Cardio Flashcards
what does the truncus arteriosus give rise to
ascending aorta and pulmonary trunk
what does the bulbus cordis give rise to
smooth parts (outflow tract) of LV and RV
what does the primitive ventricle give rise to
trabeculated LV and RV
what does the primitive atria give rise to
trabeculated LA and RA
what does the left horn of sinus venosus (SV) give rise to
coronary sinus
what does the right horn of SV give rise to
smooth part of right atrium
what does the right common cardinal v.and right anterior cardinal v. give rise to
SVC
fetal erythropoiesis in yolk sac
3-10 weeks
fetal erythropoiesis in liver
6 weeks - birth
fetal erythropoiesis in spleen
15-30 weeks
fetal erythropoiesis in bone marrow
22 weeks - adult
fetal hemoglobin
alpha 2 gamma 2
adult hemoglobin
alpha 2 beta 2
umbilical vein
ligamentum teres heptatitis - falciform ligament
umbilical arteries
medial umbilical ligaments
ductus arteriosus
ligamentum arteriosum
ductus venosus
ligamentum venosum
foramen ovale
fossa ovalis
allantois
urachus - median umbilical ligament
urachus - allantoic duct (bladder-umbilicus)
allantois remnant
urachal sinus/cyst
notochord
nucleus pulposus of IV disc
most common site of coronary a. occlusion
LAD
what supplied SA and AV node
RCA
what determines heart domination
posterior descending/interventricular a.
when do coronary a. fill
diastole
most posteiror part of heart?
LA
LA enlargements
compress esophagus –> dysphagia
compress L. recurrent laryngeal n. (vagus) –> hoarseness
what to listen to at aortic area
systolic murmur - aortic stenosis, flow murmur, aortic valve stenosis
what to listen to at left sternal border
diastolic murmur - aortic and pulmonic regurg
systolic murmur - hypertrophic cardiomyopathy
what to listen to at pulmonic area
systolic ejection murmur - pulmonic stenosis, flow murmur (ASD, PDA)
what to listen to at tricuspid area
pansystolic murmur - tricuspid regurgitation, VSD
diastolic murmur - tricuspid stenosis, ASD
what to listen to at mitral area
systolic murmur - mitral regurg
diastolic murmur - mitral stenosis
where to listen to a PDA and what it sounds like
left infraclavicular region - machine-like murmur
inspiration effect –>
RILE
increase intensity right heard sounds
expiration effect –>
RILE
increase intensity left heart sounds
what does handgrip cause
increase systemic vascular resistance
hand grip effect –>
increase intensity MR, AR< VSD murmurs
decrease intensity AS, hypertrophic cardiomyopathy mumurs
MVP - increase murmur intesnity - later onset of click/murmur
what does valsava cause
decrease venous return
valsava effect –>
decrease intensity of most murmurs
increase intensity of hypertrophic cardiomyopathy mumurs
MVP - decrease murmur intensity - earlier onset click/murmur
what does rapid squatting cause
increase venous return, increase preload, increase afterload with PROLONGED squatting
rapid squatting effect –>
decrease intensity of hypertrophic cardiomyopathy mumurs
MVP - increase murmur intensity, later onset click/murmur
what are the systolic heart sounds
aortic/pulm stenosis, mitral/tricuspid regurg, VSD
what are the diastolic heart sounds
aortic/pulm regurg, mitral/tricuspid stenosis
holosystolic high pitched blowing murmur
MR/TR
crescendo-decrescendo systolic ejection murmur following ejection click
AS
holosystolic, harsh-sounding murmur
VSD
late systolic crescendo murmur with midsystolic click
MVP
immediate high-pitched blowing diastolic decrescendo murmur
AR
follows opening snap –> delayed rumbling late diastolic murmur
MS
continuous machine-like murmur
PDA
what enhances MR
increase TPR (squat/hand grip) or LA return (expiration)
what enhances TR
increase RA return (inspiration)
where is MR the loudest and where does it radiate
apex –> radiates to axilla
what causes MR
ischemic heart disease, MVP, or LV dilation
where is TR the loudest and where does it radiate
tricuspid area –> radiates to right sternal border
what causes TR
RV dilation
what can can either MR or TR
rheumatic fever and infective endocarditis
what causes ejection click in AS
abrupt halting of valve leaflets
AS
LV > aortic P in systole
where does AS radiate
carotids
pulsus parvus et tardus
AS - pulses are weak with a delayed peak
what can AS lead to
SAD - syncope, angina, and dyspnea on exertion
AS cause
age-related calcific aortic stenosis or bicuspid aortic valve - WEAR AND TEAR
where is VSD the loudest
tricuspid area
what accentuates VSD
hand grip manuever –> increased afterload
what causes midsystolic click in MVP
sudden tensing of chordae tendinae (parachute)
what is the most freq valvular lesion
MVP
where is MVP best heard
apex
loudest just before S2
MVP
benign and can predispose to infective endocarditis
what can cause MVP
myxomatous degeneration, RF, or chordae rupture
what does MVP occur earlier with
manuevers that decrease venous return - standing or valsava
AR
chronic - wide pulse pressure (hyperdynamic circulation)
can present with bounding pulses and head bobbing
AR
what causes AR
aortic root dilation, bicuspid aortic valve, endocarditis, or RF
what increases AR murmur
hand grip
what decreases intensity of AR murmur
vasodilators
what causes opening snap in MS
abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips
MS
LA > LV pressure during diastole
what does MS often occur secondary to
rheumatic fever
chronic MS presentation
LA dilation
what enhances MS
manuevers that increase LA return (expiration)
where is PDA the loudest
S2
what causes PDA
congenital rubella or prematurity
what is best heard at left infraclavicular area
PDA
continuous machine-like murmur
PDA
what causes R –> L shunts
**early cyanosis - blue babies
Tetralogy of Fallot, Transposition, Truncus arteriosus, Tricuspid atresia, TAPVR (total anomalous pulm venous return)
what causes L –> R shunts
**late cyanosis - blue kids
VSD > ASD > PDA
what is the most common cause of early cyanosis
tetralogy of fallot
what do most patients with persistent truncus arteriosus have
VSD
hypoplastic RV
tricuspid atresia
what is the most common congenital cardiac anomaly
VSD
flixed splitting S2
ASD
how do you close PDA
indomethacin - decrease prostaglandins (PGE - keeeeps PDA open)
fetal alcohol syndrome
VSD
what does eisenmergers syndrome cause
late cyanosis, clubbing + polycythemia
what does tetralogy of fallot consist of
PROVe - pulmonary infundibular stenosis, RVH, overriding aorta, VSD
what is the most important determinant for tetralogy of fallot prognosis
pulmonary infundibular stenosis
boot shaped heart on xray
tetralogy of fallot
maternal diabetes
D-transpition of great vessels
infantile coarctation of aorta
proximal to insertion of PDA
adult coarctation of aorta
distal to ligamentum arteriosum
turners syndrome
infantile coarctation of aorta
adult coarctation of aorta sx
collateral circulation –> notching of ribs
UE - hypertension, LE - weak pulses
22q11 syndromes
truncus arteriosus, tetralogy of fallot
Down syndrome
ASD, VSD, AV septal defect (endocardial cushion defect)
congenital rubella
septal defects, PDA, pulmonary artery stenosis
turner syndrome
coarctation of aorta (preductal)
marfans syndrome
aortic insufficiency + dissection (late complication)
infant of diabetic mother
transposition of great-vessels
definition of HTN
> 140/90
definition of malignant HT
> 180/120
calcification in media of a.
monckeberg arteriosclerosis
fibrous plaques/atheromas in intima of a.
atherosclerosis
where do you see hyaline arteriolosclerosis
essential HTN and diabetes mellitus
***HYALINE = PINK
onion skinning in malignant HTN
hyperplastic arteriolosclerosis
incidental finding on mammogram
monckeberg arteriosclerosis
foam cells + fatty streaks
atherosclerosis
coronary a. occlusion order
LAD > RCA > circumflex
gold standard during first 6 hours of MI
ECG
MI dx
troponin I
MI reinfarction dx
CK-MB
transmural infarct
increase necrosis
affects entire wall
subendocardial infarcts
ischemic necrosis < 50% of ventricle wall
subendocardium espec. vulnerable to ischemia
transmural infarct ECG
ST elevation, Q waves
subendocardial infarct ECG
ST depression
LAD infarct - anterior wall
V1-V4
LAD infarct - anteroseptal
V1-V2
LCX infarct - anterolateral
V4-V6
LCX infarct - lateral wall
I, avL
RCA infarct - inferior wall
II, III, aVF
cardiomyopathy associated with systolic dysfunction
dilated
cardiomyopathy associated with diastolic dysfunction
hypertrophic and restrictive/obliterative
cause of sudden death in young athletes
hypertrophic cardiomyopathy
most common primary cardiac tumor in adults
myxoma
most common location of myxoma
left atrium - ball valve obstruction
most common primary cardiac tumor in kids
rhabdomyoma
what is rhabdomyoma associated with
tuberous sclerosis
asian children < 4 y/o
kawasaki disease
heavy male smokers < 40 y/o
buerfers disease
positive HBsAg
polyarteritis nodosa
wegeners granulomatosis triad
focal necrotizing vasculitis, necrotizing granulomas in lung + upper airway, necrotizing glomerulonephritis
positive p-ANCA
microscopic polyangiitis and churg strauss syndrome
positive c-ANCA
wegeners granulomatosis
henoch-schonlein purpura
URI –> IgA complex deposition –> childhood systemic vasculitis
henoch-schonlein purpura triad
skin - palpable purpura of butt/legs
arthralgia
GI - abdominal pain, melena, multiple lesions of same age
elevated IgE
churg-strauss syndrome
IgA nephropathy association
henoch-schonlein purpura
essential HTN tx
diuretics, ACE inhibitors, ARBs, CCB
CHF tx
diuretics, ACE inhibitors/ARBs, B-blockers (compensated CHF), K+ sparing diuretics
DM tx
ACE inhibitors/ARBs, CCB, diuretics, B-blockers, alpha-blockers
protective vs. diabetic nephropathy
ACE inhibitors
Ca+ channel blockers
nifedipine, verapamil, diltiazem, amlodipine
CCB MOA
block voltage gated L-type Ca channels of cardiac and smooth muscle –> reduce muscle contractility
CCB for vasc smooth muscle
amlopdipine = nifedipine > diltiazem > verapamil
CCB for heart
verapamil > diltiazem > amlodipine = nifedipine
VERAPAMIL = VENTRICLE
CCB clinical use
htn, angina, arrhythmias (not nifedipine), prinzmetal’s angina, raynaud’s
CCB toxicity
cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation
hydralazine MOA
increase cGMP –> smooth muscle relaxation
vasodilate arterioles > veins
reduce afterload
hydralazine clinical use
severe htn, CHF
first line - htn in preggers with methyldopa
freq coadminister w/ beta-blocker to prevent reflex tachycardia
hydralazine toxicity
compensatory tachycardia, fluid retention, nauseua, headache, angina, lupus-like syndrome
CI - angina/CAD
malignant htn tx drugs
nitroprusside, nicardipine, clevidipine, labetalol and fenoldopam
nitroprusside
short acting
increase cGMP via direct release NO
releases cyanide –> can cause cyanide toxicity
fenoldopam
dopamine D1 receptor agonist - coronary, peripheral, renal and splanchnic vasodilationg
decrease BP and increase natriuresis
nitroglycerin and isosorbide dinitrate MOA
release NO into smooth muscle –> increase cGMP –> smooth muscle relaxation = vasodilation veins > arteries
decrease preload
nitroglycerin and isosorbide dinitrate clinical use
angina, pulmonary edema
nitroglycerin and isosorbide dinitrate toxicity
reflex tachycardia, hypotension, flushing, headache
monday disease
nitroglycerin and isosorbide dinitrate toxicity
in industrial exposure - develop tolerance for vasodilating action during work week + lose tolerance over weekend –> tachycardia, dizziness and headache upon reexposure
goal of antianginal tx
decrease EDV, BP, HR, contractility, or ejection time –> reduce myocardial O2 consumption
nitrates vs. angina
PRELOAD
decrease - EDV, BP, Ejection time, MVO2
increase HR and contractility via reflex response
b-blockers vs. angina
AFTERLOAD
decrease - BP, contractility, HR, MVO2
increase - EDV and ejection time
nitrates and beta-blockers vs. angina
really decrease MVO2
decrease HR and BP
little/no effect on ejection time/contractility
no effect or decrease EDV
pindolol and acebutolol
partial beta-agonists CI in angina
CCB similar to nitrates/Bblockers
nifedipine - similar to nitrates in effect
verapamil - similar to b-blockers in effect
HMG-CoA reductase inhibitors
lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
HMG-CoA reductase inhibitors effect on LDL
DECREASE DECREASE DECREASE
HMG-CoA reductase inhibitors effect on HDL
increase
HMG-CoA reductase inhibitors effect on TG
decrease
HMG-CoA reductase inhibitors MOA
inhibit conversion of HMG-CoA –> mevalonate (cholesterol precursor)
HMG-CoA reductase inhibitors SE
hepatotoxicity - increase LFTs
rhabdomyolysis
Niacin
Vitamin B3
Niacin effect on LDL
DECREASE DECREASE
Niacin effect on HDL
INCREASE INCREASE
Niacin effect on TG
decrease
Niacin MOA
inhibits lipolysisin adipose tissue
reduce hepatic VLDL secretion into circulation
NIacin SE
red flushed fash - decrease by aspirin / long-term use
hyperglycemia - acanthosis nigricans
hyperuricemia - exacerbates gout
bile acid resins
cholestyramine, colestipol, colesevelam
bile acid resins effect on LDL
DECREASE DECREASE
bile acid resins effect on HDL
slightly increase
bile acid resins effect on TG
slightly increase
bile acid resins MOA
prevent intestinal reabsorption of bile acids
liver must use cholesterol to make more
bile acid resins SE
patients HATE it - tastes bad and causes GI discomfort, decrease absorption of fat-soluble vitamins
cholesterol gallstones
cholesterol absorption blockers
ezetimibe
ezetimibe effect on LDL
DECREASE DECREASE
ezetimibe MOA
prevent cholesterol reabsorption at SI brush border
ezetimibe SE
rare - increase LFT’s, diarrhea
fibrates
gemfibrozil, clofibrate, bezafibrate, fenofibrate
fibrates effect on LDL
decrease
fibrates effect on HDL
increase
fibrates effect on TG
DECREASE DECREASE DECREASE
fibrates MOA
upregulate LDL –> increase TG clearance
fibrates SE
myositis, hepatotoxicity (increase LFTs), cholesterol gallstones
cardiac glycoside
digoxin
digoxin MOA
direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchange –> increase intracellular calcium –> positive isotropy
stimualtes vagus nerve –> decrease HR
digoxin clinical use
CHF - increase contractility
atrial fibrillation - decrease conduction at AV node and depress SA node
digoxin toxicity
cholinergic - N&V, diarrhea, blurry yellow vision (van goh)
ECG - increase PR, decrease QT, ST scooping, T-wave inversion, arrhythmia, AV block
poor prognostic indicator = hyperkalemia
factors predisposing to digoxin toxicity
renal failure - decrease excretion
hypokalemia -digoxin bdining K+ binding site on Na/K ATPASE
quinidine - decrease clearance - displace digoxin
digoxin antidote
slowly normalize K+, lidocaine, cardiac pacera, anti-digoxin Fab fragments, Mg2+
antiarrhythmics class I
Na+ channel blockers
local anesthetics
slow/block conduction in depolarized cells
decrease slow phase 0 depol
increase threshold for firing in abnormal pacemaker cells
state depemdent - selectively depress tissue that is freq depolarized (tachycardia)
what causes increase toxicity for all class I drugs
hyperkalemia
Class IA antiarrhythmics
quinidine, procainamide, disopyramide
Class IA MOA
increase AP duration, effective refractory period, and QT interval
atrial and ventricular arrhythmias - reentrant and ectopic supraventricular and ventricular tachycardia
quinidine toxicity
cinchonism - headache, tinnitus
class IB antiarrhythmics
lidocaine, mexiletine, tocainide
class IB MOA
decrease AP duration
pref affect ischemic or depolarized purkinje and ventricular tissue
used in acute ventricular arrhythmias (post-MI) and digitalis-induced arrhythmias
class IB toxicity
local anesthetic, CNS stimulation/depression, CV depression
class IC antiarrhythmics
flecainide, propafenone
class IC MOA
no effect on AP duration
useful in ventricular tachycardia that progress to VF and in intractable SVT
last resort in refractory tachyarrythmias - pts w/o structural abnormalities
class IC toxicity
proarrhythmic, especially post-MI (CI)
significantly prolongs refractory period in AV node
procainamide toxicity
reversible SLE-like syndrome
disopyramide toxicity
heart failure
class IA toxicity
thrombocytopenia, torsades de pointes due to increase QT interval
IB is best…
post-MI
IC is contraindicated…
structural heart disease and post-MI
class II antiarrhythmics
beta-blockers –> metoprolol, propanolol, esmolol, atenolol, timolol
class II MOA
decrease cAMP and decrease CA current –> decrease SA and AV nodal activity
decrease slope of phase 4 - suppress abnormal pacemakers
AV node particularly sensitive - increase PR interval
very short acting class II
esmolol
class II toxicity
impotence, exacerabtion of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). may mask signs of hypoglycemia
metoprolol toxicity
dyslipidemia
metoprolol overdose tx
glucagon
propanolol toxicity
can exacerbate vasospasm in prinzmetal’s angina
class III antiarrhythmics
K+ channel blockers - amiodarone, ibutilide, dofetilide, sotalol
class III MOA
increase AP duration, ERP
used when other antiarrhythmics fails
increase QT interval
sotalol toxicity
torsades de pointes, excessive beta block
ibutilide toxicity
torsades
amiodarone toxicity
pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (40% iodine by weight), corneal deposits, skin deposits (blue/gray) –> photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF)
alters lipid membrane - has class I-IV effects
amiodarone
what do you check when using amiodarone
PFTs, LFTs, TFTs
class IV antiarrhythmics
Ca+ channel blockers - verapamil and diltiazem
class IV antiarrhythmics MOA
decrease conduction velocity, increase ERP and PR interval
used in prevention of nodal arrhythmias (SVT)
class IV toxicity
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
adenosine MOA
increase K+ out of cells –> hyperpolarize the cell + decrease intracellular calclium
very short acting (15 seconds)
drug of choice in dx/abolishing supraventricular tachycardia
adenosine
adenosine toxicity
flushing, hypotension, chest pain
effects blocked by theophylline and caffeine
effective in torsades de pointes and digoxin toxicity
Mg2+
