Approaches to UnderstandingElectrolyte and Acid-Base Physiology Dr A.Hadi Martakusumah SpPD-KGH Sub Division of Nephrology and Hypertension Department of Internal Medicine Padjadjaran University/Hasan Sadikin General Hospital Approaches to Understanding Acid- Base Physiology Traditional Approach The discussion of acid-base physiology outlined in most of this lecture is the ‘traditional’ empirical approach. The concepts and explanations of this approach are still the most common way that acid-base physiology is taught and understood by many clinicians to some extent Physico-chemical Approach An alternative approach derived from physico-chemical principles was proposed by Stewart in 1981 Basic Principles of the Various Theories of Acids & Bases Traditional Acid: a substance that has certain properties (eg sour taste, turns litmus approach red) Arrhenius Acid : H + in aqueous solution Base : OH- in aqueous solution At neutrality: [H+] = [OH-] Bronsted-Lowry Acid : H+ donor Base : H+ acceptor Conjugate acid-base pairs Lewis Acid : a potential electron-pair acceptor Base : a potential electron-pair donor Usanovich Acid: a substance that donates a cation, or accepts an anion or an electron Base: a substance that donates an anion, or accepts a cation. Water 60-90% of body weight for most life forms Essential nutrient to sustain life often neglected Good solvent NaCl attraction of ions (Na+ and Cl-) to water > attraction to each other Cohesion one water molecule capable of bonding with 4 others Water Highly reactive disassociation of water mass of H is small = proton jumping H+ H+ H+ H+ O- O- OH- + H3O + TBW as % of ECF as % of ICF as % Age body weight body weight body weight Premature 75-80 Newborn 70-75 50 35 1 Year Old 65 25 40-45 Adolescent 60 20 40-45 Male Adolescent 55 18 40 Female Adapted from Feld. (1988) RULE OF THIRD Body Weight 1/3 Total Body Water ICF ECF 1/3 Intravascular Interstitial Volume Volume 1/3 8 THE INTEGRATED VOLUME RESPONSE Perubahan Perubahan hemodinamik keseimbangan Sistemik garam + air Respons Tachycardia Haus Resistensi Retensi air dan Perifer Natrium oleh meningkat Ginjal Onset Menit Jam Aktifator Katekolamin Katekolamin Angiotensin ADH Penyebab Utama Dehidrasi Melalui Ginjal (Renal): Tidak melalui Ginjal (Extra Gangguan hormon Renal ) Diabetes Insipidus Perdarahan Penyakit Addison Melalui kulit : Gangguan tubulus : Keringat Renal Tubular Acidosis Luka Bakat (RTA) Steven Jhonson’s syndr Penyalah gunaan diuretika Melalui Traktus GI Post Obstruksi Mual muntah PNC Diare Diuresis Osmotik Fistula DM NGT Pemberian Mannitol Terapi Dehidrasi Cairan yang diberikan : NaCl 0,9 % Ringer Laktat Elektrolit Natrium dan Kalium Intra Sel Ekstra Sel + [Na + ] = 140 meq/L [Na ] = 20 meq/L [K + ] = 120 meq/L [K + ] = 4 meq/L Algoritme pendekatan Pasien dengan Hiponatremia Gejala Hiponatremia Susunan Saraf Pusat : Ringan Sakit Kepala Apatis Lethargy Sedang Agitasi Bingung dan disorientasi Psikosis Berat Sopor sampai Koma Pernafasan Cheyne Stoke Kematian Gejala Hiponatremia Saluran Cerna : Hilang nafsu makan Mual Muntah Sistim Muskulo Skeletal : Kramp Refleks tendon menghilang Tiga hal yang harus diperhatikan sebelum melakukan terapi Hiponatremia Apakah penderita menunjukkan gejala hiponatremia (simptomatik)? Sudah berlangsung berapa lama hiponatremia tersebut ? Akut ? Kronik ? Apakah penderita mempunyai faktor resiko untuk gangguan neurologis ? TERAPI HIPONATREMIA Kecepatan Terapi harus disesuaikan dengan kecepatan terjadinya hiponatremia Terapi harus agresif pada kasusHiponatremia Akut Terapi lebih lambat pada kasus Hiponatremia Kronik Terapi Hiponatremia Akut (Terjadi < jam) Naikkan kadar Na serum sebanyak 2 mmol/L/jam sampai gejala klinis menghilang Koreksi sampai kadar Na serum normal mungkin AMAN tapi biasanya TIDAK PERLU Terapi Hiponatremia Kronik (Terjadi pada kurun > 48 jam) Mula mula Naikkan kadar serum sebanyak 10% dari kadar awal atau 10meq/L dari kadar awal Lakukan pemeriksaan neurologis yang ketat .Kecepatan koreksi diperlambat jika ada perbaikan dalam gejala klinis Setiap saat Kecepatan Koreksi tidak boleh melebihi kadar 1,5 meq/L/jam atau kenaikan melebihi 15 meq per hari Periksa kadar Na serum dan Urine setiap 2 jam Periksa kadar kation urine (UNa + UK) . Kadar ini harus lebih rendah dari kadar Natrium yang diinfuskan. Untuk menjaga pengeluaran free water . Kalium Kadar normal dalam serum 3,5 – 5,5 meq/L Asupan normal 50 – 100 meq/hari Pengatur kadar kalium serum : Shift intra sel Ginjal Traktus gastro intestinal Jumlah K+ Ekstra Sel = 2% dari seluruh K+ total Hypokalemia without total body K depletion Hypokalemia with total body k depletion Treatment of hypokalemia Indikasi Pemberian Kalium Parenteral Disritmia Paralisis Otot Pernafasan Hipokalemia pada penderita Ensefalopati Hepatik Kadar kalium serum sangat rendah < 2 meq/L Diagnostic approach to Hyperkalemia Treatment of Hyperkalemia The Composition of the Human Body Figure 27.1a Strong Ions Cations Anions Na+ Cl- K+ SO4- Ca++ Lactic acid Mg++ Disassociate into ions in solution pH The term pH was coined by the Danish chemist, Soren Peter Sorensen in 1909 to refer to the negative log of hydrogen ion concentration the symbol pH meaning ‘potenz’ (power) of Hydrogen. pH = -log [H3O+] H3O+ > OH- = acidic OH- > H3O+ = basic pH = - log10 aH+ (or: aH+ = 10 (-pH) ) where aH+ is activity of H+ Relationship between pH & [H+] pH [H+] (nanomoles/l) 6.8 158 6.9 125 7.0 100 7.1 79 7.2 63 7.3 50 7.4 40 7.5 31 7.6 25 7.7 20 7.8 15 Cations and Anions in Body Fluids Figure 27.2 Normal Kation (mEq/L) Anion (mEq/L) Na+ 140 Cl– 103 K+ 4 HCO 3– 25 Ca + + 5 Protein 16 Mg + + 2 Organic 4 H+ 0.000040 Other 3 (40 nmol/L) Inorganic H+ and the Potential Threat to survival The free [H + ] is tiny and must be kept so for survival A very large accumulation of [H + ] may kill by binding to proteins in cells and changing their charge ,shape and possibly their function Acid-Base Balance Each day there is always a net production of acid by the body’s metabolic processes To maintain balance, these acids need to be excreted. The acids produced by the body are classified as : respiratory (or volatile) acids metabolic (or fixed) acids. Basal Carbon Dioxide Production Consider a resting adult with an oxygen consumption of 250 mls/min and a CO2 production of 200 mls/min (Respiratory quotient 0.8): Daily CO2 production = 0.2 x 60 x 24 l/day divided by 22.4 l/mole = 12,857 mmoles/day. Metabolic or Fixed Acids This term covers all the acids the body produces which are non-volatile. Because they are not excreted by the lungs they are said to be ‘fixed’ in the body. All acids other then H2CO3 are fixed acids. These acids are usually referred to by their anion (eg lactate, phosphate, sulphate, acetoacetate or b- hydroxybutyrate). Net production of fixed acids is about 1 to 1.5 mmoles of H+ per kilogram per day: About 70 to 100 mmoles of H+ per day in an adult. This non-volatile acid load is excreted by the kidney Dietary acid-base Impact Nutrient Product [H + ] (mmol/day ) Reactions generating [H + ] Sulfur-containing amino acid -Cysteine/cystinine,methionine [H + ] 70 Cathionic amino acids -Lysine,arginine,histidine [H + ] 140 Organic phosphates HPO42- +[H + ] 30 Reactions removing [H + ] Anionic amino acid -Glutamate ,aspartate HCO3- -110 Organic anions eg citrate HCO3- -60 Organic phosphate excretion H2PO42- -30 with [H + ] NET TOTAL [H + ] to be excreted as NH4+ 40 Role of the Kidneys The lungs are important for excretion of carbon dioxide (the respiratory acid) and there is a huge amount of this to be excreted: at least 12,000 to 13,000 mmols/day. In contrast the kidneys are responsible for excretion of the fixed acids and this is also a critical role even though the amounts involved (70- 100 mmols/day) are much smaller. The main reason for this renal importance is because there is no other way to excrete these acids and it should be appreciated that the amounts involved are still very large when compared to the plasma [H+] of only 40 nanomoles/litre. There is a second extremely important role that the kidneys play in acid-base balance, namely the reabsorption of the filtered bicarbonate. Role of the Kidneys In acid-base balance, the kidney is responsible for 2 major activities: Reabsorption of filtered bicarbonate: 4,000 to 5,000 mmol/day Excretion of the fixed acids (acid anion and associated H+): about 1 mmol/kg/day. Terminology of Acid-Base Disorders Acidosis – an abnormal process or condition which would lower arterial pH if there were no secondary changes in response to the primary aetiological factor. Alkalosis – an abnormal process or condition which would raise arterial pH if there were no secondary changes in response to the primary aetiological factor. Simple Disorders are those in which there is a single primary aetiological acid-base disorder. Mixed Disorders are those in which two or more primary aetiological disorders are present simultaneously. Acidaemia - Arterial pH < 7.36 (ie [H+] > 44 nM ) Alkalaemia - Arterial pH > 7.44 (ie [H+] < 36 nM ) The Anion Gap Anion gap = [Na+] - [Cl-] - [HCO3-] Reference range is 8 to 16 mmol/l. An alternative formula which includes K+ is : AG = [Na+] + [K+] - [Cl-] - [HCO3-]. Other Cations Unmeasured Anions Other Anions Proteins (15 mEq/L) A- Organic Acids (5 mEq/L Phosphates (2 mEq/L) HCO3- Sulfates (1mEq/L) UA = 23 mEq/L 25 Na + Unmeasured Cations 140 Calcium (5 mEq/L) Potassium (4.5 mEq/L) Cl - Magnesium (1.5 mEq/L) 103 UC = 11 mEq/L Anion gap = [Na+] - [Cl-] - [HCO3-] Other Cations When an Other Anions acid such A- lactic L- acid is Added Anions added HCO3- The HCO3- will fall Na + and 140 replaced by lactate Cl - anion 103 Metabolic Acidosis with increased anion gap Other Cations Other Anions Other Anions A- A- A- L- Added Anions HCO3- 25 HCO3- Na + 140 Cl - 103 Normal AG Increased AG Other Cations Note that Other Anions with a loss A- of HCO3- NaHCO3 HCO3- will fall but no new anions Na + will be added 140 Cl - Metabolic Acidosis with normal anion gap Other Cations Other Anions Other Anions Other Anions A- A- A- A- L- Added Anions HCO3- HCO3- 25 HCO3- Na + 140 Cl - Cl - Cl - 103 Normal AG Increased AG Normal AG The Basic Relationship between PCO2 and Plasma pH Figure 27.6 Mechanisms of pH control Buffer system consists of a weak acid and its anion Three major buffering systems: 1. Protein buffer system Amino acid H+ are buffered by hemoglobin buffer system 2. Carbonic acid-bicarbonate Buffer changes caused by organic and fixed acids 3. Phosphate Buffer pH in the ICF Protein buffer system If pH climbs, the carboxyl group of amino acid acts as a weak acid If the pH drops, the amino group acts as a weak base Hemoglobin buffer system Prevents pH changes when PCO2 is rising or falling Figure 27.8 Amino Acid Buffers Figure 27.8 Carbonic Acid-Bicarbonate Buffering System Carbonic acid-bicarbonate buffer system CO2 + H2O H2CO3 H+ + CO3– Has the following limitations: Cannot protect the ECF from pH changes due to increased or depressed CO2 levels Only functions when respiratory system and control centers are working normally It is limited by availability of bicarbonate ions (bicarbonate reserve) The Carbonic Acid-Bicarbonate Buffer System Figure 27.9a, b Maintenance of acid-base balance Lungs help regulate pH through carbonic acid - bicarbonate buffer system Changing respiratory rates changes PCO2 Respiratory compensation Kidneys help regulate pH through renal compensation Kidney tubules and pH Regulation Figure 27.10a, b Kidney tubules and pH Regulation Figure 27.10c The Central Role of the Carbonic Acid- Bicarbonate Buffer System in the Regulation of Plasma pH Figure 27.11a The Central Role of the Carbonic Acid- Bicarbonate Buffer System in the Regulation of Plasma pH Figure 27.11b Rates of correction Buffers function almost instantaneously Respiratory mechanisms take several minutes to hours Renal mechanisms may take several hours to days Acid-Base Disorders Respiratory acid-base disorders Result when abnormal respiratory function causes rise or fall in CO2 in ECF Metabolic acid-base disorders Generation of organic or fixed acids Anything affecting concentration of bicarbonate ions in ECF Respiratory acid-base disorders Respiratory acidosis Results from excessive levels of CO2 in body fluids Respiratory alkalosis Relatively rare condition Associated with hyperventilation Respiratory Acid-Base Regulation Figure 27.12a Respiratory Acid-Base Regulation Figure 27.12b Metabolic acid-base disorders Major causes of metabolic acidosis are: Depletion of bicarbonate reserve Inability to excrete hydrogen ions at kidneys Production of large numbers of fixed / organic acids Bicarbonate loss due to chronic diarrhea Metabolic alkalosis Occurs when HCO3- concentrations become elevated Caused by repeated vomiting The Response to Metabolic Acidosis Figure 27.13 Metabolic Alkalosis Figure 27.14 Detection of acidosis and alkalosis Diagnostic blood tests Blood pH PCO2 Bicarbonate levels Distinguish between respiratory and metabolic A Diagnostic Chart for Acid-Base Disorders Figure 27.15 Clinical Acid Base Problem Solving Langkah Pertama : Harus tahu harga normal parameter yang akan digunakan untuk menganalisis kelainan asam basa : a. pH 7.40 atau [H+ ] 40 nmol/L Cara merubah pH kedalam [H+ ] : Buang angka tujuh dan desimalnya jadi misal pH 7.26 didapat 26 Kurangi 40 dengan nilai tersebut jadi 40 – 26 = 14 Tambahkan 40 kedalam harga tersebut : 40 + 14 = 54 nmol/ b. pCO2 = 40 mm Hg c. [HCO3] = 25 mmol/L d. Anion gap plasma Na-Cl-[HCO3] = 12 mEq/L jika kadar albumin normal yaitu 4 gr% . Setiap penurunan albumin 1 gram % dari harga normal maka kadar AG dikurangi 4 Clinical Acid Base Problem Solving Langkah Kedua : Apakah ada Lab Error ? Cara mengetahuinya adalah masukkan harga PH , pCO2 dan [HCO3] kedalam persamaan Henderson di bawah ini : [H+ ] = pCO2 X 24/ [HCO3] Jika penderita tidak demam dan harga [HCO3 ] yang dihitung dan yang diukur berbeda lebih dari 10% maka ada lab error . Kita harus mengulangi pemeriksaan. Kita tidak ingin menganalisis hasil AGD berdasarkan hasil laboratorium yang salah . Clinical Acid Base Problem Solving Langkah Ketiga : Tetapkan hasil pH : Acidemia jika kurang dari 7.36 Alkalemia jika lebih dari 7.44 Clinical Acid Base Problem Solving Langkah Keempat : Tentukan apakah kelainan primernya respiratorik atau metabolik Alkalemia : Respiratory Alkalemia jika pCO2 kurang dari 38 Metabolic Alkalemia jika [HCO3] lebih dari 25 Acidemia : Respiratory Acidemia jika pCO2 lebih dari 44 Metabolic Acidemia jika [HCO3 ] kurang 25 Clinical Acid Base Problem Solving Langkah Kelima : Hitung anion gap (AG) serum yaitu : Kadar Na serum – ( Cl + [HCO ] serum 3 Jika AG > 10 ada kemungkinan Other Cation Other Anion metabolic acidemia A- HCO3- Jika AG > 20 dapat dipastikan (25) ada metabolic acidemia Na+ Jangan lupa factor albumin ! (140) Cl- (103) Clinical Acid Base Problem Solving Langkah Keenam : Check derajat kompensasi tubuh : Metabolic Acidemia : Setiap penurunan pCO2 = 1.3 X penurunan [HCO3] Metabolic Alkalemia : Setiap kenaikan pCO2 = 0.6 X kenaikan [HCO3] Respiratory Acidemia : Akut : Setiap pCO2 naik 10 mmHg = [HCO3] naik 1 mEq/L Kronik : Setiap pCO2 naik 10 mmHg = [HCO3] naik 4 mEq/L Respiratory Alkalemia : Akut : Setiap pCO2 turun 10 mmHg = [HCO3] turun 2 mEq/L Kronik : Setiap pCO2 turun 10 mmHg = [HCO3] turun 5 mEq/L Clinical Acid Base Problem Solving Langkah Ketujuh : Determine Delta ratio (Delta gap) = (Increase in anion gap / Decrease in bicarbonate) Guidelines for Use of the Delta Ratio in Metabolic Acid-Base Disorders Delta Ratio Assessment Guideline < 0.4 Hyperchloraemic normal anion gap acidosis 0.4 - 0.8 Consider combined high AG & normal AG acidosis Ratio often <1 in acidosis assoc. with renal failure 1 to 2 Usual for uncomplicated high-AG acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss (esp if patient not dehydrated) >2 Suggests pre-existing elevated HCO3 level: consider a concurrent metabolic alkalosis or a pre-existing compensated respiratory Other parameter to consider The Urinary Anion Gap The cations normally present in urine are Na+, K+, NH4+, Ca++ and Mg++. The anions normally present are Cl-, HCO3-, sulphate, phosphate and some organic anions. Only Na+, K+ and Cl- are commonly measured in urine so the other charged species are the unmeasured anions (UA) and cations (UC). Cl- + UA = Na+ + K+ + UC Urinary Anion Gap = ( UA - UC ) = [Na+]+ [K+] - [Cl-] Urinary Anion Gap Clinical Use Key Fact: The urinary anion gap can help to differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis. It has been found experimentally that the Urinary Anion Gap (UAG) provides a rough index of urinary ammonium excretion. Urinary Anion Gap Clinical Use In a patient with a hyperchloraemic metabolic acidosis: A negative UAG suggests GIT loss of bicarbonate (eg diarrhoea) A positive UAG suggests impaired renal distal acidification (ie renal tubular acidosis). As a memory aid, remember ‘neGUTive’ - negative UAG in bowel causes Osmolar Gap Osmolar gap = (Measured osmolality) - (Calculated osmolarity) 2 [Na+] + Glucose ( mmol/L) + Urea N (mmol/L) 0R 2 [Na+] + Glucose( mg% /18) + Urea N(mg% /2.8) The osmolar gap can be very useful in assisting diagnosis in metabolic acidosis due to toxic alcohols & glycols (eg ethylene glycol, methanol). Common Causes of Metabolic Acidosis Increased Anion Gap (Think…”MUDPILES”) Methanol intoxication* Uremic acidosis (advanced renal failure) Diabetic ketoacidosis* Paraldehyde intoxication Iron overdose L-lactic acidosis* Ethylene glycol intoxication* Salicylate intoxication D-lactic acidosis Alcoholic ketoacidosis* *Denotes most common Common Causes of Metabolic Acidosis Normal anion gap Mild to moderate renal failure* Gastrointestinal loss of HCO3- (acute diarrhea)* Type I (distal) renal tubular acidosis Type II (proximal) renal tubular acidosis Dilutional acidosis Treatment of diabetic renal tubular acidosis* Ketones lost in urine *Denotes most common Common causes of Metabolic Alkalosis Net loss of H+ from the ECF G.I. Loss Vomiting or nasogastric suctioning Chloride losing diarrhea: chronic diarrhea/laxative abuse Renal loss Loop or thiazide type diuretics esp. in CHF and cirrhosis Mineralocorticoid excess Hyperaldosteronism Cushing’s syndrome Common causes of Metabolic Alkalosis Retention of HCO3- Excess administration of NaHCO3 Milk-alkali syndrome: antacids, milk, NaHCO3 Massive (>8 units) blood transfusion (citrate) Posthypercapnia metabolic alkalosis (after correction of chronic respiratory acidosis) Mixed acid-base disorders Two or more simple acid-base disorders coexist Metabolic acidosis + Respiratory Metabolic Acidosis + Respiratory Acidosis Alkalosis pH usually very low pH may be near normal Pa CO2 too high Pa CO2 too low HCO3- too low HCO3- too low Metabolic Alkalosis + Respiratory Metabolic Alkalosis + Respiratory Alkalosis Acidosis pH usually very high pH may be near normal Pa CO2 too low Pa CO2 too high HCO3- too high HCO3- too high
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