Cardiovascular Flashcards
Risk factors for atherosclerosis
HTN HLD DM Smoking FHx Sedentary lifestyle and poor diet
Atherosclerosis role in AAA
a main risk factor (smoking biggest risk factor)
Plaque compresses underlying media -> problem with nutrient and waste diffusion
- > degeneration and necrosis of media
- > arterial wall weakness
Hyperhomocysteinemia clinical significance and treatment
risk factor for CVA, PVD, coronary heart dz
Tx: B6, B12, folic acid
Pathogenesis of atherosclerosis
- endothelial dysfunction (caused by HTN, HLD, DM, Smoking) leads to increased vascular permeability, leukocyte adhesion, and thrombosis
- Accumulation of lipoproteins - in vessel wall, mostly LDL
- Monocyte adhesion to the endothelium: migration of the monocytes into the intima and then transformation of these cells into macrophages and foam cells
- Factor release: activated platelets, macrophages, inflammatory mediators, cytokines
- Smooth muscle cell proliferation: migraiton of sm.m. cells into intima, deposition of elastin and collagen
- Lipid accumulation occurs extracelularly and within macrophages and smooth muscle cells -> bulging atherosclerotic plaque
Clinical presentation of atherosclerosis
most asx
Angina Claudication of LE Stroke sxs HTN retinal changes
Diagnostic tests for atherosclerosis
Exercise stress test - best initial test Nuclear stress test Stress test with echo Pharmacologic stress test PET myocardial imaging test Coronary angiogram - gold standard Ankle brachial pressure index Carotid U/S
Exercise stress test in atherosclerosis
best initial test to assess stable angina or worsening SOB with exertion or fatigue with exertion
Positive: CP, dizziness, claudication, decreased BP, ST changes
Nuclear stress test in atherosclerosis
Test to assess myocardial profusion
Stress test with Echo in atherosclerosis
assess wall motion abnormalities
Pharmacologic stress test in atherosclerosis
uses cardiac inotrope/chronotrope (dobutamine) or vasodilator (adenosine or dipyridamole) in place of exercise
caution with vasodilators in asthmatics and hypotensive patients
Positron emission tomography (PET) myocardial imaging in atherosclerosis
assess heart perfusion defects - lights up with adequate perfusion, black if not perfusing
Coronary angiogram in atherosclerosis
gold standard test
Assess degree of coronary artery occlusion - more invasive
Ankle brachial pressure index
Pt supine, ankle BP/brachial BP
assess peripheral artery disease
abnormal if less than 0.9 -> stress test or angiogram
Carotid ultrasound in atherosclerosis
assess carotid stenosis leading to TIA or stroke
Treatment of atherosclerosis
Stop tobacco use Normalize BP Control hyperglycemia Control hypercholesterolemia Low-fat diet exercise
Chylomicrons
lipoprotiens absorbed from gut travel to liver
VLDL
produced by liver, high in TGs
can become IDL and LDL
HDL
produced by liver
take up cholesterol deposited by LDL particles
LDL
high in cholesterol
made from VLDL
taken up into cells by endocytosis - part of atherogenesis
Secondary causes of hypercholesterolemia
T2DM Excess etOH Primary biliary cholangitis CKD Hypothyroidism Medications: oral estrogens, thiazide diruetics, B-blockers, atypical antipsychotics (clozapine, olanzapine), protease inhibitors
Xanthoma
deposits of lipid in tendons and under skin
Xanthelasma
deposits of lipid around eyes
Arcus senilis
deposits of lipids in the periphery of the corneas
Treatment of hypercholesterolemia
Goal: reduce risk of atherosclerosis and pancreatitis (TGs)
Lifestyle modifications: Wt loss aerobic exercise diet smoking cessation
2013 AHA/ACC guidelines for treating hypercholesterolemia - who gets treated?
Clinical atherosclerotic CV dz (ASCVD) - need mod-high intensity statin:
- ACS
- MI
- stable or unstable angina
- Revascularization procedures
- Stroke or TIA
- Peripheral artery disease
LDL >190
T1 or T2DM ages 40-75
10 yr ASCVD risk >7.5% ages 40-75
Causes of Angina
Decreased O2 supply: atherosclerosis obstructing blood flow, shock, hypoxemia, anemia, prinzmetal angina
Increased O2 demand: vigorous exertion, tachycardia, htn, ventricular hypertrophy, increased catecholamines
Clinical features of angina
chest discomfort/pressure - left sided or midsternal, radiates to back, jaw, or left arm
diaphroesis
SOB
Palpitations
Atypical sxs of angina
older patients, females, DM pts
Abdominal pain, exercise intolerance, worsening generalized fatigue
Stable angina
predictable CP that resolved with rest
No initiation of CP at rest
Dx: stress test - cardiac enzymes always normal
Unstable angina
Unpredictable chest pain that can occur at rest
Pain more severe and lasts longer
1/3 will have MI within 3 years
Dx:
Give aspirin and transport to ED
ECG and cardiac enzymes initially normal, sometimes ST depression
Stress test or cardiac cath when stable
MI
occlusion of coronary vessels d/t thrombus formation following a plaque rupture
Pressure sensation radiates to jaw or left arm
Tachycardia, diaphoresis, N/V, impending doom
Possible new S3, S4, or systolic murmur
Abnormal cardiac enzymes - trp I most specific (elevates within 4 hours, lasts 2 weeks)
STEMI vs NSTEMI
ECG gold standard within 6 hrs of sxs
STEMI: ST elevation, cardiac cath to locate occlusion, new LBBB
NSTEMI: no ST elevation, cardiac cath to locate occlusion
Evolution of MI on ECG
Acute: ST elevates - tomb stoning (also seen with prinzmetal angina)
Hours: ST elevated, R wave decreases, Q wave appears
Day 1-2: T wave inverts, Q wave deepens
Days later: ST normal, T wave inverted
Weeks later: ST normal, T wave normal, Q wave persists
Anterior wall MI on ECG
V2-V5 - LAD
Septal wall MI on ECG
V1-3 - LAD
Inferior wall MI on ECG
II, III, aVF - posterior descending a.
Lateral wall MI on ECG
I, aVL, V5, V6 - LAD or circumflex
Prinzmetal angina (Variant angina)
Coronary artery vasospasm
RF: smoking
More often younger pt, fewer CAD RFs
CP at rest - midnight to morning, lasts 5-15 min
Dx: recurrent CP at rest, transient ST elevation, no sign of high grade coronary artery stenosis
DDX for CP
MSK Costochondritis GERD Esophageal spasm - nitrates relieve spasms Cocaine hyperventilation Herpes zoster aortic stenosis trauma PE pneumonia pericarditis pancreatitis angina aortic dissection aortic aneurysm Infarction Neuropsych dz - depression, anxiety
Indications for CABG
> 50% stenosis in left main artery
3 vessel disease
Complications of MI
arrhythmia d/t electrical irritability - Vfib MC and lethal
LVF and pulmonary edema - decreased heart function
Cardiogenic shock - high risk of mortality
Ventricular free wall rupture -> tamponade
Papillary muscle rupture -> severe MR
Interventricular septal rupture -> VSD
Aneurysm formation 2/2 scar tissue
Fibrinous pericarditis - friction rub 3-5 days after MI
Dressler syndrome - autoimmune pericarditis weeks after MI
Equations for Cardiac output
CO = SV x HR
SV= EDV - ESV
Factors determining stroke volume
Preload
Afterload
Myocardial contractility
Preload
stretch of myocytes at the end of diastole
influenced by EDV and venous return
Increase intravascular volume increases preload
Dehydration decreases preload
Afterload
pressure against which the ventricles contract to eject blood
influenced by aortic pressure
after load and stroke volume inversely related, lower after load allows more blood to get out of the ventricle
Myocardial contractility influences
catecholamines, intracellular Ca2+, extracellular Na+
Independent of pre- and after-load
Increase calcium = increased contractility
Low extracellular sodium makes for higher intracellular calcium, increasing contractility
Fick principle
CO = (rate of O2 consumption)/(Ao2 - Vo2)
How does exercise change cardiac output?
1st: increased stroke volume
later - increased heart rate - which sustains increased cardiac output
Mean arterial pressure equations
MAP = CO - TPR (total peripheral resistance)
MAP = 2/3 DBP + 1/3 SBP
Pulse pressure equation
PP = SBP - DBP