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ACID
CC
D BASE BALANCE IPAO 5600
Clinical Laboratory Medicine IClinical Laboratory Medicine IWith Special Thanks To:
Pamela Jaffey MD
OBJECTIVESOBJECTIVES
1. Identify the sources of Hand nonvolatile acids)D ib th bi b t2. Describe the bicarbonatclinical utility in terms oId tif i di ti f3. Identify indications for athe normal values of pHO2 saturation in an arteO2 saturation in an arte
4. Define the relationship b
Dave Kotun, NSU O
H+ in the body (volatile
t b ff t d itte buffer system and its f acid base balance
t i l bl d dan arterial blood gas, and H, HCO3-, pCO2, pO2 and erial blood gaserial blood gasbetween pH and H+
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OBJECTIVES
5. Describe the normal ph5 esc be t e o a pthe lungs (the "respiratkidney (the "metabolic balance
6. Define the relationship iserum K+ concentration
balanceD ib th l ti7. Describe the regulation the central chemorecepthe peripheral receptors
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the peripheral receptorsaortic arch
hysiologic roles played by ys o og c o es p ayed byory component") and component") in acid-base
between pH and the i f id bn in terms of acid base
f th til t t bof the ventilatory rate by ptors in the medulla and s in the carotid bodies and
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s in the carotid bodies and
Introduction
• It is necessary for the body twithin a very narrow range: 7A deviation would alter enzycreate significant cardiovasc
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to maintain the blood pH 7.35-7.45.
yme function as well as cular disturbance.
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Introduction
This is a difficult task for the bodMetabolic processes produce 15 -b t th b d i bl f f tibut the body is capable of functionbetween 36- 44 nmol/L; deviationscan cause deathThe body maintains this pH balanas concerted actions of the lungs
The main buffer system utilized by thThe main buffer system utilized by thsystem.
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dy:- 20mol of H+ in the body daily, i ith l l l ning with plasma levels
s from these levels ultimately
ce with buffer systems as well and kidneys. he body is the bicarbonate buffer he body is the bicarbonate buffer
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SOURCES OF H+ IN THE
VOLATILE ACIDSVOLATILE ACIDSDerived from CO2:
CO di l i H O fCO2 dissolves in H2O fodissociates into bicarbonateCO2 + H2O H2CO3 HBICARBONATE BUFFER S
Respiration allows H+ to beDave Kotun, NSU O
Respiration allows H+ to be
E BODY
b i idorms carbonic acide and H+
HCO3- + H+ = THE
SYSTEM
e removed by the Lungs as CO2Orlando, PA Program 6
e removed by the Lungs as CO2
SOURCES OF H+ IN THE
NONVOLATILE ACIDS
Derived from Sources otheMetabolic products of sucompoundspLactic acidKeto acids (acetoacetateKeto acids (acetoacetate
Excreted by the Kidneys
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E BODY
er than CO2:ulfur and phosphorus containing
e and beta hydroxybutyrate)e and beta hydroxybutyrate)
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BICARBONATE BUFFER S
BUFFER = a weak acid (protonate(unprotonated ) that minimize chan(unprotonated ) that minimize chanacid or base
BICARBONATE BUFFER: H2CO3 H+ + HCO3-( acid) ( conjugate base )
Dave Kotun, NSU O
SYSTEM
ed) and “conjugate” base nges in H+ upon addition of nges in H upon addition of
-
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UNIQUENESS OF BICARBSYSTEM
THE BICARBONATE BUFFER THE BICARBONATE BUFFER It has a huge buffering capacityair (it is an open system)air (it is an open system)This is in contrast to other buffea closed systema c osed syste
ACID Hb : HHb Hb : HHb Proteins: Hprotein Phosphate buffer: H2PO - H
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Phosphate buffer: H2PO4 H
BONATE BUFFER
SYSTEM IS UNIQUE: SYSTEM IS UNIQUE:y because it communicates with
ers of the body which operate in
BASE LOCATION Hb- in erythrocytes Hb in erythrocytes Proteins- intracellularHPO4
2- intracellularOrlando, PA Program 9
HPO4 intracellular
INTERRELATIONSHIP OF COBICARBONATE BUFFER
THE HENDERSON- HASSELBAIn gene al the Hende son HIn general, the Henderson-Hdescribes the equilibrium betconjugate weak base (it is ubuffers)buffers)
We will apply the Henderson-pp yto the bicarbonate buffer systterms:
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OMPONENTS OF THE
ALCH EQUATION:asselbalch eq ationasselbalch equation tween pH, a weak acid, and seful in the preparation of
-Hasselbalch equation qtem after defining some
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H & H
Henderson-Hasselbalch equationConsider the ionization of a weak acid HA which has some pKa. It is oftenweak acid to the pKa of the acid and the extent of ionization. The reactionHA (reversible arrows) H+ + A-The acid dissociation constant (Ka) for this reaction would be given by the
This equation can be rearranged to isolate the hydrogen ion concentratiorelating the pH of the solution to the pKa and the extent of ionization of t
By definition, log 1/ [H+] = pH , and log 1/Ka = pKa , so that by taking t
This is the well-known Henderson-Hasselbalch equation that is often usedfor use in the laboratory, or other applications. Notice several interesting First, if the pH = pKa, the log of the ratio of dissociate acid and associatewill be the same. In other words, when the pH equals the pKa, the acid wSecond, notice that as the pH increases or decreases by one unit relative form of the acid changes by factors of 10 That is if the pH of a solution
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form of the acid changes by factors of 10. That is, if the pH of a solution the pH were 5, the ratio would be 0.01 and if the pH were 7, the ratio woAlso, note that if the pH is below the pKa, the ratio will be < 1, while if tha lot of information in the Henderson-Hasselbalch equation. You would beramifications.
n convenient to be able to relate the pH of a solution of a n would be
e equation
n on the left, because, remember, we want an equationthe weak acid. The rearranged form of the equation is
the log of the equation above, we get the equation
d to perform the calculations required in preparation of buffers facts about this equation. d acid will be zero, so the concentrations of the two species
will be half dissociated. to the pKa, the ratio of the dissociate form to the associated is 6 and the pKa is 7 the ratio of [ A ]/[ HA] will be 0 1 will if
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is 6 and the pKa is 7, the ratio of [ A-]/[ HA] will be 0.1, will if ould be 1. he pH is above the pKa, the ratio will be >1. In short, there is e wise to study this equation to understand its various
DEFINITIONS RELATED TO HHASSELBALCH EQUATIONQ
DEFINITIONSDEFINITIONS-log H+ = pH and H+ a
As H+ increases, pH deAs H + decreases, pH in-log Ka = pKa
Ka = the dissociation BICARBONATE BUFFER SDEFINED BY HENDERSOEQUATIONEQUATION:pH = pKa + log
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HENDERSON
are inversely proportionalcreasescreases
n constant of a weak acidSYSTEM EQUILIBRIUM AS N-HASSELBALCH
g HCO3- conjugate base/H CO conjugate acid
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H2CO3conjugate acid
Henderson Hassel
Two equivalent forms o
and
Here, pKa is − log10(Kacid dissociation consta
Dave Kotun, NSU Ofor the reaction:
bach
of the equation are
Ka) where Ka is the ant, that is:
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CALCULATION OF NML pH WHENDERSON-HASSELBALCH
Definitions: Definitions: pKa of bicarbonate buffer =Solubility coefficient of CO2pCO2 = the partial pressure
Normal = 40 mm HgCarbonic acid (H2CO3) = (0( 2 3) (
Normal value of HCO3- in pH = 6.1 + log 24 meq/ L
(0 03) (40 mm Hg)(0.03) (40 mm Hg)pH = 6.1 + log 20 = 6.1 +
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WITH THE EQUATIONQ
= 6.12 in water = 0. 03e of CO2 in an arterial blood gas
0.03) (pCO2) = (0.03) (40)) (p 2) ( ) ( ) an arterial blood gas = 24 mEq/L
1.3 = 7.4 ( normal pH)
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CONCLUSION
Henderson-Hasselbalch equapH to be understood on the babicarbonate to the pCO2
pH = HCO3- ::pCO2pH HCO3 ::pCO2
The lungs and kidney continubicarbonate to maintain a norm
Dave Kotun, NSU O
ation allows abnormalities in the asis of changes in the ratio of
uously work to adjust pCO2 and mal pH
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OFACID- BASE BALANCE
pCO2 = the RESPIRATORYpCO2 the RESPIRATORYbecause:
It depends upon the Rate of p pHCO3- = the METABOLIC C
It’s plasma concentration is mand is affected by amount of
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Y COMPONENT Y COMPONENT
RespirationpCOMPONENT because:maintained by the kidney, nonvolatile acids made
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REGULATION OF VENTILTHE LUNGS
CENTRAL CHEMORECECENTRAL CHEMORECEAre sensitive to pCO2 a
∴ Increase in pCO∴ Increase in pCOIncrease in Ven
RECEPTORS IN CAROTRECEPTORS IN CAROTAORTIC ARCH: Are Senpartial pressure of oxyg
When pO2 < 60 mIncreases - the “ hy
Dave Kotun, NSU O
control of ventilatio
LATORY RATE IN
PTORS IN THE MEDULLA:PTORS IN THE MEDULLA: and pH2 ( and decrease in pH )2 ( and decrease in pH ) ntilatory RateTID BODIES AND INTID BODIES AND IN nsitive to arterial pO2 (the gen)
mmHg, Ventilatory Rate ypoxic drive” takes over
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on
Significance of Hypox
These patients have embronchitisbronchitis
and chronically havIncreased pCO2 andIncreased pCO2 and
When they have exacerwith further decreawith further decreadrive takes over
Excessive O2 administraExcessive O2 administraexacerbation of COPD cdrive of respiration and
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pretention and death
ic Drive in COPD
mphysema or chronic
ve:d decreased pO2d decreased pO2
rbation of their illness ase in pO their hypoxicase in pO2, their hypoxic
ation (e g pure O2) duringation (e.g. pure O2) during could inhibit the hypoxic d cause significant pCO2
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g p 2
Regulation of Acid-Base BICARBONATE REABSORPBICARBONATE REABSORP
Occurs in the proximal aH+ EXCRETIONH+ EXCRETION
Occurs in the distal renaRemoves nonvolatile acmetabolism)Sulfuric and phosphoric
t b li metabolism Ketoacids generated fro(acetoacetate; beta hyd(acetoacetate; beta-hyd
Accumulation of these ketoain diabetics: diabetic ketoacid
Dave Kotun, NSU Ofuture lecture)
Balance by the KidneyPTIONPTIONand distal renal tubule
al tubule cids (waste products of ( p
c acids generated from protein
om fatty acid metabolism droxybutyrate; acetone)droxybutyrate; acetone)cids leads to a serious disorder dosis (further discussion in a
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(
EFFECT OF pH ON PLASMCONCENTRATION
As pH increases ( serum H+ As pH increases ( serum H+ H+ shifts from the intraccompartments, andK + shifts from the extracompartments HYPO
A H d ( HAs pH decreases ( serum HH + shifts from the extracompartments andcompartments, andK + shifts from the intraccompartments HYPE
Dave Kotun, NSU O
p
MA K+
decreases) (ALKALOSIS) decreases) (ALKALOSIS)cellular extracellular
acellular intracellular OKALEMIA
i ) (ACIDOSIS)+ increases) (ACIDOSIS)acellular intracellular
cellular extracellular ERKALEMIAOrlando, PA Program 20
ARTERIAL BLOOD GAS:AND INDICA
NORMAL VALUESpH = 7.35- 7.45pCO2 = 35 – 45 mm Hgb CO )by CO2)HCO3-= 22- 26mEq/L (cH d H lb l hHenderson-HasselbalchpO2 = 80- 100 mmHg (tO )O2)O2 Saturation = 95- 100hemoglobin saturated w
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hemoglobin saturated w
NORMAL VALUES ATIONS
(the partial pressure exerted
calculated by a machine from the h E ti )h Equation)he partial pressure exerted by
0% (the percentage of with O )Orlando, PA Program 21
with O2)
ARTERIAL BLOOD GAS: NAND INDICATIONS
Measurements of aboMeasurements of aboACCURATE from
ARTERIAL BLOOD tARTERIAL BLOOD tBecause pH and pCthat venous blood wthat venous blood w(bicarbonate will alsrelated to the pH anValues of pH and pCdrawn from differen
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NORMAL VALUES
ove are MOREove are MORE
than VENOUS BLOODthan VENOUS BLOODCO2 vary depending on site was obtained fromwas obtained from so vary because it is nd pCO2).2
CO2 from arterial blood nt parts of body are same.
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ARTERIAL BLOOD GAS: NAND INDICATIONS
The value of bicarbonThe value of bicarbonvenous blood
Is approximated froIs approximated frocontentAnd is a a few mEqAnd is a a few mEq The total CO2 is a a has dissolved pCOhas dissolved pCO2
CO2 content = dissolv
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NORMAL VALUES
nate from peripheralnate from peripheral
om the total CO or COom the total CO2 or CO2
lower than the total COlower than the total CO2
bit higher because it also
ved p CO2 + HCO3-
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ARTERIAL BLOOD GAS: C
Tell me what is a crTell me, what is a cr
pH < 7.25; > 7pCO2 < 20; > 6HCO < 15; >HCO3- < 15; >pO2 < 40O2 saturation <
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CRITICAL VALUES
ritical value?ritical value?
7.556040 40
< 75%
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INDICATIONS FOR ARTE
1. Monitor patients on ve2 Monitor critically ill non2. Monitor critically ill non3. Establish preoperative
parametersparameters4. Regulate electrolyte th5 Monitor O2 flow rates5. Monitor O2 flow rates 6. Diagnosis and treatme
metabolic disordersDave Kotun, NSU O
metabolic disorders
ERIAL BLOOD GAS
entilatorsnventilator patientsnventilator patients
e baseline
herapy
ent of significant
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ACIDPATHO
D- BASE BALANCE IIOLOGIC PROCESSES
OBJECTIVESOBJECTIVES1. Define and contrast
alkalosis2. Describe clinical sce2. Describe clinical sce
following acid base Metabolic acidosis; metMetabolic acidosis; met
respiratory acidosis
3 Describe the pattern3. Describe the patternfor the acid base dis
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t the terms acidosis and
enarios giving rise to theenarios giving rise to the disorders:tabolic alkalosis;tabolic alkalosis; ; respiratory alkalosis
ns of laboratory valuesns of laboratory values sorders above
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OBJECTIVES4. Describe how the an
(high vs. normal an( gcharacterize the etioacidosis
5. Identify mechanismmetabolic compensametabolic compensadisorders
6 Utilizing electrolyte6. Utilizing electrolyte data as well as clinicacid-base disorders
Dave Kotun, NSU O
acid base disorders
nion gap calculation ion gap) helps to g p) pology of metabolic
s of respiratory and ation for acid baseation for acid base
and arterial blood gasand arterial blood gas cal history diagnose the above
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above
DEFINITIONS Acidosis:
A process associateA process associateand an INCREASE ipH < 7.35pH < 7.35
Alkalosis:A process associateA process associateand a DECREASE inpH > 7 45pH > 7.45
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ed with a DECREASE in pHed with a DECREASE in pH n H+ concentration
ed with an INCREASE in pHed with an INCREASE in pH n H+ concentration
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DEFINI
M t b li id iMetabolic acidosis: Decrease in plasma
Metabolic alkalosis:Metabolic alkalosis:Increase in plasma
Respiratory acidosis:Respiratory acidosis:Increase in pCO2
Respiratory alkalosisRespiratory alkalosisDecrease in pCO2
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ITIONS
a HCO3-
HCO3-::
s:s:
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Metabolic Acid-Ba
They Are Called MetaboProblemProblem
Involves Nonvolatile AcidNot CO2 HCO3- and ReNot CO2, HCO3 , and Re
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ase Disorders
lic Because the Primary
dsnal Functionnal Function
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Metabolic AcidosisMetabolic Acidosis
h d d bThere is decreased bIncreased accumula
f floss of HCO3- from Classified as HIGH AANION GAP metabolANION GAP = unmeextracellular fluid co
Lactate, citrate, pyr
Dave Kotun, NSU O
, , py
b b dbicarbonate due to:lation of nonvolatile acids of
fm kidney or from GI tractANION GAP or NORMAL olic acidosis easured anions in the ompartment yruvate, phosphate, sulfate
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y , p p ,
METABOLIC ACIDOSIS
CALCULATION OF ANIONa+ - ( HCO3
- + Cl- ) Na+ ( HCO3 + Cl ) Normal Anion Gap =
8 148 – 14High Anion Gap Metaboli
> 14
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S
ON GAP =
ic Acidosis has anion gap
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METABOLIC ACID
H+ from nonvolatile acids (exH+ from nonvolatile acids (excombines with bicarbonate (Hbuffer equilibrium toward carbbuffer equilibrium toward carbfrom bicarbonate:
CO2 + H2O H2CO3CO2 H2O H2CO3
A decrease in bicarbonate (wA decrease in bicarbonate (wresults in increased anion gap
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DOSIS
x ketoacids; lactic acid) x. ketoacids; lactic acid) HCO3
- )and pulls bicarbonate bonic acid (H2CO3) and away bonic acid (H2CO3) and away
3 HCO3-+ H+
3 HCO3 H
without an increase in chloride) without an increase in chloride) p
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METABOLIC ACIDOSISHIGH ANION GAP MECaused by:y
Increased nonvolatiIncreased EndogenoIncreased Endogeno
Lactic acid, Beta- hand other organic a
ToxinsSalicylate; methano
Decreased Renal ExRenal failure ( ino
Dave Kotun, NSU O
S ETABOLIC ACIDOSIS
le acidsous Acid Productionous Acid Productionhydroxybutyrate, Acetoacetate acids
nol; ethylene glycol; ethanol
xcretion of Acidsorganic acids )
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METABOLIC ACIDOSMETABOLIC ACIDOSHIGH ANION GAP META
Lactic acidosis as a cauacidosisSerum Lactic Acid IncreI i d Ti P fImpaired Tissue Perfus
Shock and HypotensioSevere SepticemiapHypoxiaSevere congestive heSevere anemiaSevere anemia
Anaerobic conditions favincreased lactate produc
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increased lactate produc
SISSIS TABOLIC ACIDOSIS
use of high anion gap metabolic
eases In Conditions With isionon
art failure
vor glycolysis for energyction from pyruvateOrlando, PA Program 36
ction from pyruvate
METABOLIC ACIDOSMETABOLIC ACIDOSHigh anion gap metabolic aKeto acidosis as a cause of acidosis
States of insulin deficieketoacidsketoacidsDecreased Insulin iincreased acetyl CoA
ll d k t id tcalled ketoacids – acethydroxybutyrate) ke
Diabetes: patients have a laDiabetes: patients have a laStarvation: inadequate carbdecreased insulin
Dave Kotun, NSU O
Alcoholism: same mechanis
SISSIS acidosisf high anion gap metabolic g g p
ency cause an increase in
increased break down of fat increased ketones (also
t t t b tetoacetate; beta ketones in blood and urineack of insulinack of insulinbohydrate ingestion
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sm as starvation ketosis
METABOLIC ACIDOSMETABOLIC ACIDOS
High anion gap metaExogenous toxins a
t b li idgap metabolic acidoSubstances IngestedPoor Cash Flow:
Methanol (wood alcEthylene glycol (antSalicylates (aspirin)
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SISSIS
abolic acidosisas a cause of high anion
iosisd By Alcoholics With
cohol)tifreeze)
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METABOLIC ACIDOSIS
Normal anion gap mCausesCauses
Loss of bicarbonateanion gap is not incincreased reabsorptmaintain electroneu
Dave Kotun, NSU O
S
etabolic acidosis
e from GI tract or Kidney -creased, because there is tion of chloride anion to utrality
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METABOLIC ACID
GastroIntestinal Loss of BiDiarrhea is the most commi t b li id ianion gap metabolic acidosi
Pancreatic, Biliary, or IntestRenal Loss of bicarbonate-Renal Loss of bicarbonateurine due to renal tubular dis
Renal Tubular Acidosis (RTA)e.g. caused by chronic renal in
chronic obstruction from kidney
Dave Kotun, NSU O
DOSIS
carbonate Rich Fluidsmon cause of normal s
tinal Drainageloss of bicarbonate in loss of bicarbonate in
sease
nfection ( pyelonephritis ); y stones
Orlando, PA Program 40
METABOLIC ACIDOSI
NORMAL ANION GAP METALABS ASSOCIATED WITH M
DECREASED plasma HCO3HYPERCHLOREMIA occurHYPERCHLOREMIA occurMETABOLIC ACIDOSIS:
The kidney reabsorbs incre(bi b t )(bicarbonate)
ACIDOSIS CAUSES HYPERAcidosis increased serumthe cells K+ moves out ofhyperkalemia
This is a compensatory mechDave Kotun, NSU O
This is a compensatory mech
IS
ABOLIC ACIDOSISMETABOLIC ACIDOSIS3
- leads to DECREASED plasma pHrs with NORMAL ANION GAP rs with NORMAL ANION GAP
ased Cl- to balance the loss of anion
RKALEMIAm H+ concentration H+ shifts into f the cells into the serum
hanism for dealing with acidosisOrlando, PA Program 41
hanism for dealing with acidosis
METABOLIC ALKALOMETABOLIC ALKALO
Caused by loss of H+
It is called Metabolic becaunonvolatile acid (HCL) or seThere is increased bicarbonbuffer equilibrium toward inbuffer equilibrium toward in
CO2 + H20 H2CO3 HCO3-of bicarbo
Dave Kotun, NSU O
OSISOSIS
+
use primary disorder involves a loss of ecretion of H+ by kidneynate: loss of H+ drives bicarbonate
ncreased production of bicarbonate:ncreased production of bicarbonate:+H+ (reaction pulled toward direction
onate))
Orlando, PA Program 42
METABOLIC ALKALOSCAUSES
LOSS OF H+LOSS OF HGASTRIC LOSS of HC
VomitingVomitingNasogastric Suction
RENAL LOSS of H+ RENAL LOSS of H Some diureticsIncreased AldosteroneIncreased Cortisol (Cu
There is increased Na+
Dave Kotun, NSU Oincreased H+ and K+ s
IS
CL
e (Conn’s Syndrome);ushing’s Syndrome)+ reabsorption coupled with
Orlando, PA Program 43ecretion
METABOLIC ALKALOS
L b i t d ithLabs associated withIncreased bicarbonHypokalemia occurscompensatory mech
Decreased plasma Hcells into the serum
h llserum into the cells
Dave Kotun, NSU O
IS
h t b li lk l ih metabolic alkalosisate leads to increased pHs as part of a hanism
+ H+ shift from the K+ shifts from the h k lhypokalemia
Orlando, PA Program 44
COMPENSATION FOR MEDISORDERSDISORDERS
Respiratory compensmetabolic acid-base d
To assess compensa= HCO3- pCO2
Henderson-Hasselbalrelationship betweenpCO2 as indicated ab
Dave Kotun, NSU O
ETABOLIC ACID-BASE
sation occurs for disordersation, remember that pH
lch equation shows the pH, bicarbonate, and
bove
Orlando, PA Program 45
COMPENSATION FOR METADISORDERSDISORDERS
Respiratory compensap y pmetabolic acid-base diMETABOLIC ACIDOSISconcentration is high)
A primary decrease indecrease in pH; to brnormal, the pCO2 nee
Thi i li h d bThis is accomplished bventilatory rate to blow
L b A d iDave Kotun, NSU O
Labs: A decrease in
ABOLIC ACID-BASE
ation occurs for disordersS: (pH <7.35; H+(p ;
n bicarbonate results in a ring the pH up toward eds to be decreasedb i iby increasing w off CO2b th HCO d CO
Orlando, PA Program 46
both HCO3- and pCO2
COMPENSATION FOR METADISORDERSDISORDERS
METABOLIC ALKALpH > 7.45; H+ conc
Remember that pH =A primary increase
i d H tan increased pH; totoward normal, theThis is accomplisheThis is accomplisheventilatory rate to r
Labs: an increase inDave Kotun, NSU O
Labs: an increase in
ABOLIC ACID-BASE
LOSIS:centration is low= bicarbonate pCO2in bicarbonate results in b i th H do bring the pH down
pCO2 needs to be raiseded by decreasinged by decreasing retain more CO2
both HCO3- and pCO2
Orlando, PA Program 47
both HCO3 and pCO2
RESPIRATORY ACID B
They are called resthe primary problemand pulmonary funand pulmonary fun
Dave Kotun, NSU O
BASE DISORDERS
spiratory because m involves pCO2ctionction
Orlando, PA Program 48
RESPIRATORY ACID
Defect: Retention of CODefect: Retention of COhypoventilationCauses
Chronic Obstructive(COPD) emphysemb di d)be discussed)Neuromuscular Disof Respiratory Muscof Respiratory Musc
Spinal cord injury;(ALS); multiple sc
Dave Kotun, NSU O
Guillian- Barre Syn
DOSIS
O2 resulting fromO2 resulting from
e Pulmonary Disease ma; chronic bronchitis (to
orders Causing Weakness clescles; amyotrophic lateral sclerosis lerosis ( MS)
Orlando, PA Program 49
ndrome
RESPIRATORY AC
Defect: Retention ofDefect: Retention ofhypoventilationCausesCauses
Respiratory Center General anesthesiCNS brainstem paCNS brainstem pastroke)
Lung ConditionsObesity HypoventObesity- HypoventSyndrome)Flail chest from mKyphoscoliosis
Dave Kotun, NSU O
Kyphoscoliosis
CIDOSIS
f CO resulting fromf CO2 resulting from
Depressiona; sedative and narcotic drugs; thology (tumor; trauma;thology (tumor; trauma;
tilation Syndrome (Pickwickiantilation Syndrome (Pickwickian
ultiple rib fractures
Orlando, PA Program 50
RESPIRATORY ACRESPIRATORY AC
Defect: Retention of COhypoventilationCHRONIC OBSTRUCTIVE CHRONIC OBSTRUCTIVE OFRESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS
Smoking Plays An Impoof these disorders
Dave Kotun, NSU O
CIDOSISCIDOSIS
O2 resulting from
LUNG DISEASE AS A CAUSE LUNG DISEASE AS A CAUSE
ortant Role in the Pathogenesis
Orlando, PA Program 51
RESPIRATORY ACID
Defect: Retention of CO2 resultEMPHYSEMA:
Destruction of air spaces and lossDestruction of air spaces and lossprotease activity associated with sexhaling CO2
C O C O C SCHRONIC BRONCHITIS:Criteria for diagnosis- Persistent Cfor at least 3 Months in 2 Consecu
Chronic Irritation from Cigarette SmokExcessive Mucous Production in S
ObstructionDave Kotun, NSU O
Obstruction
DOSIS (cont.)( )
ting from hypoventilation
s of elasticity ( due to increased s of elasticity ( due to increased smoking ) results in difficulty
Cough and Sputum Production utive Yearske and Microbiologic Infections Small and Large Airways
Orlando, PA Program 52
RESPIRATORY ACIDO
Defect: Retention ofDefect: Retention ofhypoventilationNeuromuscular disordersNeuromuscular disordersacidosis
AMYLIOTROPHIC LATAMYLIOTROPHIC LATGherig’s Disease”
Progressive Degenerag gand Spinal Cord prmuscles needed for RD th t i ll i 3
Dave Kotun, NSU O
Death typically in 3 ye
SIS
f CO2 resulting fromf CO2 resulting from
s as a cause of respiratory s as a cause of respiratory
TERAL SCLEROSIS (ALS)- “Lou TERAL SCLEROSIS (ALS) Lou
ation of Motor Neurons in the Brain rogressive weakness and wasting of
Respiration and Movement
Orlando, PA Program 53
ears
RESPIRATORY ACDefect: Retention of CO2 reNeuromuscular disorders as
Multiple sclerosis (MS)One of the more comm
Usually characterizeUsually characterizeCourse
Pathology -Multiple armatter matter
Gillian - Barre SyndromAcute or Subacute illnsometimes requiring aCauses- preceding upinfection
Dave Kotun, NSU O
infectionImmunizations
CIDOSISesulting from hypoventilation a cause of respiratory acidosis
mon CNS Diseasesed by Chronic Remitting and Relapsing ed by Chronic Remitting and Relapsing
reas of Myelin Loss in the CNS white
meess with motor impairment,
assisted ventilationpper respiratory or gastrointestinal
Orlando, PA Program 54
RESPIRATORY ALKALO
D f t D l ti f CODefect: Depletion of CO2hyperventilationCCauses
Stimulation of the brainsEmotional states: exciteEmotional states: exciteFeverPregnancySalicylates and Sepsis: respiratory alkalosis and
Dave Kotun, NSU O
OSIS
R lti f Resulting from
stem respiratory centerment; anxietyment; anxiety
Both of these may cause a mixed d metabolic acidosis
Orlando, PA Program 55
RESPIRATORY AL
Defect: Depletion of CODefect: Depletion of COhyperventilationCauses (cont )Causes (cont.)Cardiac disease
Congestive Heart FailuCongestive Heart Failu(rapid breathing)Severe congestive heaghypoperfusion lacticacidosis
Dave Kotun, NSU OMechanical over ventila
LKALOSIS
O Resulting from O2 Resulting from
re Pulmonary Edema re Pulmonary Edema
art failure results in c acidosis metabolic
Orlando, PA Program 56ation
LABS IN RESPIRATORY ALABS IN RESPIRATORY A
Respiratory acidosisRespiratory acidosispH decreases; pCOHyperkalemia (H+ gothe plasma)
Respiratory alkalosipH increases; pCOpH increases; pCO2
Hypokalemia (H + go i t th ll )
Dave Kotun, NSU O
goes into the cells)
ACID-BASE DISORDERSACID BASE DISORDERS
ssO2 increasesoes into cells; K + goes into
sdecreasesdecreases
oes into the plasma; K +
Orlando, PA Program 57
COMPENSATION FOR RESACID-BASE DISORDERSACID BASE DISORDERS
Metabolic compensation Metabolic compensation base disorders
When assessing compeWhen assessing compedetermined by the ratio
Respiratory acidosis (pHp y (pA primary increase in pretention) results in a deTo bring the pH up towacompensates by reabso
Dave Kotun, NSU O
SPIRATORY
occurs for respiratory acid – occurs for respiratory acid
ensation, remember that pH is ensation, remember that pH is of bicarbonate to pCO2
< 7.35; high H+)g )pCO2 (from excessive CO2ecrease in pHard normal, the kidney orbing MORE bicarbonate
Orlando, PA Program 58
COMPENSATION FOR RESACID-BASE DISORDERSACID BASE DISORDERS
M t b li tiMetabolic compensationbase disorders
Wh i When assessing compedetermined by the ratio
Respiratory alkalosis (pHRespiratory alkalosis (pHA primary decrease in results in a increase in results in a increase in To bring the pH down tcompensates by reabso
Dave Kotun, NSU O
SPIRATORY
f i t id occurs for respiratory acid –
ti b th t H i ensation, remember that pH is on of bicarbonate to pCO2H > 7 45; low H+)H > 7.45; low H )pCO2 (from hyperventilation) pH pHtoward normal, the kidney orbing LESS bicarbonate
Orlando, PA Program 59
CALCULATION OF COMPECALCULATION OF COMPE
Purpose:Purpose:1. To determine if the c
i f h iappropriate for the primmaintain a HCO3
-/ pCOpH (and if compensatopH (and if compensatoappropriate for primary2 To determine if it is 2. To determine if it is respiratory acid-base ddisorder
Dave Kotun, NSU O
ENSATION FACTORENSATION FACTOR
compensatory change in pCO2 is h i HCO mary change in HCO3
- to O2 ratio compatible with normal ory change in bicarbonate is ory change in bicarbonate is y change in pCO2) a “ simple” metabolic OR a simple metabolic OR isorder, or a mixed acid – base
Orlando, PA Program 60
CALCULATION OF COMPEN
Purpose:A simple acid-baseA simple acid base there is only 1prima(e.g. metabolic acidA mixed acid-base dthere are 2 or moreoccurring at the sam
If the calculated competh it i i l dithen it is a simple disorIf the compensation is n
b i d di dDave Kotun, NSU O
may be a mixed disorde
NSATION FACTOR
disorder is one in whichdisorder is one in which ary acid-base disturbance dosis)disorder is one in which e acid-base disturbances me timeensation is appropriate, drdernot what is expected, it
Orlando, PA Program 61
er
CALCULATION OF RESPIRAFACTOR FOR METABOLIC AFACTOR FOR METABOLIC A
M t b li id iMetabolic acidosispCO2 should decrea2in 1.0 mEq/L of HCO
Metabolic alkalosispCO should increapCO2 should increaeach rise of 1.0 mEq
Dave Kotun, NSU O
ATORY COMPENSATION ACID BASE DISORDERSACID-BASE DISORDERS
se by 1.2 mmHg for each fall 3-
se by 0 4 0 7 mmHg for se by 0.4 – 0.7 mmHg for q/L of HCO3-
Orlando, PA Program 62
CALCULATION OF COMPENSRESPIRATORY ACID-BASE DRESPIRATORY ACID BASE D
Respiratory acidosisRespiratory acidosisACUTE
HCO3- rises 1 mEq/L for ea3 qCHRONIC
HCO3- rises 3-4 mEq/L for eR i t lk l iRespiratory alkalosisACUTE
HCO3 falls 2-3 mEq/L for eHCO3- falls 2 3 mEq/L for eCHRONIC
HCO3- falls 5 mEq/L for eac
Dave Kotun, NSU O
SATION FACTOR FOR DISORDERSDISORDERS
ach rise of 10 mmHg in pCO2g p 2
each rise of 10 mmHg in Pco2
ach decrease of 10 mmHg in pCO2ach decrease of 10 mmHg in pCO2
ch decrease of 10 mmHg in pCO2
Orlando, PA Program 63
CONCLUSIONSMetabolic acid – basPrimary Problem is with NPrimary Problem is with Nand Kidney
Metabolic acidosis: decrMetabolic acidosis: decrMetabolic alkalosis: incr
C ti i b AdjCompensation is by AdjuspCO2 (occurs over minute
Metabolic acidosis: decrMetabolic alkalosis: incr
Dave Kotun, NSU O
se disordersNonvolatile Acids HCONonvolatile Acids, HCO3-
rease in bicarbonaterease in bicarbonaterease in bicarbonate
ti V til t R t d sting Ventilatory Rate and es/ hours)rease in pCO2
rease in pCO2
Orlando, PA Program 64
CONCLUSIONSSummary of labs:
Metabolic acidosisMetabolic acidosispH decreased; HCO3
- decreased;3 ;pCO2 decreased
Normal Anion Gap MetaHyperchloremia
Metabolic alkalosispH increased;HCO3
- increased;
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pCO2 increased
abolic Acidosis:
Orlando, PA Program 65
CONCLUSIONSRespiratory acid – baPrimary Problem is with pPrimary Problem is with p
Respiratory acidosis: incRespiratory alkalosis: deRespiratory alkalosis: de
Compensation is by Adjusby the Kidney (occurs ovby the Kidney (occurs ov
Respiratory acidosis: incR i t lk l i dRespiratory alkalosis: de
Dave Kotun, NSU O
ase disorderspCO2 and lungspCO2 and lungscrease in pCO2
ecrease in pCOecrease in pCO2
sting Reabsorption of HCO3-ver days)ver days)crease in bicarbonate
i bi b tecrease in bicarbonate
Orlando, PA Program 66
CONCLUSIONSSummary of labs:
Respiratory acidosisRespiratory acidosispH decreasedpCO2 increased2
HCO3- increased
Respiratory alkalosispH increasedpCO2 decreasedHCO3
- decreased
Dave Kotun, NSU OOrlando, PA Program 67
Conclusions
Changes in serum K+ concentin pHin pH
ACIDOSIS HYPERKALEMIAALKALOSIS HYPOKALEMIAALKALOSIS HYPOKALEMIA
Note – this concept is ve
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tration resulting from changes
AAAery important in diabetes
Orlando, PA Program 68
CONCLUSIONSCONCLUSIONS
Si l id b diSimple acid – base disOne primary problem (re
Mixed acid – base disoTWO ( or more ) PRIMAO ( o o e )Examples of Mixed Acid
COPD with shock and LAcidosis and MetabolicPregnancy with excess
d M t b li Alk l iDave Kotun, NSU O
and Metabolic Alkalosis
d orders espiratory or metabolic)
ordersARY PROBLEMSO S
- Base DisordersLactic Acidosis = Respiratory p y
c Acidosissive Vomiting = Respiratory Alkalosis
Orlando, PA Program 69
s
Time for QuestionsQ
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s ???????????
Orlando, PA Program 70