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Page 1: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Acid-Base DisturbanceAcid-Base Disturbance

Department of PathophysiologyDepartment of Pathophysiology

Shanghai Jiao-Tong University School of MedicineShanghai Jiao-Tong University School of Medicine

Page 2: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

main topicsmain topics

Acid Base PhysiologyAcid Base Physiology

Acid Base disturbancesAcid Base disturbances

Page 3: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Concept of Acid Base disturbanceConcept of Acid Base disturbance

Acid Base parameter/Arterial Blood Gases Acid Base parameter/Arterial Blood Gases (ABGs)(ABGs)

Clinical Acid Base disordersClinical Acid Base disorders

Pathogenesis of Acid Base disordersPathogenesis of Acid Base disorders

Influence of Acid Base disordersInfluence of Acid Base disorders

Mixed Acid/Base disorders

Acid Base disturbancesAcid Base disturbances

Page 4: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

The concept of Acid Base balanceThe concept of Acid Base balance

Page 5: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Acid-base balance refers to the mechanisms the Acid-base balance refers to the mechanisms the

body uses to keep its fluids close to neutral pH (that body uses to keep its fluids close to neutral pH (that

is, neither basic nor acidic) so that the body can is, neither basic nor acidic) so that the body can

function normally.function normally.

Arterial blood pH is normally closely regulated Arterial blood pH is normally closely regulated

to between 7.35 and 7.45.to between 7.35 and 7.45.

Acid Base balanceAcid Base balance

Page 6: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

acidsacids ??

basesbases ??

Any ionic or molecular substance Any ionic or molecular substance that can act as a proton donor.that can act as a proton donor.

Strong acidStrong acid :: HCl, HHCl, H22SOSO44, H, H33POPO44..

Weak acidWeak acid :: HH22COCO33, CH, CH33COOH.COOH.

Any ionic or molecular substance Any ionic or molecular substance that can act as a proton acceptor.that can act as a proton acceptor.

Strong alkaliStrong alkali :: NaOH, KOH.NaOH, KOH.Weak alkaliWeak alkali :: NaHCONaHCO33, NH, NH33, ,

CHCH33COONa.COONa.

Page 7: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Lactic acid

Ketone bodies

Sulfuric acid

Phosphoric acid

Intracellular metabolism

Volatile acids

300~400L 300~400L COCO2 (15(15molmol

HH++) )

Fixed acids

50~100 50~100 mmol mmol HH++

NHNH33 , sodium citrate, sodium lactate

Origin of acids Much more

Origin of basesOrigin of bases less

CO2+H2O=H2CO3

Page 8: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Acid Base balance & regulationAcid Base balance & regulation

Page 9: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

pHpH- - pH of ECF is between 7.35 and 7.45.pH of ECF is between 7.35 and 7.45.

Deviations, outside this range affect Deviations, outside this range affect membrane function, alter protein membrane function, alter protein function, etc.function, etc.

- - You cannot survive with a pH <6.8 or You cannot survive with a pH <6.8 or >7.7>7.7

- Acidosis- below 7.35 Acidosis- below 7.35

Alkalosis- above 7.45Alkalosis- above 7.45

CNS function deteriorates, coma, cardiacCNS function deteriorates, coma, cardiac

irregularities, heart failure, peripheral irregularities, heart failure, peripheral

vasodilation, drop in Bp.vasodilation, drop in Bp.

Page 10: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Given that normal body pH is slightly alkaline and that normal metabolism produces acidic waste products such as carbonic acid (carbon dioxide reacted with water) and lactic acid, body pH is constantly threatened with shifts toward acidity.

In normal individuals, pH is controlled by two major and related processes; pH regulation and pH compensation. Regulation is a function of the buffer systems of the body in combination with the respiratory and renal systems, whereas compensation requires further intervention of the respiratory and/or renal systems to restore normalcy.

Page 11: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

H + load

ECF lung ICF Renal Bone

Buffers RBC Respiratorycontrol

Buffers

HH++ excretion excretion

bicarbonate bicarbonate reabsorptionreabsorption

Release Release bone saltbone salt

H +- K +

exchange

Hbbuffers

others

CaCa22 ++++ HH22POPO44

In chronic In chronic metabolic metabolic acidosisacidosis

H2CO3 CO2

Acid excretion

Expiration

Immediately minutes hours days Very slowVery slow

Page 12: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Buffering systemBuffering system ECF

Plasma NaHCO3/ H2CO3 NaPr/HPr* Na2HPO4/NaH2PO4

intercellular NaHCO3/ H2CO3 Na2HPO4/NaH2PO4

fluid

ICF** KPr/HPr K2HPO4/KH2PO4 KHCO3 /H2CO3

organic acids

RBC KHb/HHb KHbO2/HHbO2 K2HPO4/KH2PO4

KHCO3/ H2CO3

* HPr : protein ; ** muscle cells 。

Page 13: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

buffering?

HAHA HH+ + + + AA

Ka =Ka =[ H[ H+ + ] ] [ A [ A ]]

[ HA ][ HA ]

[ H[ H+ + ] =] = Ka Ka [ HA ][ HA ]

[ A[ A ]]

pH =pH = pKa pKa ++ lglg[ HA ][ HA ]

[ A[ A ]]

Page 14: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.
Page 15: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Henderson-Hasselbalch equationHenderson-Hasselbalch equation : :

pH pH pKa pKa + + loglog (( HCOHCO33 -- // H H22COCO33 )) pH pKa + log ( HCO3 - / ·PaCO2)pH 6.1 + log ( 24 /0.226·5.32 )pH 6.1 + log ( 24 / 1.2 )pH 6.1 + 1.3

pH 7.4

( : the factor which relates PCO2 to the amount of CO2 dissolved in plasma )

Page 16: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

plasma RBC

Cl¯ transfer

Primary changing

Hb buffering

COCO22 CO2 + H2O

H2CO3

H+

C l

CA : carbonic anhydrase

CA

CA

C l

HCOHCO33 HCO3

The compensation effect of RBC The compensation effect of RBC

Page 17: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

NaNa++-H-H++ exchange exchange of proximal tubule. of proximal tubule.HH++ secretion in collecting tubule is mediated by secretion in collecting tubule is mediated by HH++ ATPase ATPase pump in luminal pump in luminal membrane and a Cl-HCO3- exchanger in basolateral membrane. The Hmembrane and a Cl-HCO3- exchanger in basolateral membrane. The H++ ATPase ATPase pump is pump is influenced by aldosteroneinfluenced by aldosterone, which stimulates increased H, which stimulates increased H++ secretion. secretion. Hydrogen ion secretion in the collecting tubule is the process primarily Hydrogen ion secretion in the collecting tubule is the process primarily responsible for acidification of the urine, particularly during states of acidosis. The responsible for acidification of the urine, particularly during states of acidosis. The urine pH may fall as low as 4.0. urine pH may fall as low as 4.0.

BicarbonateBicarbonateReabsorptionReabsorption

Page 18: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Excretion of titratable acids is dependent on the quantity of phosphate is dependent on the quantity of phosphate filtered and excreted by the kidneys, which is dependent on one's diet, and filtered and excreted by the kidneys, which is dependent on one's diet, and also PTH levels. As such, the excretion of titratable acids is not regulated also PTH levels. As such, the excretion of titratable acids is not regulated by acid base balance and cannot be easily increased to excrete the daily by acid base balance and cannot be easily increased to excrete the daily acid load. acid load.

Page 19: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

NHNH44++ excretion excretion

The major adaptation to an increased acid load is increased ammonium production and excretion. Because the rate of NH4+  production and excretion Because the rate of NH4+  production and excretion can be regulated in response to the acid base requirements of the body.can be regulated in response to the acid base requirements of the body.

●●The process of ammoniagenesis occurs within The process of ammoniagenesis occurs within proximal tubular cells..

●●The generation of new HCO3¯ ions is probably the most important feature of this process.

Ammoniagenesis Ammoniagenesis

Page 20: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

SummarySummary

Buffers only provide a temporary solution.

Kidney: are the ultimate H+ ions balance. Slow acting mechanisms can eliminate any imbalance in H+ levels.

Lung: responds rapidly to altered plasma H+ concentrations, and keep blood levels under control until the kidneys eliminate the imbalance.

Page 21: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.
Page 22: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Acid base disturbanceAcid base disturbance

Page 23: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

An acid base disorder is a change in the a change in the normal value of extracellular pHnormal value of extracellular pH that may result when renal or respiratory function is abnormal or when an acid or base load overwhelms excretory capacity.

Definition of acid-base disordersDefinition of acid-base disorders

Page 24: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Simple Acid-Base DisordersSimple Acid-Base Disorders

Since PCO2 is regulated by respiration, abnormalities that primarily alter the PCO2 are referred to as respiratory acidosis (high PCO2) and respiratory alkalosis (low PCO2).

In contrast, [HCO3¯] is regulated primarily by renal processes. Abnormalities that primarily alter the [HCO3¯] are referred to as metabolic acidosis (low [HCO3¯]) and metabolic alkalosis (high [HCO3¯]).

Clinical disturbances of acid base metabolism classically are defined in terms of the HCO3HCO3¯̄  /CO  /CO22   buffer system. Acidosis – process that increases [H+] by increasing PCO2 or by reducing [HCO3-]Alkalosis – process that reduces [H+] by reducing PCO2 or by increasing [HCO3-]

Henderson Hasselbalch equation: 

pH = 6.1 + log [HCO3-]/ 0.03 PCO2

Page 25: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.
Page 26: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Acid Base parameterAcid Base parameter/Arterial Blood Gases (ABGs)/Arterial Blood Gases (ABGs)

Page 27: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

AArterial rterial BBlood lood GGas Samplingas Sampling

Page 28: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

pHpHpH is a measurement of the acidity of the blood,

reflecting the number of hydrogen ions present. pH = - log [H+]

pHpH7.457.45 : alkalosis

pHpH7.357.35 : acidosis

pH 7.35 - 7.45pH 7.35 - 7.45 : ①Acid-base balance.②Acidosis or alkalosis with complete compensation.③A mixed acidosis and alkalosis, both events have

opposite effects on pH, may also have a normal pH.

Page 29: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

PaCOPaCO22

(Partial Pressure of Carbon Dioxide)(Partial Pressure of Carbon Dioxide)

The amount of carbon dioxide dissolved in arterial

blood.

Normal: 4.39 Normal: 4.39 ~ ~ 6.25kPa6.25kPa (( 33 33 ~ ~ 46 mmHg46 mmHg ))Average: 5.32 kPaAverage: 5.32 kPa (( 40 mmHg40 mmHg ))Respiratory acidosis: > 46 mmHg (> 6 .25kPa)Respiratory acidosis: > 46 mmHg (> 6 .25kPa)

Respiratory alkalosis: <33 mmHg (< 4.39 kPa)Respiratory alkalosis: <33 mmHg (< 4.39 kPa)

The PaCO2 reflects the exchange of this gas through the lungs to the outside, so it is called “respiratory parameter”.

Page 30: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

SB, ABSB, ABThese two parameters are designed for HCO3¯ concentration

in plasma.

SB is measured under “standard condition”, AB is measured under “actual condition”. The difference between two cases is that the former rules out the respiratory effect on HCO3¯ concentration measurement, but the later does not.

HCO3¯HCO3¯

----------------------------------------------------

Normal: 22Normal: 22 ~~ 27mmol/L27mmol/L

Metabolic acidosis: <22 mmol/LMetabolic acidosis: <22 mmol/L

Metabolic alkalosis: > 27 mmol/LMetabolic alkalosis: > 27 mmol/L

[Standard Bicarbonate: Calculated value. Similar to the base excess. It is defined as the calculated bicarbonate concentration of the sample corrected to a PCO2 of 5.3kPa (40mmHg).

Page 31: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

BE (base excess)BE (base excess)

The base excess indicates the amount of excess or insufficient level of bicarbonate in the system. (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess.

Normal: -3 to +3 mmol/LNormal: -3 to +3 mmol/L

Metabolic acidosis: < -3 mmol/LMetabolic acidosis: < -3 mmol/L

Metabolic alkalosis: > +3 mmol/LMetabolic alkalosis: > +3 mmol/L

Base excess (BE) is the mmol/L of base that needs to be removed to bring the pH back to normal when PCO2 is corrected to 5.3 kPa or 40 mmHg. During the calculation any change in pH due to the PCO2 of the sample is eliminated, therefore, the base excess reflects only the metabolic component of any disturbance of acid base balance.

Page 32: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

AG (anion gap)AG (anion gap)Difference between undetermined anions and

undetermined cations.

Anion gap = NaAnion gap = Na++ - [Cl - [Cl¯̄ + HCO3 + HCO3¯̄]]Based on the principle of electrical neutrality, the serum

concentration of cations (positive ions) should equal the serum concentration of anions (negative ions).However, serum Na+ ion concentration is higher than the sum of serum Cl¯ and HCO3¯ concentration. Na+ = Cl¯ + HCO3¯ + unmeasured anions (gap).

Normal: 12Normal: 122mmol/L (10 - 14 mmol/L)2mmol/L (10 - 14 mmol/L)These “undetermined anions” are generally accounted

for by negatively charged proteins, phosphate, sulfate and organic anions. Except for a few relatively uncommon circumstances, an increase in the AG is synonymous with the accumulation of nonvolatile acids in body fluids, and suggests metabolic acidosis.

Page 33: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

pH—Determine Acidosis versus alkalosis

Determine MetabolicDetermine Metabolic

——the concentration of

HCO3¯, controlled by non-HCO3¯, controlled by non-

respiratory factors.respiratory factors.

SB (standard bicarbonate)

BE (base excess)

Determine RespiratoryDetermine Respiratory

——the concentration of COCO22 。

PaCOPaCO22

HCO3¯HCO3¯—influenced by Metabolic and Respiratory factors—influenced by Metabolic and Respiratory factors 。。AG AG —— ■ ■ Helpful in Metabolic AcidosisHelpful in Metabolic Acidosis ■■ Helpful in mixed acid-base disorders Helpful in mixed acid-base disorders

Page 34: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Once the acid-base disorder is identified as respiratory or Once the acid-base disorder is identified as respiratory or metabolic, we must look for the degree of compensation that metabolic, we must look for the degree of compensation that may or may not be occurring. This compensation may be may or may not be occurring. This compensation may be complete (pH is brought into the normal range) or partial (pH is complete (pH is brought into the normal range) or partial (pH is still out of the normal range but is in the process of moving still out of the normal range but is in the process of moving toward the normal range.) toward the normal range.)

In pure respiratory acidosis (high PaCOIn pure respiratory acidosis (high PaCO22, normal [HCO3, normal [HCO3¯̄], and ], and

low pH) we would expect an eventual compensatory increase in low pH) we would expect an eventual compensatory increase in plasma [HCO3plasma [HCO3¯̄] that would work to restore the pH to normal. ] that would work to restore the pH to normal. Similarly, we expect respiratory alkalosis to elicit an eventual Similarly, we expect respiratory alkalosis to elicit an eventual compensatory decrease in plasma [HCO3compensatory decrease in plasma [HCO3¯̄]. ].

A pure metabolic acidosis (low [HCO3A pure metabolic acidosis (low [HCO3¯̄], normal PaCO], normal PaCO22, and a , and a

low pH) should elicit a compensatory decrease in PaCOlow pH) should elicit a compensatory decrease in PaCO22, and a , and a

pure metabolic alkalosis (high [HCO3pure metabolic alkalosis (high [HCO3¯̄], normal PaCO], normal PaCO22, and high , and high

pH) should cause a compensatory increase in PaCOpH) should cause a compensatory increase in PaCO22. .

All compensatory responses work to restore the pH to the All compensatory responses work to restore the pH to the normal range (7.35 - 7.45)normal range (7.35 - 7.45)

Page 35: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Pathogenesis of Acid Base Pathogenesis of Acid Base disordersdisorders

Page 36: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Metabolic Metabolic acidosisacidosis

generategenerate

intakeintake

Incr

ease

d A

GIn

crea

sed

AG

AcidsAcids Fixed acidsFixed acidsSource

Exclusion

Lactic acidosisLactic acidosis

ketoacidosisketoacidosis

Salicylic acidosisSalicylic acidosis

:: renal failurerenal failure

BasesBases

Source —— —— impossibleimpossible

Loss From GIFrom GI :: diarrheadiarrhea

From kidneyFrom kidney :: proximal/distal tubular acidosisproximal/distal tubular acidosis

Consume :: ammonium chloride have been administeredammonium chloride have been administered

Primary [HCO3]

Nor

mal

AG

Nor

mal

AG

Page 37: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Metabolic alkalosis

Fixed acids

Source

Loss

——impossible

From GI:: vomiting, gastric suctionvomiting, gastric suction

From kidney

KK++ or Cl or Cl¯̄ deficiency deficiency

HyperaldosteronismHyperaldosteronismCushing’s syndromeCushing’s syndrome

Diuretic therapyDiuretic therapy

BasesSource ————Alkali administrationAlkali administration :: NaHCONaHCO33 、、 sodium sodium

lactate .lactate .

Exclusion ——impossible

Primary [HCO3]

Page 38: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Severe vomiting

Loss of HLoss of H++

Loss of ClLoss of Cl

Loss of KLoss of K++

Loss body fluidLoss body fluid Ald Ald

Page 39: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Respiratory alkalosis

Respiratory acidosis

Volatile acid

Generation ————impossibleimpossible

Exhalation :: failure of ventilationfailure of ventilation

inhalation :: inhale COinhale CO2 2 at high concentrationat high concentration

Generation ——impossibleVolatile acid

hypoxemia, anxiety, hysteria, Salicylate intoxicationCNS diseases

Exhalation

Primary [H2CO3 ]

Primary [H2CO3 ]

Page 40: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Compensation to acidosisCompensation to acidosis metabolic respiratorymetabolic respiratory

FeatureFeature HCOHCO33-- ,, BBBB,SB,SB,AB,AB,BE(,BE( -- )) HH22COCO3 3 ,, PaCOPaCO22 AB>SB AB>SB

Blood Blood HA + HCOHA + HCO33--AA--+ H+ H22COCO3 3 plasma protein, RBC Hb plasma protein, RBC Hb

bufferingbuffering (No compensation to acute(No compensation to acute

COCO2 2 + H+ H22O O repiratory acidosis)repiratory acidosis)

Lung Lung increased breathing no compensationincreased breathing no compensation

(Kussmaul Respiration)(Kussmaul Respiration)

ICF ICF HH+ + + KPr+ KPrKK+++ HPr+ HPr ;;buffering Hbuffering H+ + + K+ K22HPOHPO44KK+++ KH+ KH22POPO44 ;; [K[K+ + ]e]e

Kidney Kidney unless the acidosis is due to renal dysfunction, unless the acidosis is due to renal dysfunction,

the kidneys respond by increasing hydrogen ion secretion andthe kidneys respond by increasing hydrogen ion secretion and ammoniaammonia production, this result in HCOproduction, this result in HCO33¯̄ reabsorption reabsorption..

Bone CaBone Ca33(PO(PO44))2 2 + 4H+ 4H++3Ca3Ca2+ 2+ + 2H+ 2H22POPO44--

Results PaCOResults PaCO22, , HCOHCO33-- recovery BB recovery BB,SB,SB,AB,AB,BE(+),BE(+)

Page 41: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

In general, respiratory compensation results in a 1.2 mmHg reduction In general, respiratory compensation results in a 1.2 mmHg reduction in PCO2  for every 1.0 meq/L reduction in the plasma HCO3- in PCO2  for every 1.0 meq/L reduction in the plasma HCO3- concentration down to a minimum PCO2 of 10 to 15mmHgconcentration down to a minimum PCO2 of 10 to 15mmHg..     For example, if an acid load lowers the plasma HCO3- concentration to 9 For example, if an acid load lowers the plasma HCO3- concentration to 9 meq/L, then:meq/L, then:Degree of HCO3- reduction is  24 (optimal value) – 9 = 15.Degree of HCO3- reduction is  24 (optimal value) – 9 = 15.Therefore, PCO2 reduction should be  15 × 1.2 =  18.Therefore, PCO2 reduction should be  15 × 1.2 =  18.Then PCO2 measured should be 40 (optimal value) – 18 = 22mmHg.Then PCO2 measured should be 40 (optimal value) – 18 = 22mmHg.   Winter's FormulaWinter's FormulaTo estimate the expected PCO2 range based on respiratory compensation, To estimate the expected PCO2 range based on respiratory compensation, one can also use the Winter's Formula which predicts: one can also use the Winter's Formula which predicts: PCO2 = (1.5 × PCO2 = (1.5 × [HCO3-]) + 8 ± 2 [HCO3-]) + 8 ± 2 Therefore in the above example, the PCO2 according to Winter's should be Therefore in the above example, the PCO2 according to Winter's should be (1.5 × 9) + 8 ± 2 = 20-24 (1.5 × 9) + 8 ± 2 = 20-24

Another useful tool in estimating the PCO2 in metabolic acidosis is the Another useful tool in estimating the PCO2 in metabolic acidosis is the recognition that the recognition that the pCO2 is always approximately equal to the last 2 pCO2 is always approximately equal to the last 2 digits of the pH.digits of the pH.

Compensatory Responses: Metabolic AcidosisCompensatory Responses: Metabolic Acidosis

Page 42: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Compensation to alkalosisCompensation to alkalosis metabolic respiratorymetabolic respiratory

Feature Feature HCOHCO33-- ,, BBBB,SB,SB,AB,AB,BE(,BE( ++ )) HH22COCO3 3 ,, PaCOPaCO22 , , AB<SBAB<SB

Blood limited effectBlood limited effect on alkali on alkali HCOHCO33-- enterenter RBCRBC ;; COCO22 diffusediffuse in plasmain plasma

Buffering Buffering OHOH--+ H+ H22COCO33(HPr)(HPr)HCOHCO33--(Pr(Pr--)+ H)+ H22O HCOO HCO33

-- ++ HBuf HBuf H H22COCO33 ++ BufBuf --

Lung PHLung PH (( HH++ ) ) deceased breathingdeceased breathing

COCO22 exhalationexhalation PaCO PaCO22 no compensation no compensation

ICF HICF H++KK++ exchange, [Kexchange, [K++]] ,,

Buffering Buffering oxygen dissociation curveoxygen dissociation curve left shift, left shift, glucolysis glucolysis , , HH++ 。。

Kidney excrete the excess load of HCOKidney excrete the excess load of HCO33¯̄

Results Results HH22COCO33 ,, HCOHCO33-- recovery chronic recovery chronic :: BBBB 、、 SBSB 、 、

BE(-)BE(-)

Page 43: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

On average the pCO2 rises 0.7 mmHg for every On average the pCO2 rises 0.7 mmHg for every 1.0 meq/L increment in the plasma [HCO3-]. 1.0 meq/L increment in the plasma [HCO3-].

For example, if an alkali load raises the the plasma For example, if an alkali load raises the the plasma HCO3- concentration to 34 meq/L, then:HCO3- concentration to 34 meq/L, then:Degree of HCO3- elevation is  34 – 24 (optimal Degree of HCO3- elevation is  34 – 24 (optimal value)= 10.value)= 10.

Therefore, PCO2 elevation should be  0.7 × 10 =  7.Therefore, PCO2 elevation should be  0.7 × 10 =  7.Then PCO2 measured should be 40 (optimal value) Then PCO2 measured should be 40 (optimal value) +7 = 47mmHg.+7 = 47mmHg.

Compensatory Responses: Metabolic AlkalosisCompensatory Responses: Metabolic Alkalosis

Page 44: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Effects of Acid Base disordersEffects of Acid Base disorders

Page 45: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Effects of acidosisEffects of acidosisRespiratory Effects Hyperventilation ( Kussmaul respirations) Shift of oxyhaemoglobin dissociation curve to the right Decreases 2,3 DPG levels in red cells, which opposes the effect above. (shifts

the ODC back to the left) This effect occurs after 6 hours of acidemia.

Cardiovascular Effects Depression of myocardial contractility (this effect predominates at pH < 7.2 ) Sympathetic over-activity ( tachycardia, vasoconstriction, decreased arrhythmia

threshold) Resistance to the effects of catecholamines (occur when acidemia very severe) Peripheral arteriolar vasodilatation ■■ Venoconstriction of peripheral veins Vasoconstriction of pulmonary arteries ■■ Effects of hyperkalemia on heart

Central Nervous System Effects Cerebral vasodilation leads to an increase in cerebral blood flow and intracranial

pressure (occur in acute respiratory acidosis) Very high pCO2 levels will cause central depression

Other Effects Increased bone resorption (chronic metabolic acidosis only) Shift of K+ out of cells causing hyperkalemia (an effect seen particularly in

metabolic acidosis and only when caused by non organic acids) Increase in extracellular phosphate concentration

Page 46: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Increased rate and depth of breathing ("Kussmaul breathing")

Decreased heart rate (bradycardia)

Page 47: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Effects of alkalosisEffects of alkalosisRespiratory Effects Shift of oxyhaemoglobin dissociation curve to the left (impaired unloading of

oxygen The above effect is however balanced by an increase in 2,3 DPG levels in

RBCs. Inhibition of respiratory drive via the central & peripheral chemoreceptors

Cardiovascular Effects

Depression of myocardial contractility Arrhythmias

Central Nervous System Effects Cerebral vasoconstriction leads to a decrease in cerebral blood flow (result in

confusion, muoclonus, asterixis, loss of consciousness and seizures) Only seen in acute respiratory alkalosis. Effect last only about 6 hours.

Increased neuromuscular excitability ( resulting in paraesthesias such as circumoral tingling & numbness; carpopedal spasm) Seen particularly in acute respiratory alkalosis.

Other Effects

Causes shift of hydrogen ions into cells, leading to hypokalemia.

Note: Most of the above effects are short lasting.

Page 48: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

Mixed acid base disordersThe simple, or primary, acid-base disorders (respiratory and metabolic acidosis and alkalosis) evoke a compensatory response that produces a secondary acid-base disturbancesecondary acid-base disturbance and reversion of the blood pH towards (rarely to) normal; e.g., a simple metabolic acidosis will result in a secondary respiratory alkalosis, both of which will ordinarily be reflected in the patients’ acid-base-related analytes in blood. When two primary acid-base disturbances arise simultaneously in the same patient, the complex is called a mixed acid-base mixed acid-base disorderdisorder. If three primary disturbances occur together, the patient is described as having “triple acid-base disordertriple acid-base disorder.”

More than one acid base disturbance present. pH may be pH may be normal or abnormal.normal or abnormal.

Page 49: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.
Page 50: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

A 50 year old insulin dependent diabetic woman was A 50 year old insulin dependent diabetic woman was brought to the ED by ambulance. She was semi-comatose brought to the ED by ambulance. She was semi-comatose and had been ill for several days. Current medication was and had been ill for several days. Current medication was digoxin and a thiazide diuretic for CHF.digoxin and a thiazide diuretic for CHF.

Lab resultsLab results

Serum chemistry: Na 132, K 2.7, Cl 79, Glu 815,Serum chemistry: Na 132, K 2.7, Cl 79, Glu 815,

Lactate 0.9 urine ketones 3+ Lactate 0.9 urine ketones 3+

ABG: pH 7.41 PCOABG: pH 7.41 PCO22 32 HCO3 32 HCO3¯̄ 19 pO 19 pO22 82 82    

Case studyCase study

What is the acid base disorder? Why?What is the acid base disorder? Why?

Page 51: Acid-Base Disturbance Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine.

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