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Saturday, June 26, 2021

Myocardial infarction (MI): Cause Symptoms Treatment | Heart Attack Treatment

Myocardial infarction (MI) 

 Myocardial infarction (MI) commonly known as a heart attack, one or more areas of the heart experience a prolonged decrease or cessation in oxygen supply because of insufficient Coronary blood flow; subsequently, necrosis or death to the affected myocardial tissue occurs. The onset of the MI process may be sudden or gradual, and the progression of the event to cell death takes approximately 3 to 6 hr. 

Pathophysiology and Cause of MI

1. Acute coronary thrombosis ( partially or total)  associated with 90% of MI 

  • Severe atherosclerosis (>70% narrowing of the artery) precipitate thrombus.
  • Thrombus formation begins with plaque rupture and platelet adhesion to the damaged area.
  • Activation of the exposed platelets causes expression of glycoprotein IIb/IIIa receptors that bind fibrinogen.
  • Further platelet aggregation and adhesion occurs, enlarging the thrombus and occluding the artery.

2. Other etiologic factors include coronary artery spasm, coronary artery embolism, infectious disease-causing arterial inflammation, hypoxia, anaemia, and severe exertion or stress on the heart in the presence of significant CAD.

3. Different degrees of damage occurs to the heart muscle

  • Zone of necrosis: death to the heart muscle caused by extensive and complete oxygen deprivation; irreversible damage.
  • Zone of injury: region of the heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygenation can be restored.
  • Zone of ischemia: region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs.
4. Classification of MI 

  • STEMI: whereby ST-segment elevations are seen on ECG. The area of necrosis may or may not occur through the entire wall of the heart muscle.
  • NSTEMI: no ST-segment elevations can be seen on ECG. ST depressions may be noted as well as positive cardiac markers. T wave inversions, and clinical equivalent ( chest pain). Area of necrosis may or may not occur through the entire myocardium.
5. The region of the heart muscle that becomes affected depends on which coronary artery is obstructed.

  • Left ventricle is a common and dangerous location for an MI because it is the main pumping chamber of the heart. The left anterior descending artery supplies oxygen to this part of the heart.
  • Right ventricular infarction commonly occur with damage to the inferior and posterior wall of the left ventricle. Occlusion in the right coronary or circumflex arteries can lead to this type of infarct.
6. The severity and location of the MI determines the prognosis

Dalteparin (Fragmin) Anticoagulant+ Low-Molecular-Weight Heparin: Action and Uses

Signs and Symptoms of MI

1. Chest pain 

  • Severe, diffuse, steady substernal pain: may be described as crushing. Squeezing, or dull.
  • Not relieved by rest or sublingual vasodilator therapy such as nitroglycerin, but requires opioids (ie, morphine ).
  • May radiate to the arms ( usually the left), shoulder, neck, back and jaw.
  • Continues for more than 15 minutes.
  • May produce anxiety and fear, resulting in increased heart rate, blood pressure, and respiratory rate.
2. Diaphoresis; cool clammy skin, facial pallor.
3. Hypertension or hypotension.
4. Bradycardia or tachycardia.
5. Premature ventricular and atrial beats.
6. Palpitations, severe anxiety, dyspnea.
7. Disorientation, confusion, restlessness.
8. Fainting, marked weakness
9. Nausea, vomiting, hiccups.
10. Atypical Symptoms: epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, extreme fatigue.

Diagnostic Evaluation of MI

Ecg Changes

1. Generally occurs within 2 to 12 hours, but may take 72 to 96 hours.
2. Necrotic, injured, and ischemic tissues alter ventricular depolarization and repolarization.
  • ST-segment depression and T- wave inversion indicate a pattern of ischemia.
  • ST-elevation indicates an injury pattern.
  • Q waves indicate tissue necrosis and are permanent. A pathologic Q wave is one that is greater than 3 mm in depth or greater than one third the height of the R wave.
3. Location of the infarction (anterior, anteroseptal, inferior, posterior, lateral) is determined by the leads in which the ST changes (elevation vs depression ) are seen. Of note, the changes must be in two contiguous or related leads to be diagnostic.

Cardiac Markers

1. Cardiac enzymes ( biochemical markers) are not diagnosis of an acute MI with a single elevation; serial markers are drawn.
  • Marker elevation is then correlated to the extent of heart muscle damage.
  • Characteristic elevation over several hours confirms MI.
Other Findings
  • Elevated CRP and lipoprotein (s) due to inflammation in the coronary arteries.
  • Abnormal coagulation studies (prothrombin time [PT], partial thromboplastin time [PTT]).
  • Elevated white blood cell (WBC) count and sedimentation rate due to the inflammatory process involved in heart muscle cell damage.
  • Radionuclide imaging allows recognition of areas of decreased perfusion.
  • PET determines the presence of reversible heart muscle injury and irreversible or necrotic tissue extent to which the injured heart muscle has responded to treatment can also be determined.
  • Cardiac muscle dysfunction noted on echocardiography or cardiac magnetic resonance imaging (MRI).
Treatment and Management of Myocardial Infarction

The goals for UA/NSTMi therapy are immediate relief of ischemia and prevention of severe outcomes such as death or myocardial infarction or reinfarction. To achieve this requires administration of anti-ischemic therapy. ( rest, supplemental oxygen, nitroglycerin, beta-blockers, ACE inhibitors ); antithrombotic therapy ( aspirin, clopidogrel, ticlopidine); and ongoing risk stratification and use of invasive procedure ( cardiac catheterization) to provide early restoration of coronary blood flow.

Pharmacologic Therapy

Pharmacologic therapy for MI is standard. Use the MONA acronym to outline immediate pharmacologic interventions.
  • M (morphine ) IV rather than intramuscular (I. M) administration to prevent spurious elevation in serial biomarkers. Used to treat chest pain. Endogenous catecholamine release during pain imposes an increase in the workload on the heart, thus causing an increase in oxygen demand. Morphine's analgesic effects decrease the pain, relieve anxiety, and improve cardiac output by reducing preload and afterload.
  • O (oxygen) given via nasal cannula or face mask. Increases oxygenation to ischemic heart muscle.
  • N (nitrates) given sublingually via spray or through IV administration. Vasodilation therapy reduces preload by decreasing blood return to the heart and decreasing oxygen demand.
  • A ( aspirin) immediate dosing by mouth is recommended to halt platelet aggregation.

Other medications

1. Fibrinolytic agents such as tissue plasma activator, streptokinase, and reteplase reestablish blood flow in coronary vessels by dissolving thrombus.
  • No effect on the underlying stenosis that precipitated the thrombus to form.
  • IV administration.
2. Antiarrhythmic, such as amiodarone, and correction of electrolyte Imbalance decrease the ventricular irritability that occurs after MI.
  • Bolus of amiodarone is given via IV line over 10 minutes, then an infusion is given in varying doses over 24 hours ( 1 mg/minute for 6 hours then 0.5 mg/minute for 18 hours).
Percutaneous Coronary Interventions
  • Mechanical openings of the coronary vessel can be performed during evolving.
  • Percutaneous coronary interventions (PCIs), including Percutaneous transluminal coronary angioplasty, coronary stenting, and atherectomy, can be used instead of or as an adjunct to fibrinolytic therapy. Fibrinolytic therapy is considered inSTMI patients if PCI is not able to be performed within 90 minutes.
  • Should be performed within 90 minutes of the patient's arrival.
Surgical Revascularization
  • Cardiac surgery (ie. CABG) following STMI is associated with high mortality in the first 3 to 7 days, thus the benefit of revascularization must be weighed against the risk of cardiac surgery.
  • Benefits of this therapy include definitive treatment of the stenosis and less scar formation on the heart.
Complications of Myocardial Infarction
  • Dysrhythmias
  • Sudden cardiac death due to ventricular arrhythmias.
  • Infarct expansion (thinning and dilation of the necrotic zone).
  • Infarct extension ( additional heart muscle necrosis occurring after 24 hours of acute infarction).
  • Heart failure (with 20% 35% left ventricle damage ).
  • Cardiogenic shock.
  • Reinfarction.
  • Ischemic cardiomyopathy.
  • Cardiac rupture.
  • Papillary muscle rupture.
  • Ventricular mural thrombus.
  • Ischemic stroke.
  • Thromboemboli.
  • Ventricular aneurysm.
  • Cardiac Temponade.
  • Pericarditis.
ACS Medications 

  • Antiplatelet drug that blocks prostaglandin synthesis and thromboxane A2 formation.
Clinical Considerations
  • Administer as soon as acute coronary syndrome is suspected.
  • Give patientb160-325 mg; if not already taking aspirin, patient should chew this dose.
  • If patient is allergic to aspirin, give clopidogrel or ticlopidine instead.
Clopidogrel, ticlopidine
  • Antiplatelet drugs that inhibit platelet aggregation
Clinical Considerations
  • Alternatives for patients who cannot use aspirin.
  • Recent research indicates that using clopidogrel and aspirin concurrently reduces the risk of myocardial infarction (MI), stroke and death.
Unfractionated heparin, low-molecular-weight heparin ( dalteparin, enoxaparin)
  • Potentiate antithrombin III activity, inactive thrombin, prevent conversion of fibrinogen to fibrin.
Clinical Considerations

1:Unfractionated heparin
  • Weight-adjusted dosage is given to achieve therapeutic partial thromboplastin time (PTT) and activated clotting time.
  • Reversible with protamine sulfate.
2:Low-molecular-weight heparin
  • PTT is not monitored.
  • Give by subcutaneous injection.
  • Effects are not reversible.
Glycoprotein (GP) llb/llla inhibitors
  • Block GP sites on platelet, preventing platelet aggregation.
Clinical Considerations
  • Indicated for intermediate or high-risk ACS or with Percutaneous coronary intervention.
  • Each drug has specific indications and dosage ranges. Consult the package insert for specifics.
Fibrinolytics (alteplase, tenecteplase, streptokinase, reteplase)
  • Break up the fibrin meshwork in clots.
Clinical Considerations
  • Indicated in ST-segment elevation ACS only.
  • Certain agents require weight-adjusted dose. See package inserts for details.
Beta-adrenergic blockers (metoprolol, atenolol)
  • Reduce cardiac output and heart rate, reduce ventricular remodeling, and decrease endothelial dysfunction.
Clinical Considerations
  • Start all ACS patients on a beta-adrenergic-blocker as tolerated.
  • As ordered, titrate dosage to meet the therapeutic goals: heart rate, 60 beats/ minute; blood pressure (BP), greater than 90 mm Hg systolic.
Angiotensin-converting enzyme inhibitors ( captopril, enalapril)
  • Decrease endothelial dysfunction and prevent conversion of angiotensin l to angiotensin ll.
Clinical Considerations
  • Indicated for patients with heart failure, those with a heart rate above 100 beats/minutes, and those with an anterior MI, hypertension or diabetes.
  • Start with a drug with a short half-life such as captopril, with 24 hours to treat acute MI; on discharge, switch to a longer-acting drug, such as lisinopril or enalapril.
  • Dilates peripheral vessels, relaxes vascular smooth muscle, and decrease preload.
Clinical Considerations
  • Can be given sublingually, orally or via IV line spray in an acute care setting.
  • Do not allow BP to drop below 90 mm Hg systolic.
  • Switch the patient to topical patch or an oral form for long-term use.
  • Acts as an analgesic and sedative.
Clinical Considerations
  • Indicated in acute care setting only; not for prolonged use.
  • Give until the patient is free from chest pain or to relieve pulmonary congestion.
  • Monitor BP, level of consciousness and respiratory rate.

Nursing Assessment

1. Gather information regarding the Patients chest pain:
  • Nature and intensity
  • Onset and duration
  • Location and radiation
  • Precipitating and aggravating factors
2. Questions patient about other Symptoms experienced associated with the pain. Observe the patient for diaphoresis, facial pallor, dyspnea, guarding behaviours, rigid body posture, extreme weakness and confusion.
3. Evaluate cognitive, behavioural and emotional status.
4. Analysis information for Contraindications for fibrinolytic therapy and PCI.
5. Gather information about presence or absence of cardiac risk factors.

Nursing Diagnosis
  • Anxiety-related to chest pain, fear of death, threatening environment.
  • Activity intolerance related to insufficient oxygenation to perform activities of daily living, reconditioning effects of bed rest.
  • Risk for injury (bleeding ) related to dissolution of protective clots.
  • Risk for decreased cardiac tissue perfusion related to coronary restenosis, extension of infarction.
  • Ineffective coping to threats to self-esteem, disruption of sleep- rest pattern, lack of significant support system, loss of control, and change in lifestyle.

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