P A O 5600 Lecture 9 Acid Base Balance (2hrs) Dave

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

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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+

Orlando, PA Program 2

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


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.


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


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)


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 )

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SYSTEM

ed) and “conjugate” base nges in H+ upon addition of nges in H upon addition of

-


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


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


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


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:


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)


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

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ation allows abnormalities in the asis of changes in the ratio of

uously work to adjust pCO2 and mal pH


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


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

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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


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


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


(

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

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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.


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-


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%


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


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


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

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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


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


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:


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


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

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, , 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


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


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


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

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S ETABOLIC ACIDOSIS

le acidsous Acid Productionous Acid Productionhydroxybutyrate, Acetoacetate acids

nol; ethylene glycol; ethanol

xcretion of Acidsorganic acids )


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

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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


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)


METABOLIC ACIDOSIS

Normal anion gap mCausesCauses

Loss of bicarbonateanion gap is not incincreased reabsorptmaintain electroneu

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S

etabolic acidosis

e from GI tract or Kidney -creased, because there is tion of chloride anion to utrality


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

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DOSIS

carbonate Rich Fluidsmon cause of normal s

tinal Drainageloss of bicarbonate in loss of bicarbonate in

sease

nfection ( pyelonephritis ); y stones


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

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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))


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

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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


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


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


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


both HCO3 and pCO2

RESPIRATORY ACID B

They are called resthe primary problemand pulmonary funand pulmonary fun

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BASE DISORDERS

spiratory because m involves pCO2ctionction


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

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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)


ndrome

RESPIRATORY AC

Defect: Retention ofDefect: Retention ofhypoventilationCausesCauses

Respiratory Center General anesthesiCNS brainstem paCNS brainstem pastroke)

Lung ConditionsObesity HypoventObesity- HypoventSyndrome)Flail chest from mKyphoscoliosis

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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


RESPIRATORY ACRESPIRATORY AC

Defect: Retention of COhypoventilationCHRONIC OBSTRUCTIVE CHRONIC OBSTRUCTIVE OFRESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS

Smoking Plays An Impoof these disorders

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CIDOSISCIDOSIS

O2 resulting from

LUNG DISEASE AS A CAUSE LUNG DISEASE AS A CAUSE

ortant Role in the Pathogenesis


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


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

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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


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


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


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 )

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goes into the cells)

ACID-BASE DISORDERSACID BASE DISORDERS

ssO2 increasesoes into cells; K + goes into

sdecreasesdecreases

oes into the plasma; K +


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

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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


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


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

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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


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


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

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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-


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

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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


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

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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


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:


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

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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


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


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


s

Time for QuestionsQ

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s ???????????


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P A O 5600 Lecture 9 Acid Base Balance (2hrs) Dave

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