Presentation on theme: "(2) Respiratory acidosis 1) Concept 2) Causes and Pathogenesis 3) Compensation 4) Effects on the body 5) Principle of treatment."— Presentation transcript:
(2) Respiratory acidosis 1) Concept 2) Causes and Pathogenesis 3) Compensation 4) Effects on the body 5) Principle of treatment
1) Concept Respiratory acidosis refers to the primary increase of [H 2 CO 3 ], which is initiated by an elevation of carbon dioxide tension (increased PaCO 2 ). The increase of [H 2 CO 3 ] is also called hypercapnia.
2) Causes and Pathogenesis The basic reasons: (a) decreased ventilation, which leads to the decreased elimination of CO 2 from lung; (b) increased inhalation of CO 2. Acute Chronic
(a) Acute respiratory acidosis a) depression of respiratory center by cerebral diseases (trauma, infections) and drugs (over- dosage of anesthetics, sedatives), b) neuromuscular disorders (acute hypokalemia, poliomyelitis 脊髓灰白质炎, Guillain-Barre syndrome 脊神经根炎 ), c) cardiopulmonary arrest. d) obstruction of respiratory tract. e) Chest wall diseases (fracture of rib), f)mis-operating of respirator. (b) increased inhalation of CO 2.
(b) Chronic respiratory acidosis Chronic obstructive pulmonary diseases (emphysema, chronic bronchitis with hypoventilation) cause the chronic respiratory acidosis. Brain tumors (affecting the respiratory center in which the ventilation is decreased)
3) Compensation against respiratory acidosis (a) Non- [HCO 3 ¯ ]/[H 2 CO 3 ] buffering systems (b) Cellular compensation H + moves into the cell CO 2 moves into the cells (c)The renal compensation for chronic resppiratory acidosis. ( How about buffer pair: [HCO 3 ¯ ]/[H 2 CO 3 ] and respiratory compensation? )
(c) CO 2 moves into the cells When CO 2 in ECF(serum) is increased, CO 2 will move into the cells, CO 2 combines H 2 O to form carbonic acid, then H 2 CO 3 dissociates to form H + and HCO 3 ¯. The HCO 3 ¯ moves out of the cells as a exchange for electric neutrality, at the same time Cl ¯ moves into the cells for electrical balance. HCO 3 ¯ and Cl ¯ exchange
Predicted compensatory formula of acute respiratory acidosis ΔHCO 3 - = 0.1x ΔPaCO 2 ± 1.5 HCO 3 - = 24+ 0.1x ΔPaCO 2 ± 1.5 Secondary compensation, primary change The maximal increased value up to 30 mmol/L Decompensation
(c) The renal compensation The renal compensation in respiratory acidosis is the same as the renal compensation in metabolic acidosis. a) The activity of carbonic anhydrase (CA) increases, b) The activity of glutaminase is increased, more NH 4 + is excreted into tubular lumen. c) The end urine is more acidic. (NaH 2 PO 4 )
Predicted compensatory formula of chronic respiratory acidosis ΔHCO 3 - = 0.4x ΔPaCO 2 ± 3 HCO 3 - = 24+0.4x ΔPaCO 2 ± 3 Secondary compensation primary change Value measured > value predicted: with metabolic alkalosis Value measured < value predicted: with metabolic acidosis. Maximal compensatory value up to:45mmol/L
Changes of laboratory parameters Primary increase of [H 2 CO 3 ]: PaCO 2 ? Secondary compensation: AB,SB,BB ??? AB ?? SB BE ? pH ?
Changes of laboratory parameters Primary increase of [H 2 CO 3 ]: PaCO 2 increases Secondary compensation: AB,SB,BB increases AB > SB BE positive value increases pH tends to decrease.
4)Effects on the body In metabolic acidosis the [H + ] in plasma is increased. In respiratory acidosis both [H + ] and CO 2 concentration are increased. The main manifestations are: (A) depression of mental activity (B) effects on the cardiovascular system. (C) hyperkalemia
(A) Depression of mental activity (a) Manifestations Obtundation (thinking slowly), headache, somnolence 嗜睡, confuse, coma and asterixis (fluttering-like tremor ) may be noted. These effects on CNS caused mainly by elevated CO 2 have been termed “CO 2 narcosis”. Pulmonary encephalopathy 肺性脑病 in respiratory failure. l
(b) Mechanisms a) Increased [H + ] cause cerebral vasodilatation, then cause brain edema. Increased blood volume will cause high intracranial pressure. b) High [H + ] increases the permeability of cerebral blood vessels. Decreased plasma COP and increased interstitial COP can lead to brain edema.
Glutamic acid Glutamate decarboxylase gama r-GABA, r- gama aminobutyric acid r-GABA transaminase Succinic acid Kreb’s cycle C) The production of GABA (gama aminobutyric acid, a inhibitory transmitter) is increased due to the activity of enzyme for the production is increased, and the activity of enzyme for the decomposition is decreased in low pH (acidosis). C) The production of GABA (gama aminobutyric acid, a inhibitory transmitter) is increased due to the activity of enzyme for the production is increased, and the activity of enzyme for the decomposition is decreased in low pH (acidosis).
d) Increased CO 2 leads to ( brain ) vasodilation directly. (higher intracranial pressure) Increased [CO 2 ] stimulates via chemoreceptor sympathetic activity, then leads indirectly to stronger vasoconstriction than vasodilation. There is no α-receptor in cerebral vessels, so vasodilation in brain.
(B) Effects on the cardiovascular system (a) Impairment of myocardial contraction (b) The hemodynamic effect (c) Arrhthmias due to hyperkalemia (C) hyperkalemia
5) Principle of treatment (a) Treat the primary diseases which cause respiratory acidosis. (antibiotic, antispastic drugs) (b) Improve properly the ventilation. (c) Prevent from (respiratory alkalosis) over- ventilation during artificial respiration.
Case Discussion No.3 Female, 11 years old. Guillain-Barre syndrome before respirator after respirator pH 7.29 7.56 PaCO 2 (mmHg) 85 45 BE(mmol/L) +9.9 +16 BB(mmol/L) 56 61 SB(mmol/L) 32.8 39 AB(mmol/L) 39.5 39
Before:Decompensatory respiratory acidosis After: Decompensatory metabolic alkalosis. Reasons: too fast elimination of CO 2 slow renal elimination of HCO 3 -
(c) Can we replenish alkaline (HCO 3 ¯, sodium lactate ) to the patients with respiratory acidosis? (d) pay attention to [K + ] in serum during the treatment of acidosis.
Case Discussion A 52-year-old man with chronic obstructive lung disease was admitted to the hospital with worsening dyspnea. He appeared cyanotic and in respiratory distress. The laboratory data: Arterial blood: pH=7.34 PaCO 2 =60 mmHg PaO 2 =50 mmHg [HCO 3 - ]=31mmol/L. ΔHCO 3 - = 0.4x ΔPaCO 2 ± 3=??
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