3.1 Pressure curves / loops Flashcards
Cardiac cycle
1 compelete systole /disatole
at rate 72bpm - takes 0.8secs
Draw the pressure time curve for LV & aorta
page 39 Kerry
What are the phases of systole and disatole
- Isovolumetric contract 0.05s
First phase of systole
Mitral valve closure until AV open - Isotonic contraction - pid & reduced ejection
- Prodiastole 0.04 - Last phase of systole - ejection finished - pressure falls & AV closes
Diastole
- Isovol relax - closure AV -> MV opens
- Rapid filling phases
- Diastasis - reduced filling
- atrial systole
Whats happening during sytsole
- Pressure LV rises rapidly - closure of MV
- AV doesnt open until LVP > Ao root P
Vol blood ventricle not change isovolemetric contraction
Rapid ejection - AV open
fianl phase -pressure ventircle falls below aortic - no ejection pressure continues fall - end closure AV
Diastole
Pressure LV rapidly falls ~0 isometric relaxation
Ventricle closed cavity
A+M closed - initial retrograde flow in prox aorta =
small rise in pressure - incisura in Aorta - when kietic energy converted pteotnial energy closed AV valve
No incisura on VP pressure curve
Ventricles rapidly filla fter MV & TV open
60% in rapid filing 10% daistsis
Atrial systole remain 30% - atrial kick imprant in some pathology - AS
Heart sounds
First closures AV valves - systole
- M&T may not close exact same - spltting S1
Second - closure Ao & pulm -
S3 1/3 Daistole - vibrations inrush blood
S4 Before S1 - high Atrial Pressue-> Stiff ventricle
Curve different if RV & PA
Shape similar - pressure less - peak 25/8
Differences if patient 70 y.o
Ventricular compliance & aortic complaince - reduced
Slower rate rise during contraction
High peak pressuer in LV & aorta
Heart slower - high vagal tone
Pressure wave travel quicker - stiffer aortic walls
Draw Pressure vol & atrial pressure
diagram 41
A wave- atrial contraction
C - isvol contraction - bulging MV into LA - pressure rise-
x desc pressure fals open aortic valve opens
V wave - rise in LAP return venous blood - av closed
y Descent - pressure LA falls MV opens end iso vol relax
What causes drop Atrial pressure after AV opens
X descent - shortening of ventricles - pulls fibrous av ring down
- Length atria - increase capacity - drop in pressure - atrial pressure negative
Pressure Volume loop - draw Diastolic elastance curve for LV
Draw page 42
How measure elastance
Curve pressure on Y and volume on X
Slope curve - ventricular elastance / stiffness
compliance - inverse slope of line at point
Curve not straight line - elastance increasing as LVV increase
end disasplic point - both volume -edv & EDP - indices as preload
Increase in elastance - esp large edc - relationship not linear
What is the significance pf Shape of LV pressure vol relationship
Over typical physiological range - curve flat - slowly curves upward
LV volume - increase without much increase in pressure - ventricle easily to fill
curve rise steeply outside typical value for LVVEDV
Heart difficult overfill - increas pressure imped excess increase in LVEDV - stiffere heart harder fill
Sarcmere doesnt increase much above optimal 2.23um- contraction not adversely affected
Draw pressure volume loop for LV
PV loop for LV - page 43
where doe the vavles open
Preload increased on PV Loop
page 43 - increased sv, afterload contractility same - afterload parller - same after
What is the best index of preload
End diastole is LVEDV
Best index of preload -
If increased afterload how does this affect curve
Aortic valve closing at higher pressure less volume ejected
Best index of afterload of PV loop
Slope line connectivn lvedv w/ end ssytolic point -
afterload line foor loop 2 large angle w/ x than loop 1 = afterload higher
How show preload & contractility the same
LVEDV same - preload sontant
Index contractility - slow of end systolic pressure volume line
points on same contractility line - contractility constant
If contractility increased - pv line increased slow rotate up and to left
Effect contractility of LV PV loop
draw = page 45
increase sv
1 increase slop end systolic pv line - index contractilty
end sytolic point both line same - afterload same
LVEDV is same - preload same
Area within LV - LV loop represent
Pressure x Volume = work
Area inside loop represent exetranl work performed for lv by cardiac cycles
Icnreased cotnractily a/w incrased area - increased external work ejecting increased SV
Determinanats of myocardial performance
How performance assesd - primary function heart pump blood
Assesd index - how well perform
Pump effectives - blood volume / unit time
Cardiac index = CO / BBSA - corrects for body size
Co = SVxHR
S
SV determined by
Preload
Afterload
contractility
Preload
Load on muscle prior onset cotnract
Load determine length myocardial cell start contraction
- intital fiber lengh
incrased cause increased length
Refine index performance
eg heat pump5l w/ low preoload perfomaing better heart need high preload
Graphs - CO plott vs wedge pressure as index preload
How is preload assesd in living
Initial fibver length determine sarcomere length - onset contract - cnat be determin intract human = indices preload
Increased volume blood - causes increased length - cells at end disatole
Volume blood in lv – LVEDV good index preload - estimate using echo
NIV - not readily avail
-
LVEDV - related to LVEDP by compliance of ventricular wall
LV compliance = LVEDV/LVEDP
LVEDP
Filling pressure - LV almost same as LAP
diastole mitral open == pathway LA to LV low resistance
LVEDP & LAP useful indices preload
diffiuclt measure
require RHC
RAP & CVP
Indices filling pressure & preload RH
MAY correlate well to LSide- cannot guranteed
CVP advantage easier measure
PCWP or PAOP est left filling pressure from right side
PAOP correlat well with LAP most circumstance
Swan in PA - limits
Why Does PAOP/wedge corrleate well w/ LAP
Occlsion stops flow thru vells - no pressure drop along length vessl - at same level
Pressure mesaure tip same as pressure downstream -site at which flow first occurs due to joining with other vessels
Pressure corrleate well w/ LAP path PV to LAP low ressitance - same level
Presv metion LAP correla well w/ LVEDP (not Mitral stenosis)
mark diff - PAOP not useful LV preload
Sarcomere length mx tension in contract
2.2 um
What is afterload / how is it assesed
impedance to ejection blood from heart into arterial circulation
simplest index is MAP
MAP - systole better only during systole blood ejected
End systolic pressure loop used index after
How define contractility
Factor responsible changes in perfomrance not d/t HR Preload or afterload
Mechansim - Ca++
Is (Dp/Dt) max a good index of contracility
Maximum change pressure in LV during isovol cotnraction - more force - greater rise pressure
Dorrelate contrac some circum problem - not indep loading factors (preafter)
requires LV cath - high performance electromanometer -
If return in venous increases - co increase so that venous return always = CO - what mechanism respon for this
Increase - autoregulation
hteremetric atuoreg - preload
- Increase for - d/t preload - sv d/t starling - mechanism
- Increase stretch SA node - cause modest increase HR
important
rapidly respond acute change vr
Keep LV & RV eqaul over time
Problem - two pump lv rv - not matched
Factor equal output
1. Maintaining same rate contraction -
phsical a/w - shared conduction system
- Maint SV * automatically adjust minor diffce
starling most important match SV over time
Homemetric autoreg
Increase contract d/t contractility - interanl change increase Ca avial myocardial
Change contractily indep preafter
Advan no ventricular distenion
excessive distension disadv - law laplace
Cardiac output normal
what value can it increase yooung healthy athlete
Noramlly about 5L min
Increase up to 25-30l min
Maj increase goes to skeltal muslce - can reveice excess 20l
Cerebal constant ml/min = decrease % return
Requirements to increase caridac output in exercise
Acts as demand pump
deliver amt floqw require
CO sum all tissue flows
Increase return becomes the increase co
Intense sympathetitc activity - hr contractility peripheral vcon
Cardiac output & Venous return difference
Complete circuit - total flow must same
VR - total blood flow as returns to r side
CO - flow as leaves left
Must at all times be equal
may be minor diffcs short period time d/t pulsatile nature
If not equal - pooling
tendency for venous return =- venocontricion increase tendency VR = increases CO
EDV typucal vol
SV
EF
Can Co determ if sv is known
EDV 120
SV 70
SV/EDV
CO =- SVxHR
If healthy was given atropine - hr increase 60 -120 - what would be change in CO
No significant change
Heart acts as demand puimp
Tissues demand blood suplly - signal heart to pump
Blood flow tissues - determind arteriolar adj - metabolic autoreg
Sum all flows - VR
Normal heart pumps return as CO
Tissue signal / communicate flow requirme - alter VR
Increase tendency VR increase preload - CO increase
Change hr sv alone do not affect CO - if no demands
if Brady a/w pump fail - heart may not pump suffic blood increase HR - a/w improvement in CO
If a fixed SV - dependent on CO
What is the mechainsm preventing increase Co
HR raised - heart notpump extrab lood extrahotraic vein drain heart collapse - if pumping deamnd excessd return blood
venous pressure < atm pressure - increaesd HR a/w decreased SV
Not increase CO hr unless other changes in circulation - increase venous return
Muscular exercise - muscle arteriole dilate - capillary open & muscle demand blood supply
Drop SVR - increase VR & CO increase
How does increase
Sympathetic stumil make fibre contract great strength at length - para decrease
Effect CO
Not alter over wide range - low & high rates falls off
Low SV - max - EDV & SV max - decrease a/w fall in CO
fast hr - short diastolic time - compromise vent filling - co fall
Change HR occur w/ VR - change CO
Change demand flow - tissues rather hr chagne - brady drop VR spinal - hypovol
Patient CHB - c/o low CO w/ low rates
PPM - 70 restor CO - decrease filling pressure
