Acid – Base Acid – Base balancebalance

By By Dr. Khaled Al nadiDr. Khaled Al nadiKHMC \ JORDANKHMC \ JORDAN

Objectives of this presentationObjectives of this presentation

• Introduction• Refresh the knowledge of the major buffer

system • Learn to operate the Henderson-Hasselback

equation• Viewing simple and mixed acid-base disorders• Interpretation of plasma parameters

characterizing acid-base disorders

IntroductionIntroduction

• Human physiology has evolved to maintain ECF.PH at a value of 7.40

• H+ is a proton ( hydrogen atom without its orbital electron )

AcidAcid: is a substance that acts as proton donor.: is a substance that acts as proton donor.

BaseBase: is a substance that accept protons in: is a substance that accept protons in

solution.eg.HCO3-, phosphate ion( HPO4-)solution.eg.HCO3-, phosphate ion( HPO4-)

ammonia(NH3-) and acetate(CH3COO-) ammonia(NH3-) and acetate(CH3COO-)

Acid↔Base + HAcid↔Base + H++

Who do we express [H+]Who do we express [H+]??

1. Direct as [H+] which give H+ concentration in mol/L or Eq/L

2. Indirect as PH: PH=Log10 1/[ H+]=-Log 10[H+]

***so PH + [H+] are inversely related ***

****The range of [H+] that is compatible with life is 20-126nEq/L which is equivalent to PH range of7.7-6.9

PH]H[=7.7020

7.6257.5327.4407.3507.2647.1807.01016.9128

Sources of HSources of H++

The greatest source of acid in the body is CO2,produced as an end products of metabolism

Forms of acid in the body: •Carbonic or volatile acid(H2CO3) •Non carbonic or non volatile

Pathways for acid removal • Kidneys •Lungs •GIT

How body maintained acid base How body maintained acid base balancebalance??

• Its maintained primarily through the control of 2 organs: Lungs+ kidneys

Henderson –Hasselbalch Henderson –Hasselbalch equationequation

• CO2↔CO2 +H2O↔H2CO3↔H+ + HCO3-

• Body use this equation to control PH

• At equilibrium there are approximately 500mmol of CO2 for every 1mmol of H2CO3.

• 4000mmol of H2CO3 for every 1mmol of H+.• Using H-H equation:

• PH=PK+log [H2CO3] \ [HCO3]…..• [H+] =24 X PCO2/ [HCO3]

•

Advantage of H-H equationAdvantage of H-H equation

• [H+] is determined by ratio of PCO2 & [HCO3-].

• It is a useful mean to verify the accuracy of the laboratory data by calculating one of the variable from the other two.

CO2CO2• Under basal conditions, the average adult

produce about 300L (13.5mol) of CO2 per/day through the metabolism of CHO+fat

• These excreted by the lungs at a rate of 200ml /min during resting condition.

Blood forms of CO2Blood forms of CO2

• CO2 is transported in the blood in 3 forms:

• 1. HCO3- = 90% of total CO2in plasma

• 2. Carbamino compounds (carbametes of • Hb + proteins)= 5% of total CO2

• 3. CO2 gas dissolved in plasma = 5% of total CO2

Total CO2Total CO2[total CO2]= [ HCO3 -] +( S.PCO2)

S : solubility constant for CO2 in plasma = 0.03mmol /L / mmHg

Dissolved CO2 = S.PCO2 = 0.03 xPCO2 at PCO2 = 40mmHg , dissolved CO2 = 1.2mmol / L

***total CO2 in clinical laboratory is a measure of [HCO3]

***total CO2 gives little information about functional status of the lungs

HCO3HCO3--• HCO3- is added to the blood by :• A. diet • B. metabolisim• C. diseases

• **HCO3 has no rule in buffering of H2CO3

Non carbonic acids (NCA)Non carbonic acids (NCA)

• Sources of NCA:• 1. diet (proteins, phospholipids)• 2. inter mediary metabolism (keto-acids , lactic

acid)• 3. stool through HCO3 loss• • *** excretion of NCA is through kidneys as the

body can not convert NCA to CO2

BODY BUFFER SYSTEMBODY BUFFER SYSTEM

• Buffer: is a solution consisting of a weak acid + its conjugate base

• * * * * *• Buffering is the primary mean by which large

changes in [H+] are minimized .• The most effective buffers are : H2CO3, H2PO4,

Plasma protein( Hb)

HCO3- BUFFER SYSTEMHCO3- BUFFER SYSTEM

• we use HCO3- buffer system to • determined acid base status depending on

the isohydric -principle which states • that all buffer pairs are in equilibrium with • the same [H+].

Acid base disturbancesAcid base disturbances• Acidosis: is due to either accumulation of acid or loss of base…

PH<7.36• Alkalosis: is due to either accumulation of base or loss acid …

PH>7.44• Respiratory: denote that the primary event is alveolar ventilation

dysfunction• Metabolic: denote that the primary event is abnormal gain or loss

of NCA. • Simple: consist of one primary event and its compensatory

response • Mixed: a combination of primary events are present • e.g.. :patient with respiratory acidosis from COPD with metabolic

acidosis from uncontrolled DM. or from large doses of steroids.

Disorders & Primary EventsDisorders & Primary Events

DisordersPrimary events

R. acidosis↑ PCO2

R. alkalosis↓PCO2

M. acidosis↑ NCA. Or ↓ HCO3

M. alkalosis↓ NCA. Or ↑ HCO3

Total CO2 in acid-base Total CO2 in acid-base disturbancesdisturbances

DisordersTotal CO2

R. acidosis↑

R. Alkalosis↓

M. Acidosis↓

M. alkalosis↑

Base excessBase excess (BE)(BE)

• It refers to the change in the concentration of buffer base (BB)

• [BB] = [ HCO3-]+[Protein-] +[ Hb / HbO2] = 48 mEq /L

• BE. Associated with abnormality in [HCO3] so it is influenced by metabolic process

• M. alkalosis associated with BE.> +5• M. acidosis associated with BE.< -5

Anion gapAnion gap

• AG = ( [Na+] + [K+]) – ( [HCO3-] + [Cl-])

• Normal AG =12 ± 4 m Eq\L

why?

Low of electro-neutrality

Low of electro-neutralityLow of electro-neutrality• In any solution, • positive charges = negative charges• In serum→ [cations]=[anions],

• If we measured all cations + anions • We measured every cations & only

fraction of anions

True if

but

Examples of unmeasured anionsExamples of unmeasured anions

• 1. Negative charged proteins• 2. In organic phosphate• 3. Sulfate• 4.Ions of organic acids: (…lactic-acids ,

keto-acids …)

RULERULE

AG↑↑↑ by all metabolic-acidosis except Hyper chloremic acidosis.

Why?

• If the acid in H-H equation is HCl : HCl + NaHCO3↔ NaCl +H2CO3 the net effect will replacement of

ECF. HCO3- by Cl-

so

Anionssame

why?

RULERULE

AG is not ↑in Resp. acidosis as acid is derived from H2CO3, not from NCA.

AG is not ↑in Resp. acidosis As the acid is derived

from H2CO3, not from NCA.

AG & HCO3AG & HCO3

In simple metabolic acidosis: AG = ∆HCO3

***By this can differentiate between simple and mixed disorders

Osmolar GapOsmolar Gap

• Refers to the disparity between the measured and the calculated serum osmolarity .

• =2[Na+] + (BUN/2,8) +(glucose/18)

It is good screen for toxins

as circulatory toxins ↑measured osmolarity but not the calculated

Compensation For Primary Acid - Base Compensation For Primary Acid - Base AbnormalitesAbnormalites

• **It is physiologic process occuring in response to events toward normalization of PH

• **Corrected or compensated means that PH is returned to normal

• **It is important to understand the degree of expected compensation for each disturbance as deviation from prediction will indicate a mixed disorder.

If patient has metabolic acidosis + normal PCO2

element of Resp. acidosis as 2nd primary event.

Basic mechanism for compensationBasic mechanism for compensation

1. Buffer of ECF. : represent the 1st mechanism.

2. Respiratory compensation: ∆ in PH ±Effect on respiratory center3. Carbomate ion released from bone ( predominant source of alkali

neutralizing NCA.)4. Renal compensation

Respiratory AcidosisRespiratory Acidosis

•It caused by •any process that reduce the effectivness of alveolar ventilation.

Compensation

AcuteRespiratory Acidosis

ChronicRespiratory Acidosis

Acute Respiratory AcidosisAcute Respiratory Acidosis

• ***In pure acute Resp. acidosis , [HCO3-] should not exceed > 30mEq/l***

PCO2 ↑ by 10mmHg → ↑ HCO3- by 1mEq/l

∆[H+] = 0.8 ∆ PCO2

Chronic Respiratory AcidosisChronic Respiratory Acidosis

PCO2 ↑ by 10mmHg → ↑ HCO3 by 3.5mEq/l

] ∆H = [+0.3 X ∆ PCO2

If ↑PCO2 persist Kidneys compensate by ↑ excretion of acid primarily NH4Cl + synthesis of HCO3

↑HCO3

↓ Cl-

Respiratory AlkalosisRespiratory Alkalosis

Caused by ↑ alveolar ventilation

↑CO2 excretion→ ↓PCO2

Acute Respiratory Alkalosis / Acute Respiratory Alkalosis / compensationcompensation

• *** Acute ↓pco2→ rapid ↓[HCO3-] within minutes / independent of any renal compensation (Buffer system)

↓PCO2 by10mmHg →↓HCO3- by 2mEq/l

∆[H+] = 0.8 X ∆PCO2

ChronicChronic Respiratory Alkalosis / Respiratory Alkalosis / compensationcompensation

↓PCO2 by10mmHg →↓HCO3- by 5mEq/l

*** ]H = [+0.17 X ∆PCO2∆

ChronicChronic Respiratory AlkalosisRespiratory Alkalosis

Most individual with PCO2 >20mmHg

Will have normal range of PH Even the cause is unknown

Most individual with PCO2 >20mmHg

Will have normal range of PH Even the cause is unknown

Metabolic AcidosisMetabolic Acidosis

** Produced by any process that ↓ [HCO3] either as HCO3- loss,

or via retention of NCA .That cannot be excreted by lungs

Metabolic Acidosis / CompensationMetabolic Acidosis / Compensation

↓[HCO3] by 1mEq/l →↓PCO2 by 1.0_1.3mmHg

Example: Patient with CRF.& [HCO3]=16

PCO2 compensation range →29.6_32mmHg

If PCO2 = 24→→coexistent Resp. Alkalosis

If PCO2 = 40 24→→coexistent Resp. Acidosis

Metabolic AcidosisMetabolic Acidosis / PCO2 & PH // PCO2 & PH /

*** During chronic steady state PCO2 ≈ last 2 digit of the PH

If PH = 7.25→PCO2≈ 25mmHg

***All these compensations are applicable only when acidosis being >

24hr***.

Primary respiratory events*** Rapid compensation (Buffers)

Primary metabolic eventsRespiratory compensation is late

<{ 24hr }due to slow penetration of H+ into CSF

Metabolic AlkalosisMetabolic Alkalosis

Produced by any process that ↑[HCO3] in plasma

It is clinically useful to be divided into 2 types: 1. Chloride responsive 2. Chloride resistant

****** depending on urinary [ Cl- ] ****

Metabolic Alkalosis/ CompensationMetabolic Alkalosis/ Compensation

Highly variable

↑ [HCO3-] by 1mEq/l → ↑PCO2 by 0.6_0.7mmHg

*** Any PCO2 exceeding 55mmHg → coexistence primary Resp. acidosis ***