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29 Cards in this Set

  • Front
  • Back
Describe the embryonic formation of the foramen ovale?
1. septum primium grows towards endocardial cushions closing ostium primum
2. ostium secundum forms in septum primium
3. septum secundum migrates downward leaving septum primum at the bottom for a valve
What do the following structures become in the adult heart (HINT: Draw it out):
1. sinus venosus
2. truncus arteriosus
3. bulbus cordis
4. primative ventricle
1. sinus venosus: R-smooth R heart/L-coronary sinus
2. truncus arteriosus-outflow tracts of aorta/pulmonary a.
3. bulbus cordis: R ventricle
4. primative ventricle: L ventricle
Where does fetal hematopoesis occur and what are the timelines for this? (4)

What are the two components of the ventricular septum?
Yolk Sac (2 months in), Liver, Spleen, Bone marrow (2 weeks out)

1. muscular septum (inferior)
2. membranous septum from aorticopulmonary septum
What chemicals keep the PDA open or closed?

What causes the normal closure of the foramen ovale?
open: prostaglandins
closed: indomethacin

↓in pulmonary resistance causes ↑L atrial blood flow and pressure which closes the one way valve
1. What is the ductus arteriosus? What adult remnant does it become?
2. What is the ductus venosus? What adult remnant does it become?
3. What does the notochord become?
1. arteriosus: shunt pulm artery → aorta; becomes ligamentum arteriosum
2. venosus: shunt umbillical v. to → vena cava; becomes ligamentum venosum
3. pulp of the vertebrae
1. How many umbilical arteries and veins are there? Oxygenated or deoxygenated?
2. Where do the umbilical arteries originate in the fetus?
1. Two Arteries Deox (TAD); One Vein Ox (OVA)
2. Originate from the internal illiacs
1. What are the adult remnants of the umblical vein?
2. What are the adult remnants of the umbilical arteries?
3. What are the adult remnants of the allantointois
1. ligamentum teres
2. medial umbilical ligaments
3. median umbilical ligament
Draw/Diagram/List the derivatives of the aortic arches?
SEE SHEET
1. Draw/diagram/list the derivatives of the aortic arches?
2. Which coronary artery supplies the anterior septum?
3. What is the most posterior portion of the heart? What can enlargement of this portion cause?
1. See your sheet
2. LAD
3. L atrium: horseness/dysphagia
1. Draw the arteries that supply the heart
2. How does a ASD present on auscultation?
1. SEE SHEET
2. ↑pulmonic flow murmer (early) → pulmonic regurgitation (later as pulmonary artery dilates to accomodate pressures)
1. How does the heart cause ↑CO in early exercise and late exercise?
2. What is MAP equation?
3. What is another term for preload?
4. What is another term for afterload?
1. early: ↑SV, late: ↑HR
2. 2/3 diastolic + 1/3 systolic
3. End Diastolic volume
4. Mean Arterial Pressure (MAP)
1. What is the mechanism of digitalis?
2. Compare action of venodilators and vasodilators on the cardiovascular system?
3. What is a normal EF?
1. digitalis blocks the Na/K+ pump → ↑intracellular Na+ inhibits the Na+/Ca+2 pump → ↑Ca+2
2. veno: ↓preload, vaso: ↓afterload
3. >60%
1. What section of the cardiovascular system provides the greatest amount of resistance?
2. Apply Ohm's Law to the heart?
3. What does the starling curve graph?
1. arterioles which regulate capillary beds
2. MAP = TPR X CO
3. EDV(preload) versus CO
1. What does a cardiac/vascular curve plot? DRAW it and give the 2 lines and the x-intercept meaning?
2. What are the causes of wide splitting S2? (2)
1. SEE SHEET
2. pulmonic stenosis or RBBB
1. What causes S3?
2. What causes S4?
3. What causes fixed splitting of S2?
1. S3=fluid overload (sloshing during diastole)
2. S4=stiff ventricle (atrial kick against ventricle)
3. Atrial Septal Defect (ASD)
What are the causes of the following points in the JVP wave: (HINT: DRAW IT)
1. a wave
2. c wave
3. v wave
1. a wave: atria contracting
2. c wave: tricuspid bulge during ventricular contraction
3. v wave: filling against closed tricuspid
1. Describe paradoxical splitting?
2. What are the causes of paradoxical splitting of S2? (2)
3. Describe a mitral stenosis murmur?
1. at rest, split; on inspiration, P2 approaches A2
2. LBBB or aortic stenosis
3. opening snap (after S2), partial-diastolic murmur
1. What pathology is most likely to be associated with mitral prolapse murmur?
2. Describe a mitral regurgitation murmur?
3. Describe an aortic stenosis murmur?
1. infective endocarditis
2. holosystolic, at apex radiating to axilla
3. ejection click, partial systolic crescendo/decrescendo radiating up neck
1. What is an opening snap?
2. What is an ejection click?
3. What is a midsystolic click?
1. opening snap: mitral valve opening during mitral stenosis
2. ejection click: aortic valve opening during aortic stenosis
3. mitral valve prolapsing
Compare a PDA murmur and a VSD murmur?
PDA: continuous/machine like (P=part of the time)
VSD: holosystolic/harsh
What is the channel responsible for the plateau during Phase 2 of the cardiac action potential? What is another name for it?
L-type Ca+2 channel aka voltage-gated Calcium receptor
1. Draw the cardiac myocyte action potential and the currents responsible for it?

2. What is Wolff-Parkinson-White syndrome?

3. How is WPW seen on EKG?
1. SEE SHEET

2. Accessory pathway from atria to ventrical causes ventricular pre-excitation

3. delta wave before QRS
1. Draw the pacemaker action potential and the currents responsible for it?

2. What is the name of the accessory pathway in WPW syndrome?

3. What is Prinzmetal's angina? What drug is used to treat it?
1. SEE SHEET

2. Bundle of Kent

3. angina at rest d/t coronary artery vasospasm; nifedipine
1. What are the S/S of cinchonism? (4)
2. What phase of the cardiac AP do class I anti-arrhythmias effect?
3. What is the antidote to digoxin toxicity?
1. QRST: QT Prolongation, Ringing ears, Sore head, Thrombocytopenia
2. phase 0 (upstroke)
3. magnesium
What tissues/arrhythmias tend to be treated with the following drug classes?
1. IA
2. IB
3. IC
4. IV
1. 1A: supraventricular/ventricular
2. 1B: ischemic ventricular
3. 1C: supreventricular/ventricular
4. AV node sensitive
1. Describe the specificities of the following drugs: verapamil, nifedipine, and diltiazem?

2. What is the mechanism by which B-blockers alter cardiac myocyte activity?
1. cardiac: V>D>N
vascular: N>D>V

2. Gs→ ↑cAMP → ↑PKA → phosphorylates Ca+2 channels → ↑Ca+2
1. What is the "dig effect" seen on EKG? (3)

2. What are the normal pressures in each of the cardiac chambers?
1. ↓QT/↑PR/scooping ST

2. RA: 5 (nickle), LA: 10 (dime), RV: 25 (quarter), LV: 125 (dollar)
1. What is the pulmonary capillary wedge pressure a good indicatio of?

2. What metabolites cause autoregulation of brain bloodflow?

3. What metabolites cause autoregulation of heart bloodflow?
1. L atrium function

2. brain: pH/CO2

3. heart: O2/NO
Name the different classes of anti-arrhythmic drugs?
I: Na+ channel Blockers
II: B-Blockers
III: K+ blockers
IV: Ca+2 blockers