Lecture 7+8 Flashcards
How to alter preload?
by changing the EDV
change EDV by changing VR
VR is changed by altering blood volume, decreasing HR, or vasoconstriction/vasodilation
how to alter afterload
altering aortic pressure or total peripheral resistance
how to alter contractility
altering sympathetic activity
How does increasing preload impact the pressure-volume loop?
Draw it?
increasing VR = increasing EDV = increasing preload = increased stroke volume
C and D will shift to the right
How does increasing contractility change the P-V loop?
Draw it?
increasing contractility = increasing stoke volume and ejection fraction
Steeper ESPVR
E, F, and A change
How does increasing afterload impact the P-V loop? Draw it?
increase afterload = decreased stroke volume and ejection fraction
increased aortic pressure
D is shifted upward (looks like cone top)
Exercise and the P-V loop?
Draw it?
increases all aspects
Splitting of S2 during breathing
splitting of S1 during breathing
S2 splitting is normal: aortic valve closes BEFORE the pulmonary valve during inspiration
S1 splitting: pathological: due to conduction defect
Pathological heart sounds (S3 and S4)
S3: diastolic, low frequency
can normally occur in those younger than 35
may be pathological
mechanism: rush of blood into ventricles from atria (recoil vibration)
S4: diastolic, just before S1
can occur in those younger than 40, usually pathological
mechanism: stiff ventricle, dec compliance
Two types of valve abnormalities
- stenosis: open valve is narrowed (higher pressure is needed to push blood)
- incompetence: closed valve is leaky which leads to regurgitation
Aortic stenosis: systolic murmur
How this impacts the time-pressure graph and pressure-volume graph?
Difficult to eject blood through the aortic valve
greater LVP is seen in the T-P graph
“cone-top” is seen on P-V graph (increased afterload)
Mitral incompetence: systolic murmur
impact on T-P and P-V graphs
Blood regurgitates back into the Left atrium
T-P graph: tall T wave
P-V graph: increasing preload thus moving to right (C+D)
Aortic incompetence: diastolic murmur
aortic valves do not close properly, thus blood regurgitates back into LV from aorta
T-P graph = large aortic pulsation; rapid drop in aortic pressure
P-V graph: EDV and SV are significantly increased
Mitral stenosis: Diastolic murmur
turbulent flow across the mitral/tricuspid valves
T-P graph: LA pressure is increased; will seen above LV pressure
P-V graph: SV and EDV are reduced (move left)
What murmur’s have no isovolumetric phases?
aortic and mitral regurgitation
Ductus venosus, foramen ovale, ductus arteriosus, umbilical vein from palcenta
Roles and what happens to them after birth?
ductus venosus: bypasses the liver; becomes ligamentum venosum after birth
foramen ovale: bypasses the lungs; becomes fossa ovalis after birth
umbilical vein: blood from mother to baby; after birth it becomes ligamentum teres hepatis
ductus arteriosus: From pulmonary A. to aorta; becomes ligamentum arteriosum
What is ectopia cordis?
both types?
Heart is in an abnormal location.
thoracic ectopia cordis: heart is partially or completely exposed on the thoracic wall due to faulty development of the sternum and pericardium
abdominal ectopia cordis: the hearts protrudes through the diaphragm into the abdomen
This condition leads to death
What is the most common CHD in those with down syndrome?
Atrioventricular septal defect (AVSD)
Right to left shunts?
Cyanosis?
this allows for deoxygenated systemic venous blood to bypass the lungs and return to the body
This results in cyanosis. It can be central or peripheral.
usually needs surgery to fix the ductus arteriosus.
tetralogy of fallot
- pulmonary stenosis - uneven division of the aorta and pulmonary trunk
- right ventricular hypertrophy - due to increased workout load due to the stenosis
- VSD (membranous)
- overriding aorta - will get blood from both ventricles
common in DiGeorge, Down syndrome, fetal alcohol syndrome
Persistent Truncus arteriosus (right to left)
Failure of the neural crest cells to migrate, thus the aorticopulmonary septum is not formed
always has a VSD, the blood mixes
mild cyanosis
The aorta and pulmonary trunk do not separate, thus it is just one vessel
Transposition of the great vessels (right to left)
switching of the aorta and the pulmonary trunk due to the faulty migration of neural crest cells
This results in severe cyanosis and is immediately lethal unless VSD, ASD, or PDA is present
deoxygenated blood is pumped throughout the body and oxygenated blood is in pulmonary circulation
Total anomalous pulmonary venous return (right to left)
Abnormal drainage of the pulmonary veins into systemic circulation
leads to severe cyanosis
need VSD,ASD, or PDA to be compatible with life
common sites:
SVC, IVC, brachiocephalic, coronary, portal vein
Left to right shunts?
cyanosis?
Characterized by a “back-leak” of blood from the systemic to the pulmonary circulation. This is due to a defect in the heart wall and causes the pulmonary flow to be larger than the systemic flow.
Acyanosis - no deoxygenated blood in systematic circulation
ductus arteriosus, if not closed, will lead to L-R shunts
patent ductus arteriosus (left to right)
ductus arteriosus does not close
associated with rubella infection (effect)
associated with down syndrome
can be found in premature infants
prostaglandins will keep it open and anti-prostaglandins (NSAID- indomethacin) will close it
Eisenmenger’s syndrome
reversal of shunt
The pressure in the pulmonary circuit may ultimately exceed the systemic pressure causing reversal of blood flow from the right side of the circulation to the left (right to left shunt)
this leads to late cyanosis
Coarctation of the aorta?
theories?
location ?
congenital narrowing of a segment of the aorta
most common at the arch
theories of why this occurs?
- abnormal involution of a small distal segment of the left dorsal aorta
- muscle tissue of the ductus incorporates into the wall of the aorta which constricts after birth.
can be preductal (proximal to ductus arteriosus) or postductal (distal to the ductus arteriosus)
What is the collateral pathway when the aorta is blocked?
Subclavian→ Internal thoracic→ Anterior intercostals→ Posterior intercostals→ Descending aorta
what are signs of coarctation of the aorta?
headache and fatigue
underdeveloped lower extremities, may be cyanotic
upper limb pulses are greater than those in the lower limb
imaging: rib notching, enlarged collaterals, cardiomegaly
