Lecture 7+8 Flashcards

1
Q

How to alter preload?

A

by changing the EDV

change EDV by changing VR

VR is changed by altering blood volume, decreasing HR, or vasoconstriction/vasodilation

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2
Q

how to alter afterload

A

altering aortic pressure or total peripheral resistance

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3
Q

how to alter contractility

A

altering sympathetic activity

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4
Q

How does increasing preload impact the pressure-volume loop?
Draw it?

A

increasing VR = increasing EDV = increasing preload = increased stroke volume

C and D will shift to the right

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5
Q

How does increasing contractility change the P-V loop?

Draw it?

A

increasing contractility = increasing stoke volume and ejection fraction

Steeper ESPVR

E, F, and A change

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6
Q

How does increasing afterload impact the P-V loop? Draw it?

A

increase afterload = decreased stroke volume and ejection fraction

increased aortic pressure

D is shifted upward (looks like cone top)

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7
Q

Exercise and the P-V loop?

Draw it?

A

increases all aspects

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8
Q

Splitting of S2 during breathing

splitting of S1 during breathing

A

S2 splitting is normal: aortic valve closes BEFORE the pulmonary valve during inspiration

S1 splitting: pathological: due to conduction defect

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9
Q

Pathological heart sounds (S3 and S4)

A

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

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10
Q

Two types of valve abnormalities

A
  1. stenosis: open valve is narrowed (higher pressure is needed to push blood)
  2. incompetence: closed valve is leaky which leads to regurgitation
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11
Q

Aortic stenosis: systolic murmur

How this impacts the time-pressure graph and pressure-volume graph?

A

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)

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12
Q

Mitral incompetence: systolic murmur

impact on T-P and P-V graphs

A

Blood regurgitates back into the Left atrium

T-P graph: tall T wave

P-V graph: increasing preload thus moving to right (C+D)

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13
Q

Aortic incompetence: diastolic murmur

A

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

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14
Q

Mitral stenosis: Diastolic murmur

A

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)

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15
Q

What murmur’s have no isovolumetric phases?

A

aortic and mitral regurgitation

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16
Q

Ductus venosus, foramen ovale, ductus arteriosus, umbilical vein from palcenta

Roles and what happens to them after birth?

A

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

17
Q

What is ectopia cordis?

both types?

A

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

18
Q

What is the most common CHD in those with down syndrome?

A

Atrioventricular septal defect (AVSD)

19
Q

Right to left shunts?

Cyanosis?

A

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.

20
Q

tetralogy of fallot

A
  1. pulmonary stenosis - uneven division of the aorta and pulmonary trunk
  2. right ventricular hypertrophy - due to increased workout load due to the stenosis
  3. VSD (membranous)
  4. overriding aorta - will get blood from both ventricles

common in DiGeorge, Down syndrome, fetal alcohol syndrome

21
Q

Persistent Truncus arteriosus (right to left)

A

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

22
Q

Transposition of the great vessels (right to left)

A

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

23
Q

Total anomalous pulmonary venous return (right to left)

A

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

24
Q

Left to right shunts?

cyanosis?

A

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

25
Q

patent ductus arteriosus (left to right)

A

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

26
Q

Eisenmenger’s syndrome

A

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

27
Q

Coarctation of the aorta?
theories?
location ?

A

congenital narrowing of a segment of the aorta
most common at the arch

theories of why this occurs?

  1. abnormal involution of a small distal segment of the left dorsal aorta
  2. 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)

28
Q

What is the collateral pathway when the aorta is blocked?

A

Subclavian→ Internal thoracic→ Anterior intercostals→ Posterior intercostals→ Descending aorta

29
Q

what are signs of coarctation of the aorta?

A

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