The hemodynamic diagnosis and management of the obstetric patient– an anesthesiologist’s...

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.

“Normal BP” =

Low CO x High SVR (e.g. Hemorrhagic shock or early-onset/ severe pre-eclampsia)

“Normal BP” =

“Normal BP” =

Normal CO x Normal SVR (e.g. Healthy person)

High CO x Low SVR(e.g. Sepsis)

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.

High BP of severe pre- eclampsia =

High SVR x Low CO(vasospasm).

High BP of late onset pre- eclampsia =

Normal SVR x High CO?(?etiology)

Hemodynamic distinctions within pre-eclampsia:

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.

CAIN, STEPHEN M. Appearance of exeen lactate in anesthetizeddogs during anemic and hypoxic hypoxiu. Am. J. Physiol. aog(3):604-610. 1965.

Isovolemic anemia is well tolerated.

In dogs, lactate is produced in excess only below a Hct of 15%.

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.

Cited in Felicity Plaat* BA, MBBS, FRCA Best Practice & Research Clinical Obstetrics and GynaecologyVol. 22, No. 6, pp. 1043–1056, 2008

Detection of shock: tachypnea and tachycardia are first signs.

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?

First base excess during hemorrhage episode (negative means base deficit) mEq/L

Lowest base excess during hemorrhage episode (negative means base deficit) mEq/L

First base excess during hemorrhage episode (negative means base deficit) mEq/L

Units pRBCs

Lowest base excess during hemorrhage episode (negative means base deficit) mEq/L

First base excess during hemorrhage episode (mEq/L)

Lowest base excess during hemorrhage episode (mEq/L)

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).

Measurements Pregnant Values Nonpregnant Values

pH 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

If we plug in the midpoint values for pH (7.43) and pCO2 (29 mm Hg) from this table into the Henderson-Hasselbach equation we get a base excess for a normal pregnant patient as - 5 mEq/l.

From Creasy and Resnik’s Maternal-Fetal Medicine, 6th edition:TABLE 57-5   -- CHANGES IN ARTERIAL BLOOD GAS MEASUREMENTS IN PREGNANCYModified 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.

A. TEMPLETON AND G. R. KELMAN Br.J. Anaesth. (1976), 48, 1001

Base deficit at term = 3.10 mEq/L

Normal 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.

www.siumed.edu/~dking2/erg/images/placenta.jpg

Say “OUCH!”

Pre-E

mediators

Poor placentation

Pre-eclampsia: ischemic chorionic villi release pre-E mediators into maternal blood.

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).

Vasodilatory signals (NO, prostacyclin) decrease in pre-eclampsia

Pre-eclampsia mediators make endothelium produce vasoconstrictive signals (thromboxane, endothelin)

Endothelial cells send molecular signals to surrounding smooth muscle

Vessel lumen

Archer TL 2006 unpublished, Idea from Dandona P 2004

Arteriolar vasospasm in pre-eclampsia increases SVR.

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).

Pre-eclampsia, obesity, hyperglycemia or sepsis

WBC

Platelet

Protein (edema)

WBC

Platelets

Archer TL 2006 unpublished

Capillary endothelium (no underlying smooth muscle)

Bosio 1999

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.

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

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.

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 pre-eclampsia 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.

health.yahoo.com/topic/heart/overview/article...

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).

http://www.mamweb.org/modules.php?name=Content&pa=showpage&pid=32000

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

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_reflection.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

CI

SI

HR

90

40

8

3

100

80

0 15 30 Minutes

Archer TL and Shapiro A, UCSD, unpublished

Archer TL, Conrad BE. IJOA Jan 2011 pp 91-2.

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.

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

Archer, Rangwala SOAP 2011 Poster

CS delivery under GA, associated with acute pulmonary edema in a previously “generously” hydrated patient.

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 pre-eclampsia.

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