2. Myocardial Infarction (MI)
Introduction
• Commonly known as “Heart Attack”
results in death of heart muscle
• Occurs from partial or complete blockage
of coronary artery which decreases blood
supply to cells of heart
• Cardiac conduction, blood flow and
cardiac functions altered by MI
3. Definition
• It is necrosis of myocardium due to
insufficient oxygen and blood supply in the
myocardium leading to damage or death of
heart muscle tissue ( Myocardium).
4.
5. Etiology
• Reduced blood flow in coronary artery due
to atherosclerosis
• Complete occlusion of an artery by an
embolus or thrombus
• Sudden narrowing (vasospasm of coronary
artery)
• Acute coronary thrombosis
• Severe coronary artery disease
• Precipitate thrombus formation
• Spasm of coronary artery
• Coronary artery embolism
6. • Infectious disease causing arterial
inflammation, hypoxia
• Acute blood loss (anaemia)
• Severe exertion or stress on the heart
• Necrosis of heart muscle surrounding area.
• Inflammed and injured
• Intramural haemorrhage into atheromatous
plaques
7.
8. Risk Factors
Non-modifying factors
• Family History: Due to combination of
shared genetic, environmental and life style
factors
• Age and sex: MI is highest among white
and middle age men. However this gender
difference disappears rapidly after
menopause.
9. Risk Factors
Modifying factors
•Smoking: Nicotine in cigarette smoking causes
epinephrine and norepinephrine release
• Hypertension: Stress of constantly elevated
blood pressure increases rate of atherosclerotic
development
• Hypercholesterolemia: Risk of MI associated
with serum cholesterol level of >200mg/dl. Low
density lipoprotein (LDLs) contain more
cholesterol and have affinity for arterial wall
10. Risk Factors
• Diabetes Mellitus: Person with diabetes have
increased tendency of connective tissue
degeneration and this account for atheroma
development
• Physical Inactivity: Physically active people
have increased HDL levels and exercise enhances
fibrinolysis activity thus reducing risk of clot
formation
11. Risk Factors
• Obesity: Obese person are thought to produce
increased levels of LDL and triglycerides which
are strongly implicated in atherosclerosis
• Stress: Stress induced mechanism stimulate
sympathetic nervous system causing increased
release of epinephrine and norepinephrine. This
stimulation influences heart by increasing heart
rate and intensifying force of myocardial
contraction.
12. Pathophysiology
• Coronary artery embolism, coronary thrombosis,
coronary artery blockage, coronary artery disease
Decreased blood supply to the heart
Myocardial cells deprive of oxygen
Prolonged decreased blood supply lead to infraction
and than ischemia of myocardium muscles
13. Necrosis or death of cells
Myocardial Infraction
Chest pain, syncope, diaphoresis, Shortness
of breath, tachypnea and confusion
14. Clinical Manifestation
Chest pain:
• Severe immobilizing chest pain not relieved
by rest, position change or nitroglycerine
administration
• Persistent: Heaviness, pressure, burning,
constricting or crushing
• Sub sternal, retrosternal or Epigastric pain
• May radiate to neck, jaw, shoulders and inner
aspects upper arm usually left arm
• Duration: more than 30 min.
• Severity is more then angina
15.
16. Clinical Manifestation
Cardiovascular
• Increased Jugular Venous pressure
• Elevated blood pressure in sympathetic
stimulation or decreased blood pressure in
decreased myocardial contractility
• ECG may show tachycardia, bradycardia
or dysrhythmia
• Breathlessness/ Restlessness
• Syncope, collapse(arrhythmias)
18. Clinical Manifestation
Skin
• Cool, clammy skin, diaphoresis and pale due to
sympathetic stimulation
Neurologic
• Anxiety, restlessness and light headedness due to
decrease cerebral oxygenation
• Fear and anxiety of impending death
Psychological
• Disorientation
• Confusion
• Irritability
• Fainting marked weakness
19. Diagnostic Investigation
Patient History
• Patient history has two parts:
I. Description of presenting symptoms
II. History of previous illnesses and family history
Electrocardiogram (ECG)
• ECG should be obtained within 10 minutes from
time patient reports pain or arrives in emergency
department
20. Diagnostic Investigation
• As area of myocardial injury becomes
ischemic, myocardial repolarization is
altered and delayed causing the T wave to
invert
• Ischemic region may remain depolarized
while adjacent areas of myocardium return
to resting state
22. Diagnostic Investigation
• Injured myocardial cells depolarize normally but
repolarize more rapidly than normal cells,
causing ST segment to rise
• Elevation in ST segment in two contagious leads
is key diagnostic indicator of MI
24. Diagnostic Investigation
Cardiac Biochemical Markers:
Creatinine kinase and its isoenzymes (CK-MB).
Myoglobin
Troponin I and T
Lactic hydrogenous (LDH)
AST
Other Blood tests
Leucocytosis reaching peak on first day
Erythrocyte sedimentation rate (ESR) becomes raised
and remain so for several days
ABG
C-reactive protein (CRP) is elevated
25. Diagnostic Investigation
Cardiac angiography( Cardiac Catherization)
Chest X-Ray PA View
Echocardiogram
• Used to evaluate ventricular function
• Detect hypokinetic and akinetic wall motion and
can determine ejection fraction
26. Medical Treatment Guidelines
• Use rapid transit to hospital
• Obtain 12 lead ECG to be read within 10 minutes
• Obtain laboratory blood specimens of cardiac
biomarkers including troponin
• Obtain other diagnostics to clarify the diagnosis
Begin routine medical interventions
• Supplemental oxygen
• Nitroglycerin
• Morphine
• Aspirin
• Beta blockers
• Angiotensin converting enzyme inhibitor within 24
hours
27. Medical Treatment Guidelines
Evaluate for indications of reperfusion therapy
• Percutaneous coronary intervention
• Thrombolytic therapy
Continue Therapy as indicated
• Intravenous heparin
• Clopidrogel
• Bed rest for minimum of 12 to 24 hours
28. Thrombolytic
Purposes:
• To dissolve and lyse the thrombus in a coronary
artery (thrombolysis)
• To allow blood to flow through the coronary
artery (reperfusion)
• To minimize size of infarction
• To preserve ventricular function
29. Thrombolytic
Indication
• Chest pain for longer than 20 minutes,
unrelieved by nitroglycerin
• ST segment elevation in at least two ECG
leads
• Less than 6 hours from onset of chest pain
30. Thrombolytic
Thrombolytic Agents
• Streptokinase 1.5 million U in 100ml saline given
as intravenous infusion over 1 hour
• Alteplase, a tissue plasminogen activator (t-PA)
which activates plasminogen present on blood
clot, an IV blous is administered followed by
infusion
• Reteplase, a newer recombinant thrombolytic,
similar to alteplase, administered in two bolus
31. Thrombolytic
Nursing Consideration
• Minimize number of times the patient’s skin is
punctured
• Draw blood for laboratory test when starting IV
line
• Avoid continuous use of noninvasive blood
pressure cuff
• Check for signs of bleeding
32. Analgesics
• Morphine sulphate is administered to reduce pain
and anxiety
• It decreases workload of heart
• It relaxes bronchioles to enhance oxygenation
• Cardiovascular response should be monitored:
Blood pressure can decrease and respiratory rate
can be depressed
34. Anticoagulants
• Subcutaneous heparin (12500 U twice day)
may prevent reinfarction after successful
thrombolysis
• Intravenous heparin should be given for
48-72 hours following thrombolysis
36. Nitroglycerin
• Vasoactive agent that dilates veins causing venous
pooling of blood in body resulting in less blood
flow to heart
• IV infusion of nitroglycerin is not administered if
systolic blood pressure is <90 mm Hg
37. Medical Management
• MONATAS Or MONATAL
• M: Morphine 5-10 mg IV
• O: oxygen Therapy
• N: Nitroglycerine ( Nitrates) 300-500 mg
sublingually
• A: Aspirin 75-300 mg (Antiplatelet Therapy).
Ateplase 15 mg bolous, then followed by 0.75
mg/kg body weight over 30 min.
(Antithrombotics), Atenolol 5-10 mg IV than
oral for long term survival ( B-blocker).
38. • T: Thrombolytic agent ( Streptokinase 1.5
million unit in 100 ml NS over 1 hours.
• A: Anti coagulant, Subcutaneous heparin
(LMWH)
• S: Stool softener or L: Laxative
39.
40.
41. • Maintain ABCDE and give oxygen therapy
• Monitoring ECG contineously
• IV line should be open and collect blood sample
• Monitoring vital signs 2 hourly
• Pain control GTN 300- 500 mg sublingually
• Inj. Morphine 5-10 mg IV
• Inj. Ondecetron 4 mg IV before Morphine
administration
• Inj. Pantoprazole for stress ulcer
• Give low salt diet, low fat and low cholesteral
diet
• Patient should be connect with cardio monitoring
• Patient keep on Propped up position
44. Surgical Management
Advantages of PCI
• Provides an alternative to surgical intervention
• Performed with local anesthesia
• Patient is ambulatory 24 hours after procedure
• Length of hospital stay is approximately 1 to 3
days
• Rapid return to work (approximately 5 to 7 days
after PCI)
45. Life Style Modifications
• Do not smoke
• Maintain ideal body weight
• Take regular exercise (minimum of 20
minutes, three times a week)
• Eat diet containing fruits and vegetables
• Eat less cholesterol containing diet
• Achieve good control of hypertension
46. Nursing Diagnosis
• Acute chest pain related to imbalance between
oxygen supply and demand secondary to reduced
coronary blood flow
• Decreased cardiac output related to decreased
cardiac contractility and changes in heart rate
• Activity intolerance related to fatigue secondary
to insufficient oxygenation
47. Nursing Management
Nurses should obtain subjective data on:
Important Health information
• Past health history: Previous MI, diabetes,
hypertension, smoking
• Medications: Use of nitrates, calcium blockers,
antihypertensive medications
48. Nursing Management
Functional health pattern
• Family history of heart disease
• Nutritional-metabolic: Nausea, vomiting,
indigestion, heartburn
• Activity-exercise: Profound weakness, dyspnea
• Cognitive-perceptual: Severe sub sternal pain,
lasting more than 30 minutes
• Coping-stress tolerance: Persistent stress
49. Nursing Management
Chest pain documentation should include
following:
• Type, location and pain radiation to other areas of
body
• Vital signs, skin color and temperature
• Presence of dyspnea, labored respirations,
diaphoresis or nausea
51. Prognosis
• In almost one quarter of all cases of MI, death
occurs within a few minutes without medical
care.
• Half death occurs within 24 hours of onset of
symptoms
• 40% of all affected patients die within first month
• Prognosis of those who reach hospital is better
with 28 day survival of more than 80%
52. Prognosis
• Prognosis is worse for anterior wall infarction
than for inferior wall infarction
• Bundle branch block and high enzyme levels both
indicate extensive myocardial damage
• Old age, depression and social isolation are
associated with higher mortality
• Those who survive an acute attack more than 80%
live for a further year, 75% for 5 years, 50% for
10 years and 25% for 20 years.
53. Health Education
• Have regular blood pressure check ups and take
prescribed medications for BP control
• Reduce animal fat intake and adjust total caloric
intake to maintain ideal body weight
• Stop smoking
• Exercise regularly and maintain routine physical
activity that is done at least three or four times a
week
54. Health Education
• Alter patterns that are conducive to stress and
rushing (e.g. get up 30 minutes earlier so
breakfast is not eaten on the way to work)
• Avoid large and heavy meals
• For patient with diabetes mellitus monitor blood
glucose levels regularly and follow recommended
diet
• Gradually and progressively resume physical
activity