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fetal erythropoiesis
Young Liver Synthesizes Blood: Yolk sac (3-8wks), Liver (6wks-birth), Spleen (10-28wks), Bone marrow (18wks-adult)
allantois ->
urachus -> median umbilical ligament. urachus = part of allantoic duct between bladder and umbilicus
ductus arteriosus ->
ligamentum arteriosum
ductus venosus ->
ligamentum venosum
foramen ovale ->
fossa ovale
notochord ->
nucleus pulposus
umbilical arteries ->
medial umbilical ligaments
umbilical vein ->
ligamentum teres hepatis (contained in falciform ligament)
SA and AV nodes supplied by
RCA (usually)
LCX supplies
posterolateral LV, anterolateral papillary muscle
LAD supplies
anterior 2/3 of interventricular septum, anterolateral papillary muscle, anterior LV
PDA supplies
posterior 1/3 of interventricular septum, posterior walls of ventricles, posteromedial papillary muscle
right marginal artery supplies
RV
in 85%, PDA arises from
RCA
inc. pulse pressure in
hyperthyroid, AR, aortic stiffening, OSA, exercise
dec. pulse pressure in
AS, cardiogenic shock, cardiac tamponade, advanced HF
normal splitting
inspiration -> dec. intrathoracic P -> inc. venous return -> inc. RV filling -> inc. RV stroke volume -> inc. RV ejection time -> delayed pulmonic closure. pulm circulation also has inc. capacity during inspiration.
wide splitting
in conditions that delay RV emptying: PS, RBBB. = exaggeration of normal splitting
fixed splitting
in ASD! -> L-R shunt -> inc. RA + RV volumes -> inc. flow through pulmonic valve so that closure is always greatly delayed, regardless of breath
paradoxical splitting
in conditions that delay aortic valve closure: AS, LBBB. normal order is reversed, P2 sound is before A2, so when P2 is pushed back by inspiration, split is eliminated.
murmurs: inspiration
inc. venous return to RA -> louder R heart sounds
murmurs: hand grip
inc. afterload -> louder MR, AR, VSD; quieter hypertrophic cardiomyopathy murmur; later click in MVP.
murmurs: valsalva, standing up
dec. preload. most murmurs, including AS, get quieter. hypertrophic cardiomyopathy murmur gets louder. earlier click in MVP.
murmurs: rapid squatting
inc. venous return, inc. preload -> quieter hypertrophic cardiomyopathy murmur, louder AS murmur, later click in MVP
phase 0 - myocardial AP
rapid upstroke and depolarization - V-gated Na channels open
phase 1 - myocardial AP
initial repolarization - inactivation of V-gated Na channels. V-gated K channels start opening.
phase 2 - myocardial AP
plateau - Ca influx through V-gated Ca channels balances K efflux. Ca influx triggers Ca release from SR and myocyte contraction
phase 3 - myocardial AP
rapid repolarization - massive K efflux due to opening of V-gated slow K channels and closure of V-gated Ca channels
phase 4 - myocardial AP
resting potential - high K permeability through K channels
myocardial AP differences from skeletal AP
has a plateau, contraction is due to Ca-induced Ca release from SR.
funny current
responsible for automaticity. slow, mixed Na-K inward current
phase 0 - pacemaker AP
upstroke - opening of V-gated Ca channels. fast B-gated Na channels are permanently inactivated b/c of less neg resting V of these cells -> slow conduction v that is used by AV node to prolong transmission from atria to ventricles
phase 1, 2 - pacemaker AP
absent
phase 3 - pacemaker AP
inactivation of Ca channels and inc. activation of K channels -> K efflux
phase 4 - pacemaker AP
slow spontaneous diastolic depolarization as Na conductance increases (Ifunny). the slope of phase 4 determines HR. ACh/adenosine dec. diastolic depolarization rate and HR, catecholamines inc. depolarization and HR. sympathetic stimulation increases Ifunny.
J point
junction between end of QRS complex and start of ST seg
U wave
caused by hypokalemia, bradycardia.
drug-induced long QT mnemonic
ABCDE: antiArrhythmics (class IA, III), antiBiotics (e.g. macrolides), anti”C”ychotics (e.g. haldol), antiDepressants (e.g. TCAs), antiEmetics (e.g. ondansetron)
torsades de pointes
causes: long WT, drugs, dec. K, dec. Mg. Tx: mag sulfate
romano-ward syndrome
AD cause of congenital long QT. pure cardiac phenotype (no deafness)
jervell, lange-nielsen syndromes
AR causes of congenital long QT, sensorineural deafness
brugada syndrome
AD, often asian males. peudo-RBBB, ST elevations in V1-V3. inc. risk of V tach + SCD. Tx: ICD
WPW
most common type of ventricular pre-excitation. abnormal fast accessory pathway (bundle of Kent) bypasses rate-slowing AV node -> early depolarization -> delta wave, widened QRS, short PR interval. can -> SVT (reentry circuit)
ANP
released from atrial myocytes in response to inc. blood V and atrial P. acts via cGMP -> vasodilation and dec. NA reabsorption at renal collecting tubule. dilates afferent renal arterioles, constricts efferent arterioles -> diuresis. part of aldosterone escape mechanism.
BNP
released from ventricular myocytes in response to inc. T. similar physiologic action to ANP but longer 1/2 life. can be used to Dx and Tx HF.
aortic receptors
transmitted via vagus to solitary nucleus of medulla. respond to dec. and inc. in BP
carotid sinus receptors
trasmitted via glossopharyngeal nerve to solitary nucleus of medulla. respond to dec. and inc. in BP
carotid massage
inc. P on carotid sinus -> inc. stretch -> inc. afferent baroreceptor firing -> inc. AV node refractory period -> dec. HR
peripheral chemoreceptors
carotid and aortic bodies = stimulated by dec. PO2 (<60mmHg), inc. PCO2, and dec. blood pH.
central chemoreceptors
stimulated by changes in pH and PCO2 of brain interstitial fluid (influenced by arterial CO2). not directly related to PO2.
V1-V3 ST elevations/Q waves
anteroseptal (LAD)
V3-V4 ST elevations/Q waves
anteroapical (distal LAD)
V5-V6 ST elevations/Q waves
anterolateral (LAD or LCX)
I, aVL ST elevations/Q waves
lateral (LCX)
II, III, aVF ST elevations/Q waves
inferior (RCA) (can -> papillary muscle rupture)
myxoma
most common adult primary cardiac tumor. 90% in atria L>R). ball-valve obstruction associated w/syncope. can -> “tumor plop” sound.
rhabdomyoma
most common child primary cardiac tumor. associated w/tuberous sclerosis. usually in ventricle.
angiosarcoma
rare blood vessel malignancy. head, neck, breast. usually elderly, sun-exposed. radiation and chronic post-mastectomy lymphedema inc. risk. hepatic ones associated w/vinyl chloride (PVC pipe) and arsenic. aggressive
bacillary angiomatosis
benign capillary skin papules in AIDS pts. cause by bartonella henselae. looks like kaposi but w/neutrophilic infiltrate
cherry hemangioma
benign capillary hemangioma of elderly. does not regress. inc. frequency w/age.
cystic hygroma
cavernous lymphangioma of neck. associated w/turners
glomus tumor
benign, painful, re-blue tumor under fingernails. arises from modified smooth muscle cells of thermoregulatory glomus body
kaposi sarcoma
endothelial malignancy most commonly of skin, but can be mouth, GI, respiratory. associated w/HHV-8. looks like bacillary angiomatosis but w/lymphocytic infiltrate.
pyogenic granuloma
pollypoid capillary hemangioma that can ulcerate and bleed. associated w/trauma and pregnancy
strawberry hemangioma
benign capillary hemangioma of infancy. appears early in life. grows rapidly, regresses spontaneously by 5-8yrs.
takayasu arteritis
usually asian females weak UE pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances. granulomatous thickening and narrowing of aortic arch and proximal great vessels. Tx: steroids
polyarteritis nodosa
young adults. hep B seropositivity in 30%. Sx: fever, wt. loss, malaise, h/a, abd. pain, melena, HTN, neuro Sx, cutaneous eruptions, renal damage. LUNG = SPARED. IC-mediated. fibrinoid necrosis. string-of-pearls. Tx: steroids, cyclophosphamide
buerger dz (thromboangiitis obliterans)
heavy smokers. males gangrene, autoamputation of digits, superficial nodular phlebitis. raynauds. segmental thrombosing vasculitis. Tx: smoking cessation.
granulomatosis w/polyangiitis
we”c”ener: upper respiratory tract: perf. nasal septum, chronic sinusitis, otitis media, mastoiditis. lower respiratory tract: hemoptysis, cough, dyspnea. renal: hematuria, RBC casts. triad: focal necrotizing vasculitis, necrotizing granulomas in lung/upper airway, necrotizing glomerulonephritis. “c”-ANCA. Tx: “c”yclophosphamide, “c”orticosteroids.
microscopic polyangiitis
necrotizing vasculitis involving lung, kidneys, skin. pauci-immune glomerulonephritis and palpable purpura. looks like wegeners but w/o nasopharyngeal involvement. no granulomas, no eosinophilia. p-ANCA. Tx: cyclophosphamide, steroids.
churg-strauss
asthma, sinusitis, skin nodules/purpura, neripheral neuropathy (wrist/foot drop). can also involve heart, GI, kidneys (pauci-immune glomerulonephritis), lungs. granulomatous, necrotizing vasculitis w/eosinophilia. p-ANCA, inc. IgE.
HSP
most common childhood systemic vasculitis. often follows URI. triad: palpable purpura, arthralgia, abd. pain. 2/2 IgA immune complex deposition. associated w/IgA nephropathy (Berger dz).
hydralazine
MoA: inc. cGMP -> smooth muscle relaxation -> arteriolar vasodilation -> dec. afterload. often used w/BB to prevent reflex tachycardia. side effects: tachycardia, fluid retention, h/a, angina, lupus-like syndrome
nitroprusside
short acting, inc. cGMP via direct release of NO. can cause cyanide toxicity
fenoldopam
DA D1 receptor agonist: coronary, peripheral, renal, and splanchnic vasodilation. dec. BP, inc. natriuresis.
nitrates
vasodilate by inc. NO in vascular smooth muscle -> inc. in cGMP -> smooth muscle relaxation. dilate veins»_space; aterires. dec. preload. toxicity: reflex tachycardia, hypotension, flushing, h/a. “monday dz” in industrial exposure: tolerance during work week, then tachycardia, dizzines, h/a on monday.
bile acid resins (e.g. cholestyramine)
dec. LDL, slightly inc. HDL and TGs. MoA: prevent intestinal reabsorption of bila acids; liver must use cholesterol to make more. side effects: GI upset, dec. fat-soluble absorption.
ezetimibe
dec. LDL, no effect on HDL, TG. MoA: prevent cholesterol absorption at small intestine brush border. side effects: rare inc. LFTs, diarrhea.
fibrates
dec. TGs, slightly dec. LDL, inc. HDL. MoA: upregulate LDL -> inc. TG clearance. activates PPAR-alpha to induce HDL synthesis. side effects: myopathy (inc. risk w/statins), cholesterol gallstones
niacin
dec. LDL, inc. HDL, slight dec. TGs. MoA: inhibits lipolysis (hormone-sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis. side effects: red, flushed face (dec. w/NSAIDs or long-term use). hyderglycemia, hyperuricemia.
class IA antiarrhythmics
quinidine, procainamide, disopyramide
class IA MoA
inc. AP duration, inc. effective refratory period in ventricular AP, inc. QT interval. dec. slope of phase 0 (Na current)
class IA use
both atrial and ventricular arrhythmias, esp. re-entrant and ectopic SVT and VT
class IA toxicity
cinchonism (h/a, tinnitis w/quinidine), reversible SLE-like Sx (procainamide), HF (disopyramide), thrombocytopenia, torsades de pointes due to inc. QT
class IB antiarrhythmics
lidocaine, mexiletine, (+ phenytoin sortof)
class IB MoA
dec. AP duration. preferentially affect ischemic or depolarized purkinje and ventricular tissue. dec. slope of phase 0.
class IB use
acute ventricular arrythmias (esp. post-MI). dig-induced arrhythmias
class IB toxicity
CNS stimulation/depression, CV depression
class IC antiarrhythmics
flecainide, propafenone
class IC MoA
sig. prolongs ERP in AV node and accessory bypass tracts. no effect on ERP in purkinje and ventricular tissue. minimal effect on AP duration. dec. slope of phase 0.
class IC use
SVTs, inc. a fib. last resort in refractory VT
class IC toxicity
proarrhythmic, esp. post-MI.
class II antiarrhythmics
beta-blockers!
class II MoA
dec. SA and AV node activity by dec. cAMP, dec. Ca currents. suppress abnormal pacemakers by dec. slope of phase 4.
class II use
SVT, ventricular rate control for atrial fibrillation and atrial flutter
class II toxicity
impotence, exacerbation of COPD/asthma, CV effects *bradycardia, AV block, HF), CNS effects (sedation, sleep alterations). may mask hypoglycemia signs. Tx overdose w/saline, atropine, glucagon.
class III antiarrhythmics
K channel blockers: amiodarone, ibutilide, dofetilide, sotalol.
class III MoA
inc. AP duration. inc. ERP, inc. QT. markedly prolonged repolarization (K current)
class III use
a fib, a flutter, VT (amio, sotalol).
class III toxicity
sotalol: torsades, excessive beta-blockade. ibutilide: torsades. amio: pulm. fibrosis, hepatotoxicity, thyroid issues, acts as hapten (deposits in skin/cornea), neuro effects, constipation, CV effects (bradycardia, heart block, HF). amio: check PFTs, LDTs, TFTs. it is also lipophilic and has class I, II, III, and IV effects
class IV antiarrhythmics
Ca channel blockers: verapamil, dilt
class IV MoA
dec. conduction velocity, inc. ERP, inc. PR interval. slow rise of AP, prolonged repolarization.
class IV use
prevention of nodal arrhythmias (e.g. SVT), rate control in a fib
class IV toxicity
constipation. flushing, edema, CV effects (HF, AV block, SA node depression.
adenosine
inc. K out of cells -> hyperpolarizing the cell and dec. Ca current. drug of choice in Dx/Tx of SVT. very short action (~15sec). effects blunted by theophylline and caffeine (adenosine receptor antagonists). adverse effects: flushing, hypotension, CP, sense of doom, bronchospasm)
Mg
effective in torsades and dig. toxicity
