Physiology Flashcards Preview

Cardiology > Physiology > Flashcards

Flashcards in Physiology Deck (68)
Loading flashcards...
1
Q

Arterial pressure equation

A

A.P. = CO X TPR

2
Q

To regulate blood flow independently to each organ

A

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

3
Q

Ohm’s law

A

Q = delta P / R

4
Q

Resistance relation to radius

A

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

5
Q

flow relation to radius

A

Q = radius^4 (proportional to)

6
Q

Nace’s fave equation

A

CO = SV X HR

7
Q

Reynold’s number for turbulent flow

A

> 2000 (murmur etc)

8
Q

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

A

> 400

9
Q

Reynold’s number equation

A
Re = (d v p) / n        
n = viscosity
d = diameter 
v = velocity
p = density
10
Q

Why doesn’t increasing the diameter result in increased reynold’s number

A

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

11
Q

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

A

Local factors, SNS, circulating factors

12
Q

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

A

decrease in vessel lumen size, change in tissue vessel number

13
Q

Active hyperemia blood flow is related to

A

rate of metabolism

14
Q

graphic relationship between blood flow and rate of metabolism?

A

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)

15
Q

vasodilator metabolites

A

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

16
Q

vasodilator metabolites difference in reactive versus active hyperemia

A

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

17
Q

Angiotensin II has what effect on vasculature

A

vasoconstricts both arteries and veins

18
Q

How does N.O. vasodilate

A

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

19
Q

decreased number of blood vessels

A

rarefaction

20
Q

reduction in size of the vascular lumen

A

hypertrophic vascular remodeling

21
Q

on the left side of the heart, when is coronary blood flow greatest? why?

A

diastole –> it is a reactive hyperemia to the momentary ischemia caused during systole because of mechanical compression of the coronary arteries

22
Q

blood flow to skeletal muscle at exercise is controlled by

A

local control (NO, prostaglandins, K, ATP)

23
Q

blood flow to skeletal muscle at rest is controlled by

A

SNS (vasoconstriction increases TPR and decreases hypotension)

24
Q

rhythmic exercise has what type of hyperemia

A

elements of both reactive (after each compression, i.e. ‘ischemic episode” and overall active hyperemia due to increased muscle function

25
Q

Sympathetic innervates what part of heart

A

AV node, SA node, ventricular myocytes

26
Q

Parasympathetic (vagus) innervates what part of heart

A

AV node and SA node only

27
Q

Difference between Effective Refractory Period and Absolute RP

A

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

28
Q

Relative refractory potential

A

is when a stronger than normal stimulus elicits a weaker than normal AP

29
Q

Supranormal RP

A

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)

30
Q

The effect of PNS activity in the heart is dependent on

A

activation of K channels and deactivation of Ca channels

31
Q

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?)

A

increased PNS activity via decreased cAMP can move it to a more positive value, i.e. -30mV

32
Q

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)

A

PNS activity, that activiates IK-ach channel. Increased K channel activity

33
Q

strength of contraction is regulated by

A

intracellular Ca levels during AP and initial length of cardiac fibers which determines sensitivity of myofilaments to Ca

34
Q

receptor on Sarco Retic that releases Ca to cause myofilament activation?

A

RyR , ryanodine receptor

35
Q

how does calcium get taken up by SR

A

Active transport, ATP pump

36
Q

how does calcium get effluxed from cell

A

Antiport with sodium and also ATP pump

37
Q

catecholamines accelerate the rate of? 3 things re: cardiac cell activity

A
  1. inotropy 2. intracellular Ca decline 3. lusitropy
38
Q

Action of phospholamban

A

decreases intracellular calcium quickly and puts it in SR

39
Q

Fast and slow responses to stretch ? (corresponding to increased cardiac force)

A

Fast- increased Ca sensitivity to myofilaments by stretch … Slow- involving activation of Ca channels by stretch

40
Q

Where does the peak systolic pressure occur

A

in the aorta not the ventricle

41
Q

where does the minimum diastolic pressure occur

A

in the aorta not the ventricle

42
Q

pressure just before the mitral valve closes?

A

end diastolic pressure

43
Q

ventricular pressure during contraction

A

afterload

44
Q

afterload is equivalent to

A

diastolic aortic pressure

45
Q

impact of preload and afterload on contractility?

A

none

46
Q

How can you increase contractility

A

sympathetic stim, stress, RAAS

47
Q

SV equation

A

SV=EDV-ESV

48
Q

EF equation

A

EF=SV/EDV

49
Q

In pressure-volume loop, adjusting pre-load affects

A

Systolic pressure and Stroke volume

50
Q

In PV loop, adjusting afterload affects

A

Systolic pressure, stroke volume, ESV

51
Q

determinants of filling pressure

A

unstressed volume, compliance of blood vessels, and blood volume

52
Q

Venous return equation

A

VR = filling pressure/TPR

53
Q

Reflection coefficient =

A

1 - permeability coefficient

54
Q

Gain formula

A

(correction of error signal) / (error , abnormality still remaining)

55
Q

baroreceptors provide information to the CNS about

A

mean arterial pressure, pulse pressure, heart rate

56
Q

nerve action potentials from the carotid baroreceptor are transmitted to

A

the nucleus tractus solitarius

57
Q

baroreceptors can buffer against increases or decreases of blood pressure?

A

both

58
Q

chemoreceptors only defend against

A

decreases in blood pressure

59
Q

chemoreceptor sens hypotension via

A

low oxygen or high carbon dioxide

60
Q

chemoreceptor threshold for activtion

A

below 80 mm Hg

61
Q

Cerebral ischemia-induced response

A

below 60 mm Hg

62
Q

why does the cushing reaction result in bradycardia?

A

increase in blood pressure (to perfuse the brain) is sensed by the baroreceptor which signals the vagus nerve (PNS) to slow the heart down

63
Q

Less rapidly responding systems to BP (1min - 30min)

A

low pressure reflex (via stretch), atrial natriuretic, capillary fluid transfer, vascular stress relaxation, RAAS

64
Q

Increased atrial stretch causes increased release of

A

ANP, atrial natriuretic peptide

65
Q

physiological regulation of blood volume rapid and slow effects?

A

rapid- capillary fluid transfer Slow- renal and G.I. output

66
Q

what plays the predominant role in regulating the set point of arterial pressure

A

kidneys

67
Q

items that shift renal curve to the right

A

Ang II, aldosterone, SNS, vasopressin, renal disease obesity

68
Q

items that shift renal curve to the left

A

ANP, NO, diuretics, BBs