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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Department of Pathophysiology
Shanghai Jiao-Tong University School of Medicine
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
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.
Origin of acids
300~400L CO2(15mol H+)
50~100 mmol H+
Origin of bases
- 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.pH
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.
Release bone salt
In chronic metabolic acidosis
CO2 + H2O
CA ：carbonic anhydrase
The compensation effect of RBC
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.
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.
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
pH = - log [H+]
pH 7.35 - 7.45：
②Acidosis or alkalosis with complete compensation.
③A mixed acidosis and alkalosis, both events have opposite effects on pH, may also have a normal pH.pH
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”.
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.
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).SB, AB
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)
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: 122mmol/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)
——the concentration ofHCO3¯, controlled by non-respiratory factors.
SB (standard bicarbonate)
——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.)
From kidney：proximal/distal tubular acidosis
：ammonium chloride have been administered
：vomiting, gastric suction
K+ or Cl¯ deficiency
——Alkali administration：NaHCO3、sodium lactate .
Loss of H+
Loss of Cl
Loss of K+
Loss body fluid
Primary [H2CO3 ]
：failure of ventilation
：inhale CO2 at high concentration
Primary [H2CO3 ]
hypoxemia, anxiety, hysteria,
FeatureHCO3-，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
ICF H+ + KPrK++ HPr；
buffering H+ + K2HPO4K++ KH2PO4；
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
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.
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(-)
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.
Decreased heart rate (bradycardia)
Note: Most of the above effects are short lasting.
More than one acid base disturbance present. pH may be normal or abnormal.Mixed acid base disorders
What is the acid base disorder? Why?