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*USMLE* > Cardiovascular > Flashcards

Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

Churg-Strauss / Eosinophilic Granulomatosis with Polyangiitis

vessel size?
s/s? organs affected?
labs?

A

small/medium vessels

  • late-onset ASTHMA, rhinoSINUSITIS, migratory lung infiltrates
  • eosinophilia
  • skin NODULES
  • may also affect kidney, GI, CV
  • ASYMMETRIC multifocal NEUROPATHY due to epineural vessel involvement (eg, wrist drop via radial nerve)

labs = eosinophilia + P-anca

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2
Q

Polyarteritis Nodosa

vessel size + organs?
s/s?

A

medium vessels (some small) in…

  • kidney, heart, GI, liver (lung spared)
  • fever, weight loss, hypertension
  • renal insufficiency, nodules
  • livedo reticularis
  • rosary sign
  • mesenteric ischemia
  • myalgia/arthritis

(may cause MI, retinal ischemia + orchitis)

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3
Q

Thromboangiitis Obliterans

vessel size
mechanism
histo

A
  • small/medium vessels (esp. tibial + radial aa.) in heavy smokers before age 35
  • direct endothelial tox or HS rxn (esp. Israel, Japan + india)
  • acute/chronic inflamm. with luminal thrombi that organize + recanalize plus EXTENSION into contiguous veins/nerves (unique) which may be encased in fibrous tissue
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4
Q

Hyperplastic Arteriolosclerosis

A

results from malignant htn (diastolics > 120-130)

onion-like concentric thickening of arteriolar walls via laminated SMCs and doubled BMs

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5
Q

Temporal / Giant Cell Arteritis

in whom?
general sx (3) and specific sx (4)?
A

1 vasculitis in adults

  • general - fever, malaise, fatigue, weight loss
  • Headache - temporal; may have scalp tenderness with combing; pain, nodularity over temporal a.
  • Jaw Claudication - during chewing
  • Vision Issues - ischemic optic neuropathy, amaurosis fugax, retinal artery occlusion
  • Polymyalgia rheumatica - neck, torso, shoulder + pelvic girdle
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6
Q

Kawasaki disease

epidem?
dx criteria?
complication?

A

“mucocutaneous lymph node syndrome”; MEDIUM arteries in young CHILDREN (<5), mostly ASIANS

Dx is by HIGH FEVER FOR 5+ DAYS, plus…

  • Conjunctivitis - bilateral non-exudative
  • Cervical LAP
  • Periungual desquamation / hand+foot erythema + edema
  • Strawberry tongue and red palate/cracked lips
  • Rash - starts limbs > trunk; usually urticarial

Complication = CORONARY ANEURYSMS

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7
Q

Henoch-Schonlein purpura

A

“systemic leukocytoclastic vasculitis”; IgA complex deposition

small vessels of kidney, skin, GI and joints

palpable purpura
abdominal pain
arthralgia
acute glomerulonephritis

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8
Q

Hemolytic Uremic Syndrome

A

Shigella or E. Coli O157:H7

after bloody diarrhea, injured endothelium of preglomerular arterioles + glomerulus activates plts > microthrombi occlude vessel + break RBCs into schistocytes

thrombocytopenia (w/o purpura or active bleed)
anemia
AKI (olig-/anuria, hematuria, high creatinine)

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9
Q

Sturge-Weber Syndrome

2 s/s

A

facial port-wine stains and leptomeningeal capillary-venous malformations

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10
Q

Hereditary Hemorrhagic Telangiectasia

s/s + presentation

A

aka Osler-Weber-Rendu syndrome

multiple telangiectasias of skin + mucosa

present w recurrent epistaxis / GI bleed

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11
Q

Strawberry Hemangioma

growth + regression
lesion characteristics

A

aka infantile hemangioma; #1 benign vascular tumor in KIDS

bright-red compressible plaque with sharp borders; can have superficial + deep parts

grow for first 2 years, then regress by 5-8

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12
Q

Cherry Hemangioma

growth + regression
lesions characteristics

A

1 benign vascular proliferation in ADULTS

small, bright red cutaneous papules

dilated capillaries + post-capillary venules in papillary dermis

do NOT regress

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13
Q

Spider Angioma

A

in pregnancy, liver disease, OCP tx or estrogen supp

dilated cutaneous arterioles; central papule with radiating blanching capillaries

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14
Q

Cavernous Hemangioma

A

present at birth or later

soft blue compressible mass up to few cm diameter

histo = large dilated vascular spaces

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15
Q

Cystic Hygroma

A

aka lymphangioma; benign tumor of dilated lymph spaces lined by endothelium

mostly on NECK; lobulated, compressible and transilluminatable

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16
Q

MCC of death in athletes <35?

MCC of death in athletes >35?

A

sudden cardiac death via hypertrophic cardiomyopathy (usually asymptomatic, may report dyspnea, fatigue, chest pain or syncope)

the SCD is via V.Fib or V.Tach that progresses to V.Fib

> 35 athlete COD is coronary artery disease

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17
Q

chronic ischemic heart disease

histo findings

A

patchy fibrosis in mural endocardium
discrete scars in areas of healed infarct
diffuse subendocardial VACUOLIZATION

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18
Q

MCCs of spontaneous intracranial hemorrhage in young adults (3)

A
  1. AV malformations
  2. ruptured aneurysms
  3. sympathomimetic abuse (cocaine)
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19
Q

CV issues associated with aortic coarctation

A

often assoc. with other congenital cardiac anomalies or BERRY ANEURYSMS

BAs are especially at risk for rupture because of HYPERTENSION in branches proximal to the coarct (eg, common carotid and brachiocephalic trunk > R CCA)

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20
Q

common cancer that commonly metastasizes to heart?

effects of metastasis?

A

breast cancer

pericardial effusion, possibly tamponade > decreased RV diastolic filling

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21
Q

3 main risk factors for coronary heart disease

other major risk factors (6)

A
  1. non-coronary atherosclerosis
  2. diabetes
  3. CKD

also hypertension, hyperlipidemia, smoking, advanced age, obesity and inactivity

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22
Q

Common CODs in diabetes

A
  1. Coronary heart disease (MI) - 40%
  2. Cerebrovascular accidents (stroke) - 10%
  3. End-stage kidney - DM is leading cause of ESRD, but pt usually dies of heart disease/infection first
  4. DKA / Hyperosmolar coma - hyperosmolar coma more deadly, but neither are common CODs
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23
Q

Free wall myocardial rupture

when? what decreases risk? consequences?

A

5-14 DAYS after MI when coagulative necrosis has weakened wall and before fibrosis has strengthened it

mostly LV due to high pressures

previous MI (fibrosis) or concentric LV hypertrophy (thicker) will DECREASE risk

results in hemopericardium +/- tamponade > sudden onset intense chest pain and shock

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24
Q

hypertrophic cardiomyopathy

mutations? inheritance?

A

mutations in cardiac sarcomere proteins (thick or thin filaments)

50% cases are familial, with AD inheritance and variable expression

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25
Q

“Heart Failure Cells”

what are they? when do you see them?

A

“Siderophages” - hemosiderin-containing macrophages in alveoli

Suggestive of CHRONIC LEFT HEART FAILURE with past episodes of pulmonary congestion + edema + RBC extravasation into alveoli

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26
Q

Myocardial hibernation

what is it? result?

A

chronic myocardial ischemia > metabolism + function reduce to match reduction in coronary flow > matched demand + supply prevents necrosis

contractile + cytoskeletal proteins decrease; adrenergic control is altered; CALCIUM RESPONSE REDUCES

causes decreased contractility with LOWER EF (tx with revascularization)

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27
Q

What is “ischemic preconditioning”?

Example of it occurring in a pathological state?

A

brief repetitive episodes of myocardial ischemia followed by reperfusion protect myocardium from later prolonged ischemic episodes

ex: chronic angina prior to MI actually delays cell death during MI > greated time for myocardial salvage

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28
Q

Before 4 hours, there is not visible change on myocardial biopsy after MI…

what are the changes at…
4-12 hours
12-24 hours
1-3 days

A

4-12 h - WAVY FIBERS with narrowed, elongated myocytes

12-24 h - myocyte HYPEREOSINOPHILIA with pyknotic (small) nuclei

1-3 days - coagulative necrosis (lost nuclei/striations) and prominent NEUTROPHILs

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29
Q

Myocardial biopsy changes post-MI…

3-7 days
7-10 days
10-14 days
2 wks - 2 months

A

3-7 day - dead neutrophils + myofibers disintegrate; MACROPHAGES infiltrate borders

7-10 days - MACROPHAGE PHAGOCYTOSIS; granulation begins

10-14 days - well-developed GRANULATION + NEOVASCULARIZATION

2 wks - 2 months - COLLAGEN deposition + scar

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30
Q

Nonbacterial Thrombotic Endocarditis

associations (2 main, 3 minor)
histo
complications

A

aka “marantic endocarditis”; valvular injury via inflammatory cytokines triggers platelet deposition with underling hypercoagulability

associated with…

  1. ADVANCED MALIGNANCY - esp. mucinous adenocarcinoma
  2. SLE - Libman-Sacks endocarditis
  3. (antiphospholipid Ab syndrome; DIC; extensive burns)

histo - fibrin strands, complexes, mononuclears + platelets; no microbes!

complications - usually L-sided > can embolize to brain (stroke) or limb (acute ischemia)

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31
Q

Steps of atherosclerotic plaque formation

A
  1. Hemodynamic Stress + hyperlipidemia
  2. Endothelial injury
  3. Increased VCAMs
  4. Monocytes + T cells in intima
  5. WBCs + endothelium release PDGF, FGF, endothelin-1 and IL-1
  6. Vascular SMCs proliferate in intima
  7. VSMCs make collagen, elastin + proteoglycans > FIBROUS CAP
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32
Q

Aortic Stenosis

auscultation, MCC

A

late-peaking systolic ejection murmur heard at 2nd ICS RSB

intensity decreases with maneuvers that decrease LV blood volume - valsalva straining phase, or abrupt standing

MCC is calcific aortic valve disease

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33
Q

calcific aortic valve disease

pathogenesis

A

at first, very similar to normal atherosclerosis development

later, proteins such as OSTEOPONTIN involved in tissue calcification are produced, and fibroblasts differentiate into OSTEOBLAST-LIKE CELLS that deposit bone matrix-like material

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34
Q

HOCM vs. hypertensive heart disease

gross + micro differentiation

A

HOCM - localized, non-uniform thickening (septal); histo differentiated by DISARRAY of myocytes (other histo changes similar)

Hypertensive - uniform thickening (concentric hypertrophy via myocyte addition in parallel); transverse thickening of cells, hyperchromatic nuclei; necrosis and interstitial fibrosis if ischemic

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35
Q

Atrial Myxoma

signs? histo?

A

intermittent / positional mid-diastolic murmur (“tumor plop”); mimics mitral stenosis

amorphous ECM; stellate/globular myxoma cells; mucopolysacch. of chondroitin sulfate and hyaluronate

high vascularity –> hemosiderin macrophages

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36
Q

Wegener’s granulomatosis

vessel size, triad, other s/s

A

aka granulomatosis with polyangiitis

small vessels

triad:
1) necrotizing VASCULITIS (focal)
2) LUNG + UPPER AIRWAY GRANULOMAS
3) GLOMERULONEPHRITIS - necrotizing

upper resp. infections: perforated septum, sinusitis, otitis media, mastoiditis

lower resp. tract: cough, dyspnea, blood

hematuria, red cell casts

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37
Q

Wegener’s granulomatosis

labs, imaging, tx

A

C-ANCA (anti-proteinase 3)

CXR - large nodular densities

tx with cyclophosphamide + steroids

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38
Q

Takayasu Arteritis

who? which vessels, what kind of inflammation + histo?

A

Asian females <40

large arteries; mostly aorta + its branches

granulomatous inflammation of media
transmural fibrous thickening + luminal narrowing
(resembles temporal arteritis, but younger pts)

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39
Q

Takayasu Arteritis

S/s (3 general, 3 specific) ? Labs (2)?

A
  • fever, weight loss, fatigue
  1. OCCLUSIVE SX (claudication, BP discrepancy, bruits and pulse deficits)
  2. VISUAL + NEURO deficits
  3. ARTHRALGIA / MYALGIA

high ESR and CRP

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40
Q

Embryological cause of Tetralogy of Fallot

A

abnormal NEURAL CREST CELL migration, causes…

DEVIATED INFUNDIBULAR SEPTUM (anterior + cephalad deviation), creating…

malaligned VSD and overriding aorta

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41
Q

Anomalous pulmonary venous return

describe it

A

blood from both pulmonary (oxygenated) and systemic (deoxygenated) venous systems flows into RIGHT ATRIUM > causes DILATION of right heart chambers

there is also an ASD that allows RIGHT to LEFT SHUNT

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42
Q

Embryological cause of defects of AV septae and AV valves

consequence?

A

ENDOCARDIAL CUSHION defects (failed fusion of sup/inf endocardial cushions)

usually present as atrial and/or VSD with L-to-R shunt with eventual Eisenmenger syn.

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43
Q

Embryological cause of transposition of the great arteries

A

LINEAR (rather than spiral) AORTICOPULMONARY SEPTUM development

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44
Q

HOCM

drug contraindications + why

A

VASODILATORS - decr. afterload > more blood ejected from LV > lower LV volumes > worse LVOT (includes DHPs, nitroglycerin, ACE inhibitors)

DIURETICS - decreased preload > worse LVOT

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45
Q

HOCM

helpful drugs

A

negative inotropes

beta blockers
non-DHP CCBs - verapamil, diltiazem

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46
Q

Handgrip

does what? decreases (2) + increases (3) which murmurs?

A

Increases afterload (via BP increase)

Decreases - HOCM (incr. LV volume) and AS (decr. transvalvular P gradient > less forward flow)

Increases - AR, MR and VSD (increases backward flow in all of these)

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47
Q

Inspiration

does what to heart? increases and decreases which murmurs?

A

INCREASES RIGHT venous return
DECREASES LEFT venous return

increases most r-sided murmurs
decreases most l-sided murmurs

(but increases HOCM due to decr. LV volume)

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48
Q

Valsalva straining or abrupt standing

does what? increases and decreases which murmurs?

special effect on which murmur?

A

Decreased preload (incr. intrathoracic P / incr. leg blood pooling, respectively)

increases - HCM (via decr. LV volume)

earlier murmur onset - MVP (less blood in atrium to push against?)

decreases - most other murmurs, via decr. flow thru stenotic / regurgitant valve

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49
Q

Squatting + Passive Leg Raise

does what? increases + decreases which murmurs?

A

Squatting - incr. preload and afterload
Passive leg raise - incr. preload

Increases - most murmurs via incr. flow

Decreases - HCM

Later onset / decreased - MVP

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50
Q

Osler-Weber-Rendu syndrome

inheritance? s/s? organs affected?

A

Hereditary Hemorrhagic Telangiectasia - AD inheritance

congenital telangiectasia of skin + mucosa

mucosa - lips, oronasopharynx, resp tract, GI, urinary
(rarely in brain, liver, spleen)

rupture can cause EPISTAXIS, GI BLEEDS and HEMATURIA

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51
Q

Sturge-Weber syndrome

other name?
s/s?
special imaging sign?

A

Encephalotrigeminal Angiomatosis

rare, congenital neurocutaneous disorder with CUTANEOUS FACIAL ANGIOMA and LEPTOMENINGEAL ANGIOMA

mental retardation
seizure
hemiplegia
skull fracture

skull xray > TRAM TRACK calcifications

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52
Q

Peri-infarction pericarditis

when? (how many pts?) what? risks? tx?

A

2-4 DAYS after MI (in abt 10-20% MI pts)

reaction to necrosis near epicardium usually CONFINED TO AREA JUST OVER INFARCT

risk - later presentation of MI > more necrosis > more likely pericarditis

tx - ASPIRIN, resolves in 1-3 days

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53
Q

Dressler syndrome

what? when? where?

A

“postcardiac injury syndrome”

AUTOIMMUNE PERICARDITIS via antigens exposed/created by INFARCTION

less common + LATER ONSET (1 WEEK to SEVERAL MONTHS) than peri-infarction pericarditis

involves WHOLE PERICARDIUM diffusely

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54
Q

ECG for pericarditis

A

diffuse ST elevation

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55
Q

CV issues in Down’s (1 category, 2 examples)

A

endocardial cushion defects

ostium primum ASD
regurgitant AV valves

56
Q

CV issues in DiGeorge (2)

A

tet of Fallot

interrupted aortic arch

57
Q

CV issues in Friedreich ataxia

A

HCM

58
Q

CV issues in Marfan (2)

A

Cystic medial necrosis –> aortic dissection + aneurysm

MVP

59
Q

CV issues tuberculous sclerosis

A

cardiac rhabdomyomas > valve obstruction

60
Q

CV issues in Turner’s

A

aortic coarctation

bicuspid aortic valve

61
Q

PDA

pts at highest risk? (2)

A

premature

or

CYANOTIC congenital heart disease

62
Q

PDA auscultation

A

CONTINUOUS “machine like” murmur

INFRACLAVICULAR region, left side

max intensity at S2

63
Q

best indicator of severity of MITRAL REGURGITATION

A

presence of S3

S3 is due to ventricle not being able to accommodate excess blood flow; MR results in increased blood V/P in LA and more blood returning to ventricle in diastole

if this amt of extra blood is large > S3 is heard and MR can be assumed to be bad

64
Q

midsystolic click

heard in what? what affects it?

A

mitral prolapse - sudden chordae tendinae tensing

timing varies with LV volume > EARLIER when LV volume is LOWER (standing, valsalva)

65
Q

opening snap

when heard? what does a difference in it mean?

A

EARLY DIASTOLIC sound after S2 in MS or TS

S2-to-opening snap - time btwn aortic closure (S2) and abrupt halt of leaflet motion

SHORTER INTERVAL > MORE SEVERE STENOSIS

66
Q

3 mechs in pathogenesis of CHF

A
  1. increased SYMPATHETIC NS activity
  2. increased RAAS activity
  3. increased ADH release

all originally stimulated by decreased CO; all help to maintain CO at first, via increased HR/contractility, BP and extracellular volume

all eventually lead to deleterious cardiac remodeling

67
Q

Cavernous Sinus Thrombosis

cause?

A

contiguous spread of infection from medial 1/3 of face, sinuses (ethmoid/sphenoid) or teeth

spreads retrograde via VALVELESS veins of face (sup/inf ophthalmic vv.)

pathogens are S. aureus (#1), Strep and Mucor/Rhizopus

68
Q

Cavernous Sinus Thrombosis

s/s?

think of the nerves involved…

A

HA, fever, diplopia

Proptosis + “chemosis” (conjunctival swelling) via venous congestion

Ocular paralysis - CN III, IV, VI
Ptosis + mydriasis - CN III
Corneal reflex loss - CN V/1

Loss of upper facial sensation (CN V/1 and V/3)

69
Q

1 cardiac defect in Downs syndrome

how does it sound (2 things)?

A

Complete Atrioventricular Canal Defect

(failed endocardial cushion fusion > ostium primum ASD with VSD and a SINGLE AV VALVE)

1) AV regurgitation - holosystolic at apex
2) Increase pulm ven. return - mid-diastolic rumble at LSB

70
Q

1 cardiac defect in Downs

s/s and auscultation

A

large L to R shunt and AV regurg > excessive pulmonary flow with HF symptoms (POOR FEED, TACHYPNEA)

2 auscultation findings:
Holosystolic murmur @ apex/axilla - AV REGURG
Mid-diastolic rumble - HIGH PULM VEIN RETURN

71
Q

VSD

auscultation

A

harsh holosystolic murmur; best heard at TRICUSPID AREA but radiates over ENTIRE PRECORDIUM

PALPABLE THRILL at LSB

72
Q

Fibromuscular Dysplasia

epidem, manifestations

A

mostly in women <55 years old

fibromuscular webs causing stenosis, alternating with areas of aneurysm; vessels are tortuous and may dissect

NO INTERNAL ELASTIC LAMINA

73
Q

Fibromuscular Dysplasia

presentation (think of 4 different areas affected by dysplastic arteries)

A
  1. Renal Artery Stenosis - causes resistant hypertension via RAS activation
  2. Cerebrovascular issues - headache, TIA, stroke, aneurysms
  3. Mesenteric ischemia
  4. Limb claudication
74
Q

Fibromuscular Dysplasia

diagnosis

A

Angiography - CT, MRI or percutaneous

has a “string of beads” appearance due to multifocal aneurysms

75
Q

Isolated Systolic Hypertension

causes (4, but #1 most important))

A
  1. AGING - increased arterial STIFFNESS
  2. Severe AORTIC REGURG - via increased CO (would see decreased diastolic pressure in addition)
  3. Hyperthyroidism - also increased CO
  4. Anemia - also increased CO
76
Q

Beck triad

3 signs for what? what are the signs?

A

cardiac tamponade

  1. hypotension
  2. elevated JVP
  3. muffled heart sounds
77
Q

Pulsus alternans

what is it? what causes it?

A

beat to beat variation in pulse amplitude due to changes in systolic BP

mostly seen in SEVERE LV DYSFUNCTION

78
Q

Electrical alternans

what is it? what causes it (2)?

A

varying amplitudes / axes of the QRS complex on ECG from beat to beat

due to LARGE PERICARDIAL EFFUSION or TAMPONADE with resulting swinging motion of heart within pericardial cavity

79
Q

Dicrotic Pulse

what is it? what causes it?

A

pulse with 2 distinct peaks: one in systole and one in diastole; there is an accentuated dicrotic wave in diastole after the dicrotic notch

severe SYSTOLIC DYSFUNCTION (including LOW CO) with HIGH SYSTEMIC ARTERIAL RESISTANCE

80
Q

Hyperkinetic pulse

what is it? what causes it (3)?

A

rapidly rising + high amplitude pulse via RAPID EJECTION of blood against a DECREASED AFTERLOAD

AORTIC REGURG or high-output states like THYROTOXICOSIS or AV FISTULAs

81
Q

Pulsus parvus et tardus

what is it? what causes it?

A

WEAK (parvus) and SLOW (tardus) pulse; palpable as a slow-rising and low-amplitude pulse

via DECREASED STROKE VOLUME (parvus) and PROLONGED LV EJECTION TIME (tardus)

82
Q

what maneuver causes the murmur of mitral regurgitation to decrease or disappear?

why?

A

squatting

increased venous return + resulting increased LV volume temporarily dilates ventricle in a way that tenses chordae tendineae and prevents prolapse

results in either total disappearance or a DELAYED MID-SYSTOLIC CLICK (later = better) and shorter/lower intensity late-systolic murmur

83
Q

Primary Mitral Prolapse vs. Secondary

causes

A

Primary - sporadic myxomatous degeneration of CT of valve leaflets and chordae tendineae

Secondary - Marfan, Ehlers-Danlos or osteogenesis imperfecta

84
Q

Mitral Valve Prolapse

myxomatous lesion histo (4 features)

A
  1. SPONGIOSA PROLIFERATION - of leaflets
  2. ELASTIN FIBER FRAGMENTATION
  3. increased mucopolysaccharide
  4. increased TYPE III COLLAGEN deposits
85
Q

How soon after myocardial ischemia does contractility stop?

A

60 SECONDS - total ATP levels in the cell are relatively normal, but concentrations near the contractile fibers drop quickly due to high demand there

86
Q

How long can myocardial ischemia persist before damage is irreversible?

What happens to contractility when perfusion restarts?

A

30 minutes

MYOCARDIAL STUNNING - contractility remains impaired from several hours to days (depending on how long ischemia went on)

87
Q

What molecule released by ischemic myocardium can cause coronary vasodilation?

A

Adenosine

in hypoxia, ATP is degraded to ADP > AMP > adenosine; adenosine is a vasodilator

(but after 30 minutes, around half of myocardial adenosine is lost and ischemic injury becomes irreversible)

88
Q

What is meant by “physiological split” of S2?

A

Splitting of S2 varies with respiration

Inspiration - increased venous return increases flow thru pulmonary valve > P2 comes later than A2 as pulmonary valve stays open longer

Expiration - lower venous return > P2 and A2 occur almost simultaneously

89
Q

In what condition is there a “wide and fixed split of S2”?

A

Atrial Septal Defects

significant L-to-R shunting causes highly increased blood flow through right side of heart > pulmonary valve stays open significantly longer (“wide”) than aortic through both inspiration and expiration (“fixed”)

90
Q

Similarities + differences btwn valvular aortic stenosis and HOCM murmurs

A

Both are systolic ejection-type murmurs

valvular stenosis - standing will DECREASE the murmur (less flow through stenotic valve)

HOCM - standing will INCREASE the murmur (lower LV volume > more obstruction via interaction btwn mitral leaflet and septal hypertrophy)

91
Q

What are the “presystolic” murmurs?

what additional pathology may make the murmur disappear, even though its cause remains?

A

mitral or tricuspid regurg - if they are mild then only the “presystolic” accentuation of them via atrial contraction may be audible

atrial fibrillation can cause disappearance of the presystolic accentuation due to continuous, disorganized atrial activity

92
Q

How does inspiration change the mitral prolapse murmur?

A

the “mid systolic click” of MVP will OCCUR EARLIER

inspiration > lower LV volumes via lower venous return

(venous return to right heart increases > compresses left heart + decreases its venous return)

93
Q

How is cardiac output calculated by using a Swan-Ganz (pulmonary artery) catheter?

(what two pieces of information are needed?)

A

Fick principle

CO = rate of O2 consumption / A-V O2 difference

94
Q

Dilated Cardiomyopathy

causes (other than viral; 4 categories + examples)

A
  1. Genetic - cytoskeletal protein mutations
  2. Pregnancy
  3. Infiltrative disease - amyloidosis/hemochromatosis
  4. Drugs/toxins - anthracyclines, alcoholism
95
Q

2 causes of “secondary mitral regurgitation”

tx

A

in secondary MR the valve is anatomically normal

  1. Decompensated HF - increased LV EDV dilates valve annulus and tightens chordae > incomplete closure
  2. Hypertension - regurgitant flow pathway is relatively lower resistance than hypertensive forward pathway

tx with diuretics + vasodilators can reduce LV EDV and htn and stop the regurg

96
Q

What is the common breathing pattern seen in patients with advanced heart failure?

name + general pattern

what other conditions is it seen in?

A

Cheyne Stokes breathing

cyclic APNEIC periods followed by gradually increasing and then decreasing tidal volumes

Neuro disease - stroke, tumor, trauma

97
Q

What is the mechanism for Cheyne Stokes breathing in chronic HF patients?

A

CHF pts have CHRONIC HYPERVENTILATION with HYPOCAPNIA

due to this, when sleeping PaCO2 falls below a certain “apneic threshold” and breathing stops > CO2 builds up again and the ventilatory response results in hyperpnea and another bout of hypocapnia, continuing the cycle

(this is all worsened by longer circulation time between lungs and brain in CHF pt > greater diff btwn PaCO2 at central chemoreceptors and PaCO2 in alveolar circ)

98
Q

when is post-MI pt most at risk of fatal arrhythmia?

A

within first 48-72 hours (2-3 days) after the MI

99
Q

How does ejection fraction change in ACUTE or COMPENSATED CHRONIC MITRAL REGURG?

A

it INCREASES (greatly in acute, slightly in chronic)

(remember that EF = (EDV - ESV)/EDV … so EF has nothing to do with whether or not the ejected volume is going forward through the aorta or backward through the mitral valve

FORWARD stroke volume decreases in acute MR, but is compensated by eccentric hypertrophy in chronic MR)

100
Q

What are the changes in the heart in DECOMPENSATED CHRONIC MITRAL REGURG?

And how does this affect EF, SV and afterload?

A

ECCENTRIC hypertrophy via volume overload; compensates at first but eventually causes contractile dysfunction

SV and EF decrease

Afterload INCREASES (due to vasoconstriction to maintain BP?)

101
Q

What is “phlegmasia alba dolens”? What causes it?

A

ACUTE rise in tissue pressure that IMPAIRS ARTERIAL INFLOW > painful white “milk leg” (alba = white, dolens = painful)

usually in leg via MASSIVE ILIOFEMORAL THROMBOSIS

102
Q

Gastrointestinal effects of atrial fibrillation, mitral stenosis or mitral regurgitation?

A

LA enlargement > esophageal compression > dysphagia

103
Q

Concentrations of what 2 solutes increase in ischemic cardiomyocytes? Why?

A

Na+ and Ca++

Na+ via decreased Na/K-ATPase activity

Ca++ via SR Ca-ATPase dysfunction > failed resequestration

104
Q

Muscle biopsy in polyarteritis nodosa pt shows what?

A

segmental ischemic necrosis

105
Q

Virchow triad

A
  1. Hypercoagulability
  2. Endothelial damage
  3. Stasis / flow disruption
106
Q

3 holosystolic murmurs

A

VSD

MR

TR

107
Q

mitral regurg

heard where (and where) ?

A

heard at apex (and radiating to axilla)

108
Q

tricuspid regurg

heard where?
increases with what?

A

heard in left 2nd/3rd ICS

increases with inspiration

109
Q

VSD

heard where?

quality and associated feature?

A

left 3rd + 3th ICS

LOUD and accompanied by THRILL

110
Q

Toe cyanosis and clubbing but no finger abnormalities

Young patient recently presenting with exertional dyspnea

Suspicion?

A

Patent Ductus Arteriosus

with reversal of shunt to R-to-L; foot/hand difference is due to shunting of low O2 blood DISTAL TO LEFT SUBCLAVIAN

111
Q

Polyarteritis Nodosa

labs? histo?
associations?
imaging?
tx?

A
  • ANCA-negative
  • segmental, transmural inflamm. + fibrinoid necrosis
  • assoc. with hep B/C
  • microaneurysms on arteriography

tx with prednisone + cyclophosphamide; ACE-I for htn

112
Q

Thromboangiitis Obliterans

s/s?

A
  • calf, foot or hand intermittent claud
  • superficial nodular phlebitis
  • Raynaud’s
  • severe distal pain (even at rest, via nerves)
  • ulceration/gangrene of digits/feet
113
Q

Temporal / Giant Cell Arteritis

labs? (1 special severity correlate)
histo?
tx?

A
  • high ESR + CRP; IL-6 correlates with severity
  • medium/small branches of carotid (esp. temporal a.); granulomatous inflammation of media with thick intima, giant cells
    tx: glucocorticoids
114
Q

Changes in LV / aorta pressure tracing for AORTIC REGURG (3)

A
  1. DICROTIC NOTCH LOSS - blood no longer “caught” by valve to briefly boost aortic pressure
  2. RAPID DIASTOLIC AORTIC P LOSS - lowest diastolic P is lower than normal
  3. HIGH-PEAK SYSTOLIC P - results in wide pulse pressure
115
Q

How does surgical closure of a VSD affect…

LV pressure?
RV pressure?
LA pressure?

A

LVP - increases

RVP - decreases (less shunting)

LAP - decreases (less shunted blood returning to LA via pulmonary circ)

116
Q

Hypovolemic shock

(bleed, burn, dehydration)

skin is?
SVR is?

A

skin is COLD + CLAMMY

SVR is INCREASED (vasoconstriction to compensate)

117
Q

Cardiogenic shock (MI, HF, valves, arrhythmias)

skin is?
preload?
svr?
tx.

A

skin - cold + clammy

preload - “pcwp” can be up or down dep. on which side of heart is failing primarily

svr - INCREASED (vasoconstriction to compensate)

tx is DIURESIS and INOTROPES

118
Q

Obstructive shock

causes? (3)

A

Tension PTX
PE
Tamponade

(preload, svr, skin same as in cardiogenic)

119
Q

Distributive shock via SEPSIS / ANAPHYLAXIS

skin?
preload?
CO?
SVR?

A

skin is WARM (vasodilation)

preload - pcwp is LOW

CO is HIGHER to attempt to compensate for bp

SVR is VERY LOW via systemic dilation

120
Q

Distributive shock via CNS INJURY (usually SC)

aka “neurogenic”

skin?
preload?
CO?
SVR?

A

skin is DRY (no sweat gland innervation)

preload is LOW

CO is DECREASED

SVR is LOW due to lack of adrenergic vessel innervation

121
Q

Site of RFA for ATRIAL FLUTTER

A

in the RA at the ISTHMUS of tissue between the TRICUSPID ANNULUS and opening of the IVC

122
Q

What is a potentially troubling (to the patient) CARDIAC manifestation of ANY form of anemia?

A

palpitations

123
Q

histo sign of rheumatic fever

structure + cell

A

Aschoff body

an interstitial myocardial granuloma

pathognomonic of ARF-related myocarditis

big macro with little chromatin ribbons = ANITSCHKOW / CATERPILLAR CELLS

124
Q

Hypersensitivity myocarditis

drugs?

A

diuretics - furosemide + thiazides

abx - ampicillin + azithromycin

125
Q

Hypersensitivity myocarditis

histo?

A

eosinophil infiltrate

126
Q

Anthracycline dilated CMP

histo?

A

fibrosis + vacuolization with myocyte lysis

127
Q

HOCM

histo?

A

disorganized wavy myocytes

128
Q

T cruzi / Chagas infection

histo?

A

DISTENDED myofibers

intracellular trypanosomes (little blobs with tapered tails)

129
Q

Viral myocarditis

3 viruses?
histo?

A

adenovirus, Coxsackie B, parvo B19

LYMPHOCYTE infiltrate and FOCAL NECROSIS

130
Q

Pathological / histo finding in abdominal aortic aneurysm

A

CHRONIC TRANSMURAL INFLAMMATION

(age > 60, smoking, htn, male, family history assoc.)

macros > MMPs > degrade ECM > weakening + expansion of aorta

131
Q

What vessels supply the LV papillary muscles? (3 vessels for 2 papillary muscles)

(in a right dominant circulation)

A

anterolateral papillary m. - LCX and LAD

posteromedial pm - POSTERIOR DESCENDING (aka post. interventricular)

132
Q

What is the “conus” artery in coronary circ?

supplies what 2 things?

A

early branch of proximal RCA

supplies anterior IVS and pulmonary artery conus

133
Q

Diuretic with mortality benefit for CHF patients

A

Spironolactone / eplerenone

affect RAAS > decrease remodeling

134
Q

How is ejection fraction affected in HOCM?

A

it is either NORMAL OR INCREASED

135
Q

Pericardial friction rub associated with SLE (“skin rash and joint pain”)

What is it?

A

FIBRINOUS pericarditis

pain can radiate to L shoulder or both scapulae

136
Q

Causes of fibrinous pericarditis other than SLE (4)

A
  1. MI
  2. Uremia
  3. Viruses
  4. Other AI disease - RA

can progress to chronic constrictive pericarditis if not treated

137
Q

Changes seen in athlete heart

Hypertrophy type?
Cavity change?

A

mostly ECCENTRIC hypertrophy; small degree of concentric, with UNIFORM wall thickness increase

LV cavity is ENLARGED

(diff from smaller cavity, asymmetric thickness increase on HOCM)

*USMLE* (28 decks)

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