CARDIO Flashcards
Truncus arteriosus gives rise to
ASCENDING AORTA
and
Pulmonary Trunk
Bulbus cordis gives rise to ?
smooth parts (outflow tract) of Left and Right ventricles
Endocardial cushion
give rise to?
atrial septum
membranous interventricular septum
AV and Semilunar valves
primitive Atrium
gives rise to?
trabeculated part of :left and right Atria
primitive Ventricle
gives rise to
Trabeculated (muscular) part of left and right Ventricles
Primitive pulmonary vein gives rise to
smooth part of left atrium
LEFT horn of sinus venosus
gives rise to?
Coronary sinus
RIGHT horn of sinus venosus
Smooth part of rigjt atrium (sinus venarum)
Right Common Cardinal vein and right anterior cardinal vein
give rise to
superior vena cava
pt with down syndrone and Atrial septal defect
this is commonly due to?
endocardial cushion defect
what is responsible for development of the outflow tract formation? for example the aorticopulmonary septum
Neural crest and endocardial cell migrations –> truncal and blbar ridges that spiral and fuse to form aorticopulmonary septum –> ascending aorta and pulmonary trunk
note the ascending aorta will be posterior
and the pulmonary trunk will be anterior.
conotruncal abnormalities associated wtih failure of neural crests cells to migrate (problem w/ developing spiral septum) ?
transposition of great vessels (RV –> aorta, LV –> PA)
tetraology of fallot
Persistent truncus arteriosus ( = partial spiral development)
mitral/tricupsid valves are derived from
fused endocardial cushions of the AV canal
what virus is associated with a continous machine-like murmur (during diastole and systole)
whats the mechanism of the virus?
treatment MOA?
Congenital Rubella
the virus infects smooth muscle cells that are needed for contraction of teh patent ductus arteriosus
Indomethacin: inhibits the formation of PGE2, via COX1 and 2 inibition.
what forms the mediaN umbilical ligament?
AllaNtois –> Urachus
the urachus is part of allantoic duct bw bladder and umbilicus.
the L recurrent laryngeal n. passes udner the ligamentum arteriosum which is a derivative of?
ductus arteriosus
what forms the MediaL umbilical ligament?um
umbiLical arteries
if given an MRI of a spin with an acute disc herniation, and you see a torn anulus fibrosus allowing the nucleus pulposes to herniate. what did the nucleus pulposes derive from?
Notocord.
occlusion of the RCA can lead to?
Nodal dysfunction –> bradycardia or heart block, fatal arrthymias
bc the RCA supplies the SA and AV nodes
pt has RCA infarct or Posterior descending A occlusion –> posteromedial papillary muscle rupture –> ?
new onset mitral regurgitation
54 yo F presents with Hoarsenss and dysphagia, hx of RHD whats the cause of the hoarseness and dysphagia?
RHD –> Mitral valve stenosis –> inc in LA size –> compression of esophagus (dysphagia) and compressed left recurrent laryngeal nerve (hoarsenss) which innvervates the intrinsic muscles of the larynx.
describe the antaomy position in terms of the aorta and esophagus and the laryngeal nerve position.
left atrium sits directly infront of esophagus
left recurrent laryngeal nere loops under the ligamentum arteriosum.
normal splitting of A2 P2 is caused by?
during inspiration –> inc in intrathoracic volume –> drop (-) intrathoracic pressure –> inc venous return –> inc RV filling (inc EDV) —> inc RV stroke volume –> inc RV ejeciton time –> delayed closure of pulmonic valve
Wide splitting is caused by
conditions that delay RV emptying (pulmonic stenosis, RBBB), anything that caused delayed contraction of RV
what is the most common cause of splitting that doesnt change regardless if your in expiration or inspiration.
ASD
ASD–> left -to - Right shunt –> Inc RA and RV volumes –> inc flow through pulmonic valve.
what is it called when listening to the heart you hear splitting of P2 and A2 on expiration but not on inspisiration
paradoxical splitting
this is caused by delay in aortic valve closure.
the reason why its eliminated during inspiration is that you still get your delayed closure of P2 during inspiration moving it close to A2 sound.
what are two caused of Paradoxical splitting
aortic stenosis
LBBB
anything that delays aortic valve closure.
rapid squatting causes inc or dec in
Venous return
preload
afterload
Inc venous return (bc squatting the muscels of lower extremities are compressing the vein inc VR)
inc preload (same as VR)
inc afterload (compressing the arteries in lower limbs inc afterload
rapid squatting increases what murmurs
inc AS, MR, and VSD murmurs
DEC: hypertrophic cardiomyopathy murmur
if someone is rapidly squatting when will you hear the clickl in MVP
Later onset of click/murmur
handgrip causes and inc in afterload
what murmurs will be increased vs dec
increased: MR, AR, VSD
dec: hypertophic cardiomyopathy, AS murmurs
MVP LATER onset of click
valsalva (phase II) standing up leads to a decrease in preload.
via inc in intrathoracic pressure –> dec venous return –> dec preload.
what murmurs will be inc and dec?
ALL MURMURS WILL BE DECREASED except
HYPERTROPHIC CARDIOMYOPATHY murmur increased
MVP will have an EARILER onset click **** ( Uworld)
in a Pacemaker AP (SA and AV nodes) what is phase 0 (upstroke) caused by
in contrast to ventricular Myocardial AP occuring in myocytes, bundle his and Purkinje fibers?
Ca influx (opening of voltage gated Ca2+ channels) causes the phase 0 upstroke. and the fast voltage gated NA channels are permanently inactivated bc of thee less negative resting potential of these cells.
in contrast to the fast voltage gated NA channels in phase 0 of Ventricular AP
the upstroke caused by influx of CA2+ allows for in pacemaker cells?
slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.
phase 1 and 2 of AP is absent in?
Pacemaker AP
what phase accounts for the automaticity of SA and AV nodes.?
phase 4 = slow spontaneous diastolic depolarizatiion due to If (“funny current”)
If channels responsible for a slow mixed NA/K inward current.
abnormal fast accessory conduction pathway from atria –> ventricle (bundle of Kent) bypasses the rate slowing AV node –> ventricles begin to partially depolarize.
most cocmmon type of ventricular pre excitation syndrome.
Diagnosis
WPW
Delta wave with widen QRS complex. and shortened PR interval
on ECG.
this may result in?
re-entry circuit –> supraventricular tachycardia
tx with procainamide or amiodarone
not adenosine
WPW
name some of the drugs that cause long QT (ABCDE)
AntiArrhythmics (class IA, III)
AntiBiotics (marcorlides)
anti Cychotics (haloperidol), risperidone
antiDepressants (TCAs)
AntiiEmetics (ondansetron)
what Congenital long QT syndrome
is autosomal Dominant
pure cardiac phenotype (only K channels in heart effected)
.NO deafness
Romano-Ward syndrome
what congenitial Long QT syndrome (disorder of myocardial repolarization)
is autosomal Recessive
Cardiac K+ channels + sensorineural deafness
Jervell and Lange- Nielsen syndrome
NA channel abnormality inherited in Asians (usually MALES)
ECG: pseduo-RBBB (QRS widen), ST elevations V1-V3
inc risk for sudden ventricular tachyarrrhythmias and SCD.
what is this syndrome and what parts of the -cardium does it effect?
Brugada syndrome
dec NA influx in Epicardium and Endocardium.
Asian decent with Pseudo RBBB and ST elevations iin V1-V3. what is the tx
Implantable cardioverter-defibrillator (ICD)
In stable angina what is your classic ECG findings
ST DEPRESSION
it resolves with rest, or nitroglycerin
pt is triggered by smoking, triptans, coccaine
occurs at rest
ECG: TRANSIENT ST ELEVATIONS.
what would you tx with and whats the diagnosis?
variant (prinzmetal) angina
tx: Ca channel blockers, nitrates, and smoking cessation
what is unstable angina due to?
unstable atherosclerotic plaque thats gonna rupture.
leads to thrombosis w/ incomplete coronary artery occlusion
what are the classic ECG and BIomarkers for unstable angina
+/- ST depresions, and or T-wave inversion
biomarkers: no cardiac biomarker elevation (unlike NSTEM)
pt will complain of inc frequency, duration, or intensity of chest pain, or chest pain at rest.
