MANAGEMENT OF NURSING

SERVICES AND EDUCATION

NURSING CONFERENCE
ON

MYOCARDIAL
INFARCTION

SUBMITTED TO, SUBMITTED BY,

MRS. S. LALITHA M.Sc (N)., GROUP III
Nursing tutor Gr II B.Sc (N) IV YEAR ,
MRS. G. MEENAKSHI M.Sc (N)., COLLEGE OF NURSING,
Nursing tutor Gr II CMCH, CPT.
MRS. L. MANJULA M.Sc (N).,
Nursing tutor Gr II
COLLEGE OF NURSING,
CMCH, CPT.
 MYOCARDIAL INFARCTION
Introduction:
Myocardial Infarction(usually known as Heart attack) results from interruption of
myocardial blood flow and resultant Ischemia and is a leading cause of death worldwide.
Acute Myocardial Infarction is the most important and feared consequence of
coronary artery disease 80% to 90% of all acute myocardial infarction are secondary to
thrombus formation. Many patients may die within the first few hours of the onset, while
remainder suffer from effects of impaired cardiac function. Adequate treatment may save a
patient’s life. After treatment rehabilitation is very much important.
The incidence of myocardial infarction in India is 64.37 per 1000 men between the
ages of 29 and 69, India has the highest burden of acute coronary syndrome and ST elevation
MI in the world. During the past decades researchers have demonstrated that approximately
25% of individuals with MI have moderate to severe psychological difficulties related to
recovery.

Definition:
1. Myocardial infarction is a diseased 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.
-BRUNNER
2. Acute myocardial infarction is a clinical syndrome that results from occlusion of a
coronary artery, with resultant death of cardiac myocytes in the region supplied by
that artery.
-BRUNNER
-Current diagnosis and treatment in cardiology-

Etiology:

Causes For
myocardial
Infarction

Non
Modifiable
modifiable
risk factors
risk factors
Non-Modifiable risk factors:-
1. Age:-
Men age 45 and older and women age 55 and older are more likely to have a
heart attack than are younger men and women

2. Family history:-
Myocardial Infarction can be inherited from parents to children.

3. Gender:-
Myocardial infarction is 3 times more frequent in men than women.

Modifiable risk factors:-

1. Tobacco Use:-
This includes smoking and long-term exposure to second-hand smoke

2. Obesity:-
Obesity is linked with high BP, diabetes, high levels of tri-glycerides, bad
Cholesterol, and low levels of good cholesterol.

3. Stress:-
Emotional stress such as extreme anger, may increase the risk of a heart attack.

4. Diabetes:-
Blood sugar rises when the body doesn’t make a hormone called Insulin pr
can’t use it correctly. High blood sugar increases the risk of heart attack.

5. High Blood Pressure:-

Over time high BP can damage arteries that lead to the heart. High BP that
occurs with other conditions, such as Obesity, high cholesterol and diabetes increase
the risk even more.

6. High Cholesterol and Tri-glycerides:-

A high level of certain blood fats called tri-glycerides also increases heart
attack risks.

7. Not enough exercises:-

A lack of physical activity is linked to a higher risk of heart attacks.

8. Unhealthy diets:-
A diet high in sugars, animal fats, processed foods, trans-fat and salt increases
the risk of heart attack
 9. An auto-immune condition:-
Having a condition such as Rheumatoid arthritis or Lupus can increase the risk
of a heart attack.

10. Illegal drug use:-

Cocaine and amphetamines are stimulants, they can trigger a coronary artery
spasm that can cause a heart attack.

 MYOCARDIAL INFARCTION PATHOPHYSIOLOGY

Acute coronary syndrome is an emergent situation characterised by an

acute onset of Myocardial Ischemia that results in myocardial death. 90% of Myocardial
Ischemia is caused by Atherosclerotic obstruction, other 10% caused by emboli vessel
spasm, Visculitis, Shock, drugs, when 10% of vascular cross-sectional area of the coronary
artery is obstructed is called critical sclerosis.
In unstable angina there is reduced blood flow in a coronary artery, often due to
rupture of an atherosclerotic plaque. A clot begins to form, but the artery is no completely
occluded results in chest pain and other symptoms that may be referred to a pre infarction
angina.
Acute myocardial infarction commonly known as heart attack, when heart is starved
of oxygen because blood flow through one or more of coronary arteries- a group of vessels
that surround and supply the heart is blocked. The lack of oxygen causes chest pain and
results in irreversible damage, eventually leading to the death of heart muscle.
The area of infarction develops over minutes to hours as the cells are deprived of
oxygen Ischemia develops, cellular injury occurs , lack of oxygen results in infarction, the
death of cells.

The expression “time is muscle” reflects that urgency of appropriate treatment to

improve patient outcomes
 PATHOPHYSIOLOGY OF MI

Causative: Coronary atherosclerosis, coronary thrombosis, embolism

Progressive narrowing of Blood vessels Risk of excessive blood clot formation

Ischemia of heart muscles Thromboembolism

Hypoxia

Necrosis

Anaerobic metabolism Myocardial contractility

Release of Lysosomal enzyme

Lactic acid Formation Altered depolarisation Cardiac out

Chest pain/Muscle pain Altered repolarisation Renal Ischemia/Oliguria

Myocardial Infarction
 Irreversible Myocardial damage occurs after 30 minutes of severe
Ischemia[10% or less of blood flow]

Branches of coronaries artery

 LAD(left anterior  RCA(Right coronary  LCX(left circumflex

descending artery) artery) coronary artery)
 40%-50% damage occurs  30%-40%  15%-20%
 Anterior wall of LV  Inf/post. wall of LV  Laboral wall of left
 Anterior part of  Posterior part of IV ventricles except apex
Intraventricular septum septum
 Apex

Irreversible injury first occurs in the subendocardial region, as it is the least perfused region
of the heart because the coronary are in pericardium.
 Mainly two conditions
 I. Transmural infarct(Full thickness)
o Caused by atherosclerosis, Thrombosis
o In ECG-STEMI(STelevation)
II. Non-Transmural/ subendocardial Infarct
o Caused by lysis of the thrombotic plaque
o Sever reduced BP[shock]

Sub endocardial Infarct

Circumferential Small intramural
[global hypotension] micro infarct’s
infarct
Gross and microscopic appearance of an Infarct ;
MI less than 12 hours usually not apparently grossly, this can be highlighted by
immersing tissue in tri-phenyl-tetrazolium chloride
this can be highlighted by immersing tissues in triphenyl tetrazolium chloride

Viable myocardium is Infracted area are pale

red because it is because it leak of LDH
reserved LDH activity

Various descriptions are used to further identify an MI; the types NSTEMI, STEMI, location
of the injury to the ventricular wall (anterior, inferior, posterior, or lateral wall) and the point
in time within the process of infarction(acute, resolving or old)
 STEMI NSTEMI
 Persistent ST elevation  Transient ST segment elevation
 New ST elevation at the J-point in  Persistent or transient St segment
>= 2 contigous leads depression
 Ongoing acute coronary artery  T-wave abnormalities, including
occlusion hyperacute T wave, T wave
inversion, flat T wave
 Positive TROP

Leads with ST segment Affected myocardial area Occluded coronary artery

elevation

V1- V2 Septal Proximal LAD

V2- V4 Anterior LAD

V5- V6 Apical Distal LAD, LCX or RCA

I , aVL Lateral LCX

II , Avf, III Inferior 90% RCA, 10% LCX

V7, V8, V9[reciprocal Posteriolateral RCA or LCX

depression are frequently
evident in V1-V3]

Signs and symptoms of Myocardial Infarction:

i) Pain:
* Pain areas - in the area between shoulder chest, jaw, left arm, upper abdomen
* Pain types- Can be burning in the chest are like acleanch3d fished in the chest
* Pain circumference: Can occur during rest.
ⅱ) Whole body:
dizziness, fatigue, light. headache, Clammy skin Cold sweat or Sweating
(ii) Gastrointestinal system:
Indigestion or heart burn, nausea , Vomiting.
(iv) Neck & arm: discomfort or tightness
Common symptoms are :
anxiety, Chest pressure, feeling of impending doom, palpitations, shortness of breath.
Shoulder discomfort.

Diagnostic Evaluation!
A Myocardial infarction is diagnosed using a combination of texts and observation
including
1) Electrocardiogram
2) Cardiac biomarkers
3) Echocardiogram
4) Coronary Angiogram
5) CCTA(Coronary Ct-Angiogram)

1) Electrocardiogram:
A Simple, non-invasive test that measures the hearts electrical impulses. An ECG
Should be Obtained and interpreted within 10 minutes of patient arrival
10 Steps to read ECG:
Check: Caliberration-25mm/sec.
1. Rhythm
2. Rate
3. Axis
4. P wave
5. PR interval
6. Q Wave
7. QRS Complex
8. QT interval
9.ST Segment
10. T Wave.
i) Rhythm:
* R-R interval Irregularly irregular - Atrial fibrillation
* R-R Interval Regularly irregular- Second degree heart block type 2
ⅱ) Rate:
Regular rhythm = 300 /R-R interval (large boxes)
Rate =300/ 4 = 75 bpm
Irregular rhythm = No. of R waves in 6 sec X10 Rate
Rate =9R waves x10
= 99 bpm
III) Axis
Normal Cardiac axis is 30 to +110.
iv) Pwave:
Normal Height of Pwave <0.5mm (leadⅡ) <0.10 Sec
Width <1.5mm (vi)
* P. Pulmonale - Right atrial enlargement
* P. mitrale - Left atrial enlargement.
v) P-R interval
Normal-0.1-0.2sec (3-5 small squares)
* Prolonged- A-V blocks
* Reduced - WPW syndrome (Wolff-Parkinson. White Syndrome)
* Depressed. Pericarditis
vi) Q wave
Pathological -> 2 small squares deep.
* deep Qwave - old inferior wall MI
vii) QRS complex
0.08-0.12 Sec (2-3 Small squares)
* Broad QRS- Ventricular arrythmias.
Viii) Q-T interval:
Ventricular arrythmias - Torsade De points.
ix) ST Segment
ST Elevation- Acute Myocardial Infarction, Pericarditis
in Vi,V2: Septal Wall MI
V3.V4: Anterior Wall MI
IavL, v5v6: Lateral wall
II ,III : Inferior Wall MI
ST Depression : NSTEMI, Myocardial Ischemia, Posterior MI
x) T Wave!
Upright in all leads except Upright AVR and V1
Peaked T waves: Hyperkalemia
Hyperacute T waves: Early STEMI
Inverted T wave Myocardial Ischemia : ventricular Hypertrophy.
Depressed s wave >35mm : Left ventricular hypertrophy.
Right axis Deviation : Right ventricular hypertrophy.

2. Cardiac biomarkers
Intracellular macromolecules (protein) released from a heart muscle when it is damaged as a
result of Myocardial Infarction.
They found in the blood.
They include,1
* aspartate aminotransferase
* troponin I&T
* Creatine kinase MB (CK-MB)
* Myoglobin (Mb)
* lactate dehydragenase (LDH)
* B-type natriuretic peptide (BNP)
*C-reactive protein (CRP)
*Myeloperoxidase (MPO)
* Ischemic modified albumin (IMA)
Classification of Cardiac biomarkers
ⅰ) Myocardial injury markers:
* Myocardial of Necrosis: CK-MB, Myoglobin, troponin
* Myocardial ischemia: IMA, HFABP.
ii) Hemodynamic stress markers : natriuretic peptides
iii) inflammatory and prognostic markers- hs -CRP, SCD4OL and homocysteine
* CK-MBNormal CK-MB level for adult-5-251U1
*CK-MB peaks in 12-24 hours

3. Echocardiogram
1) transthoracic echocardiogram:
A Sonographer places a transducer on the outside of chest to send sound waves to
heart These soundwaves bounce off the different parts of heart
ii) transesophageal echocardiogram: for this test, the Sonographer guides a small transducer
down your throat and oesophagus using a long, flexible tube. This minimally invasive
procedures. It can show the heart and valves detailed manner than transthoracic

4. Coronary angiography,
It also called as Cardiac Catheterization. minimally invasive Procedure that uses a
Catheter (a long thin flexible tube) inserted into a blood vessel in The leg. arm, or neck to
take the pictures of the coronary artery opening
* It is used to measured the width of the artery and rate of blood flow.
* It is useful to perform a angioplasty or Stent, if a blockage found during angiography.

5.CCTA:
Coronary computed tomography angiography.
- It is a non-invasive SD imaging test. that identifies plaque and blockage or harrowing
(Stenosis) of the coronary arteries.
MEDICAL MANAGEMENT:-
Goals:
Goals of medical management are
  to minimize myocardial damage
 to preserve myocardial function
 to prevent complications
 to reestablish coronary flow
Treatment guidelines for Acute Myocardial Infarction:
 Use rapid transit to the hospital
 Obtain within 12 lead 10 minutes. electrocardiogram to be read within 10 minutes
 Obtain biomarkers laboratory blood including troponin specimen of cardiac
 Obtain other diagnostics to clarify the diagnosis
 Begin routine medical interventions
 Supplemental oxygen.
 Nitroglycerin
 Morphine
 Aspirin
 Beta Blocker
 Angiotensin - converting enzyme inhibitor within 36 hours
 Anticoagulation with heparin and platelet inhibitors.
 Statin.
 Evaluate for indications for reperfusion therapy
 Percutaneous coronary intervention
 Thrombolytic fibrinolytic therapy.
 Continue therapy as indicated
 IV heparin , Bivalirudin or Bondaporinux
 clopidogrel.
 Glycoprotein IIb/II a Inhibitor
 Bed rest for a minimum of 12 - 24 howls
 Statin prescribed at discharge

TIME IS MUSCLE:MUSCLE IS LIFE :-

The expression "Time is muscle" reflects the urgency of appropriate treatment
to the improve patient treatment and early recognition and improve of patients pressing with
an mI will improve changes of survival
* Time to take ECG and diagnose STEMI < 10 mins
* Door to needle time < 30 mins. Fibrinolysis can be done up to 12 hours
* Door to balloon time < 60 mins. PCI - can be done up to 48 hrs.
* Door in Door<30 minutes for patient with STEMI who arrive at STEMI referral hospital
and are transferred to STEMI receiving centre for PCI
* Fibrinolysis is equal to PCI if done within 2 hours
* Time to wire cross in PCT capable centre < 60 mins
* Time to wire cross in non-PCI capable centre<90mins [wire cross < 60+ Road cross < 30
mins]
Timely reperfusion reduce the infract size improves the left ventricular function, and
decreases the mortality. STEMI Management delays can be grouped as patient related delay
can be grouped as patient related delay and system delay. System delay is more readily
modifiable by organisational measures and it is a predictor of our comes.

Initial management of MI :

(l) OXYGEN :
Oxygen is recommended in patients with hypoxemia sao2 < 90%.Routine oxygen is
not recommended for patients without hypoxemia sao2 <90%.
(ll)PAIN:
Intravenous opioids should be considered to relieve pain .Morphine is the drug of
choice to reduce pain and anxiety .

(lll) LOADING DOSE:

Patients with symptoms of MI and ECG with ST elevation, then administer
● T.aspirin 300 mg
● T.Clopidogrel 300 mg
● T.atorvastatin 80 mg

(lV)FIBRINOLYSIS
Fibrinolysis (Thrombolysis) is the process of intravenous administration of
thrombolytics (fibrinolytics) is to dissolve the thrombus in a coronary artery, allowing blood
to flow through the coronary artery again (reperfusion) minimizing the size of infarction
preserving ventricular function .

Thrombolytic therapy is initiated when primary PCI is not available or the transport time
to a PCI capable hospital is too long .

However , although thrombolytic dissolve the thrombus ,they do not affect the
underlying athrosclerotic lesion .The patient may be referred for a cardiac catheterization and
other invasive procedures following the use of thrombolytic therapy. Thrombolytics should
not be used if the patient has bleeding disorder.

Checklist for fibrinolytics:-

Absolute contraindications:
1. Previous ICH or stroke of unknown origin at any time .
2. Ischemic stroke beyond 4.5 hours and <6 months
3. CNS damage or neoplasm or AV malformations
4. Recent major trauma /surgery /head injury with in 3 weeks
5. GI bleeding within past month
6. Known bleeding disorder (exclude menstruation)
7. Aortic dissection
8. Non-compressible punctures in past 24 hours
9. For streptokinase, previous treatment with in the previous 6 months
10. Severe uncontrolled hypertension (unresponsive to emergency therapy)

Relative contraindications :
1. Transient ischemic attack in preceding 6 months.
2. Oral anticoagulation
3. Refractory hypertension SBP>180 mmHg, DBP>100 mmHg
 4. Advanced liver disease
5. Infective endocarditis
6. Active peptic ulcer
7. Prolonged or traumatic resuscitation.

Dose of fibrinolytics agents : STAR agents

Fibrin specific:
1. Tenecteplase(TNK)- Single IV weight based bolus
2. Reteplase (r-PA) - 10 unit IV boluses given 30 min apart .
3. Alteplase (t-PA) - 90 min weight based infusion .

Non-fibrin specific:
1. Streptokinase - 1.5 million units iv given over 30-60 mins
.highly antigenic .

(lV)PERCUTANEOUS CORONARY INTERVENTION:

The patient with STEMI is taken directly to the cardiac catheterization laboratory
for an immediate PCI. The procedure is used to open the occluded coronary artery and
promote reperfusion to the area that has been deprived of oxygen early PCI can be effective
in patients of all ages .
 Primary PCI:
Performing urgent balloon angioplasty (with or without stenting ) as the
primary mode of reperfusion therapy in patients with STEMI is called primary PCI. It
is a recommended therapy for STEMI. This restores angiographically normal flow in
90 %patients PPCI should be performed with a target door to balloon time of less than
90 mins to offer maximal benefits .

● Rescue PCI
Emergency PCI performed as soon as possible in cases of failed
fibrinolytic treatment.

 Pharmaco -Invasive therapy :

It is a strategy of full dose fibrinolysis followed by transfer to PCI capable hospital for
coronary angiogram within 2-24 hours and PCI,if necessary.Pharmaco invasive therapy offers
equivalent benefits as primary angioplasty.

a) Fibrinolysis combined with rescue PCI in cases of

fibrinolysis
b) Routine early PCI strategy in cars of successful fibrinolysis.
 A PPCI strategy is recommended over fibrinolysis if anticipated time from diagnosis to
PCI is <120 mins .

If timely PPCI (<120 mims) cannot be performed in patient with a working diagnosis of
STEMI ,fibrinolytic therapy is recommended within 12 hr of symptoms onset I platiens
without contraindications .

Types of procedures in PCI :

(l) Percutaneous transluminal coronary angioplasty:

In PTCA ,a balloon -tipped catheter is used to open blocked coronary vessels and
resolve ischemia. The purpose of PTCA is to improve blood flow within a coronary artery by
compressing the atheroma .It is carried out in the cardiac catheterization laboratory .catheters
are usually prefered in femoral artery and radial artery .A balloon tiped dilation catheter is
passed through the sheath and positioned over the lesion.

The physician determines the catheter position by examining markers on the balloon that
can be seen with fluoroscopy .when the catheter is properly positioned, the balloon is inflated
with high pressure for several times and then deflated .The pressure compresses and often
cracks atheroma .The media and adventitia of the coronary artery are also stretched .

(ll) Coronary artery stent :

After PTCA ,the area that has been treated may close off partially or completely a
process called restenosis The intima of the coronary artery has been injured and responds by
initiating an acute inflammatory process .This process may include release of mediators that
leads to vasoconstriction, clotting scar tissue formation .

A coronary stent may be placed to overcome these risks. It is initially positioned over
the angioplasty balloon .When the balloon is inflated the mesh expands and presses against
the vessel wall ,holding the artery open the balloon is withdrawn ,but the stent is left
permanently in place within artery .

Because of the risks of thrombus formation within the stent ,the patient receives antiplatelet
medications , usually aspirin and clopidogrel aspirin should be continued and clopidogrel is
continued for 1 year following stent placement.

(V) CORONARY ARTERY REVASCULARIZATION

CABG- coronary artery bypass grafting

CABG- is a surgical procedure in which a blood vessel is grafted to an occluded

coronary artery so that blood can flow beyond the occulsion .it's also called bypass graft.

Indications:
● Alleviation of angina that cannot be controlled with medication or PCI
● Treatment for left main coronary artery stenosis or multivessel CAD
● Prevention of and treatment for MI, dysarrythiamias or heart failure
● Treatment for complications from an unsuccessful PCI

Traditional coronary artery bypass graft :

CABG- procedures are performed with the patient under general anesthesia .In
traditional CABG the surgeon performs a median stenotomy and connects the patient to the
cardipulmonary bypass (CPB) machine .Next a blood vessel from another part of the patient
body (eg. saphenous vein ) is grafted distal to the coronary artery lesion ,bypassing the
obstruction CAP machine mechanically circulates and oxygenates blood for the body while
bypassing the heart and lungs .CAP maintains perfusion to the body organs and tissues and
allows the surgeon to complete the anastomoses in a motionless bloodless surgical field.CAP
is then discontinued, chest tubes ,epicardial pacing wires are placed and the incision is
closed .
Alternative coronary artery bypass grafting:

Off -pump coronary artery bypass grafting surgery (OPCAB) involves a standard
median sternotomy incision ,but the surgery is performed without CPB,A B- adrenergic
blocker may be used to slow the heart rate .The surgeon also uses a myocardial stabilization
device to hold the site still for the anstomosis of the bypass graft into the coronary artery
while the heart continues to beat.

Research suggests that OPCAB is associated with reduced short term postoperative
morbidity, including stroke ,and other complications.

Complications of cardiac surgery:-

Cardiac complications:
● Hypovolemia
● Persistent bleeding
● Cardiac tamponade
● Fluid overload
● Hypothermia
 ● Hypertension
● Tachydysarythmias
● Bradycardia
● Cardiac failure
● Myocardial infarction

Pulmonary complications :
● Impaired gas exchange

Neurologic complications :
● Neurologic changes ,stroke

Kidney injury & Electrolyte imbalance.:

● Acute kidney injury
● Electrolyte imbalance

Other compalications :
● Hepatic failure
● Infection

Nursing management:-

● Continous monitoring of patient with MI to detect complications and changes in status

● Asessing for chest pain ,shortness of breath and other symptoms
● If an MI is suspected in any patient don't allow the patient to walk and to drink
anything. make them to be calm and quiet and in supine position relaxed manner.
● If the patient is in Thrombolysis therapy, watch for any bleeding symptoms
● Time is very important to manage patient with MI
● Monitor the hemodynamic parameters to assess cardiac output ,volume status and
vascular tone .
● Monitor urine output and maintain intake and output chart
● Monitor ABG ,tidal volume ,peak inspiratory pressure ,and extubation parameters.
● Auscultate chest for breath sounds
● Sedate patient adequately as prescribed and monitor respiratory rate and depth
● Suction tracheobronchial secreations as needed ,using strict aseptic technique.
● Encourage routine pain medication dosing for the first 24- 72hours .and observe for
side effects of lethargy hypotension, tachycardia , respiratory depression.

Prevention:-
● Follow healthy lifestyle:
 Don’t smoke .maintain a healthy weight with a heart healthy diet .get regular
exercise &manage stress.

● Manage other health conditions:

Certain conditions, such as high blood pressure &diabetes can increase the risk of
heart attack .so as your health care provider how often you need checkups.

● Get enough sleep:

A for 7to 9 hours sleep per night

● Exercise :
Get regular physical activity, such as at least 150 minutes a weeks of moderate
aerobic exercise or 75 mins a week of vigrous aerobic exercise.

● Healthy eating:
Eat a healthy , balanced diet that low in fat and high in fiber .This includes eating
plenty of fresh fruits and vegetables, whole grains and unsaturated fats like oily fish,
avacados, nuts and seeds ,limit saturated fats

● Don't smoke:
Avoid smoking and all forms of tobacco exposure

● Manage stress
Try to manage stress by meditation ,yoga ,& listening music

● Take medications as directed:

Your health care provider may prescribe drugs to improve your heart health.
BIBLIOGRAPHY :

 Archith baloor – textbbook of ABC of ECG, published by jaypee brothers

 Brunner and suddarth’s – textbook of medical surgical nursing volume I , published
by WOLTERS KLUWER, page no: 471 – 679
 Reena George – textbook of cardiac nursing , published by jaypee brothers page no:
114-159
 Thomas kochuthresiamma – textbook of medical and surgical nursing volume 1,
published by jaypee brothers, page no: 214 – 264

NET SOURCES :
 www.slideshare.com
 www.wikipedia.com
 www.clevelandclinic.org
 www.mayoclinic.org’