FETAL ACID-BASE, CORD GAS INTERPRETATION, & SUPPLEMENTAL OXYGEN: KEEPING IT SIMPLE, KEEPING IT SAFE
with Lisa A. Miller, CNM, JD
DISCLOSURE In the interest of full disclosure, I wish to disclose my relationship with Clinical Computer Systems, Inc., as a consultant and co-developer of their “E-Tools” software. I am also on the medical advisory board of LifeWave, Inc., a company developing a new external fetal monitoring modality.
DISCLAIMER Although I am a member of the Illinois State Bar Association and a licensed attorney in the state of Illinois, I am here today as a nurse educator, not a lawyer. Nothing in the program should be construed as legal advice. In other words, if you need legal advice, retain a practicing attorney!
Additionally, I am co-author of two EFM textbooks -
DISCLOSURE
Mosby’s pocket guide: “Fetal Monitoring: A Multidisciplinary Approach”, and “Fetal Monitoring” by Lippincott
And published in 2014, the EFM workbook, a companion workbook to the Mosby Pocket Guide, allowing practice with NICHD terminology & tracing interpretation
Fetal oxygenation involves the transfer of oxygen from the environment to the fetus…
And the subsequent fetal physiologic response if oxygen transfer is interrupted…
LET’S TALK ABOUT INTRAPARTUM HYPOXIA AND NEONATAL ENCEPHALOPATHY What is the relationship between metabolic acidemia and “potential injury” as illustrated here? Why is respiratory acidemia not included in this pathway?
TO UNDERSTAND THE RELATIONSHIP BETWEEN INTRAPARTUM EVENTS AND NEONATAL ENCEPHALOPATHY, WE NEED TO UNDERSTAND FETAL ACID-BASE, AND THE DIFFERENCES BETWEEN RESPIRATORY, METABOLIC, AND MIXED ACIDEMIA IN CORD GAS ANALYSIS. Fetal umbilical artery pH less than 7.0, or base deficit greater than or equal to 12 mmol/L, or both, increases the probability that neonatal encephalopathy, if present, had an intrapartum hypoxic component; lesser degrees of acidemia decrease that likelihood. If the cord arterial gas pH levels are above 7.20, it is unlikely that intrapartum hypoxia played a role in causing neonatal encephalopathy ACOG & AAP, 2013
UNDERSTANDING ACID-BASE To understand acid-base balance we will review four things: aerobic vs. anaerobic metabolism, and respiratory vs. metabolic acidemia In a healthy, well-oxygenated fetus, the primary mode of producing energy is via aerobic metabolism which is oxygen dependent.
AEROBIC METABOLISM CO2
O2
H2O
METABOLISM GLUCOSE
ATP (36)
HEAT (417 kcal)
ANAEROBIC METABOLISM When oxygen isn’t available for this process, the fetus uses anaerobic metabolism, which depends upon glucose and conversion of glycogen stores. The energy produced by anaerobic metabolism is much less than that produced by aerobic metabolism and is used to cover basal metabolic needs.
ANAEROBIC METABOLISM LACTIC ACID
GLUCOSE and stored GLYCOGEN
METABOLISM
ATP (2)
HEAT (32 kcal)
RESPIRATORY VS. METABOLIC ACIDEMIA Respiratory Acidemia: During normal aerobic metabolism, the end products are CO2 & H2O. If blood flow slows (often due to cord compression) then these by products are not efficiently cleared and will accumulate, turning into hydrogen & bicarbonate ions.
RESPIRATORY VS. METABOLIC ACIDEMIA Respiratory Acidemia: It is the accumulation of these free hydrogen ions in the blood that cause the drop in pH. This is respiratory acidemia and is related to the inability to effectively clear the accumulation of CO2. The first breath at birth easily corrects this.
RESPIRATORY VS. METABOLIC ACIDEMIA Metabolic Acidemia: If the decrease in blood flow becomes significant, or there is a problem with sufficient oxygen getting to the placental intervillous space (recall the O2 pathway) then the peripheral tissues will shift into anaerobic metabolism which uses glucose and stored glycogen.
RESPIRATORY VS. METABOLIC ACIDEMIA Metabolic Acidemia: This anaerobic metabolism results in the by-product lactic acid, which much be buffered. When the amount of lactic acid exceeds buffering capacity, this results in metabolic acidemia, which can extend from peripheral tissues to vital organs if uncorrected.
UMBILICAL CORD BLOOD ANALYSIS
UMBILICAL CORD BLOOD ANALYSIS
APPROXIMATE NORMAL CORD BLOOD VALUES FOLLOWING LABOR VEIN
ARTERY
pH
7.30 - 7.40
7.20 - 7.30
p02
25 - 35 mmHg.
15 - 25 mmHg.
pC02
35 - 45 mmHg.
45 - 55 mmHg.
HCO3
18 - 22
20 - 24
-4 + 2 mEq/Liter
-4 + 2 mEq/Liter
Base Excess
KEY POINTS FOR CORD GAS ANALYSIS Base deficit is more reliable than HCO3 as a measure of acidemia, and pH alone is not helpful Umbilical vein samples will always have a higher pH, higher PO2, and a lower PCO2 You must obtain both venous and arterial samples, or you cannot prove you have an arterial sample.
LABOR EFFECTS ON BASE DEFICIT Latent phase has minimal effect on base deficit Active phase of first stage results in the mean base deficit increasing by approximately 1mmol/L every 3 hours, due to an increase in the frequency and intensity of UCs In second stage, with the increase in both strength and frequency and the additional pushing efforts, base deficit will increase by 1mmol/L every hour These effects are greater if uterine activity is greater than normal, making the evaluation of contractions key to fetal acid-base issues
Pop Quiz on cord gas analysis Determine whether the following arterial cord gas values represent normal, respiratory acidemia, metabolic acidemia or mixed acidemia: 1.
2.
3.
4.
pH
6.96
PCO2
104
BD
13
pH
7.10
PCO2
70
BD
11
pH
6.79
PCO2
40
BD
25
pH
7.26
PCO2 BD
51 4
Bonus questions -- Explain these cord gases: UV pH 7.19
PCO2 66
BD 5
UA pH 7.18
PCO2 68
BD 5
UV pH 7.25
PCO2 65
BD 1
UA pH 7.29
PCO2 55
BD 1
And now, back to the oxygen pathway…
What does the fetal heart rate tracing reveal about this pathway?
Start at the top What information does the FHR tracing provide regarding oxygen transfer?
NOT ALL FHR DECELERATIONS HAVE A RELATIONSHIP TO THE OXYGEN PATHWAY… To draw conclusions regarding the significance of any FHR deceleration, we must understand the underlying physiology. But most of us were taught very simplistic phrases, like “head compression”, “cord compression” or “uteroplacental insufficiency”. Let’s see if we can go a bit deeper and perhaps draw some conclusions about FHR decelerations and fetal oxygenation
PHYSIOLOGY: EARLY DECELERATIONS
Mechanism of Late Deceleration Transient hypoxemia
Recurrent or sustained disruption of oxygenation
Chemoreceptor stimulation Tissue hypoxia
Sympathetic outflow
Anaerobic metabolism
Peripheral vasoconstriction
Lactic acidosis
Blood pressure rise Baroreceptor stimulation Vagal outflow
Metabolic acidemia Direct myocardial depression
Deceleration
MECHANISM OF VARIABLE DECELERATION VENOUS COMPRESSION Decreased venous return Relative hypovolemia Reflex increase in FHR
ARTERIAL COMPRESSION Increased SVR, elevated BP Baroreceptor stimulation Vagal outflow
Reverse
Junctional / Idioventricular Rate
All FHR decelerations that have any potential clinical significance have the same common trigger… Interruption of oxygen transfer from the environment to the fetus at one or more points along the oxygen pathway So, when we see a late, variable, or prolonged decel, we can agree …
Principle #1 Variable, late or prolonged decelerations signal interruption of the oxygen pathway at one or more points
The second half of the pathway What information can the FHR tracing provide regarding the fetal response to interruption of the oxygen pathway?
“In a fetus exhibiting either moderate variability or accelerations of the FHR, damaging degrees of hypoxia‐ induced metabolic acidemia can reliably be excluded”
Intrapartum Management of Category II Fetal Heart Rate Tracings Towards Standardization of Care • • • • • • • • •
Steven L. Clark, M.D. Michael P. Nageotte, M.D. Thomas J. Garite, M.D. Roger K. Freeman, M.D. David A. Miller, MD. Kathleen Rice Simpson, R.N. Ph.D. Michael A. Belfort, M.D., Ph.D. Gary A. Dildy, M.D. Julian T. Parer, M.D.
• • • • • • • • •
Richard L. Berkowitz, M.D. Mary D’Alton, M.D. Dwight J. Rouse, M.D. Larry C. Gilstrap, M.D. Anthony M. Vintzileos, M.D. J. Peter van Dorsten, M.D. Frank H. Boehm, M.D. Lisa A. Miller, CNM, JD Gary D. V. Hankins, M.D.
American Journal of Obstetrics and Gynecology April 2013
“The superb reliability of accelerations and moderate variability in excluding any degree of hypoxia-related central nervous system depression or risk of ongoing hypoxic injury would allow observation of patterns with these features and adequate labor progress regardless of the deceleration pattern”
Principle #2 Moderate variability or accelerations exclude ongoing hypoxic injury
Principle #1 Variable, late or prolonged decelerations signal interruption of the oxygen pathway at one or more points Principle #2 Moderate variability or accelerations exclude ongoing hypoxic injury
WHAT DO WE DO ABOUT IT? The objective of a “standardized management” protocol is to minimize the opportunities for preventable error Risk factors for error include clinicians relying on random recall (memory will fail you), lack of a checklist, unnecessary complexity, and lack of a shared mental model among team members Additionally, even the best scenarios for practice cannot prevent all poor outcomes - in those cases, the obstetric team must be able to articulate the rationale for their actions in order to defend their practice.
Management (n.) The act of handling or controlling something successfully Success = Safe delivery Safe delivery = Birth free from injury caused by interrupted oxygenation
Thus, the objective of a “standardized management” protocol is to minimize all potential sources of preventable error
Intrapartum Fetal Heart Rate Management Decision Model “ABCD”
Confirm FHR and uterine activity
“A” – Assess oxygen pathway “B” – Begin corrective measures
I FHR Category?
FHR Category?
III
II
II or III
Presence of moderate variability or accelerations Yes
I
and
Absence of clinically significant decelerations No/unsure
“C” – Clear obstacles to rapid delivery “D” – Determine decision to delivery time
Is the patient low‐risk? No
Yes
Is vaginal delivery likely before the onset of metabolic acidemia and potential injury?
Yes
Routine Surveillance •Every 30 min in the 1st stage of labor •Every 15 min in the 2nd stage of labor
No/unsure
Heightened Surveillance •Every 15 min in the 1st stage of labor •Every 5 min in the 2nd stage of labor
Expedite Delivery
Intrapartum FHR Monitoring Management Decision Model Confirm FHR and uterine activity
“ABCD” “A” - Assess oxygen pathway and other causes* “B” - Begin corrective measures if indicated
II or III
FHR Category?
FHR Category?
I
III
II
I
Presence of moderate variability or accelerations Yes
and
Absence of clinically significant decelerations No or unsure
Is the patient “low-risk”?
“C” - Clear obstacles to rapid delivery “D”- Determine decision to delivery time
No
Yes
Yes
Is vaginal delivery likely before the onset of metabolic acidemia and potential injury? No or unsure
Routine Surveillance • Every 30 min in the active phase of the • Every 15 min in the second stage
Heightened Surveillance 1st
st stage • Every 15 min in the active phase of the 1 stage • Every 5 min in the second stage
Expedite Delivery
Fetal Heart Rate Categories
I
Category I includes all of the following: • Baseline rate 110-160 bpm • Moderate variability • No late decelerations • No variable decelerations • No prolonged decelerations
Category II includes all tracings not assigned to Category I or Category III
II
III
Category III includes at least one of the following: • Absent variability with recurrent late decelerations • Absent variability with recurrent variable decelerations • Absent variability with bradycardia for at least 10 min • Sinusoidal pattern for at least 20 min
A Practical “ABCD” Checklist Approach to FHR Management
Lungs
Heart
“A”
“B”
Assess Oxygen Pathway
Begin Corrective Measures
Airway and breathing
Position changes Heart rate and rhythm Fluid bolus
Blood pressure Vasculature Volume status
Uterus Placenta
Cord
Supplemental oxygen
Correct hypotension
Contraction strength Contraction frequency Baseline uterine tone Stop or reduce stimulant Exclude uterine rupture Consider uterine relaxant
“D”
Clear Obstacles to Rapid Delivery
Determine Decision to Delivery Time
Facility
Confirm: OR availability Equipment availability
Consider Facility response time Location of OR
Staff
Consider notifying Obstetrician Surgical assistant Anesthesiologist Neonatologist Pediatrician Nursing staff
Consider: Staff availability Training Experience
Mother
Fetus
Check for bleeding Exclude abruption
Vaginal exam Consider amnioinfusion Exclude cord prolapse
“C”
Labor
Two Principles of Fetal Heart Rate interpretation Environment Lungs Heart Vasculature Uterus Placenta Cord
1. Decelerations (late, variable or prolonged) signal interruption of the oxygen pathway at one or more points
Fetus Hypoxemia Hypoxia Metabolic acidosis
Metabolic acidemia
Consider Informed consent Anesthesia options Laboratory tests Blood products Intravenous access Urinary catheter Abdominal prep Transfer to OR
Surgical considerations (prior abdominal or uterine surgery ) Medical considerations (obesity, hypertension, diabetes) Obstetric considerations (parity, pelvimetry, placentation)
Consider: Estimated weight Gestational age Presentation Position
Consider: Numer of fetuses Estimated fetal weight Gestational age Presentation Position Anomalie
Consider IUPC
Consider: Arrest or protraction disorder Remote from delivery Poor expulsive efforts
2. Moderate variability or accelerations exclude hypoxic neurologic injury
Potential Injury
*Other Causes of Fetal Heart Rate Changes Fetal Maternal Fever Fever Infection Infection Medications Medications Anemia Hyperthyroidism Arrhythmia Heart block Congenital anomaly Extreme prematurity Preexisting neurologic injury Sleep cycle
Intrapartum Fetal Heart Rate Management Decision Model
A Standardized Intrapartum FHR Management Model Four Central Concepts
“ABCD” A – Assess the oxygen pathway/review differentials B – Begin conservative corrective measures C – Clear for delivery (the 5 “p”s) D – Decision to delivery time
Do “conservative measures” improve fetal oxygenation? Measures
Evidence
Supplemental oxygen
Direct – Pulse oximetry
Maternal position changes
Direct – Pulse oximetry
IV fluid bolus
Direct – Pulse oximetry
Correcting hypotension
Indirect – FHR
Amnioinfusion
Indirect – FHR
Reducing uterine activity
Indirect – FHR, pulse oximetry
Altered pushing technique
Indirect – FHR, pulse oximetry
Altered breathing technique
Indirect ‐ FHR
KR Simpson J Midwifery Womens Health. 2007 May‐Jun;52(3):229‐37
Does this mean you need to use all seven conservative corrective measures in every case? Of course not! Use the conservative corrective measures that you deem appropriate for the clinical situation
For example, amnioinfusion might be helpful in the setting of frequent variable decelerations due to cord compression But it would not be expected to be beneficial in the setting of recurrent late decelerations
A FEW WORDS ON INTRAUTERINE RESUSCITATION & OXYGEN SUPPLEMENTATION Although the classic triad of intrauterine resuscitation has been position changes, IV fluids, and oxygen, there is little evidence on potential adverse effects (both hypoxia and hyperoxia can cause free radical production & oxidative stress) More research is needed on the risks of oxygen, both short- & long-term, on the duration of use, the types of FHR tracings where it is indicated, and algorithms for intrauterine resuscitation Simpson, KR. Semin Fetal Neonat Med, 2008
AJOG August 2014
AJOG April 2015
MCN March/April 2015
TAKE-HOME POINTS ON OXYGEN USE DURING LABOR Avoid oxygen as a first line response, try other measures first Avoid oxygen if there is moderate variability in the FHR tracing Discontinue oxytocin before using oxygen Limit the length of oxygen use – discontinue as soon as fetal response warrants Adapted from: Simpson, KR. Semin Fetal Neonat Med, 2008