MEDICINE I

Approach to Acid base disorders

Proper management may be life-saving

ACID-BASE DISORDERS
Principles of A-B homeostasis and disturbances Recognition of A-B disorders Specific disorders: common etiologies, pathogenesis, clinical features, general principles of management Interpretation of ABG and electrolyte results Normal Arterial Blood Values (memorize!) pH: 7.35 - 7.45 (midline: 7.40) pCO2: 35 - 45 mmHg (midline: 40)

NORMAL ACID-BASE 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. Arterial CO2 tension (PaCO2) controlled by central nervous system and respiratory system Plasma bicarbonate (HCO3-)- controlled by the kidneys Regulation of both will stabilize the arterial pH by either excretion or retention of acid or alkali PaCO2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production To further understand this: remember that hypercapnia underexcretion CO2, is related to hypoventilation, meaning you retain the CO2 rather than increased CO2 production (hypocapnea on the other hand is overexcretion of CO2 which is related to hyperventilation) The kidneys regulate plasma [HCO3] through three main processes: a. "Reabsorption" of filtered HCO3 b. Formation of titratable acid c. Excretion of NH4+ in the urine Importance of Acid-Base Disorders one of the most common clinical problems encountered in hospitalized patients, especially ICU (intensive care unit) patients o Pneumonia hypoxia hyperventilation respiratory alkalosis; remember if you hyperventilate, you
overexcrete your CO2 ,thus it will decrease your PaCO2 and increases the HCO3/ PaCO2 ratio, thus increasing pH

Note:

HCO3: 22 26 mmol/L (midline: 24) pO2, O2 saturation, base excess/deficit

o HCO3 is not measured but just calculated from H-H

equation

o A chemistry panel shows the [total CO2], [Cl-], [K+] and

[Na+], [glucose], [BUN] and [creatinine]

o Normal [H+] = 35-45 nmol/L or neq/L

Chemistry panel: Sodium: 135 - 145 mmol/L Potassium: 3.5 - 5 mmol/L Chloride: 96 109 mmol/L Total CO2: 23 -30 mmol/L Glucose, BUN, Creatinine Maintenance of blood pH

o Diarrhea + dehydration accumulation of lactate

metabolic acidosis; In Harrisons , with diarrhea you also
lose your bicarbonate which leads to your acidosis

o Persistent vomiting metabolic alkalosis; when you

vomit, you lose fluid and NaCl which leads to extracellular fluid volume contraction.Volume contraction through a reduction in GFR results in an enhanced capacity of the renal tubule to reabsorb HCO3.

Example: When given is CO2 = 40, HCO3 = 24 [CO2] = (40)(0.0301) = 1.204 mmol/L [HCO3] / [pCO2] = 24/1.204 = 20 pH = 6.1 + log20 = 6.1 + 1.301 = 7.401 Note: Equation describes the relationship between blood pH, pCO2 and HCO3. (pCO2)(0.0301) = [CO2] in mmoles/liter

Normal ratio of [HCO3]:[CO2] is 20:1 [HCO3] (pCO2)(0.0301)

Lead to significant physiologic effects o Metabolic acidosis >>>> predisposes to cardiac arrhythmias, pulmonary congestion; bone calcium loss (chronic) o Respiratory acidosis >>>> transient increase ICP, headache, hypertension o Respiratory alkalosis >>>> decreased ionized calcium >>>>signs of hypocalcemia (muscle cramping, tetany, aggravation of arrhythmias)

pH = 6.1 + log

pH [HCO3] [CO2] pH [HCO3] pH 1/ pCO2 Note:

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 May use the H-H equation to determine if the results are accurate If [HCO3]/[pCO2] > 20 increased pH; if < 20 decreased pH Regulation of pCO2 CO2 production CO2 elimination o CO2 production glucose metabolism o CO2 elimination ventilatory forces neural drive system; bellows apparatus; airways Note:

mechanism (the PaCO2 is expected to decrease 1.25 mmHg for each mmol per liter decrease in HCO3 )

o Incr.HCO3 incr. pH (met. alkalosis) incr. pCO2

hypoventilation

Primary respiratory disturbance Compensatory

metabolic response o Decr. PCO2 incr. pH (resp. alkalosis) decr HCO3 o Incr. PCO2 decr pH (resp. acidosis) incr. HCO3 Rules of Compensation: Respiratory compensation is immediate; renal compensation is not Overcompensation does not occur. Compensation is not complete. Abnormal acid-base with pH of 7.40 implies mixed disorder with opposing effects on pH. Prediction of Compensatory Responses on Simple Acid Base Disorders Primary Expected Range of Limits of Acid-Base Compensation Compensation Disorder Metabolic PCO2 =12 PCO2 =1.5[HCO3-] + 8 2 Acidosis -14mmHg Metabolic PCO2 = 0.6 mm Hg for each PCO2 =55 mmHg Alkalosis 1 mEq/L [HCO3-] [HCO3-] = 1 (acute) 4 Respiratory [HCO3-] = 45 (chronic) mEq/L for each 10 Acidosis mEq/L mmHg PCO2 [HCO3-] = 2 (acute) -5 Respiratory [HCO3-] = 12-15 (chronic) mEq/L for each 10 Alkalosis mEq/L mm Hg PCO2 Note: Important rule: compensation is not complete. Compensation does not result in over correction of pH. Harrison: Resp Alk HCO3 decreases by 4/10 pCO2; in metabolic acid-base disorder compare computed level of PCO2 with the ABG result, if ABG is higher or lower than expected there is mixed disorder Disorder Metabolic Acidosis Metabolic Alkalosis Respiratory Alkalosis Respiratory Acidosis pH Low High High Low HCO3Low High Low High PaCO2 Low High Low High

The respiratory-neural drive system is the chief determinant of pCO2 The components of the respiratory neural drive system include the central and peripheral chemoreceptors, respiratory neurons, lower respiratory motor neurons. Organ system of elimination: respiratory system Bellows apparatus = chest and lungs o Kyphoscholiosis causes stiffness of the chest when breathing; even if the requirement for CO2 elimination is high, it may not be able to elicit that requirement

Ventilatory system problem has more of an effect on the CO2 levels in the blood rather than CO2 production because the ventilatory system adapts to the CO2 production o if CO2 production is low, the ventilatory system will tend to lessen its ventilation so that CO2 elimination will also be low

Regulation of plasma HCO3 Via kidneys: o Reabsorption of filtered HCO3 o Formation of titratable acid o Excretion of NH4+ in urine

NUAE = UTA + UNH4 UHCO3

Note: o Titratable acids: sulfuric, phosphoric acids o NH4 weak acid (excluded from term titratable) o Net urine acid excretion tends to be positive in normal conditions o Net urine acid excretion = urine volume([urine titratable acid] + [urine NH4] [urine HCO3}]) Maintenance of blood pH Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs Chemical buffering: o includes HCO3, phosphates, proteins, hemoglobin, bone carbamates Note: Normal ratio is 20:1

Compensation for Acid Base Disorders Primary metabolic disturbance Compensatory

respiratory response o Decr. HCO3 decr. pH (met. acidosis) decr. pCO2 Hyperventilation

AcidBase Nomogram

stimulates the medullary chemoreceptors to

increase ventilation and to return the ratio of [HCO3] to PaCO2,

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So if you have metabolic acidosis, expect your patient to have a decreased PaCO2 as a compensatory

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High Anion Gap Lactic Acidosis Ketoacidosis Renal Failure or End Stage Renal Disease Methanol Ingestion Ethylene glycol ingestion Salicylate Toxicity

Normal Anion Gap Diarrhea Isotonic Saline Infusion Early Renal Insufficiency Renal tubular acidosis (RTA) Acetazolamide Ureteroenterostomy

Anion Gap AG = Na+ - (Cl- + HCO3) Normal: 10 - 12 e.g. AG = 140 - (105 + 24) = 140 129 = 11 Represents those unmeasured anions in the plasma Increase in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cations Note:

Note: NAG acidosis = hyperchloremic acidosis Lactic acidosis secondary to poor tissue perfusion or aerobic disorders Ketoacidosis secondary to increased fatty acid metabolism (DKA, AKA, starvation) Salicylates produce combined high AG acidosis (salicylates, lactic acid) and respiratory alkalosis Salicylate toxicity = combined metabolic acidosis and resp alkalosis Clinical Effects: Kussmaul breathing, dyspnea [due to respiratory response] Headache, nausea, vomiting, confusion, stupor, coma Decreased myocardial contractility and response to catecholamine; peripheral vasodilatation with central venoconstriction predisposing to pulmonary edema; arrhythmias Management: Identify and treat underlying cause. Give alkali therapy (oral or i.v.) to patients with normal AG acidosis, mixed hyperchloremic and AG acidosis, and AG acidosis due to nonmetabolizable anion in the face of renal failure. Give modest quantities of i.v. alkali in patients with pure AG acidosis due to metabolizable organic acid anion Goal: increase pH to 7.15 or [HCO3] to 10 mEq/L

Normal values: [Na+]: 135-145 mEq/L; [K+]: 3.5-5.0 mEq/L; [Cl-]: 96-109 mEq/L; [total CO2] :24-30 mEq/L If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3. Harrison normal AG is 10-12 Determinants of AG Unmeasured Anions Albumin (15mEq/L) Organic Acids (5 mEq/L) Phosphate (2 mEq/L) Sulfate (1 mEq/L) ---------------------------Total UA (23 mEq/L) Unmeasured Cations Calcium (5 mEq/L) Potassium (4.5 mEq/L) Magnesium (1.5 mEq/L) --------------------------Total UC (11 mEq/L)

Metabolic Alkalosis
Pathogenesis: Due to net gain of HCO3 or loss of volatile acid (usually HCl by vomiting) 2 stages: 1. GENERATIVE STAGE: loss of acid 2. MAINTENANCE STAGE: failure of kidneys to compensation by excreting HCO3, because of volume contraction, low GFR, or depleted K+ or ClNote: Addition of alkali is unusual Causes: Exogenous bicarbonate loads Effective ECFV contraction o Gastrointestinal o Renal ECFV expansion, hypertension Liddles syndrome Clinical Effects: Increases the affinity of hemoglobin for oxygen decrease tissue unloading Decreases ventilation

AG = UA UC = 12 mEq/L Note: AG represents those unmeasured anions in the plasma If albumin is decreased by 50%, AG = 4-5 mEq/L Increase in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cations If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.

Metabolic Acidosis
Pathogenesis: May be due to: a. Increased endogenous acid production (e.g. lactate and ketones) b. Loss of bicarbonate (e.g. diarrhea) c. Decreased excretion of endogenous acids (e.g. renal failure) Common Causes of Metabolic Acidosis

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Decreases ionized calcium neuromuscular hyperirritability Supraventricular and ventricular arrhythmias Management Identify and correct the underlying stimulus for HCO3 generation Remove the factors that sustain HCO3 reabsorption (e.g. ECF contraction or hypoK+) Acetazoleamide Dilute 0.1N HCl or NH4Cl Hemodialysis

May be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemoreceptors (e.g. hypoxemia 2o to pneumonia), chest receptors (e.g. PTE). Clinical Effects: Panic, weakness, and sense of impending doom Paresthesias about the hands and feet Trousseaus and Chvosteks signs [hypocalcemia] Possible tetany, seizures Harrisons: Reduced cerebral blood flow as a consequence of a rapid decline in PaCO2 = dizziness, mental confusion, and seizures, even in the absence of hypoxemia. The cardiovascular effects of acute hypocapnia in the conscious human are generally minimal Chronic respiratory alkalosis is the most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis. Respiratory alkalosis is common during mechanical ventilation. Management: Directed toward alleviation of underlying disorder Change in dead space, tidal volume and respiratory frequency, if on MV Re-breathing from paper bag during symptomatic attacks of hyperventilation syndrome

Respiratory Acidosis
Etiology and Pathogenesis: May be due to severe pulmonary disease (e.g. advanced COPD), respiratory muscle fatigue, or abnormalities in ventilatory control (e.g. stroke) and is recognized by an increase in PaCO2 and decrease in pH Clinical Effects: Depends on severity and acuteness May be dyspneic or tachypneic Systemic vasodilation especially cerebral vasodilation increased ICP pseudotumor cerebri A rapid increase in PaCO2 causes: anxiety, dyspnea, confusion, psychosis, and hallucinations and may progress to coma. Lesser degrees of dysfunction in chronic hypercapnia include: sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor, myoclonic jerks, and asterixis.

INTERPRETATION OF ACID BASE DISORDERS

Determine if sample is arterial or venous. Compare HCO3 on ABG and electrolyte panel to verify accuracy Determine if pH or pCO2 are normal or abnormal. If any of above are abnormal determine primary A-B disturbance Compute for expected compensation to determine presence of mixed disorders.

Acute hypercapnia follows sudden occlusion of the upper airway or generalized bronchospasm as in severe asthma, anaphylaxis, inhalational burn, or toxin injury. Chronic hypercapnia and respiratory acidosis occur in end-stage obstructive lung disease; high metabolic cost of
respiration causes ventilatory muscle fatigue (possibly you hypoventilate and retain the CO2)

Note:

o The HCO3 value on the ABG result should fall within 2 mmol/L o The
of the measured [HCO3] or total CO2 on the electrolyte panel. [total CO2] is the sum of the measured [CO2] + [HCO3-]. Thus the [HCO3-] from the blood gas and the [total CO2] from the electrolyte panel usually are within 2 mEq/L. Otherwise the measurements are in error or were taken at different times. If pH and pO2 are normal, check AG: if normal then normal A-B

Management: Depends on severity and rate of onset Acute respiratory acidosis can be life threatening, and measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilation.
This may necessitate tracheal intubation and assisted mechanical ventilation.

Calculate the Anion Gap

Oxygen administration should be titrated carefully in patients with severe obstructive pulmonary disease and chronic CO2 retention who are breathing spontaneously Avoid rapid correction of hypercapnea; Rapid correction of
pCO2 may cause the same complications noted with acute respiratory alkalosis (e.g. cardiac arrhythmias, reduced cerebral perfusion, seizures)

o RULE: If AG > 20 high AG metabolic acidosis is present

regardless of the pH or HCO3.

Compare the change in AG (AG) with change in HCO3

(HCO3). o RULE: If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis. o RULE: If AG is > HCO3, there is combined high AG metabolic acidosis and metabolic alkalosis. Note: If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3. AG = patients AG 10 (normal AG)

Respiratory Alkalosis
Etiology and Pathogenesis: Develops when a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed its metabolic production in the tissues

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HCO3 = 24 (Normal HCO3) minus patients HCO3 If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis. If AG is > HCO3, there is combined high AG metabolic acidosis and metabolic alkalosis. Maintenance of blood pH (as mentioned earlier, but this is how to derive it using log) pH = 6.1 + log 24/(40)(0.0301) pH = 6.1 + log 24/1.204 pH = 6.1 + log 20 pH = 6.1 + 1.301 pH = 7.401 Note: If HCO3- is 24 and pCO2 is 40, then blood pH is 7.40 For the pH to remain at 7.40, the ratio of [HCO 3]/[pCO2] should be 20

7.33. biochem: Na 130, HCO3 9, Cl 116. This is metabolic acidosis. Expected pCO3 is 23 so using the +/- 2 rule, 22 is acceptable. AG is low maybe because the patient has hypoprotenemia. Low AG has no significance. Case 5: A 56 year old man presents with anorexia and unremitting emesis for 4 days. ABG: HCO3 18, pCO2 30, pH 7.40. biochem: Na 130, HCO3 18, Cl 89. Here, the pH is normal but the pCO2 is abnormal. In this case, it is still abnormal even though the pH is normal. The conclusion here is respiratory alkalosis because the pCO2 is low. Now, refer again to the table for respiratory alkalosis. The HCO3 should go down by 2 if this is acute. If this is chronic which seems to be the case, the HCO3 should go down by 5. So it should be 19 +/- 2, so 18 is still acceptable. However, when the pH is exactly 7.40, chances are you are dealing with mixed disorder. *Kasi nga naman nakakapagtaka na normal yung pH and yet the ABG is abnormal. The conclusion here is respiratory alkalosis combined with a metabolic acidosis because the HCO3 is a little lower than expected. There is high AG metabolic acidosis because the Na is higher than the combined Cl and HCO3. If the AG is more than 20, whatever the pH and pCO2, there is high anion gap metabolic acidosis.

Cases mentioned in lecture (from 2012B trans) Case 1:A 20 year old female, s/p craniotomy for debulking of a large posterior fossa tumor, was placed on mechanical ventilation. No significant past history. She is on dexamethasone 4 mg 6th hourly, ranitidine and phenytoin. ABG: pH 7.51, pCO2 32, pO2 154, HCO3 25. This is respiratory alkalosis because the pCO2 is low so the high pH is due to it. The change in pCO2 is: (40 - 32) = 8, so the change in HCO3 should be approximately ([8/10]x2) = 1.6. *Refer to the table again para hindi kayo ma-confuse. The HCO3 should compensate by going down(to make the blood less basic). But here, it increased instead of compensating. Therefore, the conclusion is that there is combined respiratory alkalosis and metabolic alkalosis. The respi alkalosis is probably due to increased respiratory minute ventilation on the mech-vent. The metab alkalosis was maybe due to the dexamethasone. Case 2: A 56 year old man with a history of DM and alcoholism presents after having eaten no food and taken no insulin for the last 3 days and drinking lots of alcohol. He is hypotensive, tachycardic, and markedly tachypneic (RR of 36). He smells strongly of acetone and is dehydrated, and clinical findings are consistent with left lower lobe pneumonia. Results of ABG: PaO2 68, PaCO2 17, HCO3 6, pH 7.30. This is metabolic acidosis because the HCO3 is low. pCO2 is low because it is compensating. Using the table for metabolic acidosis: ([1.5x6]+8) = 17. So the pCO2 of 17 is appropriate. Therefore the conclusion is simple metabolic acidosis. Case 3: A 41 year old man with a history of delirium tremens presents with multiple seizures. He has been drinking heavily and has neglected to take his anticonvulsant medication for 4 days. He is drowsy but tremulous with fever, tachycardia, and hypertension. ABG: PaO2 62, PaCO2 30, HCO3 13, pH 7.17. biochem: Na 146, HCO3 12, Cl 112. This is metabolic acidosis because the HCO3 and pCO2 is low. For the expected level of pCO2: ([13x1.5]+8) = 27. The pCO2 should only be 27, 29 at max. The conclusion is that there is a concomitant respiratory acidosis because the pCO2, which is 30 in this case, is higher than expected value of 27. AG = 146 (112+12) = 22. This is high. So you are dealing now here with high anion gap metabolic acidosis combined with a respiratory acidosis. Case 4:A 74 year old man, taking diuretics for heart failure, presents with weakness and diarrhea of 2 days duration. On examination he is markedly dehydrated and hypotensive. ABG: pCO2 22, HCO3 10, pH

From 2013B Trans ROME = Respiratory Opposite, Metabollic Equal. Explanation: Usually when pH decreases it is called acidosis and increase in pH is called alkalosis. There is no confusion to this point. Also I hope that you know that changes in PCO2 will lead to Respiratory acidosis / alkalosis and that in HCO3 will lead to Metabolic acidosis / alkalosis. You can remember this by thinking that you respire PCO2 outside. Next, take the mnemonic ROME - In Respiratory alkalosis / acidosis, the pH and PCO2 levels are Opposite; This means that in Respiratory acidosis (which means pH is low) the PCO2 will be high or in other words low pH with high PCO2 is called Respiratory acidosis. In respiratory alkalosis there is high pH and low PCO2. In Metabollic acidosis / alkalosis, the pH and PHCO3 levels are Equal (Not quantitively, but it means that increased pH and increased PHCO3 is the situation in Metabollic alkalosis and both are decreased in Metabolic acidosis). To remeber this in another way: In METabollic acidosis / alkalosis the values of pH and HCO3 MEET. In Respiratory there are like RX - 'X' denotes into mark for opposite.

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