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
Determinants of end systolic wall stress
= afterload o Constantly changing throughout systole o Determined by inotropic state
26
Volumes in PV loops
* SV: total volume of blood ejected * EDV: end diastolic volume * EDS: end systolic volume o incr wall stress (afterload) => decr ESV
27
Def elastance
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
Def compliance
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
Def isovolumetric periods
* 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
What is Emax curve and what are principal determinants
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
Factors creating steep Emax slope
(↓ESV for any afterload) → ↓ volume or ↑ pressure  + inotrope  ↑ contractility  ↓ afterload
32
Factors creating flat Emax slope
(↑ESV for any afterload)  - inotrope  ↑ afterload  ↓ contractility
33
What is AUC of Emax
external work done by LV o Cardiac external work = systolic P x SV
34
What is Ed curve and what are principal determinants
end diastolic pressure/volume relationship * COMPLIANCE → determines how much end diastolic volume
35
Factors creating flat Ed slope
↓ pressure per volume o ↑ Compliance * Hyperdynamic function (ex. CVD) * ↓ Myocardial stiffness (ex. DCM in early disease)
36
Factors creating steep Ed slope
↑ pressure per volume unit o ↓ compliance * HCM * Pericardial disease
37
What is external work
energy used for blood ejection → Emax AUC o Stroke work = systolic pressure x SV
38
What is potential work
energy generated w each cardiac cycle but not converted into kinetic energy (or external work)
39
What is internal work
* 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
PV loop changes w/ incr afterload
↓ 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
PV loop changes w/ decr afterload
* ↑ 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
PV loop changes w/ incr preload
* ↑ 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
PV loop changes w/ decr preload
* ↓ end diastolic volume and pressure = primary change o ↓ SV * ↓ volume into Ao → ↓ Afterload * ↓ myocardial stretch → ↓ SV via Frank Starling * Normal IVCT hypovolemia, PH
44
PV loop changes w/ DCM
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
PV loop changes w/ HCM
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
PV loop changes w/ RCM/peric constriction
 ventricular compliance * EDPVR: steep slope → LEFTWARD AND UPWARD SHIFT o decr EDV + incr EDP * ESPVR: RIGHTWARD SHIFT
47
PV loop changes w/ SAS
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
PV loop changes w/ AI
* ↑ 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
PV loop changes w/ MR
* ↑ 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
PV loop changes w/ PDA
* 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
PV loop changes w/ MS
* 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
RV PV loop
* ↑ 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