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39 Cards in this Set

  • Front
  • Back
What is VO2? What is its value in the myocardium? In systemic circulation?
The amt of O2 taken up per unit time.
*myocardium = 12vol%
*systemic = 4vol%
What is the ratio relationship bwtn CO, myocardial VO2, and coronary flow? Does this ratio change in rest vs. work? What implications does this have for coronary flow and VO2?
The ratio must ALWAYS be kept at 1:1:1. B/c CO can increase up to 5 times its resting value, coronary Q and VO2 must also be able to increase five-fold.
As the need for O2 increases, cardiac myocytes can extract more from each RBC.
False: O2 extraction from RBC in the myocardium is always at a maximum - at work and rest.
The myocardium has no capillary reserve - i.e. all capillary beds are always open.
True: this is not a means that can be used to increase flow or VO2 during work.
How can coronary flow be increased to accomodate a rise in CO? How is this accomplished?
Through dilation of resistance vessels. H+, adenosine, and CO2 cause vasodilation in this functional hyperemia response.
How is ischemic pain on exertion caused in patients with arterial plaques?
The arterioles are dilated at rest to maintain flow past increased resistance. When CO increases with work it may not be able to dilate them further (loss of dilator reserve). Ischemia is due to inadequate flow.
What determines O2 demand in the myocardium?
CO...thus increases in PL, AL, CTY, or HR can also increase O2 demand.
In CHF, the LV can become dilated and effaced. What effects can this have in terms of SV and tension?
The "r" increases and "h" decreases, thus tension is greatly increased. The LV must generate more force to overcome tension. SV decreases, allowing blood to pool in the LV. This increases tension more.
What are the treatment goals in a patient with a dilated and effaced LV?
*give diuretic to reduce vol, which reduces PL, which reduces LV radius
*use NTG to cause vasodilation to reduce PL further
What effect does AL have on O2 demand?
They are directly related - an increase in AL increases the amt of work the heart must perform and thus increases O2 demand.
How can AL be reduced in CHF patients?
Tx w/a vasodilator will lower SVR and thus lower MAP, effectively reducing AL.
How are CTY and O2 demand related? Inversely or directly?
In patients in CHF, the SNS seeks to remedy the problem by increasing stimulation of the heart. What are the problems with this?
Increased SNS stim causes increased HR and CTY, both of which will increase the O2 demand of the heart. Also, increased HR decreases diastole and thus coronary perfusion
When does most of the coronary blood flow occur? Why?
During diastole during rebound dilation, b/c during systole extravascular compression occludes the coronary vessels.
Why does tachycardia exacerbate coronary ischemia?
B/c the length of diastole, when coronary perfusion occurs, decreases.
What causes rebound dilation of coronary vessels at the end of systole?
Low [O2] and increased metabolic vasodilators.
Why is extrinsic control less important in regulation of coronary circulation? Of what benefit is this?
SNS nerves and receptors are not well distributed. Neither are hormonal receptors. This prevents coronary vasoconstriction during fight-or-flight response.
How long can cerebral blood flow be stopped before neuron inactivity occurs? Before irreversible damage occurs?
4 seconds before inactivity, 4 minutes before damage.
What is the average CBF?
50 mL/min/100g
What are the 3 separate fluid volumes inside the cranium?
*interstitial fluid
What is normal intracranial pressure? Does this change with activity?
10mmHg. This must remain relatively constant because of ltd space.
How far above its basal level is CBF able to rise? Why?
CBF can rise to only twice its basal level due to ltd space.
What is the primary determinant of CBF?
Which is more important in regulation of CBF, extrinsic or intrinsic mechanisms?
Intrinsic myogenic and metabolic regulators play the central role.
The total CBF remains relatively constant, although regional vasodilation and vasoconstriction does occur.
True: the ltd space of the cranium prevents much change in total CBF.
What are 5 ways that ICP can be raised?
1.Excessive capillary filtration
2.blockade of cerebral aqueducts
3.inflammation of arachnoid villi
4.intracranial hemorrhage
5.tumor growth
Which has more drastic local effects on CBF, PO2 or PCO2?
PO2 is only detected during extreme hypoxia, thus PCO2 has a more drastic effect on CBF.
How would hypoventilation affect CBF?
The resulting increase in PCO2 would cause vasodilation and increased CBF.
How would hyperventilation affect CBF?
The resulting drop in PCO2 would cause vasoconstriction and a decrease in CBF.
What are the standard values for:
Pulm arterial pressure
Pulm venous pressure
Pulm capillary pressure
Pulm arterial = 15mmHg
Pulm venous = 5
Pulm capillary = 10
How is pressure in the pulmonary circuit held low?
The RV is a weak pump.
How is resistance in the pulmonary circuit held low?
The length of the vessels is small, their diameter is quite large, and they are quite distensible.
What is the importance of low pressure in the pulm circuit?
It prevents excess capillary filtration and allows for good gas exchange.
Which area of the lung is better perfused, the base or the apex? Why?
The base is much better perfused. Gravity greatly reduces pressures in the apex.
Which area of the lung is most prone to TB infection? Why?
The apex - low perfusion creates a high O2 environment.
Which area of the lungs is most prone to edema? Why?
The base - gravity increases perfusion and increases cap. pressure which favors filtration.
Is pulmonary circulation regulated more by myogenic, metabolic, or extrinsic mechanisms?
None of the above! Autocoids and PO2 play the most important roles in regulating pulm circulation.
In the lungs, low PO2 causes vasodilation.
Here, low PO2 causes vasoconstriction to prevent perfusion of tissue surrounding blocked airways.
What does O2 control of pulm circulation seek to maintain?
A constant ventilation-to-flow ratio.