Cardiology Flashcards
First pharyngeal arch
CN V, maxillary artery
Second pharyngeal arch
CN VII, stapedial artery (regresses)
Third pharyngeal arch
CN IX, common carotid, prox internal carotid artery
Fourth pharyngeal arch
CN X, true aortic arch, subclavian arteries
5th pharyngeal arch
Oblitered!
6th pharyngeal arch
CN X (recurrent laryngeal), pulmonary arteries, ductus arteriosus
Down syndrome
endocardial cushion defects (ostium primum) ASD, regurgitant AV valves
DiGeorge
TOF, interrupted AA
Friedreich ataxia
Hypertrophic cardiomyopathy
Marfan
Cystic medial necrosis (dissection, aneurysm), MV prolapse. Cardiovascular dz most likely cause of death (esp aortic dissection)
Tuberous schlerosis
cardiac rhabdomyomas -> valvular obstruction
Turner
Aortic coarction, bicuspid valve
Vancomycin MOA, SE
blocks glycoprotein polymerization by binding to D-ala, D-ala; redman syndrome, nephrotoxicity
Daptomycin MOA, SE
Depolarization of bacterial (cannot penetrate GN bacteria outer cell membrane, is inactivated by lung surfactant); myopathy & CK elevation
Linezolid MOA, SE
Inhibit protein synthesis by binding to 50s subunit; thrombocytopenia, optic neuritis, serotonin syndrome
Post-MI: 0-4 hours
Minimal change
Post MI: 4-12 hours
Early coag necrosis: edema, hemorrhage, wave fibers
Post MI: 12-24 hours
Coag necrosis, marginal contraction band necrosis
Post MI: 1-5 days
Coag necrosis, PMN infiltrate
Post MI: 5-10 days
MO phagocytosis of dead cells
Post MI: 11-14 days
Granulation tissue, neovascularization
Post MI: 2 weeks - 2 months
Collagen deposition, scar formation
Local amyloid production: cardiac, thyroid, pancreatic islets, cerebrum/cerebral blood vessels, pituitary gland
atrial naturietic protein, calcitonin, islet amylin protein (TIID), beta-amyloid protein, prolactin
Systemic amyloid protein
IG light chain, esp gamma light chains; associated with MM
Malignancy re: exposure to arsenic, thorotrast, polyvinyl chloride; cells express CD-31 (PECAM-1)
Hepatic angiosarcoma from vascular endothelial cells
Familial chylomicronemia syndrome (Type I)
Lipoprotein lipase/ApoC-II (cofactor) defect; elevated chylomicrons; pw acute pancreatitis, eruptive skin xanthelomas, HSM, lepemia retinalis
Familial hypercholesterolemia (Type II A)
LDL receptor/ApoB-100 defect; elevated LDL; pw premature CAD, corneal acrus, tendon xanthomas, xanthelesmas
Familial dysbetalipoproteinemia
ApoE; chylomicrons/LDL; pw premature CAD/PVD, palmar xanthelomas
Familial hypertriglyceridemia
ApoA-V; VLDL; pancreatitis, obesity/insulin resistance
Atrial myxoma
preference for LA; mid-diastolic rumble; histo: scattered cells w/ mucopolysaccharide stroma; VEGF & IL6
Sx of wide pulse pressure
head pounding, head bobbing
m/c cause of AR
aortic root dilatation, bicuspid aortic valve
CABG: LAD alone, multile arteries
Left internal mammary; great saphenous vein
IVDU endocarditis
R-side, TR, Staph A, early systolic murmur accentuated by inspiration
MI healing require what kind of collagen, when?
Type I; 2 weeks post-MI
Type II collagen
Cartilage, vitreous humor, nucleus pulposus
Type III collagen
skin, lung, GI, blood vessels, lympatic, granulomatous tissue
Type IV collagen
Basement membrane (Alport)
Niacin SE, mediated by, rx
Flushing, prostaglandin, aspirin
Vanc SE, mediated by
Redman syndrome, histamine
Capsaicin MoA
Decrease pain by decreasing substance P
Digoxin toxicity induced by; rx
hypokalemia, hypovolemia, renal failure; anti-digoxin antibody fragments
Heart sound: Loud P2
Pulmonary HTN
Post-MI complication days 3-7
Rupture LV free wall
TOF/truncus arteriosus/TGV embryology
NC cells migrate into truncus arteriosus and bulbar ridges to induce aorticopulmonary septation
Nitroglycerin MoA
venodilator of large veins, reduces pre-load and oxygen demand to rx angina pectoris
Arterial baroreceptors: where? nerves?
Carotid, glossopharyngeal; aortic arch, vagus nerve
atrial myoxoma pw, histo, cytokines
large pedunculated mass on LA with mid diastolic rumble @ apex, SOB w/ sitting up, fever; scattered cells with mucopolysaccharide stroma, abnormal blood vessels, hemorrhage; VEGF (angiogenesis), IL-6 (weight loss, fever)
AR pw, etiology
Early diastolic murmur (if severe, holodiastolic) with palpitations, head pounding, head bobbing; aortic root dilatation, bicuspid aortic valve
CABG: vessel source if LAD alone, multiple arteries
left internal mammary; great saphenous vein (surgeons access the vein inside femoral triangle)
R-side tricuspid regurgitation moa, pw
IV drug use, staph endocarditis; early systolic, accentuated by inspiration
Vertebral levels at which IVC branches into renal veins, common iliac veins
L1/L2, L4
MI healing culminates in what type of collagen? how long does deposition last?
type I collagen, 1 week - 2 months
niacin-induced flushing mediated by what molecule? rx with what drug?
prostaglandin; aspirin
Digoxin toxicity induced by what situations?
hypokalemia, hypoveolemia, renal failure
Digoxin toxicity pw, rx
nonspecific GI (anorexia, N/V), neuro (confusion, fatigue, weakness, color vision change), arrhythmia (most dangerous); rx with anti-digoxin antibody fragments
constrictive pericarditis moa, pw
thick, fibrous tissue in percardial space that restricts ventricular filling during diastole, reduces CO, and causes RHF (kussmaul sign: JVP increases with inspiration); pw pulsus paradoxicus, pericardial knock, increased JVP
constrictive pericarditis etiologies
idiopathic, viral, cardiac surgery/radiation, tuberculosis
heart sounds: loud P2
pulmonary HTN
heart sounds: S3
dilated ventriclesdecreased ventricular wall compliance (intrinsic in restrictive cardiomyopathy, extrinsic in constrictive cardiomyopathy)
pulsus paradoxicus moa
during inspiration, increased systemic venous return; but if pericardium cannot expand (2/2 tamponade, constrictive/restrictive pericarditis, severe obstructive lung dz), then RV pushes into LV and CO/BP decreases
Post-MI rupture of LV free wall moa
days 3-7 after coagulative necrosis, PMN infiltration, and enzymatic lysis of connective tissue reduces stability
Asthma: beta-agonist, steroid moa
Stimulated beta-2 adrenergic receptor on lungs, stimulation of Gs receptor leads to increased activation of AC and increased cAMP; steroids impair eosinophilic degranulation
Recent respiratory illness may lead to what heart condition?
serous viral pericarditis, significant acute pericardial effusion, and tamponade
rheumatic heart dz most commonly affects what valve?
MV (but can affect both MV and AV in a quarter of cases)
tetrology of fallot pw and development
most common cause of cyanotic congenital heart disease (may not present in neonate if pulmonary stenosis is mild); in beginning, VSD allows L to R shut, thus infrequent cyanotic episodes; however, over time pulmonary HTN develops and R to L shunt leads to frequent cyanotic episodes
ToF, truncus arteriosis, TGV developmental misfortune
aorticopulmonary septation requires NC cells to migrate into truncal (truncus arteriosis) and bulbar ridges (bulbus cordis) in order to grow into the aorta and pulmonary artery; failure of this process
main myocardial energy source:
FA oxidation (60%), but FA oxidation requires more O2, produces more ATP, thus shift of FA to glucose oxidation can improve stable angina
longer QT means highe rrisk of torsades; which anti-arrhythmic, thought it increases QT interval, does not increase risk of torsades?
amiodarone
adenosine moa
binds to A1 receptors on cardiac cells and activates K+ channels and increases K+ clearance; results in transient conduction delay through AV and briefly treats SVT
nitrate limitation on use
around-the-clock administration results in tolerance; thus give nitrate-free interval at night
statins 2 moa, main se
- lower cholesterol, 2. stabilize atheromatous plaque (decrease chance of second MIA); risk of myositis (increased CK), myalgias (normal CK)
statin risk of myositis increases with which drugs?
niacin, fibrates
persistent lymphadema increases risk of what disease?
lymphangiosarcoma, rare malignancy of the endothelial lining of lymph system
cavernous hemangioma
benigh neoplasm of small blood endothelial cells
carvernous lympangioma
network of endothelium lined lymph spaces below epidermis
cystic hygroma
cavernous lympangioma + absence of luminla blood cells, common in H&N, turner’s syndrome
pyogenic granuloma
capillary form of cappilary hemangioma, exophitic red nodules attached by stalk to oral mucucosa and skin;
MS-related enlargement impinges on what nerve and causes what symptom?
L recurrent laryngeal nerve, hoarseness
PDA associated with what congenital dz?
rubella
ventricular septal defect associated with what pregnancy condition?
fetal alcohol syndrome
MVP increases or decreases with squatting?
decreases. squatting increases preload and PVR; thus it increases LV volume. this returns leaves to normal arrangement (in MVP, mitral redundancy occurs 2/2 elongation, overlap of leaflets).
native valve bacterial endocarditis (NVBE): most common etiology
MVP among 15-60 yo americans; upon which plt and fibrin deposit and is colonized by bacteria
nitroglycerin moa
converts to NO at vascular SM cell membrane; NO converts GTP to cGMP; increased cGMP decreases Ca in cytosol, which decreases activity of myosin LC kinase, myosin LC dephosphorylase; muscle relaxation
congenital QT prolongation: responsible mutation
K+ channel protein
After contraction, how does myocyte achieve Ca efflux?
Ca-ATPase (SR) and Na/Ca exchange mechanism (plasma membrane)
cystic medial degeneration moa, histology
myxomatous changes in the media of large arteries; fragmentation of elastic tissue (“basket weave”), separation of elastic/fibromuscular componenets that produce small cleft-like spots with amorphous ECM filling
lysyl oxidase fxn, required cofactor
cross-link collagen fibers, elastin; copper (Menkes)
organ susceptibility to infarction
CNS (5 min), myocardium (20-30 min), kidney (30 min), spleen, liver (less likely 2/2 dual blood supply, unless transplanted)
Class I anti-arrhythmic: binding strength to Na channel
1C>1A>1B
Anti-arrhythmic medication for ischemia-induced ventricular arrhythmias
1B (lidocaine, mexiletine, tocainide) as dissociation is rapid with minimal cumulative effective
ANP fxn
- kidney (increase diuresis); 2. adrenal gland (increase naturesis by inhibiting aldosterone secretion); 3. blood vessels (vasodilation)
Veramapil fxn, SE, c/i
rate control for A-fib with RVR; negative ionotrope (helpful for angina, HTN); bradycardia, AV block, constipation; CHF pt (2/2 negative ionotropic effect)
Which statin is not metabolized by P-450 system?
pravastatin
P-450 inducers
phenytoin, phenobarbitol, rifampin, griseofulvin, carbamazapine
P-450 inhibitors
macrolides (erythromycin/clarithromycin) , ketoconazole, isoniazid, cipro, grapefruit
turner’s syndrome: unusual findings
cystic hygroma (located in neck, cystic spaces rich in lymphoid tissue); aortic co-arction
atherosclerotic plaques, likely locations
aorta > coronary arteries > popliteal > internal carotid > circle of willis
muscular/elastic arteries
coronary, poplitleal/ aorta, carotid, iliac
hypertrophic cardiomyopathy mutation
AD mutations of sarcomere protein leads to deficiency in force generation
what is unique about staph a in infectious endocarditis?
sports a surface adhesion molecule that can invade intact valvular endothelium; thus, can affect pts without pre-existing valvular dz
embryology: vein development (vitilline, umbilical, cardinal)
vitilline - portal veins; umbilitcal veins - degenerate; and cardinal - systemic veins
furosemide moa, effect on K, Ca
at ascending limb, loop diuretic that blocks Na/K/2Cl symporter; decreases K, Ca
thiazide moa, effect on K, Ca
at distal tubule, blocks Na/Cl symporter; decreases K, increases Ca
amiloride moa, effect on K
block ENaC, at apical membrane of principal cells K sparing
primary pulmonary HTN
medial hypertrophy of arteries/arterioles, concentric laminar intimal fibrosis that reduces lumina
most common cause of cor pulmonale
COPD-related obliteration of segments of pulmonary vasculature
intimal injury 2/2 athersclerosis: key cytokines in reactive intimal hyperplasia
PDGH: encourage SMC migration, proliferation; VCAM: adherence of monocytes/lymphocytes
syndenham chorea moa
anti-strep antibodies cross-react w basal ganglia
TGA: moa, aorta position relative to pulmonary artery
failure of aorticopulmonary septum to spiral normally; aorta lying anterior to (normally posterior)
Gq pathway
activates phospholipase C, degrades membrane lipids into DAG (activate protein kinase C) or IP3 (release Ca from SR)
nitroprusside SE, rx
cyanide poisoning (altered mental status, lactic acidosis); rx with Na thiosulfate, which adds sulfate to liver rhodonase to help with metabolism
ebstein’s anomaly: what is it, what causes it
apical displacement of tricuspid valve, decreased RV volume, atrialization of RV; lithium
nitroglycerin + sildenafil
hypotension
milrinone moa
phosphodiesterase isoenzyme 3 inhibitor, increases conductance of Ca channels on SR at the heart; at the periphery, can lead to vasodilation so don’t use in hypotensive patient
ACE-I and bilateral renal artery stenosis
do not use ACE-I - can limit efferent arteriole constriction to maintain renal artery perfusion
aortic coarctation adults vs children
adults: stenosis is post-PDA; children: pre-PDA
pritzmetal angina: dx
ergonavine (ergot alkaloid that acts via alpha-adrenergic receptor to induce vascular smooth muscle constriction )
carcinoid heart dz: moa, why limited to R side?
fibrous intinal thickening and endocardial plaques; limited to R-heart because serotonin and bradykinin inactivated by pulmonary vascular endothelial monoamine oxidase
hemosiderin-laden MO in alveoli: histo, how to differentiate with lipofuschin (age-related byproducts of lipid oxidation)
golden-yellow/brownish cytoplasmic capsule; prussian blue stain (blue=hemosiderin)
normal aging and effect on heart macro/micro appearance
macro: decreased LV size 2/2 ventricular septum becoming sigmoidal; micro: increased interstitial CT with concomitant amyloid deposition (w/i myocites, progressive accumulation of lipofuscin)
PDA more likely with
prematurity, rubella
functional heart murmur
2/2 acute hemodynamic change
VSD: heart sound, pulse ox finding
loud, holosystolic murmur over LLSB with Sp02 difference between RA and RV
class III anti-arrhythmics
amiodarone, ibutilide, dofetilide, sotalol
dopamine low, medium, high dose effect
low: kidney (increased GFR, Na excretion); med: cardiac (increased contractility, SBP, pulse pressure via beta-1); high: vasculature (increased SVP, decreased CO 2/2 alpha-1 )
epi/phenylephrine difference
phenyl: pure alpha-1 (vasoconstriction, decreased HR); epi: added beta effect (increased SBP, decreased DBP, increased HR, increased contractility)
likelihood of plaque rupture is associated with
mechanical strength of overlying fibrous cap
cellular sign of irreversible cardiac injury
mitochondrial vacuolization: myofibril relaxation, polysome disaggregation, TG droplet accumulation
niacin SE
vasodilation (decrease HTN meds), insulin resistance (increase DM meds), increase uric acid (careful in gout)
digoxin deadly SE
AV block, ventricular tachyarrhythmias
digoxin electrolyte SE that reflects serum toxicity
hyperkalemia
class III antiarrhythmic with beta-adrenergic blocking abilityes and QT prolongation
sotalol
verapamil vs diltiazam
more cardioselective
TGF-beta
arrest of cell cycle, angiogenesis, stimulation of fibroblasts to lay down ECM
hypertrophic cardiomyopathy histo findings
myocyte hypertrophy, haphazard arranged myocyte and myocyte bundles and fibrosis in interstitial spaces
thiamine deficiency leads to what cardiac outcome
wet beriberi leads to DCM
acute rheumatic fever pw
pericarditis: weak heart sound, increased HR, pericardial friction rub, arrhythmias; myocarditis: dilatoin, MR and acute heart failure; chronic ARF: MS
aortic rupture occurs most often at what location?
isthmus, tethered by ligamentum arteriosum, relatively fixed/immobile place
BB overdose rx
glucagon (increased cAMP, Ca, independent of adrenergic receptors)
PE prefers what lobes?
lower lobes
isoprotenolol
nonselective beta agonst (beta 1: increased contractility, beta 2: vasodilation)
labetolol moa
combined alpha, beta blocker (beta 1 blocker: decreased contraction; beta2 blocker/alpha1 blocker: decreased SVR)
fenoldopam moa, function
rx for HTN emergencies, esp in pt with renal insufficiency; selective DA-1 agonist: at periphery, decreases blood pressure and at kidney, increases renal blood flow)
NE in peripheral vein causes what, and how to you reverse
extravation can cause vasoconstriction, induration/pallor of tissue; prevent with alpha-1 antagonist like phentolamine
congenital QT prolongation: two kinds
jervell and lange-nelson (AR) with neurosensory deficiency; romano-ward (AD) no deafness
congenital DCM moa
cardiac cell cytoskeleton (problem with force transfer) and mitchondrial enzymes of oxidative phosphorylation (problem of force generation)
spontaneous intracranial hemorrhage: m/c etiology
AVM, ruptured aneurysm, cocaine
What’s the basis of association between cerebral aneurysm and coarction of aorta?
HTN means more likely to rupture
hallmarks of lightning strike
lichtenburg figures (fern-leaf pattern erythema) + second degree burns; most common reason for death is arrhythmias, respiratory failure
acute pericarditis most common causes
MI, rheumatic fever, uremia, viral
embryo: truncus arteriosus
ascending aorta, pulmonary trunk
embryo: bulbus cordis
smooth part of L/R ventricles
embryo: primitive atrium
trabeculated part of L/R atria
embryo: primitive ventricle:
trabeculted part of L/R ventricles
embryo: primitive pulmonary vein
smooth part of left atrium
embryo: right horn of sinus venosus
smooth part of right eatrium
embryo: left horm of sinus venosus
coronary sinus
embryo: right common cardinal vein and right anterior cardinal vein
SVC
Defect in L/R dynein (Kartagener’s) affects what organ and what time in development?
looping of the primary heart tube at week 4
PFO moa
failure of septum primum and septum secundum to fuse
VSD moa
membranous septum
sequence of fetal erythropoiesis organs
yolk sac, liver, spleen, bone marrow
allantois/urachus
median umbilical ligament
foramen ovale
fossa ovalis
notocord
nucleus pulposus
umbilical arteries
medial umbilical ligaments
umbilical vein
ligamentum teres hepatis (in falciform ligament)
coronary blood flow peaks during
early diastole
arterioles provide most of; veins provide most of
TPR, blood storage capacity
organ remove has what effect on TPR and CO?
increase TPR and decrease CO
speed of conduction
purkinje > atria > ventricles > AV node
pacemaker pace
SA > AV > bundle of his/purkinje/ventricles
ABCDE of drugs that induce long QT
anti Arrhythmics (IA, III), antiBiotics (macrolides), anti Cychotics (e.g. haloperidol); anti-Depressants (TCA); antiEmetics (ondansetron)
rx for torsades
give magnesium sulfate
brugada syndrome
AD d/o of asian males, ECG shows pseudo-RBB with ST elevation in V1-V3; increased risk of ventricular tachyarrhythmias and SCD; preven with implantable cardioverter-defibrillator
WPW anatomic cause, pw, complication
abnormal fast accessory conduction pathway (bundle of Kent); delta wave, widened QRS, shortened PR; supraventricular tachycardia
lyme dz heart problemz
3rd degree heart block
BNP and ANP difference
BNP has longer half life
hypoxia: pulmonary vs systemic reaction
vasoconstriction (to move blood to well-perfused areas), vasodilation
ApoB-48
mediates chylomicron secretion (chylomicron)
ApoB-100
binds LDL receptor (VLDL, IDL, LDL)
ApoC-II
lipoprotein lipase cofactor (VLDL, chylomicron)
ApoA-I
activates LCAT (HDL, chylomicron)
ApoE
mediates remnant uptake (all but LDL)
dystrophic calfcification
hallmark of cell injury and necrosis; m/c in age/damaged cardiac valve or atheromatous plaques; pw fine, gritty white clumps with dark purple, sharp-edged granules on H&E
dofetelide moa
class 3 (K+ blocking in cardiac myocytes in phase 3)
ARF: aschoff bodies
interstitial granulomas in cardiac cells
ARF: anotschkov cells
macrophages with abundant cytoplasm and central nucleus that become aschoff giant cells
prostacycline synthesized by, role, disease
synthesized in capillary endothelium by prostacyclin synthase; maintain capillary patency by promoting vasodilation and inhibiting platelet adhesion; damaged endothelial cells can’t synthesized PG so increased risk of thrombus formation
beta-1 antagonist moa
receptors on cardiac and renal tissue (JG cells) that blocks catecholamine-induced renin release and inhibits RAS
digoxin moa
- slow depolarization and increase diastolic filling time; 2. reduced Na influx slows Ca efflux, thus allowing more Ca inside
Class 1C and Class III different effect on QT duration
1C prolong QRS more with high HR (“use dependence”); III prlonged more with low HR (“reverse use dependence”)
phentolamine moa
reversible, competitive non-specific alpha-antagonist used in catacholamine induced HTN crisis (pheo, MAOI crisis, cocaine)
phenoxybenzamine moa
irreversible non-specific alpha antagonist, used in pheo
very important difference between epi and NE
epi has more beta-2 effect than NE
hydralazine/minoxidal moa, SE
direct arterial vasodliators; tachycardia and edema
ulcertaed atherosclerotic plaque with partially obstructive thrombus leads to what conditions
UA, subendocardial MI, and sudden death
ruptured plaque with fully obstructed thrombus
transmural MI
Post-catheterization atheroembolic dz presents with
renal failure, toe gangrene, livedo reticularis; light microscopy showing cholesterol emboli obstructing renal arterioles
cilostazol 2 moa
decreased plt phosphodiesterase, increase cAMP, reduce plt aggregation; direct arterial vasodilator
churg-strauss moa
antibodies against PMN myeloperoxidase (p-ANCA); pw adult-onset asthma, eosinophilia, atopia, neuropathy
plt dysfunction
increased bleeding time, mucocutaneous bleeding
intrinsic/extrinsic coagulation pathway measured by
aPTT; PT
during exercise, what changes occur? what does not change? why?
increased CO, venous constriction, arterial constriction (all but muscles); MAP does not change; decreased SVR 2/2 vasodilation of muscle arterioles
myocardial “hibernation”
reduced metabolism 2/2 persistant hypoperfusion or reptitive ischemia
ventricular tachycardia: preferred treatment
amiodarone
drug-inced SLE
hyralazine, procainimide, isoniazide; positive ANA, anti-smith; negative dsDNA
HCM: obstruction etiology
abnormal systolic anterior motion of the anterior leaflet of MV toward hypertrophied interventricular septum
CXR findings of CHF
cardiomegaly, pleural effusion, kerley B lines (edema of intralobular septa)
NBTE etiology, pw
hypercoagulable state (2/2 pro-coagulant mucin of mucinous adenoma of pancreas/lungs); small, sterile, nondestructive fibrinous vegetations along the closure lines of cusps (bland thrombus without inflammation or valvular damage); if cancer-related, called “morantic”
Silly reason to get secondary pulmonary HTN
extended consumption of appetite suppresants like fenfluramine, phentemine
most common cause of death in MI patient pre-hospital, in-hospital
cardiac arrhythmia, ventricular failure
coagulase-negative staphlococcal infection of prosthetic valve is most likely what bacteria, and what is the rx?
S. epidermidis (polysaccharide slime); vanc with rifamin or gent
digeorge syndrome
maldevelopment of third/fourth branchial pouches 2/2 deletion on chromosome 22
precapillary spincters sensitive to
epi, NE; histamine, low Ox
AV block: origin of conduction
AV node
nitroprusside effect
balanced venous/arterial vasodilator
AVM effect on preload and afterload
increase preload, decrease afterload
eruptive skin xanthomas
hypertriglyceridemia
tendon xanthomas/xanthelasmas
hypercholesterolemia
thromboangiitis obliterans (buerger’s dz)
vasulitis of medium/smal arteries (tibial, radial); acute/chronic inflammation of arterial walls, thrombosis of lumen with recanalization; segmental, and fibrosis extends into contiguous veins and nerves
polyarteritis nodosa
transmural inflammatoin of the arterial wall
noncyanotic congenital heart defect
ASD, VSD, PDA, coarctation
within 60 seconds of the onset of total ischemia
loss of cardiomycocyte contractility
NO mechanism
stimulate GC, increase cGMP, decrease Ca, decrease myosin LC kinase, myosin LC dephosphorylation and smooth muscle relaxation
constrictive pericarditis: chronic or acute
chronic process
