SEMINAR ON Myocardial infarction FOR NURSING STUDENT B.Sc. M.Sc.

1. VIVEKANANDA COLLEGE OF NURSING
SEMINAR ON;
PRESENTED BY- APURVA DWIVEDI [M.Sc. Nsg. 2st Yr.]

2. MYOCARDIAL INFARCTION

3. INTRODUCTION
ACS (Acute Coronary Syndrome) is an emergent situation characterized by
an acute onset of myocardial ischemia that results in myocardial death (i.e.;
MI) if definitive interventions do not occur promptly. (Although the terms
coronary occlusion, heart attack, and MI are used synonymously, the
preferred term is MI.) The spectrum of ACS includes unstable angina, non–
ST segment elevation MI (NSTEMI), and ST-segment elevation MI
(STEMI).

4. CONTI.
A myocardial infarction occurs when an atherosclerotic
plaque slowly builds up in the inner lining of a coronary
artery and then suddenly ruptures, causing catastrophic
thrombus formation, totally occluding the artery and
preventing blood flow downstream.

5. INCIDENCE OF MYOCARDIAL
INFARCTION
The total death rate for all myocardial infarctions was 46 per cent, but if
sudden deaths are excluded, the rate becomes 24 per cent. The annual
incidence of myocardial infarction per 1,000 in the practice population of
11,195 was 4.1 and the total annual death rate per 1,000 was 1.9.

6. Types of
heart attacks
•ST segment elevation myocardial infarction
(STEMI)
•Non-st segment
elevation myocardial
infarction (NSTEMI)
•Coronary spasm,
or unstable angina

7. STEMI: THE CLASSIC OR MAJOR
HEART ATTACK
When most people think of a heart attack, they often think of a STEMI. A
STEMI occurs when a coronary artery becomes completely blocked and a
large portion of the muscle stops receiving blood. It’s a serious heart attack
that can cause significant damage.

8. NSTEMI HEART ATTACKS
• Unlike in a STEMI, the affected coronary artery is only
partially blocked in a NSTEMI. A NSTEMI won’t show
any change in the ST segment on the
electrocardiogram.
• A coronary angiography will show the degree to which
the artery is blocked. A blood test will also show
elevated troponin protein levels. While there may be
less heart damage, an NSTEMI is still a serious
condition.

11. CORONARY SPASM, OR UNSTABLE
ANGINA
A coronary artery spasm is a quick tightening of
the blood vessels that deliver blood to your
heart muscle. These spasms may cause chest
pain, or you may not feel any symptoms. You
often have coronary spasms late at night or early
in the morning. Treatment focuses on relieving
chest pain and preventing spasms.

12. SIGNS AND SYMPTOMS
Areas where pain is experienced in myocardial infarction, showing
common (dark red) and less common (light red) areas on the chest
(left) and back (right).

13. CONTI.
Chest Pain
Shortness Of Breath
Nausea
Feeling Faint
Cold Sweat
Feeling Tired
Arm, Neck, Back, Jaw, Or
Stomach Pain

14. CONTI.
• Chest pain is one of the most common symptoms of acute myocardial infarction
and is often described as a sensation of tightness, pressure, or squeezing.
• Pain radiates most often to the left arm, but may also radiate to the lower jaw,
neck, right arm, back, and upper abdomen.
• The pain most suggestive of an acute MI, with the highest likelihood ratio, is
pain radiating to the right arm and shoulder.
• Similarly, chest pain similar to a previous heart attack is also suggestive.
• The pain associated with MI is usually diffuse, does not change with position,
and lasts for more than 20 minutes.

15. CONTI.
• It might be described as pressure, tightness, knifelike, tearing, burning sensation
(all these are also manifested during other diseases).
• It could be felt as an unexplained anxiety, and pain might be absent altogether.
Levine's sign, in which a person localizes the chest pain by clenching one or
both fists over their sternum, has classically been thought to be predictive of
cardiac chest pain, although a prospective observational study showed it had a
poor positive predictive value.
• Typically, chest pain because of ischemia, be it unstable angina or myocardial
infarction, lessens with the use of nitroglycerin, but nitroglycerin may also relieve
chest pain arising from non-cardiac causes.

16. OTHER
• Chest pain may be accompanied by sweating, nausea or vomiting, and fainting, and
these symptoms may also occur without any pain at all.
• In women, the most common symptoms of myocardial infarction include shortness of
breath, weakness, and fatigue.
• Women are more likely to have unusual or unexplained tiredness and nausea or
vomiting as symptoms.
• Women having heart attacks are more likely to have palpitations, back pain, labored
breath, vomiting, and left arm pain than men, although the studies showing these
differences had high variability.

17. CONTI.
• Women are less likely to report chest pain during a heart attack and more likely to report
nausea, jaw pain, neck pain, cough, and fatigue, although these findings are inconsistent
across studies.
• Women with heart attacks also had more indigestion, dizziness, loss of appetite, and loss
of consciousness.
• Shortness of breath is a common, and sometimes the only symptom, occurring when
damage to the heart limits the output of the left ventricle, with breathlessness arising either
from low oxygen in the blood, or pulmonary edema.
• Other less common symptoms include weakness, light-headedness, palpitations, and
abnormalities in heart rate or blood pressure.

18. CONTI.
• These symptoms are likely induced by a massive surge of catecholamines from the
sympathetic nervous system, which occurs in response to pain and, where present,
low blood pressure.
• Loss of consciousness due to inadequate blood flow to the brain and cardiogenic
shock, and sudden death, frequently due to the development of ventricular
fibrillation, can occur in myocardial infarctions.
• Cardiac arrest, and atypical symptoms such as palpitations, occur more frequently in
women, the elderly, those with diabetes, in people who have just had surgery, and in
critically ill patients.

19. ABSENCE
• "Silent" myocardial infarctions can happen without any symptoms at all.
• These cases can be discovered later on electrocardiograms, using blood enzyme
tests, or at autopsy after a person has died.
• Such silent myocardial infarctions represent between 22% and 64% of all infarctions,
and are more common in the elderly, in those with diabetes mellitus and after heart
transplantation.
• In people with diabetes, differences in pain threshold, autonomic neuropathy, and
psychological factors have been cited as possible explanations for the lack of
symptoms. In heart transplantation, the donor heart is not fully innervated by the
nervous system of the recipient.

20. BE ALERT FOR THE FOLLOWING
SIGNS AND SYMPTOMS:
Cardiovascular
• Chest pain or discomfort not relieved by rest or nitroglycerin palpitations. Heart sounds may include S3,
S4, and new onset of a murmur.
• Increased jugular venous distention may be seen if the MI has caused heart failure.
• Blood pressure may be elevated because of sympathetic stimulation or decreased because of decreased
contractility, impending cardiogenic shock, or medications.
• Irregular pulse may indicate atrial fibrillation.
• In addition to ST-segment and T-wave changes, ECG may show tachycardia, bradycardia, or other
dysrhythmias.

21. RESPIRATORY
• Shortness of breath
• Dyspnea
• Tachypnea
• crackles if MI has caused pulmonary congestion
• Pulmonary edema may be present

22. GASTROINTESTINAL
Nausea and vomiting

23. GENITOURINARY
Decreased urinary output may indicate cardiogenic
shock

24. SKIN
Cool, clammy, diaphoretic, and pale appearance due to
sympathetic stimulation may indicate cardiogenic shock

25. NEUROLOGIC
• Anxiety
• Restlessness
• Lightheadedness may indicate increased sympathetic
stimulation or a decrease in contractility and cerebral
oxygenation.
• The same symptoms may also herald cardiogenic
shock.

26. PSYCHOLOGICAL
Fear with feeling of impending doom, or denial that
anything is wrong.

27. Causes
Coronary artery
disease
(atherosclerosis)
Blood clot
Coronary artery
spasm

28. CONTI.
• Coronary artery disease (atherosclerosis). Plaques made up mostly of cholesterol
build up on your artery walls and restrict blood flow. Atherosclerosis is the most
common cause of myocardial ischemia.
• Blood clot. The plaques that develop in atherosclerosis can rupture, causing a blood
clot. The clot might block an artery and lead to sudden, severe myocardial ischemia,
resulting in a heart attack. Rarely, a blood clot might travel to the coronary artery from
elsewhere in the body.
• Coronary artery spasm. This temporary tightening of the muscles in the artery wall
can briefly decrease or even prevent blood flow to part of the heart muscle. Coronary
artery spasm is an uncommon cause of myocardial ischemia.

29. CHEST PAIN ASSOCIATED WITH MYOCARDIAL ISCHEMIA
CAN BE TRIGGERED BY:
•Physical
exertion
•Emotional
stress
•Cold
temperatures
•Cocaine use
•Eating a heavy
or large meal
•Sexual
intercourse

30. PATHOPHYSIOLOGY

32. ASSESSMENT AND DIAGNOSTIC
FINDINGS
Diagnostic
Evaluation
Patient History Electrocardiogram Echocardiogram Laboratory Test

33. CONTI.
• The 12-lead ECG and laboratory tests (e.g., serial
cardiac biomarkers) are performed to clarify whether
the patient has unstable angina, NSTEMI, or STEMI.
• The prognosis depends on the severity of coronary
artery obstruction and the presence and extent of
myocardial damage.
• Physical examination is always conducted, but the
examination alone does not confirm the diagnosis.

34. PHYSICAL EXAMINATION
Steps
Additional Information
1. Conduct a focused interview related to
cardiovascular and peripheral vascular
disease.
Ask relevant questions related to chest
pain, palpitations, shortness of breath
(dyspnea), cough, edema, fatigue, cardiac
risk factors, leg pain, skin changes, swelling
in limbs, history of past illnesses, history of
diabetes.

35. 2. Inspect:
• Face, lips, and ears for cyanosis
• chest for deformities, scars, visible pulsations
• bilateral arms/hands, noting color, warmth,
movement, sensation (cwms), edema, color
of nail beds, nail shape, and capillary refill
• bilateral legs, noting cwms, hair distribution,
edema to lower legs and feet, color of nail
beds, and capillary refill, numbness/tingling.
• Calf size/pain for signs of deep venous
thrombosis (dvt)
• Cyanosis is an indication of decreased
perfusion and oxygenation.
• To check capillary refill, squeeze nails or
pads of fingers until they blanche; release
compression and observe how many
seconds the original color returns. Normal
is 2 seconds or less.
• Assess capillary refill on bilateral lower
legs.

36. • Alterations and bilateral inconsistencies in CWMS may
indicate underlying conditions or injury.
• While checking for capillary refill, inspect the nail base
angle. The normal angle of the nail base is 160 degrees.
• Assessing for clubbing fingers however, if the angle of
nails become greater than 160 degrees, they are called
clubbing fingers. Clubbing fingers are related to chronic
hypoxemia.

37. Sudden onset of intense, sharp muscle pain
that increases with dorsiflexion of foot is an
indication of DVT, as is increased warmth,
redness, tenderness, and swelling in the calf.
Note: DVT requires emergency referral
because of the risk of developing a pulmonary
embolism.

38. 3. Auscultate:
Aortic/Pulmonic/ ERB’s point/ Tricuspid/Mitral
Auscultate apical pulse for one minute. Note the rate and
rhythm.
•Heart Sounds
• Have the patent breathe normally. Use the
diaphragm side of the stethoscope to hear the five
landmark areas:
• Aortic Area – 2nd ICS on the right sternal border.
• Pulmonic Area – 2nd left ICS
• ERB’s Point – 3rd
left ICS
• Tricuspid Area – 4th left ICS (for children 4th or 5th
left ICS)
• Mitral Area (Apical) – 5th left ICS medial to the MCL
• Auscultate for rate, rhythm, and pitch (the quality of
the sound).
• Auscultate apical pulse at the fifth intercostal space
and midclavicular line.
• Note the heart rate and rhythm. Identify S1 and S2
and follow up on any unusual findings.

39. 4. Palpate:
•Inspect and palpate of the heart
•Bilateral radial, brachial, dorsalis pedis, and
posterior tibialis pulses.
•Skin turgor
•edema
•The ball of the hand (at the base of the fingers)
is the most sensitive at detecting thrills. Inspect
and palpate for:
• Pulsations- are more visible when patients
are thin. Pulsations may indicate increased
blood volume or pressure.
• Lift or heaves- these are forceful cardiac
contractions that cause a slight to vigorous
movement of sternum and ribs.
• Thrills- these are the vibrations of loud
cardiac murmurs. Thrills occur with
turbulent blood flow.

40. • The finger pads are more sensitive in detecting
pulsations. Use the finger pads of index and middle
fingers and apply light pressure on the pulsation site.
If pulses cannot be felt, a Doppler to amplify the
sounds can be used. While palpating the artery, note
the rate (normal 60-100 beats/min), rhythm (normal:
regular), amplitude (normal: easily palpable, 2+), and
contour (normal: smooth and rounded).
• Pulse Amplitude (strength): 0 = absent; 1+ =
decreased, barely palpable; 2+ = normal; 3+ = Full
volume; 4+ = bounding pulse

41. • Absence of pulse may indicate vessel constriction,
possibly due to surgical procedures, injury, or
obstruction.
• To check skin turgor, use the thumb and index fingers to
pinch an area of the skin and release it. It should
instantly return to place.
• To check edema, press down the skin and release the
pressure, the skin normally will return to place right
away. Assessing Edema. When the indentation of the
thumb or any fingers remain in the skin, it is pitting
edema. Documenting Pitting Edema

42. 5. Report and document assessment findings
and related health problems according to
agency policy.
Accurate and timely documentation and
reporting promote patient safety.

43. PATIENT HISTORY
The patient history includes the description of the
presenting symptom (e.g., pain), the history of previous
cardiac and other illnesses, and the family history of
heart disease. The history should also include
information about the patient’s risk factors for heart
disease.

44. ELECTROCARDIOGRAM
• The 12-lead ECG provides information that assists in ruling out or diagnosing an acute MI.
• It should be obtained within 10 minutes from the time a patient reports pain or arrives in the
emergency department.
• By monitoring serial ECG changes over time, the location, evolution, and resolution of an MI
can be identified and monitored.
• The ECG changes that occur with an MI are seen in the leads that view the involved surface of
the heart.
• The classic ECG changes are T-wave inversion, ST-segment elevation, and development of an
abnormal Q wave. Because infarction evolves over time, the ECG also changes over time.

45. CONTI.
• The first ECG signs of an acute MI occur as a result of myocardial ischemia and
injury.
• Myocardial injury causes the T wave to become enlarged and symmetric.
• As the area of injury becomes ischemic, myocardial repolarization is altered and
delayed, causing the T wave to invert.
• The ischemic region may remain depolarized while adjacent areas of the
myocardium return to the resting state.
• Myocardial injury also causes ST-segment changes.

46. CONTI.
• The injured myocardial cells depolarize normally but repolarize more rapidly
than normal cells, causing the ST segment to rise at least 1 mm above the
isoelectric line (the area between the T wave and the next P wave is used
as the reference for the isoelectric line) when measured 0.06 to 0.08
seconds after the end of the QRS, a point called the J point.
• This elevation in the ST segment in two contiguous leads is a key diagnostic
indicator for MI (i.e., STEMI).

47. CONTI.
• The appearance of abnormal Q waves is another indication of
MI. Q waves develop within 1 to 3 days because there is no
depolarization current conducted from necrotic tissue.
• The lead system then views the flow of current from other parts
of the heart.
• A new and significant Q wave is 0.04 seconds or longer and 25%
of the R-wave depth (provided the R wave exceeds a depth of 5
mm).
• An acute MI may also cause a significant decrease in the height
of the R wave.

48. CONTI.
• During an acute MI, injury and ischemic changes are usually present.
• An abnormal Q wave may be present without ST- segment and T-
wave changes, which indicates an old, not acute, MI.
• For some patients, there are no persistent ECG changes, and the MI
is diagnosed by blood levels of cardiac biomarkers.

51. USING THE PREVIOUS INFORMATION, PATIENTS ARE DIAGNOSED
WITH ONE OF THE FOLLOWING FORMS OF ACS:
• Unstable angina: The patient has clinical manifestations of coronary ischemia, but
ECG and cardiac biomarkers show no evidence of acute MI.
• STEMI: The patient has ECG evidence of acute MI with characteristic changes in
two contiguous leads on a 12-lead ECG. In this type of MI, there is significant
damage to the myocardium.
• NSTEMI: The patient has elevated cardiac biomarkers but no definite ECG
evidence of acute MI.

52. CONTI.
• During recovery from an MI, the ST segment often is the first ECG
indicator to return to normal (1 to 6 weeks).
• The T-wave becomes large and symmetric for 24 hours, and it then inverts
within 1 to 3 days for 1 to 2 weeks.
• Q-wave alterations are usually permanent.
• An old STEMI is usually indicated by an abnormal Q wave or decreased
height of the R wave without ST-segment and T-wave changes.

53. ECHOCARDIOGRAM
• The echocardiogram is used to evaluate ventricular
function.
• It may be used to assist in diagnosing an MI,
especially when the ECG is nondiagnostic.
• The echocardiogram can detect hypokinetic and
akinetic wall motion and can determine the ejection
fraction.

54. LABORATORY TESTS
• Cardiac enzymes and biomarkers are used to diagnose an acute MI.
• Cardiac biomarkers, which include myoglobin and troponin, can be
analyzed rapidly, expediting an accurate diagnosis.
• These tests are based on the release of cellular contents into the
circulation when myocardial cells die.

56. CONTI.
Creatine kinase
and its isoenzymes
Myoglobin
Troponin

57. CREATINE KINASE AND ITS
ISOENZYMES
• There are three creatine kinase (CK) isoenzymes: CK-MM (skeletal muscle),
CK-MB (heart muscle), and CK-BB (brain tissue).
• CK-MB is the cardiac-specific isoenzyme; it is found mainly in cardiac cells and
therefore increases only when there has been damage to these cells.
• Elevated CKMB assessed by mass assay is an indicator of acute MI; the level
begins to increase within a few hours and peaks within 24 hours of an MI.
• If the area is repercussed (e.g., due to thrombolytic therapy or PCI), it peaks
earlier.

58. MYOGLOBIN
• Myoglobin is a heme protein that helps transport oxygen.
• Like CK-MB enzyme, myoglobin is found in cardiac and skeletal
muscle.
• The myoglobin level starts to increase within 1 to 3 hours and peaks
within 12 hours after the onset of symptoms.
• An increase in myoglobin is not very specific in indicating an acute
cardiac event; however, negative results are an excellent parameter for
ruling out an acute MI.

59. TROPONIN
• Troponin, a protein found in the myocardium, regulates the myocardial contractile
process.
• There are three isomers of troponin: C, I, and T. Troponins I and T are specific for
cardiac muscle, and these biomarkers are currently recognized as reliable and critical
markers of myocardial injury (Carreiro Lewandowski, 2006).
• An increase in the level of troponin in the serum can be detected within a few hours
during acute MI.
• It remains elevated for a long period, often as long as 3 weeks, and it therefore can
be used to detect recent myocardial damage.

60. MANAGEMENT

62. MEDICAL MANAGEMENT
• The goals of medical management are to minimize myocardial
damage, preserve myocardial function, and prevent complications.
• These goals are facilitated by the use of guidelines developed by the
American College of Cardiology (ACC) and the AHA.
• These goals may be achieved by reperfusion the area with the
emergency use of thrombolytic medications or by PCI.

63. CONTI.
• Minimizing myocardial damage is also accomplished by reducing
myocardial oxygen demand and increasing oxygen supply with
medications, oxygen administration, and bed rest.
• The resolution of pain and ECG changes indicate that demand and
supply are in equilibrium; they may also indicate reperfusion.
• Visualization of blood flow through an open vessel in the
catheterization laboratory is evidence of reperfusion.

65. PHARMACOLOGIC THERAPY
• The patient with suspected MI is given aspirin, nitroglycerin, morphine, an IV beta-blocker,
and other medications as indicated while the diagnosis is being confirmed.
• Patients should continue the beta-blocker throughout hospitalization and after discharge
because long-term therapy with betablockers can decrease the incidence of future cardiac
events.
• Unfractionated heparin or an LMWH is prescribed along with platelet-inhibiting agents to
prevent further clot formation.
• Nonsteroidal anti-inflammatory drugs (NSAIDS) carefully, particularly the blood pressure,
which can decrease, and the respiratory rate, which can be depressed.
• Because morphine decreases the sensation of pain, ST-segment changes may be a better
indicator of subsequent ischemia than reported pain.

66. ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS
• Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II.
• In the absence of angiotensin II, the blood pressure decreases and the kidneys excrete sodium and fluid
(diuresis), decreasing the oxygen demand of the heart.
• Use of ACE inhibitors in patients after MI decreases mortality rates and prevents remodeling of
myocardial cells that is associated with the onset of heart failure.
• It is important to ensure that a patient is not hypotensive, hyponatremic, hypovolemic, or hyperkalemic
before administering ACE inhibitors.
• Blood pressure, urine output, and serum sodium, potassium, and creatinine levels need to be monitored
closely.

67. THROMBOLYTICS
• Thrombolytics are used to treat some patients with acute MI.
• These agents are administered IV according to a specific protocol (Chart 28-8).
• The purpose of thrombolytics is to dissolve (i.e., lyse) the thrombus in a coronary artery (thrombolysis),
allowing blood to flow through the coronary artery again (reperfusion), minimizing the size of the
infarction and preserving ventricular function.
• Thrombolytics can be used as first-line therapy in facilities that lack the resources to perform PCIs
(Boden, Eagle & Granger, 2007).
• However, although thrombolytics may dissolve the thrombus, they do not affect the underlying
atherosclerotic lesion.
• The patient may be referred for a cardiac catheterization and other invasive interventions.

68. CONTI.
• Thrombolytics dissolve all clots, not just the one in the coronary artery.
• Thus, they should not be used if the patient has formed a protective clot elsewhere, such as
after major surgery or hemorrhagic stroke.
• Because thrombolytics reduce the patient’s ability to form a clot, the patient is at risk for
bleeding.
• Thrombolytics should not be used if the patient is bleeding or has a bleeding disorder.
• All patients who receive thrombolytic therapy are placed on bleeding precautions to minimize
the risk for bleeding.
• This means minimizing the number of punctures for inserting IV lines, avoiding IM injections,
preventing tissue trauma, and applying pressure for longer than usual after any puncture.

69. CONTI.
• To be effective, thrombolytics must be administered as early as possible after the
onset of symptoms that indicate an acute MI, generally within 3 to 6 hours.
• They are given to patients with ECG evidence of acute MI.
• The selected thrombolytic agent should be initiated within 30 minutes of presentation
to the hospital (ISCI, 2006a).
• This is called door-to-needle time, and hospitals monitor their ability to administer the
thrombolytic agent within the recommended time period as an indicator of quality of
care.

70. CONTI.
• The thrombolytic agents used most often are alteplase (Activase) and reteplase (r-PA,
TNKase).
• Alteplase is a tissue plasminogen activator (t-PA) that activates the plasminogen present on a
blood clot.
• An IV bolus dose is given and followed by an infusion.
• Aspirin and unfractionated heparin or LMWH may be used with t-PA to prevent another clot
from forming at the site of the lesion.
• Reteplase, a newer recombinant thrombolytic, is similar to alteplase and has similar effects.
• It is administered in two bolus doses, followed by a heparin infusion.

72. ANALGESICS
• The analgesic of choice for acute MI is morphine administered in IV boluses to
reduce pain and anxiety.
• It also reduces preload and afterload, which decreases the workload of the heart
and relaxes bronchioles to enhance oxygenation.
• The cardiovascular response to morphine is monitored carefully, particularly the
blood pressure, which can decrease, and the respiratory rate, which can be
depressed.
• Because morphine decreases the sensation of pain, ST-segment changes may be a
better indicator of subsequent ischemia than reported pain.

73. EMERGENT PERCUTANEOUS CORONARY INTERVENTION
• The patient with STEMI may be 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.
• Superior outcomes have been reported with use of PCI compared to thrombolytics (Antman,
et al., 2007).
• Early PCI has been shown to be effective in patients of all ages, including those older than
75 years (Chart 28-9).
• PCI may also be indicated in patients with unstable angina and NSTEMI who are at high risk
due to persistent ischemia (King, Smith, Hirshfeld, et al., 2007).

74. CONTI.
• The procedure treats the underlying atherosclerotic lesion.
• Because the duration of oxygen deprivation is directly related to the number of
myocardial cells that die, the time from the patient’s arrival in the emergency
department to the time PCI is performed should be less than 60 minutes.
• This is frequently referred to as door-to-balloon time.
• A cardiac catheterization laboratory and staff must be available if an emergent PCI
is to be performed within this short time.

75. HEALTH PROMOTION
To extend and improve the quality of life, a patient who has had an MI must
adjust his or her lifestyle to promote heart healthy living. With this in mind, the
nurse and patient develop a program to help the patient achieve desired
outcomes.

76. LIFESTYLE RECOMMENDATIONS DURING
CONVALESCENCE AND HEALING
Adaptation to an MI is an ongoing process and usually requires some modification of lifestyle.
Instruct patients to make the following specific modifications:-
• Avoid any activity that produces chest pain, extreme dyspnea, or undue fatigue.
• Avoid extremes of heat and cold and walking against the wind.
• Lose weight, if indicated
• Stop smoking and use of tobacco; avoid secondhand smoke.
• Modify meals to align with the Therapeutic Lifestyle Changes (TLC) or other recommended
diet.

77. CONTI.
• Develop heart-healthy eating patterns and avoid large meals and
hurrying while eating
• Adhere to medical regimen, especially in taking medications
• Follow recommendations that ensure blood pressure and blood glucose
are in control
• Pursue activities that relieve and reduce stress.

78. ADOPTION OF AN ACTIVITY PROGRAM
Additionally, the patient needs to undertake a structured program of activity and exercise for long-term
rehabilitation. Advise patients to:-
• Engage in a regimen of physical conditioning with a gradual increase in activity duration and then a
gradual increase in activity intensity.
• Walk daily, increasing distance and time as prescribed.
• Monitor pulse rate during physical activity.
• Avoid physical exercise immediately after a meal.
• Alternate activity with rest periods (some fatigue is normal and expected during convalescence).
• Participate in a daily program of exercise that develops into a program of regular exercise for a lifetime.

79. MANAGING SYMPTOMS
The patient must learn to recognize and take
appropriate action for recurrent symptoms. Make sure
that patients know to do the following:-
• Call 108 if chest pressure or pain (or prodromal
symptoms) is not relieved in 15 minutes by
nitroglycerin.
• Contact the physician if any of the following occur:
shortness of breath, fainting, slow or rapid heartbeat,
swelling of feet and ankles.

80. RESEARCH ARTICLE
Influence of coronary nursing management follow
up on lifestyle after acute myocardial infarction.
1.R. Carlsson,
2.G. Lindberg,
3.L. Westin,
4.B. Israelsson
Department of Medicine, Central Hospital,
Karlstad, Sweden

81. Abstract
OBJECTIVE: To examine the ability of a secondary prevention programme to improve
the lifestyle in myocardial infarction patients aged 50-70 years.
DESIGN: Habitual physical activity, food habits, and smoking habits were assessed from
questionnaires at admission to hospital and at the one year follow up. Initially, all patients
were invited to join an exercise programme and were informed about cardiovascular risk
factors. Four weeks after discharge from the hospital, 87 patients were randomised to
follow up at the coronary prevention unit by a special trained nurse (the intervention
group), and 81 to follow up by their general practitioners (the usual care group). After
randomisation, the intervention group was educated about the effects of smoking
cessation, dietary management, and regular physical activity. The intervention group also
participated in a physical training programme two to three times weekly for 10-12 weeks.

82. MAIN RESULTS: 89% of the patients referred to the intervention group improved their
food habits compared with 62% of the patients referred to the usual care group (P =
0.008). Furthermore, 50% of the smokers referred to the intervention group stopped
smoking compared to 29% in the usual care group (P = 0.09). Changes in physical
activity did not differ between the groups.
CONCLUSIONS: This secondary prevention programme based on a nurse rehabilitator
was successful in improving food habits in patients with acute myocardial infarction.
Initiating the smoking cessation programme during the hospital stay followed by repeated
counselling during follow up might have improved the results. The exercise programme
had no advantage in supporting physical activity compared to usual care.

83. NURSING
MANAGEMENT
The nursing management involved in MI is critical
and systematic, and efficiency is needed to
implement the care for a patient with MI.

84. NURSING ASSESSMENT
• Assess for chest pain not relieved by rest or medications.
• Monitor vital signs, especially the blood pressure and pulse rate.
• Assess for presence of shortness of breath, dyspnea, tachypnea,
and crackles.
• Assess for nausea and vomiting.
• Assess for decreased urinary output.
• Assess for the history of illnesses.
• Perform a precise and complete physical assessment to detect
complications and changes in the patient’s status.
• Assess IV sites frequently.

85. DIAGNOSIS
• Ineffective cardiac tissue perfusion related to reduced coronary
blood flow.
• Risk for ineffective peripheral tissue perfusion related to decreased
cardiac output from left ventricular dysfunction.
• Deficient knowledge related to post-MI self-care.

86. PLANNING & GOALS
• Relief of pain or ischemic signs and
symptoms.
• Prevention of myocardial damage.
• Absence of respiratory dysfunction.
• Maintenance or attainment of adequate
tissue perfusion.
• Reduced anxiety.
• Absence or early detection of
complications.
• Chest pain absent/controlled.
• Heart rate/rhythm sufficient to sustain
adequate cardiac output/tissue
perfusion.
• Achievement of activity level sufficient for
basic self-care.
• Anxiety reduced/managed.
• Disease process, treatment plan, and
prognosis understood.
• Plan in place to meet needs after

87. NURSING
INTERVENTIONS
• Administer oxygen along with medication therapy to assist with relief of symptoms.
• Encourage bed rest with the back rest elevated to help decrease chest discomfort
and dyspnea.
• Encourage changing of positions frequently to help keep fluid from pooling in the
bases of the lungs.
• Check skin temperature and peripheral pulses frequently to monitor tissue perfusion.
• Provide information in an honest and supportive manner.
• Monitor the patient closely for changes in cardiac rate and rhythm, heart sounds,
blood pressure, chest pain, respiratory status, urinary output, changes in skin color,
and laboratory values.

88. DISCHARGE AND HOME CARE
GUIDELINES
• Education. This is one of the priorities that the nurse must teach the patient about
heart-healthy living.
• Home care. The home care nurse assists the patient with scheduling and keeping
up with the follow-up appointments and with adhering to the prescribed cardiac
rehabilitation management.
• Follow-up monitoring. The patient may need reminders about follow-up
monitoring including periodic laboratory testing and ECGs, as well as general health
screening.
• Adherence. The nurse should also monitor the patient’s adherence to dietary

89. THANK YOU..