Tommy has a resting cardiac output (Q) of 5 L/min. His end-diastolic volume (EDV

Question

Tommy has a resting cardiac output (Q) of 5 L/min. His end-diastolic volume (EDV) at rest is 150 ml and resting blood pressure (BP) of 135/90 mmHg.

A) If I injected Tommy with epinephrine in his veins, what would happen to his EDV? Why?

B) If Tommy would decrease his BP to 120/80 mmHg, what would happen to his resting SV?

C) I decide to draw 1 L of blood (a lot!) from Tommy, how will this impact his SV?

D) If I can completely block the effect of the sympathetic nervous system in Tommy’s body and he began to exercise. What would his max HR be? How would this affect his EDV? How would this affect his ESV?

E) During exercise, Tommy holds in a really deep breath, how does this change his EDV? Why? If he continued the same exercise while doing this, what would you expect to happen to his HR?

Explanation / Answer

A) As you know epinephrine is a sympathetic neurotransmitter. Function of sympathetic nervous system on heart is excitatory. So epinephrine injection will have excitatory effec on heart--> Increased heart rate---> increased heart rate means decreased cardiac cycle time ( normal is 0. 8 second) --> As the time for each cardiac cycle is reduced , time for venous return to heart is also reduced (reduced ventricular filling time)--> result less venous return from periphery to to heart -----> result reduction in End diastolic volume.

So the answer is: Epinephrine injection will cause reduction in the EDV.

B) Decrease blood pressure ---> Decresed after load of heart ---> Result is increased SV ( Stroke Volume)

explanation: we know that SV = EDV - ESV ( after load, End systolic volume ), so you see , decreased ESV due to decreased blood pressure leads to increased Stroke Volume.

C) Due to blood loss there will reduced preload ( less amount of total blood in the body-> less filling of ventricle) , as stroke volume is directly proportional to preload ---> result will be decreased Stroke volume (SV)

D) If sympathetic tone is totally blocked , then on exercise there will be no change in the heart rate. During exercise there is tissue hypoxia( as exercising muscle will consume oxygen vigorously)--> chemoreceptor will sense this hypoxia---> signal will be sent to brain---> brain will try to send signal via sympathetic stimulation to increase heart rate --> as the sympathetic system is blocked--> there will be no respons---> so heart rate will remain same.

Heart rate remains normal, but due to exercising muscle will compress the venous system --> this will increase the venous return to heart ---> so EDV will increase as a result increased venous return

Though there will no sympathetic tone to increase the contractility of heart, according to frank sterling law --> increased preload ---> increased contractility of heart ( as the heart muscle will be more stretched due to increased end diastolic volume ) ----> more blood will go out of heart ( increased SV) ---> result will decreased ESV

E) Due to deep inspiration --> diaphragm will go downward --> increased intra-abdomina pressure ---> squeezing of abdominal muscle and viscera ----> incresed blood return to right atrium ----> increased ventricular filling ---> increased EDV.

If tommy continue to do so --> there will be reduction in venous return( as all the blood has already been returned to heart and due to continuous increased intra-abdominal pressure abdominal structure will receive less amount of blood consequently --> decreased venous return ---> decreased preload --> decreased stroke volume----> exercising muscle will ask for more oxygen and nutrients by incresing blood flow----> Heart rate will be increased.

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