Acid-base balance and disturbance Normal acid-base balance Parameters of acid-base balance Simple acid-base disturbance Mixed acid-base disturbance
Dec 27, 2015
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
H2CO3=H++HCO3-
HHb=H++ Hb-
H2PO4-=H++HPO4
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
H2CO3=H++HCO3-
H2PO4-=H++HPO4
2-
HPr=H++Pr-
HHb=H++Hb-
HHbO2=H++HbO2-
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+
HCO3- Cl-
Intracellular buffer systems
H2PO4-/HPO4
2-
HPr/Pr-
Respiratory regulation of acid-base
Central chemoreceptor
Peripheral chemoreceptor
Respiratory center
ventilation
H+, PaCO2, PaO2H+
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 NH4+ and NH3
Parameters of acid-base balance
pH 7.35-7.45
H2CO3=H++HCO3-
[H+]=pKa.[H2CO3]/[HCO3-]
[H2CO3]=0.03PaCO2=1.2
PaCO2
PaCO2 is the partial pressure of CO2 dissolved in artery plasma, the normal range is 33-46mmHg with a average value of 40mmHg.
PaCO2 reflects the situation of alveolar ventilation.
PaCO2↑ respiratory acidosis or metabolic alkalosis after compensation
PaCO2↓ 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-+HCO3-)=140-104-
24=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 HCO3-
loss of intestinal juice, bile, and pancreatic juice
renal tubular acidosis II
Excessive intake of exogenous acids
NH4Cl, aspirin (acetylsalicylic acid)
hyperkalemia
Classification
Normal AG metabolic acidosis
loss of HCO3- 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↑→PaCO2↓
△PaCO2=1.2 HCO△ 3-±2
Compensation by the kidney
Changes of acid-base parameters
pH ↓, SB ↓, AB ↓, BE ↓PaCO2 ↓ 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 Ca2+ with troponin and influence the influx of Ca2+ from extracellular space and the release of Ca2+ 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 NaHCO3
Attention should be paid to prevent hypokalemia and convulsion induced by decreased free Ca2+
Principles of prevention and treatmen
Respiratory acidosis
Respiratory acidosis is defined as a decrease of pH induced by primary increase in plasma H2CO3 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 CO2
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 HCO3
-↑
△[HCO3-]=0.1 PaCO△ 2±1.5
△[HCO3-]=0.4 PaCO△ 2±3
Changes of acid-base parameters
pH ↓, PaCO2↑ SB ↑, AB ↑, BE ↑ AB>SB
Alterations of metabolism and function
Central nervous system
Cardiovascular system
Nervous system
CO2 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
NaHCO3, 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↓→PaCO2↑
△PaCO2=0.7 HCO△ 3-±5
Compensation by the kidney
pH ↑, SB ↑, AB ↑, BE ↑ AB>SB PaCO2↑
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, CaCl2
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 H2CO3 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- -HCO3- exchange
△[HCO3-]=0.2 PaCO△ 2±2.5
Chronic respiratory alkalosis
Kidney excretion of H+ and NH4+↓,reabsorption of HCO3
-↓
△[HCO3-]=0.5 PaCO△ 2±2.5
Compensation
Changes of acid-base parameters
pH ↑, PaCO2 ↓ ,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% CO2