12.  In a general way, the treatments for these problems are
obvious from the causes but we need to consider sodium bicarbonate
in the treatment of acute lactic acidosis, a controversial area.
For a very clear and incisive review of this topic, please review
the elegant paper by Dr. Brad Hindman from our Department
(Anesthesiology, June,1990).
 
     a.  The development of a lactic acidosis during the course of
     an illness signals a dangerous disruption of normal oxygen
     use.  If not reversed, there is progressive intracellular and
     extracellular acidosis and eventually death.  In the past, an
     acute lactic acidosis was treated with sodium bicarbonate.
     In vitro data generally demonstrate that either respiratory
     or metabolic acidosis below a pH of about 7.1 decreases
     myocardial contractility and causes CNS depression.
 
     b.  The role of sodium bicarbonate has recently been
     challenged with several studies showing it to be ineffective
     and potentially detrimental by actually promoting lactic acid
     production.  The American Heart Association now recommends
     that sodium bicarbonate be used only late in the course of
     the cardiopulmonary resuscitation, if at all.
 
     c.  The major problem is that when exogenous bicarbonate is
     administered during acidemia, bicarbonate      reacts with
     hydrogen ions to form carbonic acid.  The carbonic acid
     dissociates to CO2 and water and the CO2 partial pressure
     increases.  When CO2 cannot be eliminated, the pH of the
     system is only minimally changed or in fact worsened.
 
     d.  Therefore, during states of severe hypoperfusion, such as
     CPR, there is very little benefit from sodium bicarbonate
     administration.
 
     e.  In other settings, sodium bicarbonate does have a role in
     the treatment of lactic acidosis because of the severe
     hemodynamic deterioration that can occur with a pH much below
     7.1.  Small titrated doses of bicarbonate should be used to
     temporize while attempts to improve tissue oxygenation
     continue.
 
          1)  In such cases, generally treat if the pH is less
          than 7.20, as long as a respiratory acidosis does not exist.
          If it does, treat the respiratory acidosis first. The dose of
          bicarbonate can be determined by he following :
 
     Body weight in kg.  X  deviation of HCO3 from 24  X  0.2
     0.2 = extracellular fluid volume as a fraction of body wt.
     0.4 = extracellular fluid volume as a fraction of body weight
           in infants.
 
          2)  Besides the problems mentioned, other problems with
          bicarbonate include:
             Intraventricular hemorrhage
             Hypernatremia
             Hyperosmolarity
             Left shift of the oxy-Hb dissociation curve due to
                rebound alkalosis
 
       

13.  Temperature correction of ABGs:
 
     a.  The solubility of O2 and CO2 are temperature dependent.
 
     b.  At higher temperatures, more molecules enter the gas
     phase and are sensed as partial pressure compared to the
     lower temperatures.  The same amount of gas is present at 37
     and 28 degrees, but not all is measurable at 28 degrees.
     Therefore, a sample warmed to 37 degrees will have a higher
     measured PCO2 and PO2 value than a sample at 28 degrees.
 
     c.  It is probably unnecessary to correct PCO2 and pH for
     variations in body temperature from the temperature of the
     electrodes that are usually maintained at 37 degrees
     centigrade.
 
     d.  Carbon dioxide was traditionally added to maintain PCO2 =
     40 mmHg, with the intention of preserving physiologic
     homeostasis at hypothermic temperatures.  This has been
     termed the "pH stat" strategy, because the pH is maintained
     at about 7.4 regardless of temperature.  Recently, this has
     been questioned.  It has been argued that enzyme system
     function is more physiologic when the pH and PCO2 are allowed
     to vary as occurs with hypothermia.  No carbon dioxide is
     added according to this "alpha stat" strategy.  Additionally,
     the addition of carbon dioxide has been questioned because of
     its potential to cause cerebral vasodilation and interfere
     with normal cerebral autoregulation.
 
       

14.  There is considerable confusion when it comes to defining
acid-base abnormalities as primary, secondary, or compensatory
processes.  If both respiratory and metabolic problems are an
acidosis or if both are an alkalosis, then both processes are
primary.  If they are opposite, then the primary problem is
defined by the pH.
 
       

15.  Reading a blood gas is easy, as long as you approach it
systematically.  There are four important steps:
 
     a.  First, determine the net acid-base status as defined by
     the pH.  Second, determine the respiratory component of the
     acid-base disorder as defined by the PaCO2.  Third, determine
     the metabolic component of the acid-base disorder as defined
     by the bicarbonate.  And fourth, determine the presence of
     primary, compensatory, and mixed acid-base processes.
 
       

16.  With all of this a background, lets use the information we
have reviewed to evaluate some clinical problems.
 
     a.  Case I.   The first case, is an easy one.  A patient has
     been admitted through the emergency room with a pH of 7.32, a
     PCO2 of 30, and the following electrolytes:  Na+=135, K+=4.5,
     Cl-=105, and HCO3=19.  How would you read and interpret this
     blood gas.
 
     pH status:  mild acidemia, the pH is less than 7.35.  Recall
     that the normals are 7.35-7.45.
 
     resp status:  respiratory alkalosis, recalling that the
     normal CO2 is 35-45.
 
     met status:  metabolic acidosis with the bicarbonate of 19.
     Recall that the normal is between 20-26.

     compensation:  Yes.  There has been hyperventilation to
     compensate for the acidemia.  The expected PCO2 is nearly
     equal to the last two digits of the pH.  Since the metabolic
     process is different than the respiratory process, the
     primary process is defined by the pH therefore the metabolic
     acidosis is primary.
 
     diff dx:  Is this a normal non-anion gap or an increased
     anion gap acidosis.  Na+ - Cl + HCO3 = 11.  Recall that the
     normal is 8-16.  Therefore, we must consider causes for a
     normal non-anion gap acidosis including bicarbonate loss
     from, for example, diarrhea or renal processes such as renal
     tubular acidosis, hypoaldosterone states, and early
     glomerular insufficiency.  The history and physical exam will
     probably allow us to make these determinations.
 
     b.  Case II:  pH= 7.26, PCO2= 37, Na+ 140, K+ 4.0, Cl- 103,
         HCO3- 16
     For those interested, the anion gap is 18.
 
     pH status:  acidemia
 
     respiratory status:  essentially normal
 
     metabolic status:  metabolic acidosis
 
     compensation:  Is there appropriate compensation for this
     apparent primary metabolic acidosis.  No.  The expected
     decrease in the PCO2 should approximate the last two digits
     of the pH.  Therefore, the PCO2 should be around 26 rather
     than 37.  This indicates there is inappropriate respiratory
     hypoventilation.  The clinical setting could be any increased
     anion gap acidosis (remember LUK SEMP) complicated by
     sedation or drug overdose, pneumothorax,  or severe pulmonary
     edema.

     c.  Case III.  pH 7.39, PCO2 24, Na+ 140, K+ 4.0, Cl- 106,
     HCO3- 14.  (Anion gap:  20)
 
     pH status:  normal
 
     respiratory status:  respiratory alkalosis
 
     metabolic status:  metabolic acidosis, with an increased
     anion gap of 20 (normal 8-16).

     compensation:  not appropriate.  In simple metabolic acidosis
     the expected decreased PCO2 should be about the same as the
     last two digits of the pH.  The PCO2 should be 39 not 24.
     Since the measured PCO2 is actually much lower, a primary
     respiratory hyperventilation is occurring.  Clinical settings
     would include salicylate overdose, sepsis (primary
     respiratory alkalosis with lactic acidosis).
 
       

17.  Besides being able to read a blood gas systematically, it is
critical that you know how to use the basic information which
blood gases convey at the bedside in taking care of patients.  We
must be able to apply the information that we gain from an
arterial blood gas:  to evaluate the status of the acid-base
balance, the status of oxygenation and ventilation, the need for
emergent intubation, and the appropriateness of extubation, to
name a few.
 
     a.  Let's review the indications for intubation, some of the
     most important elements embodied in the results of an
     arterial blood gas.  There are three factors to consider:
     mechanics, oxygenation and ventilation.  In terms of . . . .
.
          1)  Mechanics
               a)  Respiratory rate greater than 35/min.
               b)  VC less than 15 cc/kg for adults and 10 cc/kg
               for children
               c)  MIF less than 20 cm H2O
 
          2)  Oxygenation
               a)  PaO2 less than 70 mmHg on FiO2 40%
               b)  The A-a gradient is greater than 350 torr with
               FiO2 100%
 
          3)  Ventilation
               a)  PaCO2 is greater than 55 except in patients
               with chronic hypercarbia.
               b)  Vd/Vt it greater than 0.6 (normal is 0.3)
 
     b.  Decisions about extubation frequently are also aided by
     the results of a blood gas.  Criteria for extubation:
 
          1)  Awake and alert with stable vital signs, good grip,
          and sustained head lift.
 
               a)  Stable vital signs includes respiratory rate
               less than 30-35
               b)  Stable blood pressure and pulse
               c)  No inotropic support
               d)  Patient afebrile
 
          2)  ABG good on 40%, with PaO2 greater than 70 and PaCO2
          less than 55
 
          3)  MIF more negative than a negative 20 cm H2O.
 
          4)  VC greater than 15 cc/kg.
 
     c.  Weaning from mechanical ventilation is accomplished in a
     number of ways, blood gases being one important parameter of
     many of them.  There are two basic techniques, the T-piece
     technique and the intermittent mandatory ventilation
     technique.  You should review these at this time.
 
          1)  T-piece technique
 
               a)  If patient meets extubation criteria a T-piece
               adaptor and is attached to the endotracheal tube.
               b)  Sit patient up.
               c)  Set FiO2 slightly higher (about 5%) than the
               patient had with mechanical ventilation
               d)  Check vital signs (including respiratory rate,
               depth, and work) and saturation.  This should be
               done on a very frequent basis during the first hour
               or two.
               e)  If the patient tolerates weaning, he is
               extubated after 2-4 hours.
 
          2)  Intermittent mandatory ventilation technique
 
               a)  The IMV is gradually decreased so that
               eventually the patient begins spontaneous
               ventilation.
 
       

18.  In reviewing blood gas questions from previous exams, it is
clear that a memorization of umbilical vein and artery gases is
important.  They expect you to know the normal values, so that you
can interpret the gas and thereby the needs of the patient.
 
 
 

 
 
a.  Normals
 
             UMBILICAL       UMBILICAL        60
             VEIN-BIRTH      ARTERY-BIRTH     MIN
------------------------------------------------------------
pH           7.35            7.28             7.30-7.35
             (7.30-7.40)     (7.23-7.33)
 
pCO2         40              50               32-42
             (33-43)         (42-58)
 
pO2          30              20               50-70
             (25-35)         (12-25)
 
 
     b.  As one would expect, umbilical artery blood (which has
     circulated through the fetus) is lower in pH and oxygen and
     higher in carbon dioxide than umbilical venous blood.
 
       

19.  Notes on acid-base-pKa-ionization-lipophilic issues.  (This
is important information for the Written examination.  I've never
seen it put together in quite this way.  It may be worth 2-3
questions on the exam.)
 
     a.  Neutral pH 7.0
     b.  pKa:  The pH at which 50% ionization occurs.
     c.  "Weak acids":  pKa about 3.0-7.5
     d.  "Weak bases":  pKa about 8.0-10
     e.  Two important questions:
          1)  What is the ionizing group?
          2)  It is charged with the proton on or off?
     f.  There are two common ionizing groups in biologic systems:
          1)  Amines (narcotics, local anesthetics):
          RNH3+ ´ RNH2  +  H+
 
          The amines are the main ionizing group in most drugs.
          They are charged in the protonated form.  Therefore, as
          the system becomes more acidic, they are more charged
          and less lipophilic.  As the system becomes more basic,
          they are less charged and more lipophilic.  This is how
          the term "free basing" comes about.  Cocaine is an
          amine.  When sodium hydroxide or sodium bicarbonate is
          added to make the solution more alkaline, the free base
          forms, which is uncharged, less water soluble (being
          ionized leads to greater water solubility), very lipid
          soluble, and rapidly absorbed through mucous membranes.
 
          2)  Carboxylic acids (Thiopental):
          R-COOH ´ RCOO-  +  H+ ;  RSH ´ RS-  +  H+
 
          The carboxylic acids are the second most common ionizing
          group in biologic systems.  They are uncharged in the
          protonated form.  Therefore, as the physiologic system
          becomes acidic, they are less charged and more
          lipophilic.  As the system becomes more basic, they are
          more charged and less lipophilic.
 
          3)  Thiols are another type of ionizing group.  Consider
          them in the same way as carboxylic acids, except they
          have higher pKa.  The major ionizing group on thiopental
          are thiols.
 
     g.  Recall this information:
                                      pH           pKa
          Thiopental:                 10.5         7.6
          Narcotics (morphine):       2.5-6.0      6.1
          Local anesthetics :         5.0-7.0      8.0-9.0
 
     h.  In assessing lipophilicity, one must therefore know the
     major ionizing group as well as the the pKa.  If the pKa is
     high enough it moves it out of the range where pH adjustments
     are relevant at all.  If the pKa is 11 then at any
     physiologically reasonable pH the materal will be almost
     exclusively in the protonated form.
 
     i.  Local anesthetics and narcotics are subject to fetal ion
     trapping.  In the more acidic fetal environment, the
     dissociation is to the left--the charged form which has
     difficulty crossing the placental barrier (and thus "traps"
     the compound).  What about thiopental?  It is not trapped.
     In the more acidic fetal environment, dissociation is the
     left--to the uncharged form which can more easily cross the
     placental barrier.
 
       

20.  In conclusion, we must be able to quickly read and interpret
arterial blood gases.  This is best done with a systematic
approach and with the pH-bicarbonate diagram in mind.  In the
stress of the oral examinations, take the time to read and
interpret an arterial blood gas before you rush to treatment, then
be prepared to treat, being especially knowledgeable about
indications for intubation and the appropriateness of extubation.
These are the keys to handling these sometimes difficult and
confusing scenarios (both in the exam room and at the bedside).
 
 
          A Question From Dr. Jensen's Tutorial
 
K type
Which of the following would indicate the need for a mechanical
ventilator?
 
 1)  Vd/Vt of 0.8
 2)  A-aDO2 of 150 torr at FIO2 1.0
 3)  Inspiratory force of 5 cm H2O
 4)  Vital capacity of 20 ml/kg
 
B.
Know the list, indications for intubation.  Two points:
1.  They really do expect you to know this stuff!
 
2.  Big Blue will serve you well if you serve it well.
 
 
NFJs Key Quotes
 
Life is what happens to you while you're making other plans
     --John Lennon
 
       

NOTES:
 
1. Smith, H, and Lumb, PD. Acid Base Balance.  Clinical
Anesthesia, 2nd edition, Barash, PG,
Cullen, BF, and Stoelting, RK (eds.), Lippincott, 1992, p. 237-
250.
 
2. Moon, RE, and Camporesi, EM. Respiratory Monitoring.
Anesthesia, 3rd edition. Miller, RD
(ed.), Churchill Livingstone, 1990, p. 1129-1160.
 
3. Stoelting, RK, Miller, RD. Acid-Base Balance and Blood Gas
Analysis. Basics of Anesthesia, 3rd edition, Stoelting, RK,
Miller, RD (eds.), Churchill Livingstone, 1994, p. 217-231.
 

Note: Each detailed notes section in Big Blue is followed by recurrent key words from recent years. I have categorized every key word for the past 7 years, all 8,400 of them. This enables me to correlate key words with questions (old and remembered) and to focus the notes section. In other words, the program is quite highly integrated.--NFJ

 
ABG Keywords 1993-95
 
Bicarbonate
1.   Side effects: Bicarbonate  (93)
 
Capnography
1.   End tidal gases with air embolism  (93)
 
Content
1.   Factors affecting arterial oxygen content (94)
2.   O2 Transport, HCT and Viscosity (95)
3.   Determinants of oxygen delivery (95)
 
Interpretation
1.   Interpretation ABG  (93)
2.   ABG and respiratory depression  (93)
3.   ABG interpretation during hypothermia  (94)
4.   PA blood gas interpretation  (94)
 
Mixed venous oxygenation
1.   Determinants:  Low SvO2  (93)
2.   Interpretation:  Mixed venous oxygen  (93)
3.   Factors decreasing SvO2 (94)
4.   Factors increasing SvO2  (94)
 
V/Q Mismatch
1.   Factors affecting V/Q mismatch (also Respiratory)  (93)
 
Oxy-Hb Dissociation curve
1.   Fetal vs. adult hemoglobin  (93)
2.   Hemoglobin dissociation curves  (93)
3.   Oxyhemoglobin Shift:  Causes (95)
4.   Altered P50 and Tissue O2 Delivery (95)
 
 

All of the above are covered in the notes or below. Notice the importance of mixed venous blood gas interpretation. Score! Additional important keywords from the past several years are found below. The reference is first, followed by the underlined key word, and its year(s) as a key word. The space following the keyword is for your notes. The keywords are ordered to correlate to one of the topics above.

Bicarbonate
Schwartz, A. and F. Campbell.  Cardiopulmonary Resuscitation.
Clinical Anesthesia, P. Barsh, B. Cullen and R. Stoelting, 2nd ed.,
JB Lippincott, New York, 1992, p. 1649-50.
 
ABGs
Blood/CSF Effects:  Bicarbonate Administration (91, 92)
1.  The use of sodium bicarbonate during resuscitive efforts has
become controversial.  This controversy is reviewed throughly
in Big Blue.  The reason for concern with sodium bicarbonate
administration relates to several factors.  (Review chapter.
This comes up too often to neglect it.)
     a.  Blood.  Carbon dioxide is generated when NaHCO3 is given
in association with suboptimal ventilation.  HCO3 + H yields
H2CO3 which dissociates to  H2O + CO2.  As blood CO2
accumulates pH decreases.  Other adverse effects include
hypernatremia,  hyperosmolarity, an increased risk of
intraventricular hemorrhage, and rebound alkalosis.
Overzealous use of NaHCO3 can shift hemoglobin saturation
curve to the left inhibiting O2 release to tissues.
     b.  CSF.  CO2 diffuses rapidly across the blood-brain barrier
into the CSF.  Because HCO3- crosses the BBB much more
slowly, a paradoxical CSF acidosis results despite a normal or
high blood pH.
 
 
 
 
 
Interpretation
Ralston, D. . Perinatal pharmacology. Anesthesia for Obstetrics,
2nd ed., S. Shnider and G. Levinson, (ed.), Williams and Wilkins,
1987, vol. 1, p. 53-55.
ABGs
Acidosis- fetal ion trapping (90, 91,92)
1.  The pKa is the pH at which the concentrations of free base
and cation are equal.
2.  Local anesthetics and narcotics are weak bases.  The pKa's
of local anesthetics range from 7.6 to 8.9.  As pH decreases,
more of these drugs exist in their ionic form.
3.  In the case of fetal acidosis there is a greater tendency for
local anesthetics to exist in their ionized forms, a form which
does not allow them to diffuse back across the placenta into the
maternal plasma.  This is referred to as "ion trapping." This
would be especially important in the setting of fetal asphyxia,
situations which could potentiate local anesthetic toxicity
secondary to fetal ion trapping.
4.  A similar phenomenon may occur with opiods.
 
 
 
 
 
Interpretation
Moon, R. and E. Camporesi . Respiratory monitoring. Anesthesia,
3rd ed., R. Miller, (ed.), Churchill Livingstone, 1990, vol. 2,
p. 1136-1137.
ABGs
Effect of Fever on ABG Values (91)
1. Let's simplify.
2.  PO2 and PCO2 values from a hyperthermic patient will be
artifactually elevated.  The rise in PCO2 will lead to a fall
in pH.
     a.  Blood gas electrodes are maintained at 37 degrees in most
hospitals.  Heating results in decreased solubility in plasma and
increased gas tension.  As solution temperature increases, more
molecules enter the gas phase and are sensed as partial pressure.
3.  The PCO2 of blood decreases about 4.5% and the pH increases
about 0.015 unit/degree centrigrade with cooling.
 
 
 
 
 
Interpretation
Jensen, N.  Clinical Arterial Blood Gas Analysis.   Essentials for
the Anesthesiology Written  Board Examination, N. Jensen,
2nd ed., Privately published, Iowa City, 1992, p. 12.
ABGs
Postoperative Metabolic Alkalosis (90)
1.  The chapter on arterial blood gases is probably the best in my
book.  We need to understand these disorders in great detail.
2.  In a metabolic alkalosis, the primary abnormality is an
increase in bicarbonate usually from the loss of bicarb poor fluid.
The body store of bicarbonate is therefore contained in a smaller
volume and bicarbonate concentration increased.  Common causes
of metabolic alkalosis include vomiting and nasogastric suction
in which H+ rich gastric fluid is lost and diuretic drugs that
result in the excretion of a large volume of acidic urine, such as
loop diuretics and thiazides.
     a.  Consider the acute state as well as the compensation.
Consider the acute increase from 24 mmoles/liter to
35 mmoles/liter.  The increase occurs along the isobar for PCO2
of 40 mmHg since respiratory function remains unchanged in the
acute state.  The compensatory response to the increase in pH is
eflex alveolar hypoventilation.  I would expect this reflex
alveolar hypoventilation to be at the heart of any question on
this area.   The kidneys eventually aid in the compensation by
excreting bicarbonate-- however this only occurs after the
plasma volume has been corrected by  the administration of
suitable fluids.
 
 
 
 
 
Interpretation
Jensen, N.  Clinical arterial blood gas analysis.   Essentials for
the Anesthesiology Written  Board Examination, N. Jensen,
3rd ed., Privately published, Iowa City, 1993, p. 5.
ABGs
ABG:  Sampling Errors (92)
1.  Blood gas samples are highly susceptible to pre-analytic error
 due to improper methods in obtaining  and handling samples.
     a.  Glass syringes should be used if possible because CO2 and O2
don't dissolve into the wall of a glass syringe and the minimal
friction of glass minimizes the risk of introducing air bubbles into
the syringe.
     b.  Heparin is the recommended anticoagulant.  EDTA, citrates,
and oxalates alter the pH.
     c.  Samples must be obtained under anaerobic conditions because
the introduction of air bubbles.  If an air bubble is introduced into
a blood gas sample what changes  will occur in the sample?  This
was the basis for one of their old questions and it could be repeated.
In short, the PaO2 will increase in the sample secondary to the
bubble and the PaCO2 will decrease.  Here's why:  Oxygen in room
air is about 105 mm Hg and in a blood gas sample (FiO2 0.21) about
75-100 mm Hg.  Therefore, oxygen will go from a higher
concentration to a lower concentration and will go from the
bubble to the sample,raising the PaO2 in the sample.  What
about CO2?  It is negligible in the bubble and is about 40 mm Hg
in the sample.  Therefore, carbon dioxide will go from the
higher concentration in the sample to the lower concentration in
the bubble.  The PaCO2 will therefore decrease in the sample.
     d.  FiO2, Temperature, Source, Ventilator Settings are
obviously necessary for interpretation.
     e.  Mixed venous samples are interpretable only when
withdrawn slowly from the pulmonary artery, preventing
contamination by capillary blood.
     f.  Samples must be stored in an iced slurry because blood is a
living tissue and cooling it to 4 degrees centigrade will reduce
the metabolism.
     g.  It is important to analyze samples as soon as possible but
when properly stored, several hours will result in little
change in the blood gas measurements.
 
 
 
 
 
Mixed venous oxygenation
Jensen, N. . Clinical arterial blood gas analysis. Essentials for
the Anesthesiology Written  Board Examination, 3rd ed.,
N. Jensen, (ed.), privately published, 1993, vol. 1, p. 3.
ABGs
Mixed venous oxygen tension (91)
Interpretation:  Mixed venous oxygen (93)
Determinants:  Low SvO2  (93)
Factors decreasing SvO2  (94)
Factors increasing SvO2  (94)
PA blood gas interpretation  (94)
Determinants of O2 Delivery (95)
Mixed SVO2 Measurement (95)
 
1.  An important way of assessing the tissue oxygen delivery is
by evaluating the mixed venous oxygen level.
     a.  Mixed venous oxygen saturation provides one of the most
important assessments of tissue oxygen metabolism.
     b.  Recall that accurate sampling of true mixed
venous oxygen saturation requires sampling from PA.
     c.  The normal PvO2 is 35-45 mmHg and the
normal saturation is 65-75%.  What factors determine PvO2?
There are several, can be remembered by the mnemonic COALS,
and include:
          1)  Cardiac output
          2)  Oxygen consumption
          3)  Amount of hemoglobin
          4)  Loading of hemoglobin
          5)  Saturation of hemoglobin
2.  For your interest, the determinants of venous oxygen are
identified by rearranging the Fick equation:
SvO2 = SaO2 - (VO2/Q X Hb X 13)
3.  What factors cause low mixed venous oxygenation--
manifested by a low SvO2 or low PvO2?  As you would predict
from above:  low cardiac output, high oxygen consumption,
anemia, a severe right shift of the oxy-hemoglobin dissociation
curve causing increased unloading of hemoglobin at the tissue
level (sickle cell disease), and hypoxia or any other factor
causing a low hemoglobin saturation.
4.  What factors cause a high SvO2?  Two examples would be
decreased oxygen consumption at the tissue level caused, for
example, by the poisoning of the cytochrome P450 system by
sodium nitroprusside or by a severe left shift of the oxy-Hb
dissociation curve resulting in decreased unloading of
hemoglobin at the tissue level (carboxyhemoglobinemia).
 
 
 
 
 
Oxy-Hb dissociation curve
Jensen, N. . Clinical arterial blood gas analysis. Essentials for
the Anesthesiology Written  Board Examination, 3rd ed.,
N. Jensen, (ed.), privately published, 1993, vol. 1, p. 3-4.
ABGs
Causes:  Decreased P50 (91)
Determinants of O2 Delivery (95)
Altered P50 (95)
1.  There are many important issues related to oxygenation,
including oxygen content, the oxy-Hb dissociation curve,
V/Q mismatch, shunt, and the A-a gradient.
     a.  In  terms of arterial oxygen content, recall that oxygen is
present in the blood in two forms:  First,   bound to hemoglobin
and second dissolved in plasma.
     [CaCO2 = (1.34  X HgB X  Sat) + (0.003 PaO2)]
Arterial oxygen content is perhaps the most critical factor in
evaluating the adequacy of oxygen delivery to tissues.  Looking
at this equation it is obvious that by far the greatest amount of
oxygen in normal arterial blood is bound to hemoglobin.   In fact,
only about 1.5% of the total content of oxygen in arterial blood
is dissolved in plasma.  Clearly then, the most efficient way
to increase oxygen content is to increase hemoglobin.
     b.  We have seen how important it is that there be
appropriate quantities of hemoglobin.  It is also important how
easily the hemoglobin releases its oxygen to the tissues.  This is
reflected by the oxy-hemoglobin dissociation curve.  The P50 is
the partial pressure of oxygen at which hemoglobin is 50% s
aturated.
     c.  Recall that the normal P50 in adults is about
27 mm Hg and in infants about 19 mm Hg, as a result of increased
levels of fetal hemoglobin.
          1)  A right shift in this curve results in increased unloading
of oxygen at the tissue level and is caused by a number of factors
including increased hydrogen ion (acidosis), increased carbon
dioxide, increased temperature, and increased 2,3-DPG.
          2)  A left shift of the oxy-hemoglobin dissociation curve
results in decreased unloading of oxygen at the tissue level and
is caused by alkalosis, decreased temperature, and hemoglobin
variants such as methemoglobin, carboxyhemoglobin, or fetal
hemoglobin.  (Most hemoglobinopathies result in a left shift
of the oxy-Hb dissociation curve.  Sickle cell disease is one
exception.  It results in a right shift of the oxy-Hb dissociation
curve.)
 
 
 
 
 
Oxy-Hb dissociation curve
Jensen, N. . Arterial blood gas analysis. Essentials for the
Anesthesiology Written Board Examination, 2nd ed.,
N. Jensen, (ed.), privately published, 1993, vol. 1, p. 1.
ABGs
P50-O2 Dissociation Curve (92)
1.  This is covered in detail in the ABG notes.  If you have any
questions about this topic, please review Big Blue.
2.  We simply cannot afford to miss a question related to this, no
matter the guise.  Work hard.
 
 
 
 
 
Pyloric stenosis
Stoelting, R.  Pediatric patients.   Anesthesia and Co-Existing
Disease, R. Stoelting, S. Dierdorf and R. McCammon, 2nd ed.,
Churchill Livingstone, New York, 1988, p. 834-35.
ABGs
Pediatrics
Metabolic Effects:  Pyloric Stenosis (91)
1.  Incidence of pyloric stenosis: 1 in every 500 live births.
2.  Presentation is generally at 2 to 5 weeks of age with the
development of persistent vomiting.
3.  Etiology.  Unknown
4.  Effects.  Hyponatremic, hypokalemic, hypochloremic metabolic
alkalosis, with a compensatory respiratory acidosis.  (see the
pH-Bicarbonate diagrams in the chapter.  You should be able to
visualize these--any place and at anytime.  In fact, I will be
calling you at 0300 some night just to test you!  We'll also have
a number of "spiels" for the Oral exam that need to be on the tip
of your brain.  The Oral is very challenging and a lot of fun.  We'll
beat this beast in a few months.  Don't worry about it now.)
5.  Treatment.  This is a medical, NOT a surgical emergency.
Surgery can proceed after rehydration and correction of electrolyte
imbalances.  Na+ should be greater than 130 mEq/L, K+ at least
3 mEq/L,  Cl-at least 85 mEq/L, and  urine output 1-2 ml/kg/hr.
 
 
 
 
 
V/Q Mismatch
Bowe, E. and E. Klein.  Acid base, blood gas, electrolytes.   Clinical
Anesthesia, P. Barash, B. Cullen and R. Stoelting, 1st ed.,
JB Lippincott, New York, 1989, p. 684.
ABGs
Shunt Calculation (90)
1.  Calculations should be performed using numbers obtained with
the patient breathing 100% O2 (with FiO2=1.0, areas of relative
shunt should be either masked by the high PAO2 or converted to
absolute shunt by absorption atelectasis).  The value then reflects
absolute shunt.  If the patient is breathing less than 100%, it
combines relative and absolute shunt.
 
 
     Qs          CcO2 -CaO2
    _____  =    ____________
 
     Qt          CcO2- CVO2
 
Qs=physio shunt flow
Qt=CO
CcO2=O2 content of idealized pulmonary capillary (PcO2=PaO2)
CaO2=arterial O2 content
CVO2=mixed venous O2 content