Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Most common symptom of coronary artery disease (CAD) secondary to coronary vascular obstruction from atherosclerosis.
B.Three types.
1.Stable angina.
a.Secondary to fixed atherosclerotic plaques that narrow coronary vasculature.
b.Occurs because of an imbalance between myocardial blood supply and oxygen demand.
2.Unstable angina (UA).
a.Progression from stable angina, leading to total vessel occlusion.
b.Indication that narrowing of coronary vasculature has increased via thrombosis, hemorrhage, or plaque rupture.
c.Myocardial oxygen demand unchanged, but blood supply decreased because of reduced coronary flow.
3.Prinzmetal angina: Transient coronary vasospasms in the setting of fixed atherosclerosis (75% of cases) or healthy coronary arteries.
Incidence
A.Estimated 9.8 million Americans experience angina yearly.
B.Age-adjusted prevalence of angina is higher in females than males.
C.Annual incidence rates are highest in African Americans as compared to other ethnicities.
D.Incidence and prevalence of angina and CAD increase with age.
Pathogenesis
A.Coronary atherosclerosis causes narrowing of the coronary arteries, thereby reducing blood flow through the system.
B.Myocardial ischemia (damage) results when the amount of blood flow through the coronary arteries is insufficient to meet myocardial oxygen demand.
C.Sensation of angina is caused by the stimulation of the sensory nerve fibers in the coronary vessels.
1.The nerve fibers extend from the spinal nerves (via the spinal cord) to the thalamus to the cerebral cortex to convey pain.
2.Adenosine is thought to be the chemical mediator of angina by stimulating the afferent cardiac nerve fibers.
Predisposing Factors
A.Diabetes mellitus.
B.Hyperlipidemia (elevated low-density lipoprotein [LDL], low high-density lipoprotein [HDL], or elevated triglycerides [TGs]).
C.Hypertension (HTN).
D.Tobacco use.
E.Increased age (males >45 years and females >55 years).
F.Family history of premature CAD or MI in first-degree relative (males <45 years and females <55 years).
G.Obesity or metabolic syndrome.
H.Sedentary lifestyle.
I.Underlying valvular heart disease such as aortic stenosis.
Subjective Data
A.Common complaints/symptoms.
1.Stable angina.
a.Retrosternal chest discomfort: Described as pressure, heaviness, burning, squeezing.
b.Can be located in central chest, epigastrium, neck, back, or shoulders (pain below mandible and below epigastrium is rarely angina).
c.Can radiate to jaw, left arm, or shoulders.
d.Typically preceded by exertion, eating, cold exposure, or emotional upset.
e.Usually does not change with positions or respiration.
f.Typically lasts 1 to 5 minutes and relieved by rest or use of nitroglycerin.
2.Differentiating features of UA.
a.Symptoms occur at rest.
b.Any new-onset angina or change in usual stable anginal symptoms.
c.Angina unrelieved by rest or nitroglycerin.
d.Typically lasts longer than stable angina.
B.History of the present illness.
1.Obtain information regarding onset, provoking and alleviating factors, duration, quality, severity, and timing of the anginal-type discomfort.
2.Assess for associated symptoms, including:
a.Fatigue.
b.Diaphoresis.
c.Shortness of breath.
d.Decreased exercise tolerance.
e.Nausea/vomiting.
C.Family and social history.
1.Family history of premature CAD or MI in first-degree relative (males <45 and females <55 years).
2.Tobacco use, alcohol consumption, and illegal substance use (especially cocaine).
3.Lifestyle, including exercise and dietary habits.
D.Review of systems.
1.General: Fatigue or diaphoresis.
2.Cardiovascular: Chest pain or palpitations.
3.Pulmonary: Dyspnea on exertion or shortness of breath.
4.Abdominal: Epigastric discomfort, nausea, or vomiting.
5.Peripheral vascular: Claudication or skin changes related to venous stasis and HTN.
Physical Examination
A.Unremarkable in most patients with stable angina.
B.Vital signs: Assess heart rate and rhythm, blood pressure, oxygen saturation, and respiration rate.
C.General: Observe patient’s level of distress.
1.Levine sign: Fist clenched over sternum is suggestive of angina.
D.Skin: Diaphoresis and evidence of poor lipid metabolism (xanthoma) are possible.
E.Neck: Carotid bruits and increased jugular venous pressure are possible.
F.Cardiovascular: Inspect, palpate (pain on chest wall palpation is not usually cardiac in nature), and auscultate (partially audible S3, S4 due to left ventricular dysfunction and/or murmur of mitral regurgitation as sign of papillary muscle dysfunction).
G.Pulmonary: Auscultate lungs for evidence of rales/crackles (concern for congestive heart failure and pulmonary edema).
H.Abdomen: Auscultate for bruits, palpate for discomfort, assess for a pulsatile abdominal mass.
I.Peripheral vascular: Assess peripheral pulses, possible venous stasis changes, and peripheral edema.
Diagnostic Tests
A.ECG: Usually normal in patients with stable angina (if prior MI, could see Q-waves).
B.Chest radiograph: Usually normal but evaluate for cardiomegaly, pulmonary edema, pericardial effusion.
C.Cardiac biomarkers: Serial troponins, troponin T (cTnT), and troponin I (cTnI) to rule out MI.
D.Lipid panel to assess for risk of atherosclerosis.
E.Complete blood count to assess for underlying exacerbating cardiac factors such as evidence of anemia.
F.Complete metabolic panel to assess electrolytes (metabolic dysfunction can lead to arrhythmias) and kidney function (important if cardiac catheterization with contrast dye is needed).
G.Stress testing.
1.For a positive stress test and when deemed appropriate by the cardiologist and interventional cardiologist, a cardiac catheterization with coronary angiography is performed. During this intervention, contrast dye is injected into the coronary vasculature to aid in the visualization and revascularization of the affected vessel(s).
2.Exercise stress testing.
a.Stress ECG: An ECG is performed before, during, and after treadmill exercise. The test is 75% sensitive if heart rate reaches 85% of maximum predicted value for age. Exercise-induced ischemia results in subendocardial ischemia (ST-segment depression on ECG); can also see hypotension or ventricular arrhythmias.
b.Stress echocardiography: Cardiac echocardiography is performed before and after exercise.
i.Exercise-induced ischemia is detected by cardiac wall-motion abnormalities not present at rest.
ii.It is more sensitive for detecting ischemia than stress ECG and beneficial for determining left ventricular function.
3.Pharmacologic stress testing (for patients unable to walk on treadmill).
a.Intravenous adenosine or dobutamine can be used to replace treadmill activity.
b.These agents create cardiac stress, and they can be combined with an ECG, echocardiogram, or nuclear imaging.
4.Nuclear stress testing.
a.Thallium or technetium 99m Tc sestamibi are used in patients with baseline ECG abnormalities to localize ischemia.
b.Areas of damage will be ill-perfused on imaging.
H.Other cardiac diagnostic testing.
1.Computed tomography coronary angiography (CTCA).
a.Relatively new test.
b.Utilizes electron-beam or multidetector CT imaging to evaluate the coronary arteries for level of calcium (coronary artery calcium [CAC] score).
c.Useful in detecting the amount of atherosclerosis within the coronary arteries.
I.The flow chart in Figure 3.2 can help with diagnosis and risk stratification in angina.
Differential Diagnosis
A.MI.
B.Coronary vasospasm.
C.Pulmonary embolus.
D.Pericarditis.
E.Congestive heart failure.
F.Acute gastritis.
G.Cholecystitis.
H.Ruptured abdominal or thoracic aortic aneurysm.
I.Anxiety/panic attack disorders.
J.Gastroesophageal reflux/peptic ulcer disease.
K.Cocaine toxicity.
L.Hypertensive urgency or emergency.
M.Valvular abnormalities.
N.Hiatal hernia.
O.Costochondritis.
Evaluation and Management Plan
A.General plan.
1.Prevention of MIs and reduction of angina-type symptoms; can consider the ABCDE mnemonic.
A: Aspirin and antianginal agents.
B: Beta-blockers and blood pressure management.
C: Cholesterol management and cigarette smoking abstinence.
D: Diet and diabetic management.
E: Education and exercise.
2.Treatment using risk stratification considerations.
a.Mild disease (normal cardiac function and mild angina): Aspirin, nitrates, and beta-blockers (possibly calcium channel blockers).
b.Moderate disease (moderate angina, normal cardiac function, two-vessel coronary disease): Use of medications for mild disease and cardiac catheterization for revascularization.
c.Severe disease (decreased cardiac function, three-vessel/left main/left anterior artery disease with severe angina): Pharmacologic and consideration of coronary artery bypass grafting (CABG).
3.Evaluation of patients with anginal symptoms for acute cardiac ischemia (ST-elevation MI or non-ST-segment elevation MI).
4.For patients with UA, hospitalization for monitoring, stabilization, and possible cardiac catheterization (or stress testing if determined safe by cardiologist).
B.Patient/family teaching points.
1.Compliance with medications and primary care provider appointments.
2.HTN: Tight blood pressure (BP) control decreases CAD risk, especially in those with diabetes mellitus.
3.Diabetes mellitus: Strict control of blood sugars to reduce macrovascular (CAD) disease.
4.Hyperlipidemia: Using lifestyle modifications and the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors to reduce cholesterol.
5.Obesity: Weight loss, which is imperative for cardiovascular health.
FIGURE 3.2 Diagnosis and risk stratification in angina.
EF, ejection fraction
Source: Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J. L., & Loscalzo, J. (Eds.). (2015). Chronic stable angina. Harrison’s principles of internal medicine (19th ed.). New York, NY: McGraw-Hill.
6.Diet: Reducing saturated fat (<7% of total calories) and total cholesterol (<200 mg/d).
7.Physical activity: Imperative for cardiovascular health; recommend aerobic exercise for 30 minutes/day for 5 to 7 days/week.
8.Tobacco cessation to decrease risk of CAD.
C.Pharmacotherapy.
1.Aspirin: Antiplatelet that decreases risk of MI.
2.Beta-blockers: Decrease cardiac work (decrease pulse, BP, contractility), thus lowering myocardial oxygen demand.
3.Nitrates: Work via vasodilation.
a.Alleviate angina via reduction of cardiac preload and myocardial oxygen demand.
b.Can be administered sublingually, orally, transdermally, or intravenously.
c.Side effects: Flushing, headache, dizziness, and/or hypotension.
4.Phosphodiesterase inhibitors: Caution necessary with medications such as sildenafil, tadalafil, and vardenafil; risk of hypotension.
5.Calcium channel blockers: Decrease cardiac afterload and cause coronary vasodilation to increase coronary blood flow.
6.Lipid lowering agents: HMG-CoA reductase inhibitors to decrease atherosclerosis and risk of MIs.
Follow-Up
A.Important issues during follow-up visits for patients with angina.
1.Increased or decreased exercise tolerance.
2.Any change in anginal symptoms.
3.Problems with medication compliance.
4.Any changes in modifiable risk factors (diet, activity level, tobacco cessation).
5.Monitoring of management of comorbid conditions that contribute to CAD.
B.Additional recommendations.
1.Annual treadmill stress testing for patients with stable CAD.
2.Stress imaging in patients with change in CAD status or who underwent initial stress imaging due to known risk factors.
3.Use of echocardiography to evaluate left ventricular function and wall motion in CAD patients with worsening congestive heart failure or recent MI.
Consultation/Referral
A.Consult with a cardiologist in patients with angina/CAD for proper risk stratification, diagnostic testing, treatment regimen planning, and ongoing monitoring.
B.Consult with an interventional cardiologist for patients requiring cardiac catheterization.
C.Consult with a cardiothoracic surgeon for patients requiring CABG or those with severe valvular disease requiring repair/replacement.
Special/Geriatric Considerations
A.Prinzmetal angina.
1.Also known as variant angina caused by coronary vasospasms.
2.Rare diagnosis: Usually occurs in patients 40 to 60 years of age.
3.Can be provoked by factors such as cold exposure, tobacco use, cocaine use, emotional stress, thyrotoxicosis, excessive alcohol use, and medications (histamine, serotonin).
4.Underlying atherosclerosis in 75% of patients.
5.Chest pain episodes: Very painful; last approximately 15 minutes and usually occur at rest.
6.Can mimic symptoms of MIs; very difficult to differentiate on history and physical examination.
7.Hallmark: Transient ST elevation on ECG during chest pain episodes.
8.Coronary angiography is test of choice: Will see evidence of coronary vasospasm when IV ergonovine is administered (to stimulate chest pain).
9.Can be relieved by antianginal medications.
10.Use of calcium channel blockers and nitrates can be helpful for treatment.
B.Geriatric considerations.
1.Age: Not a limitation for evaluation and treatment of CAD.
2.Presentation: Possibly atypical symptoms.
3.Higher incidence of multivessel coronary disease.
4.Greater prevalence of renal impairment (concern for use of contrast dye during catheterization).
5.Higher incidence of polypharmacy: Potential drug interactions and medication compliance.
6.Possibly too risky for surgical intervention, thus requiring only conservative (medical) management.
7.Important to assess baseline cognitive status and comorbidities when discussing treatment
plan and to involve family when necessary.
Bibliography
Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed.). Philadelphia, PA: Wolters Kluwer.
Alaeddini, J., & Shirani, J. (2018, July 19). Angina pectoris. In E. Yang (Ed.), Medscape. Retrieved from http://emedicine.medscape.com/article/150215-overview
Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J., & Loscalzo, J. (Eds.). (2015). Chronic stable angina. In Harrison’s manual of medicine (19th ed.). New York, NY: McGraw-Hill.