Week 4 CAD, MI, and Vascular Disease Flashcards
Blow flow of systemic circulation
Heart
arteries
arterioles
capillary bed
venules
veins
vena cave
Atherosclerosis
a hardening of the arteries
Coronary artery disease prevalence
1 cause of mortality in the U.S., with almost 1 million deaths in 2020
Coronary artery disease risk factors
HTN
Diabetes + metabolic syndromes
Tobacco use
Sedentary lifestyle
Nonmodifiable risk factors – age, gender, family hx
Pathophysiology of coronary artery disease
development of fatty streak
Progressions of plaque
Plaque disruption
Fatty streak
liquid foam cells proliferating in tunica intima -> fibrous plaque/lesion
smooth muscle cells (SMC), macrophages, ECM, lipids
Fatty streak is most com in
arterial branches (carotids, coronary arteries)
Fatty streak may be present in
most adults by age 20
asymptomatic
Fatty streak cellular processes
Increased permeability of endothelium increased LDL in inner layer of vessel that binds to ECM
Increased leukocyte activation
Release of catecholamines, nitric oxide, other vasoactive substances
Change in normal anti-clotting properties of the vasculature
Progression of plaque
Muscle cells produce additional ECM that traps lipoproteins and increases size of lesion/plaque
Over time, turns into fibrous cap with lipid core of varying size + stability
Not always detected by imaging
Plaque disruption
Plaque increases in size and occupies more space in arterial lumen
Lipid core can become less stable
Structure of plaque contributes to risk of rupture
Primary prevention for plaque
Lifestyle promotion
Wellness
ASCVD risk factor estimation starting at age 40
Health diet
75 min vigorous activity OR 150 min mod intensity activity
Tobacco cessation
PT management for plaque
Exercise – decreased insulin resistance, decreased BP, decreased endothelial dysfunction
Education on smoking cessation – decreased endothelial dysfunction, decreased platelet aggregation
lifestyle modifications for pt with coronary artery disease
tobacco cessation
body mass index
moderate-intensity activity for 30 to 60 min seven days a week
alcohol consumption in moderation
low-sodium diet
two to three servings a day each fruit and vegetables
saturated fat less than 10 % of daily calories
Medical management for coronary artery disease
statin for managing LDL levels
Beta-blockers for HTN
Aspirin or plavix
Ischemic conditions
caused by variation in myocardial O2 supply and demand
Myocardial ischemia causes
vasoconstriction, increased thrombosis, vessel stenosis d/t atherosclerosis, dysfunction of endothelium, vasospasm
Other causes of myocardial ischemia
Other causes: acute respiratory failure, cardiogenic or septic shock, hemorrhage, hypovolemia, severe HTN, aortic stenosis
Unstable angina
Sudden change in frequency, intensity, type of angina symptoms that may preclude acute MI
Stable angina
Chest pain/discomfort at specific intervals, activities, etc. – chronic and predictable
Variant/prinzmetal angina
Vasospasm without presence of known/visible plaques or change in O2 demand, and which may often occur at rest
Stable angina last
several seconds to minutes
Where is stable angina pain
diffuse chest, UE, jaw, neck
Stable angina clinical manifestations
tachycardia, SOB, nausea/GI symptoms, diaphoresis, fatigue
stable angina can be treated and resolved with
sublingual nitroglycerin
What is the gold standard for testing angina
angiogram
medical treatment for angina
PCI
CABG
Medications – nitroglycerin (acute), B-blocker and calcium channel blockers to decrease O2 demand
PT considerations for angina
Awareness of patient’s baseline angina (if chronic)
Monitoring onset of symptoms, duration, intensity
Ensuring angina is relieved with normal amount of rest or with sublingual nitro
Acute coronary syndromes
stemi
nstemi
unstable angina
stemi
ST-elevation MI
Caused by occlusive thrombus resulting in myocardial tissue damage, which can lead to impaired contractility and ventricular remodeling
stemi clinical manisfestation
acute chest pain, SOB, fatigue, dyspnea, diaphoresis, GI symptoms, S4
Nstemi
non st elevation MI
Type 1 nstemi
O2 supply/demand mismatch caused by plaque/thrombus
type 2 nstemi
O2 supply/demand mismatch not caused by ACS
Can be due to respiratory failure, shock, anemia, arrhythmia, electrolyte imbalance, CKD
Unstable angina
Changes in typical angina with regards to frequency, intensity, type, quality of discomfort
Caused by CAD with nonocclusive thrombus, plaque rupture, tachycardia, vasoconstriction
No ST-elevation on EKG
Can progress to NSTEMI or STEMI
Unstable angina red flags
lasts >20 min, lower threshold for onset, change in usual pattern
Acute coronary syndrome diagnosis and treatment
Combination of EKG, clinical biomarkers, symptoms, imaging
Pharmacologic – B-blocker, Aspirin, heparin, morphine for pain, oxygen
Surgical/interventional – PCI/DES, CABG
Patients may develop arrhythmias
Acute coronary syndrome PT management
Vitals: HR and rhythm, BP, O2 needs
Symptom onset/prevalence with physical activity
Labs – ensuring that troponin is downtrending
Lines/tubes/drips
Monitoring activity tolerance and capacity for exercise via self-reported symptoms, RPE, or other scale
Patient education and referral to cardiac rehab
Cardiac symptoms can often mimic
GI, pulmonary, or MSK pain
GI discomfort often relieved by
by antacids, worse with certain foods, and occurs after meals
MSK pain may have more
focal tenderness and is worse with movement
Differential diagnosis from chest pain
GERD
peptic ulcer disease
costochondritis
bronchospasm
Medicare Part B will cover cardiac rehab if the patient has been diagnosed with certain conditions
MI in last 12 months, CABG, angioplasty, transplant, stable angina, valve repair/replacement
