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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++HCO3HHb=H++ Hb-
H2PO4-=H++HPO42HPr=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.
Volatile acid
Acid
carbonic acid
Nonvolatile acid or fixed acid
sulfuric acid, phosphoric acid, lactic
acid, acetoacetic acid, βhydroxybutyric 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++HCO3H2PO4-=H++HPO42HPr=H++PrHHb=H++HbHHbO2=H++HbO2-
Buffer acid
Weak acid
buffer base
conjugate base
Converting strong acid or base into weak
acid or base
Buffer effect of cells
Ion exchange between intracellular and
extracellular fluids
H+
HCO3-
k+
Cl-
Intracellular buffer systems
H2PO4-/HPO42HPr/Pr-
Respiratory regulation of acid-base
Central
chemoreceptor
Peripheral
chemoreceptor
H+
H+, PaCO2, PaO2
Respiratory center
ventilation
Renal regulation of acid-base balance
Excretion of H+ and reabsorption of HCO3in proximal convoluted tubule
Excretion of H+ and reabsorption of HCO3in 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 3346mmHg 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-)=140-10424=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 HCO3loss 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△HCO3-±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 ↓
Principles of prevention and
treatmen
Correction of underlying disorders
Administration of NaHCO3
Attention should be paid to prevent
hypokalemia and convulsion induced by
decreased free Ca2+
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
Acute radiculitis
Acute poliomyelitis
Disease of
respiratory muscles Organophosphorus
pesticide poisoning
Severe hypokalemia
Disease of chest
wall
Pneumothorax, hydrops of
thoracic cavity, chest deformity
Drowning
Aspiration of foreign bodies
Obstruction of
airways
Laryngeal edema
Laryngospasm
Chronic obstructive pulmonary
disease
Extensive inflammation
Pulmonary
disease
Consolidation
fibrosis
Excessive inspiration of CO2
compensation
H+-K+ exchange
Acute respiratory
acidosis
Buffer effect of red blood
cells Cl- -HCO3- exchange
△[HCO3-]=0.1△PaCO2±1.5
Chronic respiratory
acidosis
Kidney excretion of H+
and NH4+↑,reabsorption of
HCO3-↑
△[HCO3-]=0.4△PaCO2±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
and hypoxia
hypercapnia
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△HCO3-±5
Compensation by the kidney
Changes of acid-base parameters
pH ↑, SB ↑, AB ↑, BE ↑ AB>SB
PaCO2↑
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
Compensation
H+-K+ exchange
Acute respiratory
Buffer effect of red blood cells
alkalosis
Cl- -HCO3- exchange
△[HCO3-]=0.2△PaCO2±2.5
+ and
Kidney
excretion
of
H
Chronic respiratory
NH4+↓,reabsorption of HCO3-↓
alkalosis
△[HCO3-]=0.5△PaCO2±2.5
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