1 mohammed a. almeziny bpharm.rph. msc. phd clinical pharmacist

ACID AND BASE BALANCE AND

IMBALANCE

1

Mohammed A. Almeziny BPharm.RPh. Msc. PhD

Clinical Pharmacist

The Body and pH

Homeostasis of pH is tightly controlled Extracellular fluid = 7.4 Blood = 7.35 – 7.45 < 6.8 or > 8.0 death occurs Acidosis (acidemia) below 7.35 Alkalosis (alkalemia) above 7.45

2

Small changes in pH can produce major disturbances

Most enzymes function only with narrow pH ranges

Acid-base balance can also affect electrolytes (Na+, K+, Cl-)

Can also affect hormones

4

Small changes in pH can produce major disturbances cont’d Cardiovascular

(e.g., impaired contractility, arrhythmias), Pulmonary

(e.g., impaired oxygen delivery, respiratory muscle fatigue, dyspnea),

Renal (e.g., hypokalemia)

Neurologic (e.g., decreased cerebral blood flow, seizures,

coma).

The body produces more acids than bases

Acids take in with foods Acids produced by metabolism of lipids

and proteins Cellular metabolism produces CO2.

6

Maintenance of BalanceBalance maintained by: Buffering systems

Lungs

Kidneys

H2CO3…..HCO3

1-Buffer systems Prevent major changes in pH Act as sponges… 3 main systems• Bicarbonate-carbonic acid buffer• Phosphate buffer• Protein buffer

H+

H+H+

Control of Acids

Bicarbonate buffer

Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)

Maintain a 20:1 ratio : HCO3- : H2CO3

HCl + NaHCO3 ↔ H2CO3 + NaCl

NaOH + H2CO3 ↔ NaHCO3 + H2O

9

Phosphate buffer

Major intracellular buffer H+ + HPO4

2- ↔ H2PO4-

OH- + H2PO4- ↔ H2O + H2PO4

2-

10

Protein Buffers

Includes hemoglobin, work in blood and ISF Carboxyl group gives up H+ Amino Group accepts H+

11

2. Respiratory mechanisms

Exhalation of carbon dioxide respiratory control center in the medulla to

increase the rate and depth of ventilation. Peripheral chemoreceptors (located in the carotid

arteries and the aorta) activated by arterial acidosis, hypercarbia (elevated

PaCO2), and hypoxemia (decreased PaO2).

Central chemoreceptors (located in the medulla). activated by cerebrospinal fluid (CSF) acidosis and by

elevated carbon dioxide tension in the CSF

12

2. Respiratory mechanisms Cont’d

Powerful, but only works with volatile acids

Doesn’t affect fixed acids like lactic acid CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3

-

Body pH can be adjusted by changing rate and depth of breathing

13

3. Kidney excretion

Can eliminate large amounts of acid Can also excrete base Can conserve and produce bicarb ions Most effective regulator of pH If kidneys fail, pH balance fails

14

Rates of correction

Buffers function almost instantaneously Respiratory mechanisms take several

minutes to hours Renal mechanisms may take several

hours to days

15

Acid-Base Imbalances

pH< 7.35 acidosis pH > 7.45 alkalosis The body response to acid-base

imbalance is called compensation May be complete if brought back within

normal limits Partial compensation if range is still

outside norms.

17

Compensation

If underlying problem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation.

If problem is respiratory, renal mechanisms can bring about metabolic compensation.

18

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

19

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

20

Four Basic Types of Imbalance

Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

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

23

Respiratory Acidosis cont’d

Acute conditons: Adult Respiratory Distress Syndrome Pulmonary edema Pneumothorax

24

Compensation for Respiratory Acidosis

Kidneys eliminate hydrogen ion and retain bicarbonate ion

25

Signs and Symptoms of Respiratory Acidosis

Breathlessness Restlessness Lethargy and disorientation Tremors, convulsions, coma Respiratory rate rapid, then gradually

depressed Skin warm and flushed due to

vasodilation caused by excess CO2

26

Treatment of Respiratory Acidosis

Restore ventilation Treat underlying dysfunction or disease

27

Respiratory Alkalosis

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

29

Respiratory Alkalosis cont’d

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

30

Compensation of Respiratory Alkalosis

Kidneys conserve hydrogen ion Excrete bicarbonate ion

31

Treatment of Respiratory Alkalosis

Treat underlying cause Breathe into a paper bag IV Chloride containing solution – Cl- ions

replace lost bicarbonate ions

32

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+

34

Common Causes of Metabolic AcidosisNormal AG Hypokalemic

Diarrhea Fistulous disease Ureteral diversions Type 1 RTA Type 2 RTA Carbonic anhydrase

inhibitors Hyperkalemic

Hypoaldosteronism Hydrochloric acid or

precursor Type 4 RTA Potassium-sparing

diuretics Amiloride Spironolactone Triamterene

Elevated AG Renal Failure Lactic Acidosis (see

Table 10-5) Ketoacidosis

Starvation Ethanol Diabetes mellitus

Drug Intoxications Ethylene glycol Methanol

Salicylates

AG, anion gap; RTA, renal tubular acidosis.

Symptoms of Metabolic Acidosis

Headache, lethargy Nausea, vomiting, diarrhea Coma Death

36

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)

37

Treatment of Metabolic Acidosis

Treat underlying cause IV Bicarbonate solution

38

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

40

Compensation for Metabolic Alkalosis

Respiratory compensation difficult – hypoventilation limited by hypoxia

41

Symptoms of Metabolic Alkalosis

Respiration slow and shallow Hyperactive reflexes ; tetany Often related to depletion of electrolytes Atrial tachycardia Dysrhythmias

42

Treatment of Metabolic Alkalosis

Treat underlying disorder Electrolytes to replace those lost IV chloride containing solution

0.1 N HCL Infusion rate 0.2 mmol/kg/hr Central line

Acetazolamide

43

Laboratory Values in Simple Acid-Base Disorders

Disorder Arterial pH

Primary Change

Compensatory Change

Metabolic acidosis ↓ ↓HCO3

- ↓PaCO2

Respiratory acidosis ↓ ↑PaCO2

- ↑HCO3-

Metabolic alkalosis ↑ ↑HCO3

- ↑PaCO2

Respiratory alkalosis ↑ ↓PaCO2

- ↓HCO3-

Interpreting Lab data

Arterial Blood Gas (ABG) Arterial carbon dioxide tension (PaCO2). Serum bicarbonate (HCO3

-). Arterial oxygen tension (PaO2)

pH <7.35, the patient is considered academic >7.45, the patient is considered alkalemic

ABGs Normal Range

pH 7.36–7.44

PaO2 90–100 mmHg

PaCO2 35–45 mmHg

HCO3- 22–26 mEq/L

Normal Arterial Blood Gas (ABG) Values

Anion Gap (AG)

The concentration of all the unmeasured anions in the plasma eg lactate, acetoacetate, sulphate.

Anion gap = [Na+] - [Cl-] - [HCO3-] Reference range is 8 to 16 mmol/l.

Adjusted AG = AG + 2.5 × (normal albumin – measured albumin in g/dL

Anion Gap (AG) cont’d

Clinical Use of the Anion Gap To signal the presence of a metabolic

acidosis and confirm other findings Help differentiate between causes of a

metabolic acidosis To assist in assessing the biochemical

severity of the acidosis and follow the response to treatment

Osmolal gap OG

Osmolality mOsm/kg H2O= (1.86[Na])+([glucose (mmol/L)])+([BUN mmol/L])

Osmolal gap= measured Osmolality- Calculated Osmolality

exists when the measured and calculated values differ by >10 mOsm/kg

Evaluation of Acid-Base Disorders

Obtain a detailed patient history and clinical assessment.

Check the arterial blood gas, sodium, chloride, and HCO3

-. Identify all abnormalities in pH, PaCO2, and HCO3

-.

Evaluation of Acid-Base Disorders Cont’d

Determine which abnormalities are primary and which are compensatory based on pH. If the pH is <7.40, then a respiratory or

metabolic acidosis is primary. If the pH is >7.40, then a respiratory or

metabolic alkalosis is primary. If the pH is normal (7.40) and there are

abnormalities in PaCO2 and HCO3-, a mixed

disorder is probably present because metabolic and respiratory compensations rarely return the pH to normal.


Consider other laboratory tests to further differentiate the cause of the disorder. If the AG is normal, consider calculating the

urine AG. If the AGis high and a toxic ingestion is

expected, calculate an osmolal gap. If the AG is high, measure serum ketones and

lactate.


Always calculate the AG. If ≥20, a clinically important metabolic acidosis is usually present even if the pH is within a normal range.

If the AG is increased, calculate the excess AG(AG-10). Add this value to the HCO3

- to obtain corrected value. If corrected value >26, a metabolic alkalosis is

also present. If corrected value is <22, a nonanion gap

metabolic acidosis is also present.


Consider other laboratory tests to further differentiate the cause of the disorder. If the AG is normal, consider calculating the

urine AG. If the AGis high and a toxic ingestion is

expected, calculate an osmolal gap. If the AG is high, measure serum ketones and

lactate.


Compare the identified disorders to the patient history and begin patient-specific therapy.

Questions?

59

END

ACID - BASE BALANCE

1 mohammed a. almeziny bpharm.rph. msc. phd clinical pharmacist

Documents