Question 5. Dr. Campbell used an elliptical trainer for 40 minutes at the gym. Although the workload remained constant, Dr. Campbellâs heart-rate rose to 150 beats per minute during the first 5 minutes, stayed at that level for the next 25 minutes and then started to rise. It was 180 beats per minute at the end of the exercise period.
What was the time interval between QRS complexes when Dr. Campbellâs heart rate was 180 beats per minute?
a. 3.3 ms
b. 33 ms
c. 333 ms
d. 3333 ms
Question 6. In the question 5 above, Dr. Campbellâs heart rate is most likely to have risen during the last 10 minutes of exercise because his:
a. lungs were becoming congested
b. atrial cells were fatigued
c. extracellular Ca2+ concentration had increased
d. hematocrit increased due to sweating
Question 7. A Physiology student is sitting still in a cold igloo. After 30 minutes, she stands up, walks slowly around the igloo, and suddenly starts to shiver.
The student preserved their core temperature while they were sitting by:
a. depressing their Frank-Starling mechanism
b. decreasing the extracellular Ca2+ concentration
c. relaxing smooth muscles in their peripheral circulation
d. increasing the resistance of arterioles in their arms and legs
Question 8. In the question 7 above, the student started to shiver soon after walking because:
a. their atria started to fibrillate
b. their ventricles started to fibrillate
c. blood moved to the periphery, became cold, and chilled the core when it returned to the chest
d. the ATP concentration in their skeletal muscles had dropped to zero
Please use the following scenario for answering the questions 9 and 10.
A newly discovered drug binds to myosin molecules in cardiac muscle (and nowhere else) and increases the probability that myosin molecules in ventricular cells will bind to actin filaments when the intracellular Ca2+ concentration rises. The drug is being tested as a potential therapy for patients with heart failure.
Question 9. This drug might help people who have low cardiac output by:
a. increasing peripheral resistance
b. increasing the force developed by ventricular cells
c. increasing the isovolumic contraction time
d. increasing heart rate
Question 10. The increased binding of cardiac myosin molecules to actin might prevent the drug from being a useful treatment by:
a. slowing ventricular relaxation
b. decreasing the duration of systole
c. decreasing resistance of capillaries
d. slowing heart rate
Question 5. Dr. Campbell used an elliptical trainer for 40 minutes at the gym. Although the workload remained constant, Dr. Campbellâs heart-rate rose to 150 beats per minute during the first 5 minutes, stayed at that level for the next 25 minutes and then started to rise. It was 180 beats per minute at the end of the exercise period.
What was the time interval between QRS complexes when Dr. Campbellâs heart rate was 180 beats per minute?
a. 3.3 ms
b. 33 ms
c. 333 ms
d. 3333 ms
Question 6. In the question 5 above, Dr. Campbellâs heart rate is most likely to have risen during the last 10 minutes of exercise because his:
a. lungs were becoming congested
b. atrial cells were fatigued
c. extracellular Ca2+ concentration had increased
d. hematocrit increased due to sweating
Question 7. A Physiology student is sitting still in a cold igloo. After 30 minutes, she stands up, walks slowly around the igloo, and suddenly starts to shiver.
The student preserved their core temperature while they were sitting by:
a. depressing their Frank-Starling mechanism
b. decreasing the extracellular Ca2+ concentration
c. relaxing smooth muscles in their peripheral circulation
d. increasing the resistance of arterioles in their arms and legs
Question 8. In the question 7 above, the student started to shiver soon after walking because:
a. their atria started to fibrillate
b. their ventricles started to fibrillate
c. blood moved to the periphery, became cold, and chilled the core when it returned to the chest
d. the ATP concentration in their skeletal muscles had dropped to zero
Please use the following scenario for answering the questions 9 and 10.
A newly discovered drug binds to myosin molecules in cardiac muscle (and nowhere else) and increases the probability that myosin molecules in ventricular cells will bind to actin filaments when the intracellular Ca2+ concentration rises. The drug is being tested as a potential therapy for patients with heart failure.
Question 9. This drug might help people who have low cardiac output by:
a. increasing peripheral resistance
b. increasing the force developed by ventricular cells
c. increasing the isovolumic contraction time
d. increasing heart rate
Question 10. The increased binding of cardiac myosin molecules to actin might prevent the drug from being a useful treatment by:
a. slowing ventricular relaxation
b. decreasing the duration of systole
c. decreasing resistance of capillaries
d. slowing heart rate