Coronary artery disease

19 Coronary artery disease




Overview/pathophysiology


Coronary artery disease (CAD) is the leading cause of death in the United States, affecting more than 13 million Americans. 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, which is the result of 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 unstable angina (USA), non–ST-elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).


USA is defined as an increase in severity, frequency, or intensity of anginal pain or a new onset of prolonged rest angina. This definition is based largely on clinical presentation. NSTEMI is defined by clinical presentation 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 elevation. Diagnosis of STEMI is based on elevated cardiac biomarkers plus ST-segment elevation on ECG signifying ischemia. Of the three, STEMI is the most serious and life threatening.


Time is of the essence in determining the treatment plan. All patients presenting to the emergency department (ED) with STEMI are considered high-priority triage cases. Primary angioplasty is widely viewed as therapy of choice for reperfusion in acute myocardial infarction (AMI). However, not all acute care hospitals in the United States have availability for percutaneous coronary intervention (PCI). Because time is so critical in patients presenting with STEMI, a decision must be made by the ED physician 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 onset is key to reducing mortality and morbidity. If 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, 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 CAD. Weakness, diaphoresis, nausea, vomiting, shortness of breath, and acute anxiety also can occur. Heart rate (HR) may be abnormally slow (bradycardia), especially in right coronary artery (RCA) infarct, or it may be rapid (tachycardia). Stable or progressively worsening angina occurs when myocardial demand for O2 is more than the supply, such as during exercise. Pain usually is 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 it is relieved by discontinuation of exercise or administration of nitroglycerin (NTG).



Physical assessment:


Acute syndromes may include the physical findings of anxiety, hypertension, tachycardia, tachypnea, and dynamic ECG changes. Severe hypotension may occur in shock states. Temperature elevations can occur secondary to the inflammatory process. Intensity of S1 and S2 heart sounds may be decreased. Pulmonary congestion may occur if ventricular failure is present, and S3 and S4 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. Obesity, glucose intolerance, and a sedentary, stressful lifestyle also contribute to increased risk. Chest pain often occurs with exertion.



Diagnostic tests




ECG:


Reveals dynamic changes in the presence of ischemia. When the ECG is performed during chest pain, characteristic 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 determined on ECG as well as dysrhythmias. Serial ECGs are often done on patients with ACS. As ischemia advances, the muscle does not transmit electrical impulses, and the ECG is therefore used to determine the area and extent of the infarct.



Cardiac biomarkers:


Creatine phosphokinase (CPK), CK-MB, and troponin are proteins released in response to ischemia or MI. Troponin may not be elevated on initial presentation. Serial enzymes q8h for 24 hr are recommended for accurate assessment of myocardial damage.



C-reactive protein:


If elevated from normal range of 0.03-1.1 mg/dL, signals that coronary artery plaques are inflammatory and patient is at higher likelihood 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 pressures. The part of the heart that moves weakly may have been damaged during a heart attack or may be receiving too little oxygen.



Chest x-ray examination:


Usually normal unless heart failure is present.



Total lipid panel:


Obtained during 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 considered more valid when they are obtained before hospital discharge.)



Stress tests:


Over the past two decades, stress testing with concurrent imaging of the heart has become a standard means of noninvasive evaluation. Stress tests typically are prescribed to assess coronary artery flow.



Exercise treadmill test:

To determine 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 or dipyridamole is used as a stress agent in combination with an echocardiogram for patients who cannot exercise.



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 MI resulting from lack of blood flow.

• Commonly used radiopharmaceutical agents are thallium-201 and technetium-99m sestamibi. Adenosine and dipyridamole are pharmacologic stress agents used in combination with a radiopharmaceutical agent if patient is unable to exercise or fails to reach 85% of age-predicted maximum HR.

• Single photon emission computed tomography (SPECT) is used to develop three-dimensional views of cardiac processes 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 acquisition 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 dissection in patients with severe, tearing back pain and associated dyspnea and/or syncope.



Ambulatory monitoring:


A 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 intervention (PCI) is determined. For details, see “Cardiac Surgery,” p. 147.



Intravascular ultrasound:


A flexible catheter with a miniature 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.




Nursing diagnosis:


Acute pain (angina)

related to decreased oxygen supply to the myocardium


Desired Outcomes: Within 30 min of onset of pain, patient’s subjective perception of angina decreases, as documented by a pain scale. Objective indicators, such as grimacing and diaphoresis, are absent or decreased.



































































ASSESSMENT/INTERVENTIONS RATIONALES
Assess location, character, and severity of pain. Record severity on a subjective 0 (no pain) to 10 (worst pain) scale. This assessment monitors degree, character, precipitator, and trend of pain for initial check and subsequent comparisons.
Assess HR and BP during episodes of chest pain. Be alert to and report significant findings. Increases in HR and changes in systolic blood pressure (SBP) greater than 20 mm Hg from baseline signal increased myocardial O2 demands and necessitate prompt medical intervention.
Record amount of NTG or morphine sulfate needed to relieve each episode, the factor or event that precipitated pain, and alleviating factors. Document angina relief obtained, using pain scale. Continue to assess vital signs frequently. Intravenous (IV) NTG drip should be increased in increments of 10 mcg if pain persists. SBP should be maintained at 90 mm Hg or higher until pain is relieved to avoid worsening ischemia secondary to hypotension. IV morphine sulfate is added in small increments (2 mg). NTG and morphine may lower HR and BP.
Administer sublingual NTG at the onset of pain (if not on an IV NTG drip), and explain to the patient that it is to be administered as soon as angina begins, repeating q5min × 3 if necessary. NTG increases microcirculation, perfusion to the myocardium, and venous dilation. Venous dilation causes pooling in the periphery so that less blood comes back to the right side of the heart, which in turn lowers O2 demand. If pain is unrelieved or returns very quickly, emergency medical treatment is advised.
Obtain ECG as prescribed. ECG patterns may reveal ischemia, as evidenced by dynamic ST- or T-wave changes, evidence of new Q waves, or left bundle branch block.
Stay with patient and provide reassurance during periods of angina. These measures reduce anxiety, which might otherwise worsen the angina.
Monitor for presence of headache and hypotension after administering NTG. These are side effects of NTG as a result of vasodilation.
Keep patient recumbent with head of bed (HOB) elevated no higher than 30 degrees during angina and NTG administration. This position minimizes potential for headache/hypotension by enabling better blood return to the heart and head.
Administer O2 as prescribed. Hypoxia is common because of the decreased perfusion and adds stress to the compromised myocardium.
Deliver O2 with humidity. Humidity helps prevent oxygen’s convective drying effects on oral and nasal mucosa.
Emphasize to patient importance of immediately reporting angina to health care team. Early treatment decreases morbidity and mortality.
Instruct patient to avoid activities and factors known to cause stress. Stress may precipitate angina.
Discuss value of relaxation techniques, including tapes, soothing music, biofeedback, meditation, or yoga. See Deficient Knowledge (relaxation techniques) later. Relaxation helps reduce stress and anxiety, which otherwise may precipitate angina.
Administer beta-blockers (e.g., metoprolol, atenolol, carvedilol) as prescribed. These drugs block beta stimulation to the sinoatrial (S-A) node and myocardium. HR, BP, and contractility are decreased, subsequently reducing workload of the heart and myocardial oxygen demand, ultimately improving myocardial oxygenation. Metoprolol may be administered IV as initial treatment.
Administer long-acting nitrates (isosorbide preparations) and/or topical nitrates as prescribed. Nitrates are given for anginal prophylaxis via vasodilation, lowering of BP, and decreasing O2 demand.
Administer angiotensin-converting enzyme (ACE) inhibitor (e.g., enalapril, captopril, quinapril, ramipril) as prescribed. ACE inhibitors reduce BP, down-regulate the renin-angiotensin aldosterone system (RAAS), and improve long-term survival.
Administer calcium channel blockers (e.g., nifedipine, diltiazem) as prescribed. Calcium channel blockers decrease coronary artery vasospasm, a potential cause of ischemia and subsequent angina. They also cause the vessels to dilate, increasing blood flow to the heart.
Administer aspirin as prescribed. Aspirin reduces platelet aggregation, which aids in preventing obstruction of the coronary arteries.
Administer antihyperlipidemic agents (e.g., atorvastatin, rosuvastatin) as prescribed. These agents, also known as “statin” drugs, are used to reduce hyperlipidemia and can stabilize plaque.
Administer stool softeners as prescribed. Straining at stool or constipation can increase myocardial work.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Coronary artery disease

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