Advanced Editing (pics/ sounds) Flashcards
(Heart embryo) What does the truncus arteriosis become?
Truncus Arteriosis—> The ascending aorta and the pulmonary trunk

(Heart embryo) What does the bulbous cordis become?
Bulbous cordis—> The smooth outflow tracts of the RV and LV (example: forms the infundibulum/ conus arteriosus= smooth muscle funnel from RV to pulmonic arteries)

(Heart embryo) What does the primitive ventricle become?
Primitive Ventricle—> The trabeculated part of the RV and LV

(Heart embryo) What does the primitive atrium become?
Primitive Atrium—> The trabeculated part of the RA and LA

(Heart embryo) What does the right horn of the sinus venosus become? Left horn of the sinus venosus?
Right horn—> smooth part of the RA (sinus venarum)
Left horn—> Coronary sinus

(Heart embryo) What do the endocardial cushions become?
They contribute to the formation of the atrial and ventricular septum and all the valves (**defects of this are common in Down syndrome)
What does dextrocardia mean?
Your heart is on the right side of your chest
What is this?

Aortic regurgitation (aortic pressure is falls in diastole- when blood is leaking back from the aorta to the LV)
What is this?

Aortic stenosis (LV pressure has to get really high compared to aortic pressure to push blood through the stenotic aortic valve)
What is this?

Mitral regurgitation (LA pressure is only high during systole when blood from the LV flows back into the LA as it’s trying to pump)
What is this?

Mitral stenosis (LA pressure is always higher to get blood through stenosed valve to the LV)
What kind of cells in embryo are involved in forming the atriopulmonary septum (to separate the pulmonary arteries and aorta)?
NCC’s (neural crest cells) & endocardial cells (**truncal abnormalities like transposition of the great vessels, tetrology of Fallot, and persistent truncus arteriosis are due to NCC’s not being able to migrate)
What’s the difference between eccentric and concentric hypertrophy?

Describe the mechanism of Digoxin (digitalis).
Digoxin inhibits the K+/Na+ pump on myocytes—> increases Na+ in the myocytes—> makes the Na+/Ca2+ pump not work as well because Na+ won’t want to come into a high [Na+] environment—> build up of Ca2+ in the myocyte available for contraction= increases contractility

EKG: what is the P wave? QRS? T wave?
P wave= atrial depolarization
QRS= ventricle depolarization (atrial repolarization embeddded in here)
T wave= ventricle repolarization

EKG: what does the PR interval tell you?
PR interval= AV conduction delay (the AV node slows the rate of conduction and this shows it because it is the interval where atrial depolarization is spreading to the AV node—> ventricles for contraction)

EKG: What does the QRS interval tell you? How about the QT interval?
QRS interval= speed of ventricular excitation (if wide that means the ventricles are depolarizing slowly—> slow HR)
QT interval= period of ventricular excitation and refractoriness (the entire systole= depolarization + depolarization)

EKG: what does the ST segment mean? What does R to R mean?
ST segment= plateau phase where ventricles are fully depolarizer and refractory (before ventricular repolarization)
R to R segment= ventricular diastole (ventricles are relaxing and refilling with blood **note: R to R segment includes the T wave which is ventricle repolarization and repolarization is technically part of contraction, but it’s starting to relax at this point)

What is the conduction pathway (order of the spread of excitation through the heart)?
SA node—> atria—> AV node—> bundle of His—> right and left bundle branches—> Purkinje fibers—> ventricles (apex and then rest of ventricles)

When might you see a U wave following a T wave on EKG?
U waves- in hypOkalemia or bradycardia (slow HR)

What might a T wave inversion on EKG indicate?
Ischemia or recent MI (T wave= ventricular repolarization)
What’s a normal PR interval? What’s a normal QRS interval?
Normal PR interval= 3-5 small boxes (<200 msec)
Normal QRS interval= <3 small boxes (<120 msec)

Describe how the myocyte action potential graph (showing electrical activity of a single myocyte) matches up with an EKG reading (showing electrical activity across lots of myocytes).
Phase 4 (ventricular diastole) matches up with the P wave (atrial systole= ventricular diastole). Phase 0 (ventricle depolarization) matches up with QRS (ventricle depolarization). Phase 2 (refractory period) matches up with the ST segment (ventricles are fully depolarizer & refractory). Phase 3 (ventricle repolarization) matches up with the T wave (ventricle repolarization). REMEMBER THIS: the EKG from Q- T (QRS and T wave= ventricular repolarization and depolarization) matches up to phase 0-3 (ventricular systole) and the P wave and flat part (ventricular diastole) matches up to phase 4 (ventricular diastole).

What is the difference between ASD (atrial septal defect) and PFO (patent foramen ovale)? Which is more likely to cause a paradoxical emboli?
ASD= ostium/ foramen secundum or (more rarely) ostium/ foramen primum don’t form properly—> hole in the atrial septum between the RA and LA
PFO= ostium/ foramen secundum or ostium/ foramen primum don’t fuse (in 25% of people)—> hole in the atrial septum between the RA and LA
PFO is more likely to cause a paradoxical emboli (blood clot using shunt to move from RA—> LA, bypass lungs, and become systemic leading to a stroke)
*note that PFO is present in 25% of people- usually doesn’t cause problems, but paradoxical emboli is the one potential problem it can cause. ASD is more rare and requires surgery so the shunt doesn’t reverse directions (Eisenmenger syndrome)










































































































































