Magder Flashcards
What is the formula for compliance?
∆V/∆P = 1/E
What is Hooke’s Law?
Tension = Ex(L-L0)= elastance*stressed volume
What is the formula for Poiseuille’s Law?
Q = ∆P/R, where R = Ln8/r^4*π
What is the relationship between flow and velocity?
Q = V*A (cross sectional area)
In what condition does the flow coming to the heart is 0?
Pra = MSFP
How does the heart control the CO?
By regulating the pressure in the right atrium
How can we calculate venous return?
VR = MSFP - Pra/Rv = stressed volume = unstress volume/Rv*Cv
Where MSFP = V/Cv
What are the determinants of cardiac function?
- Heart Rate
- Stroke Volume
*Together, they give the CO
What are the determinants of the SV?
- Preload
- Afterload
- Contractility
How long does the plateau phase of the AP last?
What does it mean for the heart?
280 sec → time for which calcium is available
Time the heart has to contract (isovolumetrically and isotonically)
What are the 2 curves the determine the SV depending on preload and afterload?
Stuck between Systolic elastance and Diastolic elastance
What determines the best venous return the heart can get?
Pra <= 0
What are the 2 limits to CO?
Cardiac function curve and Venous Return curve (where the meet = working CVP)
What is the effect of an increase in contractility of the heart on CO?
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
What is the effect of an increased HR on the CO?
Increase CO with out increasing SV, just more contractions/min
Increase in cardiac function curve →increase in CO with a decrease in Pra
What is the effect of a change in Volume to the CO?
(effect on working CVP?)
*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
What does the intersection of the cardiac function curve and the venous return curve point represent?
The working Central Venous Pressure (CVP)
How does vessel constriction affect the cardiac function - venous return diagram?
Increase in stressed volume → more CO with higher Pra
Depends where they constrict?
How does a change in capacitance affect the cardiac function - venous return diagram? The CO?
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
How can we increase CO with a Pra = 0?
We can’t, Pra = 0 → heart is at its best, has the maximal venous return, can’t eject more than it gets back
How does a decrease in venous resistance affect the cardiac function - venous return diagram? The CO?
Decreasee in venous resistance (with dilation during exercise or septic shock) → allows more blood to come back → increased CO with rise in Pra
What are the average BP of the right and left ventricles
Left ventricle = 100 mm Hg (80-120)
Right ventricle = ~18 mm Hg (5-25)
What is the impact of not having a right ventricle? What are the limitations?
*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.
What allows efficient O2 delivery and saturation?
Low pulmonary pressure → delicate alveoli
High perfusion pressure
What is the time-varying elastance concept of K Sagawa?
The higher the afterload, the lower the SV (less time for ejection)
What is the typical value of the MSFP?
Measured in right atrium → 7.6 mm Hg > RVEDP
Why does the RV not have an isovolumic phase?
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
What are the 4 valves?
RA → RV: Tricuspid
RV → PA: Pulmonary (semilunar)
LA → LV: Mitral
LV → Aorta: Aortic (semilunar)
At what pressures do the aortic and pulmonary valve open?
At 15 mm Hg and 80 mm Hg
Why does a slight increase in the pulmonary valve opening pressure decrease SV?
*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
Why is important that we have a constant pressure MCFP > 0? (not 0)
- 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
Which pressure/flow is responsible for the regional flow in individual organs?
CO → Aortic pressure/flow
Where is the MSFP measured?
In the veins (vena cava) → fill the RV which is responsible for CO determination
How does compliance affect the steady-state levels?
It doesn’t, only resistance, upstream pressure (MSFP) and downstream pressure (Pra)
How does CO change with an increase in Pulmonary Vascular Resistance (PVR)? (For nomal individual and for individual with no RV)
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?
What is the effect of a lower elastance an increase in Pulmonary Artery diasotlic pressure?
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
What is the definition of elastance?
P/V → ability of vessels to stretch and recoil at every cycles, measure of stiffness/rigidity
What are the limitations of the RV?
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
How is the LV linked to pulmonary edema?
LV function determines pulmonary venous pressure → risk of pulmonary edema
What 2 changes in RV will decrease SV when limitation occurs?
- Increase in pulmonary opening pressure
- decrease in RV function
What changes can help increase SV when there is RV dysfunction?
- Increase in HR
- decrease in PAP (afterload)
What is the formula for O2 consumption according to the Fick’s Principle?
VO2 = Q x (CaO2 - CvO2)
What is the formula for O2 delivery?
DO2 = Q x Hb x k x Sat (arterials ~ 98%)
*Q is really the only place where we can get improvement
What do baroreceptors react to?
Detect high BP, act to decrease BP
In case of low BP, they just inhibit their function
Why does MSFP remain relatively constant?
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
What determines the steady-state CO?
Drainage of the veins
What pressures should be used to calculate systemic resistance?
R = Pa-Pc/Q
Use Pc instead of Pv because of the curvilinear effect (Pin - Pout slope)
Which type of animal has a complete 4 chamber heart?
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
What is the highest priority of the circulatory system?
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
What variable is the most closely regulated in the ciruclatory system?
PRESSURE
-Brain blood flow kept constant by adjusting local resistances (not pressures) → allows upright posture
- Load on the heart kept constant
What variables are changed for regional flow to increase?
Resistance is lowered, pressure stays relatively constant at all times
What valves open and close during systole?
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
What is the V-wave in the heart pressures?
When Mitral valve opens → pressure drops a lot in the atrium
What was the artifact from Otto Frank’s experiment?
A decrease in systole with higher diastolic pressure~preload → the heart phsyically doesn’t go the that point unlike cardiac muscles
What does Frank-Starling relationship states?
The greater the initial stretch (preload), the greater the force produced
What is the difference between the M-line and the Z-line?
M-line = between the thick myosin filaments (with myosin heads)
Z-line = where the thin actin filaments are attached
What happens when we increase CVP?
It is the same as an increse in preload (EVD) → increase in SV
What is backwards failure?
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
When does forward failure occur?
When the heart cannot reach a high ESP/ESV (elastance) in the allotted cycle time
*Problem with the heart function → decreases SV
Explain the dilution technique.
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
What are possible wasy to measure flow?
- Doppler Probe
- Pulmonary catheter → pulse pressure → proportional to SV → x HR = CO
What are the sources of volume reserves for the blood?
- Unstressed volume
- Recruitment of interstitial volume (14L)
What is the formula for elastic energy?
E = P + pgh + 1/2pv2
P = 760 mm Hg on a normal tube (atm pressure on the top)
How does our body compensate for gravity?
- Venous valves
- Muscle “pump”
- Increased venous tone
- Maintain blood volume
Does pressure determine CO?
NO
CO determines pressure!!
CO is determined by Cardiac function + venous return
What factors can bring P arterial down?
- Decrease in CO
- Decrease in SVR
What are the effects of the baroreceptor response?
- Decrease HR
- Decrease contractility
- Vasodilatation
What mechanisms are responsible for the curvilinear pressure-flow curve relationship?
- Distension → lower resistance by increasing volume
- Recruitement → open more vessels
What pressures do you use to calculate resistance?
P atrium and P critical (instead of Pv)
When does forward failure occur?
Occurs when heart can’t reach a high ESP/ESV in the alloted time because of decreased heart function
What is the difference between the permissive and restorative functions of the heart?
Permissive → lowers pressure to accept blood from the veins (venous return)
Restorative → pumping out to be able to refill (cardiac function)
What are non volume ways to increase Q?
- improve Cardiac function: (decrease Pra → let more comeback)
- Increase HR
- Increase contractility
- Decrease afterload - Increase venous return: (increase Pra → more preload)
- Decrease venous resistance
- Redistribute flow to less compliant vessels (muscles)
- Muscle contractions
What will an increase in afterload result in in terms of volumes?
An increased end systolic volume
