acid base disorders for mbbs

8/12/2019 Acid Base Disorders for MBBS

1/42

Acid Base Disorders


2/42

Acid Base Disorders

Hydrogen ion (H+) homeostasis

Essential for life:e.g. mitochondrial function

charge & shape of proteins

ionisation of Ca++, Mg++

The concentration H+ ion is 35-45

nmol/L


3/42

Hydrogen ion units

H+ conc. as nanomoles per litre (nmol/L)

H+ as pH pH = 1/ log10H+ in mol/L

e.g. 100 nmol/L = 1/ log10100 x 10-9

pH = 1/log 10-7

pH = 7


4/42

In vivo production of

protons

The human body is a net-producer of

protons (non-carbonic acids)

Intracellular and extracellular proton

concentration still needs to be kept withinnarrow limits


5/42

Understanding Normal Acid-Base Handling

Metabolic processes in the body lead to the production of acid

The catabolism of glucose and fatty acids produces CO2and H2O,

effectively carbonic acid.

About 1 mmol/Kg body weight of H+is produced a day in the body.

Respiratory elimination of CO2and cellular buffers handle this acid load.

Renal excretion of acid must be maintained.


6/42

Daily H+turnover (mmol/24hrs)

Source of acid Production Amount Disposal

CO2 tissue respiration 20,000 lungs

Lactate glycolysis 1300 gluconeogenesis

& oxidation

FF/acids lipolysis 600 re-esterification& oxidation

Ketoacids ketogenesis 400 oxidation

Urea synthesis ureagenesis 1140 oxidation ofamino

acids

H2SO4 S-containing 40 renal excretion &

amino acid buffered acids


7/42

EXTERNAL

FLUID

BLOOD IN

CAPILLARIES

Sources of Daily acid load

CELL

METABOLISM

Volatile H+

CO2

Non-volatile H+

abnormal

metabolic acids

(lactic,

acetoacetic,

hydroxybutyric,

formic,glycolic)

DIET

Proteins,

acidic or alkali foods

Toxins

drugs


8/42

Acid- tends to donate a proton

Definitions, buffers, equations, pH, pKa

Base- tends to accept a proton

HAH++ A-

pH -log[H+]

B + H+ BH+


9/42

HAH++ A-

Taking minus logs:

Ka

[H+][A-]

[HA]

Rearrange: [H+]= Ka

[HA]

[A-]

-log [H+] = -log [Ka] - log[HA]

[A-

]pKa -log Ka

and pH = -log[H+]


10/42

-log[H+

] = -log[Ka] - log

[HA]

[A-]

pH = pKa + log

[A-]

[HA]

This is the Henderson-Hasselbalch Equation


11/42

Use of biological buffersNeeded for buffering of protons produced

by the production of CO2 from cells (15,000 mmol/24 h)

by catabolism of sulfuric amino acids (100 mmol/24 h)

by intermediary metabolism, e.g. lactic acid, acetoaceticacid, beta-hydroxybutyric acid


12/42

plasma H++ HCO3- H2CO3 pKa ~ 6.1

Common buffer systems in the body

urine H++ NH3 NH4 + pKa = 9.0

urine H++ HPO4--H2PO4

- pKa = 6.8

cell H++ protein- proteinH pKa = 7.0


13/42

Buffering

Buffering: Limitation of the change in H+in theface of a tendency to change

Base-

+ H+

Hbase

HBase + OH- H2O + Base-

HCO3-+ H

+ H2CO3

H2CO3 + OH- HCO-3 + H2O

Bicarbonate buf fer ing s ystem most important


14/42

The CO2- HCO3-buffer system

is important in the plasma

The pKa = 6.1

pH = 6.1 + log

[HCO3-]

[H2CO3]

Since H2CO3= pCO2x (0.03)

H+

+ HCO3- H2CO3 CO2+ H2O

pH = 6.1 + log[HCO3

-]

[.03 x pCO2]


15/42

Other buffers: haemoglobin

CO2

Cl- Cl-

CO2 + H2O H2CO3 H+ + HCO-3 HCO

-3

Hb-

HbH

CO2from tissue respiration

Carbonatedehydratase

erythrocyte


16/42

Other buffers: haemoglobin

CO2

Cl- Cl-

CO2 + H2O H2CO3 H+ + HCO-3 HCO

-3

Hb-

HbH

CO2loss inalveoli

Carbonatedehydratase

erythrocyte


17/42

Recovery of Filtered Bicarbonate in Kidneys

Recovery of Filtered Bicarbonate in Kidneys


18/42

Generation of Additional Bicarbonate in Kidneys


19/42

The Kidney

Reabsorbs 4500 mmol of HCO3 per day

Generates new HCO3 to replenish bufferstores

The Proximal tubule does most of the work

The Distal tubule eliminates H+ = to thenonvolatile acid production


20/42

Hydrogen ion excretion

Lungs: rapid and sensitive compensation bycontrolling CO2 excretion

Kidneys: (only method for direct H+excretion)

H+ excretion directly and as H2PO42-

Ammonium excretion (oxoglutarate goes

to liver; H+used for gluconeogenesis)

Liver: Lactate used for gluconeogenesisOxoglutarate from kidney used for

gluconeogenesis


21/42

Simple Acid-Base Disturbances

pH = pK + log10 [HCO3]

(0.030)(paCO2)

pH = 6. 1 + log ( metabolic component)

(respiratory component)

HCO3_ & CO2 = pH

CO2 & HCO3_

= pH


22/42

DISORDERS OF ACID BASE

STATUS

RESPIRATORYACIDOSIS pCO2

ALKALOSIS pCO2

METABOLICACIDOSIS BICARB.ALKALOSIS BICARB.


23/42

Metabolic acidosis


24/42

Anion GapA mathematical concept

(Na+ + K+ ) - ( Cl- + HCO3-) < 7-17 mmol/L

The gap consists of other ions, mainly Ca2+, Mg+, PO42-,

sulfate-, organic anions (e.g. lactate, acetoacetate)

The sum of anion and cation in plasma must be the same

(electroneutrality)

Overproduction of e.g. lactate will increase the anion gap,

indicating that the concomitant acidosis is of the metabolic type

as will decreased excretion of acid anions as in renal failure.

Therefore an increased anion gap is a useful marker of

metabolic acidosis


25/42

Evaluating a low serum

HCO3-

A low serum HCO3- can be due to:

Metabolic acidosis

High anion gap acidosis Hyperchloremic acidosis

Respiratory alkalosis


26/42

High anion gap: MUDPILES

Methanol

Uremia

Diabetic ketoacidosis

Paraldehyde

Isopropyl alcohol

Lactic acidosis

Ethylene glycol

Salicylates


27/42


28/42

Classification of Metabolic Acidosis


29/42

Compensatory Response

In simple metabolic acidosis the high [H+] stimulates

respiration resulting in a compensatory fall in the

PCO2 (secondary respiratory alkalosis) which

brings the [H+] back towards, but never to,

normal.

(1) Maximum compensation occurs in 12-24 hours

(2) For a given [HCO3] the final PCO2 level can be

calculated from:PCO2 = 1.5 x [HCO3] + 8 (+/- 2)

(3) The limit of compensation is a PCO2 of about 10

mmHg


30/42

Metabolic alkalosis

Loss of Hydrogen IonsVomiting

Ingestion of Alkali

Potassium Deficiency


31/42

Metabolic alkalosis


32/42

MetabolicAlkalosisSaline Responsive (ECV contraction, Urine [Cl] 20

mmol/L)

Mineralocorticoid excess

Primary hyperaldosteronism,

Cortisol & Mineralocorticoid excess

Cushing's syndrome

Metabolic Alkalosis: pathophysiology


33/42

Metabolic Alkalosis: pathophysiology

Pathophysiology:The development of a metabolic alkalosis

requires two simultaneous processes: bicarbonate generation, &plasma bicarbonate maintenance

(1) Generation of bicarbonate:

Loss of H+:Gut, Renal, Exogenous HCO3

The normal kidney responds to a high plasma [HCO3] by

increasing urinary excretion of the ion. This is a very efficient

process and for the development of a metabolic alkalosis a

second mechanism to maintain the high plasma [HCO3] is

required: the maintenance mechanism.


34/42

Metabolic Alkalosis:

pathophysiology (Cont'd)

Maintenance of high plasma bicarbonate:

This is carried out by the kidney (renal bicarbonate retention)

and occurs in the following situations:

Volume depletion

Potassium depletion

Hypercapnia

Thus when evaluating the subject with metabolic alkalosis

attention should be given to the possible causes of generation

and of maintenance.

From a management point of view metabolic alkalosis can be

classified as either saline responsive or saline unresponsive


35/42

Metabolic Alkalosis: pathophysiology(Cont d)Response to IV saline therapy

The response of the subject with metabolic alkalosis to a saline

(NaCl) infusion provides a further classification of the disorder.

Saline responsive metabolic alkalosis

If the patient is hypovolaemia (dehydrated) a saline infusion willresolve the disorder, ie remove the maintenance process and

allow bicarbonate to be excreted by the kidney; hence "saline

responsive"

Saline unresponsive metabolic alkalosisIf the patient is euvolaemic, eg the metabolic alkalosis of

mineralocorticvoid excess, a saline infusion will not alleviate the

condition: hence "saline unresponsive".


36/42

Compensation

The compensatory process is decreased respiratory

exchange and high pCO2

Response reaches its maximum in 12-24 hpCO2~ 60 mmHg.

For each 1mmol/L rise of HCO3-, pCO2should increase

by 0.7 mmHg

Expected pCO2mm Hg: 0.9 X (HCO3-) + 9


37/42


38/42

Respiratory disorders


39/42

Compensation by increase


40/42

Compensation by increase

in HCO3

In the acute phase there is a rise of 2-4 mmol/L of HCO3Will result in plasma level 28-30mmol/L

In the chronic phase there is a slow, consistent increase

in the HCO3 due to renal generation

reaches maximum in 2-4 days

The maximum level is 45 mmol/L(HCO3) mmol/L = 0.44 X pCO2+7.6


41/42


42/42

Compensatory response

Secondary metabolic acidosis

HCO3level will decrease

Acute: HCO3will decrease upto 18mmol/L

Chronic:HCO3 will decrease upto 12 mmol/L

Resp.alkalosis; Can be completely compensated.

pH will be normal

acid base disorders for mbbs

Documents