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4. Physiology and pathophysiology > Cardiac cycle and PV loops > Flashcards

Cardiac cycle and PV loops Flashcards

1
Q

Determinants of cardiac cycle duration

A

systole + diastole
o Reciprocal of HR: 1/HR
o ↑ HR → ↓ cycle length
 Significant ↓ in diastolic time > systole

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2
Q

ECG events

A

Electrical events precedes mechanical systole
* P wave: electrical depol of atria → atrial contraction
* QRS: electrical depol of ventricles
o Occurs before ventricular contraction
* T wave: repol of ventricles
o Occurs before end of ventricular contration

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3
Q

Atrial pressure waves

A
  • a-wave: atrial contraction
    o Slight ↑ in atrial P: RAP = 4-6, LAP = 7-8 mmHg
  • c-wave: early ventricular contraction
    o Bulging of closed AV valves in atrium from ↑ ventricular P
  • v-wave: ventricular systole and atrial diastole
    o Atrial filling and slow blood flow from PVs → ↑ atrial P
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4
Q

Function of atrial contraction

A

function as a primer pump
* 80% of blood flows from atria → ventricles before atrial contraction
* Atrial contraction contributes to 20% of filling
* Heart can function normally w/o atrial contraction: resting state has capability to pump 300-400% > required by body (WAY TO GO)

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5
Q

Define diastole

A

ventricular filling
* Start with AoV closure, before MV open

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6
Q

What/when IVRT

A
  • Start with AoV closure, before MV open
    o Isovolumic relaxation time (IVRT): rapid decrease in LVP while volume is constant
    o Rate of pressure decrease => determined by Ca2+ mvt off contractile proteins
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7
Q

Diastolic phases

A
  • When LVP < LAP => MV open => start of LV filling
    o Pressure nadir is early diastole
    o Slow rise with ventricular filliing

a) Period of rapid filling (1/3 of diastole) = rapid flow of blood into LV → rapid ↑ LV volume curve
* E wave on PW Doppler: wide opening on MV
o Peak filling at the E point on M-mode
* Corresponds to S3
b) Diastasis: equalization of pressure atria = ventricles → very little blood mvt
* Abbreviated w/ ↑ HR
* M-mode: MV leaflets drift partially closed as blood flow through mitral valve orifice slows
c) Atrial contraction (final 1/3): ↑ ventricular filling by 20%
* A wave on PW Doppler
* M-mode: A point → partial reopening of MV
* Correspond to S4: gallop sound

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8
Q

EDV

A

End diastolic volume (EDV): volume in LV at end of diastole

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9
Q

Define systole

A

period of contraction
AoV opening → closure

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10
Q

What/when IVCT

A
  • Starts with AV valve closure when LVP > LAP (correspond to S1)
    o Isovolumic contraction time (IVCT): rapid rise in LVP w constant volume (closed MV and AoV)
     Rate of pressure rise => indicator of myocardial contractility
     Pressure build up necessary to open AoV
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11
Q

Phases of systole

A

a) Rapid ejection (1/3 of systole): ejection of 70% of blood
* Rate of blood flow into Ao > rate of blood flow into arteries
* LVP > 80mmHg and RVP > 8mmHg
b) Peak: rate of blood flow into Ao = rate of blood flow into arteries
c) Reduced ejection (2/3 of systole): ejection of 30% of blood
* decr blood flow from LV
* Ejection last until end of systole
o AoV closure mark end of systole = S2
o Immediately after T wave

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12
Q

ESV

A

End systolic volume:(ESV) volume in LV at end of systole
* Smallest LV volume

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13
Q

SV

A

Total stroke volume: amount of blood ejected in systole = EDV - ESV

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14
Q

AoP curve

A
  • When AoV open → rapid ↑ in pressure with rapid LV ejection → peak = 120mmHg
    o Entry of blood into peripheral arteries → wall stretch
  • When ventricular ejection ceases → ↓ pressure
    o Remain high since arterial wall maintain pressure in diastole
    o Incisura: short period of backward flow before AoV closure
  • After AoV closure: slow ↓ in pressure during diastole
    o Blood stored in distended elastic arteries
    o Continuous flow in peripheral vessels
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15
Q

Heart sounds 2nd to

A

vibration of surrounding fluid and sudden pressure changes
o Closure of the valve itself is a slow process → makes no noise

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16
Q

Heart sounds

A
  • S1: AV valve closure when ventricles contract
  • S2: semilunar valve closure at end of systole
    o Rapid snap
  • S3: early ventricular filling
  • S4: atrial contraction
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17
Q

Normal RAP

A

Syst. 8
Diast. 8
Mean 2-6

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18
Q

Normal RVP

A

Syst. 20-30
Diast. 0-5
Mean 2-6

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19
Q

Normal PAP

A

Syst. 20-30
Diast. 10-15
Mean 10-20

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20
Q

Normal LAP

A

Arterial. 12-15
Venous. 12-15
Mean 4-12

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21
Q

Normal LVP

A

Syst. 100-140
Diast. 0-5
Mean 5-12

22
Q

Normal AoP

A

Syst. 100-140
Diast. 60-80
Mean 70

23
Q

Normall PAWP

A

Arterial. 12-15
Venous. 12-15
Mean 4-12

24
Q

Determinants of end diastolic wall stress

A

= preload
o Determined by lusitropic properties
 EDV and compliance

25
Q

Determinants of end systolic wall stress

A

= afterload
o Constantly changing throughout systole
o Determined by inotropic state

26
Q

Volumes in PV loops

A
  • SV: total volume of blood ejected
  • EDV: end diastolic volume
  • EDS: end systolic volume
    o incr wall stress (afterload) => decr ESV
27
Q

Def elastance

A

pressure change required to elicit volume change
* Maximal elastance = beginning of systole
* Ability to returning to its normal volume after stretching force is released

Pressure/volume

28
Q

Def compliance

A

diastolic property → volume of blood that can be stored in given portion of circulation
* Elastic deformation/change in volume secondary to an applied pressure
* Opposite of elastance

volume/pressure

29
Q

Def isovolumetric periods

A
  • Constant volume, all valves are closed
  • IVCT = start of systole
    o Rapid rise in ventricular pressure
    o Until reach Ao or PA pressure and semilunar valve open
  • IVRT = start of diastole
    o Rapid fall in ventricular pressure
    o Until under atrial pressures and AV valve open
30
Q

What is Emax curve and what are principal determinants

A

end systolic pressure/volume relationship
* Line connecting several end systolic wall-stress volume point
o Slope is Emax (end systolic pressure-volume curve) → maximal elastance of ventricle
o V0: theoretic volume that chanber should empty if afterload was 0
* Affected by contractility and volume

31
Q

Factors creating steep Emax slope

A

(↓ESV for any afterload) → ↓ volume or ↑ pressure
 + inotrope
 ↑ contractility
 ↓ afterload

32
Q

Factors creating flat Emax slope

A

(↑ESV for any afterload)
 - inotrope
 ↑ afterload
 ↓ contractility

33
Q

What is AUC of Emax

A

external work done by LV
o Cardiac external work = systolic P x SV

34
Q

What is Ed curve and what are principal determinants

A

end diastolic pressure/volume relationship
* COMPLIANCE → determines how much end diastolic volume

35
Q

Factors creating flat Ed slope

A

↓ pressure per volume
o ↑ Compliance
* Hyperdynamic function (ex. CVD)
* ↓ Myocardial stiffness (ex. DCM in early disease)

36
Q

Factors creating steep Ed slope

A

↑ pressure per volume unit
o ↓ compliance
* HCM
* Pericardial disease

37
Q

What is external work

A

energy used for blood ejection → Emax AUC
o Stroke work = systolic pressure x SV

38
Q

What is potential work

A

energy generated w each cardiac cycle but not converted into kinetic energy (or external work)

39
Q

What is internal work

A
  • Internal work: total work of the heart for each contraction
    o Total mechanical work = external + potential work
    o Proportional to myocardial O2 consumption
  • Increase w heart dz
40
Q

PV loop changes w/ incr afterload

A

↓ SV → ↑ volume
* ↑ IVCT → longer time to reach pressure
* ↑ end diastolic volume and pressure
o Compensatory
o Not infinite mechanism: at some point → LVH → ↓ compliance
* Volume ↓
* Pressure ↑
* Disease progression
o Normal contractility at onset
o Contractility ↓ → ↓ SV over time
* Systolic PG in Aortic curve can be present depending on disease

SAS

41
Q

PV loop changes w/ decr afterload

A
  • ↑ SV → can eject more volume against lower pressure
  • ↓ IVCT → shorter time to reach pressure
    o Primary change
  • ↓ End diastolic volume and pressure
    o Cycle starting from a lower pressure and volume

systemic vasodil

42
Q

PV loop changes w/ incr preload

A
  • ↑ End diastolic volume and pressure
    o ↑ contractility via Frank Starling
  • Initially
    o ↓ end systolic pressure and volume
    o Afterload ↑ → higher SV
  • Overtime
    o ↑ SV → more blood into Ao/syst vasculature
    o Afterload ↑ from ↑ arterial blood pressure
  • If inotrope positive
    o ↑ contractility normalize afterload
  • Normal IVCT

AI, PDA

43
Q

PV loop changes w/ decr preload

A
  • ↓ end diastolic volume and pressure = primary change
    o ↓ SV
  • ↓ volume into Ao → ↓ Afterload
  • ↓ myocardial stretch → ↓ SV via Frank Starling
  • Normal IVCT

hypovolemia, PH

44
Q

PV loop changes w/ DCM

A

decr inotropy => decr SV + compensatory incr preload
* Incomplete ventricular emptying → incr EDV and ESV
o ↓SV and CO
* Curve slopes
o ESPVR: flat slope from ↓ end systolic pressures => incr ESV
o EDPVR: flat slope from ↑ compliance in early disease
* RIGHTWARD SHIFT
* decr stroke work

45
Q

PV loop changes w/ HCM

A

Ventricular filling depends on venous return and compliance of ventricle in diastole
* HCM → impaired relaxation and decr ventricular compliance
* EDPVR: steep slope → LEFTWARD AND UPWARD SHIFT
o decr EDV + incr EDP
* decr SV until compensation w/ ↑ preload occurs
* No change in IVRT or IVCT

46
Q

PV loop changes w/ RCM/peric constriction

A

 ventricular compliance
* EDPVR: steep slope → LEFTWARD AND UPWARD SHIFT
o decr EDV + incr EDP
* ESPVR: RIGHTWARD SHIFT

47
Q

PV loop changes w/ SAS

A

High outflow resistance caused by reduced valve orifice area => impaired LV emptying
* ↑ peak systolic ventricular pressure → incr systolic wall stress
o ↑ afterload → ↓ SV and ↑ ESV
* decr SV: velocity of fiber shortening decr 2nd to incr afterload
o decr further w development of systolic and diastolic dysfct
* incr ESV
o incr EDV because ESV added to venous return = incr preload
o Activate Frank starling => incr contractility
 Can be sufficient in mild AS to maintain normal SV
 Compensatory incr in EDV limited by LVH due to chronic  in afterload
* Can lead to large incr EDP + decr EDV because of incr stiffness
* Contractility is unchanged

48
Q

PV loop changes w/ AI

A
  • ↑ preload: LV fills from AI + atrial volume
    o  ventricular filling   EDV
     Activate Frank Starling →  contractility → incr SV
  • incr LV peak systolic pressure
     As long that not in failure = small incr in ESV
  • If failure: incr ESV => decr SV
    o Dilation of LV secondary to AI
     incr ventricular compliance
     Also contributes to incr EDV
  • ↑ afterload: ↑ wall stress during ejection
  • Absence of true IVRT: blood flows from the Ao when diastole start + blood continue to flow even when MV open (AoP > LVP)
    o No vertical line from Ao closure and MV opening
  • Absence/brief IVCT: LV start contraction and incr LVP
    o AI still flows until LVP > AoP
    o ↓ diastolic pressures
  • Contractility unchanged
49
Q

PV loop changes w/ MR

A
  • ↑ preload: regurgitant volume ↑ LAP → ↑ LV filling pressure
    o EDPVR: steep curve
  • decr afterload: MR is a = resistance pathway
    o ↓ total outflow resistance
    o decr ESV (can incr if CHF) w/ unchanged contractility
  • Absence of true IVRT: blood continue to flow back into LA as LVP > LAP
  • Absence of true IVCT: blood start to flow across MV before AoV open
  • Dilation secondary to incr EDV => incr LV compliance
    o Would normally incr afterload, but not in case of MR
  • SV is incr = volume ejected into Ao + LA
    o But decr CO => net forward flow in Ao in reduced
50
Q

PV loop changes w/ PDA

A
  • incr preload
    o EDPSV: steep curve
    o incr EDV because of overciculation of the blood in pulmonary circulation
    o incr venous return to LA
  • incr SV with stable ESV
    o Frank starling activation 2nd to incr EDV
51
Q

PV loop changes w/ MS

A
  • decr preload from impaired LV filling => ↓ EDV
    o decr SV => decr CO (Frank Starling)
  • ↓ afterload from ↓ LV filling and ↓ AoP
    o decr wall stress
    o decr ESV slightly
52
Q

RV PV loop

A
  • ↑ preload compared to LV
    o Same SV as both sides have same SV
  • ↓ afterload from low PVR
    o Much of RV ejection occurs after systolic pressure is reached
    o RV very sensitive to changes in afterload
  • ↓ contractility
    o Dependent on coordinated contraction w/ LV (IVS)
     ↓ LV contractility or BBB can ↓ contractility

4. Physiology and pathophysiology (18 decks)

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