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Nursing Diagnosis for Myocardial Infarction | Acute Pain

Nursing diagnosis: acute pain related to tissue ischemia (coronary artery occlusion)

Possibly evidenced by
Reports of chest pain with or without radiation
Facial grimacing
Restlessness, changes in level of consciousness
Changes in pulse, BP

Desired Outcomes/Evaluation Criteria—Client Will
Pain Level
Verbalize relief or control of chest pain within appropriate period for administered medications.
Display reduced tension, relaxed manner, and ease of movement.
Pain Control
Demonstrate use of relaxation techniques.

Nursing care plan intervention with rationale:
1. Monitor and document characteristics of pain, noting verbal reports, nonverbal cues, for example, moaning, crying, restlessness, diaphoresis, clutching chest, rapid breathing, and hemodynamic response (BP and heart rate changes).
Rationale: Variation of appearance and behavior of clients in pain may present a challenge in assessment. For example, men and women consistently present differently, or an individual may present differently from one episode to another. However, most clients with an acute MI appear ill, distracted, and focused on pain. Verbal history and deeper investigation of precipitating factors should be postponed until pain is relieved. Respirations may be increased as a result of pain and associated anxiety; release of stress-induced catecholamines
increases heart rate and BP.

2. Obtain full description of pain from client including location, intensity (0 to 10), duration, characteristics (dull or crushing), and radiation. Assist client to quantify pain by comparing it to other experiences.
Rationale: Pain is a subjective experience and must be described by client. Provides baseline for comparison to aid in determining effectiveness of therapy, resolution or progression of problem.

3. Review history of previous angina, anginal equivalent, or MI pain. Discuss family history if pertinent.
Rationale: May differentiate current pain from preexisting patterns as well as identify complications, such as extension of infarction, pulmonary embolus, or pericarditis.

4. Instruct client to report pain immediately.
Rationale: Delays in reporting pain hinders pain relief and may necessitate increased dosage of medication to achieve relief. In addition, severe pain may induce shock by stimulating the sympathetic nervous system, thereby creating further damage and interfering with diagnostics and relief of pain.

5. Provide quiet environment, calm activities, and comfort measures, for instance, dry or wrinkle-free linens and backrub. Approach client calmly and confidently.
Rationale: Decreases external stimuli, which may aggravate anxiety and cardiac strain and limit coping abilities and adjustment to current situation.

6. Assist or instruct in relaxation techniques, such as deep, slow breathing and distraction.
Rationale: Helpful in decreasing perception of or response to pain. Provides a sense of having some control over the situation, increase in positive attitude.

7. Check vital signs before and after administration of opioid medication.
Rationale: Hypotension and respiratory depression can occur as a result of opioid administration. These problems may increase myocardial damage in presence of ventricular insufficiency.

Collaborative management:
1. Administer supplemental oxygen by means of nasal cannula or face mask, as indicated.
Rationale: Increases amount of oxygen available for myocardial uptake and thereby may relieve discomfort associated with tissue ischemia.

2. Administer medications, as indicated, for example: Aspirin (ASA)
Rationale: Giving aspirin as soon as possible (unless contraindicated) inhibits platelet activity, interrupting platelet aggregation at the site of plaque rupture—a key mechanism in the unfolding acute MI. Patients who receive aspirin in the acute phase have a 15% lower mortality rate than those who don’t (Lackey, 2006).

3. Anti-anginals, such as nitroglycerin (Nitro-Bid, Nitrostat, Nitro-Dur), isosorbide dinitrate (Isordil), and mononitrate (Imdur)
Rationale: Nitrates are useful for pain control by coronary vasodilating effects, which increase coronary blood flow and myocardial perfusion. Peripheral vasodilation effects reduce the volume of blood returning to the heart (preload), thereby decreasing myocardial workload and oxygen demand.

4. Angiotensin-converting enzyme (ACE) inhibitors, such as lisinopril (Zestril), captopril (Capoten), and benazepril (Lotensin)
Rationale: May be given to reduce hypertension and reduce risk of developing heart failure following MI in client with diminished ventricular EF and in those with hypertension, diabetes, or
chronic kidney disease, unless contraindicated (Smith et al, 2006).

5. Angiotensin receptor blockers (ARBs), such as candesartan (Atacand), olmesartan (Benicar), and valsartan (Diovan)
Rationale: May be used in patients who are intolerant to ACE inhibitors and have heart failure (HF) or have had an MI with left ventricular EF less than or equal to 40%. They block the action
of angiotensin II that causes the blood vessels to dilate and reduce BP.

6. Aldosterone blockers, such as eplerenone (Inspra) and spironolactone
Rationale: May be used in post-MI patients who have had an MI, ACS, or left ventricular dysfunction with or without HF symptoms, unless contraindicated. They block the effects of aldosterone on the kidneys, allowing the kidneys to excrete extra sodium and water, thereby reducing BP.

7. Analgesics, such as morphine sulfate
Rationale: Although intravenous (IV) morphine is the usual drug of choice, other injectable opioids may be used in acute-phase or recurrent chest pain unrelieved by nitroglycerin to
reduce severe pain, provide sedation, and decrease myocardial workload. IM injections should be avoided, if possible, because they can alter the CPK diagnostic indicator and are not well absorbed in underperfused tissue.
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