Acid base disturbance
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Acid-Base Disturbance. Department of Pathophysiology Shanghai Jiao-Tong University School of Medicine. Acid Base Physiology Acid Base disturbances. main topics. Concept of Acid Base disturbance Acid Base parameter/Arterial Blood Gases (ABGs) Clinical Acid Base disorders

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Acid-Base Disturbance

Department of Pathophysiology

Shanghai Jiao-Tong University School of Medicine

Acid Base Physiology

Acid Base disturbances

main topics

Concept of Acid Base disturbance

Acid Base parameter/Arterial Blood Gases (ABGs)

Clinical Acid Base disorders

Pathogenesis of Acid Base disorders

Influence of Acid Base disorders

Mixed Acid/Base disorders

Acid Base disturbances

The concept of Acid Base balance

Acid-base balance refers to the mechanisms the body uses to keep its fluids close to neutral pH (that is, neither basic nor acidic) so that the body can function normally.

Arterial blood pH is normally closely regulated to between 7.35 and 7.45.

Acid Base balance



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

Strong acid:HCl, H2SO4, H3PO4.

Weak acid:H2CO3, CH3COOH.

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

Strong alkali:NaOH, KOH.

Weak alkali:NaHCO3, NH3, CH3COONa.

Lactic acid

Ketone bodies

Sulfuric acid

Phosphoric acid

Origin of acids

Much more

  • Intracellular metabolism

Volatile acids


300~400L CO2(15mol H+)

50~100 mmol H+

Fixed acids

Origin of bases


  • NH3, sodium citrate, sodium lactate

Acid Base balance & regulation

- pH of ECF is between 7.35 and 7.45. Deviations, outside this range affect membrane function, alter protein function, etc.

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

Acidosis- below 7.35

Alkalosis- above 7.45

CNS function deteriorates, coma, cardiac

irregularities, heart failure, peripheral

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











H+ excretion

bicarbonate reabsorption

Release bone salt






In chronic metabolic acidosis

H2CO3 CO2

Acid excretion






Very slow


Plasma NaHCO3/ H2CO3 NaPr/HPr* Na2HPO4/NaH2PO4

intercellularNaHCO3/ H2CO3 Na2HPO4/NaH2PO4



organic acids



* HPr:protein; ** muscle cells。

Buffering system

H+ + A


[ H+ ]  [ A ]

Ka =

[ HA ]

[ HA ]

[ H+ ] =

Ka 

[ A ]

[ A ]

pKa +

pH =


[ HA ]


pH  pKa + log(HCO3-/ H2CO3)

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)

Henderson-Hasselbalch equation:

Primary changing


CO2 + H2O









C l

C l

Hb buffering

Cl¯ transfer

CA :carbonic anhydrase

The compensation effect of RBC



  • Na+-H+ exchange of proximal tubule.

  • H+ secretion in collecting tubule is mediated by H+ ATPase pump in luminal membrane and a Cl-HCO3- exchanger in basolateral membrane. The H+ ATPase pump is influenced by aldosterone, which stimulates increased H+ secretion.

  • Hydrogen ion secretion in the collecting tubule is the process primarily responsible for acidification of the urine, particularly during states of acidosis. The urine pH may fall as low as 4.0.

  • Excretion of titratable acids is dependent on the quantity of phosphate 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 by acid base balance and cannot be easily increased to excrete the daily acid load.


NH4+ excretion

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

●The process of ammoniagenesis occurs within proximal tubular cells.

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

uBuffers only provide a temporary solution.

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

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


Acid base disturbance

An acid base disorder is a change in the normal 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 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¯]).

Simple Acid-Base Disorders

Clinical disturbances of acid base metabolism classically are defined in terms of the HCO3¯  /CO2 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 parameter/Arterial Blood Gases (ABGs)

Arterial Blood Gas Sampling

pH is a measurement of the acidity of the blood, reflecting the number of hydrogen ions present.

pH = - log [H+]



pH 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.


PaCO2(Partial Pressure of Carbon Dioxide)

The amount of carbon dioxide dissolved in arterial blood.

Normal: 4.39 ~ 6.25kPa(33 ~ 46 mmHg)

Average: 5.32 kPa(40 mmHg)

Respiratory acidosis: > 46 mmHg (> 6 .25kPa)

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”.

These 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.



Normal: 22~27mmol/L

Metabolic acidosis: <22 mmol/L

Metabolic 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).


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/L

Metabolic acidosis: < -3 mmol/L

Metabolic 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.

BE (base excess)

Difference between undetermined anions and undetermined cations.

Anion gap = Na+ - [Cl¯ + 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: 12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.

AG (anion gap)

pH—Determine Acidosis versus alkalosis

Determine Metabolic

——the concentration ofHCO3¯, controlled by non-respiratory factors.

SB (standard bicarbonate)

BE(base excess)

Determine Respiratory

——the concentration of CO2。


HCO3¯—influenced by Metabolic and Respiratory factors。

AG —■ Helpful in Metabolic Acidosis

■Helpful in mixed acid-base disorders

  • Once the acid-base disorder is identified as respiratory or metabolic, we must look for the degree of compensation that may or may not be occurring. This compensation may be 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 toward the normal range.)

  • In pure respiratory acidosis (high PaCO2, normal [HCO3¯], and low pH) we would expect an eventual compensatory increase in plasma [HCO3¯] that would work to restore the pH to normal. Similarly, we expect respiratory alkalosis to elicit an eventual compensatory decrease in plasma [HCO3¯].

  • A pure metabolic acidosis (low [HCO3¯], normal PaCO2, and a low pH) should elicit a compensatory decrease in PaCO2, and a pure metabolic alkalosis (high [HCO3¯], normal PaCO2, and high pH) should cause a compensatory increase in PaCO2.

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

Pathogenesis of Acid Base disorders

Metabolic acidosis

Primary [HCO3]

Lactic acidosis




Increased AG


Fixed acids


Salicylic acidosis


:renal failure

Source 

—— impossible

From GI:diarrhea


Normal AG

Loss 

From kidney:proximal/distal tubular acidosis

Consume 

:ammonium chloride have been administered

Metabolic alkalosis

Primary [HCO3]


Source 

Fixed acids

From GI

:vomiting, gastric suction

K+ or Cl¯ deficiency

Loss 


Cushing’s syndrome

From kidney

Diuretic therapy

Source 

——Alkali administration:NaHCO3、sodium lactate .


Exclusion 


Severe vomiting

Loss of H+

Loss of Cl

Loss of K+

Loss body fluid

Ald 

Respiratory acidosis

Primary [H2CO3 ]



:failure of ventilation

Volatile acid

Exhalation 


:inhale CO2 at high concentration

Respiratory alkalosis

Primary [H2CO3 ] 


Generation 

Volatile acid

Exhalation 

hypoxemia, anxiety, hysteria,

Salicylate intoxication

CNS diseases

metabolic respiratory

FeatureHCO3-,BB,SB,AB,BE(-)H2CO3 ,PaCO2 AB>SB

Blood HA + HCO3-A-+ H2CO3 plasma protein, RBC Hb

buffering (No compensation to acute

CO2 + H2O repiratory acidosis)

Lung increased breathing no compensation

(Kussmaul Respiration)

ICF H+ + KPrK++ HPr;

buffering H+ + K2HPO4K++ KH2PO4;

[K+ ]e

Kidney unless the acidosis is due to renal dysfunction,

the kidneys respond by increasing hydrogen ion secretion and

ammoniaproduction, this result in HCO3¯ reabsorption.

Bone Ca3(PO4)2 + 4H+3Ca2+ + 2H2PO4-

Results PaCO2, HCO3- recovery BB,SB,AB,BE(+)

Compensation to acidosis

Compensatory Responses: Metabolic Acidosis

In general, respiratory compensation results in a 1.2 mmHg reduction in PCO2  for every 1.0 meq/L reduction in the plasma HCO3- concentration down to a minimum PCO2 of 10 to 15mmHg.

For example, if an acid load lowers the plasma HCO3- concentration to 9 meq/L, then:Degree of HCO3- reduction is  24 (optimal value) – 9 = 15.Therefore, PCO2 reduction should be  15 × 1.2 =  18.Then PCO2 measured should be 40 (optimal value) – 18 = 22mmHg.

Winter's FormulaTo estimate the expected PCO2 range based on respiratory compensation, one can also use the Winter's Formula which predicts: PCO2 = (1.5 × [HCO3-]) + 8 ± 2

Therefore in the above example, the PCO2 according to Winter's should be (1.5 × 9) + 8 ± 2 = 20-24

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

Compensation to alkalosis

metabolic respiratory

Feature HCO3-,BB,SB,AB,BE(+)H2CO3 ,PaCO2, AB<SB

Blood limited effecton alkali HCO3-enterRBC;CO2diffusein plasma

Buffering OH-+ H2CO3(HPr)HCO3-(Pr-)+ H2O HCO3-+HBuf  H2CO3+Buf-

Lung PH(H+) deceased breathing

CO2exhalation PaCO2 no compensation

ICF H+K+exchange, [K+],

Buffering oxygen dissociation curveleft shift, glucolysis , H+。

Kidney excrete the excess load of HCO3¯

Results H2CO3,HCO3- recovery chronic:BB、SB、 BE(-)

Compensatory Responses: Metabolic Alkalosis

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

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

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

Effects of Acid Base disorders

Effects of acidosis

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

Decreased heart rate (bradycardia)

Effects of alkalosis

Note: Most of the above effects are short lasting.

The simple, or primary, acid-base disorders (respiratory and metabolic acidosis and alkalosis) evoke a compensatory response that produces a secondary 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 disorder. If three primary disturbances occur together, the patient is described as having “triple acid-base disorder.”

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

Mixed acid base disorders

Case study

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

  • Lab results

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

  • Lactate 0.9 urine ketones 3+

  • ABG: pH 7.41 PCO2 32 HCO3¯ 19 pO2 82

 What is the acid base disorder? Why?

Thank You

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