Response to Exercise and Haemorrage Flashcards
What is dyspnoea?
Breathlessness
Is hyperventilation during exercise caused by using PO2 and producing more PCO2?
No because these values are virtually unchanged during exercise
Why might PCO2 fall a little during exercise?
Because Co2 is being blown off
Is hyperventilation during exercise causes by a change in H+ ion concentration?
No as it remains unchanged in the arterial blood
What is it about breathing that means there are oscillation in PO2 and PCO2?
Since there are more beats that there are breathes not every lot of blood going to the left atrium will have the same PCO2 and PO2 concentration which means there are oscillations in the PCO2 and PO2 on a beat by beat basis
How are these oscillations involved in influencing the effect on peripheral chemoreceptors and therefore breathing during exercise?
Excerise increases these ossilations which can change the activity of the peripheral chemoreceptors
Apart from the changes in the ossiclations in PO2 and PCO2 what 4 other factors influence breathlessness during exercise?
- Increased body temperature
- Neural input from limbs
- Secretion of noradrenaline and adrenaline
- Input from higher centres
Why does exercise lead to a fall in total peripheral resistance?
As muscle activity increases metabolite production increases which cause local dilation of arterioles
How does a fall in total peripheral resistance affect cardiac output?
Because since blood pressure = TPR x CO, CO must increase to maintain blood pressure
Is there a fall in blood pressure during exercise?
No
Why is there no fall in blood pressure during exercise?
Because systolic volume rises and diastolic volume falls so there is overall no change (BP = DBP + (MBP/3)
What would happen to lead to an increase in cardiac output when TPR decreases?
Starlings law of the heart says the more you stretch the ventriles the greater the force of contraction so if metabolite generation as a result of exercise leads to vasodilation and a decrease in TPR there is an increase venous return and therefore the ventriles are stretched more leading to an increased force of contraction (stroke volume) and since CO = SV x HR that leads to an increase in CO
Apart from increase in SV to increase cardiac output what is another response to the decrease in TPR
The increase in venous return and therefore increase in the force of blood being pumped out by the ventricles causes arterial stretch reflex which then increases HR and therefore CO
What is the problem with the starling mechanism of how exercise increases cardiac output?
The heart diameter of patients exercising does not increase
What is the evidence that the nervous system is involved in increasing CO?
Heart rate increases in anticipation of exericise (feed forward mechanism activating the sympathic nervous system)