Transcript Obstetric Anesthesia— What the obstetrician should know.

The hemodynamic diagnosis and
management of the obstetric patient–
an anesthesiologist’s perspective.
Tom Archer, MD, MBA
Director, Obstetric Anesthesia
UCSD
August 24, 2011
Topics
• BP = CO x SVR, examples in OB
• PPH, differing OB and anesthesia
perspectives
• ABGs– role in PPH management
Topics
• Intraoperative cell salvage (“cellsaver”) in
OB.
• “Dynamic indices” of “volume status” and
limitations.
Topics
• Review: pre-eclampsia damages
endothelium in capillaries, arterioles and
muscular arteries.
Topics
• Detection of endothelial damage by
– Brachial BP, proteinuria, CNS changes, liver
enzymes, thrombocytopenia, DIC (old).
– CO and SVR estimation (new)
– Central BP estimation (new)
Clinical examples
• Electrical cardiometry to measure CO and
SVR
• Applanation tonometry to measure central
BP.
Blood pressure, while important, does not tell the whole story
about health of the circulation. CO and SVR are important too.
Anesthesia’s recurring paradigm is: BP = CO x SVR.
“Normal BP” =
“Normal BP” =
“Normal BP” =
Normal CO x Normal SVR
(e.g. Healthy person)
Low CO x High SVR
(e.g. Hemorrhagic
shock or early-onset/
severe pre-eclampsia)
High CO x Low SVR
(e.g. Sepsis)
Hemodynamic distinctions within pre-eclampsia:
High BP of severe
pre- eclampsia
=
High BP of late onset
pre- eclampsia
=
High SVR x Low CO
(vasospasm).
Normal SVR x High CO?
(?etiology)
Do these distinctions have therapeutic implications or value?
We don’t know yet.
Selander study supports idea that mild pre-eclampsia has high
CO / low SVR and severe pre-eclampsia has low CO / high
SVR.
What if we could easily
measure CO and SVR?
• Assist both intensive and general obstetric care?
• Fine tune medications (e.g. antihypertensives, other
pre-eclampsia palliation)?
• Detect and monitor disease (e.g. pre-eclampsia,
hemorrhage, sepsis, heart failure)?
• Encourage healthy life style (diet, weight loss, exercise)?
Conditions decreasing SVR directly:
• Anemia (viscosity is component of resistance)
• Fever, hyperthyroidism (increased O2 demand)
• Sepsis
• Anaphylaxis
• Neuraxial and other anesthetics
Conditions increasing SVR directly:
• Severe pre-eclampsia
• Essential hypertension?
• Diabetes?
• Smoking?
• Obesity?
Conditions decreasing CO:
• Directly: Heart failure or cardiogenic shock
(MI, tamponade, cardiomyopathy,
bradyarrythmia)
• Indirectly: Baroreceptors and sympathetic
nervous system increase SVR in compensation
for decreased CO, in attempt to maintain BP.
Conditions increasing CO directly:
• Pain, fear.
• However– increased CO requires increased
venous return.
• Healthy heart pumps out what it receives
(Frank-Starling mechanism).
CO and SVR– next vital signs?
• Currently, measurement of CO and SVR is
invasive, risky, uncomfortable, labor-intensive
and non-continuous.
• Easy and continuous estimation of CO and SVR
might improve care of multiple conditions
affecting the heart, muscular arteries,
resistance arterioles and capacitance veins.
• CO and SVR might be the next vital signs.
CO and SVR in Obstetrics:
• Postpartum hemorrhage / hemorrhagic
shock
• Low venous return  Low CO  Low
MAP increased sympathetic tone
increased arteriolar resistance High
SVR.
CO and SVR in Obstetrics:
• Severe pre-eclampsia
• Arteriolar vasospasm (sFLT, thromboxane,
endothelin, etc) High SVR high
MAP decreased CO.
CO and SVR in Obstetrics:
• Sepsis
• Pathologic arteriolar relaxation (Nitric
oxide, prostacyclin, etc) low SVR
decreased MAP increased CO.
OB and Anesthesia perspectives on
post partum hemorrhage (PPH)
(matter of emphasis only)
• OB’s question: “How much blood did we lose?”
• OB’s definition: vaginal delivery 600 mL, CS
1000 mL.
• QBL (Quantitative blood loss) is the
overwhelming emphasis of California Maternal
Quality Care Collaborative.
Anesthesia approach to PPH:
• Volume definition simple but simplistic.
• What is the hemodynamic status of the
patient?
• How is organ perfusion?
• Anesthesia question: “Does the patient
need more volume and / or blood?”
Key anesthesia insight:
• IV volume trumps blood administration.
• Normovolemic anemia is well tolerated.
• Severe hypovolemia with normal Hct =
death.
Isovolemic anemia
is well tolerated.
In dogs, lactate is
produced in excess
only below a Hct of
15%.
CAIN, STEPHEN M. Appearance
of exeen lactate in anesthetized
dogs during anemic and hypoxic
hypoxiu. Am. J. Physiol. aog(3):
604-610. 1965.
Transfusion Requirements in
Critical Care (TRCC) Study:
• Heavy influence on anesthesia and ICU
communities.
• Suggests that RBC transfusion usually not
needed down to Hgb of 7 and maybe
lower (in non-ischemic heart patients).
• Transfusion risks: infectious, immune
suppression, allergic, more?
Hemodynamic management
of PPH
QBL definition has problems– How much IV
crystalloid and colloid already given? Size of
patient? Starting Hct? Normal Hct may mean
lack of IV fluid.
Detection (order of deterioration: mental
changes and RR, then HR, then BP).
Dx is clinical and decision to transfuse should
be clinical.
Detection of shock: tachypnea and tachycardia are first signs.
Cited in Felicity Plaat* BA, MBBS, FRCA Best Practice & Research Clinical Obstetrics and Gynaecology
Vol. 22, No. 6, pp. 1043–1056, 2008
Hemodynamic management
of PPH
What do we emphasize: QBL vs. hemodynamic
status?
Treatment and endpoints:
Anemia + normovolemia are OK.
Normal Hct + hypovolemia is bad.
Normothermia – often forgotten
Insufficient IV fluid– end organ ischemia
Excess IV fluid– edema, bowel + wound
ischemia
Need for “Three Bears”
Approach to resuscitation.
Too little fluid is bad– known for a long time.
Too much fluid + edema increasingly
recognized as bad in colon and other
surgeries (anastomosis and wound healing).
Anesthesia may be slow to recognize this
because our emphasis is preventing shock
ABGs in post-partum hemorrhage:
When and why to get them?
Hemorrhage and hypotension activate sympathetic nervous system which
decreases blood flow to skeletal muscle and abdominal viscera  these tissues
don’t receive oxygen and metabolism of glucose becomes anerobic:
http://www.google.com/imgres?imgurl=http://jeramedic.files.wordpress.com/2010/06/a
Can initial base deficit in trauma patients predict
volume of fluid resuscitation required?
In a very general way, yes.
Higher initial base deficits are associated with increased
total volume resuscitation (RBCs plus crystalloid).
Davis et al J Trauma 1988
Higher initial base deficits are associated with increased total RBC
administration.
However, RBC administration can be relatively low, even in severe acidosis.
Volume expansion is key, not RBC administration.
Davis et al J Trauma 1988
With adequate volume resuscitation, base deficit should
correct within hours. (If base deficit does not correct, occult
hemorrhage should be sought.)
Davis et al J Trauma 1988
Can arterial base deficit predict
transfusion requirement in
peripartum hemorrhage patients?
Does the rule of thumb of: “One unit
of blood per mEq of base deficit”
make sense?
For example, severe postpartum
hemorrhage is recognized and…
• ABG is drawn and base excess is -8 mEq/L.
• Can we estimate that 8 units of blood will be
required over the course of the woman’s
treatment?
• Short answer is, “No!”
UCSD experience with arterial base excess and RBC
transfusion in peripartum hemorrhage:
• 51 hemorrhage patients (pre and post partum) had
ABGs drawn in calendar 2009-2010.
• 36 patients had unanticipated hemorrhage.
• 15 patients were known placenta accreta patients
undergoing planned C-hysterectomy.
• Does initial or lowest base excess predict transfusion
of RBCs in these groups?
Does first base excess predict total RBC transfusion,
for all hemorrhage patients combined?
35
30
25
20
Units pRBCs
15
10
5
0
-12
-10
-8
-6
-4
-2
0
2
4
First base excess during hemorrhage episode (negative means base deficit) mEq/L
Does lowest base excess predict total RBC transfusion,
for all hemorrhage patients combined?
35
30
25
20
Units pRBCs
15
10
5
0
-16
-14
-12
-10
-8
-6
-4
-2
0
2
4
Lowest base excess during hemorrhage episode (negative means base deficit) mEq/L
Does first base excess predict total RBC transfusion,
in unanticipated hemorrhage?
25
20
15
Units pRBCs
10
5
0
-12
-10
-8
-6
-4
-2
0
2
4
First base excess during hemorrhage episode (negative means base deficit) mEq/L
Does lowest base excess predict total RBC transfusion,
in unanticipated hemorrhage?
25
20
15
Units pRBCs
10
5
0
-16
-14
-12
-10
-8
-6
-4
-2
0
2
4
Lowest base excess during hemorrhage episode (negative means base deficit) mEq/L
Does first base excess predict total RBC transfusion
for patients with known placenta accreta?
35
30
25
20
Units pRBCs
15
10
5
0
-6
-5
-4
-3
-2
-1
First base excess during hemorrhage episode (mEq/L)
0
1
Does lowest base excess predict total RBC transfusion
for patients with known placenta accreta?
35
30
25
20
Units pRBCs
15
10
5
0
-12
-10
-8
-6
-4
-2
Lowest base excess during hemorrhage episode (mEq/L)
0
A large base deficit means: “there has been– and may
still be-- a problem.”
• First actions in PPH should be:
– Call for help
– Large bore IV access (preferably > or = 2)
– Consider second IV as part of blood draw if
ordered.
– Keep patient warm.
– Volume expand with warm crystalloid or colloid.
– Ensure blood availability.
– Diagnose the problem
– Go to OR early
ABG in peripartum hemorrhage
• Of value, but initial diagnosis of hemorrhage
and its severity should be on clinical grounds
(respiratory rate, mentation, heart rate, blood
pressure, visible EBL).
• Consider placement of arterial line for serial
ABGs and other blood draws after initial
resuscitation is under way and patient is
quasi-stable.
Another reason why base deficit
is not a good guide to total volume / transfusion
requirements in peripartum hemorrhage patients.
• Normal base excess in pregnant patients
at term is -3 to -5 mEq/L (from Creasy
and Resnik data).
If we plug in the midpoint values for pH (7.43) and
pCO2 (29 mm Hg) from this table into the HendersonHasselbach equation we get a base excess for a
normal pregnant patient as - 5 mEq/l.
Measurements
pH
Pregnant Values
Nonpregnant Values
7.4–7.46
7.38–7.42
Pco2 (mm Hg)
26–32
38–45
Po2 (mm Hg)
75–106
70–100
HCO3− (mEq/L)
18–21
24–31
O2 saturation (%)
95–100
95–100
From Creasy and Resnik’s Maternal-Fetal Medicine, 6th edition:
TABLE 57-5 -- CHANGES IN ARTERIAL BLOOD GAS MEASUREMENTS IN PREGNANCY
Modified from Dildy G, Clark SL, Phelan J P, et al: Maternal-fetal blood gas physiology. In Critical Care Obstetrics, 4th ed. New York, Blackwell, 2004.
Normal base deficit at term = 3.10 mEq/L.
A. TEMPLETON AND G. R. KELMAN Br.J. Anaesth. (1976), 48, 1001
Base deficit at term =
3.10 mEq/L
Hemodynamic management
of hypovolemia
HR, BP, mentation, urine output.
“Volume status” means: will CO increase if we
give IV volume? Called “volume responsivity
of CO to volume challenge”.
“Dynamics indices” are by far best index of this.
CVP is worthless for this decision!
Dynamic indices of “volume status”:
• Systolic pressure variation (SPV), pulse
pressure variation (PPV) and stroke
volume variation (SVV) during ventilatory
cycle.
• Require: arterial line
• Are valid only with positive pressure
ventilation!
Dynamic indices work because positive pressure ventilation
provides periodic “volume challenges” and answers question
“where is the heart on its Starling Curve?”
How to judge volume status in
spontaneously breathing patients:
• Clinical signs already discussed (mental
status, RR, HR, BP, urine output).
• BP and CO response to IV volume
challenge.
• CO response to a phenylephrine bolus?
Intraoperative cell salvage (IOCS)
Intraoperative cell salvage (IOCS)
•
•
•
•
•
Pure, washed red cell product.
Platelets, debris, K+, junk is washed out.
RBC’s 2,3-DPG stays good.
RBC deformability stays good
Earlier worries about coagulation problems
were due to using unwashed cells.
Wash volume can be varied depending on the
“dirtiness” of the surgery, from 1-3 liters of
normal saline or plasmalyte per unit of RBCs.
Downside of IOCS:
• Best global recovery of RBCs is 50%.
• In other words, of1000 RBCs bled out, at
best, 500 RBCs can be returned o the
patient.
• In orthopedics, the figure is 33%.
IOCS in cesarean delivery
• Hundreds of reported cases of cell salvage
used successfully in cesarean delivery.
• Best practice is to use abundant wash (2-3
L) to remove essentially all debris.
• Best to not suction amniotic fluid into the
reservoir.
• Best to re-administer blood through
“leukocyte” reduction filters (the purpose of
which is to eliminate fetal squamous cells)
Hemodynamics of pre-eclampsia is initiated by failure
of dilation of spiral arteries and resultant chorionic
villus ischemia.
Pre-eclampsia: ischemic chorionic villi release pre-E mediators into maternal
blood.
Say “OUCH!”
Pre-E
mediators
Poor placentation
www.siumed.edu/~dking2/erg/images/placenta.jpg
Endothelial damage causes problems
in 3 types of blood vessels:
• Leaky capillaries proteinuria (glomerulus)
and edema of liver, skin, muscle and brain.
• Spasm of arterioles (<0.1 mm) increased
SVR
• Spasm of muscular arteries (0.1 mm—5
mm) increased pressure wave reflection,
central BPs and augmentation index (AIx).
Should we go beyond brachial
BP in looking at vascular
malfunction in pre-eclampsia?
Clinical detection of vascular
dysfunction (beyond brachial BP):
• Leaky capillaries detected by proteinuria,
increased liver enzymes, CNS changes,
thrombocytopenia and edema.
• Constricted arterioles detected by calculating
SVR from CO and MAP.
• Constricted muscular arteries detected by
measuring central BP and AIx with
applanation tonometry (SphygmoCor).
Endothelial cells send molecular signals to surrounding smooth muscle
Pre-eclampsia
mediators make
endothelium produce
vasoconstrictive
signals (thromboxane,
endothelin)
Vessel lumen
Vasodilatory
signals (NO,
prostacyclin)
decrease in preeclampsia
Arteriolar vasospasm in pre-eclampsia increases SVR.
Archer TL 2006 unpublished, Idea from Dandona P 2004
Pre-eclampsia, obesity, hyperglycemia and sepsis all “activate”
(damage) endothelium, white cells and platelets, leading to
white cell adhesion and infiltration, thrombosis and edema
(inflammation).
WBC
WBC
Pre-eclampsia, obesity,
hyperglycemia or sepsis
Platelet
Platelets
Capillary endothelium (no underlying
smooth muscle)
Protein (edema)
Archer TL 2006 unpublished
CO measurement in OB: by
echocardiography in this
study.
In pre-eclampsia, early phase
(28-36 weeks) may involve
an increased CO.
After 36 weeks, CO falls and
SVR rises.
Hyperdynamic early phase of
pre-eclampsia, followed by
arteriolar constriction (high
SVR)?
Bosio 1999
Gestational hypertension (no
proteinuria), by contrast,
appears to involve persistent
high CO and low-normal
SVR.
So, hemodynamically,
gestational hypertension
and pre-eclampsia are
different diseases.
Bosio 1999
Italian study of
hemodynamics of
pre-eclampsia:
early onset pre-E
(<34weeks) is
predicted at 24
weeks by high
SVR and low CO.
Late onset (>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
Italian study of hemodynamics of pre-eclampsia: early onset pre-E
(<34weeks) is predicted at 24 weeks by high SVR and low CO. Late onset
(>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
Emerging technology in pre-eclampsia research:
central blood pressures via SphygmoCor
applanation tonometry
• Evaluates stiffness of aorta and spasm of
muscular arteries (0.1 mm – 5 mm), which
causes pressure wave reflection back to
the heart.
• “Augmentation index” is extra systolic
pressure, caused by wave reflection,
which the LV has to pump against.
For Khalil et al, AIx is
an important part of
pre-eclampsia
predictive model
Khalil: Uterine artery
pulsatility index,
placental protein 13
and augmentation
index (AIx-75) all
help predict preeclampsia in first
trimester.
SphygmoCor system for measuring central blood
pressures
Systolic
augmentation
pressure is a
deadly backdraft
of pressure
which exhausts
the heart over
time.
LV “sees” the
SBP 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...
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
The author of this
1891 book about
“examining patients for
life insurance” makes
prominent reference to
pulse wave analysis,
and the author, Dr.
Keating, was an
obstetrician!
Tom Archer, 58 y.o., good general health. Takes
Crestor for high cholesterol.
Radial and predicted ascending aortic pressure
waveform when subject is cold.
Run animation
• Wave reflection animation can be
found at:
• http://atcormedical.com/wave_ref
lection.html
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. Could see this in
Pre-E.
AIx = 6%
Tom Archer, 58 yo, after exercise and
wine.
AIx = 1%
Tom Archer, 58 y.o., while squatting.
AIx = 21%
Tom Archer, seated, very cold from being
outside in winter.
AIx = 27%
“Central blood pressure” is a
tool for following endothelial
function, muscular artery
spasm and aortic stiffness.
Impedance cardiography (IC)
• Non-invasive and continuous. Little training
required. “Hands-free”.
•
• Long history (NASA, 1960’s) and multiple
iterations and algorithms.
• Bo-Med, Cardiodynamics, Cheetah, Cardiotronic).
• All look at same signal but interpret it in different
ways.
All IC systems work with the same signal– but process it differently.
Processing algorithms are patented “intellectual property”.
Bo-Med and
Cardiodynamics work
with impedance change
during systole (-dZ(t).
Cheetah and
Cardiotronic work with
rate of impedance
change during systole
dZ(t)/dt.
C. Schmidt et al British Journal of
Anaesthesia 95 (5): 603–10 (2005)
Cardiac and stroke indices increase with uterine contractions
8
CI
3
90
SI
40
100
HR
80
0
Archer TL and Shapiro A, UCSD, unpublished
15
Minutes
30
In severe pre-eclampsia, MgSO4 and labetalol decrease SVR
and increase CO (data from electrical cardiometry)
Archer TL, Conrad BE. IJOA Jan 2011 pp 91-2.
In severe pre-eclampsia, hydralazine and magnesium decrease SVR and
increase CO. FHR deceleration is associated with decreased maternal CO.
Archer TL, Conrad BE. IJOA Jan 2011 pp 91-2.
Electrical cardiometry shows normal CV changes due to delivery and
oxytocin at elective CS. Delivery and oxytocin occur at line (D/O)
Archer, Conrad, Suresh, Tarsa. Accepted 2010 J Clin Anesth
CS delivery under GA, associated with acute pulmonary edema in a
previously “generously” hydrated patient.
Archer, Rangwala SOAP 2011 Poster
Summary
• Much can be learned about hemorrhage,
pre-eclampsia and sepsis by breaking
down BP into CO and SVR.
• Technology is now available to do this
easily and non-invasively, such as EC.
• Whether this approach will lead to better
outcomes remains to be seen.
Summary
• ABGs are an important tool for assessment
of the adequacy of the circulation, but they
should not be a first priority in obstetric
hemorrhage.
• ABG base deficits do not predict RBC
transfusions at UCSD in 2009-10.
Summary
• Elevated “dynamic indices” (SPV, PPV
and SVV during the ventilatory cycle) are
the best indicators that CO will increase in
response to IV volume expansion. CVP is
worthless for this.
• Intraoperative cell salvage (“Cellsaver”) is
quite safe in OB and should be considered
in appropriate cases.
Summary
• Central blood pressure (BP in ascending
aorta) is an emerging concept in obstetrics,
and hypertension, diabetes, renal disease
and other inflammatory disorders.
• Central blood pressure can be measured
using brachial BP and applanation
tonometry of the radial artery.
Summary
• Central blood pressures are elevated in
pre-eclampsia and other inflammatory
states and may be able to predict preeclampsia.
Key Words for
Literature Searches
• Cardiac output, systemic vascular
resistance, electrical cardiometry,
electrical velocimetry, augmentation index,
augmentation pressure, dynamic indices,
systolic pressure variation, pulse pressure
variation, cell salvage, applanation
tonometry, SphygmoCor, central blood
pressure, impedance cardiography.
The End