Acid-Base Balance

Aims and Objectives

AIM To give an understanding of arterial blood gases to students and new starters. Objectives To give a basic understanding of normal blood gases parameter To Recognize abnormalities and differences between a metabolic & respiratory problems Indications It is essential in evaluation of critical ill in ICU, CCU & HDU patients, giving an idea about his acid base balance and oxygenation .

The Balance is Beauty

Misbalanced ?

Acid & Base

Definition
An acid is a proton donor and a base is a proton acceptor. Physiologically, there are two groups of important acids:

Carbonic acid (H2CO3) Non carbonic acid

Sources of Hydrogen Ions

Volatile Acids (carbonic acids) Dietary CHO & Fats Oxidation 15,000 mmol/day as CO2 Removed by lungs No significant change in ABG (if ventilatory functions are normal)

Non-volatile Acids or (Fixed Acids) (Non carbonic acid) metabolism of sulphate & phosphate
containing amino acids from diet. 50-100 mEq Nonvolatile acids mainly excreted by the kidneys

Acid-Base Balance

Normal pH of body fluids Arterial blood is 7.4 Venous blood and interstitial fluid is 7.35

pH limit of 6.8 or 7.8 are incompatible with life.

Alkalosis or alkalemia arterial blood pH rises above 7.45 Acidosis or acidemia arterial pH drops below 7.35

Maintenance of Balance
Balance maintained by: Buffering systems
Lungs Kidneys

Buffer Systems

Prevent major changes in pH Act as sponges 3 main systems Bicarbonate-carbonic acid buffer Phosphate buffer Protein buffer
Bicarbonate buffer - most important

H+ H+

H+

Active in ECF and ICF

Phosphate buffer Active in intracellular (ICF) fluid, (HPO42 ), (H2PO4)

Protein buffer - Largest buffer store

Albumins and globulins (ECF) Hemoglobin (ICF)

Any drifts in pH are resisted by the entire chemical buffering systems.

Time course of distribution, buffering, respiratory compensation and renal excretion of an acid load
H+ Load
Cell buffering Respiratory compensation

100

Renal H+ secretion

50

12 Hours

24

72

Henderson-Hasselbalch Equation
pH = pK+ log({HCO3-}/{PCO2 x 0.03})
Blood pH = 6.10 + log (24/40 x 0.03) = 6.10 + log (20) = 7.40 Hence pH is an anti log of H+ion concentration Modified HHE [H+] = 24 x PCO2/[HCO3-] H = 24 x (40/24) = 40 nEq/L

To diagnose an acid-base imbalance, ask 3 questions: Does the pH indicate acidosis or alkalosis? Is the cause of the pH imbalance respiratory or metabolic? Is there compensation for the acidbase imbalance? ACID-BASE Parameters

CO2

< 7.40
> 40 < 24

7.40
40 mmHg 24 mmol/L

> 7.40
< 40 > 24

HCO3- + H+

HCO3-

H+

Patient evaluation The presence of an acid-base disturbance may be suspected on the basis of clinical presentation or by results of laboratory data (e.g., a low HCO3-). Evaluation of any acid-base disorder can then be approached in a stepwise manner.

ACID-BASE Parameters

< 7.40 > 40 < 24

7.40

> 7.40

40 mmHg < 40 24 mmol/L > 24

Acid Base Disorder

Primary change

Compensatory change

Respiratory acidosis

PaCo2

HCo3

Respiratory alkalosis

PaCo2
HCo3

HCo3

Metabolic acidosis

PaCo2
PCo2

Metabolic alkalosis

HCo3

Metabolic Acidosis
Can be seen when: 1. Increased Hydrogen ion production 2. Impaired excretion of H+ (dRTA)

3. Bicarb. loss from GIT fistulae

4. Renal HCO3- loss (type II RTA)

Anion Gap (AG) = (Na+ + K+) (Cl- + HCO3-) Normal AG = 12 2

Causes of high Anion gap Acidosis

Causes of non-anion gap acidosis

Lactic acidosis (type A & type B) Ketoacidosis (diabetic, alcoholic & starvation) Toxins/drugs Methanol, Ethylene glycol salicylates Renal failure

(HCMA) Distal Renal tubular Acidosis Proximal renal tubular acidosis Pancreatic fistula Ingestion of NH4Cl/HCl Ureteral diversions Type IV RTA Hypoaldosteronism (primary)

` Clinical Effects of Metabolic Acidosis

Compensated Hyperventilation Kussmaul Breathing Neuromuscular Irritability Possibility of Hyperkalemia Cardiac Arrhythmias Risk of Arrest

Example of normal physiological acid-base dynamics

Exercise induces dramatic changes in body chemistry: O2 used up, CO2 produced, H+ produced, lactic acid produced, pH lowered. Why doesnt this cause a severe problem?

CO2

Compensatory Response

Compensatory Response
pco2 = 1.5 x HCO3- + 8 2 (Winters formula) ( pco2 not <10 mmHg )
60-year-old diabetic lady with a long history of not taking her insulin. She is admitted to the hospital and you receive the following data on her: pH 7.26, PaCO2 32, HCO3- 14

What is the defect? Compensated ?

Acid-Base Imbalances
Normal
1.2 mEq/L 1 7.4 24 mEq/L 20

H2CO3 HCO3

Metabolic Alkalosis

7.58

30

Metabolic Alkalosis

Compensation: Problem = too much base Response: Lungs compensate by hypoventilation Retain CO2, increase PaCO2

Metabolic alkalosis

pH, HCO3 , pCO2 Common Causes

Vomiting Antacid abuses Diuretics Chronic diarrhea Primary Hyperaldosteronism Cushing synd. Renal Artery stenosis

Clinical Effects of Metabolic Alkalosis

Hypoventilation Tetany Ca2+ binds Albumin as pH

Compensatory Response: pco2 = 0.5 x [HCO3]

pH 7.48, PaCO2 45, HCO3- 34

60 years old lady taking diuretics for her overweight problem for many weeks, developed bilateral pneumonia, and was dehydrated. She was admitted in the hospital and her ABG showed: pH 7.45, PaCO2 60, HCO3- 34 for compensatory response pco2 = 0.5 x HCO3 so this is metabolic alkalosis and uncompensated respiratory acidosis ( mixed disorder)

Respiratory Acidosis

1 7.21

13

Respiratory Acidosis

Carbonic acid excess Cause = Hypoventilation Exhaling of CO2 inhibited Carbonic acid builds up pH falls below 7.40

Compensatory Response - Kidney retains HCO3

(Response .. Slow)

Respiratory Acidosis
ph, CO2, HCO3
Acute Respiratory Acidosis

< 48 hours duration

Chronic Respiratory Acidosis > 48 hours duration Common causes are: CNS (sedatives, methadone/heroin

Common causes are: CNS depression (anesthesia,

sedatives, cerebral oedema , head trauma,)

Neuromuscular impairment
(GBS,status epilepticus, tetanus, Hypokalemic periodic paralysis, organophosphorus poisoning)

Respiratory
(severe asthma, pneumothorax, severe bilateral pneumonia, ARDS)

addiction, Pickwickian syndrome, bulbar polio.) Neuromuscular impairment (polio, MS, muscular dystrophy) Ventilatory restriction (kyphosciolosis, phrenic nerve palsy, obesity, hydrothorax) Respiratory (COLD, interstitial fibrosis)

Clinical Manifestations

- Shallow breathing (Hypoventilation)

- Hypercapnic almost always occur with some degree of hypoxemia. - Hypercapnic encephalopathy includes irritability, headache mental cloudiness, confusion, papillodema, myoclonic jerks & flapping tremors. - hypotension due to myocardial depression.

- cyanosis

Compensatory Response

For Acute Respiratory Acidosis

[HCO3] = 0.1 x pco2

(HCO3 not > 30 mEq/L)
4 yrs old child while playing in the garden swallowed some foreign body and suddenly became short of breath and blue. He was rushed to the hospital. His initial ABG data shows: pH 7.10, PaCO2 100, HCO3- 30

What is the defect ? Compensation ?

Compensatory Response

For Chronic Respiratory Acidosis [HCO3] =0.4 x pco2 (HCO3 not >45 mEq/L)

45 yrs man known to have COLD admitted for evaluation and complaining of progressive difficulty breathing. His acid-base data are: pH 7.29, PaCO2 70, HCO3- 36

what is the ABG disorder ? compensation ?

Respiratory Alkalosis

1
7.70

40

Compensatory Response: Kidney excretes excess more bicarbonate

Respiratory Alkalosis pH , pco2 , HCO3I

Clinical manifestations:

Hyperventilation, Paresthesias, chest discomfort, Circumoral numbness

Light-headedness, confusion Tetany or generalized seizures

Compensatory Response

For acute respiratory alkalosis (< 48 hours )

[HCO3-] = 0.2 x pco2

For chronic respiratory alkalosis ( > 48 hours) [HCO3-] = 0.5 x pco2

A 1st year medical student was anxious about her performance on the 1st biochemistry test. She felt numbness around her mouth and tingling in her hands and went to the clinic. A workup revealed: pH 7.50, PaCO2 30, HCO3- 22
I knew I should have studied my Biochemistry notes.

[HCO3-] = 0.2 x pco2

what is the ABG disorder ?

compensation ?

24 weeks pregnant lady presented with gradually increasing fatigue & weakness O/E she was pallor, no edema, 120/80 was her BP, she was mild hyperventilating. Her chest was clear & she was afebrile. Her ABG data showed: pH - 7.42, pCO2 - 32, HCO3 - 20

[HCO3-] = 0.5 x pco2

What is the ABG disorder ? What are causing this ABG disorder ? Compensation ?

Acid-base disorders

Remember, these can be either respiratory or metabolic in nature. Respiratory ones can be chronic or acute; metabolic ones always chronic. Renal and respiratory systems work together reflexly to compensate for one another.

Normal physiological compensation will never bring the pH to the normal, there will always be mixed disorder when pH is normalized but the other parameters are not.