Coronary artery disease (CAD) is a condition in which plaque builds up inside the coronary arteries. Coronary arteries are arteries that supply the heart muscle with oxygen-rich blood. Plaque is made up of fat, cholesterol, calcium, and other substance found in the blood. Plaque narrows the arteries and reduces blood flow to your heart muscle. It also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow. When the coronary arteries are narrowed or blocked, oxygen-rich blood can’t reach the heart muscle. This can cause angina or a heart attack. Without quick treatment, a heart attack can lead to serious problems and even death.
The classic symptom of coronary artery disease (CAD) is angina—pain caused by loss of oxygen and nutrients to the myocardial tissue because of inadequate coronary blood flow. In most but not all patients presenting with angina, CAD symptoms are caused by significant atherosclerosis. Unstable angina is sometimes grouped with MI under the diagnosis of acute coronary syndrome.
Angina has three major forms:
- stable: precipitated by effort, of short duration, and easily relieved,
- unstable: longer lasting, more severe, may not be relieved by rest or nitroglycerin; may also be new onset of pain with exertion or recent acceleration in severity of pain.
- variant: chest pain at rest with ECG changes due to coronary artery spasm.
CAD is the most common type of heart disease. Lifestyle changes, medicines, and/or medical procedures can effectively prevent or treat CAD in most people. Other names for coronary artery disease are atherosclerosis, coronary heart disease, hardening of the arteries, heart disease, ischemic heart disease and narrowing of arteries.
Nursing Care Plans
- Acute Pain
- Deficient Knowledge
- Risk for Decreased Cardiac Output
- Other Possible Nursing Care Plans
- See Also and Further Reading
Acute Pain: Unpleasant sensory and emotional experience arising from actual or potential tissue damage or described in terms of such damage; sudden or slow onset of any intensity from mild to severe with anticipated or predictable end and a duration of <6 months.
May be related to
- Decreased myocardial blood flow
- Increased cardiac workload/oxygen consumption
Possibly evidenced by
- Reports of pain varying in frequency, duration, and intensity (especially as condition worsens)
- Narrowed focus
- Distraction behaviors (moaning, crying, pacing, restlessness)
- Autonomic responses, e.g., diaphoresis, blood pressure and pulse rate changes, pupillary dilation, increased/decreased respiratory rate
- Report anginal episodes decreased in frequency, duration, and severity.
- Demonstrate relief of pain as evidenced by stable vital signs, absence of muscle tension and restlessness
|Instruct patient to notify nurse immediately when chest pain occurs.||Pain and decreased cardiac output may stimulate the sympathetic nervous system to release excessive amounts of norepinephrine, which increases platelet aggregation and release of thromboxane A2. This potent vasoconstrictor causes coronary artery spasm, which can precipitate, complicate, and/or prolong an anginal attack. Unbearable pain may cause vasovagal response, decreasing BP and heart rate.|
|Assess and document patient response to medication.||Provides information about disease progression. Aids in evaluating effectiveness of interventions, and may indicate need for change in therapeutic regimen.|
|Identify precipitating event, if any: frequency, duration, intensity, and location of pain.||Helps differentiate this chest pain, and aids in evaluating possible progression to unstable angina.|
|Observe for associated symptoms: dyspnea, nausea and vomiting, dizziness, palpitations, desire to micturate.||Decreased cardiac output (which may occur during ischemic myocardial episode) stimulates sympathetic and parasympathetic nervous system, causing a variety of vague sensations that patient may not identify as related to anginal episode.|
|Evaluate reports of pain in jaw, neck, shoulder, arm, or hand (typically on left side).||Cardiac pain may radiate. Pain is often referred to more superficial sites served by the same spinal cord nerve level.|
|Place patient at complete rest during anginal episodes.||Reduces myocardial oxygen demand to minimize risk of tissue injury.|
|Elevate head of bed if patient is short of breath.||Facilitates gas exchange to decrease hypoxia and resultant shortness of breath.|
|Monitor heart rate and rhythm.||Patients with unstable angina have an increased risk of acute life-threatening dysrhythmias, which occur in response to ischemic changes and/or stress.|
|Monitor vital signs every 5 min during initial anginal attack.||Blood pressure may initially rise because of sympathetic stimulation, then fall if cardiac output is compromised. Tachycardia also develops in response to sympathetic stimulation and may be sustained as a compensatory response if cardiac output falls.|
|Stay with patient who is experiencing pain or appears anxious.||Anxiety releases catecholamines, which increase myocardial workload and can escalate and/or prolong ischemic pain. Presence of nurse can reduce feelings of fear and helplessness.|
|Maintain quiet, comfortable environment. Restrict visitors as necessary.||Mental/emotional stress increases myocardial workload.|
|Provide light meals. Have patient rest for 1 hr after meals.||Decreases myocardial workload associated with work of digestion, reducing risk of anginal attack.|
|Provide supplemental oxygen as indicated.||Increases oxygen available for myocardial uptake and reversal of ischemia.|
|Administer antianginal medication(s) promptly as indicated:|
||Nitroglycerin has been the standard for treating and preventing anginal pain for more than 100 yr. Today it is available in many forms and is still the cornerstone of antianginal therapy.|
||Rapid vasodilator effect lasts 10–30 min and can be used prophylactically to prevent, as well as abort, anginal attacks.|
||Long-acting preparations are used to prevent recurrences by reducing coronary vasospasms and reducing cardiac workload. May cause headache, dizziness, light-headedness, symptoms that usually pass quickly. If headache is intolerable, alteration of dose or discontinuation of drug may be necessary. Note: Isordil may be more effective for patients with variant form of angina. Reduces frequency and severity of attack by producing continuous vasodilation.|
|Reduces angina by reducing the heart’s workload. Note: Often these drugs alone are sufficient to relieve angina in less severe conditions.|
|Produces relaxation of coronary vascular smooth muscle; dilates coronary arteries; decreases peripheral vascular resistance.|
||Usually sufficient analgesia for relief of headache caused by dilation of cerebral vessels in response to nitrates.|
||Potent narcotic analgesic may be used in acute onset because of its several beneficial effects, e.g., causes peripheral vasodilation and reduces myocardial workload; has a sedative effect to produce relaxation; interrupts the flow of vasoconstricting catecholamines and thereby effectively relieves severe chest pain. MS is given IV for rapid action and because decreased cardiac output compromises peripheral tissue absorption.|
|Monitor serial ECG changes.||Ischemia during anginal attack may cause transient ST segment depression or elevation and T wave inversion. Serial tracings verify ischemic changes, which may disappear when patient is pain-free. They also provide a baseline against which to compare later pattern changes.|