CARDIAC SG Flashcards
3 cardiac layers
epicardium-visceral
myocardium- muscle
endocardium- inner
4 valves
tricuspid RA and RV
pulmonic RV and pulmonary artery
mitral- LA and LV
Aortic- LV and aorta
systole
contractions of ventricles and ejection of blood
diastole
relaxation and filling of ventricles
heart landmarks
base 2nd and 3 rd costal
Apex 5th and 6th costal
PMI 5th intercostal and midclavicular
conduction system
SA node RA- pacemaker of the heart
AV node in atrial septum-transmits signal to Bundle of His
FETAL circulataion
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
neonatal circulation if PFO and PDA closes
SVC -> RA -> RV -> pulmonary artery -> lungs oxygenate blood -> pulmonary veins -> LA -> LV ->
Aorta -> body/tissue
fetal shunts
- Ductus arteriosus
(extracardiac) - Foramen ovale (intracardiac)
- Ductus venosus (extracardiac)
cardiac output
amount of blood pumped into the aorta by the LV or pulmonary trunk by RV.
CO=SVxHR.
stroke volume
amount of blood that is pushed out of the heart with each beat. This is contingent on
Preload, afterload and cardiac contractility
preload
amount of blood in the ventricle BEFORE a
heartbeat
afterload
pressure the heart must overcome AFTER filling to contract and eject blood
contractility
the innate ability of the heart to generate force in order to contract
Frank-Starling Law adults and infants
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.
Frank-starling Law fetus
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
PFO
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
PDA
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
ductus Venosus
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
Cardiac defect MATERNAL DM
CHD: VSD AND TGA, ToF, double outlet RV
reversible hyperthropic cardiomyopathy
cardiac defect maternal Lupus
fetal conduction abnormalities: 2nd degree AV block; RX with bathamethasone ; if not treated might result with hydrops fetalis
when conduction system is mature?
8 weeks
normal pulmonary blood flow DX
i) Aortic Stenosis
ii) Coarctation of the Aorta
iii) Pulmonary Valvar Stenosis
increased pulmonary blood flow
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
decreased pulmonary blood flow
Intracardiac defects and obstructions to PBF, Cyanotic
(1) Tetralogy of Fallot
(2) Tricuspid Atresia
Ductal Dependent Systemic Circulation (left-sided lesions
i) HLHS
ii) Coarctation of the Aorta
iii) Interrupted Aortic Arch
Ductal Dependent Pulmonary Circulation (right-sided lesions)
i) D-Transposition of the Great Arteries
ii) TOF
iii) Pulmonary Atresia
iv) Pulmonary Stenosis
v) Tricuspid Atresia
vi) Severe Ebsteins Anomaly
CYANOTIC
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)
ACYANOTIC
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)
normal blood volumes
i) Premature infant: 90-105 ml/kg
ii) Term Newborn: 82-86 ml/kg
iii) 1-7 days: 78-86 ml/kg
diminished or absent pulses suggest what?
aortic arch obstruction
what can create the thrill?
PULMONARY OR AORTIC outflow obstruction. A restrictive VSD with low RV pressure
systolic BP 10-15 higherthan diastolic suggests what?
coarctation of the aorta (COA)
when to use bell?
low-pitched sounds. Use for mid-diastolic murmur of mitral stenosis or S3 in heart failure.
when to use diaphragm?
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
lub sound
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
dub sound
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
positive chronotropic meds
increase HR;
i) Atropine.
ii) Dopamine (INOTROPIC AND CHRONOTROPIC)-
iii) Epinephrine (INOTROPIC AND CHRONOTROPIC)-
iv) Isoproterenol.
v) Milrinone.
vi) Theophylline.
negative chronotropic meds
decrease HR:
Beta blockers such as propranolol
Digoxin
