Cardiovascular Flashcards
Churg-Strauss / Eosinophilic Granulomatosis with Polyangiitis
vessel size?
s/s? organs affected?
labs?
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
Polyarteritis Nodosa
vessel size + organs?
s/s?
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)
Thromboangiitis Obliterans
vessel size
mechanism
histo
- 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
Hyperplastic Arteriolosclerosis
results from malignant htn (diastolics > 120-130)
onion-like concentric thickening of arteriolar walls via laminated SMCs and doubled BMs
Temporal / Giant Cell Arteritis
in whom? general sx (3) and specific sx (4)?
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
Kawasaki disease
epidem?
dx criteria?
complication?
“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
Henoch-Schonlein purpura
“systemic leukocytoclastic vasculitis”; IgA complex deposition
small vessels of kidney, skin, GI and joints
palpable purpura
abdominal pain
arthralgia
acute glomerulonephritis
Hemolytic Uremic Syndrome
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)
Sturge-Weber Syndrome
2 s/s
facial port-wine stains and leptomeningeal capillary-venous malformations
Hereditary Hemorrhagic Telangiectasia
s/s + presentation
aka Osler-Weber-Rendu syndrome
multiple telangiectasias of skin + mucosa
present w recurrent epistaxis / GI bleed
Strawberry Hemangioma
growth + regression
lesion characteristics
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
Cherry Hemangioma
growth + regression
lesions characteristics
1 benign vascular proliferation in ADULTS
small, bright red cutaneous papules
dilated capillaries + post-capillary venules in papillary dermis
do NOT regress
Spider Angioma
in pregnancy, liver disease, OCP tx or estrogen supp
dilated cutaneous arterioles; central papule with radiating blanching capillaries
Cavernous Hemangioma
present at birth or later
soft blue compressible mass up to few cm diameter
histo = large dilated vascular spaces
Cystic Hygroma
aka lymphangioma; benign tumor of dilated lymph spaces lined by endothelium
mostly on NECK; lobulated, compressible and transilluminatable
MCC of death in athletes <35?
MCC of death in athletes >35?
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
chronic ischemic heart disease
histo findings
patchy fibrosis in mural endocardium
discrete scars in areas of healed infarct
diffuse subendocardial VACUOLIZATION
MCCs of spontaneous intracranial hemorrhage in young adults (3)
- AV malformations
- ruptured aneurysms
- sympathomimetic abuse (cocaine)
CV issues associated with aortic coarctation
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)
common cancer that commonly metastasizes to heart?
effects of metastasis?
breast cancer
pericardial effusion, possibly tamponade > decreased RV diastolic filling
3 main risk factors for coronary heart disease
other major risk factors (6)
- non-coronary atherosclerosis
- diabetes
- CKD
also hypertension, hyperlipidemia, smoking, advanced age, obesity and inactivity
Common CODs in diabetes
- Coronary heart disease (MI) - 40%
- Cerebrovascular accidents (stroke) - 10%
- End-stage kidney - DM is leading cause of ESRD, but pt usually dies of heart disease/infection first
- DKA / Hyperosmolar coma - hyperosmolar coma more deadly, but neither are common CODs
Free wall myocardial rupture
when? what decreases risk? consequences?
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
hypertrophic cardiomyopathy
mutations? inheritance?
mutations in cardiac sarcomere proteins (thick or thin filaments)
50% cases are familial, with AD inheritance and variable expression
“Heart Failure Cells”
what are they? when do you see them?
“Siderophages” - hemosiderin-containing macrophages in alveoli
Suggestive of CHRONIC LEFT HEART FAILURE with past episodes of pulmonary congestion + edema + RBC extravasation into alveoli
Myocardial hibernation
what is it? result?
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)
What is “ischemic preconditioning”?
Example of it occurring in a pathological state?
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
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
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
Myocardial biopsy changes post-MI…
3-7 days
7-10 days
10-14 days
2 wks - 2 months
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
Nonbacterial Thrombotic Endocarditis
associations (2 main, 3 minor)
histo
complications
aka “marantic endocarditis”; valvular injury via inflammatory cytokines triggers platelet deposition with underling hypercoagulability
associated with…
- ADVANCED MALIGNANCY - esp. mucinous adenocarcinoma
- SLE - Libman-Sacks endocarditis
- (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)
Steps of atherosclerotic plaque formation
- Hemodynamic Stress + hyperlipidemia
- Endothelial injury
- Increased VCAMs
- Monocytes + T cells in intima
- WBCs + endothelium release PDGF, FGF, endothelin-1 and IL-1
- Vascular SMCs proliferate in intima
- VSMCs make collagen, elastin + proteoglycans > FIBROUS CAP
Aortic Stenosis
auscultation, MCC
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
calcific aortic valve disease
pathogenesis
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
HOCM vs. hypertensive heart disease
gross + micro differentiation
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
Atrial Myxoma
signs? histo?
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
Wegener’s granulomatosis
vessel size, triad, other s/s
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
Wegener’s granulomatosis
labs, imaging, tx
C-ANCA (anti-proteinase 3)
CXR - large nodular densities
tx with cyclophosphamide + steroids
Takayasu Arteritis
who? which vessels, what kind of inflammation + histo?
Asian females <40
large arteries; mostly aorta + its branches
granulomatous inflammation of media
transmural fibrous thickening + luminal narrowing
(resembles temporal arteritis, but younger pts)
Takayasu Arteritis
S/s (3 general, 3 specific) ? Labs (2)?
- fever, weight loss, fatigue
- OCCLUSIVE SX (claudication, BP discrepancy, bruits and pulse deficits)
- VISUAL + NEURO deficits
- ARTHRALGIA / MYALGIA
high ESR and CRP
Embryological cause of Tetralogy of Fallot
abnormal NEURAL CREST CELL migration, causes…
DEVIATED INFUNDIBULAR SEPTUM (anterior + cephalad deviation), creating…
malaligned VSD and overriding aorta
Anomalous pulmonary venous return
describe it
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
Embryological cause of defects of AV septae and AV valves
consequence?
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.
Embryological cause of transposition of the great arteries
LINEAR (rather than spiral) AORTICOPULMONARY SEPTUM development
HOCM
drug contraindications + why
VASODILATORS - decr. afterload > more blood ejected from LV > lower LV volumes > worse LVOT (includes DHPs, nitroglycerin, ACE inhibitors)
DIURETICS - decreased preload > worse LVOT
HOCM
helpful drugs
negative inotropes
beta blockers
non-DHP CCBs - verapamil, diltiazem
Handgrip
does what? decreases (2) + increases (3) which murmurs?
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)
Inspiration
does what to heart? increases and decreases which murmurs?
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)
Valsalva straining or abrupt standing
does what? increases and decreases which murmurs?
special effect on which murmur?
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
Squatting + Passive Leg Raise
does what? increases + decreases which murmurs?
Squatting - incr. preload and afterload
Passive leg raise - incr. preload
Increases - most murmurs via incr. flow
Decreases - HCM
Later onset / decreased - MVP
Osler-Weber-Rendu syndrome
inheritance? s/s? organs affected?
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
Sturge-Weber syndrome
other name?
s/s?
special imaging sign?
Encephalotrigeminal Angiomatosis
rare, congenital neurocutaneous disorder with CUTANEOUS FACIAL ANGIOMA and LEPTOMENINGEAL ANGIOMA
mental retardation
seizure
hemiplegia
skull fracture
skull xray > TRAM TRACK calcifications
Peri-infarction pericarditis
when? (how many pts?) what? risks? tx?
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
Dressler syndrome
what? when? where?
“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
ECG for pericarditis
diffuse ST elevation
CV issues in Down’s (1 category, 2 examples)
endocardial cushion defects
ostium primum ASD
regurgitant AV valves
CV issues in DiGeorge (2)
tet of Fallot
interrupted aortic arch
CV issues in Friedreich ataxia
HCM
CV issues in Marfan (2)
Cystic medial necrosis –> aortic dissection + aneurysm
MVP
CV issues tuberculous sclerosis
cardiac rhabdomyomas > valve obstruction
CV issues in Turner’s
aortic coarctation
bicuspid aortic valve
PDA
pts at highest risk? (2)
premature
or
CYANOTIC congenital heart disease
PDA auscultation
CONTINUOUS “machine like” murmur
INFRACLAVICULAR region, left side
max intensity at S2
best indicator of severity of MITRAL REGURGITATION
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
midsystolic click
heard in what? what affects it?
mitral prolapse - sudden chordae tendinae tensing
timing varies with LV volume > EARLIER when LV volume is LOWER (standing, valsalva)
opening snap
when heard? what does a difference in it mean?
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
3 mechs in pathogenesis of CHF
- increased SYMPATHETIC NS activity
- increased RAAS activity
- 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
Cavernous Sinus Thrombosis
cause?
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
Cavernous Sinus Thrombosis
s/s?
think of the nerves involved…
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)
1 cardiac defect in Downs syndrome
how does it sound (2 things)?
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
1 cardiac defect in Downs
s/s and auscultation
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
VSD
auscultation
harsh holosystolic murmur; best heard at TRICUSPID AREA but radiates over ENTIRE PRECORDIUM
PALPABLE THRILL at LSB
Fibromuscular Dysplasia
epidem, manifestations
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
Fibromuscular Dysplasia
presentation (think of 4 different areas affected by dysplastic arteries)
- Renal Artery Stenosis - causes resistant hypertension via RAS activation
- Cerebrovascular issues - headache, TIA, stroke, aneurysms
- Mesenteric ischemia
- Limb claudication
Fibromuscular Dysplasia
diagnosis
Angiography - CT, MRI or percutaneous
has a “string of beads” appearance due to multifocal aneurysms
Isolated Systolic Hypertension
causes (4, but #1 most important))
- AGING - increased arterial STIFFNESS
- Severe AORTIC REGURG - via increased CO (would see decreased diastolic pressure in addition)
- Hyperthyroidism - also increased CO
- Anemia - also increased CO
Beck triad
3 signs for what? what are the signs?
cardiac tamponade
- hypotension
- elevated JVP
- muffled heart sounds
Pulsus alternans
what is it? what causes it?
beat to beat variation in pulse amplitude due to changes in systolic BP
mostly seen in SEVERE LV DYSFUNCTION
Electrical alternans
what is it? what causes it (2)?
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
Dicrotic Pulse
what is it? what causes it?
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
Hyperkinetic pulse
what is it? what causes it (3)?
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
Pulsus parvus et tardus
what is it? what causes it?
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)
what maneuver causes the murmur of mitral regurgitation to decrease or disappear?
why?
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
Primary Mitral Prolapse vs. Secondary
causes
Primary - sporadic myxomatous degeneration of CT of valve leaflets and chordae tendineae
Secondary - Marfan, Ehlers-Danlos or osteogenesis imperfecta
Mitral Valve Prolapse
myxomatous lesion histo (4 features)
- SPONGIOSA PROLIFERATION - of leaflets
- ELASTIN FIBER FRAGMENTATION
- increased mucopolysaccharide
- increased TYPE III COLLAGEN deposits
How soon after myocardial ischemia does contractility stop?
60 SECONDS - total ATP levels in the cell are relatively normal, but concentrations near the contractile fibers drop quickly due to high demand there
How long can myocardial ischemia persist before damage is irreversible?
What happens to contractility when perfusion restarts?
30 minutes
MYOCARDIAL STUNNING - contractility remains impaired from several hours to days (depending on how long ischemia went on)
What molecule released by ischemic myocardium can cause coronary vasodilation?
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)
What is meant by “physiological split” of S2?
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
In what condition is there a “wide and fixed split of S2”?
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”)
Similarities + differences btwn valvular aortic stenosis and HOCM murmurs
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)
What are the “presystolic” murmurs?
what additional pathology may make the murmur disappear, even though its cause remains?
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
How does inspiration change the mitral prolapse murmur?
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)
How is cardiac output calculated by using a Swan-Ganz (pulmonary artery) catheter?
(what two pieces of information are needed?)
Fick principle
CO = rate of O2 consumption / A-V O2 difference
Dilated Cardiomyopathy
causes (other than viral; 4 categories + examples)
- Genetic - cytoskeletal protein mutations
- Pregnancy
- Infiltrative disease - amyloidosis/hemochromatosis
- Drugs/toxins - anthracyclines, alcoholism
2 causes of “secondary mitral regurgitation”
tx
in secondary MR the valve is anatomically normal
- Decompensated HF - increased LV EDV dilates valve annulus and tightens chordae > incomplete closure
- 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
What is the common breathing pattern seen in patients with advanced heart failure?
name + general pattern
what other conditions is it seen in?
Cheyne Stokes breathing
cyclic APNEIC periods followed by gradually increasing and then decreasing tidal volumes
Neuro disease - stroke, tumor, trauma
What is the mechanism for Cheyne Stokes breathing in chronic HF patients?
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)
when is post-MI pt most at risk of fatal arrhythmia?
within first 48-72 hours (2-3 days) after the MI
How does ejection fraction change in ACUTE or COMPENSATED CHRONIC MITRAL REGURG?
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)
What are the changes in the heart in DECOMPENSATED CHRONIC MITRAL REGURG?
And how does this affect EF, SV and afterload?
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?)
What is “phlegmasia alba dolens”? What causes it?
ACUTE rise in tissue pressure that IMPAIRS ARTERIAL INFLOW > painful white “milk leg” (alba = white, dolens = painful)
usually in leg via MASSIVE ILIOFEMORAL THROMBOSIS
Gastrointestinal effects of atrial fibrillation, mitral stenosis or mitral regurgitation?
LA enlargement > esophageal compression > dysphagia
Concentrations of what 2 solutes increase in ischemic cardiomyocytes? Why?
Na+ and Ca++
Na+ via decreased Na/K-ATPase activity
Ca++ via SR Ca-ATPase dysfunction > failed resequestration
Muscle biopsy in polyarteritis nodosa pt shows what?
segmental ischemic necrosis
Virchow triad
- Hypercoagulability
- Endothelial damage
- Stasis / flow disruption
3 holosystolic murmurs
VSD
MR
TR
mitral regurg
heard where (and where) ?
heard at apex (and radiating to axilla)
tricuspid regurg
heard where?
increases with what?
heard in left 2nd/3rd ICS
increases with inspiration
VSD
heard where?
quality and associated feature?
left 3rd + 3th ICS
LOUD and accompanied by THRILL
Toe cyanosis and clubbing but no finger abnormalities
Young patient recently presenting with exertional dyspnea
Suspicion?
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
Polyarteritis Nodosa
labs? histo?
associations?
imaging?
tx?
- ANCA-negative
- segmental, transmural inflamm. + fibrinoid necrosis
- assoc. with hep B/C
- microaneurysms on arteriography
tx with prednisone + cyclophosphamide; ACE-I for htn
Thromboangiitis Obliterans
s/s?
- calf, foot or hand intermittent claud
- superficial nodular phlebitis
- Raynaud’s
- severe distal pain (even at rest, via nerves)
- ulceration/gangrene of digits/feet
Temporal / Giant Cell Arteritis
labs? (1 special severity correlate)
histo?
tx?
- 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
Changes in LV / aorta pressure tracing for AORTIC REGURG (3)
- DICROTIC NOTCH LOSS - blood no longer “caught” by valve to briefly boost aortic pressure
- RAPID DIASTOLIC AORTIC P LOSS - lowest diastolic P is lower than normal
- HIGH-PEAK SYSTOLIC P - results in wide pulse pressure
How does surgical closure of a VSD affect…
LV pressure?
RV pressure?
LA pressure?
LVP - increases
RVP - decreases (less shunting)
LAP - decreases (less shunted blood returning to LA via pulmonary circ)
Hypovolemic shock
(bleed, burn, dehydration)
skin is?
SVR is?
skin is COLD + CLAMMY
SVR is INCREASED (vasoconstriction to compensate)
Cardiogenic shock (MI, HF, valves, arrhythmias)
skin is?
preload?
svr?
tx.
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
Obstructive shock
causes? (3)
Tension PTX
PE
Tamponade
(preload, svr, skin same as in cardiogenic)
Distributive shock via SEPSIS / ANAPHYLAXIS
skin?
preload?
CO?
SVR?
skin is WARM (vasodilation)
preload - pcwp is LOW
CO is HIGHER to attempt to compensate for bp
SVR is VERY LOW via systemic dilation
Distributive shock via CNS INJURY (usually SC)
aka “neurogenic”
skin?
preload?
CO?
SVR?
skin is DRY (no sweat gland innervation)
preload is LOW
CO is DECREASED
SVR is LOW due to lack of adrenergic vessel innervation
Site of RFA for ATRIAL FLUTTER
in the RA at the ISTHMUS of tissue between the TRICUSPID ANNULUS and opening of the IVC
What is a potentially troubling (to the patient) CARDIAC manifestation of ANY form of anemia?
palpitations
histo sign of rheumatic fever
structure + cell
Aschoff body
an interstitial myocardial granuloma
pathognomonic of ARF-related myocarditis
big macro with little chromatin ribbons = ANITSCHKOW / CATERPILLAR CELLS
Hypersensitivity myocarditis
drugs?
diuretics - furosemide + thiazides
abx - ampicillin + azithromycin
Hypersensitivity myocarditis
histo?
eosinophil infiltrate
Anthracycline dilated CMP
histo?
fibrosis + vacuolization with myocyte lysis
HOCM
histo?
disorganized wavy myocytes
T cruzi / Chagas infection
histo?
DISTENDED myofibers
intracellular trypanosomes (little blobs with tapered tails)
Viral myocarditis
3 viruses?
histo?
adenovirus, Coxsackie B, parvo B19
LYMPHOCYTE infiltrate and FOCAL NECROSIS
Pathological / histo finding in abdominal aortic aneurysm
CHRONIC TRANSMURAL INFLAMMATION
(age > 60, smoking, htn, male, family history assoc.)
macros > MMPs > degrade ECM > weakening + expansion of aorta
What vessels supply the LV papillary muscles? (3 vessels for 2 papillary muscles)
(in a right dominant circulation)
anterolateral papillary m. - LCX and LAD
posteromedial pm - POSTERIOR DESCENDING (aka post. interventricular)
What is the “conus” artery in coronary circ?
supplies what 2 things?
early branch of proximal RCA
supplies anterior IVS and pulmonary artery conus
Diuretic with mortality benefit for CHF patients
Spironolactone / eplerenone
affect RAAS > decrease remodeling
How is ejection fraction affected in HOCM?
it is either NORMAL OR INCREASED
Pericardial friction rub associated with SLE (“skin rash and joint pain”)
What is it?
FIBRINOUS pericarditis
pain can radiate to L shoulder or both scapulae
Causes of fibrinous pericarditis other than SLE (4)
- MI
- Uremia
- Viruses
- Other AI disease - RA
can progress to chronic constrictive pericarditis if not treated
Changes seen in athlete heart
Hypertrophy type?
Cavity change?
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)
