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Management of Patient with Coronary Vascular Disorders
Chapter 28
Coronary Artery Disease (CAD)
• Most prevalent type of CVD in adults
• Decreased blood flow through coronary arteries = myocardial ischemia/infarction
• Ischemia results from insufficient O2 supply to myocardium
• Atherosclerosis is leading contributor
CAD
• Describe common manifestations of Coronary Artery Disease.
• Discuss risk factors for CAD.– Modifiable– Non-modifiable
• Describe Coronary Artery Disease Risk Equivalents.
Atherosclerosis
• Describe the pathophysiology of atherosclerosis.
• Review Figure 28-1, p. 860
Acute Coronary Syndromes
• Serious manifestation of CAD
• Amount of disruption of the plaque determines the degree of obstruction of the coronary artery and specific disease process:
• Unstable angina• Non-ST elevation MI• ST elevation MI
Angina Pectoris
• “Strangling of the chest”• Imbalance between O2 supply and
demand
Compare and contrast Stable and Unstable Angina Pectoris.
Describe associated clinical manifestations.
Angina Pectoris-- Management
Medical Management
• Pharmacologic therapy– Nitroglycerin– Beta-adrenergic blockers– Calcium channel blockers– Antiplatelets– Anticoagulants
• Oxygen therapy
Nursing Management
• Treat associated symptoms– Immediate rest– Oxygen– assessment– ECG– Nitroglycerin
• Reduce anxiety • Prevent pain
Myocardial Infarction
• When does a myocardial infarction occur?
• What degree of blood flow reduction results in ischemia?
• What will occur if blood flow is not restored to the myocardium?
• What is the most common cause of coronary artery occlusion?
• What are other causes?
Process of Infarction
• Dynamic process that evolves over several hours
• Normal conduction and contractile functions are suppressed
• Automaticity and ectopy are enhanced• Heart rate and force of contraction are increased• Oxygen requirements increase
Physiologic Response to Infarction
• Will take up to six hours for obvious changes to occur in the heart (blue and swollen)
• After 48 hours (gray with yellow streaks)• By 8-10 days granulation tissue forms at edges
of necrotic tissue• Within 2-3 months scarring develops which
changes the shape of the left ventricle (ventricular remodeling)
• Remodeling may ↓ L ventricular function, cause heart failure, and ↑ morbidity and mortality
MI Assessment: History
• Query patient about chest pain– If experiencing acute chest discomfort, delay
history and treat discomfort
• Obtain information about– Management of current episode of discomfort– Current medications– Family history of CAD– Presence of modifiable risk factors
MI Assessment: Pain
• Must differentiate type of chest discomfort and identify source
• Query patient to determine characteristics of discomfort– Onset– Location– Radiation– Intensity– Duration – Precipitating and facilitating factors
MI Assessment: Pain
• Remember: – angina is ischemic pain and usually improves
when oxygen supply/demand disparity resolves.
– MI does not usually resolve with simple measures
• Associated symptoms: nausea, vomiting, diaphoresis, dizziness, weakness, palpitations, and shortness of breath
MI Assessment: Cardiovascular
• Blood pressure• Heart rate• Cardiac rhythm • Distal peripheral pulses• Skin temperature• Heart sounds• Respiratory rate• Breath sounds
MI Assessment: Psychosocial
• Denial is common early reaction– Can be normal part of adapting to stressful
event– Detrimental if denial interferes with
identification of symptom
• Other common reactions– Fear– Anxiety – anger
MI: Laboratory Assessment
• Cardiac Enzymes– Creatine kinase (CK)– CK-MB isoenzyme
• Myoglobin– Found in serum 2-3 hours after MI, but is not cardiac
specific– Always increases within 3-6 hours after MI, if not
increased at 6 hour mark can rule out MI• Troponin T and I• Increased WBC
Cardiac Markers for MI
Creatine Kinase (CK)
• Cardiac enzyme released after injury
• Levels rise 3-12 hours after acute MI
• Levels peak in 24 hours
• Levels to normal within 2-3 days
• MB band is specific to myocardial cells– >3% indicates MI
Cardiac Markers for MI
Troponin• Myocardial muscle protein released after injury• Two subtypes: T and I• Greater sensitivity and specificity for myocardial
injury• Levels rise in 3-12 hours after MI• Levels peak in 24-48 hours• Levels back to baseline over 5-14 days• Used for diagnostic purposes in conjunction with
CK and the MB fraction
Acute MI: Other Diagnostic Tests
• ECG
• Stress Test
• Thallium scans
• MRI
• Cardiac catheterization
(Discussed in Chapter 26)
ECG Changes in MI
• ST-segment elevation• T-wave inversion• Abnormal Q wave
Acute MI: Collaborative Problems
• Acute Pulmonary Edema
• Heart Failure
• Cardiogenic Shock
• Dysrhythmias/Cardiac Arrest
• Pericardial Effusion and Cardiac Tamponade
Acute MI: Interventions
Pain Management:• Nitroglycerin• Morphine Sulfate
• Supplemental O2
• Position of Comfort
• Quiet and calm environment
Acute MI: Interventions
Thrombolytics• Fibrinolytics dissolve clots and restore
myocardial perfusion• Most effective when given within 6 hours
of onset of MI• Client must be continuously monitored• Contraindications: Table 41-3, p. 850• During administration monitor for bleeding
and report any signs to physician
Acute MI: Interventions
Thrombolytics (cont)• Post administration observe closely for
signs of bleeding by:– Documenting neuro status– Observing IV sites– Monitoring clotting studies– Observing for s/s of internal bleeding
• Monitor Hemoglobin and Hematocrit
– Testing stools, urine, emesis for occult blood
Acute MI: Interventions
• Glycoprotein (GP) Inhibitors– Target platelet component of the thrombus– Prevent fibrinogen from attaching to activated
platelets at the site of a thrombus– Used in:
• Acute coronary syndromes• During and before PCTA to ensure patency • Conjunction with fibrinolytics following MI
– During administration nurse assesses closely for bleeding or hypersensitivity reactions
Acute MI: Interventions
Drug Therapy
• ASA
• Beta-adrenergic blocking agent
• ACE inhibitors
• Calcium channel blockers
Acute MI: Interventions
Cardiac Care Rehabilitation• Process which assists client with cardiac
disease to achieve and maintain optimal functioning within the limits of the heart’s ability to respond to increases in activity and stress– Phase 1: begins with acute illness, ends with
discharge from hospital– Phase 2: begins after discharge and continues
through convalescence at home– Phase 3: long term conditioning
Acute MI: Interventions
Cardiac Care Rehabilitation Phase 1• Nurse promotes rest while ensuring some limited
mobility• Assistance is given for some ADL’s• Individualized– client’s progress at their own rate• Nurse encourages progressive ambulation• Nurse assesses heart rate, BP, respiratory rate
and level of fatigue with each higher level of activity
• Nurse should stop the activity and refrain from advancing activity if client develops any signs of activity intolerance
Acute MI: Interventions
Coping• During acute phase antianxiety agents may be
prescribed• Nurse assesses current coping mechanisms
– Most common are denial, anger and depression• Denial which allows the client to minimize threat and use
problem-focused coping mechanisms may be helpful in decreasing anxiety
• Anger may represent an attempt to regain control of life• Depression may be the response to grief and loss of function
Dysrhythmias
• Cause of death in clients with MI who die prior to hospitalization
• 70-90% of hospitalized MI clients have abnormal cardiac rhythms– Identify the dysrhythmia– Assess hemodynamic status– Evaluate client for chest discomfort
• Treated when they cause– Hemodynamic compromise– Increased myocardial oxygen requirements– Predispose lethal ventricular dysrhythmias
Dysrhythmias
• Inferior MI– Bradycardias– 2nd Degree AV Blocks– Transient– Nurse monitors:
• Cardiac rate & rhythm• Hemodynamic status
– May need temporary pacer if hemodynamically unstable
• Anterior MI– Venrticular irritability
(PVCs)– 3rd Degree or Bundle
Branch Block (serious complication)
– Nurse observes closely for s/s of heart failure
– May need pacemaker
PTCA: Percutaneous Transluminal Coronary Angioplasty
• Invasive, but nonsurgical technique to reduce frequency and severity of chest discomfort– Complexity and location assessed to determine
whether client would benefit from procedure– May also be used during evolving MI
• Procedure performed under fluoroscopic guidance in cardiac cath lab– Balloon inflation may be repeated until lesion is
reduced or eliminated– Meds include: heparin, nitriglycerine or nifedipine– Stents may be placed at time of procedure
PTCA: Post-Procedure Care
• Monitor for potential problems– Acute closure of the vessel– Bleeding from insertion site– Reaction to the dye– Hypotension– Hypokalemia– dysrhythmias
• Drug Therapy– Long term nitrate– Calcium channel blockers– ASA – Beta blocker and ACE
inhibitor may be added– Glycoprotein inhibitors
during initial hours– Potassium supplements if
indicated– Coagulation with coumadin
Coronary Artery Bypass Graft
• Most common cardiac surgery• Indicated for clients who do not respond to
medical management of CAD or when disease progression is evident
• To be bypassed vessels should have proximal lesions with > 70% occlusion
• Most effective when good ventricular function remains and ejection fraction is more than 40-50%
• Requires Cardiopulmonary bypass during surgery
CABG: Post-Op Care
• Mechanical ventilation for 3-6 hours• Mediastinal tubes to waterseal drainage• Epicardial pacing wires• Hemodynamic monitoring• Observes closely for:
– Dysrhythmias (ventricular ectopics, bradydysrhythmias, or heart block)
– Fluid and electrolyte imbalances (K+ at 4-5)– Hypotension, hypothermia, hypertension– Cardiac tamponade– Altered cerebral perfusion
Cardiac Tamponade
• Blood accumulates around the heart• Medical emergency• Hallmarks in post-CABG patient:
– Sudden cessation of previously heavy mediastinal drainage
– JVD with clear lung sounds– Pulsus paradoxus – Equalization of PAWP and right artrial
pressure
Neurological Changes Post-CABG
Transient:• 75%; transient changes
due to:– Anesthesia, CPB, air
emboli, hypothermia
• Experience:– Slowness to arouse– Memory loss– confusion
• Usually return to baseline in 4-8 hours
Permanent• Changes may be
associated with stroke during surgery
• Experience:– Abn. pupillary response– Failure to awaken from
anesthesia– Seizures– Absence of sensory or
motor function
• Monitor:– Neuro status q 30-60 min
initially then q 2-4 hours