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Sushila Hamal
BNS
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
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).
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
• 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
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.
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
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
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.
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
Necrosis or death of cells
Myocardial Infraction
Chest pain, syncope, diaphoresis, Shortness
of breath, tachypnea and confusion
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
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)
Clinical Manifestation
Respiratory
• Shortness of breath
• Tachypnea
• Crackles
• Pulmonary edema
Gastrointestinal
• Nausea and vomiting
• Indigestion
• Abdominal discomfort
Genitourinary
• Decreased urinary output
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
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
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
Diagnostic Investigation
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
Diagnostic Investigation
Fig. Electrocardiogram: ST elevation in Myocardial Injury
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
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
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
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
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
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
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
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
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
Antiplatelet Therapy
Anticoagulants
• Subcutaneous heparin (12500 U twice day)
may prevent reinfarction after successful
thrombolysis
• Intravenous heparin should be given for
48-72 hours following thrombolysis
Beta - adrenergic blocking agents
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
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).
• 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
• 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
Surgical Management
Percutaneous Coronary Intervention
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)
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
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
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
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
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
MI Care
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%
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.
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
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
Complications
• Rhythm disturbances
• Pericarditis
• Cardiac failure
• Cardiac rupture
• Cardiogenic shock
• Ventricular mural thrombus
• Thromboemboli
• Cardiac temponade
• Ventricular aneurysm
• Ischemic cardiomyopathy
• Psychiatric problems :- Depression
Myocardial infraction sushila

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Myocardial infraction sushila

  • 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)
  • 17. Clinical Manifestation Respiratory • Shortness of breath • Tachypnea • Crackles • Pulmonary edema Gastrointestinal • Nausea and vomiting • Indigestion • Abdominal discomfort Genitourinary • Decreased urinary output
  • 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
  • 23. Diagnostic Investigation Fig. Electrocardiogram: ST elevation in Myocardial Injury
  • 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
  • 35. Beta - adrenergic blocking agents
  • 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
  • 55. Complications • Rhythm disturbances • Pericarditis • Cardiac failure • Cardiac rupture • Cardiogenic shock • Ventricular mural thrombus • Thromboemboli • Cardiac temponade • Ventricular aneurysm • Ischemic cardiomyopathy • Psychiatric problems :- Depression