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Acid-Base DisturbanceAcid-Base Disturbance
Department of PathophysiologyDepartment of Pathophysiology
Shanghai Jiao-Tong University School of MedicineShanghai Jiao-Tong University School of Medicine
main topicsmain topics
Acid Base PhysiologyAcid Base Physiology
Acid Base disturbancesAcid Base disturbances
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
The concept of Acid Base balanceThe concept of Acid Base balance
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
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.
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
Acid Base balance & regulationAcid Base balance & regulation
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.
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.
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
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 。
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 ]]
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 )
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
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
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.
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
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.
Acid base disturbanceAcid base disturbance
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.
或
Definition of acid-base disordersDefinition of acid-base disorders
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
Acid Base parameterAcid Base parameter/Arterial Blood Gases (ABGs)/Arterial Blood Gases (ABGs)
AArterial rterial BBlood lood GGas Samplingas Sampling
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.
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”.
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).
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.
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.
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
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)
Pathogenesis of Acid Base Pathogenesis of Acid Base disordersdisorders
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
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]
Severe vomiting
Loss of HLoss of H++
Loss of ClLoss of Cl
Loss of KLoss of K++
Loss body fluidLoss body fluid Ald Ald
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 ]
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(+)
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
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(-)
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
Effects of Acid Base disordersEffects of Acid Base disorders
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
Increased rate and depth of breathing ("Kussmaul breathing")
Decreased heart rate (bradycardia)
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.
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.
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?