Cardiovascular Flashcards

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1
Q

endocarditis etiology, RF, and sxs

A
  • MC native valve infection (strep viridans, staph aureus, enterococci)
  • IVDU: staph aureus, tricuspid
  • Prosthetic valve: staph aureus, gram neg or fungi
  • most pts have underlying regurgitant defect providing a nidus
  • sxs: fever, nonspecific sxs (dyspnea, cough, CP, arthralgias, back or flank pain, GI complaints)
  • signs: stable murmur (90%), palatal, conjunctival, or subungal petechiae, splinter hemorrhages, pallor, splenomegaly
  • diagnostic signs:
    • osler nodes (painful, violaceous, raised lesions on fingers, toes, feet)
    • janeway lesions (painless red lesions on palms/soles of feet)
    • roth spots (exudative lesions in retina)
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2
Q

endocarditis dx and tx

A
  • dx: 3 sets of blood cultures at least 1h apart, before starting abx
    • echo: required to make dx and identify involved valves (vegetation)
  • tx: empiric abx cover staph, strep, enterococci
    • native valve: vanco alone or + cefazolin
    • Ill pts w/ HF: gentamicin plus cefepime and vanco
    • aortic valve replacement if refractory or abscess (funcal infxn)
  • prophylaxis: abx recommended before invasive dental work or surgical procedures: prosthetic valves, previous IE, some congenital heart dzs (transposition, tetrology), acquired valve disorders, HCM, cardiac transplant pts with valvulopathy
    • ALL OF THE ABOVE GET AMOX 1 hr before procedure (clarith or azith if PCN allergy)
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3
Q

Modified duke criteria

A
  • For detecting endocarditis
  • must have one of the following criteria:
    • 2 major
    • 1 major and 3 minor
    • 5 minor
  • Major:
      1. two pos blood cultures of typical causative microorganism
      1. echo showing new valve regurg
  • Minor:
      1. predisposing factor
      1. fever >100.4
      1. vascular phenomena (embolic dz or pulm infarct)
      1. immunologic phenomena (glomeruloneph, osler nodes, roth spots)
        • blood cuture not meeting major criteria

coronary artery vasospasm (Prinzmetal variant) etiology, RF, sxs

  • etiology: smooth muscle constriction (spasm) of the coronary artery w/out obstruction - leads to MI, ventricular arrhythmias, sudden death
  • known triggers: hyperventilation, cocaine, tobacco use, provocative agents (acetylcholine, ergonovine, histamine, serotonin)
  • Nitric oxide deficiency: increased activity of potent vasoconstrictors and stimulators of smooth muscle proliferation
  • 50yo, females
  • sxs: nonexertional chest pain similar to unstable angina
    • normal exercise tolerance
    • pain is cyclical (most occur in morning hours, no correlaiton to cardiac workload)
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4
Q

Prinzmetal angina dx and tx

A
  • dx: EKG (ST segment or Twave abnormalities)
    • Cardiac enzyme: normal troponin, CK-MB
    • Check Mg level, CBC, CMP, lipid panel
  • tx: stress testing with myocardial perfusion imaging or coronary angiography
    • pharmacotherapy (SL, topical, or IV nitrates (initial), antiplatelet, thrombolytics, statins, BB
    • once dx made, CCB and long-acting nitrates used for long term prophylaxis (amlodipine)
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5
Q

pharm tx of ACS/chest pain (angina)

A
  • Clopidogrel: reduces incidence of MI in pts with USA compared with ASA alone
  • LMWH: continue for at least 2d; PTT not followed
  • UFH: PTT 2-2.5x normal if using UFH
  • start pt with USA or NSTEMI with high LDL on statin
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6
Q

Unstable angina

A
  • O2 demand unchanged, supply decreased, secondary to low resting coronary flow
  • sxs: chronic angina increasing in frequency, duration, or intensity of pain OR
    • new onset angina that is severe and worsening OR
    • angina at rest
  • dx: EKG shows ST segment or Twave abnl
    • cardiac enzymes show normal troponin and CK-MB
  • tx: admit to unit with continuous cardiac monitoring, establish IV access, O2, pain control with NTG and morphine
    • ASA, clopidogrel, BB (first line), LMWH, replace electrolytes, if response to med tx - stress test to determine if catheterization/revascularization necessary
    • reduce RF: stop smoking, weight loss, tx DM/HTN/HLD
    • heparin
  • NOT BENEFICIAL: thrombolytics and CCB
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7
Q

NSTEMI and STEMI etiology, RF, sxs

A
  • NSTEMI: caused by severely narrowed artery that is not 100% blocked
  • STEMI: caused by 100% blockage of a coronary artery, necrosis of myocardium (thrombotic occlusion), asx in 1/3 of pts
  • sxs: CP (intense, substernal, crushing), radiation to neck, jaw, arms, back, left side, similar to angina pectoris but more severe and lasts longer, pain doesnt respond to NTG, epigastric, SOB, sweating, nausea, vomiting, weakness fatigue, syncope
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8
Q

NSTEMI and STEMI dx and tx

A
  • dx:
    • NSTEMI: EKG shows pathologic Q waves, elevated trop and CK-MB
    • STEMI: EKG shows peaked T-waves, ST elevation, Q waves, T wave inversion
    • in both, monitor BP/HR, cardiac enzymes
  • tx: admit to ccu, establish IV access, O2, NTG/morphine
    • MONA: morphine, O2, nitrates, ASA
    • BB, ACE, heparin, statin
  • prognosis: 30% mortality rate
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9
Q

dressler syndrome

A
  • post-MI syndrome occurs 1-2 wk post-MI
  • sxs: fever, malaise
  • complications: pericarditis, pleuritis
  • dx: CBC shows leukocytosis
  • tx: ASA (first line), ibuprofen
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10
Q

Dyspnea on exertion

A
  • breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity
  • clues to need for an urgent eval inclue HR >120, resp rate >30, pulse ox <90%, accessory m use, difficulty speaking full sentences, stridor, asymmetric breath sounds or percussion, diffuse crackes, diaphoresis, cyanosis
  • CV causes = AMI, HF, cardiac tamponade
  • Resp causes = bronchospasm, PE, PTX, pulm infxn, upper airway obstruction
  • workup in emergent setting for acute dyspnea: EKG and CXR, cardiac biomarkers, US, BNP, D-dimer, ABG/VBG, CO2 monitoring, chest CT or VQ scan, peak flow and PFTs
  • management: O2, IV access, EKG and uplse ox, airway managment
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11
Q

stable angina etiology, RF, sxs

A
  • etiology: fixed atherosclerosis narrowing arteries
    • O2 supply < )2 demand
  • major RF: DM (worst), HLDL (high LDL), HTN (most common), smoking, age (m>45, w>55), FHx premature CAD or MI in 1st degree relative, low HDL
    • minor RF: obesity, sedentary, stress, ETOH
  • sxs: CP or substernal pressure (lasts <10-15m, heaviness, pressure, squeezing, tightness, rarely sharp), gradual onset pain, increases with exertion or emotion, relieved with rest or NTG
    • Levine sign: clenched fist over sternum and clenched teeth when describing CP
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12
Q

stable angina dx and tx

A
  • dx: EKG - normal, Q-waves (prior MI)
    • cardiac stress test
  • tx: sublingual NTG - IV NTG
    • coronary angiography: if severely sxatic despite medical tx
  • prognosis: depends on LVEF: <50% = increased mortality
    • vessels involved: left main = poor prognosis, 2-3 vessels total = worst prognosis
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13
Q

Pericardial effusion

A
  • secondary to pericarditis, uremia, or cardiac trauma: restrictive pressure on the heart
  • sxs: painful or painless, cough and dyspnea, atypical chest discomfort, dizziness (low BP), palps
  • signs: periph edema, distant heart sounds
  • complications: as effusion increases, CO and BP dec, falling to critical levels (tamponade)
  • dx: CXR or echo determine extent of effusion or calcification (inc pericardial fluid, cardiomeg), EKG shows nonspec T wave changes, low QRS voltage (alternans)
  • tx: pericardiocentesis to relieve fluid accumulation; if recurrent, surgery with a pericardial window
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14
Q

cardiac tamponade

A
  • fluid compromises cardiac filling and impairs cardiac output
  • signs: beck’s triad - biphasic scratching sound (muffled heart sounds), HoTN, JVD, tachycardia, tachypnea, Kussmaul’s sign, pulsus paradoxus
  • dx: echo shows increased pericardial fluid, diastolic collapse of cardiac chambers, narrow pulse pressure
  • tx: pericardiocentesis
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15
Q

hypertensive urgency

A
  • BP needs to be reduced within hours
  • Persistently elevated higher than 220 systolic or 125 diastolic or accompanied complications without end-organ damage
  • tx: oral agents: clonidine, captopril, nifedipine, labetolol
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16
Q

Hypertensive emergency (malignant hypertension)

A
  • elevated BP with papilledema or retinal hemorrhage and either encephalopathy or nephropathy, confusion, left ventricular failure, intravascular coagulation
  • Difference: HTN emergency always has retinal papilledema and flame-shaped hemorrhages and exudates
  • must be reduced within 1 h to prevent progression to end organ damage or death
  • diagnostic criteria: persistently elevated higher than 220 systolic, diastolic >130
  • Complications: encephalopathy, nephropathy, ICH, aortic dissection, pulmonary edema, unstable angina, MI, stroke
    • ​on fundoscopic: retinal hemorrhages, exudates, papilledema
  • Hallmark complication: fibrinoid necrosis of the arterioles in the kidney
  • Tx: DONT REDUCE TOO RAPIDLY - can cause ischemia
    • sodium nitroprusside (short acting, titratable, potential for thiocyanate and cyanide tox with prolonged use or renal/hep fail)
    • labetalol (alpha and beta blocker) - preferred in dissection and ESRD
    • Neuro emergencies:
      • encephalopathy, stroke, ICH, SAH: labetalol, nicardipine, esmolol. AVOID nitroprusside and hydralazine
        • reduce MAP 25% over 8h
        • for MI us NTG or BB
      • aortic dissection: use nitroprusside and BB
      • Hydralazine during preg
      • lower BP within first 24-48h by 25%
        • 90% will die after 1-2y
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17
Q

congestive heart failure

A
  • decompensated: evidence on PE or chest radiograph of pulm edema, audible 3rd heart sound or increased JVP
  • Left ventricular failure: sxs of low cardiac output and congestion (SOB) dt systolic or diastolic dysfn
  • R ventricular failure: sxs of fluid overload almost always dt LVF
  • MCC systolif HF (reduced EF): ISCHEMIC CARDIOMYOPATHY (CAD with resultant MI an dloss of fning myocardium)
  • systolic dysfn: difficulty with ventricular contraction
  • diastolic dysfn: difficulty with ventricular relaxation; results from HTN and associated with aging; related to myocardial m. stiffness and LVH
  • HF with preserved EF
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18
Q

congestive heart failure etiology, RF, and sxs

A
  • MCC: CAD, HTN, DM
    • LV remodeling: dilation, thinning, mitral valve incompetence, RV remodeling
    • 75% have preexisting HTN
    • MCC of transudative (extravascular fluid) pleural effusions
    • mostly >65yo
  • sxs:
    • exertional dyspnea (SOB), then dyspnea with rest, chronic nonproductive cough, worse in recumbent position
    • fatigue, orthopnea, night cough, relieved by sitting up or sleeping with additional pillows, paroxysmal nocturnal dyspnea, nocturia
  • signs:
    • cheyne-stokes breathing, edema (ankles, pretibial (cardinal)), RALES, additional heart sounds:
      • S4 = diastolic HF (preserved EF)
      • S3 = systolic HF (reduced EF) with volume overload - tachycardia, tachypnea
    • jugular venous pressure >8cm
    • cold extremities, cyanosis, hepatomegaly (ascites, jaundice, peripheral edema)
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19
Q

congestive heart failure dx and tx

A
  • dx:
    • labs: CBC, CMP, UA +/- gluc, lipids, TSH
    • Serum BNP: increases with age and renal impairment, elevated in HF, differentiates SOB in HF from noncardiac issues
    • 12-lead EKG
    • CXR: kerley B lines
    • Echo: differentiates HF _/- preserved LV diastolic fn
    • Reduced pulse pressure and SVR
  • tx:
    • acute management: LMNOP
      • Lasix
      • Morphine (reduces preload)
      • Nitrates (reduces preload)
      • O2
      • Position
    • ACEi
    • CCB in diastolic HF
  • poor prognostic factors: CKD, DM, low LVEF, severe sxs, old
  • 5y mortality = 50%
20
Q

when to refer HF vs admit

A
  • Refer: new sxs no explained by obvious cause, continued sxs and reduced LVEF (<35%)
  • Admit: unexplained new or worsening sxs or + biomarkers indicating acute MI, hypoxia, fluid overload, pulm edema not resolved as outpt
21
Q

Peripheral vascular dz or peripheral arterial dz

A
  • in absence of limb-threatening ischemia, sxs of PAD tend to remain stable with med tx
  • if revascularization is needed, percutaneous revasc first, reserve surgery for when arterial anatomy is unfavorable
  • clinical features used to determine if thrombolytic therapy or surg revasc is most appropriate:
    • presumed etiology (embolus vs thrombus)
    • location
    • duration of sxs
    • availability of autologous vein for bypass grafting
    • suitability of pt for surg
  • proximal embolus at bifurcation of common fem artery is ideal lesion for embolectomy
    • embolus to distal vessel Ii.e. tibial a.) may be tx with thrombolytic agent
    • major use of percutaneous transluminal angioplasty (PTA) is in the tx of underlying lesion after clot has been lysed with thrombolytic tx
  • Leriche syndrome: triad of 1) claudication, 2) absent or diminished femoral pulses, and 3) erectile dysfunction
22
Q

intermittent claudication

A
  • occurs distal to level of stenosis or occlusion (calf pain with walking 10-35% of ppl with PAD)
  • sxs: reproducible pain aggravated by sustained exercies, relieved with rest, aching, dull pain, leg pain occurs after certainwalking distances, resolving within 10min, cramping, numbess, weakness, giving way
    • Physical: hair loss on bilateral lower extremities, thinning of skin, diminished pulses
  • dx: treadmill testing using ABIs at rest and after exercise - <0.9 = diagnostic
  • tx: stop smoking (first line), graduated exercise, foot care, control HLD, HTN, weight, DM, avoid extremes of temp, ASA + ticlopidine or clopidogrel (sx relief), cilostazol (PDE inhibitors)
    • surgery: angioplasty, bypass grafting
23
Q

Asx PAD

A
  • screen in pts with abnormal/absent pedal pulses, age >70, age 50-69y with hx of smoking or DM
  • sxs: none
  • dx: ABI - if <0.9 is dx; if 0.91-1.3 normal and no further testing; if >1.3 doppler ankle waveforms and toe pressures
  • tx: preventative = ASA, lipid lowering, blood pressure control
24
Q

PAD or PVD etiology, RF, and sxs

A
  • occlusive atherosclerotic dz of lower extremities
    • superficial femoral artery is MC, popliteal, aortoiliac
  • RF: smoking HLD, DM, HTN
    • Men >40y, AA
  • MCC: atherosclerosis
    • Considered to be a coronary artery disease risk equivalent
    • Common in pts with ESRD
    • 20-50% are asx and 40-50% present with atypical leg pain
  • Sxs: pain in one or more lower extremity muscle groups (cramping thigh, calf, or buttock pain’ intermittent claudication; worse with elevation (reclining))
    • Rest pain felt over distal metatarsals, prominent at night (wakes pt up from sleep), hangs foot over side of bed or stands to relieve pain
  • signs: diminished/absent pulses, muscular atrophy, hair loss distal to obstruction, thick toenails, decreased skin temp, localized skin necrosis (toes), nonhealing, infarction, or gangrene, pallor of elevation and rubor of dependency
25
Q

PAD or PVD dx and tx

A
  • dx: hypercholesterolemia >240, hypertTG >250
    • ABI testing - if <0.9 = dx
    • doppler - reduced or interrupted flow
    • Arteriography (gold standard)
  • tx: prevention of atherosclerosis (control HLD, HTN, weight, DM
    • manage primary HLD: statins, diet exercise (walk to point of claudication, rest, then continue walking), foot care
    • reduce BP, STOP SMOKING (most important)
    • Medical intervention: ASA and ticlopidine or clopidogrel (sx relief), cilostazol (PDE inhib)
    • Surgery: angioplasty (preferred), adjunctive stenting, bypass grafting
26
Q

aortic dissection etiology and sxs

A
  • ascending = type A; descending = type B
  • etiology: weakening of the aortic wall that may lead to the development of aneurysmal dilation
  • bimodal: young pt with connective tissue disorders, age 50+ w chronic HTN
  • sxs: presentation predicts intimal disruption
    • abrupt severe CP radiates to area between scapulae (feeling of impending doom, ant chest pain = type A, abd pain = type B, 64% describe as sharp, 50% describe as tearing or ripping
    • syncope = type A; dysphageia, hoarseness, Horner syndrome
  • signs: HTN, aortic insuff, pulse def in radial or femoral arteries
27
Q

aortic dissection dx and tx

A
  • dx: EKG (ro ACS), biomarkers (D-dimer), CXR (widened mediastinum, abnl aortic contour), CT with and without (preferred - anatomy, loc, extension, signs of rupture, end organ damage
    • TEE (as sensitive and spec as CT), CT angio (dx CAD, PE, and aortic dissection - requires special contrast, increased radiation), MRI (GOLD STANDARD)
  • tx: neg inotropic agent to lower BP without inc shear force on intimal flap
    • B-blocker (propran, labet, esmolol), Definitive = segmental resection of dissection with interposition of a synthetic graft
  • complications: stroke, cardiac tamp, paraplegia, back, flank, abd pain, death
28
Q

thoracic aortic aneurysm

A
  • ascending aneurysms: medial degeneration
  • descending aneurysms: atherosclerosis
  • sx/s: asxatic, CP, SOB, cough, hoarseness, dysphagia
  • dx: CXR (widened mediastinal shadow, displacement of trachea or left main stem bronchus), echo (TTE), contrast CT, MRI, invasive aortography
    • tx: if asxatic, follow with contrast CT or MRI q6-12mos, B-blockers for Marfan syndrome or bicuspid aortic valve, repair 4-5cm, descending = >6cm, increasing 1cm/y
  • prognosis: worse if associated Marfan syndrome or dissection
29
Q

abdominal aortic aneurysm

A
  • aortic aneurysms result from conditions that cause degradation or abnormal production of the structural components fo the aortic wall (elastin and collagen)
  • MC pathology: atherosclerosis (older males >50)
  • RF: smoking, high cholesterol, aging, HTN, male sex
  • sxs: asxatic, if rupture acute pain and hoTN
  • signs: palpable, uplsatile, expansile, and nontender mass - becomes painful with expansion (chest, back, lower scrotum)
  • dx: CXR (calcified outline), abd US (serial doc of size), CT w contrast, MRI to determine loc and size
  • tx: medical emergency, endovasc placement of aortic stent graft or open surg repair with prosthetic graft (expanding rapidly, asx >5.5cm), serial noninvasive FU for <5cm
  • prognosis: related to size and severity of coexisting CAD and CVD
  • screening: men 65-75 who have smoked, siblings of indivs with thoracic aortic or peripheral arterial aneurysms
30
Q

arterial embolism or thrombosis

A
  • emboli that arise from ventricular aneurysm or from dilated cardiomyopathy can be very large and can lodge at aortic bifurcation (saddle embolus), thus rendering both legs ischemic
  • a palpable femoral pulse and absent pop and distal pulses may either be dt distal common femoral embolus (pulse being palpable above level of occlusion) or embolus to superficial femoral or pop arteries
  • arterial embolism: MC source = heart; associate = afib, subacute endocarditis, acute bacterial endocarditis, rheum hrt dz
    • sxs; no hx of prior vasc dz
    • dx: EKG (dx afib), TEE (look for cardiac source), CT (look for descending throacic and abdominal sources)
    • tx: embolectomy
  • arterial thrombosis: RF for atherosclerosis, hypercoag status
    • dx: duplex
    • tx: thrombectomy
31
Q

syncope

A
  • loss of consciousness/postural tone 2ary to acute dec in cerebral blood flow; 20% pts have 1ary dx of anxiety, mood, or substance abuse
  • Ddx:
    • seizure
    • cardiat et: arrhythmias (sick sinus, v-tach, AV block, rapid SVT), obstruction of blood flow (aortic sten, HCM, mitral valve prolapse), massive MI
    • vasovagal: ↑parasymp, ↓symp stim, MCC, emotional stress, fear, etc.; premonitory sxs = pallor, sweat, light-headed, N, dec vision, roaring in ears; Tilt table study to reproduce sxs; tx = supine, elevate legs, BB
    • orthostatic HoTN: caused by ganglionic blocking agents, DM, old, defect in vasomotor reflexes; posture is main cause, + tilt table, tx with inc sodium and fluids, fludrocortisone
    • TIA, hypoglyc, hypervent, hypersensitivity, mech reduction of venous return (valsalva, postmicturition), meds
  • EKG FOR ALL PTS, serum PRL (helps RO noonepileptic psychogenic events if w/in 10-20mins after event - will be elevated after syncope or seizures)
32
Q

Coronary artery disease

A
  • risk factor mod: SMOKING CESSATION - cuts risk by 50%
  • Medical tx: ASA + BB
    • Sublingual NTG (for angina)
    • ASA (decreases morbidity and mortality)
    • BB (atenolol and metoprolol are first-line)
    • ACEi (for pts with heart failure)
    • Morphine (venodilation, decreases preload and O2 demand)
    • Nitrates (long acting - need 8 to 10 hr nitrate free interval to prevent tolerance; dilates coronary arteries, reduces preload and myocardial O2 demand; adverse effects = HA, ortho HoTN, tolerance, syncope)
    • CCB - coronary vasodilation, afterload reduction, reduces contractility; secondary tx when BB or NTG not fully effective or maxed out
    • Statins (stabilizes plaques and lower cholesterol)
  • revascularization - does NOT REDUCE RISK OF MI, but improves sxs
    • PCI, CABG, antiplatelet tx
  • Thrombolytic tx (alteplase):first line tx
    • pts who present late and PCI contraindicated, administer ASAP upt to 24hrs after onset of CP, best if given in first 6hrs
33
Q

phlebitis

A
  • inflammation at entry site due to needle or catheter insertion
  • MCC of fever after postop day 3
  • MC in lower extremity veins
  • sxs: induration, edema, tenderness, visible signs are minimal but include redness
  • tx: remove catheters at earliest signs
  • prevention: aseptic technique during insertion, frequent change of tubing (48-72h), rotation of insertion sites q4d
    • use silastic catheters (least reactive) and hypertonic solutions in veins with substantial flow
34
Q

suppurative phlebitis

A
  • MC bug: STAPH
  • presence of infected thrombus around indwelling catheter
  • sxs: locla signs of inflammation + pus from venupuncture site, high fever
  • dx: + blood cultures
  • tx: excise affected vein, extend incision proximally to first open collateral, leave wound open
35
Q

edema

A
  • lower extrem (either inc venous or lymphatic pressures, dec intravasc oncotic pressure, inc capillary leak or infxn/local injury)
  • MCC: chronic venous insuff, common complication of DVT
  • sxs: MC sx = sensation of “heavy legs”, itching, pain
  • signs: hyperpig, stasis dermatitis, lipodermatosclerosis (thick, brawny skin), atrophie blanche (small depigmented macules), measure size of calves 10cm below tibial tuberosity, check for tenderness and pitting, ulcer located over medial malleolus (hallmark finding)
  • dx: if low suspicion D dimer indicated, use Wells criteria to rule out DVT, color duplex US as well as ABI, urine dip to ro nephrotic syndrome, SCr to check kidney fn
  • tx: treat underlying cause, if chronic venous insufficiency without volume overload, avoid diuretics (may enhance sodium retention through inc secretion of renin and angiotensin - AKI and oliguria)
    • supportive care = leg elevation above heart x 30min TID and during sleep, compression stockings, ambulatory exercise
36
Q

Shock

A
  • underperfusion of tissues
  • Presentation: tachycardia, hoTN, lactic acidosis, renal dysfn, CNS dysfn
  • tx: stabilize hemodynamically:
    • fluid bolus (500-1000 L NS or lactated Ringers)
    • CBC, CMP, Creatinine, PT/PTT, pulse ox, EKG, CXR, vasopressors (dopamine, NE) if hotn despite IVF
37
Q

Shock and how it affects cardiac output, SVR, and PCWP

A
  • Cardiogenic: dec CO, inc SVR, inc PCWP
  • Hypovolemic: dec CO, inc SVR, dec PCWP
  • Neurogenic: dec CO, dec SVR, dec PCWP
  • Septic: inc CO, dec SVR, dec PCWP
38
Q

Cardiogenic shock

A
  • heart unable to generate CO to maintain tissue perfusion
  • MCC: post-acute MI, cardiac tamponade, tension PTX, arrhythmias, PE, CM, myocarditis, valvular defects
  • sxs: altered sensorium
  • signs: SBP <90, urine outpt <20mL/h, pale cool skin, hoTN, tachycardia, JVD, pulm congestion
  • dx; EKG (ST elevation MC), echo, hemodynamic monitoring
  • tx: ABCs, identify underlying cause (vasopressors - dop ± dobutamine, NTG or nitroprusside, IVF (harmful if LV pressures elevated (may need diuretics)
39
Q

subclavian steal syndrome

A
  • stenosis of subclavian artery proximal to takeoff of vertebral artery
  • sxs: vertigo, syncope, L arm exertion, angina, or ulcerated/gangrenous findings
  • dx: unequal blood pressures in upper extrems (~45mmHg dec in systolic pressure in arm supplied by vessel)
  • tx: vascular consult, elective hosp, bypass grafting from common carotid to subclavian artery distal to lesion or transposition of subclavian beyond the lesion to the side of the nearby common carotid
40
Q

thombolysis

A
  • absolute CI: recent stroke, intracranial malig, brain mets, intracranial surgical intervention
  • relative CI: renal dz, allergy to contrast, cardiac thrombus, DM retinopathy, coagulopathy, recent arterial puncture, or surgery
41
Q

embolectomy

A
  • absolute CI to thrombolysis:
    • established CVA events (including TIA and CVA) w/i last 2mo
    • active bleeding diathesis
    • recent (<10d) GI bleed
    • neurosurg within last 3 mo
    • intracranial trauma w/i last 3 mo
    • intracranial malig or mets
42
Q

Acute limb ischemia

A
  • sudden loss of limb perfusion up to 2 wk after initiating event; 1-2% of pts with PAD age 50+
  • MCC: embolism, native vessel tthrombosis, reconstruction thrombosis, trauma, and complications of peripheral aneurysm
  • MC location: fem bifurcation
  • RF: DM (4x), smoking (3x), hypercholesterol (2x)
  • sxs: pain - abrupt, severe, gradually increasing in severity, progresses proximally
    • paresthesias - loss of sensory or motor fn, numbness, tingling
  • signs: pulselessness, pallor, paralysis, poikolothermia or perishing cold
  • dx: ABI (0.5-0.9 = claudication; <0.5 = rest pain, necrosis), contrast angio (gold standard - if prior vascular procedure or hx of lower extrem claudication), baseline labs and Cr
  • tx: thrombolysis less effective if >2wk duration (anticoag with IV hep bolus - continusous hep infusion ASAP; start IVF and foley, gradual clot dissolution) embolectomy or thrombectomy, amputation if nonviable limb
  • complications: stroke
43
Q

blue toe syndrome

A
  • embolic occlusion of foot (digital) arteries with atheroembolic material from prox source (aorta); small vessel occlusion
  • sxs: sudden-onset, cool, painful, cyanotic toe, or forefoot
  • signs: normal pedal pulses and warm foot, scattered petechiae or cyanosis of soles
  • tx: same as acute limb ischemia
44
Q

thomrboangiitis obliterans, buerger dz

A
  • difficult to diff from PVD, lesions on toes and pt younger than 40
  • nonatherosclerotic, segmental, inflammatory dz affecting small-to medium sized arteries and veins of extremities; typically in younger heavy smokers
    • MC arteries affects = plantar, digital vessels of foot and lower leg - fingers/hands in advanced stages
  • sxs: digit ischemia (MC), inttermittent claud uncommon, but rest pain in toes frequent
  • dx: MRA or invasive angio
  • tx: stop smoking
  • prognosis: pain progresses to tissue loss and amputation, unless pt stops smoking, prognosis better than PVD if smoking ceases
45
Q

Raynaud phenomenon

A
  • exaggerated response to cold temp or emotional stress
  • primary RP: idiopathic, onset 15-30y, young women, family hx +, symmetric involves fingers of both hands, no digital pitting, ulceration, or gangrene
  • secondary RP: rheumatic dz, unilateral, involves 1-2 fingers, nailfold abnlities
  • sxs: sharply demarcated color changes (mostly hands, but can occur on toes; begins in single finger and spreads symmetrically to both hands)
  • signs: pallor and cyanosis required, erythema, reversible with rewarming or reduction of stress, pain or ulceration of skin from ischemia
    • livedo reticularis (violacious mottling or reticular pattern of skin of arms and legs
  • dx: nailfold capillaroscopy distinguishes primary from secondary
  • tx: preventative (wear gloves or mittens, keep body warm, stop smoking, lubricate with lotion, avoid sympathomimetics (decongestants, diet pills, amphetamines))
    • for severe sxs or tissue injury/ischemia: CCB (1st line), ACEi, sympatholytic agents (prazosin), topical nitrates, PDe inhib (sildenafil, etc.), SSRIs, statins, prostaglandin E2, misoprostol
46
Q

Palpitations

A
  • unpleasant awareness of forceful, rapid, or irregular beating of the heart; mostly benign but can be lethal arrhythmias
  • r/o panic, stress, anxiety, arrhythmia, presyncope, syncope, hyperthyroid, hypovolemia, afib, other valvular defect, drug use
  • sxs: described as stop and start, fluttering, pounding in the neck
  • signs: “cannon” A waves in the JVP, visible neck pulsations, signs of hyperthyroid (tremulousness, brisk DTRs, hand tremor), signs of drug use (dilated pupils, skin, or nasal septal perforations), auscultate for midsystolic clicks, holosystolic murmurs, and changes with valsalva, displaced PMI, etc.
  • dx: 12-lead EKG and ambulatory EKG
  • tx: abstain from caffeine and tobacco, reassurance if normal workup, if abnormal tx underlying condition
    • when to admit: palps with near syncope or syncope, especially if >75yo and abnl EKG, hct <30%, SOB, RR >24/min
47
Q

orthopnea

A
  • inability to breath (SOB) in the horizontal (lying down) position that improves with sitting upright
  • differential: COPD, acute asthma, gross obesity, HF