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Acute MyocArdiAl
infArction
PPT MADE BY
DR RAJESH T EAPEN
Definition
• Otherwise know as heart attack
• An MI occurs when there is a diminished
blood supply to the heart which leads to
myocardial cell damage and ischemia.
• Contractile function stops in the necrotic
areas of the heart.
• Ischemia usually occurs due to blockage
of the coronary vessels.
Definition cont.
• This blockage is often the result of
thrombus that is superimposed on an
ulcerated or unstable atherosclerotic
plaque formation in the coronary artery.
• MI’s are described by the area of
occurrence.
• Anterior, Inferior, Lateral or Posterior.
Coronary Artery Anatomy
Coronary artery events
• Ischemia – Outer most area, source of
arrhythmias, viable if no further infarction.
• Injury – Viable tissue found between
ischemic and infarcted areas.
• Infarction/necrosis – Center area, dead
not viable tissue that turn into scar.
MI Classifications
• MI’s can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
• Transmural and Subendocardial
Diagnostic
• ST elevations (STEMI) and non ST
elevations (NSTEMI).
Epidemiology
• MI’s are the leading cause of death in the
United States, affecting one in five men
and one in six women.
• 450,000 people in the US die from
coronary disease each year.
• Incidence rates increase with age as do
mortality rates due to infarction.
Epidemiology
• The survival rate for those hospitalized
due to MI has reached approximately
95%.
• This is the result of the advancements
made in modern medical technology.
Risk Factors
• The presence of any risk factor is
associated with doubling the risk of an MI.
Non Modifiable
• Age
• Gender
• Family history
Risk Factors
Modifiable
• Smoking
• Diabetes Control
• Hypertension
• Hyperlipidemia
• Obesity
• Physical Inactivity
Smoking
• Tobacco use increases the risk of
coronary artery disease two to six times
more than non smokers.
• Nicotine increases platelet thrombus
adhesion and vessel inflammation.
Diabetes & Hypertension
• Diabetes not only increases the rate of
atherosclerotic formation in vascular
vessels but also at an earlier age.
• The constant stress of high blood
pressure has been associated with the
increased rate of plaque formation.
• Shearing Stress and inflammation of
endothelial lining begins the process.
Hyperlipidemia
• Elevated levels of cholesterol, LDL’s or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.
• Almost 50% of the
population has some
form of dyslipidemia.
Obesity and Physical Inactivity
• Mortality rate from CAD is higher in those
who are obese.
• Some evidence shows that those who
carry their weight in their abdomen have a
higher incidence of CAD
• Physically inactive people have lower HDL
levels with higher LDL levels and an
increase in clot formation.
Pathophysiology
• Ischemia develops when there is an
increased demand for oxygen or a
decreased supply of oxygen.
• Ischemia can develop within 10 seconds
and if it lasts longer than 20 minutes,
irreversible cell and tissue death occurs.
• Myocardial cell death begins at the
endocardium. The area most distal to the
arterial blood supply.
Pathophysiology
• As vessel occlusion continues cell death
spreads to the myocardium and eventually
to the epicardium.
• Severity of the MI depends on three
factors.
– Level of occlusion
– Length of time of occlusion
– Presence or absence of collateral circulation
Signs and Symptoms
• Signs and symptoms are unique to each
individual patient.
• Ranging from no symptoms to sudden
cardiac arrest.
Chest Pain
• The most common initial manifestation is
chest pain or discomfort.
• This is not relieved by rest, position
change or nitrate administration.
• Pain is described by heaviness, pressure,
fullness and crushing sensation.
• Not everyone experiences this sensation.
Chest Pain
• PQRST assessment for chest pain
• P- Precipitating events
• Q- Quality of pain
• R- Radiation of pain
• S- Severity of pain
• T- Timing
Nausea and Vomiting
• Not everyone will experience this.
• Vomiting results as a reflex from severe
pain.
• Vasovagal reflexes initiated from area of
ischemia.
Sympathetic Nervous System
Stimulation
• During an MI increased catecholamines
are released.
• This results in diaphoresis and
vasoconstriction of peripheral blood
vessels.
• “Cool Sweat” with a temperature increase
during the first 24 hours.
Cardiovascular Changes
• Initially the BP and pulse may be elevated.
• Later, BP will drop due to decreased
cardiac output.
• Urine output will decrease
• Lung sounds will change to crackles
• Jugular veins may become distended and
have obvious pulsations.
Video
http://www.youtube.com/watch?v=LUt1xXASm
https://www.youtube.com/watch?
v=T8zkvdkzU7A
Within the first 10 minutes upon
arrival to the hospital:
• Check vital signs and evaluate oxygen
saturation
• Establish IV access
• Obtain and review 12-lead ECG
• Take a brief focused history and perform a
physical exam
• Obtain blood samples to evaluate initial cardiac
markers, electrolytes and coagulation
Diagnostics
• After collecting patient health history, a
series of EKG’s should be taken to rule
out or confirm MI.
• 12 lead EKG’s can help to distinguish
between ST-elevation MI’s and Non-ST-
elevation MI’s.
Normal Sinus Rhythm
Angina
Stable
• Chest pain caused by the build up of lactic
acid and irritation to the myocardial nerve
fibers.
• Chest pain caused by the 4 E’s (Exertion,
Emotion, Exposure To Cold, Eating )
• Pain is usually relieved with rest, pain
meds and nitrates.
Variable/Prinzmetal/Spasm
• Transient ischemia that occurs
unpredictably and almost always at rest.
• Pain is caused by vasospasm of the
arteries.
• ST segment elevations will be noted.
Unstable
• Chest pain at rest or with exercise and
tends to last greater than 15 minutes.
• This results in reversible myocardial
ischemia but is a sign that an infarct is
soon to come.
• EKG will reveal ST segment depression
and T wave inversion.
STEMI
• ST segment elevations
• T wave changes
• Q wave development
• Enzyme elevations
• Reciprocals
NSTEMI
• ST segment depressions
• T wave changes
• No Q wave development
• Mild enzyme elevations
• No reciprocals
STEMI vs. NSTEMI
Phases of a STEMI
• Hyperacute Phase
– Occurs within the first few hours of MI onset.
– Leads facing the infarcted surface: ST
segment elevation.
– Leads facing the uninjured surface: ST
segment depression (reciprocals)
– T waves become tall, widened and might be
taller than the R wave.
Phases of a STEMI
• Fully Evolved Phase
– Q wave development
– ST elevation
– T waves start to become inverted in leads
facing the injury.
Phases of a STEMI
• Resolution phase
– Weeks after there will be a gradual return of
ST segments to baseline.
– T waves will gradually return to normal but are
the last to change back.
Serum Cardiac Markers
• Myocardial cells produce certain proteins
and enzymes associated with cellular
functions.
• When cell death occurs, these cellular
enzymes are released into the blood
stream.
• CPK and troponin
CPK
• Creatine Phosphokinase
• Begin to rise 3 to 12 hours after acute MI.
• Peak in 24 hours
• Return to normal in 2 to 3 days
Troponin
• Myocardial muscle protein released into
circulation after injury.
• These are highly specific indicators of MI.
• Troponin rises quickly like CK but will
continue to stay elevated for 2 weeks.
• Myoglobin-lacks cardiac specificity.
Serum Cardiac Markers
Treatment Options
• The immediate goal for any acute MI is to
restore normal coronary blood flow to
vessels and salvage myocardium.
• There are a variety of medical and
medicinal therapies to treat an MI.
General Treatment for the MI
patient
MONA
• Morphine
• Oxygen
• Nitroglycerin
• Aspirin
Fibrinolytic Therapy
• Indicated for patients with STEMI MI’s.
• Should be given within 12 hours of
symptom onset.
• Fibrinolytics will break down clots found
within the vessles
• Contraindications: post op surgical
patients, history of hemorrhagic stroke,
ulcer disease, pregnancy, ect.
Cardiac Catheterization
• A diagnostic angiography which includes
angioplasty and possible stenting.
• Performed by an interventional
cardiologist with a cardiac surgeon on
stand by.
• Percutaneous procedure through the
femoral or brachial artery.
Cardiac Catheterization
• Upon arrival to the cath lab all actue MI
patients will receive:
– A bolus dose of plavix
– IV Integrelin
– Heparin dose either subcu or IV drip
– Angiomax : a DTI may be substituted for
heparin and integrelin.
Coronary artery bypass graft
• Surgical treatment where saphenous vein
is harvested from the lower leg and used
to bypass the occluded vessels.
Long Term Care
• Smoking Cessation and lifestyle
modifications.
• Aspirin, Beta Blockers and Clopidogrel will
be indefinite.
• Lipid lowering medication along with diet
modifications.
Nursing Management
• Nursing interventions of a patient with angina focus on:
• Early identification of myocardial ischemia.
• Assess immediately any complaints of chest pain using a
pain scale of 0 – 10, as pain (or pressure or heaviness) is an
indicator of myocardial ischemia. Immediate assessment is
important for early identification and treatment.
• Document vital signs, ECG, skin color, peripheral pulses,
level of consciousness, and overall tissue perfusion.
• Control of chest pain.
• Administer oxygen, nitrates, and analgesia as ordered.
• Use pulse oximetry to guide therapy and maintain
oxygen saturation above 90%.
• Nursing interventions of a patient with angina focus on
(Continued…):
• Patient and family education
• Educate your patient when his/ her condition has stabilised
(pain controlled).
• Teach the patient about the importance of avoiding the
Valsalva maneuver (bearing down when going to bath room).
This maneuver increases intrathoracic pressure that
decreases venous return to the right side of the heart which
is associated with hypotension and bradycardia.
• Teach the patient about risk factor modifications such as
decreasing fat intake, stopping smoking, reducing salt intake,
controlling hypertension, increasing physical activity as
tolerated, and achieving normal body weight.
• Provide information about medications; indications and side
effects.
• Teach the patient about the importance of follow up after
discharge and how to handle emotional stress and anger.
Nursing Management of MI
• Nursing interventions for a patient with acute MI
focus on:
– Achieving a balance between myocardial oxygen
supply and demand: This means that in the acute
phase, there is a need to increase myocardial oxygen
supply by oxygen administration to prevent tissue
hypoxia. Myocardial oxygen supply can be enhanced
by the administration of coronary artery vasodilators
(nitroglycerin).
– Prevention of complications: Nurses need to apply
cardiac monitoring of patient to detect early
ventricular dysrhythmias. In addition, nurses should
continue to assess for signs of ischemic pain.
Nursing Management of MI (Continued…)
– Health education: Nurses should focus on:
• Pathophysiology of acute MI.
• Description of signs and symptoms such as pain.
pressure, or heaviness in chest.
• Notification of nurses of any changes in chest pain
intensity.
• Avoidance of the Valsalva maneuver.
• Risk factors modification, including:
– Daily fat intake < 30% of total calories.
– Maintain serum cholesterol level < 200 mg/dL.
– Maintain LDL cholesterol to < 70 mg/dL.
– Stop smoking and reduce daily salt intake.
– Control hypertension and diabetes mellitus.
– Increase physical activity and reduce weight
–
Nursing Management of MI (Continued…)
– Health education (Continued…): Nurses should focus
on:
• Medication teaching: indications and side effects.
• Follow-up care after discharge.
Myocardial infarction
Nursing process
Assessment
• A careful history
• Description of symptoms (chest pain,
palpitation, dyspnea, syncope or
sweating). Each symptom must be
evaluated with regard to time, duration,
precipitating & relieving factors. In addition
complete physical assessment for:
*level of consciousness
*Heart sounds
*Peripheral pulses
*Lung sound
Nursing process (cont…)
Nursing diagnosis
– Chest pain related to reduced coronary blood flow.
– High risk for breathing pattern ineffective related to
fluid overload
– Anxiety related to fear from death
– High risk for tissue perfusion alteration related to
decreased cardiac output
– Health maintenance alteration related to no adherence
to therapeutic regimen
Nursing process (cont…)
Nursing process (cont…)
Patient's goals
• Report that pain is decreased
• Breath effectively
• Experience less anxiety level
• Have improved tissue perfusion
• Adhere to the self care program
Nursing process (cont…)
Nursing intervention
•Relief or control of chest pain
•Alleviate respiratory difficulties
•Reduce the anxiety level
•Maintain adequate tissue
perfusion
•Help the patient to adhere to the
self care program
“THANK YOU” in French

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Acute Myocardial Infarction (AMI) Guide

  • 2. Definition • Otherwise know as heart attack • An MI occurs when there is a diminished blood supply to the heart which leads to myocardial cell damage and ischemia. • Contractile function stops in the necrotic areas of the heart. • Ischemia usually occurs due to blockage of the coronary vessels.
  • 3. Definition cont. • This blockage is often the result of thrombus that is superimposed on an ulcerated or unstable atherosclerotic plaque formation in the coronary artery. • MI’s are described by the area of occurrence. • Anterior, Inferior, Lateral or Posterior.
  • 5. Coronary artery events • Ischemia – Outer most area, source of arrhythmias, viable if no further infarction. • Injury – Viable tissue found between ischemic and infarcted areas. • Infarction/necrosis – Center area, dead not viable tissue that turn into scar.
  • 6.
  • 7.
  • 8. MI Classifications • MI’s can be subcategorized by anatomy and clinical diagnostic information. Anatomic • Transmural and Subendocardial Diagnostic • ST elevations (STEMI) and non ST elevations (NSTEMI).
  • 9. Epidemiology • MI’s are the leading cause of death in the United States, affecting one in five men and one in six women. • 450,000 people in the US die from coronary disease each year. • Incidence rates increase with age as do mortality rates due to infarction.
  • 10. Epidemiology • The survival rate for those hospitalized due to MI has reached approximately 95%. • This is the result of the advancements made in modern medical technology.
  • 11. Risk Factors • The presence of any risk factor is associated with doubling the risk of an MI. Non Modifiable • Age • Gender • Family history
  • 12. Risk Factors Modifiable • Smoking • Diabetes Control • Hypertension • Hyperlipidemia • Obesity • Physical Inactivity
  • 13. Smoking • Tobacco use increases the risk of coronary artery disease two to six times more than non smokers. • Nicotine increases platelet thrombus adhesion and vessel inflammation.
  • 14. Diabetes & Hypertension • Diabetes not only increases the rate of atherosclerotic formation in vascular vessels but also at an earlier age. • The constant stress of high blood pressure has been associated with the increased rate of plaque formation. • Shearing Stress and inflammation of endothelial lining begins the process.
  • 15. Hyperlipidemia • Elevated levels of cholesterol, LDL’s or triglycerides are associated with the increased risk of coronary plaque formation and MI. • Almost 50% of the population has some form of dyslipidemia.
  • 16. Obesity and Physical Inactivity • Mortality rate from CAD is higher in those who are obese. • Some evidence shows that those who carry their weight in their abdomen have a higher incidence of CAD • Physically inactive people have lower HDL levels with higher LDL levels and an increase in clot formation.
  • 17. Pathophysiology • Ischemia develops when there is an increased demand for oxygen or a decreased supply of oxygen. • Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes, irreversible cell and tissue death occurs. • Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supply.
  • 18. Pathophysiology • As vessel occlusion continues cell death spreads to the myocardium and eventually to the epicardium. • Severity of the MI depends on three factors. – Level of occlusion – Length of time of occlusion – Presence or absence of collateral circulation
  • 19. Signs and Symptoms • Signs and symptoms are unique to each individual patient. • Ranging from no symptoms to sudden cardiac arrest.
  • 20. Chest Pain • The most common initial manifestation is chest pain or discomfort. • This is not relieved by rest, position change or nitrate administration. • Pain is described by heaviness, pressure, fullness and crushing sensation. • Not everyone experiences this sensation.
  • 21. Chest Pain • PQRST assessment for chest pain • P- Precipitating events • Q- Quality of pain • R- Radiation of pain • S- Severity of pain • T- Timing
  • 22. Nausea and Vomiting • Not everyone will experience this. • Vomiting results as a reflex from severe pain. • Vasovagal reflexes initiated from area of ischemia.
  • 23. Sympathetic Nervous System Stimulation • During an MI increased catecholamines are released. • This results in diaphoresis and vasoconstriction of peripheral blood vessels. • “Cool Sweat” with a temperature increase during the first 24 hours.
  • 24. Cardiovascular Changes • Initially the BP and pulse may be elevated. • Later, BP will drop due to decreased cardiac output. • Urine output will decrease • Lung sounds will change to crackles • Jugular veins may become distended and have obvious pulsations.
  • 26. Within the first 10 minutes upon arrival to the hospital: • Check vital signs and evaluate oxygen saturation • Establish IV access • Obtain and review 12-lead ECG • Take a brief focused history and perform a physical exam • Obtain blood samples to evaluate initial cardiac markers, electrolytes and coagulation
  • 27. Diagnostics • After collecting patient health history, a series of EKG’s should be taken to rule out or confirm MI. • 12 lead EKG’s can help to distinguish between ST-elevation MI’s and Non-ST- elevation MI’s.
  • 29. Angina Stable • Chest pain caused by the build up of lactic acid and irritation to the myocardial nerve fibers. • Chest pain caused by the 4 E’s (Exertion, Emotion, Exposure To Cold, Eating ) • Pain is usually relieved with rest, pain meds and nitrates.
  • 30. Variable/Prinzmetal/Spasm • Transient ischemia that occurs unpredictably and almost always at rest. • Pain is caused by vasospasm of the arteries. • ST segment elevations will be noted.
  • 31. Unstable • Chest pain at rest or with exercise and tends to last greater than 15 minutes. • This results in reversible myocardial ischemia but is a sign that an infarct is soon to come. • EKG will reveal ST segment depression and T wave inversion.
  • 32. STEMI • ST segment elevations • T wave changes • Q wave development • Enzyme elevations • Reciprocals
  • 33. NSTEMI • ST segment depressions • T wave changes • No Q wave development • Mild enzyme elevations • No reciprocals
  • 35. Phases of a STEMI • Hyperacute Phase – Occurs within the first few hours of MI onset. – Leads facing the infarcted surface: ST segment elevation. – Leads facing the uninjured surface: ST segment depression (reciprocals) – T waves become tall, widened and might be taller than the R wave.
  • 36. Phases of a STEMI • Fully Evolved Phase – Q wave development – ST elevation – T waves start to become inverted in leads facing the injury.
  • 37. Phases of a STEMI • Resolution phase – Weeks after there will be a gradual return of ST segments to baseline. – T waves will gradually return to normal but are the last to change back.
  • 38. Serum Cardiac Markers • Myocardial cells produce certain proteins and enzymes associated with cellular functions. • When cell death occurs, these cellular enzymes are released into the blood stream. • CPK and troponin
  • 39. CPK • Creatine Phosphokinase • Begin to rise 3 to 12 hours after acute MI. • Peak in 24 hours • Return to normal in 2 to 3 days
  • 40. Troponin • Myocardial muscle protein released into circulation after injury. • These are highly specific indicators of MI. • Troponin rises quickly like CK but will continue to stay elevated for 2 weeks. • Myoglobin-lacks cardiac specificity.
  • 42. Treatment Options • The immediate goal for any acute MI is to restore normal coronary blood flow to vessels and salvage myocardium. • There are a variety of medical and medicinal therapies to treat an MI.
  • 43. General Treatment for the MI patient MONA • Morphine • Oxygen • Nitroglycerin • Aspirin
  • 44. Fibrinolytic Therapy • Indicated for patients with STEMI MI’s. • Should be given within 12 hours of symptom onset. • Fibrinolytics will break down clots found within the vessles • Contraindications: post op surgical patients, history of hemorrhagic stroke, ulcer disease, pregnancy, ect.
  • 45. Cardiac Catheterization • A diagnostic angiography which includes angioplasty and possible stenting. • Performed by an interventional cardiologist with a cardiac surgeon on stand by. • Percutaneous procedure through the femoral or brachial artery.
  • 46. Cardiac Catheterization • Upon arrival to the cath lab all actue MI patients will receive: – A bolus dose of plavix – IV Integrelin – Heparin dose either subcu or IV drip – Angiomax : a DTI may be substituted for heparin and integrelin.
  • 47.
  • 48. Coronary artery bypass graft • Surgical treatment where saphenous vein is harvested from the lower leg and used to bypass the occluded vessels.
  • 49.
  • 50. Long Term Care • Smoking Cessation and lifestyle modifications. • Aspirin, Beta Blockers and Clopidogrel will be indefinite. • Lipid lowering medication along with diet modifications.
  • 51. Nursing Management • Nursing interventions of a patient with angina focus on: • Early identification of myocardial ischemia. • Assess immediately any complaints of chest pain using a pain scale of 0 – 10, as pain (or pressure or heaviness) is an indicator of myocardial ischemia. Immediate assessment is important for early identification and treatment. • Document vital signs, ECG, skin color, peripheral pulses, level of consciousness, and overall tissue perfusion. • Control of chest pain. • Administer oxygen, nitrates, and analgesia as ordered. • Use pulse oximetry to guide therapy and maintain oxygen saturation above 90%.
  • 52. • Nursing interventions of a patient with angina focus on (Continued…): • Patient and family education • Educate your patient when his/ her condition has stabilised (pain controlled). • Teach the patient about the importance of avoiding the Valsalva maneuver (bearing down when going to bath room). This maneuver increases intrathoracic pressure that decreases venous return to the right side of the heart which is associated with hypotension and bradycardia. • Teach the patient about risk factor modifications such as decreasing fat intake, stopping smoking, reducing salt intake, controlling hypertension, increasing physical activity as tolerated, and achieving normal body weight. • Provide information about medications; indications and side effects. • Teach the patient about the importance of follow up after discharge and how to handle emotional stress and anger.
  • 53. Nursing Management of MI • Nursing interventions for a patient with acute MI focus on: – Achieving a balance between myocardial oxygen supply and demand: This means that in the acute phase, there is a need to increase myocardial oxygen supply by oxygen administration to prevent tissue hypoxia. Myocardial oxygen supply can be enhanced by the administration of coronary artery vasodilators (nitroglycerin). – Prevention of complications: Nurses need to apply cardiac monitoring of patient to detect early ventricular dysrhythmias. In addition, nurses should continue to assess for signs of ischemic pain.
  • 54. Nursing Management of MI (Continued…) – Health education: Nurses should focus on: • Pathophysiology of acute MI. • Description of signs and symptoms such as pain. pressure, or heaviness in chest. • Notification of nurses of any changes in chest pain intensity. • Avoidance of the Valsalva maneuver. • Risk factors modification, including: – Daily fat intake < 30% of total calories. – Maintain serum cholesterol level < 200 mg/dL. – Maintain LDL cholesterol to < 70 mg/dL. – Stop smoking and reduce daily salt intake. – Control hypertension and diabetes mellitus. – Increase physical activity and reduce weight –
  • 55. Nursing Management of MI (Continued…) – Health education (Continued…): Nurses should focus on: • Medication teaching: indications and side effects. • Follow-up care after discharge.
  • 56. Myocardial infarction Nursing process Assessment • A careful history • Description of symptoms (chest pain, palpitation, dyspnea, syncope or sweating). Each symptom must be evaluated with regard to time, duration, precipitating & relieving factors. In addition complete physical assessment for: *level of consciousness
  • 57. *Heart sounds *Peripheral pulses *Lung sound Nursing process (cont…)
  • 58. Nursing diagnosis – Chest pain related to reduced coronary blood flow. – High risk for breathing pattern ineffective related to fluid overload – Anxiety related to fear from death – High risk for tissue perfusion alteration related to decreased cardiac output – Health maintenance alteration related to no adherence to therapeutic regimen Nursing process (cont…)
  • 59. Nursing process (cont…) Patient's goals • Report that pain is decreased • Breath effectively • Experience less anxiety level • Have improved tissue perfusion • Adhere to the self care program
  • 60. Nursing process (cont…) Nursing intervention •Relief or control of chest pain •Alleviate respiratory difficulties •Reduce the anxiety level •Maintain adequate tissue perfusion •Help the patient to adhere to the self care program