Obstetric Anesthesia— What the obstetrician should know.

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Transcript Obstetric Anesthesia— What the obstetrician should know.

Non-invasive
hemodynamics in OB
Tom Archer, MD, MBA
Director, OB Anesthesia
UCSD
Non-invasive hemodynamic
research at UCSD (1)
• Can emerging non-invasive hemodynamic
• measurement techniques be used to improve
• prediction or treatment of pre-eclampsia?
Two measurements and
two technologies
• Cardiac output (CO) and systemic vascular resistance
(SVR), from…
– Impedance cardiography (“Electrical velocimetry”)
• Central blood pressure and Augmentation index (AIx)
from…
– Applanation tonometry and brachial BP
Why impedance cardiography
and applanation tonometry?
Easier to perform than maternal echocardiography?
Give different information than uterine or umbilical artery
Doppler.
Systemic vascular resistance
does not = uterine artery velocimetry (UtAV)
or umbilical artery velocimetry (UmAV)
• UtAV looks at uterine artery and placenta
• SVR looks at “average” arteriolar tone (for
all vascular beds).
• Does SVR add value beyond UtAV or
UmAV?
Creasy and Resnik:
• “As many as 2/3 of of pre-eclamptic
mothers have normal uterine artery
Doppler tracings.”
• Probably their SVR is not normal.
Will CO and SVR become
vital signs in OB?
• In OB clinic for pre-eclampsia prediction /
detection?
• Inpatient management of pre-eclampsia?
– Detection of deterioration of patient condition?
– Titration of vasoactive meds (hydralazine,
labetalol)?
– Titration of other Rx?
Hemodynamics of normal
pregnancy:
CO rises early, plateaus at
28-32 weeks and falls
slightly after that.
SVR falls early, plateaus at
28-32 weeks and rises
slightly after that.
Bosio 1999
Gestational
hypertension
appears to involve
persistent high CO
and low-normal
SVR.
Hemodynamically,
gestational
hypertension and
pre-eclampsia are
different diseases.
Bosio 1999
In pre-eclampsia, early
phase (28-36 weeks) may
involve an increased CO.
After 36 weeks, CO falls
and SVR rises.
Is there a hyperdynamic
early phase of preeclampsia, followed by
arteriolar constriction (high
SVR)?
Or did they simply fail to
distinguish early and lateonset Pre-E, as in next
study?
Bosio 1999
Italian study of hemodynamics of pre-eclampsia looks at
normals, early and late onset pre-eclampsia.
Early pre-eclampsia group has UA notching, growth
restriction and preterm delivery.
Late pre-eclampsia is relatively benign.
Hypertension 2008;52;873-880; originally published online Sep 29, 2008;
Herbert Valensise, Barbara Vasapollo, Giulia Gagliardi and Gian Paolo Novelli
Early onset pre-E
(< 34 weeks) is
predicted at 24
weeks by high
SVR and low CO.
Late onset pre-E
(> 34 weeks) is
predicted at 24
weeks by low SVR
and high CO.
Hypertension 2008;52;873-880; originally published online Sep 29, 2008;
Herbert Valensise, Barbara Vasapollo, Giulia Gagliardi and Gian Paolo Novelli
Extremes of SVR at 24 weeks predict early and late onset preeclampsia
SVR > 1359 at
24 weeks
predicts early
onset (< 34
weeks) Pre-E.
SVR < 770 at 24
weeks predicts
late onset (> 34
weeks) Pre-E.
Hypertension 2008;52;873-880; originally published online Sep 29, 2008;
Herbert Valensise, Barbara Vasapollo, Giulia Gagliardi and Gian Paolo Novelli
Fetal growth restriction, with or
without pre-eclampsia or
gestational hypertension, is
associated with high SVR and
low CO.
Pre-eclampsia and gestational
hypertension, without fetal
growth restriction, are
associated with low SVR and
high CO.
Hence: Fetal growth restriction is
associated with high SVR.
Rang S, van Montfrans GA, Wolf H. Serial hemodynamic measurement in
normal pregnancy, preeclampsia, and intrauterine growth
restriction. Am J Obstet Gynecol 2008;198:519.e1-519.e9.
Early pre-eclampsia
• Associated with normal BMI, high
SVR and low CO?
• Associated with fetal growth
restriction.
Is SVR a “fundamental”
prognostic or diagnostic
measurement?
Late pre-eclampsia
• Associated with increased BMI and
increased CO?
• Relatively low impact on fetus
(compared to early pre-eclampsia)?
Gestational hypertension (GH)
vs. Pre-eclampsia (PE)
• GH associated with persistently high CO and low normal
SVR and is not associated with certain VEGF
haplotypes.
• Early onset PE associated with low CO and high SVR
and certain VEGF haplotypes are protective.
• VEGF modulates vascular tone (SVR).
• Hypothesis: GH is not mediated by VEGF deficiency. PE
is.
Molecular Human Reproduction, Vol.15, No.2 pp. 115–120, 2009
Valeria C. Sandrim1, Ana C.T. Palei2, Ricardo C. Cavalli3,
Francielle M. Arau´ jo3, Ester S. Ramos4, Geraldo Duarte3, and
Jose E. Tanus-Santos1,5
Should we be following SVR
during pregnancy?
Does early (24 weeks) elevation
of SVR predict early onset (<34
weeks) pre-eclampsia?
Just 4 EKG electrodes
connected to a small box.
Completely non-invasive.
Portable, usable in OB
clinic or OR.
Electrical impedance (resistance) of the chest
decreases during systole (inverted scale).
“Traditional” impedance
cardiography assumes
that impedance change
with heartbeat is due to
volume change in aorta.
Electrical
velocimetry tries
to improve on
this assumption
by assuming
decrease in
impedance is
due to red cell
alignment during
acceleration of
flow.
Opening of aortic valve and alignment of erythrocytes is
associated with a decrease in impedance (resistance).
Oxytocin 10 U bolus at delivery decreases SVR and
CO rises. Demonstrated with arterial line and pulse
contour analysis:
Increase in CO due to delivery and oxytocin, detected by
electrical velocimetry. No arterial line needed.
Research questions
about CO and SVR
• Is Cardiotronic system useful and easy for
routine outpatient use?
• Can we detect an early increase in SVR in preeclamptic pregnancies?
• How do hemodynamics of spinal anesthesia and
CS compare in pre-eclamptics vs. normals?
Mean BP in 30 normals and 30 preeclamptic (preterm) women
for C/S under SAB
Spinal anesthesia in pre-eclamptics causes
less hypotension than in normals
• Is this true?
• Is it due to better maintained SVR or CO?
• The teaching used to be: pre-eclampsia is
associated with hyperactive sympathetic
nervous system probably not true.
Non-invasive hemodynamic
research at UCSD (2)
• Applanation tonometry: an indirect way of
measuring ascending aortic pressure
(central blood pressure).
• Augmentation index: a measure of arterial
pressure wave reflection and increased
cardiac workload during systole.
LV “sees” the
systolic BP in
the ascending
aorta.
With normal aortic
valve, LV wall
tension depends
on pressure in
ascending aorta
(and diameter of
LV chamber).
health.yahoo.com/topic/heart/overview/article...
Heart “sees” central aortic
systolic pressure, not brachial
artery pressure.
• Obviously, it’s hard to measure ascending aorta
pressure directly.
• Ascending aortic (“central”) BP can be
extrapolated from the radial pulse, using
applanation tonometry and brachial BP.
Augmentation index
• A measure of wave reflection from
muscular arteries.
• Chronically: a measure of endothelial
function and muscular artery tone.
• Acute changes due to body temperature,
posture, wine, other drugs
Augmentation Index (AIx)
• AIx = unnecessary heart work.
• High AIx leads to LVH and
cardiomyopathy.
• Lower AIx is better.
• Treatments that lower AIx help the patient.
AIx increases in
“inflammatory” states:
•
•
•
•
•
•
•
Obesity
OSA
Hyperglycemia
Sepsis
Pre-eclampsia
Lupus
Cocaine use
Hypercholesterolemia
What makes AIx go down-chronically?
•
•
•
•
•
Exercise
Weight loss
Red wine
Statins
Control of blood pressure (ACEI and
CCB)
• NTG
Pulse analysis is an ancient practice, now
making a comeback.
http://www.itmonline.org/image/pulse2.jpg
Etienne-Jules Marey (1830-1904) invented the
sphygmograph to record the arterial pulse on
smoked paper. It was used by Engelmann,
Mackenzie and Wenckebach.
Sphygmograph 1876
http://www.mamweb.org/modules.php?name=Content&pa=showpage&pid=32000
Pulse analysis was serious
business in the 19th century
• Sphygmographs in common use.
• Insurance companies relied on their
results.
Life insurance
examination
manual from
1891 discussed
pulse analysis by
sphygmography.
Tom Archer, 58 y.o., good general health.
Radial and predicted ascending aortic pressure
waveform when subject is cold.
SphygmoCor system for measuring central blood
pressures
Augmentation
index– extra
cardiac work
due to wave
reflection
AIx =
Augmentation
Pressure /
Pulse Pressure
Kozo Hirata, MD; Masanobu Kawakami, MD; Michael F O’Rourke, MD, DSc*Circ J 2006; 70: 1231–1239
Extra cardiac
work
(“wasted
energy”)
causes LVH
chronically
and–
perhaps–
CHF acutely
in preeclampsia.
Augmentation
pressure is a
deadly
backdraft
which
exhausts the
heart over
time.
Augmentation pressure
• Reduces stroke volume and cardiac
output. Creates illusion of hypovolemia?
• Activates renin-angiotensin-aldosterone
system?
• Activates BNP?
What creates
central BP?
#2 Stiffness of
AIR
aorta (“windkessel”)
BLOOD
heart
#1 SV
Central BP
veins
arteries
#4 Wave
reflection–
#3 Systemic vascular
resistance (resistance
arterioles)
Muscular arteries
timing and
amount
Run animation
• Wave reflection animation can be
found at:
• http://atcormedical.com/wave_ref
lection.html
BJOG January 1985. Vol. 92, pp. 23-30
Fetal umbilical artery flow velocity waveforms and
placental resistance : clinical significance
BRIAN J. TRUDINGER Senior Lecturer, WARWICK B. GTLES Postgraduate Scholar, COLLEEN
M. COOK Technical Oflcer, JOHN BOMBARDIER1 Biomedical Engineer & LEE COLLINS Medical
Physicist, Fetal Welfare Laboratory, Westmead Hospital, Westmead, New South Wdes 21 45,
Australia
“There is, however, much information in the velocity waveform. With
each heart beat a pressure pulse travels down the arterial tree, and
is the resultant of forward compression waves created by the
ejection pulse of the heart and reflected waves from arteriolar
terminations and other near branching points of the arterial tree
(Taylor 1965: McDonald 1974).”
BJOG January 1985. Vol. 92, pp. 23-30
Fetal umbilical artery flow velocity waveforms and
placental resistance : clinical significance
BRIAN J. TRUDINGER Senior Lecturer, WARWICK B. GTLES Postgraduate Scholar, COLLEEN
M. COOK Technical Oflcer, JOHN BOMBARDIER1 Biomedical Engineer & LEE COLLINS Medical
Physicist, Fetal Welfare Laboratory, Westmead Hospital, Westmead, New South Wdes 21 45,
Australia
Trudinger BJ et al BJOG January 1985. Vol. 92, pp. 23-30
Diseased, high resistance umbilical arteries.
Much wave reflection.
Trudinger et al BJOG January 1985. Vol. 92, pp. 23-30
Healthy, low resistance umbilical arteries.
Little wave reflection.
Trudinger et al BJOG January 1985. Vol. 92, pp. 23-30
Trudinger et al BJOG January 1985. Vol. 92, pp. 23-30
Trudinger et al BJOG January 1985. Vol. 92, pp. 23-30
Tom Archer, 58 yo, after work, seated
comfortably. Aix = 11%.
Tom Archer, 58 y.o., while squatting.
Aix = 21%
Tom Archer, seated, very cold from being
outside in winter.
Aix = 27%
Tom Archer, 58 yo, after exercise and
wine.
AIx = 1%
Ted Archer, 30 y.o., at rest. Subject runs
marathons. Aix = -14%.
Reflected pressure wave arrives late and
perfuses coronaries in diastole.
Statins and ACE inhibitors
can lower central BPs
and AIx– is this part of their
therapeutic effect?
6 months Rx
with
atorvastatin
decreased
central aortic
pulse pressure
and
augmentation
index.
WW Nichols Curr Opin Cardiol
2002, 17:543–551
Four months
Rx with
lisinopril
decreased
central aortic
pulse pressure
and
augmentation
index.
WW Nichols Curr Opin Cardiol
2002, 17:543–551
ACE inhibitors and
aldosterone antagonists
can reverse
LV hypertrophy.
Is this due to decreased AIx and
strain on the heart?
ACE inhibitors and aldosterone antagonists
reverse LV hypertrophy– via central BP effects?.
Adams KF, Am J Health-Syst Pharm—Vol 61 May 1, 2004 Suppl 2
DO, 56 yo female, hypertensive, diabetic
May 31, 2007. Aix = 41%
DO, 56 yo female, hypertensive, diabetic
January 3, 2008. After weight loss and 3
weeks Lipitor. AIx = 26%
Augmentation index
increases in pre-eclampsia
Normotensive 29 y.o. pregnant
woman
Pre-eclamptic patient,
29 yo.
Ayten Elvan-Tas¸ pinar, Arie Franx, Michiel L. Bots,
Hein W. Bruinse, and Hein A. KoomansAm J Hypertens
2004;17:941–946
MT, 22 yo, healthy, in labor, epidural in
place and she is comfortable.
Aix = -1%.
JM, 21 yo, in labor, recent onset lupus, on
prednisone and plaquenil
Aix = 6%
At UCSD: 25 y.o. woman at 26 weeks, chronic HTN and preeclampsia, on labetalol– pressure has been well controlled at
time of this study. AIx (now 24%) might have been higher
before BP control.
BNP increases
in severe preeclampsia–
probably due
to stretching of
the left
ventricle.
American Journal of Obstetrics and
Gynecology (2005) 193, 450–
4Evaluation of B-type natriuretic
peptide (BNP) levels in
normal and preeclamptic women
Jamie L. Resnik, MD,* Christina Hong,
MD, Robert Resnik, MD,
Radmila Kazanegra, MD, Jennifer
Beede, BA, Vikas Bhalla, MD,
Alan Maisel, MD
In pre-eclampsia, we see increased SVR (arteriolar
constriction), MAP and decreased CO. Atria and ventricles
respond by increasing natriuretic peptide secretion.
Cite this article as: Tihtonen KM, Kööbi T, Vuolteenaho O, et al. Natriuretic peptides and hemodynamics in preeclampsia. Am
J Obstet Gynecol 2007;196:328.e1-328.e7.
Will BNP correlate with AIx
and MAP, as indices of left
ventricular stretch?
Other questions for
UCSD research:
• Can we develop a predictive model for
pre-eclampsia based on non-invasive
hemodynamic measurements, uterine
artery Doppler and serum markers?
• Is there a role for non-invasive
hemodynamics in patient management?
Questions:
In pre-eclampsia do increases in
SVR and AIx precede changes in
umbilical artery Doppler?
Can SVR and AIx be endpoints for
palliative treatment of preeclampsia, to improve fetal and
maternal outcomes?
Question:
For the Chronic Hypertension in Pregnancy
Study (CHIPS) should you (ideally) measure
brachial BP or central BP?
Thank you!
Questions?