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buffers, mechanism, maintenance of body pH and disorders

buffers, mechanism, maintenance of body pH and disorders

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Buffers Buffers Presentation Transcript

  • Acid-Base balance
  • Acid Base balance Acid-base balance refers to the mechanisms thebody uses to keep its fluids close to neutral pH (thatis, neither basic nor acidic) so that the body canfunction normally. Arterial blood pH is normally closely regulatedto between 7.35 and 7.45.
  • acids ? Any ionic or molecular substance that can act as a proton donor. Strong acid : HCl, H2SO4, H3PO4. Weak acid : H2CO3, CH3COOH.bases ? Any ionic or molecular substance that can act as a proton acceptor. Strong alkali : NaOH, KOH. Weak alkali : NaHCO3, NH3, CH3COONa.
  • Origin of acids Much more Intracellular metabolism Volatile CO2+H2O=H2CO3 300~400L CO2 (15mol acids H+) Lactic acid Fixed Ketone bodies 50~100 mmol H+ acids Sulfuric acid Phosphoric acid Origin of bases less NH3 , sodium citrate, sodium lactate
  • pH- pH of ECF is between 7.35 and 7.45. Deviations, outside this range affect membrane function, alter protein function, etc.- You cannot survive with a pH <6.8 or >7.7- Acidosis- below 7.35 Alkalosis- above 7.45 CNS function deteriorates, coma, cardiac irregularities, heart failure, peripheral vasodilation, drop in Bp.
  •  Given that normal body pH is slightly alkaline and that normal metabolism produces acidic waste products such as carbonic acid (carbon dioxide reacted with water) and lactic acid, body pH is constantly threatened with shifts toward acidity. In normal individuals, pH is controlled by two major and related processes; pH regulation and pH compensation. Regulation is a function of the buffer systems of the body in combination with the respiratory and renal systems, whereas compensation requires further intervention of the respiratory and/or renal systems to restore normalcy.
  • Buffer Systems in Body Fluids Figure 27.7
  • Buffering system ECF Plasma NaHCO3/ H2CO3 NaPr/HPr* Na2HPO4/NaH2PO4 intercellular NaHCO3/ H2CO3 Na2HPO4/NaH2PO4 fluid ICF** KPr/HPr K2HPO4/KH2PO4 KHCO3 /H2CO3 organic acids RBC KHb/HHb KHbO2/HHbO2 K2HPO4/KH2PO4 KHCO3/ H2CO3* HPr : protein ; ** muscle cells 。
  • Major buffer system in the bodyCarbonic acid/Bicarbonate(HCO3-/H2CO3) :The major extracellular buffer , regulated by lungsand kidneys , effective , determining the pH ofplasma.Phosphate (HPO42-/H2PO4- ) : IntracellularProtein (Pr-/HPr) : Plasma/IntracellularHemoglobin (Hb-/HHb and HbO2-/HHbO2 ) : RBC*A buffer system cannot buffer itself. fast / no permanence
  • 2) Respiratory control: Expelling more CO2 through respiration→toexclude volatile acid. H+→chemoreceptor → excite respiratorycentre → hyperventilation → exclude volatile acidFast / effectively / only excludesvolatile acid
  • PaCO2↑ (40-80 mmHg)→ Blood-brain barrierpermeable to CO2: CO2+H2O↔ H2CO3 ↔ H++HCO3-(incerebrospinal fluid, CSF)→ [H+] ↑ → Centralchemoreceptor(beneath the ventral surface of themedulla oblongata) → Respiratory center ↑ →Ventilation↑ (Main)
  • 3) Role of kidney (exclusion ofacid with conservation of base) hydrogen ion secreted ammonium excreted by renal tubularcell bicarbonate reabsorbed Effectively ( fixed acid may beexcluded ) / slowly
  • Kidney tubules and pH Regulation Figure 27.10a, b
  • Definition of acid-base disorders An acid base disorder is a change in thenormal value of extracellular pH that may resultwhen renal or respiratory function is abnormalor when an acid or base load overwhelmsexcretory capacity.
  • PLAY Animation: Relationship Between PCO2 and Plasma pH Figure 27.6
  • Simple acid-base disorder1. Metabolic acidosis1) concept: primary disturbance [HCO3-] ↓ ; PH . PaCO2 ↓2) clasification: Normal AG High AG3) pathogenesis and mechnisms: (1) lose of bases (2) gaining acids
  • Metabolic acidosis Causes:(1) lose of bases (bicarbonate decreased) Gastrointestinal losses: diarrhea Renal losses: proximal renal tubular acidosis and distalrenal tubular acidosis(2) gaining acids (bicarbonate consumed in buffering) Lactic acidosis: tissue hypoxia, impaired oxygen utilization, severe liverdysfunction, and shock Ketoacidosis: diabetic,hepatic cirrhosis, alcoholic poisoning, or starvation Renal failure: conservation of acids Exogenous acid intake: ammonium chloride, salicylate, ethyleneglycol(commonly used in antifreeze), or methanol intoxication
  • 4) Compensation:all regulation system take part in Compensation5) Effects: Effects(1) Depression of central neural system a Elevated activities of glutamate decarboxylase→GABA ↑ b.ATP ↓(2) Depression of heart and vessel(Ca2+ transportdisorder; hyperkalemia;ATP↓): cardiac output ↓ ; cardiac arrhythmias; peripheral vasodilation.(3) Skin: warm and flashed(4) Alteration of skeleton: decacification, retarding growth andosteodystrophy
  • Respiratory acidosis1) Concept: Concept Primary change : retention of CO2; pH . PaCO2↑2) Classification: Classification Acute RAC Chronic RAC
  • 3) Causes : Disorder of external respiration - Overdosage of sedatives, narcotics,etc. Cerebrovascular accidents. Cardiopulmonary arrest Central nervous system trauma, infections Poliomyelitis Inhalation of foreign bodies Chronic obstructive pulmonary disease Asthma Pneumonia Increased CO2 inhalation –
  • 4) Compensation: Compensation In acute RAC: ion exchange across the membrane andbuffering in cell
  • ( somatic cell )CO2+H2O H2CO3 HCO3- + H+ H++A- HA K+ K+
  • In chronic RAC: excretion of more H+ and ammonia ion reabsorption of more HCO3- inkindneys
  • The Central Role of the Carbonic Acid-Bicarbonate Buffer System in the Regulation of Plasma pH Figure 27.11a
  • 5) Effects: Effects (1) Neurological effects: CO2 narcosis (2) Cardiovascular effects: arrhythmias; pulmonary artery hypertension; cardiac output decrease. (3) Inducting of hyerkalemia and hypochloremia6) principle of treatment: improve ventilation
  • Metabolic alkalosis1) Concept: Concept Primary disturbance [HCO3-] ↑ ; PH . PaCO2 ↑2) Classification: Chloride – responsive Chloride – resistant
  • 3) Causes and mechanism: mechanism Mechanism: Mechanism a. Excessive gain of alkali (bicarbonate) b. Excessive loss of hydrogen ions,chloride or potassium ions
  • Causes:a.Excessive gain of alkali (bicarbonate)Bicarbonate intake:treatment of MACcitrate-containing blood transfusionsParenteral solution containing lactateb.Excessive loss of hydrogen ions, chloride orpotassium ionsGastrointestinal H+ loss:vomiting,gastric suctionRenal H+ loss:Aldosteronism,cushing’s syndromethiazidec.Volume contractionDehydrationDiuretic therapy
  • 4) Compensation: Compensation Blood buffer role limitation Respiratory regulation Ion exchange and H+ out cell to titrate bicarbonate Renal role: excluding bicarbonate and conserving H +5) Effects: Effects (1) Hypoventilation→ PaCO2 ↑, PaO2 ↓ (2) Agitation of central neural system: GABA↓ → seizures (3) Increase excitability of the neuromuscle: free [Ca2+] decrease→ muscle tremors (4) Mental dysfunction: O2 dissociated curve leftshift → impairingO2 release → ATP ↓. At 6-8 hs, 2,3-DPG↑ and curve shifts backtowards the right. (5) Hypokalemia → reduced fibrillation threshold
  • 6) Principle of treatment: treatmenta. Etiology treatmentb. Administration of KCl. or spironolactone ifK+ and Cl- deficits are presentc, Carbonic anhydrase inhibitor:acetazolamide
  • Respiratory alkalosis1) Concept: Concept Primary change : H2CO3 ↓ or PaCO2 ↓ ; pH2) Classification: Classificationa. Acute RALb. Chronic RAL
  • 3) Causes and mechanisms: mechanisms Mechanisms: Hyperventilation Causes:a. Psychogenic hyperventilation:Hysteriab. Stimulation of respiratory center: High altitude hypooxia Salicylate toxication Blood ammonia↑(Hepaticencephalopathy) Encephalitis Brain injury Fever
  • 4) Compensation: Compensation In acute RAC: Ion exchange, H+ out of cell to titrate base in ECF In chronic RAC: Decreased excretion of H+ and NH4+ Decreased reabeorption of HCO3-5) Effects: Effects(1) Increased excitability of the nerve and muscle(2) Mental dysfunction(3) Hypokalemia,hypochloridemia6) Principle of treatment: treatment a. Decreased ventilation by administration ofsedative. b. Application of a plastic bag to inspire more
  • The Central Role of the Carbonic Acid-Bicarbonate Buffer System in the Regulation of Plasma pH Figure 27.11b