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Chapter 30 Coordinating Care for Patients With Cardiac Disorders
Unit VI Promoting Health in Patients with Circulatory or Perfusion Disorders
A variation of unstable angina is variant , or Prinzmetal’s, angina . The blockage of blood flow in this disorder is caused by coronary artery spasm rather than plaque formation, but commonly atherosclerotic changes are present. It typically occurs at rest and in clusters. Interestingly, it normally occurs at night between midnight and 8 a.m.
develops when there is an imbalance between supply and demand of oxygen-rich blood to the heart tissue resulting in insufficient oxygen to meet the demands of the myocardial tissue . Infarction, or cell death, occurs when that imbalance is severe or prolonged, which causes irreversible damage. The primary patient complaint is chest pain, also called angina . Angina is classified into two categories, stable and unstable angina. Stable angina is chest pain or discomfort that is associ- ated with physical activity. It is typically linked to fixed plaque formations. Symptoms of stable angina are often alleviated with rest and/or medications. Nitrates such as nitroglycerin that dilate the coronary arteries, improving oxygen-rich blood flow to the heart, are typically prescribed for angina. Unstable angina refers to chest pain that can occur at rest. Of the two types of angina, unstable angina is the most con- cerning. It is identified as the initial phase of acute coronary syndrome (ACS), defined as a disorder caused by an acute decrease in blood flow through the coronaries to the myocar- dial tissue, and can be a precursor to MI. It should be treated as an emergency. Unstable angina is usually prolonged and may not be relieved with medication. In addition to nitroglyc- erin, these patients may z medications such as morphine. Supplemental oxygen is typically necessary.
FIGURE 30.1 Layers of the arterial wall.
Management Medical Management
Tunica adventitia
Tunica media
Tunica intima
As stated previously, the formation of plaque within the blood vessels is a silent process. Often CAD is suspected only when the individual presents with clinical symptoms. The diagnosis is made on the basis of clinical presentation and diagnostic findings. Laboratory Tests Laboratory tests diagnostic for CAD are summarized in Table 30.2. Many of the blood tests performed assess for the presence of risk factors for CAD development, such as lipid profiles, inflammation, and coagulation studies. Lipid profiles evaluate total cholesterol and triglyceride levels as well as the ratio of LDL to high-density lipoprotein (HDL) to determine if hyperlipidemia is present. Specific cardiac enzymes are used to rule out MI.
Smooth muscle
Endothelium
Basement membrane
Internal elastic membrane
External elastic membrane
part of the vessel, forming plaque. The plaque deposits in- crease in size over time causing narrowing of the coronary arteries, which impedes oxygen-rich blood flow to the heart (Figure 30.2). The next and most dangerous step in the development of atherosclerosis is potential plaque rupture. When that oc- curs, platelets aggregate on the ruptured plaque surface. The coagulation cascade is initiated, and thrombus formation is
stimulated. This further decreases or obstructs blood flow altogether leading to unstable angina, myocardial infarction (MI), or sudden cardiac death. Clinical Manifestations The clinical manifestations of CAD are virtually silent until the artery is approximately 40% blocked by plaque. Ischemia
Table 30.2 Laboratory Tests Diagnostic for Coronary Artery Disease
Laboratory Tests
Rationale
Electrolyte imbalances along with increases in renal or hepatic laboratory values may indicate damage caused by poor perfusion or may indicate the presence of risk factors for heart disease. Laboratory values included in the comprehensive metabolic profile include: l Glucose, calcium, sodium, potassium, carbon dioxide, chloride Laboratory values helpful in assessing renal function in addition to electrolytes, sodium, and potassium include: l BUN, creatinine, total protein Laboratory values helpful in assessing hepatic function include: l ALP, ALT, AST, bilirubin, total protein, and albumin
l Comprehensive metabolic panel to establish a baseline, assess electrolyte balance, and assess renal and hepatic functions
l Glucose (80–100 mg/dL) l Calcium (8.5–10.9 mg/dL) l Albumin (3.9–5.0 g/dL)
l Total protein (6.3–7.9 g/dL) l Sodium (135–145 mEq/L) l Potassium (3.5–5.0 mEq/L) l Carbon dioxide (20–29 mmol/L) l Chloride (96–106 mmol/L) l Blood/urea/nitrogen (BUN) (7–22 mg/dL) l Creatinine (0.5–1.3 mg/dL) l Alkaline phosphatase (ALP) (44–147 IU/L) l Alanine aminotransferase (ALT) (8–37 IU/L) l Aspartate aminotransferase (AST) (10–34 IU/L) l Bilirubin (0.2–1.9 mg/dL) l Inflammatory markers such as C-reactive protein l Less than 1.0 mg/L = low risk for CVD l 1.0–2.9 mg/L = intermediate risk for CVD l Greater than 3.0 mg/L = high risk for CVD
FIGURE 30.2 A comparison of a normal artery with an artery narrowed by athero- sclerotic plaque deposits on the wall.
Artery cross section
Normal artery
Endothelium
Normal blood flow
Artery wall
Narrowing artery
Atherosclerotic plaque
Assess for the presence of inflammation and/or derangements in clotting, which are both implicated in the development of atherosclerosis
Damaged endothelium
Abnormal blood flow Atherosclerotic plaque
Narrowed artery
Continued
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