Cardio Deck 1

Question 1

Where does fetal erythropoiesis occur?

Answer 1

Young Liver Synthesizes Blood. Yolk sac 3-8 weeks, Liver 6 to birth, Spleen 10-28 weeks, Bone marrow 18 weeks and forever after (note they overlap in fetal period as shown by numbers)

Question 2

How does fetal blood having better oxygen affinity?

Answer 2

Less avidly binds 2,3-BPG b/c gamma subunits. Rmember this for subunits, Alpha Always; Gamma Goes, Becomes Beta.

Question 3

What are the three shunts in fetal flow?

Answer 3

Ductus venous takes oxygenated blood from umbilical vein and bypasses liver to IVC
Foramen ovale is a straight shot from the IVC O2 rich blood to go through to left atrium then to brain with high O2
Ductus Arteriosus is for blood to go form pulm artery to descending aorta (after brain blood left) to deliver mixed blood and bypass lung circulation

Question 4

What makes Ligamentum trees? Medial umbilical ligament? median umbilical ligament?

Answer 4

Umbilical vein is ligamentum teres, umbiLical arteries are mediaL umbilical ligaments (duh, two arteries, so clearly there will be two of them), the allaNtois is the urachus-mediaN umbilical ligament. FYI urachus is part allantoic duct between bladder and umbilicus.

Question 5

What supplies SA and AV nodes?

Answer 5

RCA, infarct of it can cause bradycardia or heart block

Question 6

What is dominance in heart circulation? Which is most common?

Answer 6

Right dominance is more common meaning that PDA comes from Right Coronary Artery and not Left Circumflex artery. (note codominance is about as common as left dominance, each being about 8%)

Question 7

Where do you enter for pericardiocentesis?

Answer 7

5th intercostal

Question 8

How can you use blood gasses for CO calculation?

Answer 8

Fick equation. CO= rate of O2 consumption divided by (arterial O2 - venous O2). Remember it is mixed venous blood! so taken from vein either returning from organ you are measuring, or PA or right atrium for the entire body.

Question 9

Mean arterial pressure equation:

Answer 9

MAP=CO X TPR= 2/3 diastolic X 1/3 systolic (makes sense b/c 2/3 of time is in diastole)

Question 10

How does digitalis (cardiac glycoside) affect heart?

Answer 10

Blocks Na/KATPase. So there is more Na within the cell. The heart kicks out Ca++ through a Na/Ca++ exchanger and when there is higher intracellular Na, there is less gradient to kick out Ca, so more Ca causes more contractility.

Question 11

What is normal ejection fraction?

Answer 11

55% and it is SV/EDV. Low EF in systolic heart failure, EF is normal in diastolic heart failure

Question 12

What is the strongest determinant in terms of resistance in vasculurature?

Answer 12

Radius. Resistance is directly proportional to viscosity and length of a tube, but INVERSELY proportional to radius to the FOURTH POWER!

Question 13

Resistance in series vs parallel

Answer 13

Parallel is 1/r=1/r1+1/r2… duh you know that shit. stupid card is stupid and shouldn’t have been made

Question 14

Biggest factor of viscosity

Answer 14

hematocrit (polycythemia vs anemia). But also hyperproteinemic states (like multiple myeloma)

Question 15

How do you change after load?

Answer 15

vAsodilators (eg hydrAlAzine) decrease Afterload (Arterial). ACEi and ARBs decrease both preload and after load.

Question 16

JVD waves?

Answer 16

A wave is Atrial contraction. C wave is rv ventricle Contraction (causes bulge of tricuspid), X descent is atrial relaXation but [absent in tricuspid regurg] and V wave is high atrial pressure from filling due to filling against closed tricuspid ValVe. (page 270). Y decent is blood flow from RA to RV

Question 17

When do you hear wide splitting? What about paradoxical splitting?

Answer 17

Conditions that delay RV emptying. PULMONIC STENOSIS, RBB BLOCK. The delay in RV emptying causes delayed sound. (exaggeration of normal split). NOTE: opposite for paradoxical splitting.

Question 18

When’d o you see a fixed split?

Answer 18

ASD. Left to right shunt. Increase RA and RV volumes cause flow througgh the pulmonic valve such that regardless of breath, pulmonic closure is greatly delayed! (b/c much less pulmonic arterial pressure, so it will take longer to equalize and the split will fix)

Question 19

What causes holosystolic hipitched “blowing murmur”?

Answer 19

Mitral/tricuspid regurge. (dilation of ventricle can cause it or rheumatic fever or endocarditis among other things)

Question 20

When do you hear a crescendo-decrescendo systolic ejection murmur?

Answer 20

Aortic stenosis b/c. Think about when heart has most force in contraction vs when aortic pressure is matching it. So not loudest at first because Law of LaPlace it won’t be able to contract as forcefully, then gets louder as it contracts b/c will get stronger force, then aortic pressure will raise and there won’t be as much of a difference and blood won’t rush out as rapidly. If you think about it, it makes sense.

Question 21

Holosystolic harsh sounding murmur that is loudest at tricuspid area

Answer 21

VSD. loudest at tricuspid area and louder if higher after load (so hand grip test)

Question 22

Mid systolic click and crescendo sounding murmur.

Answer 22

Mitral valve prolapse. USUALLY BENIGN

Question 23

High pitched blowing early diastolic decrescendo

Answer 23

aortic regurg. Makes sense it is decrescendo b/c most pressure difference is right after systole with elastic recoil of aorta and relaxation of LV

Question 24

Diastolic opening snap murmor

Answer 24

Mitral stenosis. Snap from abrupt halt in leaflet motion in diastole after rapid opening due to fusion at leaflet tips. Often secondary to rheumatic fever

Question 25

Machine like murmur caused by:

Answer 25

PDA, often due to congenital rubella or prematurity.