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Myocardial Infarction

Myocardial infarction, also known as a heart attack, is caused by prolonged ischemia from an imbalance of oxygen supply and demand that causes irreversible cell damage and muscle death. It occurs when there is atherosclerosis of the coronary arteries leading to plaque rupture and thrombus formation, blocking blood flow. The location and type of infarction is determined by the occluded artery. Symptoms include chest pain and diagnostic tests involve ECGs and cardiac biomarker levels. Treatment focuses on reperfusion through fibrinolysis, percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG). Goals of nursing care are to manage pain, maintain hemodynamic stability, and promote activity tolerance.

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0% found this document useful (0 votes)
556 views8 pages

Myocardial Infarction

Myocardial infarction, also known as a heart attack, is caused by prolonged ischemia from an imbalance of oxygen supply and demand that causes irreversible cell damage and muscle death. It occurs when there is atherosclerosis of the coronary arteries leading to plaque rupture and thrombus formation, blocking blood flow. The location and type of infarction is determined by the occluded artery. Symptoms include chest pain and diagnostic tests involve ECGs and cardiac biomarker levels. Treatment focuses on reperfusion through fibrinolysis, percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG). Goals of nursing care are to manage pain, maintain hemodynamic stability, and promote activity tolerance.

Uploaded by

Odai AL Karkii
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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MYOCARDIAL INFARCTION

Definition
Myocardial infarction ( Heart Attacks ) : Prolonged ischemia caused by an
imbalance between oxygen supply and oxygen demand , causes irreversible cell
damage and muscle death

Pathophysiology
MI patients have coronary atherosclerosis

- endothelial damage ( HTN / smoking ) fatty substances, cholesterol, cellular


waste products deposited in the inner lining of an artery >> lipid plaque builds up
>> Plaque rupture >> thrombus formation result in complete occlusion of the
artery >> leading to ischemia and necrosis of the myocardium supplied by that
artery

Irreversible damage to the myocardium can begin as early as 20 to 40


minutes after interruption of blood flow

Type of Infarction
1- ST-segment elevation

 Q-wave MI
 non–Q-wave MI

2- without ST-segment elevations

 unstable angina
 NSTEMI
Location of the Infarction
1- ANTERIOR LEFT VENTRICLE / interventricular septum
 occlusion of the left anterior descending (LAD)
 high risk for heart failure, pulmonary edema, cardiogenic shock , bundle branch blocks
 V 1 through V 4 , Q waves and ST-segment elevation
2- LATERAL AND LEFT VENTRICLE
 occlusion of the left circumflex vessel
 risk for dysrhythmias of SA or AV nodes (sinus arrest)
 I, aVL, V 5 , and V 6 , Q waves and ST-segment elevations ( lateral
wall )
3- POSTERIOR LEFT VENTRICLE
 occlusion of the left circumflex vessel
 V1 and V 2, tall upright R waves with ST-segment depression; Q waves and ST-
segment elevation in V 7 through V9 ( posterior wall )

4- INFERIOR LEFT VENTRICLE


 occlusion of the right coronary artery
 dysrhythmias caused by SA and AV node dysfunction
 Q waves and ST-segment elevation in II, III, aVF
5- RIGHT VENTRICLE

 occlusion of the right coronary artery


 Q waves and ST-segment elevations in right precordial chest leads
(RV 1 through RV 6)

Assessment
- Chest pain

2
 Persistent and crushing sub sternal pain that may radiate to the left arm, jaw,
neck, or shoulder blades. Pain is usually described as heavy, squeezing, or
crushing

- Pain unrelieved by rest or sublingual nitroglycerin

- N/V, diaphoresis, dyspnea, weakness

Physical Examination
- Hypertension, and tachycardia from increased sympathetic tone

- Hypotension and bradycardia from increased vagal tone

- Pulse may be irregular and fain

Auscultation
 S3 and S4 is heard
 crackles , rhonchi in (heart failure or pulmonary edema )

Diagnostic Tests
- ECG
- Biochemical Marker
 Troponins (T/ I ) are released into the circulation after necrosis
 cTnI and cTnT are highly specific to cardiac tissue
 TnI 3 to 12 hours, remain for 5 to 10 days
 TnT 3 to 12 hours, remain for 5 to 14 days
-Angiocardiography MRI, myocardial perfusion imaging, PET, CT

Management
Early Management (ER): Patient with STEMI

1- Administer aspirin

2- Recording 12-lead (ECG), ST-segment elevations of 1 mm


3
3- Give oxygen by nasal cannula

 Hypoxemia because of pulmonary edema

4- Administer sublingual nitroglycerin

 Give 0.4 mg every 5 minutes for a total of three doses


 promote vasodilation

5- Morphine sulfate

 drug of choice to relieve the pain of an MI


 (2 to 4 mg) and can be repeated every 5 m

6- Administer β-blocker within the first 24 h

 diminish myocardial oxygen demand

7- (ACE) inhibitors lower BP

PERCUTANEOUS CORONARY INTERVENTION (PCI)


 STEMI with symptom onset within the prior 12 hours
 reestablish blood flow to ischemic myocardium

PTCA
 coronary artery is dilated with a balloon catheter , a stent may be placed
in the artery
 Aspirin and clopidogrel are given to the patient before the primary PCI

FIBRINOLYTIC THERAPY
- By converting plasminogen to plasmin >> degradation of fibrin and fibrinogen,
resulting in clot lysis

Indication:
 given to the patient with STEMI within the previous 12hours
 when PCI cannot be performed within 120 minutes
4
Administration:
- Two 18-gauge peripheral IV lines

- One line is for the fibrinolytic agent, second line for other drugs

- Subclavian and jugular sites are avoided

- assesses the patient for resolution of chest pain

- Normalization of elevated ST

- Development of reperfusion dysrhythmias

- Evidence of bleeding

Complications
1. Cardiogenic shock 6. Acute Kidney Injury
2. Recurrent MI 7. Mitral regurgitation
3. Heart failure 8. pericarditis
4. Dysrhythmia Complications ( V tach ,VF )
5. Ventricular septal rupture

NURSING PROCESS
NURSING Dx:
1- Acute pain RT tissue ischemia (coronary artery occlusion) AMB
 Reports of chest pain with/without radiation
 changes in level of consciousness
 Changes in pulse, BP

Goal: Verbalize relief/control of chest pain


5
Intervention Rationale
Monitor and document characteristic of Patients with an acute MI appear ill,
pain and BP or heart rate changes. distracted, and focused on pain
Catecholamines increases heart rate and
BP. Stress

Instruct patient to do relaxation Decreases external stimuli, which may


techniques : deep and slow breathing aggravate anxiety and cardiac strain
quiet environment, calm activities,

Antianginals: nitroglycerin increase coronary blood flow and myocardial


perfusion

Beta-blockers educing heart rate, systolic BP, and


myocardial oxygen demand

Analgesics: morphine reduce severe pain, provide sedation, and


decrease myocardial workload

2- Risk for decreased Cardiac Output RT


 Altered heart rate/rhythm
 Reduced preload
 Altered contractility—infarcted or dyskinetic muscle

Goal: Maintain hemodynamic stability, BP, cardiac output within normal rang,
absence of dysrhythmias

Intervention Rational
Inspect for pallor, cyanosis, and cool or Systemic vasoconstriction resulting from
clammy skin diminished cardiac
output

Auscultate breath sounds. Crackles reflect pulmonary congestion

6
Auscultate heart sounds: S3 is usually associated with heart failure
S3 and S4 S4 is an finding during the early stages of
acute MI

frequent BP readings Hypotension may occur related to


ventricular dysfunction
Monitor output, noting changes in urine Decreased output may reflect systemic
output perfusion problems and
may reflect heart failure

Administer supplemental oxygen, as to maintain oxygen saturation >90% to


indicated prevent hypoxemia

Review serial ECGs Provides information regarding progression


or resolution of infarction

Review chest x-ray May reflect pulmonary edema related to


ventricular dysfunction

Administer Antidysrhythmic drugs , Beta


blockers , (ACE) inhibitor

3- Activity Intolerance RT Imbalance between oxygen supply and demand

AMB Reports fatigue; exertional discomfort

Goal: Demonstrate increase in tolerance for activity with heart rate and rhythm, BP
within client’s normal limits

Intervention Rational
Document heart rate and rhythm and Trends determine client’s response to
changes in BP before, during, and after activity and may indicate
activity ,Correlate with reports of chest pain myocardial oxygen deprivation
or shortness of breath

7
Instruct patient to avoid increasing Activities that require holding the breath
abdominal pressure (straining during and bearing down, such as Valsalva’s
defecation) maneuver. reduced cardiac output

Encourage bedrest to chair rest , limit Reduces myocardial workload and oxygen
activity on basis of pain or adverse cardiac consumption
response

Explain pattern of graded increase of activity Progressive activity provides a controlled


level, such as sitting in chair demand on the heart and preventing
overexertion

Review signs and symptoms reflecting Palpitations, pulse irregularities,


intolerance of present activity development of chest pain, or dyspnea

Done BY Suhaib Allaham


8

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