Download Acid Base

Module 1: Acid Base
1.1 Introduction and Overview
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1.2 Module Objectives
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On completing this module, you will have:
 a basic knowledge of acid-base principles
 an understanding of factors that have an impact on fetal oxygenation and the
development of fetal acidosis
 knowledge of the importance of acid-base balance in labour, delivery and the
newborn transition
It should take approximately 40-45 minutes to complete this module.
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1.3 Overview of the Module
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This module includes:
1. A pretest to assess your prior knowledge of the module content:
This will not be scored, and is for your own information only
2. Basics of acid-base balance
3. Overview of fetal oxygenation
4. Physiology of fetal acidosis:
- Respiratory acidosis
- Metabolic acidosis
- Mixed acidosis
5. Interpretation of blood gas results
6. Application in practice
- Fetal scalp blood sampling
- Cord blood sampling
7. Definition of, and criteria for diagnosis of intrapartum asphyxia
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1.4 Pretest
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Please complete the short five-question pretest for this module.
Click Next to begin the pretest.
1.5 Draw from Pretest
Draw 5 questions randomly from Pretest
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1.6 Pretest Score
(Results Slide, 0 points, 1 attempt permitted)
Results for
1.5 Draw from Pretest
Result slide properties
Passing Score
0%
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1.7 Basics of Acid-Base Balance
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pH: A measurement of acidity or alkalinity. A pH of less than 7.35 is considered acidosis.
Hypoxia: A state of reduced oxygen availability to a body as a whole, or to a region or
specific tissues in a body.
Hypoxemia: Decreased oxygen content in the blood, measured by partial pressure of
oxygen (pO2) and reflected by partial pressure of carbon dioxide (pCO2).
Acidosis: An increase in hydrogen ion concentration in the body’s tissues.
Buffer: A substance that combines with hydrogen ions or acid in the body to maintain a
normal pH. The main buffer in fetal physiology is bicarbonate (HCO3).
Base deficit: A value derived from measuring the pH, the pC02, and the concentration of
bicarbonate (HC03) in the blood. This value reflects the amount of buffering required to
compensate for increasing acidity, or a rise in hydrogen ions in the blood. Record as a
positive.
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1.8 What is pH?
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pH stands for the “power of hydrogen” or “potential of hydrogen”.
The pH system was devised to measure the degree of acidity or alkalinity in solutions,
and is dependent upon the concentration of
unbuffered hydrogen ions (H+).
Because the concentration of H+ in biological fields is so low to begin with, the pH
system was devised as a negative logarithm for practical application.
Each decrease by 0.1 units means a progressively larger increase in H+:
 decrease in pH by 0.2 units = twofold increase in H+ concentration
 decrease in pH by 1.0 units = tenfold increase in H+ concentration
For example a pH of 7.0 = 10-7 = .0000007
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1.9 Common Items Acid-Base Scale: a Comparison
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Instructions
Click the concentrations in the left column to discover the pH (central column) of some
common solutions.
You can click 'Show All' to reveal all the solutions.
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1.10 Normal Acid-Base Balance
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Homeostasis requires a delicate balance of acid and base. It is reflected by normal pH,
p02, pC02, bicarbonate, and base deficit.
Normal acid-base balance occurs in an environment of adequate gas exchange.
Hypoxia is the diminished presence of O2 in the body tissues.
Hypoxia occurs in an environment of impaired gas exchange and reduced fetal
oxygenation.
Hypoxemia is a condition in which O2 levels in arterial blood are low. Hypoxemia occurs
in an environment of impaired gas exchange.
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1.11 By-products of Normal Aerobic Metabolism
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The by-products of metabolism in an oxygen-rich environment are carbon dioxide (CO2)
and water (H2O).
CO2 returns to the maternal system via the umbilical artery and is eliminated across the
placenta.
If CO2 builds up in the fetal circulation due to compromised gas exchange and the
normal fetal compensatory mechanisms are taxed, then a state of acidemia results.
Respiratory and metabolic acidosis (defined later in this module) affect pH, bicarbonate,
pO2, pCO2, and base deficit levels:
CO2 + H2O
H2CO3
H+ + HCO3-
We require 20 parts bicarbonate (buffer) to balance just 1 part of hydrogen!
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1.12 Anaerobic Metabolism
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Anaerobic metabolism is a process for removing energy (glucose) from long-term
storage compounds (carbohydrates) and putting it into a usable form (ATP) where
something besides oxygen accepts the energy electrons to be used for muscle
contraction.
This is usually short-term.
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1.13 Learning Pearls
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Aerobic metabolism is the preferred process for energy production (oxygen is readily
available and by-products are easily excreted via the lungs).
Anaerobic metabolism is the less preferred process for energy production (oxygen is
not readily available and by-products require buffers and intact kidney function).
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1.14 Fundamentals of Fetal Oxygenation
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In utero, the fetus depends on several factors to maintain adequate oxygenation,
including:
1. Maternal oxygenation
2. Placental gas exchange
3. Umbilical cord blood flow
4. Fetal hemoglobin oxygen carrying capacity
There are many factors which have an impact on fetal oxygenation, both in the
antepartum and the intrapartum period.
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1.15 Etiologies of Reduced Fetal Oxygenation
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Maternal
Anemia, cardiovascular disease, increased BP
Respiratory disease
Hypotension (supine position, blood loss, anesthesia)
Maternal medications, e.g. heroin or narcotics
Uterine
Excessive uterine activity caused by:
Spontaneous uterine activity
Prostaglandin
Oxytocin
Placental
Dysfunction (IUGR, oligohydramnios or abnormal Doppler)
Placental abruption
Chorioamnionitis/sepsis
Post-dates
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Umbilical
Cord presentation/ prolapse
Knots, entanglement
Rupture or trauma
Cord compression secondary to oligohydramnios
Fetal
Congenital malformations
Anemia - hemolytic or hemorrhagic
Infection
Carboxyhemoglobin (maternal smoking)
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1.16 The Anatomy of the Placenta
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1.17 Placental Gradient and Transfer of Oxygen
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Introduction
Oxygen transfer is accomplished by diffusion.
Diffusion depends upon:
 presence of a gradient
 capacity for exchange
 maternal blood flow rate
 fetal blood flow rate
Under normal circumstances fetal acid-base balance is determined by the mother.
Note: Fetal pH (7.3) is 0.1 unit less than that of the mother (7.4).
Close this intro and roll over the labels for more information on placental gradient and
transfer of oxygen.
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1.18 Normal Fetal Circulation: A Reminder
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Let’s take a moment to have a look at how normal fetal circulation occurs.
Original video source http://yourtotalhealth.ivillage.com/developing-human-heart.html
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1.19 Environment of Impaired Oxygenation
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Impaired gas exchange leading to abnormal acid-base balance can occur in the
antepartum and the intrapartum periods.
The oxygenation of the fetus depends on maternal oxygenation, placental circulation
and diffusion, as well as fetal circulation and the distribution of oxygenated blood to
fetal tissues.
In an environment of impaired gas exchange, due either to antepartum or intrapartum
factors, the fetus will employ circulatory compensatory mechanisms to reduce the
negative impacts of impaired oxygenation.
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1.20 Blood Flow Redistribution/Shunting
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Blood flow through the head is redistributed to favour brainstem areas:
 Decreased to the cerebellum and cerebral cortex
 Increased to the pons and medulla
 Maintained to the subcortical areas
In times of low fetal oxygenation all of the above are used to provide maximum flow of
highly oxygenated blood to the organs that need it most.
In addition, peripheral constriction ensures a 48% increase in fetal circulation to the
brain, adrenals and heart and decreased blood flow to non-essential organs (e.g.
intestine, kidneys).
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1.21 Blood Flow Redistribution/Shunting
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In labour, oxygenation of the fetus becomes cyclical: As the uterus contracts there is a
subsequent reduction in placental gas exchange, as well as an impact on umbilical cord
patency. Play the graph below for an example.
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1.22 Why Do We Need to Understand Acid-Base?
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Electronic Fetal Monitoring (EFM) was developed to prevent morbidity in labour from
decreased fetal oxygenation by indicating certain fetal heart rate patterns that
correspond with an environment of critically reduced oxygen supply beyond normal
parameters, taxing the fetal ability to compensate.
However, in practice EFM is a very non-specific tool, as at times tracings that are
considered 'abnormal' are not necessarily indicative of critical changes in fetal acid-base
balance.
It is the challenge of care providers to determine what constitutes a truly abnormal
fetal heart rate pattern, indicating need for emergent or urgent delivery.
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1.23 Why Do We Need to Understand Acid-Base?
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As seen on the previous pages, an intermittent reduction in fetal oxygenation is normal
throughout labour and is not necessarily indicative of compromised fetal status.
The fetus employs compensatory measures to adapt to an environment of reduced
oxygenation, or hypoxia.
Fetal scalp blood sampling and/or cord blood sampling at birth for the determination of
acid-base balance complement the use of EFM for a more accurate determination of
fetal status.
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1.24 Learning Pearls
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The placenta is the chief organ of homeostasis as it is the only method of gas exchange
for the fetus.
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1.25 Physiology of Fetal Acidosis
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Fetal homeostasis is dependent on an equilibrium between acid and base resulting from
normal metabolism and adequate gas exchange.
The body strives to maintain itself within a narrow margin of pH 7.35-7.45:
This is the proper balance between systemic acids and bases.
pH reflects the amount of unbuffered acid in the blood in relation to the amount of
base solution.
The main buffer in fetal blood is bicarbonate (HCO3).
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1.26 Respiratory Acidosis: Quick to Resolve
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When CO2 builds up in the fetal blood stream due to short-term impaired gas exchange,
it combines with H2O to form carbonic acid, or H2CO3.
CO2 + H2O
H2CO3
H+ + HCO3-
Carbonic acid is a volatile acid which can build up quickly, yet can also be converted back
to H2O and CO2 quickly in the environment of improved fetal gas exchange or newborn
respiratory function.
Respiratory acidosis does not use the body’s buffer bases to correct acid imbalance due
to the volatility of carbonic acid.
Therefore, when fetal/placental gas exchange returns to normal after compromise or
the fetus is delivered, CO2 is eliminated quickly through the placenta or newborn
respiration and normal pH quickly follows.
Newborns respond quickly to stimulation, O2 administration, and establishment of
respiration.
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1.27 Metabolic Acidosis: Slow to Recover
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Metabolic acidosis arises in an environment of prolonged insufficient oxygenation
resulting from a less than ideal environment, such as utero-placental dysfunction or
decreased maternal oxygenation.
The fetus becomes dependent upon anaerobic metabolism to provide sufficient energy
to the fetal brain and organ systems, resulting in the production of lactic acid, and fetal
acidosis.
The body will attempt to buffer the resultant excess H+ with bicarbonate. However,
lactic acid is a fixed acid, as opposed to a volatile acid such as carbonic acid, and is
therefore excreted very slowly from the fetal blood stream. This ultimately results in an
abnormality in fetal blood pH which is prolonged and greater than with respiratory
acidosis.
Metabolic acidosis at delivery can result in a newborn that will require extensive
resuscitation, and is associated with low Apgar scores, multi-organ failure or long term
deficits, decreased neurological function, and death.
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1.28 Respiratory versus Metabolic Acidosis
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1.29 Mixed Acidosis
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Mixed acidosis results from a combination of both respiratory and metabolic acidosis.
It may have more than one etiology, such as a placental as well as an umbilical cord
origin e.g. utero-placental insufficiency (metabolic) as well as cord occlusion resulting
from oligohydramnios and uterine contractions in labour (respiratory).
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1.30 How the Fetus Responds to Hypoxia
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Acute disturbances
 Major redistribution of blood flow
 Decreased O2 consumption to 60% of normal
 Anaerobic metabolism
Mild/gradual/chronic disturbances
 Increased O2 capacity (increased Hct)
 Increased FHR
 Lowered total O2 consumption by:
 slowing fetal growth
 decreased fetal breathing movements
 decreased fetal body movements
 Mild to moderate redistribution of blood flow (shunting).
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1.31 Fetal Hypoxic Acidemia
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Definition
“A condition of impaired gas exchange which, when persistent, leads to progressive
hypoxemia, hypercapnia and metabolic acidosis”
Key Points
The primary reason the pH alters in the fetus is decreased oxygenation via the placenta.
This results from a combination of respiratory and metabolic acidosis (respiratory first,
followed by metabolic).
Incidence
 Low risk woman/fetus 0.5-2%
 Woman/fetus with risk factors 20%
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1.32 Interpretation of Gas Results
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The key values that indicate the type of acidosis in a fetus or newborn are:
 pH
 Base deficit (BD)
 pC02
Remember: Respiratory acidosis does not mobilize the other body’s buffer bases as
carbonic acid quickly breaks down into its by-products of H2O and CO2, and hence CO2
can be quickly excreted.
Therefore with respiratory acidosis the pH is acidotic but the base deficit will be normal,
reflecting the fact that buffers were not required.
However, metabolic acidosis does require additional buffers to neutralize the circulating
lactic acid, so there will be a larger base deficit in these cases in addition to a low pH.
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1.33 Application in Practice: Scalp and Cord Gases
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In the context of atypical and abnormal classifications from electronic fetal monitoring
during labour, it is recommended that confirmation of impaired fetal oxygenation be
obtained through fetal scalp blood sampling.
In addition, collecting samples from the umbilical cord following delivery provides
information on the status of fetal and placental oxygenation at birth.
SOGC guidelines recommended that cord blood samples be taken at all deliveries.
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1.34 Fetal Scalp Blood Sampling
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In the presence of atypical and abnormal fetal heart rate tracings, the information on
fetal status obtained from fetal scalp blood sampling can reduce increased operative
and instrumental delivery rates that are associated with the use of EFM.
Fetal scalp blood is collected in the intrapartum setting using a lancet to make a
cutaneous scalp puncture.
When
 Atypical or Abnormal or uninterpretable fetal heart tracing
 Gestational age >34 weeks when delivery is not imminent
 Resources are available to perform and process sample
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1.35 Fetal Scalp Blood Sampling
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How
 By obtaining capillary blood from the fetal scalp via the sampling kit
Contraindications to fetal scalp sampling
 Parameters are normal (i.e. accelerations present)
 Gestational age <34 weeks as delay in delivery may be associated with adverse
neonatal outcomes
 Family history of bleeding disorders (i.e. hemophilia, maternal ITP)
 Mother HIV+, Hep C or has suspected chorioamnionitis
 Malpresentation (i.e. face)
 When there is no consent from the mother
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1.36 Confirmation of Fetal Hypoxic Acidemia
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1.37 Requirements for Fetal Scalp Blood Sampling
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Fetal scalp blood sampling requires:
 Cephalic presentation (not asynclitic)
 Cervix dilated at least 3cm
 Ruptured membranes
 Equipment and laboratory support
 Adequate sample to process (may be difficult with significant caput, which may result
in a falsely low pH)
A sample taken during uterine contractions, when perfusion and pH are normally lower,
may result in a falsely low pH (up to 0.05 units).
Maternal hyperventilation may result in a falsely low pH: need support in keeping
environment calm.
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1.38 Scalp Lactate Testing
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The SOGC Fetal Health Surveillance Guidelines did not recommend scalp lactate testing.
Although research was promising, there was insufficient compelling evidence to
recommend practice change.
A large RCT, published in the BMJ (June 2008) showed that scalp lactate testing was
equivalent to pH to determine outcomes, and could be used to direct clinical practice.
The pH results from fetal scalp blood do not differentiate between respiratory and
metabolic acidosis. Lactate in fetal scalp blood identifies metabolic acidosis. It is
assessed using a rapid, bedside meter and is predictive for determining which cases
warrant intervention.
BCW has implemented scalp lactate testing for use in clinical assessment of fetal
acidemia.
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1.39 Interpretation of Scalp Lactate Results
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When FBSLS is normal, testing should be repeated if the FHR abnormality persists.
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1.40 Umbilical Cord Gas Analysis
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Obtaining cord gases:
 Provides an objective measure of status at birth
 Is more accurate than the Apgar scores
 Helps exclude possibility of birth-related hypoxic acidemia as a cause of subsequent
neurological sequelae (when values are within normal range)
 Helps determine which acidosis was present in the fetoplacental unit (respiratory,
metabolic, or mixed)
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1.41 Umbilical Cord Gas Analysis
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Arterial samples best indicate fetal oxygenation at time of birth, as this is the sample
drawn from blood returning to the placenta from fetal circulation.
However, both UA and UV are needed to help determine that the sample is correct as
~25% of samples thought to be UA are, in fact, UV by mistake.
Normal Values:
 Arterial pH 7.21-7.35
 Venous pH 7.30-7.40
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1.42 Clamping and Cutting for Cord Blood Sampling
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Gather equipment:
 crushed ice for transport of sample
 heparinized 2 - 3mLs syringes with 22 gauge needles (one for UA and one
for UV)
 protective gear using universal precautions (goggles, gloves)
 laboratory equipment to process sample, or available transport to
nearest facility
It was previously believed that samples could be collected 30-60 minutes post-birth (and
up to 72 hours if cord kept on ice). Recent evidence shows that the base deficit may be
increased, compared to obtaining the sample within 2-3 minutes post-birth (and up to
20 minutes maximum).
Therefore, obtain and send the sample as soon as possible.
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1.43 Cord Blood Samples in Context of Delayed Clamping
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There is growing evidence that delayed cord clamping is beneficial to the newborn and
may decrease morbidity such as intraventricular hemorrhage, anemia, and need for
transfusions in the preterm newborn.
To this end, both the FIGO (International Federation of Gynecology and Obstetrics) and
the ICM (International Confederation of Midwives) advocate for delayed cord clamping
for at least 1 minute and/or until the cord stops pulsating.
There is recent evidence that supports that delayed cord clamping alters UA and UV gas
results; however, the alteration is not clinically significant.
SOGC recommends the collection of cord blood samples even in cases of delayed
clamping.
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1.44 Normal umbilical cord blood pH and blood gas values in term
newborns
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1.45 Newborn Hypoxic Acidemia
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“Newborn metabolic acidosis occurs at 2% of all deliveries, even in low risk women. The
majority (75%) of these babies will be asymptomatic and have no increased likelihood of
long-term sequelae.”
However, there is a chain of events progressing from hypoxic fetal acidemia through
metabolic acidosis to neonatal encephalopathy to long-term sequelae (including
cerebral palsy) which can result in a small subset of severely affected individuals.
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1.46 Association Between Cerebral Palsy and Hypoxic Acidemia
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CP Incidence : 2/1000 births (<1500g infants account for 25%).
Essential criteria for determining an association between CP and intrapartum
asphyxia:
 Evidence of metabolic acidosis in cord gas (pH <7 and BD ≥12 mmol/L)
 Early onset of severe or moderate neonatal encephalopathy in infants born at or
beyond 34 weeks gestation
 Cerebral palsy of the spastic quadriplegic or dyskinetic type
 Exclusion of other identifiable etiologies, such as trauma, coagulopathy, infectious
conditions or genetic disorders
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1.47 Neonatal Encephalopathy
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Neonatal encephalopathy can result from many conditions and 70% of cases occur
secondary to events arising before the onset of labour such as prenatal stroke, infection,
cerebral malformation and genetic disorders.
However, factors that suggest an intrapartum event for neonatal encephalopathy
include:
 A sentinel (signal) hypoxic event occurring immediately before or during labour
 A sudden and sustained fetal bradycardia or the absence of FHR variability in the
presence of persistent, late or complicated variable decelerations, usually after a
hypoxic sentinel event when the pattern was previously normal
 APGAR score of 0-3 beyond 5 minutes
 Onset of multisystem involvement within 72 hours of birth
 Early imaging study showing evidence of acute nonfocal cerebral abnormality
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1.48 Learning Pearls
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When analyzing blood gas results (scalp or cord), the key values will be pH or lactate,
Base Deficit (BD) and PCO2.
A low pH and normal BD will point towards respiratory acidosis (in conjunction with
clinical signs from neonate).
A low pH and high BD will point towards metabolic acidosis (with confirmation based on
clinical signs from neonate).
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1.49 Summary
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You have completed Module 1: Acid-Base!
After completing this module you have an understanding of:
 basic acid-base principles
 factors that impact fetal oxygenation and the development of fetal acidosis
 the importance of acid-base balance in labour, delivery and the newborn transition
Having reviewed the Introduction and Acid-base modules, you will now move on to the
Intrapartum module.
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2. Pretest
Q2.1 When the fetus is in a sub-optimal environment (reduced oxygen), it
generates energy from glucose stores via anaerobic metabolism.
The by-product of this is a buildup of lactic acid, which leads to metabolic
acidosis.
(True/False, 1 points, 1 attempt permitted)
Correct
Choice
X
True
False
Feedback when correct:
That's right! This is True
Feedback when incorrect:
Sorry, that's not right - this is True
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Q2.2 As pH decreases, Hydrogen ions increase.
(True/False, 1 points, 1 attempt permitted)
Correct
Choice
X
True
False
Feedback when correct:
That's right! This is True
Feedback when incorrect:
Sorry, that's not right - this is True
Q2.3 One of the fetal responses to hypoxia is to decrease blood flow to the
heart, brain and adrenals.
(True/False, 1 points, 1 attempt permitted)
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Correct
Choice
True
X
False
Feedback when correct:
That's right! This is False
Feedback when incorrect:
Sorry, that's not right - this is False
Q2.4 At what uterine pressure will placental perfusion virtually stop?
(Multiple Choice, 1 points, 1 attempt permitted)
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Correct
Choice
10-20 mm Hg
X
30-50 mm Hg
50-70 mm Hg
Feedback when correct:
That's right! Placental perfusion will virtually stop at 30-50 mm Hg uterine pressure.
Feedback when incorrect:
Sorry, that's not right. Placental perfusion will virtually stop at 30-50 mm Hg uterine pressure.
Q2.5 At delivery, it is normal for the fetus to be mildly…
(Multiple Choice, 1 points, 1 attempt permitted)
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Correct
Choice
X
Acidotic
Alkalotic
Feedback when correct:
That's right! At delivery, it is normal for the fetus to be mildly acidotic.
Feedback when incorrect:
Sorry, that's not right. At delivery, it is normal for the fetus to be mildly acidotic.
Q2.6 The "best case scenario" of blood coming through the umbilical
artery is a PO2 of _________ and a PCO2 of _________:
(Multiple Choice, 1 points, 1 attempt permitted)
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Correct
Choice
45 and 60
X
20 and 45
10 and 20
Feedback when correct:
That's right! The "best case scenario" of blood coming through the umbilical artery is a PO2 of
20 and a PCO2 of 45.
Feedback when incorrect:
Sorry, that's not right. The "best case scenario" of blood coming through the umbilical artery is a
PO2 of 20 and a PCO2 of 45.
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