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