Presentation on theme: "Acid Base Interpretation Part III Clinical correlation Jakub Matera."— Presentation transcript:
Acid Base Interpretation Part III Clinical correlation Jakub Matera
5 steps to analyse acid base Step 1 Look at the pH. Acidaemia or alkalaemia? Step 2 Who is responsible for this change in pH ( primary culprit )? Step 3 Calculate compensatory changes. Adequate compensation? Acute or chronic process? Step 4 Calculate AG and ∆ gaps. Is there any additional pathological process? Mixed metabolic or respiratory disturbance? Step 5 Clinical correlation? Find the diagnosis.
Analyse the following blood gas and electrolyte values: pH 7.47, PCO 2 20, HCO 3 15, Na 145, Cl 100 The pH is elevated (alkalaemia), with a low PCO 2 and a low HCO 3. Because the pH is high, the low PCO 2 represents a primary disorder (RO), so a respiratory alkalosis is present. Expected HCO 3 based on metabolic compensation should be: in acute (The 2 for 10 Rule) = 20; in chronic (The 5 for 10 Rule) = 14. At first inspection, the low HCO 3 level appears to be metabolic compensation for a chronic respiratory alkalosis. Follow the fourth step rule, however, and calculate the AG: 145 – (100+15) = 30 Because the wide anion gap exists a metabolic acidosis (WAGMA) is also present. Now calculate the ∆ AG: 30 - 12 = 18, and add it to the measured HCO 3 : 15. The sum, 33 mmol/L, is higher than a normal HCO 3 concentration, indicating a metabolic alkalosis is also present. The near-normal pH reflects the competing effects of these three primary disorders. This patient had findings of bacterial pneumonia (hence the respiratory alkalosis), history of vomiting (the metabolic alkalosis) and evidence of alcoholic ketoacidosis (causing metabolic acidosis). These three independent disorders can occur concurrently in other clinical settings. Four primary acid-base disorders cannot coexist, as a patient cannot hypoventilate and hyperventilate at the same time.
What if a patient presents with a pH of 7.10, a PCO 2 50, HCO 3 15, Na 145, Cl 100 ? The person is acidaemic with an elevated PCO 2, and low HCO 3 Because the pH is low, the increased PCO 2 (respiratory acidosis) and decreased HCO 3 (metabolic acidosis) are both primary disorders (ROME). The anion gap is increased : AG = 145 – (100+15) = 30; therefore, the metabolic acidosis is of the wide anion gap variety (WAGMA). Because the sum of the ∆ AG (18) and the measured HCO3 (15) is 33 mmol/L. So, greater than the normal HCO 3 concentration, a metabolic alkalosis is also present: three primary disorders. This patient presented in an obtunded conscious state (respiratory acidosis),with a history of vomiting (metabolic alkalosis) and laboratory findings consistent with diabetic ketoacidosis (metabolic acidosis).
Interestingly, identical blood gas values pH of 7.10, a PCO 2 50, HCO 3 15, Na 145, Cl 100 could occur in a patient with chronic respiratory acidosis and metabolic compensation in whom an acute anion gap metabolic acidosis developed. Example: Patient with COPD and T2DM who developed metformin induced lactic acidosis Although the pH, PCO 2, and HCO 3 values would be the same in both these patients, clinical correlation would readily differentiate between the two. As is the case for other diagnostic tests, acid-base abnormalities cannot and should not be interpreted without knowledge of the clinical context.
Metabolic acidosis Wide anion gap (WAGMA) increased H + consumes HCO 3 - Non anion gap (NAGMA) loss of HCO 3 - (kidney or gut) will raise Cl - hence non anion gap
Dr Adolph Kussmaul( 1822 -1902) German physician and a leading clinician of his time First to describe dyslexia. (He called it 'word blindness'.) First to describe polyarteritis nodosa. First to describe progressive bulbar paralysis. First to diagnose mesenteric embolism. First to perform pleural tapping and gastric lavage. First to attempt oesophagoscopy and gastroscopy. He described two medical signs and one disease which have eponymous names that remain in use: Kussmaul breathing - very deep and laboured breathing seen in severe metabolic acidosis Kussmaul's sign - paradoxical rise in the JVP on inspiration in constrictive pericarditis, RV strain (TS) and COPD. Kussmaul disease (also called Kussmaul-Maier disease) - Polyarteritis nodosa.
GOLD MARK: an anion gap mnemonic for the 21st century. Mehta AN, Emmett JB, Emmett M. Lancet 2008;372(9642):892. Over the past couple decades, the dynamic of conditions that can cause an anion gap metabolic acidosis has changed and a list has expanded. Metabolic acidosis due to excessive paraldehyde use has become exceedingly rare. Iron and isoniazid are just two of many drugs and toxins that cause hypotension and lactic acidosis Three “new” organic anion-gap-generating acids and acid precursors have been recognised in recent years. They are: D-lactic acid, which can occur in some patients with short bowel syndromes; 5-oxoproline (or pyroglutamic acid) associated with chronic paracetamol use, often by malnourished women; high-dose propylene glycol infusions; Propylene glycol, the solvent used for several parenteral medications including lorazepam, diazepam, phenobarbital, and others is metabolised to lactate. Therefore we propose a new anion gap mnemonic for the 21st century: GOLD MARK. This acronym represents : G- Glycols (ethylene and propylene), O- Oxoproline, L- L-lactate, D- D-lactate M- Methanol, A- Aspirin, R- Renal failure, and K- Ketoacidosis. Mnemonic aids are only helpful if they are easily remembered and we believe GOLD MARK fits that requirement.
Lactic acidosis overproduction, underutilisation, decreased excretion Type A – caused by tissue ischaemia (overproduction) Type B – caused by impaired mitochondrial O 2 utilisation and impaired excretion Type A – all state of shock (cardiogenic, hypovolaemic, septic); – excessive exercise, seizures, respiratory failure; – mesenteric ischaemia, limb ischaemia, compartment syndrome; – haemoglobin abnormality: severe anaemia, COHb (CO poisoning), MetHb (nitropruside).
Lactic acidosis Type B - impaired mitochondrial O 2 utilisation and impaired excretion B1 – systemic disease LUKE TIPS FAILURES: Leukaemia, Lymphoma, Thiamine deficiency, Infections, Pancreatitis, Short bowel syndrome (D-Lactate), Failures: hepatic, renal, diabetic; B2 – toxins and drugs: alcohols –glycols, iron, isoniazid, biguanides (metformin), salicylates, AZT (zidovudine), and cyanide poisoning; B3 – inborn metabolic errors (eg G6PD).
Non anion gap metabolic acidosis loss of HCO 3 - (kidney or gut) will raise Cl -, hence non anion gap. K + normal or ↑ Mineralocorticoid deficiency (Addison’s ) Addition of Cl (Saline) K + ↓ Lower GI losses (diarrhoea) Renal losses (CA inhibitors, RTA) Urinary diversion (vesico-colic, uretero-enterostomy)
Mnemonic for NAGMA USED CARP U- Uretero-enterostomy S- Small bowel fistula E- Extra chloride (K + normal or ↑) D- Diarrhoea C- Carbonic anhydrase inhibitor A- Addison’s disease (K + ↑) R- Renal tubular acidosis (RTA) P- Pancreatic fistula
NAGMA – kidney or gut ? NAGMA – loss of HCO 3 - (kidney or gut) will raise Cl - Urine Anion Gap (UAG) – helps differentiate between GIT and renal causes of hyperchloraemic metabolic acidosis (NAGMA with ↓K + ) UAG = Na u + K u – Cl u UAG – normal close to 0 neGUTive = GI loss of HCO3 (eg diarhoea, fistulas) Positive = impaired renal acidification (eg RTA, CAI)
Metabolic alkalosis Volume loss Saline responsive Urinary chlorine < 10 mmol/L Upper GI losses vomiting, gastric alkalinisation, gastric aspiration Lower GI losses chronic diarrhoea (Cl - ) Renal diuretic losses remote diuretic use Skin loss (Cl - ) Cystic fibrosis Milk-alkali syndrome chronic ingestion of large doses of CaCO 3. Hypercalcemia increases renal bicarbonate reabsorption Volume normal or overloaded Saline unresponsive Urine chlorine > 20 mmol/L Conn’s Syndrome primary hyperaldosteronism Cushing’s Syndrome Bartter’s Syndrome inherited thick ascending limb of the loop of Henle and excretion excessive amounts of Na, K, Cl. Renal artery stenosis stimulates the renin-angiotensin- aldosterone system Severe hypo K + and hypo Mg 2+ Current diuretics use
Respiratory disturbance Acidosis Acute Severe pneumonia Severe head injury Sedative use General anaesthetics Chronic COPD Intracranial tumours Neuromascular disease Alkalosis Central / supratentorial Mild to moderate HI CVA Pain Anxiety (fear, stress) Voluntary hyperventilation Systemic Liver failure Pregnancy Respiratory Asthma PE Pulmonary fibrosis APO Mild pneumonia
Alveolar-arterial Gradient It is simply the difference between Alveolar concentration of O 2 (PAO 2 ), and arterial concentration of O 2 (PaO 2 ). A-a gradient = PAO 2 – PaO 2 The PaO 2 is obtained from the ABG The PAO 2 is obtained from the Alveolar Gas equation: Alveolar Gas equation: PAO 2 = PIO 2 – PaCO 2 /R The PIO 2 is PO 2 inspired in trachea The PaCO 2 is a value from your ABG R – respiratory quotient ( 0.8 or 1.0 if patient is on 100% FiO 2 ) PIO 2 = (PB – 47) x FiO 2 PB is barometric pressure of the inspired air (760 mm Hg at sea level) 47 mm Hg is a water vapour pressure (47 mm Hg) PAO2 = (760-47) x FiO2 – PaCO2/R
A-a gradient Normally some A-a gradient exists b/o anatomical barriers between alveolar air and the blood that would become arterial blood: thin layer of epithelial cells of the alveolar wall, very thin layer of interstitial potential space, equally thin layer of arterial endothelial lining. Normal A-a gradient 5-25 mmHg or < age/4 + 4 < (age+10)/ 4
Is the A-a gradient helpful ? On a busy night at the ED, a nurse slips you the ABG result of a patient that you had seen 60 minutes ago. You'd almost forgotten the details of the history already; except that the patient was symptomatically breathless, but you could not identify any focal signs. You had seen another 3 patients since then, and another 3 are waiting for you.
ABG that is shown to you: pH 7.34, pO 2 94, pCO 2 40 and HCO 3 25 You probably think that it is not too bad, right ? Not too abnormal results, huh ? And if you are anything like me, you may be grumbling to yourself that your very own ABG may not be anywhere near that good. Ahaa ! The problem is that, you have forgotten that due to the symptomatic breathlessness, the patient has been on a nasal prongs oxygen at 3 L/min, which probably gives an FiO 2 of around 0.3 [30% oxygen]. So the oxygen concentration should be much higher.
pH 7.35, PO 2 94, PCO 2 40, HCO 3 25 Let's try calculating the A-a gradient and see what it tells us. Alveolar Oxygen Concentration is calculated as follows: at sea level BP = 760 mm Hg, at 37 C water pressure = 47 mm Hg PAO 2 = (760-47) x FiO 2 – PaCO 2 /R = [(760-47) x 0.30] - [40/0.8] = 164 mm Hg. Measured PaO 2 = 94 mm Hg Which gives an A-a gradient of a whopping 70 mm Hg !!!! So there are huge problems with the lungs; and the ABG is no where near as normal as initially thought ! What could be the problem ? Did you really narrow your DD ?
Calculating the A-a gradient is more academic then making a difference in diagnosis It doesn't tell you what the problem is it just tells you that there is a problem. Most of the time you would not need an A-a gradient to tell you that there is a problem and most of the time clinical history and assessment will tell you what the problem is. In general we would not do an ABG unless the patient is in severe respiratory distress and you are unable to check saturation using a non invasive sats probe. In an intubated patient ABG maybe more useful for obvious reasons. In ED, non intubated patients, it maybe quite unnecessary. The time and risk involved outweighs its clinical usefulness.. The procedure to procure an ABG is not without risk. It is only a matter of time before some patient ends up with an ischemic hand.
What we should remember? Step wise approach to acid base analysis Look at the pH: acidaemia or alkalaemia ? If pH within a normal limit but abnormal PCO 2 or HCO 3 look at pH again – whichever side of 7.40 the pH is on, the process that caused it to shift to that side is the primary abnormality Principle: The body does not fully compensate for primary acid-base disorders Indentify primary process: remember ROME Respiratory alkalosis ↑ pH, ↓ PaCO 2 acidosis ↓ pH, ↑ PaCO 2 Metabolic alkalosis ↑ pH, ↑ HCO 3 acidosis ↓ pH, ↓ HCO 3
Compensation rules and limits Expected PCO 2 Metabolic acidosis The One & a Half plus 8 Rule Winter’s formula Metabolic alkalosis The Point Nine plus Nine Rule Expected HCO 3 Respiratory acidosis acute The 1 for 10 Rule chronic The 4 for 10 Rule Respiratory alkalosis acute The 2 for 10 Rule chronic The 5 for 10 Rule
Calculate the anion gap: Na – (Cl + HCO 3 ) If AG is ≥ 20, there is a primary metabolic acidosis regardless of pH or HCO 3 Principle: The body does not generate a large anion gap to compensate for a primary disorder Calculate the excess anion gap: ∆ AG = AG – 12 Add ∆ AG to the measured HCO 3 if the sum is greater than a normal HCO 3 (>30) there is an underlying metabolic alkalosis; if the sum is less than a normal HCO 3 (<22) there is an underlying non anion gap metabolic acidosis Principle: 1 mmol of unmeasured acid titrates 1 mmol of bicarbonate (+ ∆ AG= - ∆ HC0 3 )
Clinical correlation Know the causes of WAGMA and lactic acidosis Know the causes of NAGMA – USED CARP Metabolic acidosis (kidney and gut) Metabolic alkalosis (saline responsive or not?) Respiratory disorders A-a gradient – limitations and usefulness
VAQs Describe state the characteristics or appearance of the subject, including relevant negatives. Interpret state a conclusion or conclusions which includes a differential diagnosis, but excludes management.
An 84 year old man is brought to your ED following a high speed car accident. He has sings of multiple rib fractures. Two hours after arriving in the ED he becomes more breathless and distressed. His observations are: GCS 14, HR 75, BP 100/60, RR 24. He is on 50% O 2, ABGs are performed: pH 7.14, pCO 2 60, pO 2 114, HCO 3 17, Lactate 1.4, Na 139, K 4.8, Cl 116, Glucose 11.3. Describe and interpret his results.
An 8 year old girl is brought to your ED with a 3 week history of general malaise. On the morning of presentation, she was found by her mother to be very lethargic and difficult to rouse. Her observations are: GCS 9, HR 110, BP 85/50, RR 18, temp 36 o C VBG results: pH 7.31, PCO 2 31, HCO 3 17, Na 128, K 5.9, Cl 100, Gluc 1.5 Describe and interpret the results of her investigations