PANCE Prep- Cardiology Part 2 Flashcards
What creates S1, S2, S3, S4 and what disease are associated with them. What creates split S2
S1- MV and TV closure (loudest at apex)
S2- AV and PV closure (loudest at base)
S3- right after S2, passive ventricular filling striking overly compliant ventricle
-Systolic HF, DCM, normal in kids and pregnancy
S4- right before S1 when atria contract, blood striking non-compliant LV
-Diastolic HF, HOCM, LVH
Split S2: delayed PV closure
Where do AS and MR murmurs radiate to?
AS- carotids
MR- axilla
Increase or decrease in venous return does what to murmur intensities?
Inspiration vs expiration on murmur intensities
how does handgrip and amyl nitrate impact murmur intensity
what two positions accentuate aortic murmurs?
what position strengthens mitral murmurs?
- increase venous return increases ALL murmurs except HCM and MVP–> squatting, leg raise, supine
- decreasing venous returns decreases all murmurs except HCM and MVP–> valsalva, standing
- Right sided murmurs increase w/ inspiration
- Left sided murmurs increase w/ expiration
- Hand grips increases afterload–> increases regurg murmurs (AR and MR) and decreases outflow murmurs (AS, HCM, MVP)
- Amyl nitrate decreases afterload–> decreased regurg murmurs (AR and MR) and increased outflow murmurs
- sitting up and leaning forward makes aortic murmurs stronger
- lying on left side strengthens mitral murmurs
3 Complications of AS and survivals
think AS Complications (ASC)
- Angina (increased O2 demand but fixed CO due to obstructed LV outflow)- 5 yr survival
- Syncope w/ exertion (brain not being perfused adequately)- 3 yr survival
- CHF- 2 year survival
AS murmur description
PE finding, pulse pressure?
How to dx: what might you see on EKG
How to tx: indications and pt education on things/meds to avoid
Systolic ejection murmur, crescendo-decrescendo murmur heard at RUSB that radiates to carotids
PE: pulsus parvus et tardus: small, delayed carotid pulse
narrowed pulse pressure
DX: Echo, EKG: LVH
TX: surgery is ONLY effective therapy
surgery for sxs pts, or asxs SEVERE AS (EF < 50%)
*no medical therapy is truly effective
*AVOID physical exertion,venodilators (nitrates), neg. inotropes (CCB, BB) ANYTHING THAT DEC PRELOAD
AR murmur description PE finding, pulse pressure? What sign is most sensitive for AR? two pulses associated with AR how to dx how to tx
diastolic, decrescendo, blowing murmur at LUSB
PE finding: bounding pulses (due to increased SV)
wide pulse pressure
-Hill’s sign (most sensitive): popliteal artery systolic pressure > brachial artery by 60mmHg
-Water Hammer pulse- swift upstroke and rapid fall of radial pulse accentuated w/ wrist elevation
-Corrigans pulse- similar to water hammer pulse but referring to carotid artery
DX: Echo, cath is definitive
TX:
- surgery only definitive
- afterload reduction with vasodilators (ACEI, ARBs, Nifedipine, Hydralazine)
MS murmur description MC cause of MS 3 main sxs of MS how to Dx how to Tx
-early-mid diastolic rumble at apex esp. in LLD position, OPENING SNAP, prominent S1
MC caused by rheumatic heart disease, also have to think endocarditis and signs
SXS: pulm sxs (dyspnea, hemoptysis, pulm HTN), a-fib, mitral facies (flushed cheeks with facial pallor)
DX: echo (most useful), ekg: shows left atrial enlargement (p wave > 3mm) +/- afib
TX:
- meds- diuretics to manage HF/fluid overload, BB for rate control of a-fib, if appropriate afterload reduction improves forward flow and prevents remodeling of left atrium (ACEI, ARBs),
2) . surgery is definitive
MR murmur description MC cause chronic and acute sxs PE finding how to dx how to tx
-blowing holosystolic murmur at apex w/ radiation to axilla
MC cause is MVP (rheumatic fever developing countries), also ischemia
chronic sxs: HF sxs (DYSPNEA, fatigue), a-fib
acute sxs: pulm edema, hypotension
PE finding: widely split S2
DX: echo (best noninvasive test)- hyperdynamic LV
TX: surgery (try to repair first)- if refractory to medical therapy or EF less than 60%
1. sxs pts who cannot undergo surgery benefit from afterload reducers (ACEI/ARBs, BB) and diuretics
MVP is usually asymptomatic but some may experience what sxs? how do you treat these sxs?
autonomic dysfunction: anxiety, atypical CP, painic attacks, palps–> then tx w/ BB but otherwise no tx is needed
PS murmur description
MC cause of PS
preferred tx
harsh midsystolic ejection cresc-decrecendo murmur at LUSB radiates to neck
PS almost always congenital
TX: balloon valvuloplasty
PR murmur description
MC cause of PR
preferred tx
GRAHAM-STEEL murmur: brief decrescendo early diastolic murmur at LUSB with full inspiration
PR almost always congenital
TX: none needed- well tolerated
TS murmur description
what can TS cause?
preferred tx
mid-diastolic murmur heard at LLSB at 4th ICS, opening snap
can cause right sided HF
TX:
1). meds decrease RA volume overload (diuretics and na restriction)
2). surgery: commissurotomy or replacement if RHF or dec CO
TR murmur description
what sign is seen with TR
preferred tx
holosystolic blowing high pitched murmur at subxyphoid area (L mid sternal border)
-Carvallo sign- increased murmur intensity w/ inspiration
TX:
1). meds- diuretics (volume overload/congestion)
2). surgery for severe TR
describe the pathophysiology of AS MS AR MR
AS: LV outflow obstruction–> fixed CO
-increased afterload–> LVH –> eventual LHF
MS: Obstruction of flow from LA to LV–> increased LA pressure and left atrial enlargement–> Pulm congestion and PHTN
AR: back flow of blood into LV–> LV volume overload with eventual LV dilation and HF
MR: back flow from LV into LA–> increased LA pressure –> increased pulm pressures
__ is 2nd MC cause of ESRD is US
HTN
describe the different grades of retinopathy
I: arterial nicking
II: AV nicking
III: hemorrhages and soft exudates
IV: papilledema
Electrolyte changes and Meds of:
- Thiazide diuretics: 2 cautions, 1 CI
- Loop diuretics: 2 cautions, 1 CI
- K sparing diuretics 1 ADR, 2 CI
- Thiazide diuretics (HCTZ, chlorthalidone, metolazone): HYPOK+, HYPONa+, HYPERCa++, Hyperglycemia, Hyperuricemia (caution w/ gout and DM)
* CI: NO SULFA ALLERGY - Loop diuretics (furosemide, bumetanide): HYPOK+, HYPONa+, HYPOCa++, caution: gout and DM (hyperuricemia and hyperglycemia)
* CI: sulfa allergy, ototoxic - K sparing diuretics: HyperK*, gynecomastia
* CI: renal failure, HYPO Na
When is it best to use ACEI for HTN and what are their SE
- Hx of DM and HTN, nephropathy or systolic Left-sided CHF, post MI–> renoprotective**
SE:
- hypotension w/ first dose
- azotemia/RI
- HYPERK+
- Cough- MC
- angioedema
*CI: pregnancy, lactation, bilateral renal stenosis
What are the 2 types of CCBs and how do they help with HTN?
Dihydropyridines: potent vasodilator w/ little or no effect on cardiac contractility or conduction
ex. Nifedipine and amlodipine
Non-dihydropyridines: affects cardiac contractility and conduction
- used w/ HTN w/ concomitant Afib and used for raynauds
ex. verapamil, diltiazem
SE of CCBs, one for verapamil
2 contraindications
HA, dizziness, LH, flushing, peripheral edema,
Verapamil: constipation
CI: 2nd and 3rd Heart block, CHF
SE of BB, adrs may worsen with what two things
3 contraindications
fatigue, depression, impotence, masked sympathetic sx of hypoglycemia (caution w/ diabetics)
- may worsen PVD or raynauds
- CI: 2/3 Heart block, asthma, decompensated HF
good HTN med to use w/ BPH? how do these meds help with HTN? ADRs?
A1 blockers prazosin terazosin doxazosin *alpha blockade = peripheral arterial dilation ADRs: 1st dose syncope, dizziness, HA
What antihypertensive med should you use to treat HTN w/ comorbid:
- afib
- angina
- post MI
- Systolic HF
- DM
- isolated HTN in elderly
- BPH
- AA
- Gout
- afib: BB or CCB
- angina: BB or CCB
- post MI: BB or ACEI
- Systolic HF: ACEI, ARB, BB, diuretic
- DM: ACEI
- isolated HTN in elderly: diuretic
- BPH: a1 blocker
- AA: thiazide, CCB
- Gout: CCB, Losartan (only ARB that doesn’t cause hyperuricemia)
4 groups: indication for statins
- 40-75y/o with DM 1 or 2 with LDL 70-189
- 40-75y/o w/o DM with LDL 70-189 but 7.5% or greater 10 yr ASCVD
- 21y/o or older w/ LDL 190 or higher
- known atherosclerotic CV disease (MI, stroke, CAD, PAD for example)
Best meds to:
- lower LDL
- Lower TG
- Increase HDL
- lower LDL: Statins
- Lower TG: Fibrates
- Increase HDL: Niacin
what is the only med that is safe in pregnancy to help tx hyperlipidemia? what is the trade off of using this medication?
Bile acid sequestrants
(cholestyramine, colestipol, colesevelam)
*may increase TGs
PAD signs and sxs
what is leriche’s syndrome
dx: best screening and GS
how to tx
- LE pain/discomfort brought on by exercise or walking and relieved w/ rest: CLAUDICATION
- rest pain in advanced disease
- decreased pulses, atrophic skin changes, dusky red w/ dependent rubor, lateral malleolar ulcers
Leriche’s syndrome: claudication (butt, thigh) + impotence + Decreased femoral pulses
DX:
- ABI BEST SCREENING TEST: +PAD if ABI <0.90
- Arteriography (gold standard)
- hand held doppler- used in ED
TX:
- supportive: first line is exercise, smoking cessation
- Platelet inhibitor: Pletal/Cilostazol most effective medical therapy
* maybe also ASA, plavix - Revascularization: PTA (balloon catheter) ,bypass, endarterectomy
Where do AAA typically occur and what measurement is considered aneurismal
infrarenally
> 3.0cm (>5cm = increased risk of rupture)
How do you dx AAA (three classes of pts)
- Abdominal US- best initial test for asxs pts suspected AAA and for monitoring progression in size
- CT w contrast- best for thoracic aneurysms, sxs stable pts, and for further eval of known AAA
3) . focused beside US- unstable pts with suspected AAA
* *Angiography- gold standard
Screening for AAA
How do you treat/monitor AAAs depending on size?
Screening: one time screening with abd US for men 65-75 yo who ever smoked
- 5.5cm or greater OR >0.5cm expansion in 6 months= immediate surgical repair even if asymptomatic
- > 4.5cm= vascular surgeon referral
- 4-4.5cm= monitor by US q6months
- 3-4cm= monitor by US q1yr
*BB reduces shearing forces and risk of rupture
What is an aortic dissection and where is it is the worst place to have?
tear in the innermost layer of aorta (intima)
65% ascending= highest mortality
What are risk factors of aortic dissections and which one is most important?
- HTN (MOST IMPORTANT)
- age 50-60 (M>F)
- vasculitis
- collagen disorders (Marfan’s)
Tx of aortic dissections
Surgical if: (A needs surgery ASAP)
- Acute proximal (Type A or I II)
- acute distal (type III) w/ complications
Medical management w/ labetolol (SBP 100-120 and pulse <60) for descending if no complications (B or III)
*could use sodium nitroprusside added if needed
What is Buerger’s disease?
what type of person do you suspect this in?
how to dx
how to tx
nonatherosclerotic small and medium vessel vasculitis
-distal extremity ischemia in both lower and upper extremities (foot ulcers + raynauds phenomenon)
young men who smoke w LE ulcers/gangrene
DX: aortography- occlusive lesions of small and medium vessels “corkscrew collaterals” (Gold standard)
2. abnormal Allen test (occlude radial and/or ulnar arteries)
TX:
- STOP smoking (only definitive management of Buerugers)
- Wound care/amp
- CCB for raynauds
What is virchows triad
risk factors for DVT
- Intimal damage: trauma, infection, inflammation
- stasis: immobilization or prolonged sitting
- hypercoagulability: protein C or S deficiency, Factor V mutation
what is the hypercoagulability work up?
- Factor V Leiden (MC)
- Prothrombin gene mutation
- Protein C and S def.
- Antiphospholipid Ab
- Lupus
- Factor VII def.
How do you dx and tx DVT
DX: Venous duplex (1st line imaging)
- d-dimer +/- Wells criteria
- Venography (gold standard)
TX: AT LEAST 3 MONTHS
- Novel anticoagulants preferred over warfarin (apixaban, dabigatran, rivaroxaban)
2) Heparin (unfractionated heparin or LMWH (lovenox) –> Warfarin (overlap w/ heparin for at least 5 days)
what is the MOA, duration of action, antidote, and SE of LMWH
- MOA: potentiates antithrombin III
- Duration of action: 12 hrs
- Antidote: protamine sulfate
- SE/CI: renal failure, thrombocytopenia
- better to use in pregnancy
what is the MOA, duration of action, antidote, and SE of unfractionated heparin
- MOA: potentiates antithrombin III, inhibits thrombin and other coag. factors
- Duration of action: 1hr
- Antidote: protamine sulfate
- SE: thrombocytopenia
chronic venous insufficiency: PP, CP, management
PP: venous valve incompetency leads to venous HTN
CP: leg pain worse w/ prolonged standing/sitting, foot dependency, improves w/ elevation and walking
-brownish hyperpigmentation
-medial malleolus ulcer
-pitting edema, stasis dermatitis (hemosiderin deposit)
TX: initial tx is conservative with compression stockings, exercise, leg elevation
-ulcer management and surgery for cases refractory to conservative tx
How to measure orthostatic hypotension
management of this
hypotension within 2-5 mins of quiet standing (or after a 5 minute period of being supine) defined by AT LEAST 20mmHg decline in SBP AND/OR fall in DBP 10mmHg or more
- HR usually increases on standing- absence of increase is associated with autonomic dysfunction
- increase in HR >15 may be due to hypovolemia
1st line management: increasing salt and fluid intake, gradual position changes
1st line medical management is Fludrocortisone (which should be used after conservative tx)
Describe the 4 types of shock
- Hypovolemic: loss of blood or fluid volume (increase PVR and HR to maintain CO)
- Cardiogenic: primary myocardial dysfunction- reduced CO
- Obstructive: extrinisic or intrinsic obstruction to circulation (tamponade)
- distribution: maldistribution of blood flow from essential organs to nonessential organs
“SHOCK”: sepsis (distributive), hypovolemic, obstructive, cardiogenic, kortisol
Management of Shock
ABC’s
Airway: may need intubation
Breathing: mechanical ventilation and sedation decreased work of breathing
Circulation: isotonic crystalloids (NS, LR)
Delivery of oxygen: monitor lactate levels
Endpoint resuscitation: urine output, CVP, MAP
hypovolemic shock PP, clinical signs
PP: loss of fluid volume leads to inc HR, inc SVR (vasoconstriction), hypotension, dec CO, dec PCP
- tachy, hypotensive, oliguria/anuria
- Pale, cool mottled skin
- Prolonged capillary refill
- Decreased skin turgor, dry mucous membranes
- I.e. hemorrhage, vomiting, diarrhea, severe burns
cardiogenic shock PP, clinical signs
PP: inadequate tissue perfusion leads to dec CO with inc SVR (INC PWCP) but adequate intravascular volume
- Severe respiratory distress***
- Cool clammy skin
- i.e. MI, myocarditis, valvular disease, cardiomyopathy, arrhythmia
Obstructive shock PP, clinical signs
PP: obstruction of blood flow due to PHYSICAL obstruction of heart and great vessels
- Severe respiratory distress**
- Cool clammy skin
- depends on cause
- i.e. tamponade, PE, tension pneumo, aortic dissection
Describe the 4 types of Distributive shock
- Septic- severe inflammatory immune response which leads to peripheral vasodilation (dec SVR)
- Neurogenic- sympathetic blockade which leads to unopposed vagal tone on vessels–> vasodilate (brady and hypotensive)
- Anaphylactic- severe IgE mediated HSN rxn w/ histamine release leads to vasodilation and cap. permeability
- Hypoadrenal- decreased corticosteroid and mineralocorticoid activity
Septic Shock clinical signs
only shock w/ increased CO- EARLY ON
- Warm, flushed extremities and skin: EARLY ON bc inc CO and dec SVR
- Brisk cap refill
- Bounding pulses, hypotension with WIDE pulse pressure
How do you treat hypovolemic shock
- ABCDEs
- volume resuscitation: crystalloids (NS or lactated ringer 3-4L)
- control hemorrhage source and prevent hypothermia
How do you treat cardiogenic shock
- O2, isotonic fluids (avoid aggressive IV fluid tx- use SMALLER AMOUNT of fluids*)– ONLY shock where large amounts of fluids are not given
- Inotropic support: dobutamine, epi
- tx underlying cause
How do you treat obstructive shock
- O2, isotonic fluids, inotropic support (dobutamine, epi)
2. tx underlying cause
How do you tx septic shock
- broad spectrum IV abx (get culture first, Zosyn + Ceftriaxone)
- IV fluid resuscitation: NS or LR (isotonic crystalloids)
- Vasopressors
How do you tx anaphylactic shock
- Epi 1st line
- Airway managment
- Antihistamine (diphenhydramine or Ranitidine)
- IV fluids
- Observe patient for 4-6hrs
how do you tx adrenal insufficiency (Addisonian crisis) shock?
Hydrocortisone 100mg IV
What type of antibiotic interacts with statins and what does it increase the patients risk of?
statin + macrolides (clarithromycin)
*may increase statin drug levels
*prolonged QT interval, myopathy and rhabdomyolysis
definition of hypercholesterolemia and dislipidemia?
hypercholesterolemia: total cholesterol >200, dislipidemia LDL > 130 and/or HDL <40 regardless of TC
1 treatment for high cholesterol
lifestyle modifications: dietary changes of decreased trans fatty acids, cholesterol, carbs plus exercise and weight reduction
screening guidelines for lipids and when to initiate screening
adults ages 20-79 w/o CVD every 4-6 years
initiate: people with higher risk (> 1 risk factor or severe risk factor) initiate screening at 20-25 for males or 30-35 for females
lower risk: initiate screening at 35 for males and 45 for females
MOA for statins, ADRs and contraindications, what to order before initiating statin
MOA: inhibit hepatic cholesterol synthesis (esp LDL)
ADRs: myositis, RHABDO, hepatitis
Contraindications: active hepatic dz, persistent elevated LFTs, pregnancy, breastfeeding
MUST ORDER LFTs PRIOR TO INITIATION OF MED
Bile acid sequestrants MOA, Indication, ADRs, and what meds CAN’T be taken with them
MOA: binds bile acids in intestine and causes liver to have to produce more (which uses up LDL to make more)
-often used in combo with statin to reduce LDL
*SAFE in PREG
ADRs: GI side effects, Osteoporosis with LT use, INC TG LEVELS
*impairs absorption of ABX, DIGOXIN, WARFARIN (must take these meds 1 hr before or 4 hrs after BAS)
Ezetimibe MOA, indication, ADRs
MOA: inhibits intestinal cholesterol absorption
-used in combo with statin to reduce LDL levels
ADRs: INC LFTs, HA, diarrhea
Fibrates: drugs, MOA, ADRs, contraindications
Fenofibrate, Gemfibrozil
MOA: inhibit TG synthesis and increase lipoprotein lipase (breaks down TG rich lipoproteins)
ADRs: Inc gallstones, GI symptoms, myalgias
Contraindications: active hepatobilary dz, severe renal disease, breastfeeding
Niacin MOA, ADRs, watch in pts with what two conditions
MOA: increases HDL (delays clearance)
ADRs: flushing, itchiness (take NSAID/ASA 30 mins before to reduce), GI sxs
hyperuricemia (GOUT), hyperglycemia (DM)
3 clinical signs of familial hypercholesterolemia
Xanthomas or Xanthelasmas
corneal arcus
bruits (especially carotid)
genetic pattern of familial hypercholesterolemia
autosomal dominant
two main etologies for AS
1) . degenerative: calcification (esp over age 70)
2) . congenital and bicuspid valve (common in pts under 70)
acute vs chronic causes of AR?
acute: acute MI, aortic dissection, endocarditis
chronic: aortic dilation (MARFAN’s, inflammatory disorder, syphilis)
what is an austin-flint murmur and what disease do you hear it in?
AR
diastolic rumble at the apex secondary to regurgitant flow from aortic valve competing with forward flow from left atrium
what is ortner’s syndrome and what disease is it heard in?
recurrent laryngeal nerve palsy due to compression from a dilated left atrium, which causes hoarseness
from MS
murmur description of MVP
MVP is most common cause of what in US?
most common cause of MVP
mid-late systolic ejection click
MVP most common cause of MR
MC cause of MVP: myxomatous degeneration (connective tissue diseases)
main modifiable RF for aortic aneurysm and classic CP
RF: smoking
MOST pts are asxs, but if there are sxs then abd/flank/back pain with pulsatile abdominal mass
ruptured presents with hypotension or syncope
classic presentation for aortic dissection
severe, ripping/tearing CP that may radiate into the back between scapula (esp with type B)
- unequal BP in both arms, decreased peripheral pulses
- can be hyper or hypotensive
most common imaging for aortic dissection and sign on CXR
CT angiogram**, MR angiogram, TEE
CXR: widened mediastinum
PP behind varicose veins
failure of saphenous vein valves causing dilation of the superficial veins
what criteria can you use for evaluation of DVT?
well's criteria low prob (-2 to 0) mod prob (1-2) high prob (3-8)
what is giant cell arteritis
classic sxs
how to dx
how to tx
large and medium vessel vasculitis of extracranial branches of carotid artery (i.e temporal artery)
polymyalgia rheumatica
classic sxs: headache, jaw claudication, visual changes
*may have scalp tenderness, fever, weight loss, fatigue
dx: CLINICAL, temporal biopsy for definitive
will see increased ESR and CRP
Tx: initiate high dose corticosteroids once suspected to prevent BLINDNESS (don’t wait for biopsy results to start steroids)
what is superficial thrombophlebitis? 3 things it is associated with clinical signs how to dx how to tx
inflammation or thrombosis of superficial vein
MC associated with IV, pregnancy, varicose veins
CP: tender, pain, edema, erythema, induration along course of vein, may have palpable cord
Dx: CLINICAL, venous duplex would show noncompressible vein with clot and wall thickening
tx: NSAIDs, elevation, warm compresses
*maybe phlebectomy if persistent or septic
acute arterial occlusion MC site
clinical signs
how to dx/workup
how to tx
VASCULAR EMERGENCY
THROMBOTIC MC, MC in superficial femoral artery
6P’s: paresthesias (early sign), pain, pallor, pulselessness, poikilothermia, paralysis (late finding)
dx: bedside arterial doppler to assess for pulses, CT angiogram
tx: reperfusion is key (surgical bypass, surgical thromboembelectomy), maybe thrombolytic therapy
what is pericarditis
what are the two MC causes
clinical signs
how to dx
inflammation of the pericardium, may involve the myocardium as well
Causes: idiopathic and infectious (viral)
CP: sudden onset pleuritic, peristent and positional (better when sitting forward), can have friction rub
Dx best with ECG: diffuse ST elevations (V1-V6) with associated PR segment depressions
-may use ECHO to eval for effusion/tamponade
Tx: NSAIDS or ASA 1st line (1-2 wks), colchicine 2nd line
what is dressler’s syndrome? how to tx
autoimmune condition
post MI pericarditis (usually 2-3 wks after)
tx: ASA or colchicine
what is pericardial effusion?
clinical signs
how to dx
how to tx
accumulation of fluid in pericardial space
CP: chest pain (if associated with acute pericarditis), dyspnea, fatigue, MUFFLED HEART SOUNDS
dx: ECHO test of choice (inc fluid in space), ECG see low QRS voltage and electrical alternans (alternating amplitude of QRS complex)
tx: tx underlying cause, large effusions might require pericardiocentesis
what is cardiac tamponade?
clinical signs
how to dx
how to tx
large pericardial effusion (rate more CRUCIAL than volume) that results hemodynamic instability
BECK’S TRIAD: hypotension + JVD + muffled heart sounds
-pulsus paradoxus
dx: ECG shows low voltage QRS with electrical alternans
echo: pericardial effusion + diastolic collapse of cardiac chambers
tx: immediate pericardiocentesis
criteria for SIRS
at least 2 of the following:
1) . Temp over 38C/100.4 F OR hypothermia under 36C/96.8F
2) . Pulse > 90
3) . RR > 20 or PaCO2 <32
4) . WBC > 12 OR under 4
sepsis vs severe sepsis vs septic shock
sepsis: SIRS + focus of infection (often have inc lactate)
severe sepsis: SIRS + MSOF
septic shock: Sepsis + refractory hypotension despite fluid administration
what are the diagnostic criteria for kawaski disease?
idiopathic vasculitis in kids <5 yo
fever for at least 5 days with 4 of the following:
1). conjunctivitis: bilateral, nonexudative, limbic sparing
2). mucositis: red, fissured lips/strawberry tongue
3). polymorphous rash
4). extremity changes: edema, desqamation of hands and feet, redness
5). cervical lymphadenopathy
what is the most concerning complication of kawaski disease?
coronary artery aneurysm
what is the treatment for kawaski disease?
aspirin and IVIG
