3. Pathophysiology of Coronary Artery Disease
• Development of Atherosclerosis
Atherosclerosis is a chronic inflammatory disorder that is characterized by an
accumulation of macrophages and T lymphocytes in the arterial intimal wall.
A high LDL cholesterol concentration is one of the triggers of vascular
inflammation.
The inflammation injures the wall, allowing the LDL cholesterol to move into
the vessel wall below the endothelial surface.
Blood monocytes adhere to endothelial cells and migrate into the vessel
wall. Within the artery wall, some monocytes differentiate into macrophages
that unite with and then internalize LDL cholesterol. The foam cells that
result are the marker cells of atherosclerosis
4.
5. B. Acute Coronary Syndrome
• The term acute coronary syndrome (ACS) is used to describe the array
of clinical presentations of CAD that range from unstable angina to
acute MI
• Angina
• Angina pectoris, or chest pain, caused by myocardial ischemia is not a
separate disease, but rather a symptom of CAD.
• The lack of oxygen causes myocardial ischemia, which is felt as chest
discomfort, pressure, or pain.
6.
7.
8.
9. Types of Angina
• Stable Angina.
Stable angina is predictable and caused by similar precipitating factors each
time; typically, it is exercise induced.
Patients become used to the pattern of this type of angina and may describe
it as “my usual chest pain.”
Pain control should be achieved within 5 minutes of rest and by taking
sublingual nitroglycerin.
• Unstable Angina.
Defined as a change in a previously established stable pattern of angina. It is
part of the continuum of ACS.
Unstable angina usually is more intense than stable angina, may awaken the
person from sleep, or may necessitate more than nitrates for pain relief.
10. Types of Angina ..cont.
• Variant Angina.
Variant angina, or Prinzmetal angina, is caused by a dynamic obstruction from
intense vasoconstriction of a coronary artery.
Coronary artery spasm is treated with nitroglycerin or calcium channel
blockers to vasodilate the coronary arteries
• Silent Ischemia.
Silent ischemia describes a situation in which objective evidence of ischemia
is observed on an ECG monitor but the person does not complain of anginal
symptoms.
11. Medical Management
• Aspirin (if the patient cannot tolerate aspirin, then a thienopyridine
such as clopidogrel can be given)
• Patients with definite unstable angina or non–ST elevation myocardial
infarction (UA or NSTEMI) should receive dual antiplatelet therapy on
admission if an invasive strategy is imminent.
• A glycoprotein (GP) IIb/IIIa inhibitor is administered unless bivalirudin
is chosen; and a loading dose of clopidogrel is given at least 6 hours
prior to the procedure.
12.
13. Relieving Chest Pain
• Oxygen:
All patients with acute ischemic pain are administered supplemental oxygen to
increase myocardial oxygenation.
• Nitrates:
A combination of intravenous and sublingual nitroglycerin is used to
vasodilate the coronary arteries and decrease pain.
After nitrate administration, the critical care nurse closely observes the
patient for relief of chest pain, for return of the ST segment to baseline, and
for the potential development of unwanted side effects such as hypotension
and headache.
Administration of a nitrate is avoided if the SBP is below 90 mm Hg.
14. Relieving Chest Pain …cont.
• Analgesia:
Morphine (2 to 4 mg given intravenously) is the analgesic opiate of
choice for preinfarction angina.
• Aspirin:
Chewing an oral non–enteric-coated aspirin (162 to 325 mg) at the
beginning of chest pain has been shown to reduce mortality.
15. Patient Education
• After the anginal pain is controlled, longer-term education of th
patient and the family can begin. Points to cover include:
1) Risk factor modification
2) Signs and symptoms of angina,
3) When to call the physician,
4) Medications, and
5) Dealing with emotions and stress.
17. MYOCARDIAL INFARCTION
• Myocardial infarction (MI) is the term used to describe irreversible
myocardial necrosis (cell death) that results from an abrupt decrease
or total cessation of coronary blood flow to a specific area of the
myocardium.
• Three mechanisms can block the coronary artery and are responsible
for the acute reduction in oxygen delivery to the myocardium:
1. Plaque rupture
2. New coronary artery thrombosis
3. Coronary artery spasm close to the ruptured plaque
18. Pathophysiology
A. Ischemia
The outer region of the infarcted myocardial area is the zone of
ischemia, or penumbra.
B. Injury
The infarcted zone is surrounded by injured but still potentially viable
tissue in an area known as the zone of injury
C. Infarction
The area of dead muscle (necrosis) in the myocardium is known as the
zone of infarction
19.
20. 12-Lead Electrocardiographic
Changes
• The changes in
repolarization are seen
by the presence of new
Q waves. These new,
pathologic Q waves are
deeper and wider than
tiny Q waves found on
the normal 12-lead ECG
B- inversion T wave indicated to Ischemia
C- T wave inversion and ST- segment elevation
Indicated to Ischemia and current injury
D- Q wave indicated to necrosis
A- normal ECG
21. Non–ST-Segment Elevation Myocardial
Infarction
• One reason for the lack of ST-segment elevation may be that the
infarction and subsequent necrosis are not full thickness lesions.
Because some of the muscle in the area can still be depolarized, ST-
segment elevation may not occur.
• This type of MI is also less likely to develop Q waves on a subsequent
12-lead ECG after the acute phase has passed. This situation is
diagnostically known as an NSTEMI.
24. Complications of Acute Myocardial Infarction
Sinus Bradycardia
heart rate less than 60 beats per minute [beats/min
Sinus Tachycardia.
Sinus tachycardia (heart rate more than 100 beats/min)
Atrial Dysrhythmias.
Premature atrial contractions (PACs) occur frequently in patients who sustain an acute MI.
Ventricular Dysrhythmias.
Premature ventricular contractions (PVCs) are seen in almost all patients within the first
few hours after an MI.
Atrioventricular Heart Block During Myocardial Infarction.
Heart block can occur in 6% to 14% of patients with STEMI, and those patients have
increased mortality rates.
25. Complications of Acute Myocardial Infarction … cont.
Ventricular Aneurysm After Myocardial
Infarction.
Ventricular Septal Rupture After Myocardial
Infarction
Heart Failure and Acute Myocardial Infarction
26. Medical Management
• Recanalization of the Coronary Artery
fibrinolytic therapy or PCI to open the occluded artery for the patient with an
acute STEMI
• Anticoagulation
For patients who will receive fibrinolytic therapy, an initial heparin bolus of 60
units/kg (maximum 5000 units) is given intravenously, followed by a continuous
heparin drip at 12 units/kg/hr (maximum 1000 units/hr) to maintain an
activated partial thromboplastin time (aPTT) between 50 and 70 seconds (1.5 to
2.0 times) control for 48 hours or until revascularization.
27. Medical Management … cont.
• Dysrhythmia Prevention
The antidysrhythmic with the best safety record after STEMI is amiodarone.
Beta-blockers are another class of antidysrhythmics that are recommended
for all patients after STEMI.
Beta-blockers prevent ventricular dysrhythmias, lower blood pressure, and
prevent reinfarction, especially in patients with left ventricular dysfunction.
Prevention of Ventricular Remodelling
Many patients are at risk for development of heart failure after STEMI.
Vasodilating medications (ACEIs or ARBs) can stop or limit the ventricular
remodeling that leads to heart failure.
30. HEART FAILURE
• Pathophysiology
I. a condition in which the heart cannot pump blood at a volume required to
meet the body’s needs.
II. CAD with resultant necrotic damage to the left ventricle is the underlying
cause of heart failure in most patients.
III. Other major conditions that lead to heart failure include valvular
dysfunction
31.
32. Type of heart failure.
1. Left Ventricular Failure
defined as a disturbance of the contractile function of the left ventricle,
resulting in a low cardiac output state.
This leads to vasoconstriction of the arterial bed that raises systemic vascular
resistance (SVR), a condition also described as “high afterload,” and creates
congestion and edema in the pulmonary circulation and alveoli.
Ptients presenting with left ventricular failure have one of the following:
1) decreased exercise tolerance
2) fluid retention
3) discovery during examination of noncardiac problems.
33. 2. Right Ventricular Failure
• defined as ineffective right ventricular contractile function. Pure
failure of the right ventricle may result from an acute condition such
as a pulmonary embolus or a right ventricular infarction
• The common manifestations of right ventricular failure are: jugular
venous distention, elevated central venous pressure (CVP), weakness,
peripheral or sacral edema, hepatomegaly (enlarged liver), jaundice,
and liver tenderness. Gastrointestinal symptoms include poor
appetite, anorexia, nausea, and an uncomfortable feeling of fullness
34.
35. 3. Systolic Heart Failure
The term systolic dysfunction describes an abnormality of the heart
muscle that markedly decreases contractility during systole (ejection)
and lessens the quantity of blood that can be pumped out of the heart.
4. Diastolic Heart Failure
abnormality of the heart muscle that makes it unable to relax, stretch,
or fill during diastole. Diastolic heart failure (DHF) is caused by left
ventricular dysfunction.
37. Pulmonary Complications of Heart Failure
• Breathlessness in heart failure is described by the following terms:
Dyspnea: the patient’s sensation of shortness of breath, which from pulmonary
vascular congestion and decreased lung compliance
Orthopnea: difficulty breathing when lying flat because of an increase in venous
return that occurs in the supine position
Paroxysmal nocturnal dyspnea: a severe form of orthopnea in which the patient
awakens from sleep gasping for air
Cardiac asthma: dyspnea with wheezing, a non-productive cough, and pulmonary
crackles that progress to the gurgling sounds of pulmonary edema
Pulmonary Edema in Heart Failure
Pulmonary edema, or protein-laden fluid in the alveoli, inhibits gas exchange
by impairing the diffusion pathway between the alveolus and the capillary. It
is caused by increased left atrial and ventricular pressures and results in an
excessive accumulation of serous or serosanguineous fluid in the interstitial
spaces and alveoli of the lungs.
38. Medical Management
A. Relief of Symptoms and Enhancement of Cardiac Performance.
Acute phase of advanced heart failure, the patient may have a pulmonary
artery catheter in place so that left ventricular function can be monitored
closely.
• Control of symptoms involves management of fluid overload and improvement of
cardiac output by decreasing SVR and increasing contractility.
• Diuretics are administered to decrease preload and to eliminate excess fluid from
the body.
• Morphine is given to facilitate peripheral dilation and decrease anxiety.
• Afterload is decreased by vasodilators such as sodium nitroprusside (Nipride) and
nitroglycerin.
• Sodium nitroprusside is a balanced vasodilator medication that relaxes arterial
resistance and venous capacitance vessels.
• Nitrates are used to decrease preload and vasodilate the coronary arteries if CAD is
an underlying cause of the acute heart failure.
39. Medical Management … cont.
A. Chronic phase
• After the acute exacerbation is resolved, the patient is transitioned to oral
agents
• patient with heart failure will receive ACEIs to inhibit left ventricular chamber
remodelling and slow left ventricular dilation.
• Digoxin may be added to the regimen, especially if the person has
concomitant AF.
42. VALVULAR HEART DISEASE appendix 3
• Mitral Valve Stenosis
The term mitral valve stenosis describes a progressive narrowing of the
mitral valve orifice.
Symptoms occur when the normal valve size is reduced to 2 cm2 or
less. Symptoms occur at rest when the valve area is reduced below 1
cm.
• Mitral Valve Regurgitation
Mitral valve regurgitation results in retrograde flow of blood into the
left atrium with each ventricular contraction.
43. VALVULAR HEART DISEASE … cont.
• Aortic Valve Stenosis
describes a narrowing of the aortic valve area.
• Aortic Valve Regurgitation
Aortic valve incompetence results in a reflux of blood back into the left
ventricle during ventricular diastole.
• Tricuspid Valve Stenosis
It often occurs in conjunction with mitral or aortic disease.
Tricuspid valve stenosis increases the pressure work of the usually low-
pressure right atrium, resulting in right atrial hypertrophy
44. Medical Management
• Management of valvular disorders includes pharmacologic therapy to
control symptoms of heart failure and then cardiac surgical repair or
replacement of the affected valve.
