approach to acid-base disorders antonio renato b. herradura, m.d. f.p.c.p, f.p.c.c.p uermmmc
TRANSCRIPT
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Approach to Acid-Base Disorders
Antonio Renato B. Herradura, M.D.
F.P.C.P, F.P.C.C.P
UERMMMC
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Importance of Acid-Base Disorders
• Among the most common clinical problems encountered in hospitalized patients, especially ICU patients
• Lead to significant physiologic effects
• Proper management may be life-saving
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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
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Normal Arterial Blood Values
• pH: 7.35 - 7.45
• pCO2: 35 - 45 mmHg
• HCO3: 22 – 26 mmol/L
• pO2, O2 saturation, base excess/deficit
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Normal Arterial Blood Values
• pH: 7.35 - 7.45
• pCO2: 35 - 45 mmHg
• HCO3: 22 – 26 mmol/L
• pO2, O2 saturation, base excess/deficit
• 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
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Maintenance of blood pH
pH = 6.1 + log [HCO3]
(pCO2)(0.0301)
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Maintenance of blood pH
pH = 6.1 + log [HCO3]
(pCO2)(0.0301)
pH α [HCO3]
pCO2
pH α [HCO3]
pH 1/α pCO2
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Regulation of pCO2
CO2 production ≈ pCO2 elimination
glucose metabolism ventilatory forces
neural drive bellows apparatus
airways
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Regulation of plasma HCO3-
• Via kidneys:1. Reabsorption of filtered HCO3
2. Formation of titratable acid
3. Excretion of NH4+ in urine
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Maintenance of blood pH
• Maintenance of the ratio of HCO3 to pCO2
via compensatory responses by the kidneys and lungs
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Maintenance of blood pH
• Maintenance of the ratio of HCO3 to pCO2
via compensatory responses by the kidneys and lungs
• Chemical buffering:– includes HCO3, phosphates, proteins,
hemoglobin, bone carbamates
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Compensation for Acid – Base Disorders
Primary metabolic Compensatory disturbance respiratory response
HCO3 pH (met. acidosis) pCO2
HCO3 pH (met. alkalosis) pCO2
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Compensation for Acid – Base Disorders
Primary respiratory Compensatory
disturbance metabolic response
pCO2 pH (resp. alkalosis) HCO3
pCO2 pH (resp. acidosis) HCO3
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Prediction of Compensatory Responses on Simple Acid - Base Disorders
Primary Acid-Base Disorder
Expected Range of Compensation
Limits of Compensation
Metabolic Acidosis
PCO2 =
1.5[HCO3-] + 8
PCO2 =
12-14 mm Hg
Metabolic Alkalosis
PCO2 =
0.6 mm Hg for each 1 mEq/L [HCO3
-]
PCO2 =
55 mm Hg
Respiratory Acidosis
[HCO3-] =
1(acute) – 4 (chronic) mEq/L for each 10 mm Hg PCO2
[HCO3-] =
45 mEq/L
Respiratory Alkalosis
[HCO3-] =
2 (acute) -5 (chronic) mEq/L for each 10 mm Hg PCO2
[HCO3-] =
12-15 mEq/L
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Acid–Base Nomogram
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Anion Gap
• AG = Na+ - (Cl- + HCO3)
• Normal: 10 - 14• 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
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Determinants of AG
Unmeasured Anions Unmeasured Cations
Albumin (15mEq/L) Calcium (5 mEq/L)
Organic Acids (5 mEq/L) Potassium (4.5 mEq/L)
Phosphate (2 mEq/L) Magnesium (1.5 mEq/L)
Sulfate (1 mEq/L)
---------------------------- ---------------------------
Total UA (23 mEq/L) Total UC (11 mEq/L)
AG = UA – UC = 12 mEq/L
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Metabolic Acidosis
PATHOGENESIS
• May be due to:– Increased endogenous acid production (e.g.
lactate and ketones)– Loss of bicarbonate (e.g. diarrhea)– Decreased excretion of endogenous acids
(e.g. renal failure)
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Common Causes of Metabolic Acidosis
HIGH ANION GAP NORMAL ANION GAP
Lactic Acidosis Diarrhea
Ketoacidosis Isotonic saline infusion
ESRD Early renal insufficiency
Methanol ingestion RTA
Ethylene glycol ingestion Acetazoleamide
Salicylate toxicity Ureteroenterostomy
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Metabolic Acidosis
CLINICAL EFFECTS
• Kussmaul breathing, dyspnea• Headache, nausea, vomiting, confusion, stupor,
coma• Decreased myocardial contractility and response
to catecholamine; peripheral vasodilatation with central venoconstriction predisposing to pulmonary edema; arrhythmias
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Metabolic Acidosis
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
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Metabolic Alkalosis
PATHOGENESIS
• Due to net gain of HCO3 or loss of volatile acid (usually HCl by vomiting)
• 2 stages:– GENERATIVE STAGE: loss of acid– MAINTENANCE STAGE: failure of kidneys to
compensation by excreting HCO3, because of volume contraction, low GFR, or depleted K+ or Cl-
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Metabolic Alkalosis
CLINICAL EFFECTS
• increases the affinity of hemoglobin for oxygen ----- decrease tissue unloading
• Decreases ventilation• Decreases ionized calcium ----- neuromuscular
hyperirritability• Supraventricular and ventricular arrhythmias
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Metabolic Alkalosis
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
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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)
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Respiratory Acidosis
CLINICAL EFFECTS
• depends on severity and acuteness• may be dyspneic or tachypneic• Systemic vasodilation especially cerebral
vasodilation ----- increased ICP ----- pseudotumor cerebri
• Myoclonic jerks, asterixis, tremors, restlessness, coma
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Respiratory Acidosis
MANAGEMENT
• Depends on severity and rate of onset• May be life-threatening• Measures to reverse underlying cause• Restoration of adequate alveolar
ventilation• Avoid rapid correction of hypercapnea
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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
• May be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemoreceptors (e.g. hypoxemia 2o to pneumonia), chest receptors (e.g. PTE).
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Respiratory Alkalosis
CLINICAL EFFECTS
• Panic, weakness, and sense of impending doom• Paresthesias about the hands and feet• Trousseau’s and Chvostek’s signs• Possible tetany, seizures
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Respiratory Alkalosis
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
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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.
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Interpretation of Acid - Base Disorders
• Calculate the Anion GapRULE: If AG > 20 high AG metabolic acidosis is present regardless of
the pH or HCO3.
• Compare the change in AG (ΔAG) with change in HCO3 (ΔHCO3).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.
RULE: If ΔAG is > ΔHCO3, there is combined high AG metabolic acidosis and metabolic alkalosis.
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Thank you for your attention!
Have a nice day!