Acid base disorders stmu

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Acid Base Change Acid base Disorders

MUHAMMAD SHOAIBM.Phil. Biochemistry

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Contents

BasicsNormal PhysiologyAbnormalitiesRespiratory Acid Base DisordersMetabolic Acid Base DisordersCase study

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ACID AND BASE Acid

Any compound which forms H ions in solution ⁺(proton donors)eg: Carbonic acid releases H ions⁺

BaseAny compound which combines with H ions in ⁺

solution (proton acceptors)eg: Bicarbonate(HCO3 ) accepts H+ ions⁻

Acids and bases can be Strong or Weak

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ACID–BASE BALANCE Normal pH : 7.35-7.45

Homeostasis of pH is tightly controlled

Extracellular fluid = 7.4

Blood = 7.35 – 7.45

< 6.8 or > 8.0 death occurs

If any of these changes causes the pH to change to a value

outside the normal range, the suffix emia is used to describe

the acid-base derangement:

Acidosis (acidemia) below 7.35

Alkalosis (alkalemia) above 7.45

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3 SYSTEMS THAT MAINTENANCE PH

• Moves or release hydrogen ions

1. Buffers

• Regulate carbonic acid by eliminating or retaining CO2

2. Respiratory system

• Long term regulation of acid-base in body by regulating bicarbonate ions.

3. Renal system

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1. BUFFER SYSTEMS Chemical buffers are available in extracellular/

intracellular compartments• Phosphate• Protiens• bicarbonate

Helps to maintain a stable pH , Removes or release H+ ions• Excess acid (acidosis) pH <7.35, buffers bind with H+

ions• Too alkaline (alkalosis) pH >7.45, buffers release H+

ions

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Bicarbonate system constituted of plasma sodium bicarbonate (NaHCO3) and carbonic acid (H2CO3) and cellular H2CO3 and potassium bicarbonate (KHCO3)

extracellular space

The phosphate system found in renal tubular fluid and intracellularly

Proteins

intracellular space

Mostl powerfull in

Most dominating in

Three buffering systems

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2. RESPIRATORY SYSTEM

Normal PaCO2 = 35- 45 mmHg

Pulmonary buffering system is as effective as the chemical buffering system . The lungs respond to deviations in pH by altering the rate and depth of ventilation. Eliminates or retains carbon dioxide

↑ carbon dioxide (acid) stimulate respiration

↑rate & depth of resp ↓ pH to normal range

Alkalosis depresses respiration

↓ rate & depth of resp retains carbon dioxide

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The kidneys are the third line of defence against wide

changes in body fluid pH

• movement of bicarbonate

• Retention/Excretion of acids

• Generating additional buffers

Long term regulator of ACID – BASE balance

May take hours to days for correction

3. Renal System

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Role of kidneys is preservation of body’s bicarbonate stores

• by controlling serum bicarbonate concentration through the regulation of H+ excretion

• bicarbonate reabsorption

• production of new bicarbonate

Proximal tubule: 70-90%

Loop of Henle: 10-20%

Distal tubule and collecting ducts: 4-7%

RENAL REABSORPTION OF BICARBONATE

i. MAINTAIN BICARBONATE

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Regeneration of titrated bicarbonate

by excretion of:

• Titratable acidity (mainly phosphate)

• Ammonium salts

ii. Regeneration Of Bicorbonate

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• TITRATABLE ACIDITY Occurs when secreted H+

encounter & titrate phosphate in tubular fluid

Refers to amount of strong base needed to titrate urine back to pH 7.4

40% (15-30 mEq) of daily fixed acid load

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• AMMONIUM EXCRETION Occurs when secreted H+

combine with NH3 and are trapped as NH4

+ salts in tubular fluid

60% (25-50 mEq) of daily fixed acid load

Very adaptable (via glutaminaseinduction)When blood acidity is significantly increased, glutamine metabolized into ammonia.

Ammonia recipient of H+.

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Normal bicarbonate 22-26 mEq/L Acidosis• Excess H+ ions • pH falls • kidneys excrete H+ and retain bicarbonate

Alkalosis• Less H+ ions• pH increases• Kidneys retains H+ ions & excrete bicarbonate

Interactions Among The Carbonic Acid–bicarbonate Buffer System And Compensatory Mechanisms In The Regulation Of Plasma pH

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Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH

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HENDERSON-HASSELBACH EQUATION

pH = pKa + log([HCO3-]/.03xpCO2)

Shows that pH is a function of the ratio between bicarbonate and pCO2

PCO₂ - ventilatory parameter (40 +/- 4) HCO₃ - metabolic parameter (22-26 mmol/L)⁻

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2

24HCO

PaCOH

Kassirer-Bleich equation

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ACID–BASE MONITORING Acid–base status can be monitored

intermittently or continuously. Arterial blood gas (ABG) analysis remains

the gold standard in assessing for acid–base disorders.

In the ICU, ABGs can be obtained by arterial puncture or through an indwelling arterial catheter

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GETTING AN ARTERIAL BLOOD GAS SAMPLE

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SAMPLE ANALYSIS The blood gas machines in most labs actually

measure the pH ,the pCO2 and the pO2. bicarbonate level -------- from a serum

sample.

The [HCO3-] and the base difference are calculated values using the Henderson-Hasselbalch equation.

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INTERPRETATION OF BLOOD GASMEASUREMENTS It is an easy mathematical exercises

immediately and rapidly get a insight into the underlying process causing the disturbance in acid–base status.

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Acidosis “is a disorder that predisposes/lead to low systemic pH. Utilizing the Henderson–Hasselbalch equation, this can be caused by a fall in systemic bicarbonate concentration or by an elevation in the pCO2 .

Alkalosis is a disorder that predisposes/lead to high systemic pH. This is usually caused either by an increase in systemic bicarbonate concentration or by a fall in the pCO2.

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FOUR BASIC TYPES OF IMBALANCE

Metabolic Acidosis

Metabolic Alkalosis

Respiratory Acidosis

Respiratory Alkalosis

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A change in either the PCO2 or the HCO3 will cause a change in the pH of extracellular fluid.

When the change involves the PCO2, the condition is called a respiratory acid-base disorder: an increase in PCO2 is a respiratory acidosis, and a decrease in PCO2 is a respiratory alkalosis.

When the change involves the HCO3, the condition is called a metabolic acid-base disorder: a decrease in HCO3 is a metabolic acidosis, and an increase in HCO3 is a metabolic alkalosis.

Acid Base Disorders

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ACID BASE DISORDERS

Disorder pH [H+] Primary disturbance

Secondary response

Metabolic acidosis

[HCO3-] pCO2

Metabolic alkalosis

[HCO3-] pCO2

Respiratory acidosis

pCO2 [HCO3-]

Respiratory alkalosis

pCO2 [HCO3-]

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ACIDOSIS Principal effect of acidosis is depression of the CNS

through ↓ in synaptic transmission. Generalized weakness Deranged CNS function the greatest threat Severe acidosis causes

Disorientationcoma death

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ALKALOSIS Alkalosis causes over excitability of the

central and peripheral nervous systems. Numbness Lightheadedness It can cause :

Nervousness muscle spasms or tetany Convulsions Loss of consciousness Death

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OUTLINE OF ACID-BASE INTERPRETATION RULESStep 1 : Determine if data is consistent using Henderson’s

Equation

Step 2 : Check pH & PaCO2 (If either of them is normal, or

both are normal, got to step 6 to diagnose

mixed acid-base disorder)

Step 3 : Determine Primary acid base

disorder

Step 4 : Check for compensation

Step 5 : Check Anion Gap/hypoalbuminemi

a or delta/delta

Step6 : Mix Acid Base disorders

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RESPIRATORY ACIDOSIS

RESPIRATORY ACIDOSIS Carbonic acid excess caused by blood

levels of CO2 above 45 mm Hg. Hypercapnia – high levels of CO2 in blood Chronic conditions:

Depression of respiratory center in brain that controls breathing rate – drugs or head trauma

Paralysis of respiratory or chest muscles Emphysema

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RESPIRATORY ACIDOSIS Acute conditions:

Adult Respiratory Distress Syndrome Pulmonary edema Pneumothorax

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COMPENSATION FOR RESPIRATORY ACIDOSIS

Kidneys eliminate hydrogen ion and retain bicarbonate ion

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ACID–BASE BALANCE DISTURBANCES

Respiratory acidosis. 35

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RESPIRATORY ALKALOSIS

RESPIRATORY ALKALOSIS Carbonic acid deficit pCO2 less than 35 mm Hg (hypocapnea) Most common acid-base imbalance Primary cause is hyperventilation

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RESPIRATORY ALKALOSIS Conditions that stimulate respiratory center:

Oxygen deficiency at high altitudes Pulmonary disease and Congestive heart failure –

caused by hypoxia Acute anxiety Fever, anemia Early salicylate intoxication Cirrhosis Gram-negative sepsis

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COMPENSATION OF RESPIRATORY ALKALOSIS

Kidneys conserve hydrogen ion Excrete bicarbonate ion

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Respiratory Alkalosis. 40

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METABOLIC ACIDOSIS

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METABOLIC ACIDOSIS Bicarbonate deficit - blood concentrations of bicarb

drop below 22mEq/L Causes:

Loss of bicarbonate through diarrhea or renal dysfunction

Accumulation of acids (lactic acid or ketones) Failure of kidneys to excrete H+

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COMPENSATION FOR METABOLIC ACIDOSIS Increased ventilation Renal excretion of hydrogen ions if possible K+ exchanges with excess H+ in ECF ( H+ into cells, K+ out of cells)

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Responses to Metabolic Acidosis

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METABOLIC ALKALOSIS

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METABOLIC ALKALOSIS Bicarbonate excess - concentration in

blood is greater than 26 mEq/L Causes:

Excess vomiting = loss of stomach acid Excessive use of alkaline drugs Certain diuretics Endocrine disorders Heavy ingestion of antacids Severe dehydration

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COMPENSATION FOR METABOLIC ALKALOSIS

Alkalosis most commonly occurs with renal dysfunction, so can’t count on kidneys

Respiratory compensation difficult – hypoventilation limited by hypoxia

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Metabolic Alkalosis

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ANION GAP This step identifies the type of metabolic acidosis

present, i.e., whether it is secondary to an anion that creates an AG on electrolyte measurement or not.

The AG is a diagnostic tool to uncover the actual anions elevated in the blood but not routinely included in our measurements under normal conditions.

It is calculated as follows:AG = serum sodium − serum chloride − serum bicarbonate. A normal anion gap is <12 mmol L−1.

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HYPOALBUMINEMIA In this step interpreting metabolic acidosis is

adjusting for factors that would falsely lower the anion gap if one existed, e.g., hypoalbuminemia and lithiumor bromide ingestion

Adjusted AG in hypoalbuminemia = observed AG + [2.5(normal albumin − observed albumin)].

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DELTA/DELTA This step is the comparison of the degree of

change in AG with the change in serum bicarbonate, aiming to assess the extent of contribution of the AG-producing process to the actual acidosis. This measurement is called delta/delta:

delta/delta= ΔAG/ ΔHCO- =(AG -12) / (24 - HCO3-).

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MNEMONIC VERSION OF EXPECTED COMPENSATORY RESPONSES TO ACID–BASE DISTURBANCES

Assuming a normal ABG of pH 7.4, pCO2 40, HCO3− 24, and utilizing meq L−1 or mmol L−1 for bicarbonate and mmHg for pCO2,

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MIXED ACID BASE DISORDER

If the Arterial pH is relatively normal and the PCO2 and/or HCO3 are abnormal, one can assume that a mixed abnormality is present.

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MIXED ACID BASE DISORDER Diagnosed by combination of clinical assessment, application of

expected compensatory responses , assessment of the anion gap, and application of principles of physiology.

Respiratory acidosis and alkalosis never coexist

Metabolic disorders can coexist

Eg: lactic acidosis/DKA with vomiting

Metabolic and respiratory AB disorders can coexist

Eg: salicylate poisoning (met.acidosis + resp.alkalosis)

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1-CASE STUDY 11 year old girl Mild bronchial asthma with fever and increased

breathing Asthmaticus diagnosed ABGs Ph 7.22 p CO2 38mmHg serum bicarbonate

15med L-1 Serum albumin level 1gdL-1 What is your interpretation …………….? Hypoalbuminemia ( primary metabolic acidosis

and acute respiratory acidosis )

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2-CASE STUDY 2 year old child was foun unconscious increased

breathing ABGs pH 7.38

pCO2 28mmHg serum bicarbonate 16 meqL-1

What is your interpretation……………? Salicylate poisoning

Acid base disorders stmu

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