Download myocardial infarction

Coronary Artery Disease
Dr. Belal Hijji, RN, PhD
September 28, 2011
Learning Outcomes
At the end of this lecture, students will be able to:
• Provide brief description of CAD and its etiology.
• Discuss the risk factors for the development of CAD and
describe its pathophysiology.
• Define unstable angina, recognise its medical and
nursing management..
• Define MI and describe its pathophysiology in brief.
• Discuss the medical and nursing management of patient
with acute MI.
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Description and Etiology
• CAD is the biggest contributor to cardiovascular-related
morbidity and mortality. Atherosclerosis is a progressive
disease that affect arteries throughout the body.
• There is a strong association between specific risk
factors and the development of CAD. These are
discussed next.
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Risk Factors for CAD
• These factors are:
– Nonmodifiable such as age (middle & old), race (people of
color & multiracial population than white people), family
history (close blood relatives who had MI or stroke before
the age of sixty).
– Modifiable such as elevated serum lipids (cholesterol,
triglycerides, HDL, LDL, VLDL). Refer to the last slide for
these abbreviations. Other factors are high-fat diet,
obesity, physical inactivity, hypertension (SBP > 140 mm
Hg or DBP > 90 mm Hg), cigarette smoking, and chronic
kidney disease.
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Pathophysiology of CAD
• CAD is a progressive atherosclerotic disorder of the
coronary arteries that results in narrowing or complete
obstruction (See picture on next slide).
• Atherosclerosis affects the medium-size arteries that
perfuse the heart and other organs.
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Acute Coronary Syndromes (ACS)
• ACS is used to describe the array of clinical
presentations of CAD that range from unstable angina to
acute MI (myocardial infarction). Both cases will be dealt
with next.
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Unstable Angina
• Unstable angina is defined as a change in a previously
established stable pattern of angina (which is
predictable, exercise induced, and results from fixed
blockages of > 75% of the coronary artery lumen).
• Unstable angina is more intense than stable angina, may
interrupt sleep, or may require than nitrates for pain
relief.
• Severe angina that lasts for more than 5 minutes, is
worsening in intensity, and is not relieved by nitroglycerin
tablet is a medical emergency. Activate Emergency
Medical Services to take the patient to hospital.
• Unstable angina may indicate atherosclerotic plaque
rupture and thrombus formation that can lead to MI.
Patient reporting to emergency dept. with recent onset of
unstable angina who has nonspecific or nonelevated ST
segment should be admitted to the CCU.
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Medical Management
• If there is ST segment elevation on 12-lead ECG, the
patient should be treated for acute MI.
Normal ECG
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An ECG showing ST-segment elevation (orange) in I, aVL and V1-V5 with
reciprocal changes (blue) in the inferior leads, indicative of an anterior wall
myocardial infarction
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Medical Management (Continued..)
• If there is no ST segment elevation but chest pain
continues, the patient should receive aspirin,
nitroglycerin for vasodilation, intravenous antiplatelet
agents such as glycoprotein inhibitors, and
unfractionated heparin.
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Nursing Management
• Nursing interventions of a patient with angina focus on:
• Early identification of myocardial ischemia.
• Assess immediately any complaints of chest pain using a
pain scale of 0 – 10, as pain (or pressure or heaviness) is an
indicator of myocardial ischemia. Immediate assessment is
important for early identification and treatment.
• Document vital signs, ECG, skin color, peripheral pulses,
level of consciousness, and overall tissue perfusion.
• Control of chest pain.
• Administer oxygen, nitrates, and analgesia as ordered.
• Use pulse oximetry to guide therapy and maintain
oxygen saturation above 90%.
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• Nursing interventions of a patient with angina focus on
(Continued…):
• Patient and family education
• Educate your patient when his/ her condition has stabilised
(pain controlled).
• Teach the patient about the importance of avoiding the
Valsalva maneuver (bearing down when going to bath room).
This maneuver increases intrathoracic pressure that
decreases venous return to the right side of the heart which
is associated with hypotension and bradycardia.
• Teach the patient about risk factor modifications such as
decreasing fat intake, stopping smoking, reducing salt intake,
controlling hypertension, increasing physical activity as
tolerated, and achieving normal body weight.
• Provide information about medications; indications and side
effects.
• Teach the patient about the importance of follow up after
discharge and how to handle emotional stress and anger.
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Myocardial Infarction
• Definition: MI is a description of an irreversible
myocardial necrosis (cell death) that results from abrupt
decrease or complete cessation of coronary blood flow
to the myocardium.
• Pathophysiology (See next slide):
– Ischemia: The outer region of infarcted myocardial area
known as zone of ischemia. It is composed of viable cells.
– Injury: The infarcted zone is surrounded by injured but still
potentially viable tissue known as zone of injury.
– Infarction: The area of dead muscle in the myocardium.
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A myocardial infarction (2) of the tip of the anterior wall of the
heart (an apical infarct) after occlusion (1) of a branch of the left
coronary artery (LCA), right coronary artery = RCA.
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Medical Management of MI
• Using the research-based guidelines developed by the
American College of Cardiology and the American Heart
Association decreases in-hospital mortality rate post MI
from 15.3% to 8.3%. Emergency treatment of acute
STEMI includes:
– Fibrinolytic therapy (Streptokinase, or alteplase, or
reteplase) are used to stimulate lysis of the clot or through
mechanical opening the occluded artery.
– Anticoagulants: Heparin co-administration with fibrinolytic
therapy. The initial dose of heparin is 60 International Units
(IU)/ kg (Maximum 4000 IU) IV, followed by continuous
heparin drip at 12 IU/kg/hr (Max 1000 IU/hr).
– Beta-blockers (metoprolol or atenolol) to prevent
dysrhythmias.
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Medical Management of MI (Continued…)
– Anti-diabetic agents for tight glucose control to improve
survival rate.
– Angiotensin-Converting Enzyme (ACE) Inhibitors: These
include lisinopril and captopril and are helpful in prevention
of heart failure.
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Nursing Management of MI
• Nursing interventions for a patient with acute MI
focus on:
– Achieving a balance between myocardial oxygen
supply and demand: This means that in the acute
phase, there is a need to increase myocardial oxygen
supply by oxygen administration to prevent tissue
hypoxia. Myocardial oxygen supply can be enhanced
by the administration of coronary artery vasodilators
(nitroglycerin).
– Prevention of complications: Nurses need to apply
cardiac monitoring of patient to detect early
ventricular dysrhythmias. In addition, nurses should
continue to assess for signs of ischemic pain.
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Nursing Management of MI (Continued…)
– Health education: Nurses should focus on:
• Pathophysiology of acute MI.
• Description of signs and symptoms such as pain.
pressure, or heaviness in chest.
• Notification of nurses of any changes in chest pain
intensity.
• Avoidance of the Valsalva maneuver.
• Risk factors modification, including:
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–
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Daily fat intake < 30% of total calories.
Maintain serum cholesterol level < 200 mg/dL.
Maintain LDL cholesterol to < 70 mg/dL.
Stop smoking and reduce daily salt intake.
Control hypertension and diabetes mellitus.
Increase physical activity and reduce weight
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Nursing Management of MI (Continued…)
– Health education (Continued…): Nurses should focus
on:
• Medication teaching: indications and side effects.
• Follow-up care after discharge.
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Abbreviations
• HDL cholesterol: High-density lipoprotein cholesterol. It is
described as good cholesterol because it has protective effect
against acute atherosclerosis.
• LDL cholesterol: Low-density lipoprotein cholesterol. It is
described as the bad cholesterol because high levels are
associated with an increased risk of CAD, stroke, and
peripheral arterial disease.
• VLDL cholesterol: Very-low-density lipoprotein cholesterol.
When the triglyceride levels are high, the VLDL level is also
high.
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