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
LV ejection fraction
Normal 55-75%
EF = SV/EDV = (EDV-ESV)/EDV
Causes of systolic heart failure
Systolic heart failure - CO doesn’t meet systemic demands
Increased preload
Increased after load
Decreased contractility
Brady or tachycardia
High output conditions:
- decreased O2 carrying capacity (anemia)
- Increased metabolic demand (hyperthyroidism, beriberi (thiamine deficiency))
Causes of diastolic heart failure
Filling problem
LVH - 2/2 chronic htn -> S4, S3, summation gallop
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy (HOCM)
AD
Chaotic, disordered hypertrophy of the LV myocytes with interstitial fibrosis - muscle fibers oriented in different directions
Hypertrophy of the inter ventricular septum -> LV outflow tract obstruction
Clinical features:
- Exertional syncope, dyspnea, CP
- Sudden cardiac death in a young athlete
- Systolic murmur (like AS), LOUDER with Valsalva (decreased preload), SOFTER with squatting (increased after load)
- Forceful, enlarged apical impulse - silver dollar sized
Dx: ECHO
Tx: B-blocker (decrease HR, prolong diastole); restrict physical exertion
AVOID volume depletion, NO diuretics
Dilated cardiomyopathy
MC
Dilation of ventricles -> systolic dysfunction
Clinical features:
- fatigue, dyspnea, systolic dysfunction
- S3
- Systolic and diastolic murmurs - leaflets separate
- CXR: globular heart
Tx: diuretics, ACE inhibitors, B-blockers
Causes of dilated cardiomyopathy
Ischemic heart disease! Idiopathic etOH Cocaine Doxorubicin Coxsackie virus B Myocarditis HIV Chagas disease (Trypanosoma cruz) Beriberi (thiamine deficiency) - wet = edema Hemochromatosis (most commonly causes dilated CM) Pregnancy - "permpartum CM"
Restrictive cardiomyopathy
Least common CM
Ventricular walls become stiff and noncompliant -> diastolic dysfunction
Causes: usually d/t infiltration of the myocardium
- Sarcoidosis
- Amyloidosis
- Hemochromatosis (less likely than dilate)
Clinical features:
Right-sided heart failure - edema, JVD, ascites
Diagnosis: ECHO, myocardial bx
Tx: identify and tx underlying cause; Diuretics, ACE-i, B-blockers
Symptoms of left heart failure
Left = lungs
DOE Orthopnea Paroxysmal nocturnal dyspnea Rales (crackles) Displaced PMI S3 heart sound - apex
Causes of left heart failure
Ischemic heart disease
HTN
Symptoms of right heart failure
JVD
Hepatomegaly
Lower extremity edema
Causes of right heart failure
Left heart failure
Valvular heart disease
COPD -> cor pulmonale
Pulmonary hypertension
Tests used to diagnosis CHF
ECHO BNP CXR Cardiac enzymes ECG
BNP and how to interpret
Hormone produced in response to ventricular stretch -> vasodilation and urinary excretion of Na+ and H2O (little)
BNP less than 100 - r/o CHF
BNP 100-400 - indeterminate
BNP >400 indicates CHF
CXR in CHF
Cardiomegaly Pulmonary edema Cephalization of pulmonary vasculature - bigger in upper lungs, normally hard to see Kerley B lines - peripheral, lower lungs Pleural effusion
Treatment of acute decompensated CHF presenting with pulmonary edema
NOLIP
Nitrates - redistributes blood outside pulmonary vasculature
O2 - only if hypoxemic
Loop diuretic - takes long time to work d/t low CO = low kidney perfusion, only help volume overload
Inotropic drugs - Dobutamine, milrinone - not first line d/t increased mortality
Positioning - pool blood in legs
Drugs proven to reduce mortality in CHF
ACE inhibitors - decrease preload and after load, increase CO
-candesartan and valsartan if intolerant to ACE-i d/t cough
B-blockers - bisoprolol, carvedilol, extended-release metoprolol
- prevents cardiac remodeling
- Avoid with acute decompensated CHF
Aldosterone antagonists - spironolactone, eplerenone
-Start after ACE-i and B-blocker
Drugs used for symptom relief in chronic CHF
Loop diuretics - decrease preload, fluid overload
Digoxin - improve contractility
Vasodilators - isosorbide dinitrate, hydrazine (decreased mortality in AA)
Cardiac resynchronization therapy
Pacemaker leads in each ventricle -> synchronized ventricular contraction
Can improve mortality and reduce sxs in patients with LVEF at or below 35%
Pulmonary capillary wedge pressure (PCWP) is a good approximation of what other pressures?
LA pressure
LV diastolic pressure
Two most common sites of pulmonary artery catheter placement
L subclavian v.
Right internal jugular v.
Causes of myocarditis
MC- viruses: parvovirus B19, coxsackie, echoviruses, adenovirus, EBV, CMV, influenza
Trypanosoma cruz - Chagas disease
Drug toxicity - chloroquine, PCNs, sulfonamides, cocaine, radiation, cyclophosphamide, doxorubicin, daunorubicin
Clinical features in myocarditis
Asx -> sudden death fatigue CP HF sxs - edema, SOB palpitations fever S3 or S4 Signs of CHF - edema, pulmonary rales, JVD
Diagnostic tests in myocarditis
ECG: normal or signs of MI - ST elevation, Q waves; peripheral or ectopic beats
Cardiac enzymes - normal or elevated - troponin I
CXR: CM or pulmonary congestion
ECHO: impaired ventricular function
Cardiac magnetic resonance (CMR) - detect inflammatory hyperemia, edema, myocyte necrosis
Definitive dx: endomyocardial bx - cx and viral PCR
Chagas disease
Trypanosoma cruz
MEGA -3
cardioMEGAly
MEGAesophagus
MEGAcolon
Treatment of myocarditis
treat underlying cause - abx for bacterial Stop offending agents Tx any significant arrhythmias Tx HF sxs \+/- immunosuppressant agents
Supportive treatment - usually viruses
Acute rheumatic fever causes
2-4 weeks after untreated group A strep pharyngitis - 3%
Due to autoantibodies that attack heart and joints - sterile vegetations
MC: MV>AV>TV=PV
Diagnosis of acute rheumatic fever
JONES criteria
-Hx of recent strep and 2 major or 1 major and 2 minor
Major: JONES
- Joints - polyarthritis - hot swollen
- Heart - pancarditis, pericarditis, endocarditis, myocarditis
- Nodules - subcutaneous on extensor surfaces - painless, back wrist, elbow, anterior knee
- Erythema marginatum - painless, trunk or medial limbs; multiple lesions with central clearing
- Sydenham chorea
Minor: PEACE
- Previous rheumatic fever
- ECG with PR prolongation
- Arthralgias
- CRP and ESR elevation (nonspecific)
- Elevated temperature
Diagnostic testing for acute rheumatic fever
Elevated ESR and CRP
Elevated WBC
90% ASO titer
Treatment for acute rheumatic fever
NSAIDs - joint inflammation
Corticosteroids - carditis severe
B-lactams (PCN) - ongoing infection
Endocarditis ppx prior to surgery or dental procedure - patient population and tx
Prosthetic cardiac valve
Previous infective endocarditis
Congenital heart disease - unrepaired cyanotic defect, palliative shunts, repaired with prosthetic device/material
Cardiac transplant with cardiac valvuloplasty
Tx: amox 2 g x1 30-60 min prior to procedure
No longer recommended if hx of rheumatic HD unless previous endocarditis
Endocarditis vegetation composition
platelets, fibrin, microorganisms, inflammatory cells
Risk factors for endocarditis
Damaged heart valves - rheumatic HD, congenital HD IV drug users poor dentition age >60 yo Male
Presentation of endocarditis
Fever, malaise, weakness, anorexia, new heart murmur, wt loss
Jane way lesions - contender, erythematous macule on palms and soles - septic emboli
Osler nodes - tender nodules on fingers and toe pads; caused by immune complexes (also in lupus and disseminated gonococcal infections)
Roth spots - retinal hemorrhages with pale centers - immune complexes
Splinter hemorrhages - nonspecific
Conjunctival hemorrhages
Bacterial causes of endocarditis
S. aureus - 31% Viridan group Strep 17% - assoc with dental procedures Enterococci 11% Coagulase-negative staph 11% S. bovis 7%
HACEK
- Haemophilus spp
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
Culture negative - intracellular
- Coxiella burnetii - Q fever
- Bartonella spp. - cat scratch
- Brucella spp - unpasturized milk, zoonotic
Complications of endocarditis
severe damage to endocardium and valves -> valve repair/replace
Septic emboli - Right side -> PE; Left side -> stroke, spleen, kidney, anywhere
Duke criteria
Endocarditis - definitive dx - positive culture/histo of vegetation
Clinical criteria - 2 major; 1 major 3 minor; 5 minor
Major:
Serial blood cultures positive
Vegetations or cardiac abscesses on ECHO - TEE
New valve regurgitaiton - MC MR
Blood cx positive for Coxiella burnetii (closely associated)
Minor:
Predisposing heart condition or IV drug use
Temp >38C
Vascular phenomenon - arterial emboli, conjunctival hemorrhages, Janeway lesions
Immunologic phenomenon - glomerulonephritis, Osler nodes, roth spots
Positive cx not meeting requirements for major criteria
Serologic evidence of infection without positive cx
Empiric antibiotic most often used for infective endocarditis
Vancomycin until sensitivities back
4-6 weeks
Nonbacterial thrombotic endocarditis (marantic)
Occurs on non-damaged valves - sterile vegetations
Associated with:
sepsis, pregnancy - hyper coagulable states
venous catheters
mutinous adenocarcinoma
Libman-Sacks endocarditis
Associate with SLE
both sides of the valve
Due to deposition of immune complexes
Chronic constrictive pericarditis
Scarred, fibrous pericardium becomes rigid -> decreased diastolic filing and cardiac output
Risk factors: cardiac surgery, radiation
Presentation:
HF sxs - DOE, fatigue, peripheral edema
Physical exam: JVD, Kussmaul’s sign (JVD with inspiration)
Confirm with ECHO - thickening of pericardium, most ventricle filling in early diastole
CXR: calcification of pericardium - specific, not sensitive
Tx: pericardiectomy - high mortality - 10%
Conditions with Kussmaul’s sign
JVD with inspiration - impaired RV relaxation and filling
Restrictive CM RV infarction tricuspid stenosis massive PE right sided CHF Chronic constrictive pericarditis
Left atrial myxoma
MC cardiac tumor in adults
75-80% left atrium
ball valve - obstruct blood flow into LV -> syncope
Physical exam: rarely - early diastolic “tumor plop”
Dx: ECHO
Tx: surgical resection
Atrial fibrillation Risk factors
Hyperthyroidism pulmonary dz CAD HTN anemia valvular disease pericarditis Rheumatic HD sepsis alcoholism
Afib
rapid, irregularly irregular rhythm
ECG: no distinct p waves
asx or SOB, CP, palpitations, irregularly irregular pulse
Afib managment
Acute: new onset less than 48 hours - electrocardioversion
Chronic:
-evaluate for thumbs with TEE
Anticoagulate with heparin and warfarin
Rhythm control with sotalol or amiodarone -> sinus rhythm
Rate control with B-blockers, NDP CCBs or digoxin
Atrial flutter
re-entrant rhythm in right or left atrium - can degenerate to afib
ECG - sawtooth pattern, >150bpm
Risk: CAD, CHF, COPD, valve dz, pericarditis
Sxs: Asx or palpitations, syncope
Tx: rate control - b-blockers, CCB; cardioversion - electrical or chemical; catheter ablation
PVCs
causes: hypoxemia, abnl electrolytes, hyperthyroidism, caffeine
Clinical: asx or palpitations, syncope, sensation of skipped, heavy, or dramatic beat
ECG: wide QRS
Tx: none if healthy - b-blockers in CAD
More than 3 in a minute concerning for other ventricular arrhythmias
V-tach
sustain -> vfib
ECG: series of 3 or more PVCs, HR of 160-240
Tx: electrocardioversion, followed by antiarrhythmic medication
Recurrent -> internal defibrillator
Clinical: asx if brief -> palpitations, syncope, hypotension
Torsades de pointes
ECG: vtach with sine wave
Tx: IV magnesium rapid bolus -> lidocaine, phenytoin
Vfib
lack of ordered ventricular contractions leading to NO cardiac output
ECG: erratic, no identifiable p waves or QRS
Tx: CPR, immediate shock
Treatable causes leading to a code - H’s
Hypovolemia -> rapid volume resuscitation through multiple IV sites and/or central lines
Hypoxemia -> correct via intubation, chest tube, or O2
H+ (acidosis) -> IV push 1-2 amps bicarbonate (common in prolonged code)
Hyperkalemia -> CaCl2 IV push, bicarbonate, insulin/glucose (common in prolonged resuscitation due to acidosis)
Hypoglycemia -> 1 amp D50 IV push - always check finger stick
Hypothermia -> warming
Treatable causes leading to a code - T’s
Tamponade -> pericardiocentesis
Tension PTX -> needle decompression then chest tube
Thombus - MI -> cardiac cath or thrombolytic
Thombus - PE -> thrombolytic or thombectomy
Trauma -> follow ATLS protocols
Toxins
Prehypertension vs hypertension BP readings
Pre: 120-139/80-89
htn: over 140/90
Diagnosis HTN after 3 separate occasions
Complications of uncontrolled htn
atherosclerosis -> CAD, ischemic stroke hemorrhagic stroke LVH -> diastolic dysfunction Thoracic aortic dissection AAA CKD (also can cause the htn) hypertensive retinopathy (AV nicking, cotton wool spots, retinal hemorrhages-flame hem)
Most likely cause of htn refractory to multiple meds? Next step to dx? tx options?
renal a. stenosis
- over 50 - atherosclerosis
- under 50, women - fibromuscular dysplasia of renal a (needs on string)
MRA of renal a. - best, least invasive
Spiral CT with con
renal a. duplex scan
renal arteriogram - gold standard, but invasive
Tx:
medical management - avoid ACE/ARBs if bilateral (decreased GFR and worsening renal fxn)
Angioplasty
Surgical revascularization - bypass
Causes of secondary hypertension
renal a. stenosis
CKD or ESRD
Drugs - OCPs over 35, NSAIDs, antidepressants, glucocorticoids
Hypercortisolism - Cushing - dx: serum cortisol, serum ACTH, dexamethasone suppression test
Primary hyperaldosteronism - Conn -
Triad: htn + hypokalemia + metabolic alkalosis
Dx: high plasma aldosterone:plasma renin ratio
Pheochromocytoma:
episodic htn with diaphoresis, tachy, palpitations, HA
Dx: 24 hr urine catecholamines and metanephrins, CT abd
Hypo- or hyperthyroidism - dx TSH
Hyperparathyroidism - calcium drives sm.m. contraction -> peripheral vasoconstriction
Dx: serum calcium, PTH
Coarctation of aorta
-BP high in arms, low in legs; weak dorsals pedis pulses
Dx: ECHO
OSA - Dx: polysomnography
Hypertensive urgency vs emergency
BP >180/120
urgency- no sxs, no end organ damage
emergency - end organ damage
-renal dz, AMS, papilledema, retinal vascular changes, unstable angina, MI, aortic dissection, pulmonary edema
Treatment of hypertensive urgency
Goal:
reduce BP to 160/100 initially
Reduce MAP no more than 25% in first 2-3 hours - risk ischemia
IV drugs: Nitroprusside Labetalol Nicardipine Clonidine Captopril Enalapril
JNC8 bp goals: Gen pop under 60 Adults with CKD Adults with DM Gen pop over 60 no CKD, no DM
less than 140/90 for:
Gen pop under 60
Adults with CKD
Adults with DM
less than 150/90 for:
Gen pop over 60 no CKD, no DM
Aortic dissection - mechanism, risk, features and dx
Tear in intimate of aorta -> blood dissects into media -> forms false lumen
Risk factors:
HTN
Dz weakening aorta - Marfans, Ehlers-Danlos, syphilis
Features:
Severe, sharp or tearing CP radiating to back
May cause syncope, TIA or decreased peripheral pulses
Dx:
Normal ECG
Widening mediastinum on CXR
Best test: CT chest with contrast - two lumens; classify as Stanford A (involves ascending aorta) or Stanford B (distal to L. subclavian A)
Aortic dissection - management
Stabilze BP with beta-blockers - decreases slope of rise in BP - anti-impulse treatment
Morphine for pain control
Stanford A - emergency surgical repair - high risk
Stanford B - treat medically unless LE ischemia, uncontrolled pain
AAA - risk factors, features, dx, screening
Focal dilation of the abdominal aorta, distal to renal a.
Risk: Tobacco use Age >55 Male Caucasian Atherosclerosis HTN FHx
Features:
Asx - possible abd/lower back pain
Exam: pulsatile abdominal mass, abdominal bruit
Ruptured AAA: hypotension, severe abd pain, pulsatile mass
Dx:
Best first test: abd u/s
CT or MRI with con
Screen: one time abd u/s all men 65-75 with hx of smoking
Indication for repair of AAA
Diameter > 5.5 cm in men or >5 cm in women
Increase in diameter by more than 0.5 cm in 6 mo - should be having abd u/s q6mo
Symptomatic - tenderness, pain in abdomen or back
Peripheral artery disease (PAD) - risk, features, dx
Atherosclerosis of peripheral arteries - legs
Risk: Smoking HTN DM HLD
Claudication - exertion leg pain improves with rest
Non-healing foot ulcers
Erectile dysfunction
Skin changes - dry, shiny skin, decreased hair growth on legs
decreased pulses in legs
Dx: ABI ratio - ankle SBP to brachial SBP -ABI >= 0.9 normal; less than 0.9 = vascular insufficiency; less than 0.4 = severe disease U/S or CT angiogram or MRA Arteriogram
Management of peripheral artery disease
Conservative medical management:
- smoking cessation
- Glucose and BP control
- Daily exercise to increase collateral flow
- Cilostazol - improves blood flow to LE and decreases claudication via arteriovasodilation; more effective than pentoxifylline (makes RBC more flexible); contra in HF d/t increased mortality
- daily aspirin or clopidogrel to reduce CV events
- Statin to reduce CV events, increase pain-free walking distance
If not responding to medical management -> angioplasty, bypass grafting, or amputation
-may have concurrent CAD
DVT - risk, features, dx, tx
Blood clot developing in deep vein - usually LE
Risk: -virchow’s triad
- Hemostasis - immobilization from illness, surgery, travel
- Hypercoagulability - inherited, cancer, high estrogen states (pregnancy, OCPs)
Features:
Often asx
Pain, warmth, and/or swelling in LE -calf
Homan’s sign - pain with dorsiflexion, found in less than 1/3
Dx:
Positive D-dimer (also high in post op) - negative r/o
Best test: doppler u/s of extremity
Tx:
elevate leg
Anticoagulate - LMWH (enoxaparin) or unfractionating heparin -> warfarin x3 mo
If anticoagulant contraindicated (high fall risk) - IVC filter
Treatment of varicose veins
Weight reduction, avoid prolonged standing, leg elevation
Compression stockings
Sclerotherapy - inject substance to cause injury and thrombosis
Thermal ablation - laser
Surgery ligation of long saphenous v or short saphenous v - lose option for CABG
Giant cell arteritis (temporal arteritis)
Large vessel vasculitis
elderly woman
Associated with polymyalgia rheumatica (PMR)
HA, tenderness of temples, jaw claudication
Transient or permanent vision loss
Histo: granulomas - multinucleate giant cells
Elevated ESR - normal r/o
Definitive dx: temporal a. bx
Tx: prednisone 1-2 mo, with long taper 9-12 mo; don’t delay start, risk blindness
Aspirin
Calcium, vit D to reduce risk of osteoporosis due to steroids
Takayasu arteritis
Large vessel vasculitis - arch of aorta and major branches off arch
Asian woman - 10-40 yo
Cerebrovascular ischemia, coronary ischemia, syncope, vertigo
Poor pulses in UE - pulseless disease
Tx: glucocorticoids
Kawasaki disease (mucocutaneous lymph node syndrome)
Medium vessel vasculitis
Asian infant, kid
“CRASH and Burn”
Conjunctivitis - b/l non exudative, painless
Rash on trunk
Adenopathy of cervical LN
Strawberry tongue and diffuse erythema of mucous membranes
Hands and feet - edema with induration, erythema or desquamation
Fever - >40 C or 104 lasting at least 5 days
coronary artery aneurysm within weeks of illness onset - risk rupture or thrombosis -> MI
Tx: IVIG within first 10 days of illness
High dose aspirin until 48 hr after fever resolution
Low dose aspirin until inflammatory markers (platelets, ESR) return to normal (usually 6 weeks)
ECHO in acute phase and 6-8 weeks later
Steroids NOT indicated, no benefit
Polyarteritis nodosa
Necrotizing inflammation of small and medium sized arteries -> ischemia
- Kidneys, GI tract
- SPARES lungs
Associated with Hep B/C - Hep with renal dz - proteinuria, hematuria
ANCA negative
Angiography - aneurysms in affected organs
Thormboangiitis obliterates (Buerger disease)
Small/medium sized arteries and veins
Heavy smoker, young male 30-40s
Ischemia of digits, Raynaud’s
Tx: stop smoking
Henoch-Schonlein purpura (IgA vasculitis)
Small vessel vasculitis
Kids - recent URI, strep Palpable purpura of LE Arthritis and arthralgia Abd pain d/t intestinal hemorrhage Renal dz (IgA nephropathy) - microscopic hematuria, mild proteinuria
Tx: hydration, pain control
Mixed cyroglobulinemia syndrome (essential mixed cyroglobulinemia)
Small vessel vasculitis
Polyclonal IgG and IgM against IgGs precipitate out at cool temps
Associated with Hep C
Melzer’s triad: palpable purpura, weakness (peripheral neuropathy), arthralgia
Raynauds Liver involvement (hep C)
20-30% kidney dz - hematuria, proteinuria
Granulomatosis with polyangiitis (Wegners)
Granulomas in:
Lung - pulmonary nodules, infiltrates, hilar LAD
Upper airway - ENT, soft palate
Kidneys
c-ANCA + (PR3-ANCA)
Dx: Kidney or lung bx
Tx: steroids and cyclophosphamide
Eosinophili granulomatosis with polyangiitis (Chrug-Strauss)
Allergic!
Assoc with asthma
Lung dz - opacities, nodules
Upper airway disease
Skin - tender skin nodules, palpable purpura
20% renal involvement
Histo: Eosinophilic inflammation + granulomas on lung bx
p-ANCA + (MPO-ANCA)
Eosinophilia
