CV Flashcards
ascending aorta arises from?
truncus arteriosus
pulmonary trunk arises from?
truncus arteriosus
smooth mm/outflow of left and right ventricles arises from?
bulbus cordis
trabeculated part of left and right atria arises from?
primitive atrium
trabeulated part of left and right ventricles arises from?
primitive ventricle
smooth part of left atrium arises from?
primitive pulmonary v
coronary sinus arises from?
left horn of sinus venosus
smooth part of right atrium arises from?
right horn of sinus venosus
SVC arises from?
right common cardinal v and right ant cardinal v
when does heart start to beat?
we 4
patent foramen ovale
d/t failure of septum primum and septum secundum to fuse after birth
VSD
most commonly occurs in membraneous septum
conotruncal abnormalities
transposition of great vessels
tetralogy of fallot
persisten truncus arteriosus
aortic and pulmonary valves arises from?
endocardial cushions of outflow tract
mitral and tricuspid valves arise from?
fused endocardial cushions of AV canal
fetal erythropiesis
young liver synthesizes blood yolk sac 3-8wks liver 6wk-birth spleen 10-28wk bone barrow 18wk+
hemoglobin
alpha always
gamma goes
becomes beta
fetal hemoglobin
alpha2 gamma2
higher affinity for O2 d/t lower affinity for 2,3 BPG
what do you give to close PDA
indomethacin
what do you give to keep PDA open?
PGs E1 and E2
median umbilical ligament arises from?
allantois -> urachus
ligamentum arteriosum arises from?
ductus arteriosus
ligamentum venosum arises from?
ductus venosus
foramen ovale arises from?
fossa ovalis
nucleus pulposus arises from?
notochord
medial umbilical ligament arises from?
umbilical aa
ligamentum teres hepatis arises from?
ligamentum hepatis in falciform ligament
SA and AV nodes get blood from?
RCA
right dominant circulation
PDA from RCA
85%
most posterior part of heart?
left atrium -> enlargement = dysphagia or horseness
CO
SVxHR
or
rate of O2 consumption/ (aaO2-vvO2)
MAP
COxTPR
or
2/3DP + 1/3SP
early exercise
CO maintained by increased HR and SV
late exercise
CO maintained by increased HR only
what does increased HR d/t diastole?
shortens it d/t increased filling time -> decreased CO
increased pulse pressure
hyperthyroidism
aortic regurg
aortic stiffening (isolated systolic HTN of elderly)
obstructive sleep apnea (increased sympathetics)
exercise (transient)
decreased pulse pressure
aortic stenosis
cardiogenic shock
cardiac tampenade
advanced heart failure
contractility increases d/t
catecholamines (increased Ca pump on SR)
increased intracellular Ca
decreased extracellular Na (decreased Na/Ca exchanger)
digitalis (blocks Na/K pump -> increased intracellular Na -> decreased Na/Ca exchange -> increased Ca
contractility decreased d/t
B1 blockade (decreased cAMP) HF w/systolic dysfunction acidosis hypoxia/hypercapnia non-dihyydropyridine Ca Ch blockers
Myocardial oxygen demand
increased myoCARDial O2 demand increased Contractility increased Afterload increased heart Rate increased Diameter of venticle (wall tension)
wall tension
(pressure x radius) / 2x wall thickness
preload
approximated by ventricular EDV
decreased by venodilators (nitroglycerin)
afterload
approximated by MAP
vasodilators (hydralazine) decrease afterload
what decreases both preload and afterload?
ACEI and ARBs
EJ
SV/EDV (EDV-ESV)/EDV normal 55% decreased in systolic HF normal in diastolic HF
increased afterload
increased aortic pressure
decreased SV
increased ESV
loop is tall and skinny
increased preload
increased SV
loop gets wider to the right
increased contractility
increased SV
increased EF
decreased ESV
loop gets wider to the left
S1
mitral and tricuspid valve closure
loudest at mitral
S2
aortic and pulmonary valve closure
loudest at left upper sternal border
S3
in early diastole during rapid ventricular filling phase
associated with increased filling pressures
mitral regurg
HF
more common in dilated ventricles
normal in prego and kids
S4
in late diastole, atrial kick
apex in LLD
high atrial pressure
ventricular hypertrophy
a wave
Atrial contraction
absent in a-fib
c wave
RV Contraction
d/t closed tricuspid valve bulging into atrium
x descent
atrial relaXation and downward displacement of closed tricuspid valve during ventricular contraction
absent in tricuspid regurg
v wave
increased right atrial pressure d/t villing against closed tricuspid
y descent
RA emptying into RV
normal splitting
inspiration -> decreased intrathoracic pressure -> increased venous return -> increased RV filling -> increased RV SV -> increased RV ejection time -> delayed closure of pulmonic valve
wide splitting
daled RV empyting
pulmonic stenosis
RBBB
present during exhalation but exaggerated in inspiration
fixed splitting
same in inhalation and exhalation
ASD -> L to R shunt - increased RA and RV volumes -> increased flow thru pulmonic
paradoxical splitting
conditions that delay aortic valve closure
aortic stenosis
LBBB
pulmonic closes before aortic
inspiration
increased intensity of R heart sounds
handgrip
increases afterload
increased MR, AR, VSD murmurs
decreased hypertrophic cardiomyopathy murmurs
MVP: later onset of click/murmur
valsalva phase II, standing up
decreased preload
decreased intensity of most murmurs
increased intensity of hypertrophic cardiomyopathy
MVP: earlier onset of click
rapid squatting
increased VR and increased preload
decreased intensity of hypertrophic cardiomyopathy
increased intensity of AS
MVP: later onset of click
AS
C/D systolic ejection murmur
LV»aortic pressure
aortic listening post -> radiates to carotids
pulsus parcus et tardus (weak pulse w/delayed peak)
SAD- syncope, angina, dyspnea on exertion
age related calcification or bicuspid valve
MR/TR
holosystolic high-pitched blowing murmur
RF or infective endocarditis can cause either
MR
loudest at mitral post, radiates to axilla
ischemic heart disease (post-MI)
MVP
LV dilation
TR
tricuspid post radiates to R sternal border
RV dilation
MVP
mitral valve prolapse
late systolic crescendo murmur w/midsystolic click
most frequent w/valvular lesion
mitral post
loudest just before S2
benign, predispose to infective carditis
can be caused by myxomatous degeneration (CT disease), RF, chordae rupture
VSD
holosystolic
harsh
loudest at tricuspid
AR
high pitched blowing early diastolic decrescendo murmur
long diastolic murmur and signs of hyperdynamic pulse when serve and chronic
often d/t aortic root dilation, bicuspid aortic valve, endocarditis, RF
progresses to LHF
MS
follows opening snap delayed rumbling late diastolic murmur LA>>LV pressure during diastole RF can lead to LA dialation
PDA
continuous machine like murmur
loudest at S2
congenital rubellla or prematurity
best heard at left intraclavicular area
PR interval
QRS
speed of conduction
purkinje >atria > ventricles > AV node
pacemakers
SA >AV >bundle of His > purkinje/venticles
conduction pathway
SA -> atria -> AV -> common bundle -> bundle brr -> fasicles -> purkinje fibers -> ventricles
torsades de pointes
long QT predisposes:
drugs
decreased K and increased Mg
Tx with Magenesium sulfate
drug induced long QT
ABCDE anti Arrhythmics (class IA, III) aBx (macrolides) anti Cychotics (haloperidol) anti Depressants (TCAs) anti Emetics (odansetron)
congenital long QT
usually d/t ion ch defects
increased risk of SCD
romano-ward syndrome
jervell and lange-nielsen syndrome
romano-ward syndrome
AD
long QT
pure cardiac phenotype
jervell and lange-nielsen syndrome
AR
long QT
sensoineural deafness
brugada syndrome
AD
asian males
pseudo RBBB and ST elevation in V1-3
increased risk of ventriculat tachy and SCD
prevent SCD w/implantable cardioverter-defibrillator
wolff-parkinson-white
MC type of ventricular pre-excitation syndrome
bundle of kent - abnormal fast accessory conduction pathway from atria -> ventricle
widened QRS
delta wave
can cause supraventricular tachy
atrial natriuretic peptide
atrial myocytes
acts via cGMP
vasodilation and decreased Na resorption in renal collecting tubules
brain natriuretic peptide
ventricular myocytes
via cGMP
longer half life the ANP
used to Dx HF (very good neg predictive value)
