2/21 Flashcards
Primitive pulmonary vein
smooth part of left atrium
Left horn of sinus venosus
coronary sinus
Right horn of sinus venosus
smooth part of right atrium
What is the first functional organ in vertebrate embryos?
-what week does it start functioning?
- heart
- week 4
When does cardiac looping happen?
-what can go wrong here?
- week 4
- Kartagener syndrome & dextrocardia
What fuses to make the membranous IV septum
- muscular interventricular septum
- aorticopulmonary septum
- little by the endocardial cushions
Where is a VSD most commonly seen?
-membranous IV septum
What are all the heart valves derived from?
-endocardial cushions
4 places that fetal erythropoiesis happens.
- Yolk sac (3–8 weeks)
- Liver (6 weeks–birth)
- Spleen (10–28 weeks)
- Bone marrow (18 weeks to adult)
*Young Liver Synthesizes Blood.
ductus venosus
-what does this bypass?
-Bypasses hepatic circulation. Blood shunted to IVC instead.
What is the formane ovale called after it closes?
-fossa ovalis
Where was most of the PGE1 & PGE2 coming from that kept the ductus artiosus open?
-placenta
# of umbilical arts? # of umbilical veins?
- 2 umb. arts
- 1 umb vein.
Umbilical vein
Ligamentum teres hepatis
-Contained in falciform ligament.
UmbiLical arteries
MediaL umbilical ligaments
Ductus arteriosus
Ligamentum arteriosum
Ductus venosus
Ligamentum venosum
AllaNtois
Urachus-mediaN umbilical ligament
- The urachus is the part of the allantoic duct between the bladder and the umbilicus.
- Urachal cyst or sinus is a remnant.
Notochord
Nucleus pulposus of intervertebral disc
which coronary art supplies the SA & AV nodes?
RCA
Right/Left dominant heart depends on whether or not its the RCA or LCX gives off which art?
Posterior descending art.
-85% of time its RCA = right dominant.
LAD occlusion: which leads STEMI?
V1-V3
Ficke principle
CO = rate of O2 use/(arterial O2 - venous O2)
Extracellular sodium conc.
-relationship to inotropy of heart?
- Na/Ca exchanger. Pumps Ca out in exchange for bringing a Na into cell down its conc. gradient.
- The less extracellular sodium = less this pump works b/c of the dec. Na gradient = more Ca stays in the cell = more contractility of cardiac myocyte.
- pretty much same thing as digitalis/digoxin except thats inc. the intracellular Na to dec. the conc. gradient to slow down the Na/Ca pump to inc. intracellular Ca.
- blocks the Na/K ATPase
Effect of acidosis on heart inotropy?
-acidosis decreases heart contractility.
Afterload equation:
Wall tension =
wall tension = (pressure * radius)/(2*wall thickness)
Ejection fraction
- in systolic failure
- in diastolic failure
- systolic failure = dec.
- diastolic failure = same
Spherocytosis
-does it inc. or dec. viscosity of blood?
-inc.
Whats the period of highest O2 consumption by the heart?
-isovolumentric contraction of left ventricle.
a wave
-positive wave
atrial contraction
c wave
-positive wave
beninning of RV contraction
-blood rushes against the close tricuspid valve, which pushes in a little and causes inc. pressure in LA.
x descent
- negative wave
- atrial relaxation. last half of RV contraction.
- downward displacement of closed tricuspid valve during RV contraction. Blood rushes past it and little vacuum forms and pulls the tricuspid down a little.
- this is absent in tricuspid regurg.
which wave is absent in tricuspid regurg?
x descent
which wave is absent in afib?
a wave
v wave
- positive wave
- filling of RA against closed tricuspid valve
y descent
- negative wave
- blood flow from RA to RV.
- so obviously the pressure is decreasing in the RA.
What causes wide splitting?
- wide splitting = P2 more delayed than usual.
- doesn’t have to do w/inspiration.
- due to dec. RV emptying; pulm stenosis, right bundle branch block.
- inspiration still delays P2 a little
Fixed splitting seen in what?
- ASD
* inspiration has no effect on P2 splitting. Thats why its called “fixed”.
Paradoxical splitting: P2 before A2
- delayed LV emptying. So A2 happens after P2.
- so during inspiration, P2 still delayed, but now moves closer to (but still before) A2 as opposed to farther away and after it.
- this = paradoxical.
- ie. aortic stenosis
Where do you hear?
- aortic stenosis
- aortic regurg
- aortic stenosis = right sternal border
- aortic regurg = left sternal border
Where do you hear
-hypertrophic cardiomyopathy
- left sternal border
- 3rd rib space
Where do you hear
-VSD
- tricuspid area
- left sternal border
- 4th/5th rib space
Hand grip (inc. systemic resistance/pressure) -increases intensity of which murmurs?
- VSD
- Mitral regurg
- aortic regurg
Valsalva
-stimulates which nerve?
-vagus nerve.
-
Occlusion of which artery leads to papillary muscle infarct?
-papillary muscle infarct can lead to what murmur?
- RCA
- mitral regurg.
Where does aortic stenosis murmur radiate to?
-“Pulsus parvus et tardus” - whats that mean?
- carotids
- “pulses are weak with a delayed peak.”
Whats the most frequent valvular lesions?
mitral valve prolapse
Valsalva
reduces venous return!
- dec. intensity of most murmurs since less volume/pressure in all chambers.
- will however inc murmur of hypertrophic cardiomyopathy.
where is the highest BP in the whole body?
LV
Mitral stenosis:
- S2-OS interval, what is it?
- what shortens that interval?
The higher the early left atrial diastolic pressure, the earlier the opening snap will be.
- The mitral valve opens the moment the pressure in the left atrium is higher than the pressure in the left ventricle.
- So if the pressure in the left atrium is higher then the opening snap will occur sooner.
-the more severe the stenosis, the higher the steady state left atrium pressure in early diastole, and the shorter the S2-OS interval.
Machine-like murmur
PDA
Name a failure of fusion
hypospadias
-failure or urethral folds to close
anterior or posterior: aorta vs pulm art?
- LV = posterior so makes sense that aorta = posterior.
- pulm art = anterior.
Beta error
-concluding that there is no difference when in actuality there is.
Sudden deceleration/blunt aortic trauma: which part of aorta most likely damaged?
- aortic isthmus
- right by where ligamentum arteriosum attached.
isoprotenerol
non selective beta agonist
Lipofuscin
result of free radicals & lipid peroxidation
-organellar membrane components - mostly lipids.
Hearts response to volume overload?
eccentric hypertrophy
-dilation
Which drug has class 3 AA activity + beta-blocking activity?
Sotalol
Fenoldopam
D1 agonist (no alpha or beta activity)
- D1 = Gs = vasodilates smooth muscle
- also causes renal natriuresis.
Gs effect on smooth muscle?
vasodilation/relaxation
Nicardipine
dihydropyridine calcium channel blocker
-vascular smooth muscle.
Where are beta-1 receptors found?
- cardiac tissue
- renal juxtaglomerular cells (afferent arteriole)
- NOT on vascular tissue
Ventricular gallop
S3
diaphragm or bell of stethoscope
- high freq
- low freq
- S1/S2
- S3
- high freq = diaphragm
- low freq = bell
- S1/S2 = high freq = diaphragm
- S3 = low freq = bell.
How do u accentuate S3 sound?
left lateral decubitus
-fully exhale
Is a thin fibrous atheroma plaque good or bad?
bad, not stable. Can rupture.
-a rich lipid core also makes it more likely to rupture.
Cardiac tissue conduction velocity
-Fastest to slowest
Park at ventura ave.
- purkinje = fastest
- atrial muscle
- ventricular muscle
- av node = slowest
ventricular action potential
-phase 0
- rapid upstroke
- QRS complex
ventricular action potential
-phase 2
- Ca influx
- plateau = ST segment
- Ca influx triggers Ca release from SR => myocyte contraction.
Which phase of ventricular AP is myocyte contraction?
phase 2: opening of Ca channels.
-the plateau.
How does PKA and Gs (ie. beta-1) cause inc. in HR?
PKA increases rate at which Ca is sequestered back into sarcoplasmic reticulum from cytosol. Increasing this rate will decrease the relaxation rate of the myocytes which will allow them to contract again sooner. So PKA -> inc rate of Ca sequestration -> dec myocyte relaxation rate -> inc. HR.
*SERCA = pumps Ca into SR. Phospholamban inhibits SERCA. PKA phoshos phospholamban and inhibits it. So PKA inhibits the inhibitor.
SO: beta-1 inc. PKA action = inc. rate of cardiac myocyte relaxation = inc. chronotropy/HR.
Nodal phase 0: influx of what?
Ventricular myocyte phase 0: influx of what?
- nodal = Ca influx @ threshold potential
- ventricular myocyte = Na influx @ threshold potential
Which phases are present in nodal action potential?
0, 3, 4
slope of which phase determines HR?
-slope of phase 4 in SA node.
ACh/adenosine: action on phase 4 (diastolic depolarization).
- dec. slope of phase 4 in SA node.
- this decreases the HR.
Catecholamines: action on phase 4 (diastolic depolarization).
- inc. slope of phase 4 in SA node.
- this increases the HR.
- basically increases chances that If channels are open, which increases the phase 4 slope.
ST segment correlates to which phase?
phase 2 = plateau, when myocytes are all depolarized for like 100-200 ms or something.
T wave correlates to which phase?
T wave = ventricular repolarization = phase 3 (rapid K efflux)
QRS complex correlates to which phase?
QRS complex = ventricular depolarization = phase 0.
-Na rushes in.
Which tissues does ANP act on?
- kidneys: dilate afferent arteriole, inhibit Na resorption, inhibit renin.
- adrenals: inhibit aldo secretion
- vasculature: vasodilate arts/veins
Niacin side effects
- flushed face, relieved w/aspirin
- hyperuricemia
- hyperglycemia (can lead to acanthosis nigricans)
arterial baroreceptors
- more or less firing w/higher BP?
- what happens when you massage them?
- higher BP = more firing = more inhibition of sympathetic drive = para takes over = vasodilation.
- massaging them stimulates high BP so u get vasodilation.
- these afferents terminate in solitary nucleus of medulla.
Wolf parkinson white
-QRS wider or more narrow?
- wider due to the delta wave
- it will become narrow if it forms a re-entrant circuit and causes tachy.
