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Blood Gas Interpretation
- 9. pH = 7.4 PaC02 = 40 HCO3 = 24
- 10. Approach 1. How is the oxygenation? 2. What is the pH? 3. Is there a respiratory component? 4. Is there a metabolic component? 5. Is there compensation?
- 11. How is the oxygenation? Pa02 A-a gradient P:F ratio
- 12. •pulmonary veins
- 13. A-a Gradient PA02 – Pa02 PA02 = (Fio2 x (Patm – PH20)) – (PaCo2/RQ) = (Fio2 x (760 - 47)) – (PaC02/0.8)
- 14. P:F Ratio pa02/Fio2 For ARDS: Mild: 200 – 300 Moderate 100 – 200 Severe < 100
- 15. What is the pH? pH = 7.4 pH > 7.4 Alkaemia pH < 7.4 Acidaemia
- 16. Is there a respiratory component? PaCO2 with pH = respiratory acidosis PaCO2 with pH = respiratory alkalosis Normal pH + abnormal PaCO2 : Two opposing primary acid-base disorders OR Primary respiratory disturbance + metabolic compensation
- 17. Is there a metabolic component? HCO3 + pH = metabolic alkalosis HCO3 + pH = metabolic acidosis What is the anion gap? What is the delta ratio?
- 18. Is there compensation? Acute Chronic Respiratory Acidosis Respiratory Alkalosis For every 10mmHg change in CO2 HCO3 ↑1 HCO3 ↑4 HCO3 ↓2 HCO3 ↓5
- 19. Metabolic Acidosis Metabolic Alkalosis C02 = 1.5 x HCO3 + 8 (+/- 2) CO2 = 0.7 x HCO3 + 20 (+/- 5)
- 20. Anion Gap Na+ 140 Cl- 104 HCO3 - 24 A- CATIONS ANIONS K+ ANION GAP (~12)
- 21. Raised Anion Gap Na+ 140 Cl- 104 HCO3 - 24 A- CATIONS ANIONS K+ ANION GAP (~12) A- HCO3 -16 ANION GAP (~20) H+ + HCO- 3 ↔ H2CO3 ↔ H20 + CO2
- 23. Normal Anion Gap Na+ 140 Cl- 104 HCO3 - 24 A- CATIONS ANIONS K+ ANION GAP (~12) HCO3 -16 Cl- 114
- 24. Normal Anion Gap
- 25. Urinary Anion Gap Na + K - Cl Approximation of ammonium excretion Positive: Renal Ne‘GUT’ive: GIT
- 26. Delta Ratio HCO- 3 AG < 0.4: NAGMA 0.4 – 0.8: mixed NAGMA + HAGMA 1-2: pure HAGMA > 2: HAGMA + metabolic alkalosis or pre-existing compensated respiratory acidosis
- 27. Anion Gap HAGMA Delta Ratio Osmolar gap, ketones, lactate NAGMA UAG Positive: Renal Negative: GIT
- 28. Fio2 0.21 pH 7.1 p02 100 mmHg pC02 17 mmHg HCO- 3 5 mmol/L cBase(ECF)c -22 mmol/L Na 130 mmol/L Cl 94 mmol/L Glucose 35 mmol/L Lactate 3 mmol/L
- 29. Fio2 0.21 pH 7.31 p02 100 mmHg pC02 27 mmHg HCO- 3 12 mmol/L cBase(ECF)c -14 mmol/L Na 136 mmol/L Cl 105 mmol/L Glucose 5.3 mmol/L Lactate 1.3 mmol/L
- 30. pH 7.1 pCo2 24 pO2 150 HCO3 8 BE – 18 Na 141 K+ 5.6 Chloride 107 AG 26 Creat 300 Lactate 25 Glucose 4
- 32. ↑ GLYCOLYSIS
- 36. pH 7.1 pCo2 24 pO2 150 HCO3 8 BE – 18 Na 141 K+ 5.6 Chloride 107 AG 26 Creat 300 Lactate 25 Glucose 4
- 37. Fio2 0.4 pH 7.5 p02 58 mmHg pC02 45 mmHg HCO- 3 35 mmol/L cBase(ECF)c 8 mmol/L Na 137 mmol/L Cl 92 mmol/L Glucose 6 mmol/L Lactate 1.0 mmol/L
- 38. Metabolic Alkalosis HCO- 3 H+ + ↓HCO- 3 excretion
- 40. Endogenous: metabolism of ketoacids Exogenous: citrate, antacid, sodium bicarbonate, calcium supplements ↑HCO- 3
- 41. Renal: diuretics, hyperaldosteronism, post- hypercapnoea, Bartter and Gitelman syndrome GIT: vomiting, NGT loss ↓H+
- 43. Fio2 0.4 pH 7.2 p02 60 mmHg pC02 60 mmHg HCO- 3 26 mmol/L cBase(ECF)c 1 mmol/L Na 140 mmol/L Cl 105 mmol/L Glucose 7 mmol/L Lactate 1.0mmol/L
- 44. Respiratory Acidosis Excess C02 in inspired gas Increased production of CO2 Decreased/insufficient alveolar ventilation
- 46. Fio2 0.21 pH 7.44 p02 105 mmHg pC02 30 mmHg HCO- 3 19 mmol/L cBase(ECF)c -4 mmol/L Na 135 mmol/L Cl 104 mmol/L Glucose 5 mmol/L Lactate 1.0 mmol/L
- 47. Respiratory Alkalosis ALWAYS due to increased alveolar ventilation
Editor's Notes
- What is an acid? A substance that dissociates in solution to form hydrogen ions (Arrhenius theory) or a substance that donates a proton (hydrogen ion) (Bronsted-Lowry theory) or a substance that acts as an electron pair acceptor (Lewis theory) What is a base? A substance that dissociates in solution to form hydroxide ions (Arrhenius theory) or a substance that accepts a proton in solution or substance that acts as electron pair donor (Lewis theory)
- What is pH? The negative logarithm to base 10 of the hydrogen ion concentration in solution– measures how acidic or basic a substance is pH = pK + log Base/Acid pH = potential hydrogen pK = negative logarithmic of the dissociation constant – the dissociation constant is a measure of the strength of an acid - ratio of concentration of dissociated form to combined form at equilibrium When pH = pKa the concentration of the conjugate base and acid are equal The smaller the pKa the greater the acidity and stability of conjugate base
- Why is pH important? Body controls pH very tightly – homeostatic mechanisms Optimal enzyme activity in cells is dependent on a certain pH (most enzymes function within a narrow range only of pH) Disrupts cell membranes Required for protein structure and function can interfere with stability and therefore function of protein may become biologically inactive Required for hormone production, release and function (we know noradrenaline doesn’t work if significant acidosis) Required for optimal organ function – cardiac contractions weaker with acidosis, predisposed to arrhythmias, peripheral vasodilatation Required for synapse function
- Buffers: substances which have the ability to minimise changes in pH when an acid or base is added to it .first line – react within seconds, bicarbonate can only buffer metabolic acids not respiratory. Do not eliminate excess acids/base – just minimise changes in pH Bicarbonate buffer: most important for ECF, buffers metabolic acids, relies on respiratory system, open at both ends Protein buffer system: important intra-cellularly, Hb important especially for co2 buffering Phosphate buffer system: has three dissociations with different pKas, important intracellular buffer
- Partial pressure – the pressure that the gas would exert if occupied that same volume on its own ctHb: measures all Hb including oxygenated, deoxygenated, carboxyhaemoglobin, methaemoglobin surrogate of potential 02 carrying capacity NOT effective o2 carrying capacity HCTc_ mathematically produced haematocrit value – ratio between volume of erythrocytes to the volume of whole blood – HCt is proportional to Hb (true if Hb calculated correctly, no intravascular haemolysis and red cells contain expected amount of Hb) So2: fraction of effective haemoglobin which is oxygenated (concentration of oxyhaemoglobin/concentration of effective haemoglobin) F02Hb: fractional oxygenated haemoglobin content - fraction of total Hb which is oxygenated (concentration of oxyhaemoglobin/concentration of total Hb) FC0Hb: fraction of total haemoglobin present as carboxyhaemoglobin – carbon monoxide has > 200 x the affinity for Hb compared to oxygen and isn’t released as easily decreased o2 carrying capacity and also binds to intracellular cytochromes which impairs aerobic metabolism. Also causes oxidative injury, activates inflammatory cascade and lipid peroxidation Symptoms: < 10% none (commonly found in smokers, normal 0.5%), 10 – 20% value or no symptoms, 30 – 40% headache, tachycardia, confusion, weakness, nausea, vomiting, 50 – 60%: coma, convulsions, arrhythmias, ECG changes, 70 -80%: circulatory and ventilatory failure, cardiac arrest and death. Increased absorption if increased CO concentration, decreased barometric pressure, increased activity, increased RR, high metabolic rate or anaemia. Half life decreases with o2. Sources: fire, stoves, heaters, automobile exhaust, charcoal grills, swimming behind motor boat Sats probe will have falsely elevated reading as COHb absorbs red light similar to O2Hb and does not absorb near IR light – probe finds it hard to differentiate between the two – normally calculates a ratio between red and infrared light FHHb: fraction of total haemoglobin present as deoxyhaemoglobin FMetHb: fraction of total haemoglobin present as methaemoglobin – altered state of Hb where Ferrous ions Fe2+ are oxidised to Ferric state Fe3+ and unable to bind oxygen. Normal < 1.2%. Causes: congenital (Hb M disease, cytochrome B5 reductase deficiency), acquired (benzene derivatives, chloroquine, dapsone, prilocaine, metoclopramide, nitrites, sulphonamides) Signs: cyanosis, decreased o2 delivery signs, sats 85 – 90%, chocolate brown blood, normal pao2 3 – 15%: minimal symptoms, 15 – 30%: cyanosis, chocolate brown blood, 30 – 50%: drowsiness, headache, dyspnoea, dizziness, 50 – 70%: seizures, coma, dysrhythmia, tachypnoea, acidosis, ischemia, > 70%: death, severe hypoxia Management: high flow o2, cease precipitants, methylene blue (electron acceptor to facilitate reduction of MetHb) cBase(ECF)c: standard base excess - amount of acid or base required to titrate anaemic blood Hb 50g/L back to a normal pH of 7.4, normal pc02 40mmHg and at 37 degrees – estimate of ECF buffering
- Good to have an approach – like ECGs system makes it less likely to miss things
- O2 Hb dissociation curve: relationship between the partial pressure of oxygen and the oxygen saturation of haemoglobin
- Saturated vapor pressure of water at body temp Normal A-a gradient: alveolar hypoventilation, low inspired oxygen (fio2 < 0.21% or atmospheric pressure < 760mmHg) Raised A-a gradient: diffusion defect, VQ mismatch, right to left shunt, increased o2 extraction Gradient varies with age and fio2 (age/4 + 4) RQ is ratio of co2 produced to oxygen consumed per unit time – glucose has RQ of 1, protein 0.8, fat 0.7
- Used as risk stratification and in severity scoring Ratio of arterial oxygen partial pressure to fractional inspired oxygen At sea level normal PF ratio is 400 – 500mmHg
- Alkalemia/acidemia is excessive base or acid in the blood Alkalosis/acidosis is the process leading to this state
- Ph and HCO3 should move in same direction
- Electroneutrality – cations = anions Most of this anion gap is due to serum proteins – especially albumin (for every 4g/L decrease in albumin there is a 1 decrease in the expected anion gap
- Why does this cause decreased HCO3?? Buffering – acid from the anions combines with HCO3 to produce carbonic acid co2 + h20
- Ketoacidosis (starvation, diabetes, alcohol), lactic acidosis (D or L lactate), renal failure includes citrate toxicity from dialysis, toxins (toxic alcohols, pyroglutamic acidosis, salicylates, citrate toxicity) Short bowel syndrome leads to an increased load of undigested carbohydrates (including simple sugars) in the colon. As a result, the amount of organic acid produced exceeds the amount that can be metabolized by healthy individuals. This leads to an accumulation of organic acids, including SCFA and lactate, resulting in a more acidic environment than normal. Interestingly, the lower pH favours the growth of bacteria responsible for producing D- and L-lactate as they are acid-resistant and this leads to a further decrease in the pH thus generating a vicious cycle.
- Gaining exogenous chloride, losing bicarb via the kidneys or the GIT Ureteric diversion, small bowel fistula, excessive chloride, exogenous acid, , diarrhoea, resolving DKA, carbonic anhydrase inhibitors, Addisons (type 4 RTA), RTA, pancreatic fistula (USEDCRAP) or (HARDUP – hyperalimentation, acetazolamide, RTA< diarrhoea, ureteroenteric fistula, pancreaticoduodenal fistula, spironolactone) Diarrhoea – sodium loss in excess of chloride loss – excess chloride Fistulas: loss of bicarb rich chloride poor fluid
- Can help differentiate between GIT and renal causes of hyperchloremic metabolic acidosis Provides rough estimate of ammonium excretion (ammonium is positively charged so a rise in its urinary concentration will cause a fall in urinary anion gap). Normally slightly positive. If there is a negative urinary anion gap it means another cation – namely ammonium is being excreted If acidosis is due to loss of base via bowel then the kidneys respond appropriately to increase ammonium excretion and cause a net loss of hydrogen from body decreased UAG If acidosis is due to loss of base via kidney then kidney not able to increase ammonium excretion UAG not increased Low urinary AG: GI loss of base No change in urinary AG: renal loss of base Negative urinary AG: severe diarrhoea Positive urinary AG: altered urinary acidification
- Assumes that each acid molecule is buffered by one HCO3 molecule so there is a net increase in unmeasured anion and a decrease in hco3 This assumes that all buffering is by HCO3 (not true some is intracellular – some by Hb and proteins)
- Nil significant a-a gradient, severe high anion gap (31) metabolic acidosis with respiratory compensation, delta ratio 1 – HAGMA Raised glucose Likely DKA – check ketones
- Nil significant A-a gradient, metabolic acidosis with respiratory compensation, raised anion gap (19) but delta ratio = 0.58 (mixed NAGMA + HAGMA) – don’t stop insulin yet
- 3 x ABGS with lactate Seizure, 2. ethylene glycol 3. Asthma with salbutamol toxicity
- Due to increased production OR decreased utilisation/clearance Lactate and pyruvate – ongoing conversion via Cori cycle (glucose -> pyruvate -> lactate in glycolysis dependent tissues such as skeletal muscle, blood cells, bone marrow, renal medulla, hypoxic tissue) (lactate:pyruvate in cells normally 10:1) Lactate -> pyruvate -> glucose in liver Lactate – mostly converted to glucose in liver, half metabolised to co2 and water in citric acid cycle. Only liver and kidneys can convert lactate to glucose Although lactate is freely filtered at the glomerulus, it is almost all reabsorbed and normally <2 % of lactate is removed from the body in urine [3]. The principal route of disposal begins with cytosolic conversion to pyruvate by the enzyme lactate dehydrogenase. This pyruvate has two principal fates. The first is oxidation to acetyl CoA by the enzyme pyruvate dehydrogenase for ultimate metabolism to carbon dioxide and water via the citric acid cycle and oxidative phosphorylation. The second is conversion to glucose, a process called gluconeogenesis. Oxidation of pyruvate via the citric acid cycle can potentially occur in all cells with mitochondrion, but gluconeogenesis is confined to liver and kidney cortex cells. For this reason liver and kidneys are the most significant organs for lactate elimination, the liver accounting for disposal of around 60 % of circulating lactate [4] and the kidneys for disposal of 25-30 % [5]. Overall, the body has immense capacity for lactate disposal, which can, if necessary (e.g. following extreme exercise), rise as high as 500 mmol/hour, considerably higher than the basal rate of production Causes Increased rate of glycolysis Due to lack of ATP (ATP produced via oxidative phosphorylation produces a lot more ATP (36 versus 2): so any cause of lack of oxygen Due to exogenous pro-glycolytic stimulus: salbutamol, adrenaline, catecholamines Pyruvate dehydrogenase issues Thiamine deficiency: cofactor in oxidative phosphorylation and coenzyme with PDH to form acetyl coA Sepsis Errors of metabolism Defects of oxidative phosphorylation/Krebs cycle Cyanide: disables electron transport chain Paracetamol: inhibits electron transport chain Salicylate: inhibits enzymes involved in Krebs cycle Metformin: inhibits pyruvate carboxylase (required to change pyruvate to oxaloacetate), inhibits electron transport chain, relative insulin deficiency Propofol: electron transport chain Toxic alcohol: increases NADH which favours production of lactate NRTI: disrupts oxidative phosphorylation Inborn errors - Decreased clearance: hepatic/renal dysfunction, decreased gluconeogenesis
- Seizure: Historical features: history, meds
- Asthma with salbutamol toxicity History, meds
- Ethylene glycol toxicity Osmolar gap Calcium oxalate crystals Ethylene glycol: lactate electrode relies on use of lactate oxidase which conversts lactate into pyruvate producing hydrogen peroxide which is reduced at cathode. Glycolic acid (product from ethylene glycol) also is substrate for enzyme falsely elevates lactate Can do lactate gap (lactate serum – lactate ABG) Also confirmed by raised osmolar gap + calcium oxalate crystals in urine Other things that can interefere: citrate, ethanol, heparin, paracetamol, salicylate and urea, isoniazid
- Raised A-a gradient (170.95), metabolic alkalosis with respiratory compensation How to investigate? History (antacids, diuretics, b lactams (act as non reabsorbable anions in renal tubule therefore promote potassium and hydrogen excretion), cystic fibrosis, Urinary Chloride < 20 (chloride responsive): - extra-renal loss: vomiting, sweat Renal loss: post hypercapnoeac, diuretics (remote use now ceased), >20: chloride resistant: - Normal/low BP: diuretics, Barters (defect in thick ascending loop of Henle NaK2CL transporter), Gilteman (defect of sodium chloride co-transporter), hypokalemia, hypomag HTN: (increased mineralocorticoid or mineralocorticoid like effects) High serum renin: diuretics, renal artery stenosis, renin secreting tumour, MH Low serum renin Low serum aldosterone: cushing, corticosteroid, 17 hydroxylase deficiency, Liddle syndrome, licourice overindulgence High aldosterone: adrenal adenoma, hyperplasia, aldosterone synthase hyperactivity, primary hyperaldosteronism
- Urinary hydrogen ion losses increase when relatively generous sodium and water delivery to the distal nephron combines with increased mineralocorticoid activity at this site. Three important actions of mineralocorticoids enhance hydrogen ion secretion by the distal renal tubule: ●Direct stimulation of the secretory H-ATPase pump ●Increased number of open epithelial sodium channels (ENaC) ●Increased activity of Na-K-ATPase These actions combine to enhance the movement of sodium from the distal tubule lumen across the cell and into the extracellular fluid. Because sodium is reabsorbed more readily than luminal anions, its reabsorption generates an electronegative charge in the tubular lumen. The electronegative lumen reduces back-diffusion of secreted hydrogen ions from the lumen into the tubular cells and also increases distal tubule hydrogen and potassium secretion, resulting in hypokalemia and total body potassium depletion.
- Have they gained alkali: from us? From themselves? Are they losing acid? From their stomach (acidic secretions) From their kidneys
- Raised A-a gradient (150), Acute respiratory acidosis with metabolic compensation
- Can occur via three mechanisms Excess co2 in inspired gas: laparoscopic surgery, rebreathing in anaesthetics Increased production: malignant hyperthermia – only if ventilation otherwise impaired
- Respiratory centre suppression: sedatives, narcotics, CNS infection/ vasculitis/infarction/trauma, OSA, obesity hypoventilation Airway obstruction: burns, ludwigs angina, trauma, anaphylaxis Mechanical ventilation: permissive hypercarbia Neuromuscular: spinal cord injury, Guillain barre, myasthenia, muscle relaxants, envenomation, polio, critical illness myoneuropathy, paraneoplastic effects, phrenic nerve damage, myopathy, hypokalemia, shock, hypermagnesemia, MND, musclular dystrophy Decreased chest wall compliance: abdo distension, burns, pleural effusion, pneumothorax, obesity, kyphoscoliosis, ank spond Loss of chest wall integrity: flail segment Increased small airways resistance: asthma, bronchiolitis, COPD Decreased lung compliance: ALI, pneumonia, pulmonary oedema, vasculitis, haemorrhage, pulmonary fibrosis
- Chronic respiratory alkalosis with metabolic compensation – normal in late pregnancy
- Central causes: via resp centre – head injury, stroke, anxiety, drugs (antiepileptics, salicylate, propanalol, SSRI, opiate, benoz), endogenous compound (progresterone in pregnancy, cytokines in sepsis, toxins in chronic liver disease, thyrotoxicosis Act on peripheral chemoreceptros: e.g. hypoxia, high altitude Act on intra-pulmonary receptors: PE, pneumonia, asthma, pulmonary oedema Iatrogenic: mechanical ventilation