Myocardial Infarction Flashcards
Myocardial Infarction (Acute Coronary Syndrome)
limited blood supply to the myocardial tissue resulting in necrosis
Characteristics:
- Unstable angina
- Non ST elevation myocardial infarct (NSTEMI)
- ST elevation myocardial infarct (STEMI)
Etiology
- Blockage in the coronary artery from CAD
- Coronary spasms (vasospasms) from illicit drug use like cocaine, which causes constriction of the coronary artery and stop blood flowing to the heart muscle
- Blood loss from anemia
- Increases in oxygen demand and supply as with thyrotoxicosis and cocaine use
(-) manifested by increased heart rate
Pathophysiology
- Development of the unstable plaque that ruptures and forms a thrombus
- Broken pieces of this unstable plaque can circulate in the blood, reaching the heart and creating an obstruction which can also result from a spasm, constriction, dysfunction or adrenergic stimuli
- Severe narrowing of the coronary lumen
- Ischemia results from the coronary artery being starved of oxygen because of the obstructed artery
What happens after an MI?
Early signs
- No physical changes to heart muscle until 6 - 8 hours
- When myocytes die, cardiac enzymes are released - CK-MB, troponin and myoglobin
24 - 36 hours
- Inflammation sets in and neutrophils come on the scene and congregate at the damaged tissue site
- Within 24 hours, heart fails to pump efficiently (cardiogenic shock) and arrhythmias can develop
10 days
- Macrophages arrive to the site to clean up dead cells
- New tissue formed from granulation is not well formed and is weak, increasing changes of cardiac rupture
2 months
- Scarring occurs, heart size and functionality is affected due to increased collagen
Clinical Manifestations
“CRUSHING”
- Chest pain
- Radiating chest pain that goes to left arm, jaw, back
- Unrelieved by nitroglycerin or rest
- Sweating
- Hard to breath (SoB)
- Increased heart rate, blood pressure or irregular heart rate
- Nausea with vomiting
- Going to be anxious and scared
Diagnostic tests
BLOOD TESTS
- Troponin: Protein released from the heart when damage is present
- Myoglobin: Early cardiac marker released after heart injury
- CK- MB (creatine kinase): form of enzyme released when their is muscle damage to the heart specifically
OTHER TEST:
- Echocardiogram
- Heart Cath
- Stress test
- ECG (Obtain a 12 lead ECG ASAP)
What are the roles of medical treatment
- Reduce cardiac damage
- Preserve myocardial function
- Prevent complications
Pharmacology treatment
Acute Angina Means Nasty Artery Blockages And Cardiac Complications
- Antithrombotic agents
- Antiplatelet e.g., Aspirin (162- 325mg) or Plavix (Clopidogrel)
- Morphine
- Nitrates
- ACE inhibitors
- Beta blockers
- ARBs receptors
- Cholesterol lowering medications
- Calcium channel blockers
Cardiac rehabilitation 1
- Diagnosis of atherosclerosis
- Education lifestyle changes
- Early low level mobilization
- Medication
Cardiac rehabilitation 2
- Last about 4-6 weeks 6 months
- Scheduled visits
- Monitored ECG exercise programmes ( stress tests)
- Support programmes
- Lifestyle changes
Cardiac rehabilitation 3
- The patient is usually stable in this stage
- Knows signs and symptoms and can manage lifestyle
Nursing Diagnosis
- Ineffective tissue perfusion
- Risk for imbalances tissue perfusion
- Fluid volume deficit
- Death and Anxiety
- Deficient Knowledge
Complications
- Acute pulmonary edema
- Heart failure
- Cardiogenic Shock
- Dysrhythmias and cardiac arrest
- Cardiac tamponade
- Pericardial effusion
Nursing Intervention
Relieving pain - Oxygen @ 2 - 4 l/min - Monitor vital signs - Bed rest (-) Elevate the HOB (-) Venous return to the heart decreases
Improving respiratory function
- Oxygen administration
- Chest auscultation
- Monitor cyanosis
- Pursed lip breathing
Promoting Adequate tissue function
- Vital signs
- Checking skin temperature
- Monitoring pulses
Patient teaching
- Avoid activity that brings on symptoms
- Avoid extremes of heat and cold
- Lose weight
- Stop smoking, avoid second hand smoke
- Develop positive coping methods
- Modify diet