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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.
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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 CO x Normal SVR (e.g. Healthy person) “Normal BP” = Low CO x High SVR (e.g. Hemorrhagic shock or early-onset/ severe pre-eclampsia) “Normal BP” = High CO x Low SVR (e.g. Sepsis) “Normal BP” =
Hemodynamic distinctions within pre-eclampsia: 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) 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?
First base excess during hemorrhage episode (negative means base deficit) mEq/L
Lowest base excess during hemorrhage episode (negative means base deficit) mEq/L
Units pRBCs First base excess during hemorrhage episode (negative means base deficit) mEq/L
Lowest base excess during hemorrhage episode (negative means base deficit) 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).
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 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. Base deficit at term = 3.10 mEq/L A. TEMPLETON AND G. R. KELMAN Br.J. Anaesth. (1976), 48, 1001
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!