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Physiology Kerry > 3.1 Pressure curves / loops > Flashcards

3.1 Pressure curves / loops Flashcards

1
Q

Cardiac cycle

A

1 compelete systole /disatole

at rate 72bpm - takes 0.8secs

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2
Q

Draw the pressure time curve for LV & aorta

A

page 39 Kerry

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3
Q

What are the phases of systole and disatole

A
  1. Isovolumetric contract 0.05s
    First phase of systole
    Mitral valve closure until AV open
  2. Isotonic contraction - pid & reduced ejection
  3. Prodiastole 0.04 - Last phase of systole - ejection finished - pressure falls & AV closes

Diastole

  1. Isovol relax - closure AV -> MV opens
  2. Rapid filling phases
  3. Diastasis - reduced filling
  4. atrial systole
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4
Q

Whats happening during sytsole

A
  1. Pressure LV rises rapidly - closure of MV
  2. 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

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5
Q

Diastole

A

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

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6
Q

Heart sounds

A

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

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7
Q

Curve different if RV & PA

A

Shape similar - pressure less - peak 25/8

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8
Q

Differences if patient 70 y.o

A

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

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9
Q

Draw Pressure vol & atrial pressure

A

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

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10
Q

What causes drop Atrial pressure after AV opens

A

X descent - shortening of ventricles - pulls fibrous av ring down
- Length atria - increase capacity - drop in pressure - atrial pressure negative

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11
Q

Pressure Volume loop - draw Diastolic elastance curve for LV

A

Draw page 42

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12
Q

How measure elastance

A

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

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13
Q

What is the significance pf Shape of LV pressure vol relationship

A

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

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14
Q

Draw pressure volume loop for LV

A

PV loop for LV - page 43

where doe the vavles open

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15
Q

Preload increased on PV Loop

A

page 43 - increased sv, afterload contractility same - afterload parller - same after

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16
Q

What is the best index of preload

A

End diastole is LVEDV

Best index of preload -

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17
Q

If increased afterload how does this affect curve

A

Aortic valve closing at higher pressure less volume ejected

18
Q

Best index of afterload of PV loop

A

Slope line connectivn lvedv w/ end ssytolic point -

afterload line foor loop 2 large angle w/ x than loop 1 = afterload higher

19
Q

How show preload & contractility the same

A

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

20
Q

Effect contractility of LV PV loop

A

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

21
Q

Area within LV - LV loop represent

A

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

22
Q

Determinanats of myocardial performance

A

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

23
Q

SV determined by

A

Preload
Afterload
contractility

24
Q

Preload

A

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

25
Q

How is preload assesd in living

A

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

26
Q

LVEDP

A

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

27
Q

RAP & CVP

A

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

28
Q

Why Does PAOP/wedge corrleate well w/ LAP

A

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

29
Q

Sarcomere length mx tension in contract

A

2.2 um

30
Q

What is afterload / how is it assesed

A

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

31
Q

How define contractility

A

Factor responsible changes in perfomrance not d/t HR Preload or afterload

Mechansim - Ca++

32
Q

Is (Dp/Dt) max a good index of contracility

A

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 -

33
Q

If return in venous increases - co increase so that venous return always = CO - what mechanism respon for this

A

Increase - autoregulation
hteremetric atuoreg - preload

  1. Increase for - d/t preload - sv d/t starling - mechanism
  2. 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

  1. 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

34
Q

Cardiac output normal

what value can it increase yooung healthy athlete

A

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

35
Q

Requirements to increase caridac output in exercise

A

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

36
Q

Cardiac output & Venous return difference

A

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

37
Q

EDV typucal vol
SV

EF
Can Co determ if sv is known

A

EDV 120
SV 70

SV/EDV

CO =- SVxHR

38
Q

If healthy was given atropine - hr increase 60 -120 - what would be change in CO

A

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

39
Q

What is the mechainsm preventing increase Co

A

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

40
Q

How does increase

A

Sympathetic stumil make fibre contract great strength at length - para decrease

41
Q

Effect CO

A

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

Physiology Kerry (17 decks)

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