Physiology Flashcards by Drew Kropilak

Arterial pressure equation

A.P. = CO X TPR

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To regulate blood flow independently to each organ

alter the resistance (only slight changes in the radius of the blood vessels required)

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Ohm’s law

Q = delta P / R

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Resistance relation to radius

R = 1 / (radius^4) [proportional to]

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flow relation to radius

Q = radius^4 (proportional to)

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Nace’s fave equation

CO = SV X HR

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Reynold’s number for turbulent flow

> 2000 (murmur etc)

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Reynold’s number at branches/arches (local vortices)

> 400

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Reynold’s number equation

Re = (d v p) / n        
n = viscosity
d = diameter 
v = velocity
p = density

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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

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Three ways to rapidly regulate vascular resistance (seconds to minutes)

Local factors, SNS, circulating factors

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Two ways to regulate vasc resistance slowly (weeks to months)

decrease in vessel lumen size, change in tissue vessel number

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Active hyperemia blood flow is related to

rate of metabolism

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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)

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vasodilator metabolites

adenosine, ATP, ADP, AMP, CO2, lactic acid, K

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vasodilator metabolites difference in reactive versus active hyperemia

reactive- not removed properly Active- generated at a higher rate than they can be removed

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Angiotensin II has what effect on vasculature

vasoconstricts both arteries and veins

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How does N.O. vasodilate

via decreasing intracellular Ca2+ –> relaxation of SM cells of vasculature

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decreased number of blood vessels

rarefaction

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reduction in size of the vascular lumen

hypertrophic vascular remodeling

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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

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blood flow to skeletal muscle at exercise is controlled by

local control (NO, prostaglandins, K, ATP)

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blood flow to skeletal muscle at rest is controlled by

SNS (vasoconstriction increases TPR and decreases hypotension)

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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

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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

1. 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