CARDIAC SG

Question 1

3 cardiac layers

Answer 1

epicardium-visceral
myocardium- muscle
endocardium- inner

Question 2

4 valves

Answer 2

tricuspid RA and RV
pulmonic RV and pulmonary artery
mitral- LA and LV
Aortic- LV and aorta

Question 3

systole

Answer 3

contractions of ventricles and ejection of blood

Question 4

diastole

Answer 4

relaxation and filling of ventricles

Question 5

heart landmarks

Answer 5

base 2nd and 3 rd costal
Apex 5th and 6th costal
PMI 5th intercostal and midclavicular

Question 6

conduction system

Answer 6

SA node RA- pacemaker of the heart

AV node in atrial septum-transmits signal to Bundle of His

Question 7

FETAL circulataion

Answer 7

Umbilical vein carries OXYGENATED blood to baby from placenta -> bypasses liver via ductus
venosus -> goes into IVC -> RA -> (majority bypasses RV and goes directly into LA via PFO -> LV ->
aorta ->body) some goes to RV -> pulmonary artery -> PDA (by passes lungs- small amount of blood
does make it to the lungs) -> aorta -> body/tissues -> umbilical arteries carry DEOXYGENATED blood
from baby to placenta

Question 8

neonatal circulation if PFO and PDA closes

Answer 8

SVC -> RA -> RV -> pulmonary artery -> lungs oxygenate blood -> pulmonary veins -> LA -> LV ->
Aorta -> body/tissue

Question 9

fetal shunts

Answer 9

1. Ductus arteriosus
   (extracardiac)
2. Foramen ovale (intracardiac)
3. Ductus venosus (extracardiac)

Question 10

cardiac output

Answer 10

amount of blood pumped into the aorta by the LV or pulmonary trunk by RV.
CO=SVxHR.

Question 11

stroke volume

Answer 11

amount of blood that is pushed out of the heart with each beat. This is contingent on
Preload, afterload and cardiac contractility

Question 12

preload

Answer 12

amount of blood in the ventricle BEFORE a

heartbeat

Question 13

afterload

Answer 13

pressure the heart must overcome AFTER filling to contract and eject blood

Question 14

contractility

Answer 14

the innate ability of the heart to generate force in order to contract

Question 15

Frank-Starling Law adults and infants

Answer 15

within limits, cardiac muscle fibers contract more forcefully with stretching. more
muscle is stretched, greater force of contraction, increased blood volume causes increased force of
contraction. Increased pressure within the atria during filling (preload) will cause an increase in SV. Can
compensate by increasing SV to 16-18 mm Hg when there is increased preload.

Question 16

Frank-starling Law fetus

Answer 16

has a narrow capacity to increase SV when there is increased preload. Typically, they reach a peak
SV of 4-5 mm Hg. This can be due to functional immaturity → decreased contractile proteins in the
myocardium, inefficient myocardial Ca uptake, limited passive ventricular filling capacity. This all makes
it very hard for the fetus to increase CO when there is an increase in atrial pressure. Also, cholinergic
nerves derived from the vagus nerve drive changes in fetal HR

Question 17

PFO

Answer 17

functional closure caused by a drop-in pressure in the inferior vena cava and RA. Pulmonary
venous return increases and L arterial pressure exceeds R arterial pressure. PFO can remain in
infants with pulmonary stenosis or other defects associated with increased R atrial pressure.
Permanent closure is obtained by age 2.5 years

Question 18

PDA

Answer 18

Functional closure in term infants is usually noted within the first 3 days. This is caused by
increasing atrial O2 saturations amid decreasing PVS as well as decreased responsiveness to
naturally synthesized prostaglandins. RDS, septicemia, excessive fluid administration, furosemide
therapy, phototherapy, and prematurity encourage delayed functional closure. Anatomic closure is
typically noted by 2-3 months of life. The remnant of the PDA is labeled the ligamentum arteriosum

Question 19

ductus Venosus

Answer 19

functional closure occurs shortly after birth. This occurs once the parallel circuitry
disappears, blood flow from the placenta through the umbilical vein and ductus venosus ceases.
Anatomic closure is complete by 2 months of age. The remnant is labeled the ligamentum venosum

Question 20

Cardiac defect MATERNAL DM

Answer 20

CHD: VSD AND TGA, ToF, double outlet RV

reversible hyperthropic cardiomyopathy

Question 21

cardiac defect maternal Lupus

Answer 21

fetal conduction abnormalities: 2nd degree AV block; RX with bathamethasone ; if not treated might result with hydrops fetalis

Question 22

when conduction system is mature?

Answer 22

8 weeks

Question 23

normal pulmonary blood flow DX

Answer 23

i) Aortic Stenosis
ii) Coarctation of the Aorta
iii) Pulmonary Valvar Stenosis

Question 24

increased pulmonary blood flow

Answer 24

Left to Right Shunts, Acyanotic

(1) PDA
(2) VSD
(3) ASD
(4) Endocardial Cushion Defect
ii) Admixture Lesions, Cyanotic
(1) Complete Transposition of the Great Arteries
(2) Truncus Arteriosus
(3) Total Anomalous Pulmonary Valvular Connection

Question 25

decreased pulmonary blood flow

Answer 25

Intracardiac defects and obstructions to PBF, Cyanotic

(1) Tetralogy of Fallot
(2) Tricuspid Atresia

Question 26

Ductal Dependent Systemic Circulation (left-sided lesions

Answer 26

i) HLHS
ii) Coarctation of the Aorta
iii) Interrupted Aortic Arch

Question 27

Ductal Dependent Pulmonary Circulation (right-sided lesions)

Answer 27

i) D-Transposition of the Great Arteries
ii) TOF
iii) Pulmonary Atresia
iv) Pulmonary Stenosis
v) Tricuspid Atresia
vi) Severe Ebsteins Anomaly

Question 28

CYANOTIC

Answer 28

i) D-Transposition of the Great Arteries (Mixing-Dependent)
ii) Tetralogy of Fallot (Restricted Pulmonary Blood Flow)
iii) Tricuspid Atresia (Restricted Pulmonary Blood Flow)
iv) Pulmonary Atresia with Intact Ventricular Septum (Restricted Pulmonary Blood Flow)
v) Ebstein Anomaly (Restricted Pulmonary Blood Flow)
vi) Total Anomalous Pulmonary Venous Connection/Return (Complete Mixing)
vii) Truncus Arteriosus (Complete Mixing)
viii) Single Ventricle Anatomy/Physiology (Variable Physiology)
ix) Hypoplastic Left Heart Syndrome (Variable Physiology)
x) Double Outlet Right Ventricle (Variable Physiology)

Question 29

ACYANOTIC

Answer 29

i) Valvar Aortic Stenosis (Obstructive)
ii) Aortic Coarctation and Interrupted Aortic Arch (Obstructive)
iii) Serial Obstructive Left Heart Defects (Obstructive)
iv) Valvar Pulmonary Stenosis (Obstructive)
v) Ventricular Septal Defect (Shunting Lesions)
vi) Atrial Septal Defect (Shunting Lesions)
vii) Atrioventricular Septal Defect (Shunting Lesions)
viii) Patent Ductus Arteriosus (Shunting Lesions)
ix) Aortopulmonary Window (Shunting Lesions)

Question 30

normal blood volumes

Answer 30

i) Premature infant: 90-105 ml/kg
ii) Term Newborn: 82-86 ml/kg
iii) 1-7 days: 78-86 ml/kg

Question 31

diminished or absent pulses suggest what?

Answer 31

aortic arch obstruction

Question 32

what can create the thrill?

Answer 32

PULMONARY OR AORTIC outflow obstruction. A restrictive VSD with low RV pressure

Question 33

systolic BP 10-15 higherthan diastolic suggests what?

Answer 33

coarctation of the aorta (COA)

Question 34

when to use bell?

Answer 34

low-pitched sounds. Use for mid-diastolic murmur of mitral stenosis or S3 in heart failure.

Question 35

when to use diaphragm?

Answer 35

high-pitched sounds. Use for analyzing the second heart sound, ejection and midsystolic clicks and for the soft but high-pitched early diastolic murmur of aortic regurgitation

Question 36

lub sound

Answer 36

S1 (lub), marks the beginning of systole (end of systole). Related to the closure of the mitral and tricuspid valves. Loudest at the apex; low pitch

Question 37

dub sound

Answer 37

S1 (lub), marks the beginning of systole (end of systole). Related to the closure of the mitral and tricuspid valves. Loudest at the apex; high pitch

Question 38

positive chronotropic meds

Answer 38

increase HR;

i) Atropine.
ii) Dopamine (INOTROPIC AND CHRONOTROPIC)-
iii) Epinephrine (INOTROPIC AND CHRONOTROPIC)-
iv) Isoproterenol.
v) Milrinone.
vi) Theophylline.

Question 39

negative chronotropic meds

Answer 39

decrease HR:
Beta blockers such as propranolol
Digoxin