Acid-base balance and disturbance Normal acid-base balance Parameters of acid-base balance Simple acid-base disturbance Mixed acid-base disturbance

Normal acid-base balance Concepts of acid and base Sources of acids and bases Regulation of acid-base balance

Concepts of acid and base H 2 CO 3 =H + +HCO 3 - HHb=H + + Hb - H 2 PO 4 - =H + +HPO 4 2- HPr=H + +Pr - Acid base H + donor H + receptor

Sources of acids and bases mainly produced during the catabolism of intracellular nutrients, with a small part of them from food. Acid Volatile acid carbonic acid Nonvolatile acid or fixed acid sulfuric acid, phosphoric acid, lactic acid, acetoacetic acid, β- hydroxybutyric acid

Regulation of acid-base balance Buffer systems Respiratory regulation of acid-base balance Renal regulation of acid-base balance

Buffer systems Buffer system in the blood Buffer effect of cells

Buffer system in the blood H 2 CO 3 =H + +HCO 3 - H 2 PO 4 - =H + +HPO 4 2- HPr=H + +Pr - HHb=H + +Hb - HHbO 2 =H + +HbO 2 - Buffer acid buffer base Weak acid conjugate base Converting strong acid or base into weak acid or base

Buffer effect of cells Ion exchange between intracellular and extracellular fluids H + k + HCO 3 - Cl - Intracellular buffer systems H 2 PO 4 - /HPO 4 2- HPr/Pr -

Respiratory regulation of acid-base Central chemoreceptor Peripheral chemoreceptor Respiratory center ventilation H +, PaCO 2, PaO 2 H+H+

Renal regulation of acid-base balance Excretion of H + and reabsorption of HCO3 - in proximal convoluted tubule Excretion of H + and reabsorption of HCO3 - in distal tubule Excretion of NH 4 + and NH 3

Parameters of acid-base balance pH H 2 CO 3 =H + +HCO 3 - [H + ]=pKa.[H 2 CO 3 ]/[HCO 3 - ] [H 2 CO 3 ]=0.03PaCO 2 =1.2

PaCO 2 PaCO 2 is the partial pressure of CO 2 dissolved in artery plasma, the normal range is mmHg with a average value of 40mmHg. PaCO 2 reflects the situation of alveolar ventilation. PaCO 2 ↑ respiratory acidosis or metabolic alkalosis after compensation PaCO 2 ↓ respiratory alkalosis or metabolic acidosis after compensation

Standard bicarbonate (SB) and actual bicarbonate (AB) SB is the bicarbonate under “standard condition” which refers to a temperature of 38 ℃, PaCO2 of 40mmHg and 100% oxygen saturation of hemoglobin. Normal range: 22-27mmol/L Average value:24mmol/L SB↑ metabolic alkalosis or chronic respiratory acidosis SB↓ metabolic acidosis or chronic respiratory alkalosis

AB AB is the bicarbonate measured under “actual condition” which refers to the actual status of the patient. A comparison between SB and AB can provide some information for the differentiation of respiratory acid-base disturbance from metabolic acid-base disturbance.

Buffer base (BB) BB is the sum of all all alkaline buffer substances in the blood, which is also measured under standard condition. Normal range: 45-52mmol/L Average value: 48mmol/L

Base excess (B E) BE describes the amount if a fixed acid or base that must be added to a blood sample to achieve a pH of 7.4 under standard condition. If an acid must be added, the BE value is positive. If an base must be added, the BE value is negative. The normal value is -3-+3mmol/L

Anion gap (AG) AG is the difference between unmeasured anion (UA) and unmeasured cation (UC). AG=UA-UC=Na + -(Cl - +HCO 3 - )= =12mmol/L AG↑ metabolic acidosis

Simple acid-base disturbance Metabolic acidosis respiratory acidosis Metabolic alkalosis Respiratory alkalosis

Metabolic acidosis Metabolic acidosis is defined as a decrease of pH induced by primary decrease in plasma bicarbonate concentration.

etiology Excessive production of fixed acid lactic acidosis (glycolysis) keto-acidosis (lipolysis) Disorders in the excretion of acidic metabolites renal failure, renal tubular acidosis I Excessive loss of HCO 3 - loss of intestinal juice, bile, and pancreatic juice renal tubular acidosis II Excessive intake of exogenous acids NH 4 Cl, aspirin (acetylsalicylic acid) hyperkalemia

Classification Normal AG metabolic acidosis loss of HCO 3 - from intestinal of renal route excessive intake of chloride- containing medicine High AG metabolic acidosis lactic acidosis, keto-acidosis renal failure, salicylic poisoning

compensation Compensation by the buffer system Compensation by the lung ventilation↑→PaCO 2 ↓ △ PaCO 2 =1.2 △ HCO 3 - ±2 Compensation by the kidney

Changes of acid-base parameters pH ↓, SB ↓, AB ↓, BE ↓PaCO 2 ↓ AB<SB

Alterations of metabolism and function Cardiovascular system Central nervous system

Cardiovascular system Cardiac arrhythmia hyperkalemia Negative inotropic action H + can competitively inhibit the combination of Ca 2+ with troponin and influence the influx of Ca 2+ from extracellular space and the release of Ca 2+ into cytoplasm from sarcoplasmic reticulum. Decreased response of vascular system to CA

Central nervous system Weakness, fatigue, lethargy, disorder of consciousness, coma Activities of Glutamate decarboxylase ↑ Gamma-aminobutyric acid (GABA) ↑ Activities of oxygenase in mitochondria ↓ ATP ↓

Correction of underlying disorders Administration of NaHCO 3 Attention should be paid to prevent hypokalemia and convulsion induced by decreased free Ca 2+ Principles of prevention and treatmen

Respiratory acidosis Respiratory acidosis is defined as a decrease of pH induced by primary increase in plasma H 2 CO 3 concentration.

Etiology Suppression of respiratory center Cerebrovascular accident Trauma or infection of brain Excessive sedatives, narcotics, alcohol Disease of respiratory muscles Acute radiculitis Acute poliomyelitis Organophosphorus pesticide poisoning Severe hypokalemia Disease of chest wall Pneumothorax, hydrops of thoracic cavity, chest deformity

Obstruction of airways Drowning Aspiration of foreign bodies Laryngeal edema Laryngospasm Chronic obstructive pulmonary disease Pulmonary disease Extensive inflammation Consolidation fibrosis Excessive inspiration of CO 2

compensation Acute respiratory acidosis H + -K + exchange Buffer effect of red blood cells Cl - -HCO3 - exchange Chronic respiratory acidosis Kidney excretion of H + and NH4 + ↑, reabsorption of HCO 3 - ↑ △ [HCO 3 - ]=0.1 △ PaCO 2 ±1.5 △ [HCO 3 - ]=0.4 △ PaCO 2 ±3

Changes of acid-base parameters pH ↓, PaCO 2 ↑ SB ↑, AB ↑, BE ↑ AB>SB

Alterations of metabolism and function Central nervous system Cardiovascular system

Nervous system CO 2 narcosis headache, fatigue, mental derangement, tremor, lethargy, coma Pulmonary encephalopathy hypercapnia and hypoxia Cardiovascular system Dilation of brain blood vessels, intracranial hypertension, brain edema Cardiac arrhythmia and decreased cardiac contractility

Principles of prevention and treatmen Keep the airway unobstructed and to improve ventilation Tracheotomy, intratrachea intubation, mechanical ventilation

Metabolic alkalosis Metabolic alkalosis is defined as a increase of pH induced by primary increase in plasma bicarbonate concentration.

Etiology Excessive loss of fixed acid loss from the stomach vomiting, gastric suction loss from the kidney diuretics, hyperaldosteroism Excessive intake of alkaline substances NaHCO 3, stored blood (citrate) Hypokalemia paradoxical acidic urine

Classification Saline-responsive alkalosis vomiting, gastric suction, diuretics Saline-resistant alkalosis hyperaldosteroism, severe hypokalemia

Compensation Compensation by the buffer system Compensation by the lung ventilation↓→PaCO 2 ↑ △ PaCO 2 =0.7 △ HCO 3 - ±5 Compensation by the kidney

pH ↑, SB ↑, AB ↑, BE ↑ AB>SB PaCO 2 ↑ Changes of acid-base parameters

Alterations of metabolism and function Central nervous system restless, mental derangement, delirium, disorder of consciousness, GABA↓ Oxygen dissociation curve of hemoglobin shifts to left Free calcium ↓ convulsion, tendon hyperreflexia hypokalemia

Principles of prevention and treatmen Saline-responsive alkalosis NaCl, KCl, CaCl 2 Saline-resistant alkalosis antisterone, potassium, carbonic anhydrase (CA)

Respiratory alkalosis Respiratory alkalosis is defined as a increase of pH induced by primary decrease in plasma H 2 CO 3 concentration.

Etiology Psychogenic factors nervousness, anxiety, hysteria Hypoxemia Some pulmonary disease ARDS Brain diseases encephalitis, meningitis Misuse of mechanical ventilation

Acute respiratory alkalosis H + -K + exchange Buffer effect of red blood cells Cl - -HCO 3 - exchange △ [HCO 3 - ]=0.2 △ PaCO 2 ±2.5 Chronic respiratory alkalosis Kidney excretion of H + and NH4 + ↓, reabsorption of HCO 3 - ↓ △ [HCO 3 - ]=0.5 △ PaCO 2 ±2.5 Compensation

Changes of acid-base parameters pH ↑, PaCO 2 ↓,SB ↓, AB ↓, BE ↓, AB<SB

Alterations of metabolism and function Disturbance in CNS vertigo, disorder of consciousness, coma Increased neuromuscular excitability, tetany, convulsion

Principles of prevention and treatmen Treatment of primary disease Prevention mechanical hyperventilation Inspiration of oxygen-containing 5% CO 2