Download Pressure – Volume Relationships

Pressure – Volume
Relationships
Richard P. Wyeth Ph.D
Gentleman’s Review
Daniel Martingano OMS I
Case Study
•
A 22 YO male athlete sees his team physician for his pre-season physical.
During examination the physician notices a spitting of the second heart
sound during deep inspiration. The most likely mechanism for this splitting
is:
A. Delayed closure of aortic valve
B. Delayed closure of pulmonic valve
C. Delayed opening of mitral valve
D. Delayed opening of pulmonic valve
Frank Starling Curve
Right Ventricular v. Left Ventricular
Systole
• Peak systolic pressure of the RV is 4 to 5 x
less than that of the LV
• RV pumps like a bellows
• LV forcefully from apex to base with slight cc
twist
• Duration of systole are approximately equal
• Isovolumetric phase of loops represent longer
time required to match afterload of Ao vs PA
Right v. Left Pressure/Volume
Relationships
• Greater LV pressure alter
phasic wave form compared
to RV
• Volumes moved are equal
• LV/RV volume mismatches
are resolved continuously
Left Ventricular PV
Loop as an Example
•
•
•
•
•
•
With opening of mitral valve LV begins to
fill passively (A)
At B, LV diastolic pressure is lowest. Rapid
filling in AB due to high LV compliance
(DP/DP)
Towards conclusion of BC atrial systole
adds ~ 20% to diastolic volume as it
stretches LV
C is LVEDV/LVEDP. CD is isovolumetric
contraction
At D LV and Ao pressures equilibrate and
Ao valve opens
Rapid ejection occurs in DE
Left Ventricular PV
Loop as an Example
• LV peak systolic pressure is developed
at E
• During EF LV systolic pressure and
volumes decline
• At F LV and Ao pressures again
equilibrate and Ao valve closes
• Isovolumetric relaxation occurs as LV
pressures rapidly drop. FA
• A represents end systolic volume
unchanged from F
• Cycle is complete
Pressure Volume Loop
Modulations and Stroke Volumes
A. Increased preload increases LVEDV not LVESV
—
SV increases
B. Increased afterload increases LVESV. LVEDV
unchanged
—
SV decreases
C. Increased contractility, a positive inotropic effect
decreases LVESV not pressure
—
SV increases
Resistance to Venous Return
• Resistance to VR causes venous distention
• Veins highly distensible (vessels of capacitance not
resistance) Little change in venous pressure
• Arteries have little capacitance and contribute ~1/3 of
resistance
• Veins contribute ~2/3 of resistance to VR
– Capillaries separate arterial from venous side
– Resistance is from venule to right atrium or left
Venous Return Determines Central
Venous Pressure
• As VR increases RAP decreases (I)
• As RAP increases VR decreases (II)
• CVP = RAP
• As VR increases CVP decreases
• As CVP increases VR decreases
• When VR = 0 RAP = MSFP
Matching CO with VR
• As VR increases –
CO increases
• As VR decreases –
CO decreases
Matching CO with VR Effects –
Increasing Volume
• Increasing volume
(“Transfusion") shifts the
vascular function curve to
the right (Return to RA)
– A match between the
cardiac output and venous
return now occurs at a
higher RAP with an
increased CO
Matching CO with VR Effects –
Contractility & Vascular Resistance
•
•
Increasing cardiac contractility
(positive inotropic effect) shifts
cardiac function curve upward
Increasing Vascular resistance
(total peripheral resistance )
shifts both CO and VR
downward
Matching CO with VR Effects – Increasing
Volume, Contractility, & Vascular Resistance
•
•
•
•
What must be done CO to raise with
increased resistance?
– Increase inotropy
Will increased resistance increase
afterload?
– Yes it will take more static work to
open aortic valve (pulmonary valve
also)
Is this a good or bad thing?
What about the converse? – decrease
in resistance
Venous v. Arterial Volume
Distribution & MSFP
• Total blood volume is sum of
venous and arterial volumes
– Venous is unstressed (D in
volume will not change MSFP)
– Arterial is stressed and will change
MSFP
Venous v. Arterial Volume
Distribution & MSFP
• Notice here that changes in venous volume must
be greater than 4 L to affect increases in MSFP.
• This also shows that little arterial blood will be
found in adult volumes < 4L.
– What does that tell you about hypovolemia and
hypotension?
• What about blood redistribution?
– Decreased venous compliance vs increased.
Measuring Contractility – Systolic
Performance
•Maximum “dp/dt” is maximal rate of
pressure change per time change
• Most accurate measure of in vivo
ventricular systolic performance
dpdt
LV
•Measured during isovolumetric
contraction
– independent of pre- and afterload
Heart Performance Summary
Heart performance is interrelated:
– Related to Frank Starling Relationship
– Autonomic Status
– Preload increases increase performance
– Afterload increases decrease performance
– Contractility is independent of pre- and afterload
– Frequency, increased HR preload decreases SV decreases.
Decreased HR preload increases SV increases
Cardiac Power Output
• CPO is a measure of overall heart function incorporating flow and
pressure generating capacities.
– Good indication of maximun contractile force of heart.
• Determining CO at rest and at VO2max allows you to determine
Cardiac Reserve (CR).
• Normal (untrained) 1 W at rest …12 W at maximum exercise (VO2
max )
– Normally patients have a 3 W or better CR.
– Less has been shown as a predictor of increased mortality.
Heart Failure – Cardiac Cycle
Inadequacy
• In failure heart can not compensate for increasing
perfusion demands (exercise) by increasing cardiac
output.
• Not only are there left and right failures, there are
diastolic and systolic failures
– Weak muscle characterizes systolic (contractility) failures
– Stiff muscles characterize diastolic (preload) failures
Heart Failure – Cardiac Cycle
Inadequacy
• Heart failure is the inability of the heart to pump
sufficient blood to maintain normal exercise.
– The greater the failure the lesser the cardiac reserve.
• Clinically, cardiac reserve can be approximated by
determining cardiac output power at rest and at VO2
max.
– Most clinical presentations have a component of several or
all of these.
Right v. Left Ventricular Pump Failure
Lf Heart Failure
Case Study
•
•
•
•
•
•
•
ID/CC. 56 year old female with COPD presents to the ER with
extreme dyspnea at rest.
HPI. Increasing productive cough and exertional dyspnea. 80
pack year hx of cigarette smoking. Currently 3 pack/day despite
sypmt and dx of COPD.
PE. JVD with large a and v waves, cyanosis, labored breathing,
ankle and sacral edema, tender hepatomegaly.
Labs. ECG= rt axis deviation, peaked p waves. Pulmonary
function tests = COPD pattern.
CXR. Rt ventricular and PA enlargement.
Rt heart catheterization. Pulmonary hypertension.
Gross Anatomy. Right ventricular hypertrophy.
Summary
•The relationship of ventricular pressures and volumes determines CO.
RV peak systolic pressure is 4 to 5 x less than the LV.
–During systole the RV pumps like a bellows .
–The LV contracts from apex to base with a counter-clockwise twist.
•Systolic durations are ~ equal; isovolumetric phase of PV loops
represent the longer time required to reach the and match aortic verses
pulmonic arterial diastolic pressure (afterload).
–Greater LV pressure alter phasic wave while the volumes moved are
approximately equal with LV/RV volume mismatches continuously being
resolved.
Summary
• Ventricles with increased contractility operate at a lower enddiastolic volume/ pressure and achieve end-systolic pressure at a
lower end-systolic volume.
– In contrast, ventricles with impaired contractility operate at a high enddiastolic volume and pressure and achieve end-systolic pressure at
higher end-systolic volumes.
• The slope of a line from the origin through the end-systolic pressure
point is measures the contractile state.
– PV loops with end-systolic points on the same line are generated when
loading conditions are changed, but contractility is unaltered.
– This measure of contractility is relatively load-independent.
Summary
• PV Loops are modulated by both intrinsic and extrinsic
phenomena.
• Increased contractility, an intrinsic cardiac property increases
contractility and decreases LV end systolic volume (ESV).
– If the systemic pressure is unaltered then the systemic
circulation receives this increased stroke volume (SV).
– Extrinsic factors like increased preload increases LV end
diastolic volume (EDV) but do not alter LVESV and SV
increases.
Summary
• As pump flow varies cardiac output changes central venous
pressure (CVP) and right atrial pressure (RAP).
– RAP responds to increasing venous return that must be matched
by an increase in cardiac function.
– That is, ventricular function must increase to increase output and
bring venous return to equilibrium.
– For example, increasing blood volume shifts the vascular
function curve to the right (Return to RA) and the match between
the cardiac output and venous return now occurs at a higher
RAP.
Summary
•
In normally compliant myocardium, contractility is the intrinsic function that
alters the end systolic pressure volume relationships.
– Expressed as the maximal rate of pressure change per time change, maximum “dp/dt”
or dpdtmax is the velocity measured during isovolumetric contraction.
– It is the most accurate measure of in vivo ventricular systolic performance and
independent of afterload.
– Cardiac catheterization is required to determine this performance parameter.
•
Heart failure is the inability of the heart to pump sufficient blood to maintain
normal exercise.
– The greater the failure the lesser the cardiac reserve.
– Clinically, cardiac reserve can be approximated by determining cardiac output power
at rest and at VO2 max.