Control of Blood Pressure & Hypertension Flashcards
what is pre-load
- the stretching of the myocytes prior to contraction
- “end-diastolic volume”
- a change in ventricular pre-load will affect the ability of the ventricle to contract
there is a specific volume at which – from that point the ability of teh ventricle to contract will be greatest
increase preload – increased SV (to a point)
decrease preloard – decrease SV
what is afterload
- the “load” the heart has to eject against
- the “opposing force” of the aortic wall pressure (wallstress)
increase afterload = decreae SV
decrease afterload = increase SV (harder to push out against a force)
what is contractility
- the force of contraction, this is INDEPENDENT of preload
think of this as the force that can be generated by th ebiochemical properites of the cells themselves – amoutn of calcium!!!
Changed with…
- SNS (norepi)
- heart rate – triggers more
what are the regulators of cardiac output (CO)
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contractibitliy of the cells
preload
afterload
HR
SV
TPR
MAP
how does contractibility impact the relationship between stroke volume and preload (EDV)?
- normally— EDV increases, & this will increase SV (to a degree)
if you increase contractibility — the cells will have more “pep” and be able to force more out & create a bigger stroke volume!
if you decrease contractibility – the cells wont have that “pep”and less will be forced out through stroke volume
what are some reasons for increased contractibility?
positive inotropic effects
- increased sympathetic response
- increased angiotensin II
- reduced sodium
- increased HR
- cardiac glycoside medications (digoxin)
**these all increase contractibility of the cells becuase they increase calcium in teh cell
what are some reasons for decreased contractibility? negative inotropic effects
- the parasympathetic system
- beta blockers
- reduced intracellular calcium (calcium channel blockers)
- some antiarrythmics
- high sodium concentrations
systolic heart failure – will decrease contractibility
explain the relationship between HR and CO and SV?
what if HR increases? what happens to CO or SV
when might we see increased HR and decreased SV??
increased HR will increase CO
but HR can increase and decrease stroke volume SV
the AMOUNT leaving in each pump may be less, even though there is more of them
times where there can be increased HR and decrease SV
- ventricular tachycardia (lots of beats, but such a small time in diastole it cant fill)
- a fib (less time in diastole – forcing atrial contraction over and over)
- heart failure with a preserved EF —> the heart is able to beat “normal” ef because it relies on diastole filling (since its so stiff and failing) – when you increase HR you decrease the distole phase
what is MAP? what are the controllers?
MAP = mean arterial pressure
MAP = CO x TPR
inputs from
- neural signals
- humoral factors (RAAs system, vasopressins, ADH)
- long term renal compensations
How does neural control impact MAP?
baro and chemoreceptors
neural control is essentaill baroreceptors and chemoreceptors
- baroreceptors: sense a drop in pressure and stop firing to the brain–> signially a need to increase in pressure!
- more stretch (pressure) = increased firing (releases ANF which triggers excretion of h20 and salts)
- less stretch ( no pressure) = decreased firing – which triggers the pressors of brain (constriction)
these are carotid sinus and arch of aorta
these adjust to SHORT term changes in blood pressures – long term changes (like HTN) are determened by blood volume control and the RAAS system
Chemoreceptors
- the peripheral chemoreceptors (in the carotid body and aortic arch) respond to changes in O2 and CO2
- when O2 drops – with hypotension – body will try to compensate with increased respirations
- this will help but wont fix it
how do vascular reflexes/changes impact MAP?
discuss smooth muscle
- the arterioles have ability to constrict and have greatest resistnace to decrease flow to specifica capillaries – thuse controlling blood flow
arterioles = smooth muscle
- they have the ability to change/contract depending on the electrical Ca+ depedning on the prescence of Epi or NE (the NE is released from adrenal medulla or spilled over from the nearby neruon or from a pheochromatoma tumor
- they also change according to heat
- endocrine hormones can change them (aldosterone, bradykinin, NE)
- paracrine (locally made) like NO or prostoglandins can impact them too
overall affects of norephinephrine & epinephrine on…
- CO
- TRP
- MAP
- HR?
NE
CO: increases
TPR: increases
MAP: increases
HR: briefly increases (but baroreceptors compensate this)
Epi
- highly responsive to beta receptors –> increases HR and inotropy
- vasoconstricts in most areas
- vasodilates in muscles and liver — specifically in the lungs think about anaphylaxis
affects of epi and NE are most predominant when released from the efferent nerves (more than when they’re released from the adrenal glands)
what is the RAAS system
- how is it stimulated
- what are the effects
RAAS system: endocrine system which regulates pressures in the body
- Renin: produced by the renal cells (JG cells)
Stimulated (to fix blood loss, hypotensions and heart failure)
- by renal hypotension (decreased pressures due to decreased BP overall or renal artery stenosis)
- decreased sodium level in the kidney – need to trigger to increase salt uptake
- by the sympathetic system (fight or flight)
Effects of RAAS (via AGII)
- directly vasoconstricts
- releases aldosterone (which will reuptake salt and water)
- ADH released (reuptake water)
- enhance NE and epi activity (SNS)
- trigger thirst in brain
what is the RAAS system
- how is it stimulated
- what are the effects
RAAS system: endocrine system which regulates pressures in the body
- Renin: produced by the renal cells (JG cells)
Stimulated (to fix blood loss, hypotensions and heart failure)
- by renal hypotension (decreased pressures due to decreased BP overall or renal artery stenosis)
- decreased sodium level in the kidney – need to trigger to increase salt uptake
- by the sympathetic system (fight or flight)
Effects of RAAS (via AGII)
- directly vasoconstricts
- releases aldosterone (which will reuptake salt and water)
- ADH released (reuptake water)
- enhance NE and epi activity (SNS)
- trigger thirst in brain
primary hypertension
- what is it
- characteristics
what
- related to excess weight (intra-abdominal), sedintary lifestyle and genetics
characterisitcs
- with increased adipose tissue – you need more perfusion to those tissues – so you compensate by increasing your cardiac output (CO) to get there
- there is an increase in sympathetic nerve activity
- angiotensis II and aldosterone levels increased
- natuersis impaired (less ability to excrete water and salt)
