myocardial infarction

1. MYOCARDIAL
INFARCTION
PRESENTED BY-
SAM MATHEW
STAFF NURSE
DH –ED

2. Objectives
 Define and understand the epidemiology of MI’s and
how they are classified
 Will be able to identify the risk factors associated with
MI’s
 Will be able to recognize signs and symptoms of MI and
what the appropriate interventions are.
 Understand the treatment options available to treat MI.
 Nursing responsibilities
 Follow up care

3. DEFINITION
. Myocardial infarction is a
disease condition which is
caused by reduced blood
flow in a coronary artery
due to atherosclerosis and
occlusion of an artery by
an embolus or thrombus
.

4. 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.

5. MI Classifications
 MI’s can be subcategorized by anatomy and clinical diagnostic
information.
 Anatomic
Transmural - atherosclerosis involving a major coronary artery, it is usually as
a result of complete occlusion of the artery in addition on ECG ST elevation and
q waves are seen(STEMI)(epicardium,myo,endocardium)
 Subendocardial - small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles. It is particularly susceptible to
ischemia,in addition to ST depression is seen on ecg(NSTEMI)
 Diagnostic
 ST elevations (STEMI)-ECG must show new ST elevation in two or
more adjacent ECG leads or new LBBB , it must be greater than 2 mm in leads
V2 and V3 or greater than 1 mm in all other leads.
 non ST elevations (NSTEMI)-ST segment depression ≥0.5mm or dynamic T-
wave inversion with pain or discomfort , and cardio specific proteinstroponin
are rises in blood in NSTEMI.

7. CORONARY ARTERIES OF HEART

8. Tunica Intima
T. Adventitia
Tunica media
plaques
Thrombus
Atherosclerosis –is a narrowing of the
arteries caused by a buildup of plaque

9. ETIOLOGY

10. NON-MODIFIABLE
RISK
FACTORS
MODIFIABLE
RISK
FACTORS
ETIOLOGY

11. NON-MODIFIABLE RISK
FACTORS
FACTOR
AGE
SEX
FAMILY
HISTORY

12. AGE: More than 40 years.
FAMILY HISTORY:
Myocardial infarction can
be inherited from parents
to children.
GENDER: Myocardial
infarction is 3 times more in
men than women.

13. MODIFIABLE RISK FACTORS
FACTOR
HIGH
BLOOD
LIPIDS
LEVEL
HYPER-
TENSION
SMOKING
PHYSICAL
INACTIVITY
OBESITY
DIABETES
MELLITUS
STRESS

14. HIGH BLOOD CHOLESTROL LEVEL
LOW DENSITY
LIPOPROTEIN
(LDL)
DANGEROUS
HIGH DENSITY
LIPOPROTEIN
(HDL)
LIPIDS
(LIPOPROTIENS)

15. HYPERTENSION
High blood pressure
our arteries are designed to pump blood at a certain
pressure. If that pressure is exceeded, the walls of the
arteries will be damaged
.
injury to endothelial lining , atherosclerosis
narrowed & thickened arterial walls
risk of M.I.

16. SMOKING
Smoking can damage the walls of your arteries.( toxic
substances in cigarette)
Atherosclerosis
narrowed & thickened arterial walls
Risk of M.I.

17. PHYSICAL INACTIVITY
Improper lipid metabolism
LDL level increases
Starts accumulating
in blood vessels
Risk of M.I.

18. OBESITY
More lipids are produced
LDL level increases
Atherosclerosis
Risk of M.I.

19. DIABETES MELLITUS
Diabetes increases the risk of MI because
it increases the rate of atherosclerotic
progression and adversely affects the lipid
profile
Risk of having M.I.

20. STRESS
Release stress hormones like adrenaline, noradrenaline, and
cortisol
increase in heart rate, and elevated blood pressure
it’s causing damage over time to all your blood vessel
That damage increases the risk of plaque buildup in coronary
arteries or can even cause a rupture of plaque
MI
The way you handle stress also matters. If you respond to it in
unhealthy ways -- such as smoking, overeating,or not exercising -
that makes matters worse.

21. PATHOPHYSIOLOGY

22. How a Heart Attack Happens

23. Cholesterol deposition within the wall of the main artery
This deposited cholesterol ultimately forms a plaque in the wall of the artery called
atherosclerotic plaque. Atherosclerotic plaque formation is a long term process, required
many years to establish.
Sometimes this plaque may rupture or erode,it leads to activate clotting mechanism so
platelet aggregation and fibrin deposition, which lead to formation of an occlusive
thrombus in a coronary artery.
This occlusive thrombus completely block a coronary artery and interrupts blood supply to
part of the myocardium (heart muscle),
It lead to irreversible changes and death of myocardial cells, and ultimately ST-segment
elevation myocardial infarction develops.
PATHOPHYSIOLOGY

24. CLINICAL MANIFESTATIONS
Chest pain due to a lack of blood and
oxygen supply of the heart muscle
Characteristics: Severe, immobilizing
chest pain.
Usually prescribed as heaviness,
pressure, tightness, burning.
Location: Substernal, Retrosternal or
Epigastric.
Radiation: It may radiate to neck, jaw,
arm or back.
Duration: Lasts for 20 minutes or more.
PAIN

25.  Cardiovascular-
 Initially the BP and pulse may be elevated.
Later, BP will drop due to decreased cardiac
output.
 palpitation.
 Jugular veins may become distended and have obvious
pulsations.

26. CONTD…..
 Respiratory-
Respiratory symptoms occur when the damaged the
heart muscle limits the pumping action of the left
ventricle, causing acute left heart failure and
consequent lung congestion.
 Shortness of breath
 Dyspnea/Tachypnea
 Crackles
 Pulmonary edema

27.  Gastrointestinal-
 Nausea
 Vomiting
Stimulation of vomiting center by severe pain causes
nausea & vomiting
FEVER
It is due to inflammatory process caused by
Myocardial cell death.

28. In response to pain and the blood flow
abnormalities that result from
dysfunction of the heart muscle
SYMPATHETIC NERVOUS SYSTEM STIMULATION
Increased catecholamine releases.(adrenal medulla)
Diaphoresis (perfuse sweating
Cold & clammy skin (“cold sweat”).
Integumentary system (Skin)
cool, clammy skin
Diaphoresis
Pallor, Cyanosis
Coolness of extremities

29. Genitourinary-
Hypoperfusion to the kidneys leads to decrease renal
perfusion pressure which is required to maintain
glomerular filteration rate in the kidney
Decrease GFR leads to decrease urinary output
Urine output (Oliguria): 30ml/HR or <400ml/day.
Myocardial damage
Failure of the pump action of the heart,
resulting in reduced cardiac output

30. CONTD…..
 Neurogenic-
due to inadequate blood flow to the brain
 Light- headedness
 Headache
 Visual Disturbances
 Altered speech
 Altered motor functions
 Altered level of consciousness

31. CONTD…..
 Psychosocial-
 Fear feeling
 Pt. may deny that anything is wrong

32. LOOK WHO IS SLEEPING?

33. DIAGNOSTIC TESTS

34. ASSESSMENT/DIAGNOSTIC FINDINGS
 It is generally based on presenting symptoms, ECG and
laboratory test results.
 Patient history-it includes
• Description of presenting
symptoms
• History of previous illness,
family health history

35. CONTD…..
 Electrocardiogram-
ECG provides information that
assists in diagnosing acute MI.
 The classic ECG changes are-
 ST segment elevation
 ST depression
 T wave inversion
 Abnormal Q wave

36. RECOGNITION OF ECG TIPS
REMEMEBER - SALI
 S-SEPTAL MI-V1 V2
 A-ANTERIOR WALL MI-V3 V4
 L-LATERAL WALL MI -V5 V6-1-AVL
 I-INFERIOR WALL MI- 11-111-AVF
 POSTERIOR WALL MI- ST V1-V3,ST V7-V9

37. S
A
L
I

38. CORONARY ARTERIES OF HEART
LATERAL MI
ANTERIOR
OR SEPTUM
INFERIOR MI

39. SERUM CARDIAC
MARKERS
CK-MB (ENZYME)
TROPONINE-T
(PROTEIN)
cardiac enzymes are proteins that are released into the
blood by dying heart muscles.

40.  CK-MB- increases 3-6 hrs after onset of chest pain,
peaks in 12-18 hrs & return to normal within 3-4 days.
 Cardiac troponin T- increases 4-6 hrs after MI &
persists for 2 weeks
 Full blood count: WBC (white blood cell) count is usually
elevated. ESR (Erythrocyte sedimentation rate) and CRP
(C-reactive protein) may also elevate.
CHEST X-RAY
To detect cardiomegaly.

41. ECHOCARDIOGRAM
PURPOSE: it is useful to assess the ability of heart
muscles to contract & relax.
It is done to evaluate ventricular function by checking
ejection rate.
CT&MEGNATIC RESONANCE IMAGING (MRI)
PURPOSE: To detect site & extent of myocardial cells.

42. ANGIOGRAPHY
Angiography is used to detect
abnormalities,including narrowing
(stenosis) or blockages in the blood
vessels (called occlusions).
This is done by injecting a radio-
opaque contrast agent into the blood vessel this
dye makes the coronary arteries visible on x-ray
pictures. This helps doctors see blockages in the
arteries.

43. MANAGEMENT
 GOALS
 Restoration of the balance between the oxygen supply
and demand to prevent further ischemia
 Pain relief
 Prevention and treatment of any complications that
may arise

44. Chest pain suggestive of ischemia
 Vital signs
 12 lead ECG
 Obtain initial
cardiac enzymes
electrolytes, cbc
lipids, bun/cr,
glucose, coags
 CXR
Immediate assessment within 10 Minutes
 Establish
diagnosis
 Read ECG
 Identify
complicatio-
ns
 Assess for
reperfusion
Initial labs
and tests
Emergent
care
History &
Physical
 Cardiac monitoring
 IV access
 Morphine
 Oxygen<94%
 Nitrates
 Aspirin

45. STEMI vs. NSTEMI

47. MEDICAL MANAGEMENT

48. ANTIPLATELET DRUG (Decrease platelet aggregation and
inhibit thrombus formation)
 Aspirin(160 to 325mg) slows the blood's clotting action
by reducing the clumping of platelets
 Clopidogrel(300mg) -works by blocking platelets from
sticking together and prevents them from forming
harmful clots. It is an antiplatelet drug.
DRUG THERAPY

49. ANALGESIC:
NITRATES.
Sublingual Nitroglycerine- Nitrates act as a vasodilator
and relief pain,Total 3 doses (can repeat 3-5mts if no
contraindication)-use only SBP ˃ 90mmhg heart rate 50-100/mt
Morphine Sulphate.
 produces central nervous system analgesia.
 Produce venodilation(it helps to reduce left ventricular
preload and oxygen demand)

50. BETAADRENERGIC BLOCKERS
(Propanolol) it inhibit SNS stimulation of heart.
reduces both heart rate & contractility
CALCIUM CHANNEL BLOCKERS
(Verapamil, Nifedipine)
It causes coronary artery vasodilatation & decreases
myocardial contractility.
Increases blood supply to myocardium & decreases
O2 demand of myocardium.
ANTI COAGULATION THERAPY (prevent the formation
of blood clots)
LMWH-ENOXAPARIN
UNFRACTIONED HEPARIN

51. ACE Inhibitors
These medicines lower bloodpressure
and reduce the strain on your heart.
They also help slow down further
weakening of the heart muscle.
Eg:enalapril, captopril

52. FIBRINOLYTIC THERAPY
TIME OF ADMINISTRATION:
Thrombolytics are given to the
patient upto 12 hours of onset of
chest pain but for best results it
should be given within 1 hr after
onset of chest pain.
ACTION: These will dissolve &
do lysis of thrombus in coronary
artery.
We are using metalyse for
thrombloysis
If STEMI is present, the goal is
to achieve a door- to –drug
time of 30 min & a door-to –
balloon time of within 90 min.
Indicated for patients with STEMI MI’s.

53. Absolute & relative contraindications
for thrombolytic therapy
 Absolute contraindications-
 Any prior ICH
 Ischemic stroke within 3 months
 Known structural cerebral vascular lesion
 Known malignant intracranial neoplasm
 Active bleeding
 Significant closed head trauma within past 3
months

54.  Relative contraindications-
 History of chronic, severe, poorly controlled
hypertension
 Severe uncontrolled hypertension on presentation
 History of prior ischemic stroke >3months
 Dementia
 Pregnancy
 Active peptic ulcer
 Current use of anticoagulants, the higher the INR the
greater the risk

55. Angioplasty
During angioplasty, a thin, flexible tube with a balloon
on the end is threaded through a blood vessel to the
blocked coronary artery. Then,the balloon is inflated
to push the plaque against the wall of the artery.This
widens the inside of the artery,restoring blood flow.
Also a small mesh tube called a stent may be put in the
artery to help keep it open.Some stents are coated with
medicines that help prevent the artery from becoming
blocked again.
SURGICAL MANAGEMENT

57. PTCA (Percutaneous
Transluminal Coronary
Angioplasty)

58. ATHERECTOMY
With Atherectomy the plaque is shaved off using a type
of rotational blade.

59. CORONARY ARTERY BYPASS GRAFT (CABG)
A form of bypass surgery that
can create new routes around
narrowed and blocked
coronary arteries, permitting
increased blood flow to deliver
oxygen and nutrients to the
heart muscle.
Coronary artery bypass graft is
an option for selected groups
of patients with significant
narrowings and blockages of
the heart arteries.
The bypass graft for a CABG
can be a vein from the leg or
an inner chest-wall artery.

60. COMPLICATIONS
 Dysrrythmias -Damaged heart muscle disrupts electrical
signals and produces arrhythmia in which heartbeat may be too
fast, too slow or irregular like VF,VT,AF
 Cardiogenic shock- It may develop after the large territory
heart muscle damage. It leads to failure of the pumping action of
the heart. The end results are very low blood pressure with an
inadequate supply of oxygen rich blood to vital organs most
significantly the brain, kidneys and heart
 Heart failure- It occurs slowly over time after an attack in
which the heart cannot pump enough blood to meet the body’s
demand
 Embolism. sometimes thrombus may dislodged from
heart and may cause stroke (if reach in the brain) or
ischemic limb (if reach in the limb)

61. mechanical complications
It is due to tear or rupture of infarcted heart muscle. It
includes-
Severe mitral regurgitation – it is due to rupture of
papillary muscle(leakage of blood backward through
the mitral valve from left ventricle to lt atrium )
Cardiac tamponade – it is due to rupture of ventricle.
Right heart failure – it is due to rupture of
interventricular septum.
Late complications:
These develop after one week of attack and include:
Dressler’s syndrome-
This syndrome is characterized by fever, pleuritis and percarditis.
It is caused by an autoimmune reaction to damage heart muscle

62. Nursing diagnosis
 Acute pain R/T myocardial ischemia resulting from
coronary artery occlusion
 Outcome- the client will experience improved comfort as
evidenced by dec. in pain rating scale.
 Interventions- assess characteristics of pain
 Assess respiration, BP, heart rate with each episode of chest
pain.
 Obtain 12 lead ECG on admission & on each episode of
chest pain.
 Monitor respond to drug therapy.
 Limit visitors.
 As morphine as ordered.
 Administer nitrates as ordered.

63.  Ineffective tissue perfusion R/T thrombus in coronary
artery
 Outcome- the client will demonstrate improved
cardiac tissue perfusion as evidenced by dec. rating of
pain.
 Interventions- provide bed rest.
 Administer oxygen as prescribed.
 Administer thrombolytics.
 Monitor ST segments.

64.  Dysrrhythmias R/T electrical instability or irritability
secondary to infarcted tissue
 Outcome- the client will have no dysrrythmias as
evidenced by normal sinus rhythm.
 Interventions- teach client & family about need for
continous monitoring.
 Assess apical heart rate.
 Give antidysrrythmic agents as ordered.
 Monitor effects of antidysrrythmics.
 Monitor serum K levels.
 Maintain patent IV line.
 Monitor ST segments & document changes.

65.  Risk for bleeding R/T coagulopathies with
thrombolytic therapy.
 Powerlessness R/T a near-death experience &
anticipated lifestyle changes.
 Anxiety & fear R/T hospital admission & fear of death.
 Risk for constipation R/T bed rest, pain medications &
NPO or soft diet.
 Ineffective health maintenance R/T MI & implications
for lifestyle changes.
 Risk for activity intolerance R/T an imbalance b/w
oxygen supply & demand.

66. Health education
Proper medication compliance (right dose and right
time)
Perform exercise
Do not smoke
follow the diet plan
Maintain a healthy weight
Manage your stress
signs and symptoms to be reported to physician

67. Conclusion :
 MI is a life threatening disease caused by many factors.
Health education must be given to the patients with
predisposing or risk factors to prevent it. Early
diagnosis is also very important for saving the life of
the patient.


68. REFERENCE
Mosby’s Comprehensive Review of Nursing
Dolores F.Saxton,Patricia M.Nugent.
The Lippincott Manual of Nursing Practice
https://en.wikipedia.org/wiki/Myocardial_infarction