1. Myocardial Infarction
NUR 409
Fall
JUST/ School of Nursing
coyright 2004 Anna Story

2. Anatomy Review Three Layers for the Heart Epicardium: Myocardium:
outer layer
Myocardium:
middle layer
Endocardium:
inner layer

3. Anatomy Review

4. Anatomy Review Myocardium Muscular wall of the heart
Atrial myocardium wraps around great vessels
2 divisions of ventricular myocardium:
Superficial ventricular muscles: surround ventricles
Deep ventricular muscles:spiral around and between ventricles

5. Coronary Arteries

6. Coronary Arteries
Coronary arteries and cardiac veins Supplies blood to muscle tissue of heart
Left and right
Originate at aortic sinuses
High blood pressure, elastic rebound force blood through coronary arteries between contractions

7. Coronary Arteries Right Coronary Artery Supplies blood to:
right atrium
portions of both ventricles
cells of sinoatrial (SA) and atrioventricular nodes
marginal arteries (surface of right ventricle)
posterior interventricular artery

8. Coronary Arteries Left Coronary Artery Supplies blood to:
left ventricle
left atrium
interventricular septum.
2 main branches:
circumflex artery
anterior interventricular artery

9. Question
Which of the following infarctions is a result of the occlusion of the left anterior descending coronary artery?
A. Anterior left ventricle
B. Lateral and posterior left ventricle
C. Inferior left ventricle
D. Right ventricle

10. Answer A. Anterior left ventricle
Rationale: Infarctions of the anterior wall of the left ventricle and the interventricular septum result from occlusion of the left anterior descending (LAD) coronary artery. The LAD coronary artery supplies oxygenated blood to the anterior wall of the left ventricle, the interventricular septum, and the ventricular conducting tissue.

11. Coronary Arteries
Ischemia, injury or death involving the right coronary artery (RCA) most often result in changes in the inferior surface of the heart: Leads II, III, AVF
Obstruction of blood flow in the circumflex artery is associated with lateral changes from ischemia or infarction: Leads I, AVL, V5, V6
Left anterior descending branch (LAD) of the left coronary artery (LCA) flow obstructions are associated with anterior wall and/or septal changes: Leads V1 and V2 (septal)…Leads 2,3,4 (anterior wall)

12. MI Definition
A result of occlusion of arterial flow to the myocardium.
Occlusion occurs via spasm, blood clot or stenosis
Irreversible damage to the myocardium

13. MI Definition
Either one of the following criteria;
-Typical rise and gradual fall (Tn) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following
Ischemic symptoms
Development of pathological Q wave
ECG changes suggesting ischemia
Pathological findings of an acute myocardial infarction

14. WHO Criteria 2 out of 3 Characteristics
MI Definition
WHO Criteria 2 out of 3 Characteristics
Typical Symptoms
Enzyme Rise and Fall
ECG Pattern Involving Development of
Q-waves

15. Myocardial Infarction
Prolonged ischemia
Plaque rupture triggers thrombus formation at the site of an atherosclerotic lesion.
Occlusion of blood flow results in MI.
Irreversible damage occurs after 20 to 40 minutes.
Tissue can be salvaged if flow is restored within 6 hours.
Cellular changes depend on extension and expansion of infarct and ventricular remodeling.

16. Atherosclerotic Plaque

17. PATHOPHYSIOLOGY

18. Atherosclerosis—Pathophysiology
Triglycerides, hypertension, and cigarette smoking cause damage to the endothelium.
Fatty substances, cholesterol, cellular waste products, calcium, and fibrin pass are deposited forming lipid plaque (atheroma).
White blood cells, smooth muscle cells, and platelets to aggregate at the site forming a fibrous plaque
Blood flow is reduced, decreasing oxygen supply to tissues.
Symptoms occur with 75% or more occlusion.

19. Pathophysiology
When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time

20. Size of the Infarction Extent, severity, and duration of ischemia
Size of the vessel
Collateral circulation
Status of intrinsic fibrinolytic system, vascular tone, and metabolic demands
Transmural—necrosis of tissue in all layers of the myocardium
Normal motion is affected.

21. Type of Infarction Q-wave Non–Q-wave Infarcted the full muscle wall
Formation of pathological Q waves in area of infarct
Greater than one small box in duration
Deeper then 1/3 of the R wave
Non–Q-wave
Infarcted only partial amount of muscle wall

22. Type of Infarction Significant Q-wave where none previously existed
Why?
Impulse traveling away from the positive lead
Necrotic tissue is electrically dead
No Q-wave in Subendocardial infarcts
Not full thickness dead tissue
But will see a ST depression
Often a precursor to full thickness MI
Criteria
Depth of Q wave should be 25% the height of the R wave
Width of Q wave is 0.04 secs
Diminished height of the R wave

23. Type of Infarction
There are two distinct patterns of ECG change depending if the infarction is:
ST Elevation ((Transmural or Q-wave), or
Non-ST Elevation (Subendocardial or non-Q-wave)

24. Location of the Infarction
Anterior left ventricle
Occlusion of left anterior descending (LAD)
Lateral and posterior left ventricle
Left circumflex artery
Inferior left ventricle
Occlusion of right coronary artery
Right ventricle

25. Location of infarction

27. Anterior MI V1, V2, V3, V4 Anterior infarct with ST elevation
Left Anterior Descending Artery (LAD)
V1 and V2 may also indicate septal involvement which extends from front to the back of the heart along the septum
Left bundle branch block
Right bundle branch block
2nd Degree Type2
Complete Heart Block

28. Lateral MI I, AVL, V5, V6 Lateral Infarction with ST elevations
Left Circumflex Artery
Rarely by itself
Usually in combo

29. Posterior MI leads V1, V2 Posterior Infarct with ST
Depressions and/ tall R wave
RCA and/or LCX Artery
Understand Reciprocal changes
The posterior aspect of the heart is viewed as a mirror image and therefore depressions versus elevations indicate MI
Rarely by itself usually in combo

30. Inferior MI leads II, III, AVF Inferior Infarct with ST elevations
Right Coronary Artery (RCA)
1st degree Heart Block
2nd degree Type 1, 2
3rd degree Block
N/V common, Brady

31. RVI
Hypotension
Jugular vein distention
Dry lung sounds

32. A 59-year-old man has been admitted
A 59-year-old man has been admitted. He has a 90-minute history of severe crushing chest pain. His ECG shows 3mm ST segment elevation in leads V1 to V4consistent with an acute anterior myocardial infarction.
He is given loading doses of aspirin and clopidogrel. Forty-five minutes after admission, he undergoes successful primary percutaneous coronary intervention (PCI) with the insertion of a drug eluting stent into his critically narrowed left anterior descending coronary artery. By the time he is returned to the coronary care unit 30 minutes after the procedure, he is pain free and there is partial resolution of his ECG changes.

33. His U + Es, full blood count, blood glucose, renal, hepatic and thyroid function are all normal.
Fasting lipid profile: cholesterol = 6.8mmol/litre; HDL cholesterol = 1.2mmol/litre; LDL cholesterol = 4mmol/litre; triglycerides = 3.5mmol/litre 
Although he has a history of asthma, it is well controlled and he has never been hospitalized for it. He uses his salbutamol inhaler rarely. He also has a history of gastro-oesophageal reflux with endoscopically confirmed oesophagitis two years ago.
He smokes 20 cigarettes per day and consumes approximately 35 units of alcohol per week. His body mass index = 26kg/m2 

34. Assessment History Physical exam Diagnostic studies Electrocardiogram
Laboratory test

35. Assessment
History
Heaviness, squeezing, choking, or smothering sensation
Substernal pain can radiate to the neck, left arm, back, or jaw
Prolonged and unrelieved by rest or nitroglycerin
Nausea/vomiting
Diaphoresis, dyspnea, weakness, fatigue, anxiety, restlessness, confusion, shortness of breath, or a sense of impending death

36. Risk Factors Associated with Acute Coronary Syndrome: Modifiable
Tobacco smoke
Hypertension
Physical activity
Obesity
Dyslipidemia
Diabetes mellitus

37. Lipid Levels Source: From Gale Encyclopedia

38. Risk Factors Associated with Acute Coronary Syndrome: Nonmodifiable
Age: Death generally occurs over age 65
Gender: Men are at greater risk than women. After menopause mortality increase in women
Heredity: Children of parents with heart disease are at greater risk

39. Risk Factors Associated with Acute Coronary Syndrome: Other
Stress
Alcohol consumption
Hormone Replacement Therapy (HRT)

40. .
Secondary Prevention Guidelines for Risk Factors Source: From Smith, S., et al. (2006). AHA/ACC secondary prevention for patients with coronary artery disease. Circulation, 113, 2363–2372

41. Secondary Prevention Guidelines for Risk Factors Source: From Smith, S
Secondary Prevention Guidelines for Risk Factors Source: From Smith, S., et al. (2006). AHA/ACC secondary prevention for patients with coronary artery disease. Circulation, 113, 2363–2372.

42. Physical Examination May appear restless, agitated, in distress
Skin cool and moist
VS, low-grade fever, hypertension, and tachycardia or hypotension and bradycardia
Irregular, faint pulse
Lack of point of maximal impulse
Diminished S1, S3 ,, and S4, pericardial friction rub
JVD, heart failure, pulmonary edema
Labored breathing, crackles, rhonchi

43. Diagnostic Tests The electrocardiogram (ECG)
Detects patterns of ischemia, injury, and infarction
Depolarization and repolarization of cardiac cells are altered causing ECG changes
Ischemia—T-wave inversion, ST-segment depression
Injury—ST-segment elevation
Infarction—T-wave, ST-segment, and Q-wave changes
Reveals the anatomical region involved

44. Question
Which biomarker is preferred for diagnosing a coronary event?
A. Creatine kinase
B. Creatine kinase isoforms
C. Myoglobin
D. Troponin

45. Answer
D. Troponin
Rationale: Troponin is a contractile protein with two subforms (troponin T and troponin I) that are highly specific for cardiac muscle. Troponin levels are not detected in the healthy person, and skeletal muscle injury does not affect the level. Troponin has been found to be a sensitive marker during the early hours after an MI. Because the cardiac troponins are highly sensitive and specific for MI, they are the preferred biomarker for diagnosing this coronary event.

46. Laboratory Tests Creatine kinase Creatine kinase isoforms Myoglobin
CK-MB specific to myocardial cell damage
Rises in 3 to 12 hours, peaks in 24 hours, returns to normal in 48 to 72 hours
Creatine kinase isoforms
CK-MB2/CK-MB1 ratio greater than 1—diagnostic for MI
Myoglobin
Rises in 1 to 4 hours, peaks in 6 to 7 hours, not specific for the diagnosis of MI

47. Laboratory Tests (cont.)
Troponin
Preferred biomarker
Troponin I rises in 3 to 12 hours, peaks at 24 hours, and remains elevated for 5 to 10 days.
Troponin T rises in 3 to 12 hours, peaks in 12 hours-2 days, and remains elevated for 5 to 14 days.
Other diagnostic tests
CXR, echocardiogram, radionuclide angiography, MRI,

48. The evolution changes in acute MI.

49. ECG Changes ST elevation & depression T-waves
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted

50. Evolving MI and Hallmarks of AMI
Q wave
ST Elevation
T wave inversion
1 year

51. ST Elevation Infarction
Before injury
Ischemia
Infarction
Fibrosis
Normal ECG
ST depression, peaked T-waves, then T-wave inversion
ST elevation & appearance of Q-waves
ST segments and T-waves return to normal, but Q-waves persist

52. Non ST Elevation Infarction
Before injury
Ischemia
Infarction
Fibrosis
Normal ECG
ST depression & T-wave inversion
ST returns to baseline, but T-wave inversion persists

53. ECG Changes Reciprocal changes
ST segment depression in the same plane of leads (ie. limb or precordial) as ST segment elevation
ST elevation is the primary event
ST depression is a passive electrical phenomenon in which the primary event is viewed from the other side of the heart

54. ECG Changes Common reciprocal changes:
ST depression in III and aVF associated with ST elevation in I and aVL
ST depression in I and aVL associated with ST elevation in III and aVF
ST depression in V1-V3 as a result of posterior MI (ST elevation in V8 and V9)

55. ECG Changes
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

56. ECG Changes

57. ECG Changes in MI
Source: Adapted from Ellis, K. (2007). EKG plain and simple. Upper Saddle River, NJ. Prentice-Hall.

58. Anterior Left Ventricle
Anteroseptal wall MIs are the most frequent type of infarction and have the potential for causing a significant amount of left ventricular dysfunction.
Patients with an anteroseptal MI are at high risk for heart failure, pulmonary edema, cardiogenic shock, and death because of an inadequate pump.
Anteroseptal wall MIs are also associated with increased risk for intraventricular conduction disturbances, such as bundle branch blocks and fascicular blocks, which are also known as hemiblocks.

59. Anterior MI
The anterior portion of the heart is best viewed using leads V1- V4.

60. Anterior MI

61. Lateral and Posterior Left Ventricle
Infarctions of the lateral and posterior walls are less common than infarctions of the anteroseptal wall.
Patients with a lateral or posterior wall MI are at risk for dysrhythmias associated with dysfunction of the SA or AV nodes. Examples include sinus arrest, wandering atrial pacemaker, sinus pause, or junction rhythm.

62. Lateral MI
Leads I, aVL, and V5- V6

63. Lateral MI

64. Posterior MI
leads V1, V2

65. Posterior MI

66. Inferior Left Ventricle
Infarctions of the inferior wall are less common than anteroseptal MIs but occur more frequently than MIs of the lateral or posterior walls.
The potential impact on left ventricular function usually is less for a patient with an inferior wall MI than for a patient with an anteroseptal wall infarction. Because the right coronary artery supplies oxygenated blood to much of the conducting tissue, patients are at frequent risk for dysrhythmias related to altered function of the SA and AV nodes.

67. Inferior
Leads II, III and aVF

68. Inferior MI

69. Right Ventricle
Patients with a right ventricular infarction and hemodynamic abnormalities with a concurrent inferior wall MI have a signifi - cantly higher mortality rate (25% to 30%).
Dysrhythmias associated with right ventricular infarction involve dysfunction of the SA and AV nodes.

70. Practice 1 Anterior MI with lateral involvement
ST elevations V2, V3, V4
ST elevations I, AVL, V5
Click for answer

71. Practice 2 Click for answer Anteroseptal MI
ST elevations V1, V2, V3, V4

72. Practice 3
Inferior MI
ST elevation 2,3 AVF
Click for answer

73. Practice 4 Inferior lateral MI ST elevations 2, 3, AVF
ST elevations V5
Click for answer

74. Practice 5
Click for answer
Acute inferior MI
Lateral ischemia

75. Management

76. Case Study
Mr. O, a 68-year-old black man, was brought to the emergency department (ED) by an ambulance at 10:30 AM. He described substernal chest pain with radiation to his back that began 1 hour ago. The pain is not relieved by rest or sublingual nitroglycerin. He describes the pain as dull and rates it an 8 on a scale of 10. He has a history of hypertension, obesity, and elevated cholesterol. He has no known drug allergies.
On physical examination, he was awake, alert, oriented, and cooperative. His skin was cool and diaphoretic. Blood pressure was 90/42 mm Hg; heart rate, 110 beats/minute and irregular; respiratory rate, 26 breaths/minute on 2 L O2 per nasal cannula; temperature, 98°F. His cardiac examination revealed S1, S2, and an S3. He had no jugular venous distension. Peripheral pulses were present but thready and there was no peripheral edema.

77. Case Study (cont…)
Auscultation of his lungs revealed bilateral basilar crackles. He had no evidence of cyanosis or clubbing. His abdominal examination showed positive bowel sounds in all four quadrants.
His abdomen was soft and nontender with no palpable masses. The nurse immediately recorded a 12-lead ECG that showed 4-mm ST segment elevation in leads V1 through V4. Blood samples were drawn that revealed an elevated CK level positive for MB. His troponin level was also abnormal. Mr. O was given an aspirin and an IV line was started. Mr. O was diagnosed with an acute anteroseptal wall MI. The plan was to perform a primary percutaneous transluminal coronary angioplasty (PTCA).

78. Management Early management Thrombolytic therapy
Primary percutaneous transluminal Coronary Angioplasty (PTCA)
Intensive and intermediate care management
Pharmacological therapy

79. Management

80. Management Treatment Goals Decrease myocardial oxygen demand
Remove physical/psychological stressors
Relieve pain
Reduce workload of the heart (BP, HR)
Inhibit further clot formation
Rapid identification/diagnosis
Transport for reperfusion therapy

81. Management Evaluate within 10 minutes of arrival.
Patient history and 12-lead ECG elevation greater than 1 mm in two or more contiguous leads=MI
ASA, oxygen, nitroglycerin, morphine, β-blocker
VS, IV access, continuous cardiac monitoring
Serum cardiac markers, CBC, chemistry, and lipid profile
CXR, echo

82. Initial Management Administer aspirin, 160 to 325 mg chewed.
After recording the initial 12-lead electrocardiogram (ECG), place the patient on a cardiac monitor and obtain serial ECGs.
Give oxygen by nasal cannula.
Administer sublingual nitroglycerin (unless the systolic blood pressure is 100 beats/min). Give 0.4 mg every 5 minutes for a total of three doses.
Provide adequate analgesia with morphine sulfate.
Administer β-blocker.

83. Management Initial Treatment: “MONA greets all patients”
Morphine sulfate, mg q 5-15 min slow IV
Maintain BP > ~ 90 mm Hg
Titrated to Pain relief
Reduce PVR and workload on the heart
O2 via nasal canula
Nitroglcerin SL
Aspirin, mg PO
Chewed & swallowed if possible
Determine if hypersensitive to ASA

84. Early management Management IV, NS, large bore
TKO with some exceptions
No dextrose containing solutions
Fluid boluses appropriate in some cases
2nd line if time permits
Minimize number of attempts
12 Lead ECG
Diagnostic evidence of AMI present
Assess for RVI

85. Management (cont.) Fibrinolytic therapy
In STEMI, door to drug within 30 minutes
Given within 3 hours of onset of symptoms
Percutaneous coronary intervention
Reestablishes blood flow
Artery is opened by balloon and stent is placed.
Used for patients who present within 12 hours

86. Fibrinolytics Thrombolytic Therapy Alteplase – tPA Tenecteplase – tNK
Tissue plasminogen activator (tPA or PLAT)is a protein involved in the breakdown of blood clots
Alteplase – tPA
Tenecteplase – tNK
Reteplase – RPA
Anistreplase (Eminase): It converts plasminogen  to plasmin
Streptokinase (Kabikinase, Streptase)
Urokinase (Abbokinase)

87. Thrombolytic Therapy
Fibrinolytics dissolve clots and restore myocardial perfusion
Most effective when given within 6 hours of onset of MI
Client must be continuously monitored
During administration monitor for bleeding and report any signs to physician

88. Thrombolytic Therapy
Post administration observe closely for signs of bleeding by:
Documenting neuro status
Observing IV sites
Monitoring clotting studies
Observing for s/s of internal bleeding
Monitor Hemoglobin and Hematocrit
Testing stools, urine, emesis for occult blood

89. Contraindications for the Use of Fibrinolytic Therapy

90. Management (cont.) Hemodynamic monitoring
Pulmonary artery catheter, arterial monitoring
Additional diagnostic testing
Computer imaging tests
Echocardiogram
Stress test
Coronary angiography

91. Intensive and Intermediate Care Management
Maximize cardiac output; minimize cardiac workload.
Frequent VS, cardiac monitoring with ST segment, pulse oximetry
Serial ECGs and serial serum cardiac markers
CBC and chemistry
Bedrest to commode for first 12 hours
Pain relief
NPO until pain free, then clear liquids to cardiac diet
Stool softeners

92. Pharmacological Therapy
Daily ASA indefinitely, clopidogrel (plavix) for 14 days in STEMI
ACE inhibitors with anterior wall MI, pulmonary congestion, or EF less than 40%
Blood glucose control with insulin, magnesium repletion
β-blocker shown to reduce morbidity and mortality
IV unfractionated heparin or low-molecular-weight heparin in STEMI with high risk for systemic emboli (anterior wall MI, atrial fibrillation, cardiogenic shock, previous embolus)

93. Pharmacological Therapy
Drug Therapy
Antidysrhythmias
IV nitroglycerin for 24-48hrs.
Calcium channel blockers

94. Question
Which of the following is used to decrease myocardial oxygen consumption?
A. ASA
B. Morphine
C. Calcium channel blockers
D. β-blockers

95. D. β-blockers
Rationale: β-Blockers may be used to decrease myocardial oxygen consumption by reducing myocardial contractility, sinus node rate, and atrioventricular (AV) node conduction velocity. The reduction in myocardial contractility reduces the work of the heart and decreases myocardial oxygen demand.
Answer

96. Hemodynamic management
Pulmonary artery catheter
PAWP greater than 18 indicates pulmonary congestion or cardiogenic shock
PAWP less than 18 indicates volume depletion
COP
Arterial line
Oxygen saturation

97. Management

98. Complications Pericarditis Extension / Ischemia Expansion / Aneurysm
Acute MI
RV Infarct
Mechanical
Heart Failure
Mural Thrombus

99. Acute MI Complications
Vascular complications
Myocardial complications
Mechanical complications
Pericardial Complications
Thromboembolic Complications
Electrical complications

100. Acute MI Complications
Vascular complications
Recurrent ischemia (15-20%)
Recurrent MI
Management goals are to Increase oxygen supply and decrease oxygen demand

101. Myocardial Complications
Cardiogenic shock is the most serious myocardial complication of MI.
Occurs because of the loss of contractile forces in the heart.
LV failure is the most common cause of cardiogenic shock complicating acute MI. The prospective SHOCK Trial Registry identified LV failure as the etiology of shock in 78.5% of patients .
Occur when necrosis involves 40% or more of the left ventricle.

102. Question
A post-MI patient with progressive dyspnea, tachycardia, and pulmonary congestion accompanied by a new holosystolic murmur most likely has which of the following?
A. Ventricular septal wall rupture
B. Pericardial effusion
C. Left ventricular wall rupture
D. Dysrhythmia

103. Answer A. Ventricular septal wall rupture
Rationale: The greatest risk for ventricular septal wall rupture is within the first 24 hours and continues for up to 5 days. The patient presents with a new, loud, holosystolic murmur associated with a thrill felt in the parasternal area. In addition, the patient has progressive dyspnea, tachycardia, and pulmonary congestion.

104. Mechanical complications
Interventricular Septal Rupture
LV Free Wall Rupture

105. Cardiac rupture syndromes complicating acute myocardial infarction
Cardiac rupture syndromes complicating acute myocardial infarction. A, Anterior myocardial rupture in an acute infarct (arrow). B, Rupture of the ventricular septum (arrow). C, Complete rupture of a necrotic papillary muscle.

106. Pericardial Complications
Pericarditis: occur during 48-72hrs.
Pericardial effusions (incidence, up to 45%)
more common with large, anterior, or both large and anterior infarcts and when CHF is present
Dressler’s syndrome:
Clinical pericarditis with fever, leukocytosis, and a high erythrocyte-sedimentation rate and may be associated with pulmonary infiltrates, effusion, or both.
It can lead to tamponade or constrictive pericarditis.

107. THROMBOEMBOLIC COMPLICATIONS
Systolic emboli originated in the wall of left ventricle.
These emboli can occlude the cerebral, renal, mesenteric, or iliofemoral artery.
Patients are systemically anticoagulated with unfractionated or low–molecular-weight heparin followed by warfarin (Coumadin) for 6 to 12 months.

108. ELECTRICAL COMPLICATIONS
Conduction Disturbances:
Because the right coronary artery is also the source of oxygenated blood for the inferior, posterior, and right ventricular walls, patients with inferior, posterior, or right ventricular wall MIs are at risk for conduction disturbances resulting from poor SA node functioning.
1st degree and mobitz type I may be appear.

109. ELECTRICAL COMPLICATIONS
Dysrhythmias – Cause of death in clients with MI who die prior to hospitalization
70-90% of hospitalized MI clients have abnormal cardiac rhythms
Identify the dysrhythmia
Assess hemodynamic status
Evaluate client for chest discomfort
Treated when they cause
Hemodynamic compromise
Increased myocardial oxygen requirements
Predispose lethal ventricular dysrhythmias

110. ELECTRICAL COMPLICATIONS
Dysrhythmias – 95% of patients with an MI experience these.
Common dysrhythmias
1. Sinus Bradycardia (Inferior MI)
2. Sinus Tachycardia (Anterior MI)
3. Atrial Fibrillation (Anterior MI)
4. Ventricular – PVCs >6/min
5. Ventricular Tachycardia/V-Fib
6. AV Block – RCA occlusion

111. Dysrhythmias Inferior MI Anterior MI Bradycardias 2nd Degree AV Blocks
Nurse monitors:
Cardiac rate & rhythm
Hemodynamic status
May need temporary pacer if hemodynamically unstable
Anterior MI
Venrticular irritability (PVCs)
3rd Degree or Bundle Branch Block (serious complication)
Nurse observes closely for s/s of heart failure
May need pacemaker

112. Nursing diagnosis Pain Ineffective Tissue Perfusion (cardiopulmonary)
Risk for ineffective tissue perfusion
Activity Intolerance
Ineffective Coping
Fear
Anxiety
Ineffective Sexuality Patterns
Impaired Physical Mobility
Decreased COP
Knowledge deficit

113. Acute MI: Collaborative Problems
Potential for Dysrhythmias
Potential for Heart Failure
Potential for Recurrent Chest Discomfort and Extension of Injury

114. Nursing interventions
Pain Management
Nitroglycerin to increase collateral blood flow, redistribute blood flow to subendocardium, and dilate coronary arteries
Morphine Sulfate to relieve pain, decrease myocardial oxygen demand, and reduce circulating catecholamines

115. Nursing interventions
Pain Management
Supplemental O2
2-4 L per minute per nasal cannula
Titrated to keep SaO2 > 92%
Position of Comfort
Semi-Fowlers
Quiet and calm environment

116. Learning Outcome
Prioritize discharge teaching for the patient who has had an acute coronary event.

117. Discharge Education Priorities for ACS
Implement the ABCDE to assist with discharge:
A = Aspirin and antianginals
B = Beta blockers and blood pressure
C = Cholesterol and cigarettes
D = Diet and diabetes
E = Education and exercise

118. Pharmacologic Therapy
Anti-anginals: Nitroglycerin
Antiplatelets: ASA,
Decrease myocardial O2 demand: Beta Blockers
Prevent ventricular remodeling: ACE Inhibitors
Cholesterol reduction: HMG-COA Reductase Inhibitors, Nicotinic Acid

119. Pharmacologic Therapy
Unless contraindicated, the patient experiencing an MI should receive:
Early administration of ASA & beta blocker
Aspirin & Beta blocker at discharge
ACE-inhibitor or angiotensin receptor blockers (ARB) at discharge
Smoking cessation counseling
Lipid Lowering agent

120. Anxiety & Depression Management
Approximately 30% of patients experience depression post-coronary event
Anxiety & depression coexist in patient with ACS

121. Anxiety & Depression Management
Psychoeducational programs:
Teach patients stress management and relaxation techniques
Assist patients in attaining the appropriate coping mechanisms
Assist patients to adapt and use the appropriate defense mechanisms for healthy control of depression and anxiety

122. Physical Activity 30 minutes of moderate exercise 5 days/week
Cardiac Rehab: promote lifestyle changes, & appropriate exercise.
Resuming sexual activity: Resume 6-8 weeks post MI and after treadmill test.

123. Nutrition Dietary changes Decrease lipids Decrease HTN
Control diabetes
Decrease obesity

125. Out

126. Nursing interventions
Cardiac Care Rehabilitation
Process which assists client with cardiac disease to achieve and maintain optimal functioning within the limits of the heart’s ability to respond to increases in activity and stress
Phase 1: begins with acute illness, ends with discharge from hospital
Phase 2: begins after discharge and continues through convalescence at home
Phase 3: long term conditioning

127. Nursing interventions
Cardiac Care Rehabilitation
Nurse promotes rest while ensuring some limited mobility
Assistance is given for some ADL’s
Individualized– client’s progress at their own rate
Nurse encourages progressive ambulation
Nurse assesses heart rate, BP, respiratory rate and level of fatigue with each higher level of activity
Nurse should stop the activity and refrain from advancing activity if client develops any signs of activity intolerance