•Postmenopausal; past history of hormone replacement therapy
•Erectile dysfunction (ED): May be associated with hypertension or antihypertensive medications
T
EACHING/L
EARNING•Family history of heart disease, MI, diabetes, stroke, hyperten- sion, peripheral vascular disease, hypercholesterolemia
•Use of tobacco; may express desire or attempts at smoking cessation
•Use of alcohol or other drugs
•Use or misuse of cardiac medications, over-the-counter (OTC) preparations
•Use of vitamins and herbal supplements such as vitamin E, ginseng, garlic, ginkgo, hawthorn, bromelain
•Vomiting
•Poor skin turgor, dry or diaphoretic skin
•Decreased urine output
•Mentation changes such as disorientation, poor memory, changes in thought processes
•Weakness
•Facial grimacing, changes in body posture; may place clenched fist on midsternum when describing pain
•Crying, groaning, squirming, stretching
•Withdrawal, lack of eye contact
•Autonomic responses: Changes in heart rate and rhythm, blood pressure, respirations, skin color and moisture, and level of consciousness
•Increased respiratory rate, shallow and labored breathing
•Color: Pallor or cyanosis
•Decreased oxygen saturation on pulse oximetry
•Breath sounds: May be clear or crackles and wheezes present
•Sputum:Clear, possibly pink-tinged
•Difficulty resting quietly
•Overemotional responses such as intense anger or fear
•Withdrawal from family
•Not willing to cooperate with treatment recommendations; not responsive to teaching
M AY E X H I B I T
(continued)(continues on page 78)
D I A G N O S T I C D I V I S I O N M AY R E P O R T
(continued)D
ISCHARGEP
LANC
ONSIDERATIONS•May require assistance with activities of daily living (ADLs), food preparation, shopping, transportation, homemaking or maintenance tasks, modifications of physical layout of home ÁRefer to section at end of plan for postdischarge considerations
M AY E X H I B I T
(continued)T E S T
W H Y I T I S D O N E D
IAGNOSTICS
TUDIES•Electrocardiogram (ECG): Record of the electrical activity of the heart to detect dysrhythmias, to identify any myocardial ischemia present, or any damage to myocardial tissue from the past.
•Cardiac catheterization with angiography: Assesses patency of coronary arteries; reveals abnormal heart size, valvular function by measuring chamber pressures; and evaluates ventricular contractility by measuring ejection fraction (EF).
•Chest x-ray:Procedure used to evaluate organs and structures within the chest
B
LOODT
ESTS•Cardiac enzymes, including troponin I and troponin T. Also possibly CPK, CK, and CK-MB: Substances released from heart muscle when it is damaged.
In the emergency setting, the ECG is the most important diagnos- tic test. High probability of myocardial infarction is indicated by ST-segment elevation greater than 1 mm in two anatomi- cally contiguous leads (indicates acute MI in 90% of people, as confirmed by serial measurements of cardiac biomarkers) or by the presence of new Q waves (Kumar, 2009). Results that indicate intermediate probability of myocardial infarction are ST-segment depression, T-wave inversion, and other non- specific ST–T-wave abnormalities. Note: Some emergency departments use an 80-lead ECG that enhances the ability to detect acute MI in the right ventricle, posterior, and high left lateral regions of the myocardium (Franks, 2012).
Cardiac catheterization defines coronary anatomy and the extent of a client’s disease. Client with intractable angina (despite medication) should immediately undergo cardiac catheteriza- tion (Coven, 2013). Most individuals with UA and NSTEMI benefit from angiography when they have a TIMI (Thrombol- ysis in Myocardial Infarction) risk score of less than 3 points (Antman et al, 2000).
Visualize changes in heart size and any infiltrates that may be present in the lung.
Troponin levels are now considered to be the criterion standard for defining and diagnosing myocardial infarction, according to the American College of Cardiology (ACC)/American Heart Association (AHA) (Zafari, 2013). Cardiac-specific tro- ponins are not detectable in the blood of healthy individuals;
therefore, they provide high specificity for detecting injury to cardiac myocytes. These molecules are also more sensitive than CK-MB for myocardial necrosis and therefore improve early detection of small myocardial infarctions. Differentia- tion is generally based on three sets of tests measured at 6- to 8-hour intervals after the client’s presentation to the emer- gency depertment. The current definition of NSTEMI requires a typical clinical syndrome plus elevated troponin (or creatine kinase isoenzyme MB [CK-MB]) levels to over 99% of the normal reference. Given this definition, nearly 25% of indi- viduals who were previously classified as having unstable angina now fulfill the criteria for NSTEMI (Coven, 2013; Lab Tests Online, 2011).
W H AT I T T E L L S M E Diagnostic Studies
Client Assessment Database
(continued)CHAPTER 4CARDIOVASCULAR—MYOCARDIAL INFARCTION
T E S T
W H Y I T I S D O N E
(continued)•Complete blood count (CBC), including red (RBC) and white blood cell (WBC) counts, hemoglobin/hematocrit (Hgb/Hct), platelets
• Metabolic profile, including blood glucose electrolytes (BUN/Cr)
•Serum lipids, including total lipids, lipoprotein electrophore- sis, isoenzymes, cholesterols (HDL, LDL, very low density lipoprotein [VLDL]), triglycerides, phospholipids:A group of tests that make up a lipid profile.
•Coagulation studies, including partial thromboplastin time (PTT), activated partial thromboplastin time (aPPT), and platelets:Injury to a vessel wall or the tissue initiates the coag- ulation cascade and formation of a thrombus.
•Arterial blood gases (ABG):Assessment of levels of oxygen (PaO2) and carbon dioxide (PaCO2).
May be done if MI is suspected in order to rule out anemia as a cause of decreased oxygen supply and prior to giving throm- bolytics. Leukocytosis is also common, but not universal, signifying an acute inflammatory state. The platelet count is necessary if a IIb/IIIa agent is considered or may become dangerously low after the use of heparin (Zafari, 2013).
Important for client with new-onset angina. Close monitoring of potassium and magnesium levels is important because low levels may predispose to dysrrhythmias. Creatinine levels must be considered before using an angiotensin-converting enzyme (ACE) inhibitor and particularly if cardiac catheteri- zation is considered
The lipid profile numbers may be low during an acute MI; there- fore, it is important to follow up. It may show that the client has hyperlipidemia that was not identified or was uncontrolled in the past, (a risk factor for CAD and MI).
Thrombus formation can potentiate ischemic damage to the myocardium as blood flow is blocked.
Should be checked and repeatedly corrected if clinical findings suggest hypoxemia, which may result from pulmonary con- gestion, atelectasis, or ventilatory impairment secondary to complications of MI.
W H AT I T T E L L S M E
(continued)Nursing Priorities
1. Relieve pain and anxiety.
2. Reduce myocardial workload.
3. Prevent, detect, and assist in treatment of life-threatening dysrhythmias or complications.
4. Promote cardiac health and self-care.
Discharge Goals
1. Chest pain absent or controlled.
2. Heart rate and rhythm sufficient to sustain adequate car- diac output and tissue perfusion.
3. Achievement of activity level sufficient for basic self-care.
4. Anxiety reduced and managed.
5. Disease process, treatment plan, and prognosis understood.
6. Plan in place to meet needs after discharge, including follow-up appointments.
N U R S I N G D I A G N O S I S : acute Pain
May Be Related To
Physical agent (tissue ischemia) Possibly Evidenced By Verbal/coded reports of pain Facial mask (grimacing) Restlessness
Changes in heart rate, blood pressure
Desired Outcomes/Evaluation Criteria—Client Will
Pain LevelVerbalize 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.
NOC
NOC
ACTIONS/INTERVENTIONS RATIONALE
Pain ManagementIndependent
Monitor and document characteristics of pain, noting verbal reports, nonverbal cues, for example, moaning, crying, rest- lessness, diaphoresis, clutching chest, rapid breathing, and hemodynamic response (BP and heart rate changes).
Obtain full description of pain from client including location, intensity (using 0 to 10 or similar scale), duration, character- istics (dull or crushing), and radiation. Assist client to quan- tify pain by comparing it to other experiences.
Note history of previous angina, anginal equivalent, or MI pain.
Discuss family history if pertinent.
Instruct client to report pain immediately.
Assist or instruct in relaxation techniques, such as deep, slow breathing and distraction.
Check vital signs before and after administration of opioid medication.
Collaborative
Administer supplemental oxygen by appropriate route.
Administer medications, as indicated; for example:
Anti-anginals, such as nitroglycerin (Nitro-Bid, Nitrostat, Nitro-Dur), isosorbide dinitrate (Isordil), and mononitrate (Imdur)
Analgesics, such as morphine sulfate NIC
Variation of appearance and behavior of clients in pain may present a challenge in assessment. For example, men and women consistently present differently (McSweeney, 2003), 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.
Pain is a subjective experience and must be described by client. Provides baseline for comparison to aid in determin- ing effectiveness of therapy, resolution or progression of problem.
May differentiate current pain from preexisting patterns as well as identify complications, such as extension of infarction, pulmonary embolus, or pericarditis.
Delays in reporting pain hinders pain relief and may necessi- tate increased dosage of medication to achieve relief. In ad- dition, severe pain may induce shock by stimulating the sympathetic nervous system, thereby creating further dam- age and interfering with diagnostics and relief of pain.
Helpful in decreasing perception of or response to pain. Pro- vides a sense of having some control over the situation, increase in positive attitude.
Hypotension and respiratory depression can occur as a result of opioid administration. These problems may increase myocardial damage in presence of ventricular insufficiency.
Increases amount of oxygen available for myocardial uptake and thereby may relieve discomfort associated with tissue ischemia.
Nitrates are useful for pain control by coronary vasodilating ef- fects, 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.
Although intravenous (IV) morphine is the usual drug of choice, other injectable opioids may be used in acute-phase or re- current chest pain (unrelieved by nitroglycerin) to reduce se- vere pain, provide sedation, and decrease myocardial workload. IM injections should be avoided, if possible, be- cause they can alter the CPK diagnostic indicator and are not well absorbed in underperfused tissue.
N U R S I N G D I A G N O S I S : risk for decreased Cardiac Output
Risk Factors May Include Altered heart rate/rhythm
Reduced preload—increased systemic vascular resistance (SVR) Altered contractility—infarcted or dyskinetic muscle
Possibly Evidenced By
(Not applicable; presence of signs and symptoms establishes actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump EffectivenessMaintain hemodynamic stability, such as BP, cardiac output within normal range, adequate urinary output, decreased frequency or absence of dysrhythmias.
Report decreased episodes of dyspnea and angina.
Demonstrate an increase in activity tolerance.
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CHAPTER 4CARDIOVASCULAR—MYOCARDIAL INFARCTION
ACTIONS/INTERVENTIONS RATIONALE
Cardiac Care: Acute Independent
Monitor mental status. Investigate sudden changes or contin- ued alterations in mentation, such as anxiety, confusion, lethargy, and stupor.
Inspect for pallor, cyanosis, mottling, and cool or clammy skin.
Monitor respirations, noting work of breathing.
Auscultate breath sounds.
Evaluate quality and equality of pulses.
Auscultate heart sounds:
Note development of S3and S4.
Note presence of murmurs and rubs.
Obtain frequent BP readings. Monitor hemodynamic pressures when invasive lines/devices are available.
Monitor heart rate and rhythm. Document dysrhythmias via telemetry.
Monitor output, noting changes in urine output. Record urine specific gravity, as indicated. Calculate fluid balance.
Note jugular vein distention (JVD) and development of dependent edema.
Weigh daily at the same time on the same scale.
Have emergency equipment and medications available.
Collaborative
Administer supplemental oxygen, as indicated.
Measure cardiac output and other functional parameters as appropriate.
Review serial ECGs.
NIC
Cerebral perfusion is directly related to cardiac output and is influenced by electrolyte and acid-base variations, hypoxia, and systemic emboli.
Systemic vasoconstriction resulting from diminished cardiac output may be evidenced by decreased skin perfusion and diminished pulses.
Cardiac pump failure and ischemic pain may precipitate respi- ratory distress.
Crackles reflect pulmonary congestion; may develop because of depressed myocardial function.
Decreased cardiac output results in diminished, weak, or thready pulses. Irregularities suggest dysrhythmias, which may require further evaluation and monitoring.
S3is usually associated with heart failure, but it may also be noted with the mitral insufficiency (regurgitation) and left ventricular overload that can accompany severe infarction.
S4is an almost universal finding during the early stages of acute MI if the patient has sinus rhythm. A fourth heart sound can occur with or without signs of heart failure (Williams, 1990).
Indicates disturbances of normal blood flow within the heart, such as incompetent valve, septal defect, or vibration of pap- illary muscle and chordae tendineae (complication of MI).
Presence of rub with an infarction is also associated with in- flammation, such as pericardial effusion and pericarditis.
Hypotension may occur related to ventricular dysfunction, hypoperfusion of the myocardium, and vagal stimulation.
However, hypertension is also a common phenomenon, possibly related to pain, anxiety, catecholamine release, and preexisting vascular problems.
Heart rate and rhythm can be affected by presence of coronary artery blockage, myocardial necrosis, and impairment of ventricular contractilitly, electrolyte and acid-base imbal- ances, and circulating catecholamines. Dysrhythmias, espe- cially premature ventricular contractions or progressive heart blocks, can compromise cardiac and become lethal.
Acute or chronic atrial flutter or fibrillation may be seen with coronary artery or valvular involvement and may or may not be pathological. (Refer to CP: Dysrhythmias.)
Decreased output may reflect systemic perfusion problems and may reflect heart failure. Inotropic drugs may be needed for support of circulation or additional fluids to enhance circu- lating volume and kidney function. Note: Specific gravity measurements reflect hydration status and renal function.
Suggests developing congestive failure or fluid volume excess.
Sudden changes in weight reflect alterations in fluid balance.
Sudden coronary occlusion, lethal dysrhythmias, extension of infarct, and unrelenting pain are situations that may precipi- tate cardiac arrest, requiring immediate life-saving therapies or transfer to CCU.
Supplemental oxygen should be given to maintain oxygen sat- uration >90% to prevent hypoxemia and resultant depres- sion of myocardial function and dysrhythmias (Zafari, 2013).
Cardiac index, preload and afterload, contractility, and cardiac work can be measured noninvasively with thoracic electrical bioimpedance (TEB) technique. Useful in evaluating re- sponse to therapeutic interventions and identifying need for more aggressive or emergency care.
Provides information regarding progression or resolution of in- farction, status of ventricular function, electrolyte balance, and effect of drug therapies.
(continues on page 82)