Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Draw the pressure time curve for LV & aorta

A

page 39 Kerry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Curve different if RV & PA

A

Shape similar - pressure less - peak 25/8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pressure Volume loop - draw Diastolic elastance curve for LV

A

Draw page 42

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Draw pressure volume loop for LV

A

PV loop for LV - page 43

where doe the vavles open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Preload increased on PV Loop

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the best index of preload

A

End diastole is LVEDV

Best index of preload -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
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
26
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
27
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
28
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
29
Sarcomere length mx tension in contract
2.2 um
30
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
31
How define contractility
Factor responsible changes in perfomrance not d/t HR Preload or afterload Mechansim - Ca++
32
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 -
33
If return in venous increases - co increase so that venous return always = CO - what mechanism respon for this
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 2. 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
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
35
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
36
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
37
EDV typucal vol SV EF Can Co determ if sv is known
EDV 120 SV 70 SV/EDV CO =- SVxHR
38
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
39
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
40
How does increase
Sympathetic stumil make fibre contract great strength at length - para decrease
41
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

Physiology Kerry (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions