Magder Flashcards

1
Q

What is the formula for compliance?

A

∆V/∆P = 1/E

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2
Q

What is Hooke’s Law?

A

Tension = Ex(L-L0)= elastance*stressed volume

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3
Q

What is the formula for Poiseuille’s Law?

A

Q = ∆P/R, where R = Ln8/r^4*π

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4
Q

What is the relationship between flow and velocity?

A

Q = V*A (cross sectional area)

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5
Q

In what condition does the flow coming to the heart is 0?

A

Pra = MSFP

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6
Q

How does the heart control the CO?

A

By regulating the pressure in the right atrium

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7
Q

How can we calculate venous return?

A

VR = MSFP - Pra/Rv = stressed volume = unstress volume/Rv*Cv
Where MSFP = V/Cv

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8
Q

What are the determinants of cardiac function?

A
  1. Heart Rate
  2. Stroke Volume
    *Together, they give the CO
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9
Q

What are the determinants of the SV?

A
  • Preload
  • Afterload
  • Contractility
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10
Q

How long does the plateau phase of the AP last?
What does it mean for the heart?

A

280 sec → time for which calcium is available
Time the heart has to contract (isovolumetrically and isotonically)

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11
Q

What are the 2 curves the determine the SV depending on preload and afterload?

A

Stuck between Systolic elastance and Diastolic elastance

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12
Q

What determines the best venous return the heart can get?

A

Pra <= 0

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13
Q

What are the 2 limits to CO?

A

Cardiac function curve and Venous Return curve (where the meet = working CVP)

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14
Q

What is the effect of an increase in contractility of the heart on CO?

A

Increase in the cardiac function curve → increase in CO with a decrease in Pra
*More goes out, more can come in
Higher Stroke Volume → increased CO

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15
Q

What is the effect of an increased HR on the CO?

A

Increase CO with out increasing SV, just more contractions/min
Increase in cardiac function curve →increase in CO with a decrease in Pra

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16
Q

What is the effect of a change in Volume to the CO?
(effect on working CVP?)

A

*Done when the BP goes down
Increase in volume → increase MSFP → shift of venous curve to right → increase in CO with an increase in Pra

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17
Q

What does the intersection of the cardiac function curve and the venous return curve point represent?

A

The working Central Venous Pressure (CVP)

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18
Q

How does vessel constriction affect the cardiac function - venous return diagram?

A

Increase in stressed volume → more CO with higher Pra

Depends where they constrict?

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19
Q

How does a change in capacitance affect the cardiac function - venous return diagram? The CO?

A

Change in capacitance → more change in pressure with smaller change in volume
→ Increase MSFP for same total volume → same as a change in volume → increased CO with increase Pra

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20
Q

How can we increase CO with a Pra = 0?

A

We can’t, Pra = 0 → heart is at its best, has the maximal venous return, can’t eject more than it gets back

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21
Q

How does a decrease in venous resistance affect the cardiac function - venous return diagram? The CO?

A

Decreasee in venous resistance (with dilation during exercise or septic shock) → allows more blood to come back → increased CO with rise in Pra

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22
Q

What are the average BP of the right and left ventricles

A

Left ventricle = 100 mm Hg (80-120)
Right ventricle = ~18 mm Hg (5-25)

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23
Q

What is the impact of not having a right ventricle? What are the limitations?

A

*Vena cava attached directly to pulmonary circuit
- Almost normal max CO and max O2 consumption
- Can’t tolerate increase in pulmonary artery pressure (RV would normally take care of that) → damages liver, gut, etc.

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24
Q

What allows efficient O2 delivery and saturation?

A

Low pulmonary pressure → delicate alveoli
High perfusion pressure

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25
Q

What is the time-varying elastance concept of K Sagawa?

A

The higher the afterload, the lower the SV (less time for ejection)

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26
Q

What is the typical value of the MSFP?

A

Measured in right atrium → 7.6 mm Hg > RVEDP

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27
Q

Why does the RV not have an isovolumic phase?

A

MSFP > RVEDP → tricuspid valve stays open
*At the end of ejection, the RV will not just relax until the pressure gets lower than in the right ventricle because it is already (MSFP in right atrium) → RA starts filling RV

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28
Q

What are the 4 valves?

A

RA → RV: Tricuspid
RV → PA: Pulmonary (semilunar)
LA → LV: Mitral
LV → Aorta: Aortic (semilunar)

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29
Q

At what pressures do the aortic and pulmonary valve open?

A

At 15 mm Hg and 80 mm Hg

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30
Q

Why does a slight increase in the pulmonary valve opening pressure decrease SV?

A

*Increase in afterload
RV has less elastance (1 mm Hg/ml instead of 3 mm Hg/ml in the RV) → as increase afterload → get compromise because start reaching the max systolic elastance (P/V) before having ejected all of the SV

31
Q

Why is important that we have a constant pressure MCFP > 0? (not 0)

A
  • If pressure was 0, when it contracts we would have to wait for the pressure wave to go around before next conctraction for volume to come back (1-2/min) → heart would have to empty at every beat
  • With a starting pressure, the heart doesn’t empty at every beat → can beat more often as it gets part of the volume back more often → always some blood coming into the heart
32
Q

Which pressure/flow is responsible for the regional flow in individual organs?

A

CO → Aortic pressure/flow

33
Q

Where is the MSFP measured?

A

In the veins (vena cava) → fill the RV which is responsible for CO determination

33
Q

How does compliance affect the steady-state levels?

A

It doesn’t, only resistance, upstream pressure (MSFP) and downstream pressure (Pra)

34
Q

How does CO change with an increase in Pulmonary Vascular Resistance (PVR)? (For nomal individual and for individual with no RV)

A

Stays constant for normal individual
*no RV → can’t handle increase in PAP →
No RV → CO decreases as PVR increases because the right ventricle can’t adjust to the increasing afterload?

35
Q

What is the effect of a lower elastance an increase in Pulmonary Artery diasotlic pressure?

A

As PA sastolic pressure increases (increase in afterload), Max SV decreases a lot faster with lower elastance than with higher elastance
*max SV = volume the blood ejects at optimal afterload

36
Q

What is the definition of elastance?

A

P/V → ability of vessels to stretch and recoil at every cycles, measure of stiffness/rigidity

37
Q

What are the limitations of the RV?

A

Systole → slope of RV Ees
Diastole:
- break in diastolic elastance curve (limit in filling/wall)
- Slope of diastolic elastance curve
- MSFP (if too low) also can limit RV SV → RV diastolic pressure can’t be higher than the upstream MSFP to keep filling

RV limit of SV limits max LV SV

38
Q

How is the LV linked to pulmonary edema?

A

LV function determines pulmonary venous pressure → risk of pulmonary edema

39
Q

What 2 changes in RV will decrease SV when limitation occurs?

A
  1. Increase in pulmonary opening pressure
  2. decrease in RV function
40
Q

What changes can help increase SV when there is RV dysfunction?

A
  1. Increase in HR
  2. decrease in PAP (afterload)
41
Q

What is the formula for O2 consumption according to the Fick’s Principle?

A

VO2 = Q x (CaO2 - CvO2)

42
Q

What is the formula for O2 delivery?

A

DO2 = Q x Hb x k x Sat (arterials ~ 98%)

*Q is really the only place where we can get improvement

43
Q

What do baroreceptors react to?

A

Detect high BP, act to decrease BP
In case of low BP, they just inhibit their function

44
Q

Why does MSFP remain relatively constant?

A

Because it is in a very compliant region → not much change in pressure for big changes in volume
Q = VR = MSFP-Pra/Rv → Pra is what really changes to change VR

45
Q

What determines the steady-state CO?

A

Drainage of the veins

46
Q

What pressures should be used to calculate systemic resistance?

A

R = Pa-Pc/Q
Use Pc instead of Pv because of the curvilinear effect (Pin - Pout slope)

47
Q

Which type of animal has a complete 4 chamber heart?

A

mammals and birds
they have respectively 12x and 16x the aerobic capacity of the next highest species
Only animals with high constant temperature
*Need efficient heart

48
Q

What is the highest priority of the circulatory system?

A

Maintain flow the organs at all times!!!
- Constant flow → brain
- Heart → considerable variations (5L/min at rest → 20-25L/min at exercise)
- Pulmonary flow → flow must vary with need of the whole body
*Flow adapts to the metabolic needs

49
Q

What variable is the most closely regulated in the ciruclatory system?

A

PRESSURE

-Brain blood flow kept constant by adjusting local resistances (not pressures) → allows upright posture
- Load on the heart kept constant

50
Q

What variables are changed for regional flow to increase?

A

Resistance is lowered, pressure stays relatively constant at all times

51
Q

What valves open and close during systole?

A

A bit after the start of systole → mitral valve closes (S1) → C wave (backwards flow in the atrium) → Systole → closure of the aortic valve (S2) → backwards flow in the ventricle

52
Q

What is the V-wave in the heart pressures?

A

When Mitral valve opens → pressure drops a lot in the atrium

53
Q

What was the artifact from Otto Frank’s experiment?

A

A decrease in systole with higher diastolic pressure~preload → the heart phsyically doesn’t go the that point unlike cardiac muscles

54
Q

What does Frank-Starling relationship states?

A

The greater the initial stretch (preload), the greater the force produced

55
Q

What is the difference between the M-line and the Z-line?

A

M-line = between the thick myosin filaments (with myosin heads)
Z-line = where the thin actin filaments are attached

56
Q

What happens when we increase CVP?

A

It is the same as an increse in preload (EVD) → increase in SV

57
Q

What is backwards failure?

A

Happens when LVEDP is too high → pressure increases in all compartements before up to lungs → pulmonary edema

*When you try increasing volume in left heart in the wall part of the diastolic elastance curve

58
Q

When does forward failure occur?

A

When the heart cannot reach a high ESP/ESV (elastance) in the allotted cycle time
*Problem with the heart function → decreases SV

59
Q

Explain the dilution technique.

A

To measure CO:
1. inject dye in small vessel
2. wait t amount of time
CO = 60* I (amount of indicator)/C(mean concentration)T

60
Q

What are possible wasy to measure flow?

A
  • Doppler Probe
  • Pulmonary catheter → pulse pressure → proportional to SV → x HR = CO
61
Q

What are the sources of volume reserves for the blood?

A
  1. Unstressed volume
  2. Recruitment of interstitial volume (14L)
62
Q

What is the formula for elastic energy?

A

E = P + pgh + 1/2pv2

P = 760 mm Hg on a normal tube (atm pressure on the top)

63
Q

How does our body compensate for gravity?

A
  • Venous valves
  • Muscle “pump”
  • Increased venous tone
  • Maintain blood volume
64
Q

Does pressure determine CO?

A

NO
CO determines pressure!!
CO is determined by Cardiac function + venous return

65
Q

What factors can bring P arterial down?

A
  1. Decrease in CO
  2. Decrease in SVR
66
Q

What are the effects of the baroreceptor response?

A
  1. Decrease HR
  2. Decrease contractility
  3. Vasodilatation
67
Q

What mechanisms are responsible for the curvilinear pressure-flow curve relationship?

A
  1. Distension → lower resistance by increasing volume
  2. Recruitement → open more vessels
68
Q

What pressures do you use to calculate resistance?

A

P atrium and P critical (instead of Pv)

69
Q

When does forward failure occur?

A

Occurs when heart can’t reach a high ESP/ESV in the alloted time because of decreased heart function

70
Q

What is the difference between the permissive and restorative functions of the heart?

A

Permissive → lowers pressure to accept blood from the veins (venous return)
Restorative → pumping out to be able to refill (cardiac function)

71
Q

What are non volume ways to increase Q?

A
  1. improve Cardiac function: (decrease Pra → let more comeback)
    - Increase HR
    - Increase contractility
    - Decrease afterload
  2. Increase venous return: (increase Pra → more preload)
    - Decrease venous resistance
    - Redistribute flow to less compliant vessels (muscles)
    - Muscle contractions
72
Q

What will an increase in afterload result in in terms of volumes?

A

An increased end systolic volume