Myocaedial infarction

Myocardial Infarctions
? Myocardial infarction, also known as a “heart attack,” occurs when the heart fails to receive adequate oxygen as a result of an occlusion in the coronary arteries
? Common causes: Atherosclerosis (hardening/narrowing of vasculature) combined with plague accumulation
? Presentation: Shortness of breath and chest pain that possibly radiates to back, neck, or shoulders. Skin may be cool, diaphoretic, and appear with pallor. Lungs are clear upon auscultation as it’s a vasculature issue, not respiratory
? Confirmation: EKG is used to distinguish MI from other pathologies and determine the location of the occlusion. Cardiac catheterization provides definitive data on location of occlusion and can also be used as a treatment by using angioplasty (balloon and stent)
? Treatment: MONA (morphine, oxygen, nitroglycerin, and aspirin), cardiac catheterization to verify location of occlusion with angioplasty to relive occlusion, and possibly coronary artery bypass graphing (CABG) surgery
? Goals of treatment: Minimize damage to the heart muscle and subsequent disability/death, prevent cardiac arrest. Get patient into cardiac catheterization lab within 30-60 minutes after admission
? Facility goals: Initiate MONA therapy as soon as possible. The first EKG should be performed within 10 minutes of arrival and patient must be prepped and in the cardiac catheterization lab within 30-60 minutes after admission!
? Nursing diagnoses: Impaired tissue profusion, acute pain, anxiety, activity intolerance
Pathophysiology
What is a Myocardial Infarction?
A myocardial infarction, also known as a “heart attack,” occurs when the heart fails to receive adequate oxygen as a result of an occlusion in the coronary arteries. Blood supply is cut off to the vasculature above the occlusion. This can result in tissue necrosis if not rapidly corrected. Early treatment and rapid identification is imperative to minimizing damage to the heart and preventing disability and death.
Etiology
Non-Modifiable Risk Factors
There are various causes of MI. Heart and vascular conditions, such as atherosclerosis and congestive heart failure, predisposition the patient to having a MI. Risk factors can be divided into modifiable (controllable) and non-modifiable (those beyond the patent’s control) categories.
Modifiable Risk Factors
? Hypertension
? Stressful lifestyle
? Smoking
? Poor diet
? Sedentary lifestyle
Non-Modifiable Risk Factors
? Family history: Genetic predisposition from family history of MI’s and heart disease
? Age: Risk increases with age
Clinical Manifestations
In the male population, common symptoms include crushing chest pain that radiates to the left arm and lower jaw. Women tend to present with a different pattern of symptoms. They may experience pain that originates in the neck radiates into the shoulder region along with symptoms similar to gastrointestinal reflux disease (GERD) such as heartburn and nausea. In the early phase, the blood pressure is low and the pulse is bradycardic. Shortness of breath, hypoxemia, and tachypnea are also common.
Atypical Symptoms in Women
? Fatigue and sleep disturbance
? Shortness of breath
? Chest pain, back pain, upper abdominal or epigastric pain
? Nausea with or without vomiting
Cardiovascular Symptoms
? Hypotension: Inflow and outflow is impeded by the obstruction.
? Bradycardia and weak/irregular pulse: The obstruction leads to cellular ischemia and necrosis (if prolonged), which alters the alters the heart’s rhythm and causes the rate to be bradycardic.
? Oxygen saturation: The blockage in the coronary arteries impairs profusion to the myocardium, resulting a low oxygenation saturation (Note: Low oxygen saturation can also be a respiratory symptom but it’s included here in the cardiovascular category as the origin is cardiovascular).
Respiratory Symptoms
? Shortness of breath (SOB): Occurs from decreased cardiac output. With less oxygenated blood in circulation, the lungs attempt to compensate, which causes respirations to be labored and distressed.
? Lungs clear upon auscultation: The clarity of lung sounds rule out respiratory pathologies as the origin of the current event.
Complications of the Anterior Wall MI
? Life-threatening dysrhythmias
? New systolic murmur at the apex
? Tissue necrosis
? Death
Diagnostics
Orders to Obtain from the Provider
? Complete blood count (CBC) and comprehensive metabolic panel (CMP)
? Cardiac enzyme panel
? Lipid panel
CBC and CMP
? CBC: Includes red blood cell (RBC) count, hemoglobin (Hgb) and hematocrit (Hct). RBC, Hgb, and Hct will usually be decreased. White blood cell (WBC) count with differential: Leukocytosis may appear within 2 days of the initial event due to the inflammatory response of the myocardial tissue.
? CMP: Electrolytes are a major focus. The serum potassium may be lowered.


Cardiac Enzyme Panel
? Troponins: Troponin 1 (cTnl) and Troponin (cTn): This level will be increased within 3-4 hours following the infarction. The troponins are the most reliable indicator of myocardial damage (damage to the heart muscle).
? Creatine kinase (CK): CK and its isoenzyme CK-MB are released in response to damaged tissue. CK level will be elevated with 3-4 hours following the myocardial event, peak at 12-24 hours, and stabilize within 72-96 hours. These levels will determine the extent of damage to the myocardium and also help zone in on the timing
? Myoglobin: Levels will increase within 1-3 hours, peak in 4-12 hours, and return to normal levels following 12 hours. This value is not specific to myocardial infarctions as it’s more of a general indication of muscle damage (not limited to the heart muscle), but a negative result can help rule out MI.
Lipid Panel
? Lipid Profile: Since patients with an MI often have underlying cardiac damage, anticipate the LDL to be high and HDL to be low.
? Triglycerides may be elevated and overall cholesterol will usually be high.
Treatment
Goals of Treatment
The primary goals of immediate interventions are to decrease the myocardial workload while increasing the available oxygenation. Rapid identification and actions will minimize the damage caused to the heart muscle and reduce tissue necrosis. Chances of survival are increased and long-term disabilities are reduced if tissue necrosis can be prevented or minimized!
Immediate Interventions
? Obtain vitals
? Establish venous access
? Administer medications (oxygen, nitroglycerin, aspirin, morphine, ACE-inhibitor)
? Draw labs
? EKG.

MONA
The “MONA” mnemonic represents the 4 priority interventions for patients suspected to be experiencing a MI. these include morphine, oxygen, nitroglycerin, and aspirin. Keep in mind that while MONA is helpful, it doesn’t actually represent the correct order or prioritization of the interventions. The mnemonic that correctly represents the order of actions is ONAM. This can be remembered by On A.M. (as is I work in the mornings: I am ON in the A.M. shift, or I am totally a morning person- I am ON in the A.M.).
Oxygen is always given first, allegedly because it’s the most important (personally, I suspect it may also be because it’s the fastest, but never think this on a NCLEX exam!) Nitro is given next in order to dilate the vessels, making it a matter of increased space. Aspirin helps disaggregate the platelets with the goal of clot reduction and prevention of additional ones. Morphine reduces pain and anxiety, which will in turn assist with the psychosocial aspects that contribute to the tachypnea, thereby reducing the oxygen demand.
MONA
O: Administer oxygen: by means of nasal cannula or face mask, oxygen administration provides more concentration for myocardial uptake in order to promote tissue profusion to meet metabolic demands. It can also decrease the discomfort associated with tissue ischemia and prevent additonal damage.
? N: Administer Nitroglycerin, IV: Nitro has a vasodilation effect, which promotes perfusion and lowers the myocardial workload and oxygen demand.
? A: Administer Aspirin: this works by inhibiting platelet activity and interrupts aggregation at the rupture site, thrombolysis
? M: Administer morphine: this relaxes the endothelial lining and promotes profusion of the heart tissue by reducing the myocardial workload. It also controls pain and reduces the risk of developing life-threatening dysrhythmias and other complications.
Nursing Care Planning
Nursing Assessment
? Assess vitals, including pain, frequently in the early phase of treatment and recovery
? Monitor cardiovascular function for dysrhythmias with an EKG (remember: the first EKG should be performed within 10 minutes of arrival)
? Heart sounds should be assessed for the emergence of a new murmur
? Once stable: Collect data from the patient about comorbidities, including hypertension, smoking, and family history or heart disease and MI’s. Inquire about stress levels, such as work-related and personal stressors.
Nursing Diagnoses
? Impaired tissue profusion
? Acute pain
? Anxiety
? Activity intolerance
Nursing Interventions
? Impaired tissue profusion related to issue ischemia secondary to coronary artery occlusion as evidenced by patient report of chest pain, EKG readings, restlessness, and changes in level of consciousness
? Acute pain: Assess pain levels and administer medications as ordered. Instruct patient to do relaxation techniques, including deep and slow breathing, distraction behaviors, visualization, and guided imagery. Assist as needed
? Anxiety: Administer medications as ordered (or via protocol per policy), including supplemental oxygen. Enhancing oxygenation may relieve anxiety associated with hypoxia
? Activity intolerance: Assess tolerance levels for activity. Cluster care activities to provide periods of uninterrupted tasks. Instruct patient to reserve energy as possible by spacing out activities
Discharge Preparation: Medication Management
? The medication regimen the patient will need must be established prior to discharge
? The provider uses the nurse’s assessment findings to determine what medications to prescribe
Possible Medication Regimen
? ACE Inhibitor: Maintains blood pressure within optimal range and promotes vascular health by reducing cardiac workload. This prevents (or slows down the process of) ventricular remodeling and reduces the risk of future cardiac events
? Beta-blockers: Maintains blood pressure within optimal range. Common beta-blockers include atenolol (Tenormin), pindolol (Visken), propranolol (Inderal), nadolol (Corgard), and metoprolol (Lopressor)
? Aspirin: A low daily dose reduces the risk of subsequent cardiac events
? A different antiplatelet agent, such as sclopidogrel (Plavix), may be given instead
? Nitroglycerin: A vasodilator that’s ordered as a sublingual tablet for the patient to use at home in the event of chest pain related to angina
? SSI: May be added to assist the patient in controlling stressors, such as ones that are work-related
? Welbutrin or Chantix: For smoking cessation, as smoking is a known risk factor for MI
Important Teaching Principles
Following a MI, it’s important to educate patients on reducing preventable risks factors. This include smoking cessation, weight control, stress reduction, dietary changes, reducing LDL while keeping HDL high, and lowering blood pressure