This is yet another stem of questions using the laws of flow physiology to elucidate the means of heart failure and compensation for different volume-ion changes in disease states. Enjoy!
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Control of Cardiac Output
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The volume of blood present in the ventricles at the end of each cardiac cycle is approximately how many millilitres?
How is ejection fraction calculated?
A Hartmann fluid bolus challenge to a patient in shock does what to the stroke volume of the patient directly?
Increases adrenergic response
Question 3 Explanation:
The direct effect is preload increase. This causes a great many things, such as atrial stretch reflex to trigger natriuresis and a greater contractile force to push additional volume.
By a powerful increase in TPR (SVR), the body's autonomous response to hypovolaemia affects stroke volume in which way described below?
A decrease in preload
An increase in the contractility of the heart
An increase in afterload
A decrease in volume of the chamber
CO = ____ x HR
Which of the following is not true of the Bainbridge atrial stretch reflex?
it utilises mechanoceptors
It transmits afferents to the medulla via the tenth cranial nerve
An increase in cholinergic efferents results
An increase in noradrenergic efferents results
Question 6 Explanation:
The sympathetic nervous system is up-regulated in the atrial stretch reflex. Thus, concomitantly, the parasympathetics are down-regulated. The former utilises noradrenergic efferents, the latter the cholinergics.
Serum pH is tightly controlled to ensure adequate perfusion of tissues. Which of the following are not related to chemoreception and its homeostasis?
Question 7 Explanation:
The carotid body - not the carotid sinus - is involved in chemoregulation. The carotid sinus role is baroreception.
What is the most powerful way to increase a patient's stroke volume?
Which of the following scenarios increase afterload?
Increase of venous compliance
An increase of cardioaccelerator nerve functionality
Increasing aortic arch pressure
Stem 1 of 4
A patient is recovering after a myocardial infarction. Under LaPlace and Starling's law his heart must necessarily work greater and the cardiologist cautions the patient is at risk of hypertrophic cardiomyopathy.Under Starling's law, what is EDV proportional to?
Stem 2 of 4In the short term, which of the below scenarios is the patient's myocardium less likely to undergo?
Increases cardioaccelerator sympathetic postganglionics
Increased myocardial contracture force
Remodelling of the heart chamber
Increase of the HR
Question 11 Explanation:
This is an example of the longer-term consequence when the patient's heart is insufficiently able to deal with an increase of EDV and thus undergoes dilatation.
Stem 3 of 4Sarcomere length, ergo Starling's law of contracture, is determined by ...
Stem 4 of 4The patient had an infarct to the artery determining coronary dominance during his MI. How would you classify this vessel functionally?
Question 13 Explanation:
PIVA, or the posterior inter ventricular branch of the coronary arteries, determine coronary artery dominance. As such, the question is asking for the classification of an artery -which is a distributive vessel.
A patient with severe dehydration would see what change to their cardiac physiology based on Frank-Starling's law?
An increase in systemic vascular resistance
A decrease in myocardial contractility
A decrease in the capacitance vasomotor activity
An increase in the vasodilation of the caval circulation
Question 14 Explanation:
FS law states that contractility is directly proportional to EDV. In the dehydrated patient, volume decrease leads - in extremis - to a decrease of stretch on the sarcomere, thus a decrease in the power provided from the sliding filament theory.
In HFrEF, what is the positive feedback loop that proves ultimately fatal?
Increase to CO increases EDV
Increase to CO decreases EDV
Decrease to CO increases EDV
Decrease to CO decreases EDV
Question 15 Explanation:
There is a decreased pump action of the heart, leading to reduced CO. This causes an increase of EDV, which Frank Starling can compensate for, but only for a time before dilation occurs and the heart muscle undergoes permanent death.
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