Cp2Wk4- 1-25 Physio Ballam Mi/fetal

Front 1

Avg pressures in large arteries, arterioles, capillaries, vena cava, pulmonary arteries, capillaries, and veins
PRU?

Back 1

systemic...
large arteries: 120/80
arterioles: 66/60
capillaries: 18
vena cava: 0-4
pulmonary....
arteries: 24/16
capillaries: 8
veins: 6
if PRU is 1 resistance of lungs is low

Front 2

What happens to TPR when the umbilical arteries and veins are clamped (after birth)?
Why?

Back 2

dramatic increase in TPR (systemic)... ductus venosus closes... and closes the foramen ovale (pressure gradient switches to L --> R)
- Placenta adds parallel resistence which decreases TPR

Front 3

In a normal neonate, what causes the ductus arteriosis to close?

Back 3

w/in few days after birth, hormone changes (drop in prostaglandins) and inc. arterial 02 sat causes it to close

Front 4

6 examples of acyanotic congenital cardiovascular defects?
What is acyanotic?
What is cyanotic?

Back 4

acya- No or left to right shunt
cya- usually right to left shunt
1. ASD,
2. VSD,
3. PDA,
4. AS,
5. post-ductal coarctation,
6. PS

Front 5

Common compensatory change in ASD?

Back 5

often L to R shunt
dilation of right atrium and ventricle

Front 6

What are common compensatory changes in VSD?

Back 6

all chambers may dilate L to R shunt
LV dilation can lead to HF
prolonged shunt may lead to inc. pulm. reistance and REVERSIBLE!!! shunt (eisenmengers)

Front 7

What is a common compensatory change in PDA (pantent ductus arteriosus)?

Back 7

LV dilation (inc. return), may lead to HF

Front 8

What is a common compensatory change in AS (aortic stenosis)?
What bout severe problems?

Back 8

LV hypertrophy (high LV systolic pressures)
- if severe R to L shunt via ductus a or L to R via foramen ovale

Front 9

What often happens in preductal coarctation?
How does postductal coarctation differ?

Back 9

pinching off before the Ductus Arteriosus
Pressure high preceding DA and low after

ductus may remain open due to lack of L side pressure, if bad enough can cause R to L shunt

POST- allows for closure

Front 10

What is a common compensatory change in PS (pulmonary stenosis)? What gradient is considered mild?

Back 10

RV hypertrophy
50 mmHg gradient considered mild

Front 11

Where are the pressures in the heart the greatest?
Therefore where are MI's most likely to occur?

Back 11

– systole
– left ventricle
– endocardium
LV, endocardium

Front 12

When is flow greatest in left coronary artery versus right coronary artery?

Back 12

1. Left- greatest at beginning of diastole
2. Right- peaks during systole

Front 13

Describe the features of an aortic pump... (balloon)

Back 13

- The balloon is deflated during systole
allowing blood to perfuse the tissues
• The balloon is inflated at the beginning
of diastole forcing blood in the aorta
back into the coronary circulation.

Front 14

Explain why HTN can cause increase in work of the heart...

Back 14

It increases cardiac work and therefore metabolic needs
ä Cardiac stroke work = SV x Mean BP
ä Cardiac work = stroke work x HR

Front 15

What are the main physiological changes to the heart with atherosclerosis?
What causes pain?

Back 15

• Acute ischemia reduces amount of ATP available within minutes
• Acidosis causes pain
• Lack of ATP causes pumps to slow
– Na+/K+ pump
– Ca++ pump
• Na+/Ca++ exchanger slows
• Less effective contraction

Front 16

What ionic changes intracellular changes occur during ischemia?

Back 16

- Increased Na+
• Increased Ca++
• Decreased K+

Front 17

What ionic changes extracellular changes occur during ischemia?

Back 17

- decreased Na
- decreased Ca
- Increased K

Front 18

Within ten minutes describe the effects of ischmemia on the action potential and ionic permeability

Back 18

Within 10 min. the membrane potential begins to depolarize increasing permeability to Ca++ and partially activates fast Na+ gates.

Front 19

What potential differences are seen by the electrodes of an ECG?
Are they negative or positive compared to normal?

Back 19

- ECG measures extra cellular potential
- more negative compared to normal

Front 20

How does ischemia effect the picture of action potential specifically phase 4 and overall AP amplitude?

Back 20

Increased intracellular Na+ and Ca++ as well as loss of K+ reduces polarization (less negative) of phase 4.
So starts higher, but AP amplitude is reduced.
But the opposite shows up on ECG due to extracellular read on Electrodes not intracellular

Front 21

1. Why would a decreased resting membrane potential be more likely to developed arrhythmias?
2. Describe the change in cross bridge interaction and contractile force and why these changes occur...

Back 21

1. closer to threshold and easier to excite

2. - cross bridge interaction inhibited (lack of ATP) and decreased contractile force (hypokinetic)

Front 22

Exercise would produce ischemia most easily in which part of the myocardium?

What type of remodeling is most likely with MI after a week?

Back 22

Endocardial portion of the LV lateral wall

- dilation

Front 23

What happens to areas adjacent to the ischemia and why?

Back 23

Areas adjacent to the ischemia can become ischemic due to increased mechanical load (preload) and increased metabolic demand causing spread of infarcted tissue.

Front 24

What is reactive hyperemia and why does it occur?
What could this do to clot busters?

Back 24

transient increase in organ blood flow that occurs following a brief period of ischemia due to vessels dilating
- could fail and not improve with clot busters

Front 25

What are short term responses to Cardiac failure related to baroreceptor response?

Back 25

• Carotid Baroreceptors increase TPR and preload
• Short term control
• Can cause tissue ischemia

Front 26

What are the hormonal responses to HF?
a. which hormone is secreted first and by which glands? What does it do to TPR?
b. What does kidney do to respond to lowering BP
c. What does Renin do?
d. What does Angiotensin do? What does it stimulate?
e. What does ADH do?

Back 26

a. Adrenal and secretion of norepinephrine epinephrine causes vasoconstriction and increased TPR.
b. Renin produced in response to lowering BP,
c. Renin causes Angiotensin production
d. Angiotensin causes vasoconstriction stimulates Vasopressin (ADH) secretion and it converted to AngII
e. Causes vasoconstriction and Na retention (fluid retention)

Front 27

What factors are released by atrium and ventricle and which is a clinical diagnostic marker for cardiac failure?

Back 27

1. Atrial natruretic factor- secreted by Atrium in response to atrial stretching causes fluid and Na secretion
2. Natriuretic factor b secreted by stretched ventricles
– Used as clinical diagnostic marker of cardiac failure