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.
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 acidFast / 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
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