Cardiac cycle and PV loops Flashcards
Determinants of cardiac cycle duration
systole + diastole
o Reciprocal of HR: 1/HR
o ↑ HR → ↓ cycle length
Significant ↓ in diastolic time > systole
ECG events
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
Atrial pressure waves
- 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
Function of atrial contraction
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)
Define diastole
ventricular filling
* Start with AoV closure, before MV open
What/when IVRT
- 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
Diastolic phases
- 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
EDV
End diastolic volume (EDV): volume in LV at end of diastole
Define systole
period of contraction
AoV opening → closure
What/when IVCT
- 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
Phases of systole
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
ESV
End systolic volume:(ESV) volume in LV at end of systole
* Smallest LV volume
SV
Total stroke volume: amount of blood ejected in systole = EDV - ESV
AoP curve
- 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
Heart sounds 2nd to
vibration of surrounding fluid and sudden pressure changes
o Closure of the valve itself is a slow process → makes no noise
Heart sounds
- 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
Normal RAP
Syst. 8
Diast. 8
Mean 2-6
Normal RVP
Syst. 20-30
Diast. 0-5
Mean 2-6
Normal PAP
Syst. 20-30
Diast. 10-15
Mean 10-20
Normal LAP
Arterial. 12-15
Venous. 12-15
Mean 4-12
Normal LVP
Syst. 100-140
Diast. 0-5
Mean 5-12
Normal AoP
Syst. 100-140
Diast. 60-80
Mean 70
Normall PAWP
Arterial. 12-15
Venous. 12-15
Mean 4-12
Determinants of end diastolic wall stress
= preload
o Determined by lusitropic properties
EDV and compliance
Determinants of end systolic wall stress
= afterload
o Constantly changing throughout systole
o Determined by inotropic state
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
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
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
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
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
Factors creating steep Emax slope
(↓ESV for any afterload) → ↓ volume or ↑ pressure
+ inotrope
↑ contractility
↓ afterload
Factors creating flat Emax slope
(↑ESV for any afterload)
- inotrope
↑ afterload
↓ contractility
What is AUC of Emax
external work done by LV
o Cardiac external work = systolic P x SV
What is Ed curve and what are principal determinants
end diastolic pressure/volume relationship
* COMPLIANCE → determines how much end diastolic volume
Factors creating flat Ed slope
↓ pressure per volume
o ↑ Compliance
* Hyperdynamic function (ex. CVD)
* ↓ Myocardial stiffness (ex. DCM in early disease)
Factors creating steep Ed slope
↑ pressure per volume unit
o ↓ compliance
* HCM
* Pericardial disease
What is external work
energy used for blood ejection → Emax AUC
o Stroke work = systolic pressure x SV
What is potential work
energy generated w each cardiac cycle but not converted into kinetic energy (or external work)
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
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
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
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
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
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
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
PV loop changes w/ RCM/peric constriction
ventricular compliance
* EDPVR: steep slope → LEFTWARD AND UPWARD SHIFT
o decr EDV + incr EDP
* ESPVR: RIGHTWARD SHIFT
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
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
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
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
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
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
