Critical Care Exam 2 latest complete
study guide 2024
Coronary Atherosclerosis (CA) An abnormal accumulation of lipid, or fatty substances, and
fibrous tissue in the lining of arterial blood vessel walls.
CA Pathophysiology: -Inflammatory response due to injury to the vascular endothelium and
progresses over many years
-Injury may be initiated by smoking or tobacco use, hypertension, hyperlipidemia, and other
factors
-Endothelium changes and stops producing normal antithrombotic and vasodilating agents,
presence of inflammation attracts inflammatory cells, such as macrophages, macrophages ingest
lipids, becoming "foam cells" that transport the lipids into the arterial wall, some of the lipid is
deposited on the arterial wall, forming fatty streaks, activated macrophages also release
biochemical substances that can further damage the endothelium by contributing to the oxidation
of low-density lipoprotein (LDL)
-Smooth muscle cells proliferate and form a fibrous cap over a core filled with lipid and
inflammatory infiltrate, these deposits (atheromas, or plaques) protrude into the lumen of the
vessel, narrowing it and obstructing blood flow
-If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can
resist the stress of blood flow and vessel movement
-If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable
plaque
-Ruptured plaque attracts platelets and causes thrombus formation, a thrombus may then obstruct
blood flow, leading to acute coronary syndrome (ACS)
-Atherosclerotic lesions most often form where the vessels branch and with turbulent blood flow,
suggesting a hemodynamic component is involved in their formation
-Other causes of decrease blood flow to the heart: vasospasm (sudden constriction or narrowing)
of a coronary artery and profound hypotension
CA Manifestations: -Depends on location, degree of narrowing, thrombus formation, and
obstruction of blood flow to myocardiaum
-Ischemia (causes angina pectoris)
-Persistently low cardiac output and heart failure
-Sudden cardiac death (decrease in blood supply from CAD may cause the heart to abruptly stop
beating)
,-Epigastric distress and pain that radiates to the jaw or left arm
-Shortness of breath
-Most common manifestation of myocardial ischemia is the onset of chest pain
-Women: indigestion, nausea, palpitations, and numbness, prodromal symptoms may occur (e.g.,
angina a few hours to days before the acute episode), or a major cardiac event may be the first
indication of coronary atherosclerosis
Nonmodifiable Risk Factors: -Family history of CAD (first-degree relative with cardiovascular
disease at 55 years of age or younger for men and at 65 years of age or younger for women)
-Increasing age (more than 45 years for men; more than 55 years for women)
-Gender (men develop CAD at an earlier age than women
-Race (higher incidence of heart disease in African Americans than in Caucasians)
-History of premature menopause (before age 40) and history of pregnancy-associated disorders
such as preeclampsia
-Primary hypercholesterolemia (a genetic condition resulting in elevated LDL)
Modifiable Risk Factors: -Hyperlipidemia
-Tobacco use
-Hypertension
-Diabetes
-Metabolic syndrome
-Obesity
-Physical inactivity
-Chronic inflammatory conditions (e.g., rheumatoid arthritis, lupus, HIV/AIDS; Chronic kidney
disease)
Other Risk Factors: -Enlarged waist circumference
-Elevated triglycerides
-Reduced HDL
-HTN
-Elevated fasting glucose
CA Treatment: -Control cholesterol: have fasting lipid profile done every 5 years (LDl
under 100, total cholesterol under 200, HDL above 40-50, and triglycerides under 150),
Mediterranean diet, vegetarian diet, weight reduction, increase physical activity, medications to
lower lipid levels (statins, fibrates, etc)
-Tobacco use: the use of medications such as the nicotine patch, nicotine lozenges, nicotine gum,
varenicline, or bupropion may assist with stopping the use of tobacco
-HTN: keep blood pressure under 130/80 for all adults
-Diabetes: treat with insulin, metformin, and other interventions to lower glucose
Angina Pectoris (AP): Chest pain or discomfort that occurs when a part of your heart doesn't get
enough blood and oxygen
, AP Pathophysiology: -Usually caused by atherosclerotic disease and most often is associated
with a significant obstruction of at least one major coronary artery
-Several factors are associated with typical anginal pain (physical exertion, exposure to cold
which causes vasoconstriction, eating a heavy meal, stress or emotion-provoking situation), these
increase oxygen demand
AP Manifestations: -Pain, mild indigestion, choking or heavy sensation in chest, apprehension
or impending death, discomfort radiates to neck, jaw, shoulders, and inner aspects of arm,
weakness, SOB, pallor, diaphoresis, lightheaded, N/V, subsides with nitroglycerin and rest
Treatment Goal: -Decrease oxygen demand and increase supply
AP Medical Management: -Pharmacologic therapy and control of risk factors, percutaneous
transluminal coronary angioplasty (PTCA), intracoronary stents, CABG
-Oxygen Therapy
AP Pharmacological Treatment: -Nitroglycerin (causes vasodilation, lower BP, decreases
oxygen demand, do not give if systolic under 90), beta-adrenergic blockers (metoprolol, reduces
heart rate, slows conduction of impulses, decreases BP, reduces myocardial contractility),
calcium channel blockers (decrease SA node and AV node conduction, dilate smooth muscle,
decrease BP, amlodipine, diltiazem), antiplatelet and anticoagulant medications (aspirin,
adenosine diphosphate receptor antagonists, heparin, glycoprotein IIb/IIa agents)
Diagnostic studies pertinent to CAD/angina diagnosis: -Patient history related to
manifestations
-12-lead ECG to show changes related to ischemia (T-wave inversion, ST-segment elevation,
abnormal Q wave)
-Cardiac biomarker to rule out ACS
-Exercise or pharmacologic stress test
-Nuclear scan or invasive procedure (cardiac catheterization, coronary angiography)
Nursing interventions & rationales for patients with angina and coronary artery disease: -Treat
Angina: sit and rest, fowler position to reduce O2 requirements, ask questions to determine if
angina is same experience usually, measure VS, observe for respiratory distress, give
nitroglycerin sublingually, give oxygen
-Reduce Anxiety: guided imagery, music therapy, provide education on illness, treatment, and
methods of preventing progression
-Prevent Pain: identify level of activity that causes pain, alternate activities with rest periods,
balance
-Continuing and Transitional Care: arrange to meet needs for patients with disability or special
needs, home health or transitional nurse, recommend modifications to lifestyle
Percutaneous coronary interventions (PCIs): -Process of mechanically dilating a blood vessel
study guide 2024
Coronary Atherosclerosis (CA) An abnormal accumulation of lipid, or fatty substances, and
fibrous tissue in the lining of arterial blood vessel walls.
CA Pathophysiology: -Inflammatory response due to injury to the vascular endothelium and
progresses over many years
-Injury may be initiated by smoking or tobacco use, hypertension, hyperlipidemia, and other
factors
-Endothelium changes and stops producing normal antithrombotic and vasodilating agents,
presence of inflammation attracts inflammatory cells, such as macrophages, macrophages ingest
lipids, becoming "foam cells" that transport the lipids into the arterial wall, some of the lipid is
deposited on the arterial wall, forming fatty streaks, activated macrophages also release
biochemical substances that can further damage the endothelium by contributing to the oxidation
of low-density lipoprotein (LDL)
-Smooth muscle cells proliferate and form a fibrous cap over a core filled with lipid and
inflammatory infiltrate, these deposits (atheromas, or plaques) protrude into the lumen of the
vessel, narrowing it and obstructing blood flow
-If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can
resist the stress of blood flow and vessel movement
-If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable
plaque
-Ruptured plaque attracts platelets and causes thrombus formation, a thrombus may then obstruct
blood flow, leading to acute coronary syndrome (ACS)
-Atherosclerotic lesions most often form where the vessels branch and with turbulent blood flow,
suggesting a hemodynamic component is involved in their formation
-Other causes of decrease blood flow to the heart: vasospasm (sudden constriction or narrowing)
of a coronary artery and profound hypotension
CA Manifestations: -Depends on location, degree of narrowing, thrombus formation, and
obstruction of blood flow to myocardiaum
-Ischemia (causes angina pectoris)
-Persistently low cardiac output and heart failure
-Sudden cardiac death (decrease in blood supply from CAD may cause the heart to abruptly stop
beating)
,-Epigastric distress and pain that radiates to the jaw or left arm
-Shortness of breath
-Most common manifestation of myocardial ischemia is the onset of chest pain
-Women: indigestion, nausea, palpitations, and numbness, prodromal symptoms may occur (e.g.,
angina a few hours to days before the acute episode), or a major cardiac event may be the first
indication of coronary atherosclerosis
Nonmodifiable Risk Factors: -Family history of CAD (first-degree relative with cardiovascular
disease at 55 years of age or younger for men and at 65 years of age or younger for women)
-Increasing age (more than 45 years for men; more than 55 years for women)
-Gender (men develop CAD at an earlier age than women
-Race (higher incidence of heart disease in African Americans than in Caucasians)
-History of premature menopause (before age 40) and history of pregnancy-associated disorders
such as preeclampsia
-Primary hypercholesterolemia (a genetic condition resulting in elevated LDL)
Modifiable Risk Factors: -Hyperlipidemia
-Tobacco use
-Hypertension
-Diabetes
-Metabolic syndrome
-Obesity
-Physical inactivity
-Chronic inflammatory conditions (e.g., rheumatoid arthritis, lupus, HIV/AIDS; Chronic kidney
disease)
Other Risk Factors: -Enlarged waist circumference
-Elevated triglycerides
-Reduced HDL
-HTN
-Elevated fasting glucose
CA Treatment: -Control cholesterol: have fasting lipid profile done every 5 years (LDl
under 100, total cholesterol under 200, HDL above 40-50, and triglycerides under 150),
Mediterranean diet, vegetarian diet, weight reduction, increase physical activity, medications to
lower lipid levels (statins, fibrates, etc)
-Tobacco use: the use of medications such as the nicotine patch, nicotine lozenges, nicotine gum,
varenicline, or bupropion may assist with stopping the use of tobacco
-HTN: keep blood pressure under 130/80 for all adults
-Diabetes: treat with insulin, metformin, and other interventions to lower glucose
Angina Pectoris (AP): Chest pain or discomfort that occurs when a part of your heart doesn't get
enough blood and oxygen
, AP Pathophysiology: -Usually caused by atherosclerotic disease and most often is associated
with a significant obstruction of at least one major coronary artery
-Several factors are associated with typical anginal pain (physical exertion, exposure to cold
which causes vasoconstriction, eating a heavy meal, stress or emotion-provoking situation), these
increase oxygen demand
AP Manifestations: -Pain, mild indigestion, choking or heavy sensation in chest, apprehension
or impending death, discomfort radiates to neck, jaw, shoulders, and inner aspects of arm,
weakness, SOB, pallor, diaphoresis, lightheaded, N/V, subsides with nitroglycerin and rest
Treatment Goal: -Decrease oxygen demand and increase supply
AP Medical Management: -Pharmacologic therapy and control of risk factors, percutaneous
transluminal coronary angioplasty (PTCA), intracoronary stents, CABG
-Oxygen Therapy
AP Pharmacological Treatment: -Nitroglycerin (causes vasodilation, lower BP, decreases
oxygen demand, do not give if systolic under 90), beta-adrenergic blockers (metoprolol, reduces
heart rate, slows conduction of impulses, decreases BP, reduces myocardial contractility),
calcium channel blockers (decrease SA node and AV node conduction, dilate smooth muscle,
decrease BP, amlodipine, diltiazem), antiplatelet and anticoagulant medications (aspirin,
adenosine diphosphate receptor antagonists, heparin, glycoprotein IIb/IIa agents)
Diagnostic studies pertinent to CAD/angina diagnosis: -Patient history related to
manifestations
-12-lead ECG to show changes related to ischemia (T-wave inversion, ST-segment elevation,
abnormal Q wave)
-Cardiac biomarker to rule out ACS
-Exercise or pharmacologic stress test
-Nuclear scan or invasive procedure (cardiac catheterization, coronary angiography)
Nursing interventions & rationales for patients with angina and coronary artery disease: -Treat
Angina: sit and rest, fowler position to reduce O2 requirements, ask questions to determine if
angina is same experience usually, measure VS, observe for respiratory distress, give
nitroglycerin sublingually, give oxygen
-Reduce Anxiety: guided imagery, music therapy, provide education on illness, treatment, and
methods of preventing progression
-Prevent Pain: identify level of activity that causes pain, alternate activities with rest periods,
balance
-Continuing and Transitional Care: arrange to meet needs for patients with disability or special
needs, home health or transitional nurse, recommend modifications to lifestyle
Percutaneous coronary interventions (PCIs): -Process of mechanically dilating a blood vessel
