Blood Pressure Flashcards
What is blood pressure?
pressure inside blood vessels or heart chambers, relative to atmospheric (unit: mmHg)
How does your brain know what your blood pressure is and what does it do about it?
- blood pressure sensors (baroreceptors) communicate blood pressure level to brain (medulla) via afferent nerves
- brain (medulla) outputs blood pressure controllers (SNS and PSNS) via efferent nerves
What are the SNS and PSNS responses to brain output?
change depending on what blood pressure is (if it decreased or increased)
What are baroreceptors?
stretch-sensitive nerve endings that feedback information to brain
Where are baroreceptors located?
- in carotid sinus – common carotid artery
- in aortic arch
What is the afferent nerve that brings info to medulla from baroreceptor in carotid sinus?
glossopharyngeal nerve
What is the afferent nerve that brings info to medulla from baroreceptor in aortic arch?
vagus nerve
At rest, what is the brain input to SNS?
no sympathetic nerve activity
At rest, what is the brain input to PSNS?
some parasympathetic nerve activity – explains why heart rate is lower than what intrinsic rate would be
What happens if BP rises acutely?
↑ stretch of baroreceptors
↑ firing of afferent nerves
↑ stimulation of PSNS
- results in ↓ HR
↑ inhibition of SNS
- results in ↓ SVR and SV
BP = HR x SV x SVR therefore blood pressure is restored to normal
What happens if BP falls acutely?
↓ stretch of baroreceptors
↓ firing of afferent nerves
↓ stimulation of PSNS
- results in ↑ HR
↓ inhibition of SNS
- results in ↑ SVR and SV
BP = HR x SV x SVR → blood pressure is restored to normal
What does the brain do to SNS and AVP release normally at rest?
inhibits SNS and AVP release
What happens when the SNS normally stimulates the kidney?
- results in renin release
- renin increases AII
- AII can affect SVR
- AII stimulates aldosterone
- aldosterone affects kidney Na+ reabsorption and water reabsorption
What does the release of AVP usually do?
- has effect on SVR – which causes vasoconstriction
- stimulates kidney – which increases water reabsorption
What does the brain do to SNS and AVP release if BP increases?
increases inhibition of SNS and AVP release
result:
- ↓ BV leads to ↓ CO
- ↓ SVR leads to ↓ BP
What does the brain do to SNS and AVP release if BP decreases?
decreases inhibition of SNS and AVP release
result:
- ↑ BV leads to ↑ CO
- ↑ SVR leads to ↑ BP
What are some cardiovascular adaptations to exercise? (6)
- ↑ left ventricle size and wall thickness (hypertrophy) –partly responsible for increase in SV
- ↑ SV (volume effect) – increase in BV, resulting in reflex increase in pumping via Frank Starling mechanism
- ↓ resting and submaximal HR
- ↑ BV
- BP does not change or slightly decrease
- CO better distributed to active muscles
Describe the difference in stroke volume between trained and untrained individuals.
- higher in trained than untrained individuals
- larger increase during exercise in trained individuals
Describe the difference in heart rate between trained and untrained individuals.
- higher in untrained than trained individuals
- trained and untrained individuals can reach close to same MHR
Describe the difference in cardiac output between trained and untrained individuals.
cardiac output is similar between trained and untrained individuals
What results in larger cardiac output?
- higher heart rate
- higher stroke volume
What is ‘training-induced’ or ‘athletic’ bradycardia?
slower resting heart rate in athletes
What are the mechanisms that cause training-induced or athletic bradycardia?
- increased vagal tone (controversial)
- passive, due to increased SV with no change in CO
- beta receptor desensitization (controversial)
How does increased vagal tone reduce heart rate?
- more vagal input to heart reduces HR
- reduced SA node pacemaker activity
Describe the ‘passive’ mechanism – due to increased SV with no change in CO.
even though HR drops, SV and CO increase at rest so CO is not altered when training vs. not training
