Cardiac Flashcards

Question 1

Q

diabetes

Answer

A

tissues that contain aldose reductase - cataracts (lens), microaneurysms in the eye (pericytes), peripheral neuropathy (Schwann cells)

NEG makes BM permeable to protein - hyaline within vessel wall

Question 2

Q

aneurysm

Answer

A

weakening –> outpouching of vessel wall

[compare this to a process in the lung? = bronchiectasis
- ex CF pt –> infection –> weakening of elastic tissue and dilatation of bronchi

GI “aneurysm” - weakening, outpouching of mucosa through a weak point in the muscular wall]

Law of Laplace - wall stress increases as radius increases –> all aneurysms will burst
P = 2T*thickness/r

abd aortic aneurysm: no vasa vasorum to aorta below the renal arteries –> outer part of the wall is most susceptible –> atherosclerosis occurs here –> rupture
-rupture triad = left flank pain (SADPUCKER), hypotension, and pulsatile mass

arch of aorta aneurysm - most common cause is tertiary syphilis (vasculitis of arterioles, arterioles surrounded by plasma cells with lumen completely occluded –> necrosis of overlying tissue, death of nerves)

key factor for causing aortic arch rupture

HTN
elastic tissue fragmentation
cystic medial necrosis - GAGs turn into cysts

proximal dissection is the most common one

closes lumen to subclavian = absent pulse left
death by cardiac tamponade
retrosternal tearing chest pain
Marfans - most common cause of death is mitral prolapse and conduction disruption, second most common cause of death is dissection
most common cause of death in Ehlers-Danlos
pregnancy - dissecting aortic aneurysm is a catastrophic aortic disease, increased plasma volume –> weakening of wall –> dissection
side note - can get dilated CM in pregnancy

Question 3

Q

pt with lung cancer comes in complaining of headaches

Answer

A

you see retinal veins are engorged, he is congested

ddx - SVC syndrome –> death

radiation to shrink tumor restore some blood flow

Question 4

Q

Sturge-Weber formation

Answer

A

vascular malformation in the face in the trigeminal nerve distribution
+ AV malformation
+ mental retardation

Question 5

Q

spider angioma

Answer

A

= AV fistulas (bypass venule)

normal in pregnant women - spider angiomas occur in pregnant women

or in alcoholics - w/ cirrhosis
in alcoholics - you will also see gynecomastia, palmar erythema, warm skin
another reason you see these in alcoholics - cant metabolize 17-ketosteroids –> will aromatize those in adipose –> more estrogen

blanchable

Question 6

Q

muscular vessel vasculitis

Answer

A

consequence is infarction

polyarteritis nodosa - males

necrotizing inflammation –> can get bead-like aneurysm formation (esp in mesenteric circulation)
p-ANCA
scenario - IVDA with chronic hep B who has a nodular, inflammed mass on LE + hematuria
- chronic hepB means pt has HbSAg

Wegener’s granulomatosis (with polyangiitis)

saddle nose defomity (bridge of nose can collapse due to perforated septum), sinusitis, glomerulonephritis
c-ANCA
treat with cyclophosphamide –> hemorrhagic cystitis (prevent with MESNA) and bladder cancer

Kawaski disease - coronary artery vasculitis –> most common cause of MI in kids
+ mucocutaneous inflammation, desquamation of skin, LAD

Question 7

Q

elastic artery vasculitis

Answer

A

in arch vessels –> pulseless disease, strokes

Takayasu’s arteritis - young, Asian lady with absent pulse

Question 8

Q

temporal arteritis

Answer

A

granulomatous vasculitis of temporal artery
-can also involve ophthalmic branch –> blindness

associated with polymyalgia rheumatica - no elevation in serum CK
- v.s. polymyositis = inflammation of muscle, elevated CK

corticosteroids on hx alone (for 1 year)

Question 9

Q

Henoch-Schonlein purpura

Answer

A

14 yo with URI last week - presents with joint pains, hematuria, palpable purpura of buttock and lower extremities

most common vasculitis in children

IC = IgA-(anti-IgA)

Question 10

Q

Rickettsial organisms

Answer

A

infect endothelial cells –> petechiae

RMSF - extremities to trunk, other rashes do the reverse

Question 11

Q

Mucormycosis

Answer

A

DKA

mucor in frontal sinuses –> invade through cribiform plate –> brain

Question 12

Q

Raynaud’s phenomena

Answer

A

100s of diseases can cause this

1) cold reacting antibodies (IgM agglutinins) and cryoglobulins (associated with hepC) - Raynaud’s in cold weather

2) scleroderma, CREST syndrome - first Raynauds, then digital vasculitis and eventually fibrosis
- C - calcinosis, centromere antibody
- R - Raynauds
- E - esophageal dismotility
- S - sclerodactyl (finger stuck in a pencil sharpener)
- T - telangiectasia

3) vasoconstriction - common in pts who take ergot derivatives for migraines
- migraines are are cause by vasodilation…

Question 13

Q

HTN

Answer

A

most common causes of death

1) MI (MI is also the most common cause of death in diabetes)
2) stroke - in BG!
3) renal failure - hyaline arteriolar sclerosis

most common abnormality in HTN - LVH

HTN (esp in AA and elderly) is a condition increased Na –> increased blood volume

Na likes to go into smooth muscle cells - peripheral resistance arterioles
Na enters muscle - opens up Ca2+ channels –> peripheral resistance arterioles are constricting
-> blood is being squeezed out arterial system –> increases diastolic pressure
treat this population with HCTZ
if pt has HLD - cant use HCTZ or b-blockers (they can produce HLD), use ACEI instead
low renin HTN - because of high plasma volume

otherwise - in primary HTN, 60% have normal renin levels and 25% have increased renin levels, 15% have low renin levels

HTN: 90% is essential
10% due to fibromuscular dysplasia (irregular thickening of large and medium sized arteries, string of beads appearance), others

HTN predisposes to many things - one of which is afib

thiazides - first line in HTN
HTN with HF - b-blockers must be used with caution, contraindicated in cardiogenic shock

HTN in pregnancy - hydralazine, labetalol, methyldopa, nifedipine

hydralazine - increased cGMP in smooth muscles –> vasodilator
- compensatory tachy (so you would NOT use it in an hypertensive ermergency, can give b-blocker to counteract), fluid retention, headache, Lupus-like syndrome

HTN emergency - clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

nitroprusside - increased cGMP via direct release of NO, can cause cyanide tox
fenoldopam - D1 agonist –> stimulates adenylyl cyclase –> raises cAMP –> vasodilation of most arterial beds (renal..)

labetalol - a1, b1, b2
- can be used in cocaine intox

Question 14

Q

CCBs

Answer

A

amlodipine (dihydropyridines), diltiazem, verapamil

block L-type Ca channels
amlodipine/nifedipine best for vascular smooth muscle
verapamil best for heart

non-dihydropines - can also be used for afib/flutter

ADRs

pines - peripheral edema, flushing, dizziness, gingival hyperplasia
non-dihydropyridines - cardiac depression, *AV block, hyperprolactinemia, constipation

Question 15

Q

nitrates

Answer

A

venodilation > vasodilation (especially arteries and not arterioles) - decrease preload

used in angina, coronary heart syndrome, pulm edema

cGMP –> decreased intracellular Ca and activation of myosin light chain phosphatase –> myosin light-chain dephosphorylation

ADRs

reflex tachy, hypotension, headaches, flushing
Monday disease in industrial exposure - tolerance during week, loss of tolerance over weekend –> ADRs when re-exposed
contraindicated in RV infarct
cyanide tox = with nitroprusside infusion
- cyanide inhibits cytochrome C –> lactic acidosis and bright red venous blood
- normally metabolized by rhodanese - enzyme that transfers a sulfur to cyanide
- in cyanide tox - give sulfur donors (sodium thiosulfate) or something that can bind to cyanide (sodium nitrite –> metHb will bind to cyanide, hydroxocobalamin)

b-blockers and nitrates are good anti-anginal therapy - reduce myocardial O2 consumption

Question 16

Q

lipid-lowering agents

Answer

A

HMG-coA reductase inhibitors - blocks HMG-coA –> mevalonate –> cholesterol

*decrease LDL, increased HDL, decrease TGs
hepatotox, myopathy esp when used with fibrates or niacin

bile acid resins - cholestyramine, colestipol, colesevelam

prevent intestinal absorption of bile acids - liver must use cholesterol to make more
decrease LDL, increase HDL and TGs
GI upset, decreased absorption of drugs and fat-soluble vitamins

ezetimibe

decrease LDL
prevent cholesterol absorption at small intestine brush border
rare LFTs, diarrhea

fibrates - gemfibrozil, -fibrates

decrease LDL, increase HDL, *decrease TGs
upregulate LPL –> increased TG clearance, activates PPAR-a to induce HDL synthesis
myopathy, cholesterol gallstones

niacin - decrease LDL, increase HDL, decrease TGs

inhibits lipolysis (HSL) in adipose tissue, reduces hepatic VLDL synthesis
red flushed face, hyperglycemia, hyperuricemia

PCSK9 inhibitors -mabs

*decrease LDL, increased HDL, decrease TGs
inactivation of LDL-R degradation –> increases amount of LDL removed from blood
myalgias, delerium/dementia

Question 17

Q

digoxin

Answer

A

binds to K+ site of Na/K ATPase - hypokalemia can lead to tox (more digoxin binds)
- decreases APD - can cause short QT interval

also stimulates vagus nerve –> AV nodal conduction –> decreased HR

uses: HF, afib (decreases conduction at AV node, depresses SA node)
- when AV conduction is slowed, atria will continue to fibrillate/flutter but ventricles will contract at a normal rate (enough time for diastolic filling)

tox: hyperkalemia, cholingeric side effects (blurry yellow vision - Van Gogh), arrhythmias and AV block
- can cause delayed afterdepolizations (because it increases intracellular Ca) –> v.tach and death

verapamil, amiodarone, quinidine can cause decreased clearance

antidote - slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

Question 18

Q

rheumatic fever

Answer

A

antibodies to M protein of S. pharyngitis…
- ddx by evidence of prior group A strep infection (anti-streptolysin O or anti-DNase B titer)

myocarditis - most common cause of death in the acute phase

Aschoff bodies = granuloma with giant cells in myocardium
Anitschkow cells - enlarged macrophages with caterpillar nucleus

acute attack- vegetations on mitral valve –> mitral valve regurg (can also have aortic valve involvement)

chronic disease = valve scarring –> mitral stenosis
occasionally, aortic valve stenosis (fishmouth)
and the complication is endocarditis

Question 19

Q

heart failure

Answer

A

ACEI/ARB, b-blockers, and spironolactone decrease mortality (other diuretics provide symptom relief)
- can add hydralazine and nitrate therapy

b-blockers - decreases cardiac work, but only use in STABLE HF

1) slows ventricular rate
2) reduces peripheral resistance by decreasing circulating levels of NE, renin, endothelin

orthopnea - due to increased venous return

pulm edema - HF cells (hemosideran-laden macrophages in lungs)

Question 20

Q

shock

Answer

A

shock = low perfusion to tissues –> lactic acid accumulation
- additionally - liver is the primary site of lactic acid clearance (converted back to glucose), hypoperfusion will affect liver

hypovolemic - …burns, cold and clammy, give IV fluids

cardiogenic/obstructive - cold clammy, decreased CO (more so than in hypovolemia), inotropes, diuresis, relieve obstruction

distributive -

sepsis, anaphylaxis- warm, increased CO and decreased SVR
- septic shock is distributive shock - means blood is trapped in small vessels rather than large - that is why you have a low PCWP and CVP but high CO
CNS injury - dry, decreased CO and SVR
pressors and fluids

Question 21

Q

HLD signs

Answer

A

cholesterol in the skin

xanthomas (lipid-laden macrophages), tendinous xanthoma (Achilles), corneal arcus (white ring around iris, common in elderly)

familial hypercholesterolemia

absent LDL receptor - put you on an HMG-coA reductase inhibitor
Achilles tendon xanthoma
death by age 20 by coronary attack

Question 22

Q

congenital cardiac defect associations

Answer

A

Septal defects:
fetal alcohol syndrome - septal defects, tet of Fallot
DS - AV septal defect (endocardial cushion defect), other septal defects
congenital rubella - PDA, pulmonary artery stenosis, septal defects

Valve defects:
Marfan - mitral valve prolapse, aneurysm/dissection/aortic regurg
Li - tricuspid displaced towards apex
Turner - bicuspid aortic, coarctation of aorta (esp in between aortic branches and PDA) –> blood from pulmonary trunk will enter the aorta (low pressure area downstream of coarctation)
- coarctation of aorta - eventually, intercostal arteries enlarge due to collateral circulation –> erode and notch ribs
- in adults, coarctation is not associated with PDA and lies distal to aortic arch
- associated with bicuspid aortic valve
- collateral circulation across intercostals

Williams syndrome - supravalvular aortic stenosis

Other:
infant of diabetic mother - transposition of great vessels
22q11 (Digeorge) - truncus arteriosus, tet fallot, transposition of great vessels

Question 23

Q

ECG abnormalities

Answer

A

AV node supplied by RCA - 100ms delay

Pacemaker rates: SA > AV > ventricular system
conduction velocity: Purkinje > atria > ventricles > AV node

PR = 200 ms
QRS = 120 ms

T wave inversion - recent MI, ischemia
U wave (mini wave that follows T wave) - hypokalemia, bradycardia

Afib = irregularly irregular

no P waves, irregularly spaced QRS
can have fine fibrillatory waves in between the QRS complexes
risk factors - HTN, CAD
precipitated by illness or increased sympathetic tone, or excessive alcohol consumption (holiday heart syndrome)

A flutter - 4:1 sawtooth pattern

3 P waves + 1 QRS + 1 T = 4:1 sawtooth
treat like afib, definitive treatment is catheter ablation

Vfib - SCD

SCD is associated with CAD (70%), HCM, long QT, Brugada, cocaine abuse, mitral valve prolapse
prevent with implantable cardioverter-defibrillator

Torsads - can progress to v fib

long QT predisposes to torsades
drug-induced - anti-arrhythmics (1A, 3), macrolides, haloperidol, TCAs, ondansetron
metabolites - hypokalemia, hypoMg
congenital
treat with MgSO4

Question 24

Q

AV block

Answer

A

first degree - PR > 200, benign and asymptomatic

second degree
Mobitz 1) progressive lengthening of PR until beat drops - P is NOT followed by QRS, regularly irregular (RR interval)
2) dropped beats, PR interval stays constant - may progress to 3rd block
- treat with pacemaker

third degree = complete

atria and ventricles beat independently of each other
atrial rate > ventricle rate
treat with pacemaker
can be cause by Lyme disease

Question 25

Q

coronary circulation

Answer

A

left coronary –> LAD, LM, LC

LAD - anterior surface, anterolateral papillary muscle
LC - lateral and posterior walls, anterolateral papillary muscle

right coronary - PDA (85% of time), RM

RCA - SA and AV nodes
PDA - …posteromedial papillary muscle, usually rises from RCA (can arise from LCX, or codominant circulation)

coronary blood flow during diastole: aortic pressure > IV pressure

RCA occlusion –> inferior wall MI –> RV dysfunction

Question 26

Q

pericardium

Answer

A

innervated by phrenic nerve (C3-C5) - pericarditis can cause referred pain to shoulder

acute pericarditis

aggravated by inspiration
relieved by sitting up and sitting forward
- sensitive to movements - coughing, radiates to neck (phrenic nerve)
widespread ST-segment elevation and/or PR depression
causes - unknown viral, Coxsackie, neoplasia, autoimmune (SLE, pericarditis), uremia, STEMI (due to transmural infarct and inflammatory exudate), Dressler syndrome, radiation therapy

fibrinous pericarditis in the 2-3 days following a STEMI - disappears with 1-3d of ASA

Question 27

Q

organs are arranged in parallel

Answer

A

mean pressure in each major artery will be approx same as the mean pressure in the aorta
- nephrectomy will increase TPR and decrease CO

systolic pressure and pulse pressure are higher in large arteries than in the aorta because of inertia of blood - pressure waves travel at a higher velocity than blood itself

Question 28

Q

compliance

Answer

A

C = dV/dP

aging decreases compliance of arteries - increased arterial pressures in the elderly

Question 29

Q

systolic and pulse pressures

Answer

A

systolic and pulse pressures are increased - …OSA (due to increased sympathetic tone)

Question 30

Q

S2

Answer

A

A2, P2 - pulmonic valve closes after

inspiration delays closure of pulmonic valve - decreased intrathoracic pressure –> venous return to RA/RV is increased –> take longer to empty RV
- also pulmonary vessels have increased holding capacity during inspiration

wide splitting - when RV emptying is delayed (pulmonary stenosis, RBBB)

fixed splitting in L –> R shunt

paradoxical splitting - when closure of aortic valve is delayed (aortic stenosis, LBBB)
- split is eliminated during inspiration

Question 31

Q

threshold potential

Answer

A

potential difference where there is a NET inward current - depolarization becomes self-sustained

Question 32

Q

ventricular AP

Answer

A

0) upstroke - Na enters cells (inactivation gates close at 20 mV)
- dV/dt depends on resting membrane potential - lower is better
- the larger the inward current –> the more rapidly local currents will spread to adjacent sites and depolarize them (does NOT depend on AP duration)

1) initial repolarization - inward Na has ceased, outward K

2) plateau - inward current = outward current
- Ca in through dihydropyridine channels (nifedipine is the inhibitor)
- Ca entry –> Ca-induced Ca-release
- K is moving out
- 150 ms in atria < ventricles < Purkinje cells

3) repolarization - slow K channels open

4) resting membrane potential = -85mV
- high K permeability, leak channels, ATPases

things that are different from skeletal muscle - plateau, Ca-induced Ca-release, gap junctions

contraction

1) as myosin head binds ATP - it detaches from actin
2) ATP is hydrolyzed –> conformational change –> actin is rebound
- cardiac muscle has high resting tension - difficult to stretch cells beyond Lmax so will only operate on ascending limb of length-tension curve

inotropy

positive inotropes increase tension, also cause faster relaxation (more time for filling)
SNS –> P-L-type Ca channels…
phosphorylation of phospholamban –> activates Ca2+ ATPase on SR –> faster relaxation

decrease inotropy - …acidosis, hypoxia/hypercapnia, non-dihydropyridine CCBs

Question 33

Q

SA node

Answer

A

unstable resting membrane potential

0) upstroke - Ca2+ entry, T-type and L-type Ca channels
- slow conduction velocity - used for delay by AV node
- fast VS-Na channels are permanently inactivated due to higher resting potential of these cells

3) repolarization - K out

4) spontaneous depolarization = longest part of AP
- If - mixed inward Na/K current, turned on by preceding repolarization
- sets HR - remember adenosine decreases HR
- sympathetic stimulation increases the chance that If channels are open

latent pacemakers - heart will beat slower if it is driven by a latent pacemaker

Question 34

Q

refractory period

Answer

A

absolute refractory period < effective RP (conducted AP cant be generated)

relative RP - AP generated will have an abnormal configuration

Question 35

Q

autonomic effects on HR

Answer

A

SNS: b1-NE

1) increase If, increased rate of phase 4 depol
2) increase in ICa (less depolarization needed to reach threshold)
- also increases conduction velocity through AV node
- and increases the total amount of trigger Ca2+ that has entered the cells
- positive staircase effect or extra beat

PSNS: M2-Ach/adenosine –> Gk (aka Gi protein)

1) decreases If
2) Gk directly increases K-Ach out
3) decreases ICa
- downstream - less Ca enters the cells

Question 36

Q

ACEIs/ARBs

Answer

A

decrease preload and afterload

Question 37

Q

cardiac work

Answer

A

W = P x V

- pressure work requires more O2 consumption - so O2 consumption increases more with aortic stenosis than with exercise

Question 38

Q

S4 sound

Answer

A

atrial kick - occurs in late diastole

- best heard at apex with pt at left lateral decubitus

Question 39

Q

JVP

Answer

A

a wave = atrial contraction (in late diastole)

a wave disappears afib
giant a wave in mitral/ tricuspid stenosis and with S4
giant c (?) wave is tricuspid regurg

c wave = RV contraction (tricuspid bulges/reflects backwords)

x descent = downward displacement of tricuspid during ventricular ejection (reduced in tricuspid regurg, HF)

v wave = RA filling
- corresponds to beginning of diastole

y descent = RA emptying into RV, prominent in constrictive pericarditis, absent in cardiac tamponade

Kussmaul sign - increase in JVP on inspiration (normally decreases during inspiration)

impaired filling of RV –> blood backs up –> JVP increased
constrictive pericarditis, restrictive cardiomyopathies, RA/RV tumors

Question 40

Q

atherosclerosis

Answer

A

thickening of intima - intimal plaque

abd aorta > coronary artery > popliteals > carotid
note coronary arteries are maximally dilated in an area of stenosis - to maintain resting blood flow

damage to endothelium –> lipid enters intima, gets oxidized, uptaken by macrophages = fatty streak
- damage due to - smoke, oxidized lipid, Chlamydia pneumonia infection, viral infections, homocysteine

fatty streak undergoes inflammation, healing, increased lipid deposition and necrosis, development of fibromuscular cap

inflammation/healing process leads to ECM and smooth muscle proliferation - involves PDGF and FGF (which are produced by monocytes and platelets)
note fibroblasts dont contribute much to the formation of atheromas - fibrous cap is due to SMC proliferation

symptomatic after > 70% stenosis

causes thickening of blood vessel wall –> wall atrophy –> weakening –> abdominal aneurysm (no vasa vasorum in abdominal aorta)

palpable pulsatile abdominal mass - rupture is feared when greater than 5 cm
rupture triad: hypotension, pulsatile abdominal mass and flank pain
dilated, calcified aortic wall with crescent shaped non-opacification on CT (flap, clot)

Question 41

Q

arteriolosclerosis

Answer

A

hyaline arteriolosclerosis
- classically produces glomerular scarring due to decreased GBF (arteriolonephrosclerosis) –> shrunken kidney with scarring/nodules on surface

hyperplastic arteriolosclerosis - due to smooth muscle hyperplasia

consequence of severe/malignant HTN
onion-skin appearance
classically causes ARF with flea-bitten appearance - surface of kidney has pinpoint hemorrhages

remember malignant HTN also has fibrinoid necrosis (so histo will show hyperplastic arteriolosclerosis and ring of pink surrounding lumen)

Question 42

Q

Monckeberg medial sclerosis

Answer

A

calcification of internal elastic lamina and media - non-obstructive, not clinically significant

incidental finding on x-ray, mammography - pipestem appearance

thought to cause isolated systolic HTN

Question 43

Q

aortic dissection and aneurysm

Answer

A

DISSECTION
most common cause is HTN
- intimal tearing is the inciting event - due to HTN
- adventitia contains vasa vasorum… –> medial degeneration and increased wall stiffness

associated with inherited defects of CT, elastic tissue - Marfans (medial cystic degeneration), Ehlers-Danlos
- other causes include HTN, bicuspid aortic valve

dissection - complication is pericardial tamponade –> most common cause of death

can have fatal hemorrhage into mediastinum (mediastinal widening on CXR), obstruction of arteries (ex renal artery lumen is squeezed shut)
blood pressure differences between arms

type A: involves ascending aorta - surgery

ahead of brachiocephalic artery - specifically in the sinotubular junction (right above aortic valve)
cant propagate distally

type B: involves descending aorta

originate close to the left subclavian
treat medically with b-blockers and vasodilators

ANEURYSM

thoracic - tertiary syphilis and end-arteritis, tree-bark appearance of aorta
- other risk factors include - bicuspid aortic valve, HTN

traumatic aortic rupture - MVC, aortic isthmus (first descending part of the aorta)

Question 44

Q

Large vessel vasculitides

Answer

A

vasculitides in general present with non-specific symptoms (fevers, fatigue, etc.)

aorta or major branches

temporal (giant cell) arteritis

associated with polymyalgia rheumatica (flu-like symptoms with joint and muscle pain)
elevated ESR
giant cells, intimal fibrosis
segmental lesions so negative biopsy does not exclude disease
treat with corticosteroids

Takayasu - same as temporal arteritis, presents in Asian women less than 40

narrowing of aortic arch and proximal vessels –> pulseless disease
visual and neuro symptoms
elevated ESR
treat with corticosteroids

Question 45

Q

Medium vessel vasculitides

Answer

A

muscular arteries that supply organs

polyarteritis nodosa

necrotizing vasculitis that involves most organs, lung is spared = GI/melena, HTN and renal damage, neuro damage, etc.
IC mediated
associated with HbsAG - usually occurs in middle aged men
string of pearls lesions = early lesions have transmural inflammation with fibrinoid necrosis –> wall of blood vessel weakens –> aneurysm, lesions heal to form fibrosis
treat with corticosteroids and cyclophosphamide (remember this causes transitional cell carcinoma and SIADH)

Kawasaki dz = mucocutaneous LN syndrome

CRASH and burn
conjunctivitis, rash (palms and soles), adenopathy (cervical LN), strawberry tongue, hand and foot changes, fever
coronary artery involvement - thrombosis, aneurysms
treat with ASA - decreases risk of thrombus development
give IVIG - modulates complement activation, saturates Fc receptors on macrophages, suppresses idiotypic antibodies
disease is self-limited

Buerger dz (thromboangiitis obliterans) - segmental thrombosing vasculitis, necrotizing vasculitis involving digits

ulcers/gangrene/autoamputation of digits and toes
associated with Raynaud’s (vasospasm in response to cold/stress - white –> blue –> red fingers)
associated with smoking = pt is heavy male smoker < 40 yo
- treat with smoking cessation

Question 46

Q

Small vessel vasculitides

Answer

A

99% of time due to type 3 HSR

IC deposition –> complement –> fibrinoid necrosis of blood vessels –> palpable purpura
- complement is called in via alternate/lectin pathway

Wegners - nasopharynx, lungs, kidneys

PR3-ANCA/c-ANCA
large necrotizing granulomas with adjacent necrotizing vasculitis - 1) granulomas in lung and upper airway, 2) glomerulonephritis, 3) vasculitis
treat with cyclophosphamide and steroids - relapses are common

Microscopic polyangiitis

lung, kidney (glomerulonephritis), skin, palpable purpura
distinguish from Wegners - NO nasopharyngeal involvement, NO granulomas
p-ANCA
treat with cyclophosphamide and steroids - relapses are common

………………………

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) - necrotizing granulomatous vasculitis with eos

asthma, peripheral eosinophilia, increased IgE
peripheral neuropathy - foot drop
p-ANCA

Henoch-Schonlein purpura - vasculitis due to IgA IC deposition

common in kids - follows URI
triad: palpable purpura on LE + butt, GI bleeding, arthralgias
assoc with IgA nephropathy
self-limiting but may recur, treat with steroids if severe

Question 47

Q

tumors

Answer

A

most common tumor is melanoma met
- most commonly involves pericardium –> pericardial effusion

myxoma - LA –> ball-valve obstruction –> multiple syncopal episodes

may hear a tumor plop sound during early diastole
classically embolizes to leg

rhabdomyoma - kids, think TS
- ventricle

strawberry hemangioma - skin, liver

initally GROW to proportion of the child, then regress spontaneously before puberty
v.s cherry hemangioma in elderly

angiosarcoma - malignant proliferation of endothelial cells, aggressive and difficult to resect

skin, head/neck, breast, liver
usually on sun-exposed areas, associated with radiation therapy and chronic post-mastectomy lymphedema
liver angiosarcoma in particular - associated with exposure to PVC, arsenic, throtrast (outdate radiocontrast agent)

Kaposi sarcoma - HHV8

Eastern European males, AIDS, transplant recipients
lymphocytic infiltrate
v. s Bacillary angiomatosis - AIDS, neutrophilic infiltrate
visualize with silver stain, treat with sulfa drug

Question 48

Q

hereditary hemorrhagic telangiectasia

Answer

A

Osler-Weber-Rendu syndrome

blanching skin lesions, recurrent epistaxis, skin discolorations, AV malformations, GI bleeds, hematuria

Question 49

Q

embryology

Answer

A

bulbus cordis - RV/LV outflow tracts
cardinal veins - SVC

endocardial cushion - AV septums, AV and SL valves

left horn of sinus venosus - coronary sinus
right horn of sinus venosus - smooth part of RA
primitive pulm vein - smooth part of LA

heart is the first functional organ in the embryo - beats by week 4
- week 4 = looping to establish L-R polarity

Question 50

Q

septation

Answer

A

atria

1) septum primum grows towards endocardial cushions - narrowing foramen primum
2) septum secundum forms in septum primum (foramen primum disappears)
3) foramen secundum forms
4) septum secundum expands
- residual foramen (between septums) is foramen ovale - septums fuse and FO closes soon after birth because of increased LA pressure

ventricles

1) muscular ventricular septum forms, IV foramen
2) aorticopulmonary septum rotates and fuses with muscular IV septum to form membranous IV septum
3) endocardial cushions grow to separate atria from ventricles

outflow tract formation - neural crest and endocardial cells migrate…. –> aorticopulmonary septum

Question 51

Q

congenital cardiac malformations

Answer

A

VSD: most common

membranous part of septum (from aorticopulmonary septum and endocardial cushions)
shunt-reversal
holosystolic, harsh-sounding murmur, loudest at tricuspid area

ASD

defect is that septa are missing (v.s. PFO, where septa dont fuse)
most common type is ostium secudum, ostium primum is associated with DS
loud S1
wide, fixed split S2

PDA - after branches come off aorta

associated with congenital rubella
holosystolic machine-like murmur, loudest at S2, best heard at left infraclavicular area
shunt reversal - cyanosis of LE
treat with indomethacin - decreases PGE

Tet of Fallot
1&2) aorta overriding VSD
3&4) stenosis of right outflow tract and RVH
- R–>L shunt - cyanotic baby
- squatting reverses cyanotic spell
- tet spells are caused by crying, fever, and exercise due to exacerbation of RV obstruction
- boot-shaped heart on XR

Transposition of great vessels - have to introduce a shunt, maintain PDA in the meantime

associated with mat DM
due to failure of aorticopulmonary septum to spiral

Total anomalous pulmonary venous return

pulmonary veins drain into right heart (as do SVC, coronary sinus)
associated with ASD and sometimes PDA

Truncus arteriosus - early cyanosis
- most pts also have VSD

Tricuspid atresia - no valve
- need ASD and VSD for viability

Question 52

Q

angina

Answer

A

stable angina: >70% stenosis

reversible injury to myocytes (occurs if blood flow is decreased for <20 min)
ST depression - endocardium is most susceptible to damage
- why? because coronary arteries begin in the epicardium and dive down
- ST DEPression in V5 = subendocardial infarct

unstable angina - due to RUPTURE of atherosclerotic plaque and incomplete occlusion of coronary artery

again reversible injury and ST-depression
high risk of progression to MI - thrombus can easily occlude entire vessel

Prinzmetal angina - vasospasm

transmural ischemia - blood vessel has completely clamped down - ST elevation
can also have T wave inversion
smoking is a risk factor

treat all with nitrates (decreases preload), add CCB for Prinzmetal

Coronary steal syndrome - distal to coronary stenosis, vessels are maximally dilated at baseline

giving vasodilators dilates normal blood vessels and shunts blood towards well-perfused areas –> diverts flow from stenosed vessels –> myocardial ischemia
principle behind pharmacologic stress tests with vasodilators

Question 53

Q

MI

Answer

A

necrosis of cardiac myocytes - complete occlusion of coronary artery

presentation - crushing pain…dyspnea (due to blockage of blood flow –> pulm congestion)
- symptoms are not relieved by NG

arteries
- usually LAD, next most common is RCA –> in general, LV is more affected

EKG

STEMI (V5) - transmural infarct, can also have Q waves
- EKG localization of STEMI:
- anteroseptal (LAD) - V1-2
- anteroapical (distal LAD) - V3-4
- anterolateral (LAD, LCX) - V5-6
- lateral (LCX) - 1, aVL
- inferior (RCA) - 2, 3, aVF
- posterior (PDA) - V7-9 and ST-dep in V1-3 with tall R waves
NSTEMI- subendocardial infarcts (esp inner 1/3)
other findings: peaked T waves, T wave inversion, new LBBB, pathologic Q waves or poor R wave progression (evolving or old transmural infarct)

labs/tests:

EKG is gold standard in first 6 hrs
trop I - rises 2-4 hrs after infarction, peaks at 24hrs, normal by 7-10 days
CK-MB - rises 4-6 hrs after, peaks at 24 hrs, returns to normal by 48-72 hrs
- CK-MB can also be released by skeletal muscle

treat with ASA/heparin, supplemental O2, nitrates, b-blocker, ACEI

fibrinolysis or angioplasty
- contraction band necrosis - returning blood returns Ca2+
- reperfusion injury - cardiac enzymes continue to rise
unstable angina/NSTEMI - medical treatment
STEMI - meds, percutaneous coronary intervention preferred over fibrinolysis (due to lower rates of hemorrhage and recurrent MI)

changes with time:

first 4hrs - no microscopic changes, arrhythmia
- arrhythmia is an important cause of death before reaching the hospital and within the first 24 hrs
1 day of coagulative necrosis (cells will be eosinophilic) - susceptible to reperfusion injury and contraction band necrosis
1 week of inflammation - during macrophage phase, complication is rupture of weakened ventricular free wall or septum –> cardiac tamponade, mitral insufficiency (if RCA is affected), shunt
- ventricular pseudoaneurysm is a contained free wall rupture
1-3 weeks - granulation tissue, gross exam will show red border at the edge of the infarct
months - type 1 collagen scar (which is not as strong as the original myocardium)
- ventricular aneurysm
- Dressler syndrome - inflammation in pericardium exposes new antigens –> pericarditis 6-8 weeks after infarction
- Dressler syndrome can also involve other serosal surfaces (aka autoimmune polyserositis), treat with ASA/NSAIDs/glucocorticoids

Question 54

Q

cardiomyopathy

Answer

A

Dilated cardiomyopathy

valvular regurg
causes: idiopathic, genetic (AD), Coxsackie myocarditis, alcohol abuse, drugs (doxorubicin, cocaine), pregnancy, Chagas, hemachromatosis, sarcoidosis, wet Beriberi
eccentric hypertrophy
treat …. implantable cardioverter, heart transplant
Takotsubo cardiomyopathy - ventricular apical ballooning, due to SNS input (stressful situations)

HCM (AD) - genetic mutations in sarcomere proteins

outflow obstruction - septal hypertrophy, mitral valve obstruction outflow tract
myocyte hypertrophy
can be associated with Friedrich ataxia
treat - b-blockers, non-dihydropyridine CCBs, ICD if pt is at high risk

Restrictive cardiomyopathy

normal ejection fraction
usually normal wall-thickness but can have increased LV thickness
decreased compliance of endomyocardium
causes: amyloidosis, sarcoidosis, endocardial fibroelastosis (kids), Loeffler syndrome (eosinophilic infiltrate + endocardial fibrosis), postradiation fibrosis
- amyloidosis - light chains, mutated transthyretin, wild-type transthyretin (senile systemic amyloidosis
- endomyocardial fibrosis - occurs in tropical regions (Uganda)
classic finding is low voltage EKG

Question 55

Q

SNS and catecholamines

Answer

A

a1 - NE*, epi, phenylepi
b1 - *Epi, dopamine, dobutamine, isoproterenol
b2 - *Epi, isoproterenol, terbutaline
- b2– > cAMP-PKC –> augmented Ca2+ uptake by SR –> vasodilation

isoproterenol is stronger than epi on b-receptors
- isoproterenol will increase cardiac contractility and decreased SVR

b-blockers - will decrease contractility, can precipitate asthma attack in pts with asthma or COPD

a-neuron blockers - gaunethidine, inhibit NE rlease

Question 56

Q

endocarditis

Answer

A

disrupted normal endocardial surface –> fibrin-platelet nidus –> bacteriaf]

in general multiple blood cultures necessary for ddx:
S aureus - acute, large vegetations

subacute - S. viridans, small vegetations on susceptible valves

associated with dental procedures
adheres to tooth enamel and fibrin-platelet aggregates on damaged heart valves - because it produces dextrans (from sucrose)

culture negative orgs are: Coxiella, Bartonella, and HACEK (Haemophilus, Aggregatibaceter, Cardiobacterium, Eikenella, Kingella)

mitral valve is most frequently involved
- tricuspid in IVDA - S aureus, Pseudomonas, Candida

other features:
Anemia, murmur
Fever
Roth spots - round white spots on retina
Osler nodes - raised lesions on finger/toe pads due to IC deposition
Janeway lesions - erythematous lesions on palms, soles
Emboli, splinter hemorrhages
- emboli, Janeway lesions are = embolic
- IC - osler nodes, Roth spots

endocarditis can be non-bacterial (aka thrombotic or marantic endocarditis)

secondary to malignancy (mucinous adenocarcinomas), hypercoagulable state, lupus (NOT associated with systemic sclerosis)
hypercoagulable state and cytokines create a setting where thrombi can deposit on heart valves

Question 57

Q

heart murmurs

Answer

A

Aortic stenosis = wear-and-tear disease, dystrophic calcifications

compensation leads to prolonged asymptomatic stage - systolic ejection click followed by crescendo-decrescendo murmur
- murmur - loudest heart at base –> radiates to carotids
- pulses are weak with a delayed peak (pulsus parvus et tardus), syncope/etc. on exertion
complications - …microangiopathic hemolytic anemia
treat - valve replacement after onset of complications

Aortic regurg - blowing (descrendo) murmur in early diastole

can be heard at the left or right (if caused by aortic root dilation) sternal border
widened pulse pressure - head bobbing, pulsating uvula and nail beds, waterhammer pulse
recurrent laryngeal wraps around aortic arch –> hoarseness
LV dilation –> LH failure
- LV dilation allows for an increase in stroke volume to maintain CO (this only occurs chronically)
- in acute AR - LV is not large enough to maintain CO –> decrease in CO, increase in HR
treatment is valve replacement when LV dysfunction develops

Mitral valve prolapse

most frequent valvular lesion
mid-systolic ejection click (due to sudden tensing of chordae tendinae), followed by regurg murmur
asymptomatic
valve degeneration (Marfans, Ehlers-Danlos) or papillary muscle rupture
again treat with valve replacement

Mitral regurg

holosystolic blowing murmur
- loudest at apex and radiates towards axilla
- louder with squatting and expiration
- squatting - increased TPR send more blood flowing backwards
- expiration - increases blood that enters LA and LV
bounding pulse with brisk upstroke (due to increased LV volumes)
functional mitral regurg - transient hemodynamic factors that cause LV dilatation and or papillary muscle ischemia

Mitral stenosis

opening snap followed by diastolic rumble
- opening snap due to abrupt half in leaflet motion in diastole
- decreased interval between S2 and OS correlates with increased severity - probably because this means valve is more stenosed
chronic rheumatic fever
chronic MS can result in LA dilatation

Question 58

Q

maneuvers during auscultation

Answer

A

inspiration - increases venous return
- widens S2 split

hand grip - increases afterload

increased intensity of MR, AR, and VSD murmurs
decreases hypertrophic cardiomyopathy and AS murmurs
MVP - later onset of click/murmur

Valsalva, standing up - decrease preload

decrease intensity of most murmurs (including AS)
increase intensity of HCM murmur
MVP - earlier onset of click/murmur

Rapid squatting - increases venous return/preload, increases afterload

decreased intensity of HCM murmur
increased intensity of most other murmurs
MVP - later onset of click/murmur

MVP - maneuvers that increase LV volume maintain tension on the chordae longer –> click occurs later

Question 59

Q

palpable skin rash

Answer

A

N. gonorrhea infection - meningococcemia or disseminated

begins on trunk and spreads over entire body
fever, hypotension, tachy = septic

Question 60

Q

long QT

Answer

A

congenital - due to genetic mutations in K+ channel - decreased K outflow

Romano-Ward syndrome - AD, pure cardiac phenotype
Jervell and Lange-Nielsen syndrome - AR, sensorineural deafness

Question 61

Q

conduction defects

Answer

A

Brugada - AD, Asian males

pseudo RBBB and ST elevations in V1-V3
increased risk of vtach and SCD (use ICD)

WPW = pre-ventricular excitation syndrome

fast accessory conduction pathway from atria to ventricle (bundle of Kent) that bypasses the AV node
ventricles begin to partially depolarize earlier - delta wave (curve where Q should be) and widened QRS
may result in reentry circuit –> supraventricular tachy

Question 62

Q

cardiac tamponade

Answer

A

equilibration of pressures in all heart chambers

Beck’s triad - hypotension, distended neck veins, distant heart sounds

will see late diastolic collapse of RA - pericardial fluid displaces with ventricular expansion
HR increased
pulsus paradoxus - SBP <10mmHg during inspiration, because of increased venous return and RA volume, constant pericardial effusion and RV volume –> septum pushes towards LV…
also seen in asthma, COPD, OSA, pericarditis, croup
- mechanism in COPD - exaggerated drop in intrathoracic pressure –> transmitted to extrathoracic structures –> excessive drop in BP during inspiration
Korotkoff sounds (hear when you are taking BP, deflating the cuff) - during inspiration –> increased RH volumes. When you cant expand pericardium –> IV septum blows towards LV –> LV stroke volume and SBP decrease

EKG - low voltage and electrical alternans (swinging movement of heart in effusion)

Question 63

Q

anti-arrhythmics

Answer

A

Class 1 - Na channel blockers

decrease conduction (esp in depolarized cells)
- decrease slope of phase 0 depol

dissociation of drug occurs during resting state of the channel

binding strength: 1C > 1A > 1B

1A) quinidine, procainamide, disopyramide

increase AP duration and ERP (in vent. AP), increased QT, slows conduction velocity
some K channel blocking effects - prolongs APD and QT
use in atrial and vent arrhythmias, esp SVT and VT
ADRs: cinchonism (headache, tinnitus with quinidine), procainamide (lups), HF (disopyramide), thrombocytopenia, torsads

1B) lidocaine, mexiletine, phenytoin

decrease AP duration, no effect on conduction velocity
good for ischemic or depolarized ventricular tissue
use in acute VT (esp post MI), digitalis-induced arrhythmias
1B is Best post-MI - because these tissues have a reduced resting potential that delays the transition from the inactivated to the resting state –> increased drug-channel binding
CNS stim/dep, CV dep (think lidocaine)

1C) flecainide, propafenone

prolongs ERP in AV node and accessory tracts (no effect on ventricles), slows AP conduction velocity
use in SVTs, afib
proarrhythmic (esp post MI)
- 1C binds with the greatest affinity –> effects accumulate over many cardiac cycles and effect is enhanced with tachycardia –> delay in conduction speed that is out of proportion to prolonged refractory period –> this is why it is proarrthymic

………………………………………………………….
anti-arrhythmics class 2
b-blockers

slows sinus node discharge rate, slows AV node conduction

[decreases SA and AV node activity (less cAMP), decreases Ca currents (also suppresses abnormal pacemakers, decreases slope of phase 4)]

use in SVT, ventricular rate control for afib and aflutter

ADRs:
may mask the signs of hypoglycemia
metoprolol - dyslipidemia
propanolol can exacerbate Prinzmetal
contraindicated in pheo and cocaine tox

treat OD with saline, atropine, and glucagon
- glucagon increases cAMP and cardiac contractility

...................................................................
anti-arrhythmics class 3
K-channel blockers

amiodarone, ibutilide, dofetilide, sotalol = AIDS

block - slow delayed rectifier K channels (Iks)

increase AP duration, ERP, and QT
- does NOT affect AP conduction velocity

used in afib, aflutter, vtach (amiodarone, sotalol)

ADRs:
sotalol - torsads, excess b-blockade
ibutilide - torsads
amiodarone - pulmonary fibrosis, hepatotox, hypo/hyperthyroid (drug = 40% iodine), acts as hapten (eye deposits, skin deposits that are photosensitive, blue-grey skin discoloration), neuro effects, CV depression
- amiodarone - PFTs, LFTs, TFTs
- amiodarone has class 1-4 effects
- interestingly, amiodarone has the lowest risk of torsads

...................................................................
anti-arrhythmics class 4
Ca-channel blockers

verapamil, diltiazem

same action as b-blockers (class 2)

prevents nodal arrhythmias (SVT), rate control in afib

ADRs: constipation, flushing, edema, CV depression

Question 64

Q

other anti-arrhythmics

Answer

A

adenosine - shifts K+ out of cells –> hyperpolarizes cells and decreases Ica –> decreased AV node conduction

drug of choice for SVT (certain types)
15s acting time
effects are blunted by theophylline and caffeine (adenosine receptor antagonists)
ADRs: flushing, hypotension, CP, sense of impending doom, bronchospasm

Mg2+ - torsads and digoxin tox

Answer 65

A

HR increases, CO increases
PaO2 and PaCO2 unchanged - respiratory rate increases to eliminate the additional CO2 produced and improved V/Q matching
- venous blood concentrations will change!

vasodilators - adenosine and NO during exercise dilate coronary blood vessels
- so increase in HR doesnt limit coronary blood flow

when would arterial blood pH decrease - if you get lactic acidosis

Answer 66

A

carotid sinus –> glossopharyngeal nerve (afferent) –> medulla –> vagal nerve

reflex PSNS simulation of SA node, atrial myocytes, and AV node

can be used acutely terminate PSVT
- Valsava and cold water immersion can also be used

Answer 67

A

selective inhibition of If - prolongs phase 4 and decreases SA node firing

use in chronic stable angina pts who dont take b-blockers, chronic HF with reduced ejection fraction

ADRs: luminous phenomena/visual brightness, HTN, bradycardia

Answer 68

A

cardiac and smooth muscle - Ca-induced Ca-release and Ryr

cardiac muscle - Ca binds troponin
smooth muscle - Ca binds calmodulin

skeletal muscle

L-type Ca channels directly interact with RyR –> Ca released from SR –> Ca binds to troponin
mechanical coupling - so Ca2+ influx across plasma membrane isnt required
verapamil would have no effect

T-tubules are NOT present in smooth muscle

Answer 69

A

DS - most common congenital cardiac anomaly in DS

failure of endocardial cushion fusion –> ostium primum atrial septal defect, VSD, and single AV valve
–> L-R shunting, AV regurg –> excess pulmonary blood flow symptoms

increased pulmonary venous return - mid-diastolic rumble
AV valve regurg - holosystolic, best heard at apex

Answer 70

A

endothelial damage

homocysteine –> cystathionine –> cysteine

methylene THF reductase, FAD - used to regenerate methyl-THF
- MTHFR deficiency is the most common genetic cause of hyperhomocyestinemia

methylmalonic acid = neurotoxic
- lethargy, seizures, paresthesias, hypotonia

Answer 71

A

due to increased venous stasis (uterus compresses IVC and internal iliacs), endothelial injury (during delivery), and hypercoagulability
- hypercoag - because of increase in factors 1, 2, 7, 8,9, 10 and a drop in protein S levels

use LMWHs - heparins dont cross placenta, short elimination times
- enoxaparin

Answer 72

A

clopidogrel - blocks platelet adenosine diphosphate receptor –> limits platelet aggregation

ASA - prescribed in preelampsia

Answer 73

A

cephalization of pulm vessels (diameter of upper lobe vessels > lower lobe vessels), Kerley B lines (edema of interlobular septa)

cocaine can cause acute decompensated heart failure

Answer 74

A

acts on M2 and M3 receptors

vasodilates via NO release

Answer 75

A

due to TGs (not cholesterol)

chylomicrons - TGs that you eat

less than 3% cholesterol in chylomicrons
have to fast to get an accurate TG level, but not to get an accurate cholesterol and HDL level

VLDL is what we make in the liver from G3P

Answer 76

A

increased pCO2 in tissues –> increased pH in erythrocytes

H+ buffered on histidine residues on Hb - stabilize deoxygenated Hb –> decreased affinity for O2

Answer 77

A

NE: a1 > a2 > b1 –> increased MAP (widened pulse P) –> reflex bradycardia
= CO unchanged/changed
- use in hypotension, septic shock

isoproterenol: b1 = b2&raquo_space; a –> increase HR and vasodil (decreased MAP)
= everything but MAP is increased, pulse pressure widens more than with NE or epi
- use to evaluate tachy, can worse ischemia

epi: b > a, doesnt increase HR as much as NE, b2 > a1
= all parameters increased
- a effects predominate at high doses

Answer 78

A

contractile function is normal, diastolic function is decreased

Answer 79

A

aka innominate vein

Answer 80

A

subclavian artery is stenosed proximally to the origin of the vertebral artery

most pts are asymptomatic
- when symptoms occur –> arm ischemia or vertobasilar insufficiency (dizziness, vertigo, drop attacks)

retrograde flow through vertebral artery on the affected side - because of the lower pressure in the subclavian downstream of the stenosis

coronary -subclavian steal phenomenon

in pts who have had coronary bypass surgery with internal mammary artery graft
blood flow through the IMA reverses during increased demand
chest pain

Answer 81

A

breach of all 3 layers of the blood vessel –> hematoma outside the vascular wall, held “in” by the surrounding CT

Answer 82

A

atherosclerosis –> aortic aneurysm

HTN –> dissection

Answer 83

A

reversible competitive a-antagonist
- drug can still get to Vmax (if you increase the concentration enough)

compare to phenoxybenzamine - irr a-agonist
= will decrease Vmax

Answer 84

A

urgency >180/120 and no end-organ damage

hypertensive emergency
- end organ damage - papilledema, hemorrhage/AKI (elevated serum creatinine)/ACS, encephalopathy

Answer 85

A

seen during severe systolic dysfunction - pulse with 2 peaks

hyperkinetic pulse - rapidly rising pulse with high amplitude
- aortic regurg, high CO

Answer 86

A

biventricular pacemaker

lead in RA, lead in RV
lead in AV groove on posterior face of heart

Answer 87

A

occurs upon necrosed tissue - ex aortic valve

aortic sclerosis - benign calcifications in elderly
aortic stenosis - occurs over time

in the setting of hypercalcemia - calcium will deposit on alkaline tissues
- kidneys, lungs, systemic arteries, gastric mucosa

Answer 88

A

antianginal drug
inhibits late phase inward Na channels in ischemic myocardial cells - during cardiac repolarization

less Na - slows down Na/Ca exchanger –> less intracellular calcium –> reduces myocardial O2 consumption

Answer 89

A

moderate increases in capillary fluid transudation can be offset by a compensatory increase in lymphatic drainage

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Cardiac Flashcards

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