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BSCI 440; Spring, 2003
Round II; PRACTICE EXAM ANSWERS
W. J. Higgins
 

DISCLAIMER:  This examination is meant for practice.  It is intended to provide you with some measure of how well you understand the material for Examination II.  It may not include questions on all subjects.  I think the answer key is correct, but alternate interpretations may be possible.  Please be sure to run all questions or explanations by Dr. Higgins before or after class.
 

#1
         Just to get us rolling along with some easy points (and expected questions!),
         predict the effects of each of the following agents (or of only the agonist if
         given after an antagonist!) with I for INCREASE, D for DECREASE, and NC
         for NO CHANGE.
 
 
AGENT HR TPR SV CO DP BPave
phentolamine _NC____ _D/NC____ _NC____ _NC____ _NC____ _NC____
Muscarine _D____ _D____ _I____ _D____ _D____ _D____
Atropine + 
Nicotine (High dose)
_I____ _I____ _I____ _I____ _I____ _I____
Propranolol + NE _NC____ _I____ _NC/~I____ _NC____ _I____ _I____
Phentolamine + NE _I____ _D/NC____ _I____ _I____ _I____ _I____
H2 agonist _NC____ _D____ _D____ _D____ _D____ _D____
Nicotine (low dose) _D____ _NC____ _I____ _D____ _D____ _D____
The BP tracings for some of the above may be found in the figures located elsewhere on the Web site ( see BP tracings)
 

#2.
         Consider an individual (i.e., your lab partner) who has been accidentally jabbed
         with a syringe containing ACh.

a.     Please draw the expected response in his/her BP tracing below:  (Be accurate &
        complete; do not include the homeostatic response.)

Please see the BP response to ACh found elsewhere on the Web site.  (Obviously I cannot draw it in Word document.)  Note that the DP decreases, PP increases, HR decreases, and SP should be somewhere near the pre-treatment level.

b.     In FEWER THAN 10 WORDS , explain the effects of the ACh's actions on each of
       the cardiovascular factors listed below (i.e., tell us WHY you see the effect you predict):

HR: muscarinic receptors = sames as parasymp = decreased HR

SV: Increased filling time = increased EDV = increased SV due to......

DP: more time between beats = longer time for DP to fall

PP: increased SV (see above) = increased PP

CO: decreased due to decreased HR

Capillary filtration & reabsorption: decreased BP = decreased filtration & increased reabsorp

Baroreceptor sensory nerve: decreases due to decreased BP

Pressor Area:   Increased due to decreased input from Depressor

Depressor Area:  Decreased due to decreased stimulation by baraorecptor sensory nerve

Vagus afferent nerve:  Decreased due to dcecreased depressor area activity

Vagus efferent nerve:  due to decreased aortic arch sensory barorecptor nerve activity

Sympathetic NS output: Increased due to increased pressor area activity

Interval between P waves of ECG:  decreased to increased HR via symp activity to raise BP back to normal

End Diastolic Volume:  Increased due to symp --> increased VR & contractility
 

3.    In the BP experiments in the lab, you noticed an effect on BP when you injected lactic acid i.v. into the rat.  What was this change and why did it occur?

Lactic acid in blood ---> shifts HCO3- towards CO2  Thus as CO2 increases, it stimulates peripheral chemoreceptors (some) and diffuses into CNS where it stimulates medullary chemoreceptors.  This decreases depressor activity which results in less inhibition of pressor area and increased pressor area activity to increase sympathetic output:  increased SV (you know the mechanism), increased HR, increased CO and VR, AND decreased parasypathetic output (due to decreased depressor area activity).

4.    Draw or diagram the feedback cycle for the decline of cardiovascular function following the formation of a myocardial infarct:

Infarct = area of non-functional tissue --> rest of ventricle must work harder -> increased O2 demand and hypertrophy --> work harder --> etc.
 

5.    During exercise, a highly trained athlete may actually decrease her TPR while increasing her CO by 2 or 3 fold.  How does this happen???

Possible because as symp stimulation and autoregulation dilate BVs to skeletal muscle, the ventricles can maintain venous return by increased SV (symp stimulation; do you know the intracellular pathway or mechanism?)

6.    Describe the ionic events occuring during an action potential in the SA node of the heart.  Describe the actions of ACh and NE on the ionic channels and events in the SA node.

See pages 380 - 382 for a detailed list of the events.  Symp and parasymp effects are also discussed on 382.

7.    As promised, a few UP/DOWNS!!  Please use D, I, or NC.
 
a. As [Epi] increases, the SA node's Na+ conductance _I_______
b. As digitalis is administered to a subject, her TPR will _D_______
c. As renal blood flow decreases, renal artery diameter will _I_______
d. As an individual ages, venous blood vessel compliance _D_______
e. As blood vessel compliance decreases, diastolic BP _I_______
f. Immediately after the T wave of the ECG, ventricular pressure _D_______
g. As plasma [CO2] increases, vagal afferent nerve activity _I_______
h. As cardiac EDV decreases, SV will _I_______
i. Immediately after the P wave of the ECG, ventricular pressure _I_______
j. Immediately after the QRS complex, the mitral valve is _Closed_______
k. As pressor area activity decreases, venous return _D_______
l. As plasma [beta 2 agonist], red blood cell [2,3-DPG] _I_______