Acido-basic disorders Spac Jiri Hendersonova-Hasselbalchova equation > • pKa = 6,1 • [HCO3-] = 24 mmol.l-1 • [H2CO3] = 1,2 mmol.l-1 > Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory system and the control of plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Normal acido-basic homeostasis Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms Preanalytic phase The most suitable sample is arterial blood. Most often it is taken from a. Radialis into a capillary on a thin needle or into a modified syringe; lithium heparin is used as an anticoagulant. In the intensive care units, an arterial catheter is often inserted to allow repeated donations. In any case, ensure that the sample is taken without air bubbles. . Preanalytic phase arterialized capillary blood, most commonly from the fingertip or the earlobe. The capillary sample should be composed as much as possible of arterial blood. Therefore, it is necessary to increase the blood flow through the capillaries at the place of collection (“arterialization”) - by heating, massages, etc. as much as possible venous blood should be sampled from the central venous bed (central venous catheter, port). Peripheral venous blood does not adequately report the overall metabolic status of the organism, especially in patients with severe centralized circulation. Central venous blood is collected into a syringe with balanced lithium heparin, even in this case the collection must be anaerobic. The actual pH is determined electrochemically, typically by a miniaturized glass electrode. The partial pressure of carbon dioxide (pCO2) is determined electrochemically by a Severinghaus electrode. It is also a glass electrode but is coated with a layer of water and separated from the sample by a gas permeable membrane. CO2 from the sample diffuses through the semipermeable membrane into distilled water, the pH of the resulting solution depends on pCO2. Current and standard bicarbonates are calculated from the measured pH and pCO2 values, Current HCO3 - This parameter indicates the current concentration of bicarbonate in the blood being examined. Since it depends on both the metabolic and respiratory components of acid-base balance, its interpretation is complicated. Standard HCO3 - what would be the concentration of bicarbonate in the blood sample examined after elimination of the respiratory disorder, ie after saturation of the blood to pCO2 = 5.3 kPa. It therefore only informs about the metabolic component of the acid-base balance. Base excess, BE evaluates only the metabolic component of the acid-base balance. It is defined as the amount of strong acid that would need to be added to the sample to reach a pH of 7.4, provided that the respiratory disorder ABR (ie pCO2 = 5.3 kPa) is excluded. In metabolic acidosis, a strong base would have to be added; the corresponding parameter is referred to as base deficiency, base deficiency, BD, or (more often) expressed as negative BE. logo D:\SCContent\9780443100574\graphics\fullsize\F00574-016-f011.jpg Downloaded from: StudentConsult (on 18 September 2008 02:34 PM) © 2005 Elsevier Acidosis Metabolic acidosis – increased H+, decreased HCO3- Respiratory acidosis – increased H+, increased PaCO2 Simple metabolic acidosis Compensation of metabolic acidosis ABR and electroneutrality lElectroneutrality must be maintained l lDeviations in ion concentration are most easily compensated by changing the HCO3- Ca2+ Na+ K+ Mg2+ Cl– HCO3- prot- SO42-, HPO42-, laktát, ketokyseliny Anion gap (AG) Na+ K+ Cl– HCO3- AG •The difference between main measured cations (Na + K) and the measured anions (Cl + HCO3) •Normally 13 to 15 mmol/l •Unmeasured anions (P- - albumin, SO4, PO3, ORG- ) Na – (Cl+HCO3) = anion gap •High anion gap (normal Cl) –Increased unmeasured anions (albumine, inorganic, organic) Acid-base disorders •Metabolic acidosis lead to hyperkalaemia –Shift H/K or Na • •Decrease of 0,1 PH increase plasma K by 0,6 mmol/l –Diabetic ketoacidosis, lactic acidosis, diarrhea and RTA often associated with low K intracellulary !! Metabolic acidosis – clinical features •Increased ventilation (Kussmauls) •Increased tachycardia •Decreased cardiac contractility •Periferal arterial dilatation + central venous contraction → pulmonary edema with minimal overload •CNS – headache, lethargy, stupor, coma Causes of metabolic acidosis 1 •Disorder Mechanism •Normal anion gap •Inorganic acid addition Therapy or poisoning with NH4Cl, HCl •Gastrointestinal base loss Loss of HCO3 in diarrhoea, small bowel fistula, urinary diversion procedure •Renal tubular acidosis Urinary loss of HCO3 in proximal RTA, impaired tubular acid secretion in distal RTA Causes of renal tubular acidosis •Type Examples •Proximal RTA (type 2) Congenital (Fanocon, cystinosis, Wilsons disease) • Paraproteinaemia, amyloidosis • Heavy metal toxicity (Pb, Cd, Hg) • Hyperparathyreosis • Carboanhydrase inhibitors (ifosfamide) • •Classical distal RTA Congenital, hyperglobulinaemia, •(type 1) Autoimunne connective tissue disease (SLE) • Toxins and drugs (toluene, lithium, amphotericin) • •Hyperkalemic distal RTA Hypoaldosteronism, •(type 4) Obstructive nephropathy • Drugs (amiloride, spironolactone) • Renal transplant rejection Acid-base disorders Disturbance Blood PH Primary change Compensatory response Predicted compensation Metabolic acidosis < 7,40 HCO3 < 24 mmo/l PCO2 < 5,33 kPa PCO2 fall in kPa = 0,16 x HCO3 fall in mmol/l Metabolic alkalosis > 7,40 HCO3 > 24 mmol/l PCO2 > 5,33 kPa PCO2 rise in kPa = 0,08 x HCO3 rise in mmol/l Respiratory acidosis < 7,40 PCO2 > 5,33 kPa HCO3 > 24 mmol/l Acute: HCO3 rise in mmol/l = 0,75 x PCO2 rise in kPa Chronic: HCO3 rise in mmol/l = 2,62 x PCO2 rise in kPa Respiratory alkalosis > 7,40 PCO2 < 5,33 kPa HCO3 < 24 mmo/l Acute: HCO3 fall in mmol/l = 1,50 x PCO2 fall in kPa Chronic: HCO3 fall in mmol/l = 3,75 x PCO2 fall in kPa PH of 7,4 = H+ of 40 nmol/l PCO2 of 5,33 kPa = 40 mmHg, PCO2 does not rise above 7,33 kPa (55 mmHg), not adequate oxygenation Simple respiratory acidosis Acute compensation of respiratory acidosis Chronic compensation of respiratory acidosis Causes of respiratory acidosis •Severe pulmonary disease •Respiratory muscle fatigue •Increase of PaCO2 (central respiratory control) •Renal compensation by reabsorbtion of bicarbonate (about 3 days) • Respiratory acidosis clinical features •Acute –Anxiety, dyspnoea, halucination, coma • •Chronic –Sleep disturbances, sleep inversion somnolence, loss of memory, tremor, myoclonics jerks, asterixis Respiratory acidosis treatment •Acute –Adequate alveolar ventilation –Intubation, mechanical ventilation –Oxygen administration titrate carefully in CHOPD –No rapid correction (respiratory alcalosis symptoms) –Sufficient Cl and K to enhance renal excretion of bicarbonate •Chronic –Improve lung function (bronchodilatans, glucocorticoids, diuretics) Alkalosis Metabolic alkalosis – decreased H+, increased HCO3- Respiratory alkalosis – decreased H+, decreased PaCO2 Causes of respiratory alcalosis •Hyperventilation •Critically ill patients •Mechanical ventilation •2 to 6 hour hypocapnia → decrease of renal amonium and titrable acid excretion •Full adaptation take several days •Many causes and diseases –Drugs (salycilates, methylxantines) direct stimulation of respiration –Progesterone (gravidity) –Liver failure –Gramnegative septikaemia before fever with hypotension and hypoxemia Simple metabolic alkalosis Compensation of metabolic alkalosis Causes of metabolic alkalosis 1 •Exogenous bicarbonate load –Milk alkali syndrome –Acute alkali administration • •Effective ECFV contraction, normotension, K deficiency and secondary hyperreninemic hyperaldosteronism –Gastrointestinal origin •Vomiting, gastric aspiration •Congenital chloridorhea •Villous adenoma –Renal origin •Diuretic, edematous states, posthypercapnic state, recovery of acidosis •Hypercalcemia/hypoparthyreoidism, Mg, K deficiency •Barttters syndrome –Gitemans syndrome Causes of metabolic alkalosis 1 •ECFV expansion, low K, hypertension –High renin •Renal artery stenosis, accelerated hypertension •Renin secreting tumors, estrogen therapy –Low renin •Primary aldosteronism –Adenoma, primary hyperplasia, carcinoma •Adrenal enzyme defects –11 beta hydrochylase deficiency –17 alfa hydroxylase deficiency •Cushings syndrome –Ectopic corticotropin –Adrenal adenoma –Primary pituitary •Other –Licorice, carbenoxolone, chewers tobaco –Liddles syndrome Metabolic alkalosis clinical features •Changes in central and peripheral nervous system –Similar to those hypocalcemia –Mental confusion, obtundation, seizures –Paresthesia, muscular cramping, tetany, aggravation of arrythmias •Hypoxemia in chronic obstructive pulmonary disease •Hypokalemia and hypophosphatemia Metabolic alkalosis treatment •Correcting the underlying stimulus for generating bicarbonate –Discontinuation of diuretics –H2 blockers or proton pump blockers •Remove the factors that sustain bicarbonate reabsorption –ECF contraction –K deficiency • •ECF expansion (NaCl, KCl) •Acetazolamide •Arginin hydrochloride •NH4Cl oraly •Hemodialysis Simple respiratory alkalosis Acute compensation of respiratory alkalosis Chronic compensation of respiratory alkalosis Respiratory alkalosis clinical features •Reduced cerebral blood flow –Dizziness, mental confusion, seizures •Cardiac arrhythmias –Intracellular shift of Na, K –Decreased Ca2+ •Paresthesia, circumoral numbness, tetany Respiratory alkalosis treatment •Ventilator management (dead space, tidal volume and frequency) •Rebreathing from paper bag •Betablockers in hyperadrenergic states Na (140) + K (5) = Cl (105) – HCO3 –(25) + Gap (15) If Gap > 30 – clinically important acidosis Summary •Individualize patient and correcting underlying stimulus •ECF volume clinical examination (contraction or edema) •Laboratory plasma –Na, K, Cl, Ca, Mg, –Proteins and albumin, urea, kreatinin, AST,ALT –Bicarbonate –PaCO2 •Laboratory urine –Na, K, Cl, free water, Ca –Poisoning