Nate extra, non DIT, FA cardio flash cards
(90 cards)
Truncus arteriosus gives rise to
Ascending aorta and pulmonary artery
Bulbus cordis gives rise to
Smooth parts of the R. and L ventricle (outflow tract)
Primitive ventricle gives rise to
Trabeculated R and L ventricle
Primitive atria gives rise to
Trabeculated R and L atria
Right horn of sinus venosus (SV) gives rise to
Smooth part of R. atrium
Absorbed pulmonary veins give rise to
Smooth part of left atrium
Left horn of sinus venosus (SV) gives rise to
Coronary sinus
Right common cardinal vein and right anterior cardinal vein give rise to
SVC
What two structures fuse to form the aorticopulmonary septum? What embryologic tissue are they derived from?
The truncal and bulbar ridges (migrations of the neural crest)
What structure closes the interventricular foramen? What two tissues fuse to form this structure?
The interventricular foramen is closed by the membraneous inverventricular septum. It is formed via fusion of the dorsal aorticopulmonary septum and the ventral endocardial cushion tissue.
What causes a PFO?
Failure of the septum primum and secundum to fuse after birth
Fetal erythropoiesis occurs in which tissues? When?
"Young liver synthesizes blood" Yolk sac (week 3-10) Liver (week 6- birth) Spleen (week 15-30) Bone marrow (week 22-adult)
Which bones have erythropoiesis occurring in them?
Ribs, skull, sternum, pelvis and vertebrae.
**Up until age 25, also have erythropoiesis occurring in the tibia and the femur also
What does fetal hemoglobin have higher affinity for oxygen than maternal hemoglobin?
The fetal gamma unit has lower affinity for 2,6 BPG and therefore higher affinity for oxygen than the mothers beta unit of hemoglobin
Are the umbilical vessels named according to the relation of flow to moms heart or the fetus’ heart? How many umbilical vein(s) and artery(ies) are there?
Named according the how flow relates to the fetal heart. Therefore, flow towards the fetal heart is a umbilical vein. There is one umbilical vein bring oxygenated blood to the fetal heart and there are two umbilical arteries bring deoxygenate blood away from the fetal heart and back towards the mother
During the late stages of exercise how is CO maintained?
By HR only b/c stroke volume plateaus. Excessively high HRs decrease CO b/c diastole is too short too completely fill the ventricles.
How do catecholamines increase heart contractility?
How do catecholamines increase HR?
They act on beta 1 receptors -> increasing cAMP via AC. PKA then increases the activity of the Ca++ pump on the SR. This allows more calcium to be released (Ca++ induced Ca++ release) via the ryanodine receptor thus increasing contractility.
Heart rate is increased via the same mechanism above, but specifically they increase the likelihood that funny channels controlling the phase 4 depolarization (diastolic depolarization) are to be open, thus increasing HR.
What is the equation for resistance in a blood vessel? What things can alter the viscosity?
R = (8 x viscosity x length) / (pi x r^4)
Viscosity depends mainly on hematocrit. Increased viscosity is seen in polycythemia, hyperproteinemic states (ie multiple myeloma) and hereditary spherocytosis, Viscosity is decreased in anemia.
In general, do left heart valves or right heart valves close first?
Left heart is under higher pressure so they tend to close first (mitral and aortic valves before tricuspid and pulmonic valves).
What is the physiological mechanism of a S3 heart sound? What pathological conditions it is seen in? When is it normal?
An S3 heart sound is due to rapid ventricular filling in early. It is associated with elevated filling pressures (mitral regurgitation, CHF, L -> R shunts (VSD, ASD, PDA)) and is also more common in DILATED hearts. Normal in pregnant women, young athletes and children.
What is the physiological mechanism of a S4 heart sound? What pathological conditions it is seen in? When is it normal?
S4 heart sounds are heard at end of diastole right before S1. They are caused by “atrial kick” against a stiff ventricle. They are associated with ventricular hypertrophy. Never normal.
What are the 5 parts of the Jugular Venous Pulse (JVP)? And what causes each?
“At Carter’s crossing (X) vehicles yield”
a wave- atrial contraction
c wave- RV contraction (tricuspid bulges back into RA)
x descent- atrial relaxation, further ventricle contraction causes downward displacement of tricuspid b/c RV has ejected most of its blood
v wave- incr RA pressure d/t filling against closed tricuspid
y descent- rapid ventricular filling
What is the dicrotic notch? Why does it occur and what important function does it serve?
The dicrotic notch is a rebound in the aortic pressure after the aortic valve closes, while ventricular pressure continues to fall. It is due to the elastic property of the aorta. The wall of the aorta stretches during ventricular contraction and then this rebounding of the wall increases pressure in the aorta. It is important b/c it pushes blood back against the aortic valve and into the coronary arteries (remember: coronary arteries undergo DIASTOLIC FILLING).
What is normal splitting of the second heart sound?
Normally, the pulmonary valve will close slightly after the aortic valve. During inspiration, this split is widened. This happens because during inspiration decreased intrathoracic pressure pulls more blood into the right heart, thereby increase RV SV and increasing ejection time -> delayed closure of the pulmonic valve -> increased split.
**There is also an effect on the left heart during inspiration. Increased RV size pushes intenrventricular septum into the LV -> decreasing LV volume -> early aortic valve closure