MEDICAL-SURGICAL NURSING: Cardiovascular Care Plans Activity Intolerance Cardiac Surgery 151

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OVERVIEW/PATHOPHYSIOLOGY

Coronary artery disease (CAD) is the leading cause of death in the United States, affecting more than 17 million Ameri- cans. The coronary arteries supply the myocardial muscle with oxygen and the nutrients necessary for optimal function. In CAD, the arteries are narrowed or obstructed, potentially resulting in cardiac muscle death. Atherosclerotic lesions, arterial spasm, platelet aggregation, and thrombus formation all may cause obstruction. The most common symptom of CAD is angina, affecting 50% of patients with this disease.

Angina results from the decreased blood flow and insufficient oxygen supply to the heart muscle.

Acute coronary syndrome (ACS) refers to an imbalance between myocardial oxygen supply and demand secondary to an acute plaque disruption or erosion. ACS is an umbrella term that includes stable coronary artery disease (SCAD), unstable angina (USA), non–ST-elevation myocardial infarc- tion (NSTEMI), and ST-segment elevation myocardial infarc- tion (STEMI).

USA is defined as an increase in severity, frequency, or intensity of anginal pain or a new onset of rest angina, lasting more than 20 min. NSTEMI is defined by clinical presenta- tion of chest pain with an elevation in cardiac biomarkers and electrocardiograph (ECG) changes that may include T-wave inversion or ST-segment depression but no ST-segment eleva- tion. Diagnosis of STEMI is based on elevated cardiac bio- markers plus ST-segment elevation on ECG signifying ischemia. Of the three, STEMI is the most serious and life threatening.

Time is essential in diagnosing and treating patients with ACS. Patients presenting with a STEMI are high priority for intervention. An ECG is the primary assessment tool that guides the intervention strategy. Primary angioplasty is the therapy of choice for reperfusion in acute myocardial infarc- tion (AMI). However, not all acute care hospitals in the United States can provide percutaneous coronary interven- tion (PCI). Because time is so critical in patients presenting with STEMI, a decision must be made by the health care provider to proceed with either fibrinolytic therapy or primary PCI within 10 min of presentation. The goal for door-to- needle time is within 30 min and door-to-balloon time within 60-90 min. Initiating thrombolysis within 70 min of symptom

catheterization laboratory facilities for primary intervention are not available within this “golden hour,” fibrinolytics are administered until transport can be arranged.

HEALTH CARE SETTING

Primary care, acute care, intensive/coronary care unit

ASSESSMENT

Signs and symptoms:

Chest pain, substernal pressure and burning, and pain that radiates to the jaw, shoulder, or arm are the most common symptoms of ischemia. Weakness, dia- phoresis, nausea, vomiting, shortness of breath, and acute anxiety also may occur. Heart rate (HR) may be abnormally slow (bradycardia), especially in right coronary artery (RCA) infarct, or it may be rapid (tachycardia). Stable or progres- sively worsening angina occurs when myocardial demand for O

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is more than the supply, such as during exercise. Pain is often described as a feeling of pressure or as a crushing or burning substernal pain that radiates down one or both arms.

It can be felt also in the neck, cheeks, and teeth. Usually anginal pain is relieved by discontinuation of exercise, rest, or administration of nitroglycerin (NTG).

Physical assessment:

Anxiety, hypertension, tachycardia, tachypnea, and dynamic ECG changes are the most common symptoms of acute ischemia. Severe hypotension may occur in shock states. Temperature elevations can occur secondary to the inflammatory process. Intensity of S

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and S

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heart sounds may be decreased. Pulmonary congestion may occur if ventricular failure is present, and S

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and S

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sounds may be auscultated.

History and risk factors:

Family history, increasing age, male gender, smoking, low high-density lipoprotein (HDL) values, hypercholesterolemia, diabetes mellitus, hypertension, and metabolic syndrome. Obesity, glucose intolerance, and a sedentary, stressful lifestyle also contribute to increased risk.

Chest pain occurring with exertion is a warning sign of CAD.

DIAGNOSTIC TESTS

ECG:

Reveals dynamic changes in the presence of ische-

mia. When the ECG is performed during chest pain, charac-

teristic changes may include ST-segment elevation or

depression greater than 0.05 mV in leads over the area of

ischemia. The presence of a bundle branch block also can be



Coronary Artery Disease

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CardiovascularCarePlans

PART I: Medical-Surgical Nursing

Cardiac nuclear imaging modalities:

Myocardial perfusion imaging:

• Detection of CAD is found by differential blood flow through the left ventricular myocardium. Normal blood flow and normal tracer uptake are seen with unobstructed coronary arteries; diminished flow and diminished tracer uptake are found with coronary stenosis. An abnormality will be present in an area of myocardial infarction (MI) resulting from lack of blood flow.

• Commonly used radiopharmaceutical agents are thal- lium-201 and technetium-99m sestamibi. Dobutamine, adenosine, and dipyridamole are pharmacologic stress agents used in combination with a radiopharmaceutical agent if patients are unable to exercise or fail to reach 85%

of age-predicted maximum HR.

• Single-photon emission computed tomography (SPECT) is used to develop three-dimensional views of cardiac pro- cesses and cellular level metabolism by viewing the heart from several different angles and using tomography methods to reconstruct the image. SPECT enables clearer resolution of myocardial ischemia and better quantification of cardiac damage.

Radionuclide angiography: Used to evaluate left and right ventricular ejection fraction (EF), left ventricular volume, and regional wall motion. The first-pass technique is a fast acquisi- tion of myocardial images. Gated pool ejection or multiple- gated acquisition (MUGA) scan permits calculation of the amount of blood ejected with ventricular contraction and is used for risk stratification of patients after MI or with CAD.

CT:

May be helpful in differentiating AMI from aortic dis- section in patients with severe, tearing back pain and associ- ated dyspnea and/or syncope.

Ambulatory monitoring:

24-hr ECG monitoring (Holter monitor) can show activity-induced ST-segment changes or ischemia-induced dysrhythmias.

Coronary arteriography via cardiac catheterization:

The gold standard of diagnostic testing for CAD. Arterial lesions (plaque) are located and the amount of occlusion determined. During this test, feasibility for coronary artery bypass grafting (CABG) or percutaneous coronary interven- tion (PCI) is determined. For details, see

Chapter 18, “Cardiac

Surgery,” p. 149.

Intravascular ultrasound:

A flexible catheter with a minia- ture transducer at the tip is threaded to the coronary arteries to provide information on the interior of the coronary arteries.

Ultrasound is used to create a cross-sectional image of the three layers of the arterial wall and its lumen to assess the degree of atherosclerosis.

often done on patients with acute syndromes. As ischemia advances, the muscle does not transmit electrical impulses, and the ECG helps determine the area and extent of the infarct.

Cardiac biomarkers:

Creatinine phosphokinase (CPK), CK-MB, and troponin I and T are proteins released in response to ischemia or MI. Elevations of these biomarkers usually occur 4-6 hr after ischemic damage. Serial tests q8h for 24 hr are recommended and help determine the extent of myocar- dial damage.

C-reactive protein:

If elevated from the normal range of 0.03-1.1 mg/dL, this signals that coronary artery plaques are inflammatory and the patient is at higher risk of an acute coronary event.

Echocardiogram:

Assesses ventricular function, chamber size, valvular function, ejection fraction, wall motion, and hemodynamic measurements. Heart muscle damage may alter ventricular function, wall motion, and hemodynamic pres- sures. A heart muscle that moves weakly may have been damaged during an acute ischemic attack, or it may be receiv- ing too little oxygen.

Chest x-ray examination:

Usually normal unless heart failure is present.

Total lipid panel:

Obtained during the patient’s evaluation and treatment to assess for hyperlipidemia, a risk factor in CAD. Low HDL (value less than 40 mg/dL) and high low- density lipoprotein (LDL) (value greater than 100 mg/dL) are linked to atherosclerotic heart disease. (Values may change in the presence of acute ischemia, and therefore are consid- ered more valid when they are obtained before hospital discharge.)

Stress tests:

Stress testing with concurrent imaging of the heart is the standard means of noninvasive cardiac evaluation.

Stress tests are prescribed to assess coronary artery flow, val- vular function, and wall motion abnormalities.

Exercise treadmill test: To determine the amount of exercise-induced ischemia, hemodynamic response, and ECG changes with exercise. Significant findings include 1 mm or more ST-segment depression or elevation, dysrhythmias, or a sudden decrease in blood pressure (BP).

Stress echocardiogram: Typically performed using either a treadmill or bicycle. Echocardiograms are obtained before and immediately after exercise. A stress-induced imbalance in the myocardial supply/demand ratio will produce myocardial ischemia and regional wall motion abnormality (the area of ischemia affects muscle contraction). Stress echocardiography is particularly useful for identifying CAD in patients with multivessel disease.

Stress echocardiogram: Dobutamine, adenosine, or dipyri-

damole is used as a stress agent with echocardiogram imaging

for patients who cannot exercise.