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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?.

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Non-invasive hemodynamics in OB


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    1. Non-invasive hemodynamics in OB Tom Archer, MD, MBA Director, OB Anesthesia UCSD

    2. Non-invasive hemodynamic research at UCSD (1) • Can emerging non-invasive hemodynamic • measurement techniques be used to improve • prediction or treatment of pre-eclampsia?

    3. 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

    4. Why impedance cardiography and applanation tonometry? Easier to perform than maternal echocardiography? Give different information than uterine or umbilical artery Doppler.

    5. 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?

    6. 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.

    7. 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?

    8. 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

    9. Gestational hypertension appears to involve persistent high CO and low-normal SVR. Hemodynamically, gestational hypertension and pre-eclampsia are different diseases. Bosio 1999

    10. 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 pre-eclampsia, followed by arteriolar constriction (high SVR)? Or did they simply fail to distinguish early and late-onset Pre-E, as in next study? Bosio 1999

    11. 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

    12. 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

    13. Extremes of SVR at 24 weeks predict early and late onset pre-eclampsia 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

    14. 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.

    15. Early pre-eclampsia • Associated with normal BMI, high SVR and low CO? • Associated with fetal growth restriction.

    16. Is SVR a “fundamental” prognostic or diagnostic measurement?

    17. Late pre-eclampsia • Associated with increased BMI and increased CO? • Relatively low impact on fetus (compared to early pre-eclampsia)?

    18. 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

    19. Should we be following SVR during pregnancy? Does early (24 weeks) elevation of SVR predict early onset (<34 weeks) pre-eclampsia?

    20. Just 4 EKG electrodes connected to a small box. Completely non-invasive. Portable, usable in OB clinic or OR.

    21. Electrical impedance (resistance) of the chest decreases during systole (inverted scale).

    22. “Traditional” impedance cardiography assumes that impedance change with heartbeat is due to volume change in aorta.

    23. Electrical velocimetry tries to improve on this assumption by assuming decrease in impedance is due to red cell alignment during acceleration of flow.

    24. Opening of aortic valve and alignment of erythrocytes is associated with a decrease in impedance (resistance).

    25. Oxytocin 10 U bolus at delivery decreases SVR and CO rises. Demonstrated with arterial line and pulse contour analysis:

    26. Increase in CO due to delivery and oxytocin, detected by electrical velocimetry. No arterial line needed.

    27. 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 pre-eclamptic pregnancies? • How do hemodynamics of spinal anesthesia and CS compare in pre-eclamptics vs. normals?

    28. Mean BP in 30 normals and 30 preeclamptic (preterm) women for C/S under SAB

    29. 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.

    30. 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.

    31. 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...

    32. 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.

    33. 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

    34. 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.

    35. Obesity OSA Hyperglycemia Sepsis Pre-eclampsia Lupus Cocaine use Hypercholesterolemia AIx increases in “inflammatory” states:

    36. What makes AIx go down-- chronically? • Exercise • Weight loss • Red wine • Statins • Control of blood pressure (ACEI and CCB) • NTG

    37. Pulse analysis is an ancient practice, now making a comeback. http://www.itmonline.org/image/pulse2.jpg

    38. 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

    39. Pulse analysis was serious business in the 19th century • Sphygmographs in common use. • Insurance companies relied on their results.

    40. Life insurance examination manual from 1891 discussed pulse analysis by sphygmography.

    41. Tom Archer, 58 y.o., good general health. Radial and predicted ascending aortic pressure waveform when subject is cold.

    42. SphygmoCor system for measuring central blood pressures

    43. 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

    44. Extra cardiac work (“wasted energy”) causes LVH chronically and– perhaps– CHF acutely in pre-eclampsia.

    45. Augmentation pressure is a deadly backdraft which exhausts the heart over time.

    46. Augmentation pressure • Reduces stroke volume and cardiac output. Creates illusion of hypovolemia? • Activates renin-angiotensin-aldosterone system? • Activates BNP?

    47. What creates central BP? #2 Stiffness of aorta (“windkessel”) AIR BLOOD heart Central BP #1 SV veins arteries #4 Wave reflection– timing and amount #3 Systemic vascular resistance (resistance arterioles) Muscular arteries

    48. Run animation • Wave reflection animation can be found at: • http://atcormedical.com/wave_reflection.html

    49. 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).”