculation when myocardial cells die.

o Creatine Kinase and its Isoenzymes- CK-MM (skeletal muscle), CK-

MB (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-MBassessed by mass assay is indicator of acute MI (begins toincrease within few hr and peaks within 24 hrs of MI). If areareperfused, peaks earlier.

o Myoglobin- heme protein transport O2. Found in cardiac andskeletal muscle. Starts to increase within 1-3 hrs and peaks within12 hrs after onset of symptoms.

Increase not very specific in indicating acute cardiac event.Negative results rule out acute MI

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Medical management of ACS/MI

o Goal is to minimize myocardial damage, preservemyocardial 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, O2administration, and bed rest.

o

Resolution of pain and ECG changes indicatedemand in equilibrium as well as reperfusion.

o Visualization of blood flow through open vessel incath lab

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Pharmacologic therapy

o Aspirin, nitro, morphine, IV beta-blocker

o Should continue beta-blocker thru

hospitalization and after D/C bc long termtherapy 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

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Pharmacologic therapy

1. Analgesics- morphine by IV bolus to reduce pain and anxiety. Reduces preloadand afterload which decrease workload of heart and relax bronchioles toenhance O2. Monitor BP (will decrease), and RR (slows).

2. Angiotensin-Converting enzyme inhibitors- (ACE-I) prevent conversion ofangiotensin 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 nothypotensive, hyponatremic, hypovolemic, or hyperkalemic before giving.Monitor BP, UO, serum Na, K, and CREA.

3. Thrombolytics- tx acute MI. Given IV. Dissolve thrombus in coronary artery andminimize size of infarction as well as preserving ventricular fx. First line therapy.Dissolve ALL clots, not just ones in coronary arteries. Dont use if pt formedprotective clot such as after major sx or hemorrhagic stroke. Pt at risk forbleeding. Given as early as possible, usually within 30 of presentation of ER.

o Alteplase and reteplase- Alteplase is tissue plasminogen activator that activatesplasminogen present on blood clot. IV bolus given and followed with infusion.Aspirin and Heparin/LMWH used with t-PA to prevent another clot from formingat site of lesion. Reteplase administered in 2 bolus doses, followed by heparininfusion.

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Emergent Percutaneous Coronary

Intervention

o STEMI may be taken directly to cardiac cath

for immediate PCI.

o

Open occluded coronary artery and promotereperfusion to area deprived of O2.

o Tx atherosclerotic lesion.

o

Perform asap less than 60 from admit

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Cardiac Rehabilitationo 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 livingcan 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.

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Phases of cardiac rehab

o Phase I begins with the diagnosis of atherosclerosis, whichmay occur when pt admitted to hospital for ACS.

Low level activities and initial education for pt and familyimprove pt outcomes

Teach S/S of need for 911, meds, rest-activity balance, andfollow up appointments.

o Phase II is after pt D/C. Attends sessions 3 times a week for4-6 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 termconditioning. Pt self directed.

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Assess of pt with ACS

1. Chest pain/discomfort

2. SOB/dyspnea

3. Palpations

4. Unusual fatigue or faintness5. Diaphoresis

6. Complete physical assessment

7. Monitor IV sites (when stable change to saline lock)

o Each symptom evaluated in regard to time, duration,and factors that precipitate symptom and relieve itand in comparison with previous symptoms

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Collaborative problems of ACS

1. Acute pulmonary edema

2. HF

3. Cardiogenic shock4. Dysrhythmias and cardiac arrest

5. Pericardial effusion and cardiac tamponade

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Nursing interventions

1. Balancing myocardial O2 supply with demand top priority

2. O2 along with meds to assist with relief of symptoms. O2 raises the circulationof O2to reduce pain associated with low levels of myocardial O2. Usually 2-4Lnasal cannula

3. Vitals assessed frequently as long as pt experiencing pain and/or other S/S ofacute ischemia.

4. Physical rest in bed with backrest elevated help decrease chest discomfort anddyspnea. Elevation helps tidal volume bc reduce pressure from abdominalcontents on diaphragm and better lung expansion, drainage of upper lung lobesinprove, and venous return to heart(preload) decreases, reducing work of theheart.

5. Improve respiratory fx- monitor fluid volume status to prevent overloading heartand lungs and encourage pt to breathe deeply and change positions frequently.

Monitor RR and pulse ox.6. Adequate tissue perfusion- bed or chair rest during initial phase of tx helps

reduce myocardial O2 consumption. Check skin temp and peripheral pulsesfrequently

7. Reduce anxiety- decreased sympathetic stimulation decreases the workload ofthe heart which relieves pain and other S/S ischemia.

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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 care-

facilitate pt involvement in cardiac rehab.Home care nurse for assistance if necessary.

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Percutaneous coronary interventions

o Types of procedures1. 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 forother 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 arterys 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.

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2. Coronary Artery stent- release mediators which leadsto vasoconstriction, clotting, and scar tissueformation.

Stent is metal mesh that provides structural supportto the vessel at risk of acute closure. It is positionedover the balloon. Balloon inflated and meshexpands/presses against the vessel wall, holdingartery open.

Some stents coated w med such as sirolimus orpaclitaxel which minimize formation of thrombi orscar tissue within stent.

Antiplatelet meds (aspirin and clopidogrel) given.Clopidogrel cont for a month following placement ofbare metal stent and for a year following drug elutingstents.

3. Atherectomy- removal of atheroma from coronary

artery by cut, shave, or grind.

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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 thanbradytherapy.

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Complications of PCI

During PCI

1. Dissection

2. Perforation3. Abrupt closure

4. Vasospasm of coronaryartery

5. Acute MI6. 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

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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 inhibitorduring 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 sitemay 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 sitefor bleeding or develop of hard mass indicative of hematoma.

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Coronary Artery Revascularizaion

o CABG sx procedure in which blood vessel graftedto occluded coronary artery so blood can flowbeyond occlusion. Also called bypass graft

o Major indications for CABG:1. Alleviation of angina that cant be controlled w

med or PCI

2. Tx of L main coronary artery stenosis ormultivessel CAD

3. Prevention and tx of MI, dysrhythmias, or HF

4. Tx for complications from unsuccessful PCI

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Coronary Artery Revascularizaion

o Recommendation for CABG determined by number of diseasedcoronary vessels, degree of L ventricular dysfx, presence of otherhealth problems, pt symptoms, and previous tx.

o CABG may be preferred tx for high risk pt such as those with severetriple 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 blockageor 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 andcoronary artery distal to lesion.

o Common adverse effect of vein removal is edema in extremity fromwhich vein taken.

o R and L internal mammary arteries and radial and gastroepiploicarteries used occasionally.

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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.

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Cardiopulmonary bypasso

Machine circulated and O2 blood for body while bypassingheart and lungs. Maintains perfusion to body organs and tissuesand allows surgeon to complete anastomoses in motionless,bloodless field.

o CPB accompanied by putting cannula in R atrium, vena cava, orfemoral vein to withdraw blood from body. Cannula connected

to tubing filled with isotonic crystalloid solution. Venous bloodremoved fro body by cannula filtered, O2, cooled/warmed bymachine, and returned to body. Cannula used to return O2blood usually inserted in ascending aorta, or inserted in femoralartery. Heart is stopped by injection of K rich cardioplegiasolution into coronary arteries. Pt given heparin to preventclots. Protamine sulfate administered to reverse heparin.

o During procedure, hypothermia maintained (82.4-89.6). Bloodcooled during CPB and returned to body. Lowers basalmetabolic rate, decreasing O2 demand. Crystalloid solutiongiven to prevent blood from being viscous. After sx bloodwarmed and put back in body.

o

UO, ABG, electrolytes, and coagulation monitored.

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Alternative CABG

o OPCAB involves standard median sternotomyincision without CPB. Beta adrenergic blockermay be used to slow HR. My use myocardialstabilization device to hold the site still for

anastomosis of bypass graft into coronaryartery while heart continues to beat.

o OPCAB decrease incidence of stroke andneurological complications, renal failure, and

postoperative complications.o Pt with multiple bypass grafts to arteries on

dorsum of heart may not be candidate oftechnique.

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Complications of CABG

1. hemorrhage

2. Dysrhythmias

3. MI

o CABG isnt a cure for CAD, and angina,exercise intolerance, or other symptomsexperienced before CABG may recur.

o Medications required sx may need to becontinued.

o Lifestyle modifications recommended.

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o Preoperative management

1. Assessment for baseline for postoperative comparison

2. Evaluate pt understanding of sx procedure, informed consent, and adherence totx protocol

3. Preoperative testing- chest x-ray, ECG, lab tests, coagulation studies, and bloodtyping 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 anxiolyticagents 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 mechanicalventilaion for 2-24 hours after sx. Answer questions and teach about deepbreathing/cough, incentive spirometer and foot exercises. Also about earlyambulation and frequency

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o Intraoperative management

1. Comfort and safety

2. Chest tubes inserted to evacuate air and drainagefrom mediastinum and thorax. Temporary epicardial

pacemaker electrodes may be implanted on surfaceof R atrium and R ventricle. Epicardial electrodes canbe connected to an external pacemaker if ptpersistent bradycardia perioperatively.

3. Possible intraoperative complications include low CO,dysrhythmias, hemorrhage, MI, stroke, embolization,and organ failure from shock, embolus, or adversedrug reactions.

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Nursing interventionso Postoperative nursing management1. Achieve and maintain hemodynamic stability and

recovery from general anesthesia.

2. Pt transferred to PACU; sx team and anesthesia reportoff

3. Once cardiac and respiratory status stable, pttransferred 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 hrsafterwards.

Neurological status: LOC, pupil size and reaction tolight, reflexes, facial symmetry, movement ofextremities, and hand grip strength.

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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 pulmonaryvascular 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 invasivelines.

Renal fx: UO, urinary specific gravity and osmolality

Fluid and electrolyte status: Intake, output from drainage tubes, COparameters, 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, SvO2monitor, 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

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7. Monitor for complications

8. Decreased CO- preload alterations occur when little blood volumereturns 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 bealtered if too much volume returns to the heart, causing fluidoverload.

Afterload alterations occur when arteries are constricted as resultof postoperative HTN or hypothermia, increasing workload of theheart. HR alterations from bradycardia, tachycardia, anddysrhythmias can lead to decreased CO, and contractility can bealtered in cardiac failure, MI, electrolyte imbalances, and hypoxia.

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9. Fluid volume and electrolyte imbalance- monitor weight, I and O,hemodynamic parameters, hematocrit levels, distention of neckveins, edema, liver size, breath sounds, and electrolyte levels

Dangerously high or dangerously low levels of K, Mg, Na, and Ca areextremely important to monitor.

Elevated glucose common postoperatively. IV insulin may be give to

pt with or without diabetes achieve glycemic control necessary topromote wound healing and recovery.

10. Impaired gas exchange- endotracheal tube with ventilatorassistance may be used for 24 hrs or more.Stable pt may beextubated 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 detectpulmonary congestion and monitor lung expansion. ABG, SpO2, andend tidal CO2 are assessed for decreased O2 and increased carbondioxide.

After extubation, turning, coughing, deep breathing, and earlyambulation to prevent atelectasis and pneumonia.

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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, handgrip strength, presence of pedal and popliteal pulses, and temp and color ofextremities.

Hypoperfusion or microemboli may produce central nervous system injury aftercardiac sx.

12. Restoring CO- measure BP, HR, CVP, arterial pressure, and pulmonary arterypressures

Renal fx related to cardiac fx, BP and CO drive glomerular filtration. UOmeasured. UO of less than 30mL/hr indicate decrease in CO or inadequate fluidvolume

Body tissues depend of CO for O2 blood for body and organ systems. Observefor cyanosis or duskiness as possible sign reduced CO. Distention of neck veinswhen head of bed elevated 30 degrees or more may signal R sided HF. If COdecreased, skin cool, moist, and cyanotic.

Dysrhythmias may develop w decreased perfusion to/irritation of myocardiumfrom sx. (a-fib, bradycardia, tachycardia, and ectopic beats.

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Nursing interventions13. 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 manualresuscitation bag before and after suction to minimize risk of hypoxia that can result fromsuctioning procedure. ABG determinations compared with baseline data.

Body position is changed every 1-2 hrs. Provides optimal pulmonary ventilation and perfusionby allowing the lungs to expand more fully.

Before being extubated, pt should have cough and gag reflex and stable VS, lift head off bedor have firm hand grasp, adequate vital capacity, negative inspiratory force, and minutevolume appropriate for body size, and have acceptable ABG while breathing warm humidifiedO2 without assistance of ventilator.

Encourage deep breathing an coughing at least every 1-2 hrs to clear secretions, openalveolar sacs, and promote effective ventilation.

14. Maintain fluid and electrolyte balance

15. Minimize sensory perception imbalance- clinical manifestations of delirium includerestlessness, agitation, visual and auditory hallucinations, and paranoia. Appears after 2-5 daystay in intensive care. Causes include anxiety, sleep deprivation, increased sensory input,meds, and physiologic problems such as hypoxemia and metabolic imbalance.

16. 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 afterremoval of chest tubes. Pain causes tension which releases catelcholamines resulting inconstriction of arterioles and increase HR. Increase afterload and decreased CO. Opioidsusedand help sleep as well as reduce metabolic rare and O2 demand. Adverse effects ofopioids include respiratory depression, hypotension, constipation, ileus, or urinary retention.( Narcan antagonist)

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Nursing interventions17. 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 andreduce blood flow to kidneys.

Monitor blood urea nitrogen, CREA, glomerular filtration rate, and electrolyte levels.

18. 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, urinarytract, incisions, and intravascular cath. Use aseptic tech to changedressings 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 frictionrub, and arthralgia. May occur days to weeks after sx. Anti-inflammatory improve symptoms.

19. Promote home and community care-

Specific instructions provided about incision care, S/S infection,diet, activity progression and exercise, deep breathing, incentivespirometry, smoking cessation, weight and temp monitor, medregimen, follow up visits, and rehabilitation.

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