Physiology Flashcards
Arterial pressure equation
A.P. = CO X TPR
To regulate blood flow independently to each organ
alter the resistance (only slight changes in the radius of the blood vessels required)
Ohm’s law
Q = delta P / R
Resistance relation to radius
R = 1 / (radius^4) [proportional to]
flow relation to radius
Q = radius^4 (proportional to)
Nace’s fave equation
CO = SV X HR
Reynold’s number for turbulent flow
> 2000 (murmur etc)
Reynold’s number at branches/arches (local vortices)
> 400
Reynold’s number equation
Re = (d v p) / n n = viscosity d = diameter v = velocity p = density
Why doesn’t increasing the diameter result in increased reynold’s number
diameter and velocity are inversely related, in a squared function. Here’s why
1) velocity is inversely proportional to the cross sectional area of the pipe
2) cross sectional area is proportional to the square of the radius (or 1/2 of the diameter) –> pi r ^2
3) therefore, velocity depends on the inverse square of the radius
4) as you increase the diameter, you get an exponential decrease in velocity that prevents you from increasing reynold’s number
Three ways to rapidly regulate vascular resistance (seconds to minutes)
Local factors, SNS, circulating factors
Two ways to regulate vasc resistance slowly (weeks to months)
decrease in vessel lumen size, change in tissue vessel number
Active hyperemia blood flow is related to
rate of metabolism
graphic relationship between blood flow and rate of metabolism?
non-linear because of ‘blood flow reserve’ that is utilized with increase metabolic need (slow slope at first due to reserve, slope increases more rapidly according to metabolic need)
vasodilator metabolites
adenosine, ATP, ADP, AMP, CO2, lactic acid, K
vasodilator metabolites difference in reactive versus active hyperemia
reactive- not removed properly Active- generated at a higher rate than they can be removed
Angiotensin II has what effect on vasculature
vasoconstricts both arteries and veins
How does N.O. vasodilate
via decreasing intracellular Ca2+ –> relaxation of SM cells of vasculature
decreased number of blood vessels
rarefaction
reduction in size of the vascular lumen
hypertrophic vascular remodeling
on the left side of the heart, when is coronary blood flow greatest? why?
diastole –> it is a reactive hyperemia to the momentary ischemia caused during systole because of mechanical compression of the coronary arteries
blood flow to skeletal muscle at exercise is controlled by
local control (NO, prostaglandins, K, ATP)
blood flow to skeletal muscle at rest is controlled by
SNS (vasoconstriction increases TPR and decreases hypotension)
rhythmic exercise has what type of hyperemia
elements of both reactive (after each compression, i.e. ‘ischemic episode” and overall active hyperemia due to increased muscle function
Sympathetic innervates what part of heart
AV node, SA node, ventricular myocytes
Parasympathetic (vagus) innervates what part of heart
AV node and SA node only
Difference between Effective Refractory Period and Absolute RP
ARP is dependent on sodium channels (at a more positive membrane potentials, inactivation is closed) no stimulus can generate AP. –> it includes phase 0, 1, 2 and a tiny bit of 3
ERP includes all of the ARP and the first half of the relative refractory period. –> it is the time when no stimulus generated by surrounding cells can elicit an AP
Relative refractory potential
is when a stronger than normal stimulus elicits a weaker than normal AP
Supranormal RP
when weaker than normal stimulus elicits AP, as you don’t have the normal opposition K channels (they aren’t activated yet, and can’t stabilize the membrane potential)
The effect of PNS activity in the heart is dependent on
activation of K channels and deactivation of Ca channels
how can you increase (make more positive) the threshold potential from its original value of -40mV? (i.e. how can you make it more difficult to reach threshold and fire a potential?)
increased PNS activity via decreased cAMP can move it to a more positive value, i.e. -30mV
how could you create a more negative MDP (maximal diastolic pressure) in SA nodes (i.e. decreasing the most negative potential reached during phase 4)
PNS activity, that activiates IK-ach channel. Increased K channel activity
strength of contraction is regulated by
intracellular Ca levels during AP and initial length of cardiac fibers which determines sensitivity of myofilaments to Ca
receptor on Sarco Retic that releases Ca to cause myofilament activation?
RyR , ryanodine receptor
how does calcium get taken up by SR
Active transport, ATP pump
how does calcium get effluxed from cell
Antiport with sodium and also ATP pump
catecholamines accelerate the rate of? 3 things re: cardiac cell activity
- inotropy 2. intracellular Ca decline 3. lusitropy
Action of phospholamban
decreases intracellular calcium quickly and puts it in SR
Fast and slow responses to stretch ? (corresponding to increased cardiac force)
Fast- increased Ca sensitivity to myofilaments by stretch … Slow- involving activation of Ca channels by stretch
Where does the peak systolic pressure occur
in the aorta not the ventricle
where does the minimum diastolic pressure occur
in the aorta not the ventricle
pressure just before the mitral valve closes?
end diastolic pressure
ventricular pressure during contraction
afterload
afterload is equivalent to
diastolic aortic pressure
impact of preload and afterload on contractility?
none
How can you increase contractility
sympathetic stim, stress, RAAS
SV equation
SV=EDV-ESV
EF equation
EF=SV/EDV
In pressure-volume loop, adjusting pre-load affects
Systolic pressure and Stroke volume
In PV loop, adjusting afterload affects
Systolic pressure, stroke volume, ESV
determinants of filling pressure
unstressed volume, compliance of blood vessels, and blood volume
Venous return equation
VR = filling pressure/TPR
Reflection coefficient =
1 - permeability coefficient
Gain formula
(correction of error signal) / (error , abnormality still remaining)
baroreceptors provide information to the CNS about
mean arterial pressure, pulse pressure, heart rate
nerve action potentials from the carotid baroreceptor are transmitted to
the nucleus tractus solitarius
baroreceptors can buffer against increases or decreases of blood pressure?
both
chemoreceptors only defend against
decreases in blood pressure
chemoreceptor sens hypotension via
low oxygen or high carbon dioxide
chemoreceptor threshold for activtion
below 80 mm Hg
Cerebral ischemia-induced response
below 60 mm Hg
why does the cushing reaction result in bradycardia?
increase in blood pressure (to perfuse the brain) is sensed by the baroreceptor which signals the vagus nerve (PNS) to slow the heart down
Less rapidly responding systems to BP (1min - 30min)
low pressure reflex (via stretch), atrial natriuretic, capillary fluid transfer, vascular stress relaxation, RAAS
Increased atrial stretch causes increased release of
ANP, atrial natriuretic peptide
physiological regulation of blood volume rapid and slow effects?
rapid- capillary fluid transfer Slow- renal and G.I. output
what plays the predominant role in regulating the set point of arterial pressure
kidneys
items that shift renal curve to the right
Ang II, aldosterone, SNS, vasopressin, renal disease obesity
items that shift renal curve to the left
ANP, NO, diuretics, BBs
