Acid-Base Disorders

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Slide 1:

Acid-Base Disorders CSN Vittal

Normal Values:

Normal Values pH : 7.35 – 7.45 PaCO 2 : 35 – 45 mm Hg PaO 2 : > 70 mm Hg HCO 3 - : 22 – 26 mEq/L BE : -2.0 to +2.0 mEq/L


pH Depends on Acid : Base Proportional to HCO 3 - / H 2 CO 3 pH change to HCO 3 - is metabolic pH change to H 2 CO 3 (CO 2 ) is respiratory

Base Excess:

Base Excess Difference between patient’s actual buffering capacity and normal buffering capacity Normal Values : +/- 2.0 mEq/L Follows changes in HCO 3 -

Sources of acid gain::

Sources of acid gain: 1. Carbon dioxide (since CO 2 and H 2 O form HCO 3 - , and H + in the presence of carbonic anhydrase) 2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules 3. Loss of bicarbonate in faeces or urine 4. Intake of acids or acid precursors Sources of acid loss: Use of hydrogen ions in the metabolism of various organic anions Loss of acid in the vomitus or urine

Primary & Compensatory Chages:

Primary & Compensatory Chages Primary Change Compensation Resp. Acidosis h PaCO 2 h HCO 3 - Resp. Alkalosis i PaCO 2 i HCO 3 - Met. Acidosis i HCO 3 - i PaCO 2 Met. Alkalosis h HCO 3 - h PaCO 2

Slide 7:

An Approach to Acid-Base Disorders

Diagnosis of Acid-Base Disorders:

Diagnosis of Acid-Base Disorders Consider the history Look for clues on physical exam Examine the electrolytes PCO 2 Potassium Anion Gap Review other laboratory data Analyze the arterial blood gas


History Loose Stools and decreased Intake Polyphagia, Polydipsia of DM History of Renal Insufficiency Possibilty of Poisoning in Toddlers Fever and Increasing Sickness Any signs of CNS Disorder Any Medication History


Examination Any Signs of Sepsis Any Signs of Dehydration Any Signs of Meningeal irritation Any Signs of Addison’s Disease Any Signs of Neuromuscular Disease

5 Step Approach:

5 Step Approach pH: Normal, acid or alkaline? Respiratory component – Is it like pH? Metabolic component – Is SBE like pH? Magnitude of change – minor, moderate or major? Recognizing compensation

Step 1:

Step 1 Acidemic or Alkalotic? Acidemic : pH < 7.35 Alkalotic : pH > 7.45 A normal pH does not rule out acid base disorder

Step 2 Respiratory Component : PCO2:

Step 2 Respiratory Component : PCO 2 If the respiratory change is like the pH, i.e., both acid, then the cause is respiratory The exception : when the metabolic component is also acid -> both are contributing to the acid pH. If the PCO 2 is not like the pH, i.e., the PCO 2 is low (alkaline), then the primary problem is not respiratory; the low PCO 2 is a compensation for the metabolic acidosis.

Step 3 Metabolic Component : SBE:

Step 3 Metabolic Component : SBE If the Standard Base Excess (SBE) is the component which is like the pH, i.e., both acid (a negative base excess), then the cause is metabolic . The exception , - is when the respiratory component is also acid; then both contribute to the acid pH. If the SBE is not like the pH, i.e., the SBE is alkaline, then the primary problem is not metabolic; the high SBE is a compensation for the respiratory acidosis.

Step 4 Magnitude of Disturbance:

Step 4 Magnitude of Disturbance Just try to judge minor, moderate, or major, for clinical comment. Whenever the pH is normal, i.e., pH = 7.4. then the PCO 2 and the SBE are equal and opposite. The slope for BE / PCO 2 when pH = 7.4 gives us this ratio: 3 units of change in SBE = 5 mm Hg change in PCO 2 . Adjective PCO 2 mmHg SBE mEq/L Alkalosis Severe <18 <13 Marked 18 to 25 13 to 9 Moderate 25 to 30 9 to 6 Mild 30 to 34 6 to 4 Minimal 34 to 37 4 to 2 Normal Normal 37 to 43 2 to -2 Acidosis Minimal 43 to 46 -2 to -4 Mild 46 to 50 -4 to -6 Moderate 50 to 55 -6 to -9 Marked 55 to 62 -9 to -13 Severe > 62 to <-13

Step 5 Recognizing compensation :

Step 5 Recognizing compensation If a pt. with a respiratory problem has a high PCO 2 , e.g., 60 mmHg (raised by 20mmHg) then for "complete compensation" the SBE would have to be about 12 (using the 5 to 3 ratio given above) . If the SBE were zero = "no compensation" - typical of an acute process of recent onset. Most likely - the patient is somewhere in the middle (SBE = 6 mEq/L) which is typical for "compensation for chronic respiratory acidosis”.

Step 5 Recognizing compensation :

Inverse example: if a patient with a metabolic problem has a low SBE, e.g., -12, then the PCO 2 would have to be reduced by hyperventilation to about 20 mmHg to achieve "complete compensation". If the PCO 2 were still normal then there would be "no compensation". Again, far the most likely, the patient is somewhere in the middle (30 mmHg) which is typical for "compensation for metabolic acidosis". Step 5 Recognizing compensation

Logical Approach to an Acid pH :

Logical Approach to an Acid pH Are the pH and the PCO 2 both acid? If so the PCO 2 contributes to the condition. If not (i.e., PCO 2 is alkaline) then the metabolic component is the cause and the PCO 2 is compensatory. Is either PCO 2 or SBE normal? Because, if so, there is no compensation and you have a pure acidosis: (pure respiratory acidosis occurs fairly frequently, metabolic rarely) To be typical the compensation must lie roughly half way between no compensation and complete compensation - use the rule 3 mEq/L = 5 mmHg to work out complete compensation. If both components are acid, you don't have a typical single condition, you have a combined metabolic and respiratory acidosis.

Example A:

Example A pH = 7.2, PCO 2 = 60 mmHg, SBE = 0 mEq/L Overall change is acid. Respiratory change is also acid - therefore contributing to the acidosis. SBE is normal - no metabolic compensation. Therefore, pure respiratory acidosis. Typical of acute respiratory depression. Magnitude: marked respiratory acidosis

Example B:

Example B pH = 7.35, PCO 2 = 60 mmHg, SBE = 7 mEq/L Overall change is slightly acid. Respiratory change is also acid - therefore contributing to the acidosis. Metabolic change is alkaline - therefore compensatory. The respiratory acidosis is 20 mmHg on the acid side of normal (40). To completely balance plus 20 would require 20 * 3 / 5 = 12 mEq/L SBE The actual SBE is 7 mEq/L, which is roughly half way between 0 and 12, i.e., a typical metabolic compensation . Magnitude: marked respiratory acidosis with moderate metabolic compensation

Example C:

Example C pH = 7.15, PCO 2 = 60 mmHg, SBE = - 6 mEq/L Overall change is acid. Respiratory change is acid - therefore contributing to the acidosis. Metabolic change is also acid - therefore combined acidosis. The components are pulling in same direction - neither can be compensating for the other Magnitude: marked respiratory acidosis and mild metabolic acidosis

Example D:

Example D pH= 7.30, PCO 2 = 30 mmHg, SBE = -10 mEq/L Overall change is acid. Resp. change is alkaline - therefore NOT contributing to the acidosis. Metabolic change is acid - therefore responsible for the acidosis. The components are pulling in opposite directions. SBE is the acid component so it is primarily a metabolic problem with some respiratory compensation The metabolic acidosis is 10 mEq/L on the acid side of normal (0). To completely balance 10 would require 10 * 5 / 3 = 17 mmHg respiratory alkalosis (= 23 mmHg) The actual PCO 2 is 30 mEq/L which is roughly half way between 23 and 40, i.e., a typical respiratory compensation.. Magnitude: marked metabolic acidosis with mild respiratory compensation.

Slide 23:

Respiratory Acidosis

Respiratory Acidosis:

Respiratory Acidosis Acute The PaCO 2 is elevated above the upper limit of the reference range (i.e., > 45 mm Hg) with an accompanying acidemia (i.e., pH < 7.35). Chronic The PaCO 2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (i.e., HCO 3 - > 30 mEq/L.)

Respiratory Disturbances:

Respiratory Disturbances Is it Acute or Chronic ? Respiratory Acidosis Acute : pH decrease = 0.008 X (PaCO 2 – 40) Respiratory Alkalosis Acute : pH Increase = 0.008 X (PaCO 2 – 40) Chronic : pH decrease = 0.003 X (PaCO 2 – 40) Chronic : pH Increase = 0.003 X (PaCO 2 – 40)

Respiratory Acidosis - Acute:

Respiratory Acidosis - Acute Abrupt failure of ventilation, h PaCO 2 Neuromuscular disorders CNS Depression Brain stem Injury Musculoskeletal Disorders GBS Myasthenia Airway Obstructive Disease Asthma Foreign Body Laryngeal Edema Pulmonary Embolism Drugs Sedatives Barbiturates

Respiratory Acidosis - Chronic:

Respiratory Acidosis - Chronic COPD Obesity hypoventilation syndrome (i.e., Pickwickian syndrome) Neuromuscular disorders Amyotrophic lateral sclerosis Severe restrictive ventilatory defects Interstitial fibrosis and Thoracic deformities

Respiratory Acidosis:

Respiratory Acidosis Symptoms: Symptoms of the disease that causes respiratory acidosis are usually noticeable shortness of breath easy fatigue chronic cough, or wheezing. When respiratory acidosis becomes severe, Confusion irritability, or lethargy may be apparent.

Respiratory Acidosis:

Respiratory Acidosis Treatment: Treat the underlying cause Improve alveolar gas exchange Assisted ventilation Bicarbonate must not be infused to treat the acidosis because it generates more CO 2

Slide 30:

Respiratory Alkalosis

Respiratory Alkalosis:

Respiratory Alkalosis Hyperventilation, i PaCO 2 Catastrophic CNS Events Hemorrhage Hysterical Assisted ventilation Drugs Salicylates (early stages) Interstitial Lung Disease Cirrhosis, Liver Failure Anxiety Gram negative Septicemia Hypoxia and severe anemia or high altitude

Respiratory Alkalosis:

Respiratory Alkalosis Symptoms Tingling and numbness Parasthesias Lethargy Tetany Unconsciousness Vasospasm of cerebral vassals - Hypercapnia

Respiratory Alkalosis:

Respiratory Alkalosis Treatment Treat underlying cause

Slide 34:

Metabolic Acidosis

Metabolic Acidosis:

Metabolic Acidosis Increased H + Load Increased HCO 3 - Loss

Metabolic Acidosis:

Metabolic Acidosis What is anion gap? Anion gap = (Na + ) – ( Cl - + HCO 3 - ) Usually 12 + 2 Major unmeasured anions albumin Phosphates sulfates organic anions Anion gap Met. Acidosis : AG > 12 Non Anion gap Met. Acidosis : AG < 12

Anion Gap Metabolic Acidosis:

Anion Gap Metabolic Acidosis Accumulation of unmeasured anions Low HCO 3 and h AG ethanol remia iabetic ketoacidosis araldehyde nfection actic acid thylene glycol alicylates M U D P I L E S Na + Cl - HCO 3 - AG Na + Cl - HCO 3 - AG

Differential Dx of high-anion gap acidosis: "SLUMPED"::

Differential Dx of high-anion gap acidosis: "SLUMPED" : Salicylates Lactic acidosis Uremia Methanol intoxication Paint sniffing (toluene) / Paraldehyde Ethylene glycol intoxication DKA or alcoholic ketoacidosis

Non Anion Gap Metabolic Acidosis:

Non Anion Gap Metabolic Acidosis Loss of HCO 3 or External acid infusion Low HCO 3 AG < 12 GI Losses of Bicarbonate (Diarrhoea) Renal Losses Renal Tubular Acidosis Renal Toxins Carbonic Anhydrase Inhibitors Ureteral Diversion Compensation for Resp. Acidosis HCl or NH 4 Cl Infusion, TPN

Decrease in Anion Gap Metabolic Acidosis Defined as < 6:

Decrease in Anion Gap Metabolic Acidosis Defined as < 6 P araproteinemias, Multiple myeloma L ithium intoxication E xcessive Calcium and Magnesium A lbumin is low (hypoalbuminemia) B romism

Metabolic Acidosis:

Metabolic Acidosis Increased work of breathing : Deep rapid breathing (Kussmaul’s) Peripheral Vasodilatation, collapse, shock, impaired cardiac function Lethargy, drowsiness, confusion, stupor Hyperkalemia Nonspecific : Nausea, Vomiting Chronic Acidosis: Osteopenia – CaCo 3 loss Muscle weakness – Glutamine loss Clinical Features

Metabolic Acidosis:

Metabolic Acidosis Principles: Identify cause Initial goal : Bring the pH ~ 7.25 (For cardiac contractility & responsiveness to catecholamines) Sodabicarb : 1-2 mEq/Kg [1 ml of 7.5% NaHCO 3 = 0.9 mEq] [ Bicarb deficit (mEq/L) = Body wt.(Kg) X 0.3 X Base excess] Half as bolus Half as infusion over 12 – 24 hrs. Management

Metabolic Acidosis:

Metabolic Acidosis Potassium replacement : Serum K + should be > 3.5 mEq/L before administering HCO 3 - THAM (tromethamine; tris-hydroxymethyl aminomethane) An amino alcohol Indication : In partients with CHF who may not be able to tolerate additional Na+ burden if treated with Sodabicarb. Dose : Body wt. (Kg) X Base excess Administration: As infusion over 3 - 6 hours Management – Contd.

Metabolic Acidosis:

Metabolic Acidosis DKA Lactic Acidosis RTA Uremia Salicylate toxicity Specific Treatment

Slide 45:

Metabolic Alkalosis

Slide 46:

Metabolic Alkalosis Very Dangerous: Shifts O 2 dissociation curve to Lt. Causes vasoconstriction of all vessels except pulmonary circulation Suppresses ventilation Decreases ionized Ca ++ and shifts K + into cells – hypocalcemia and hypokalemia Increase in extra-cellular pH (above 7.45) due to primary increase in plasma bicarbonate

Slide 47:

Metabolic Alkalosis Issues to Ponder over: What generated the alkalosis? What is maintaining the alkalosis – what is preventing kidney from excreting the alkali ?

Slide 48:

Metabolic Alkalosis - Causes Loss of acid: GI Losses Vomiting NG suction Acid diarrhoea (Congenital chloridorrhoeas, villous adenomas) Renal H+ Loss Diuretics (thiazides, furosemide) Bartter’s Syndrome Mg deficiency Hyperaldosteronism, Cushing’s Infusion of HCO 3 : Iatrogenic Milk Alkali syndrome Massive blood transfusion (citrated blood) Rapid correction of chronic hypercapnia

Slide 49:

Metabolic Alkalosis What’s maintaining 1. Volume contraction (Chloride responsive) NG Suction, vomiting, diuretics 2. Potassium deficiency 3. Chloride depletion 4. Increased mineralocorticoids (Chloride resistant)

Slide 50:

Metabolic Alkalosis What’s maintaining Volume contraction (Chloride responsive) Adrenal Disorders Exogenous Steroids Alkali Ingestion Licorice Bartter’s Syndrome

Slide 51:

Metabolic Alkalosis Clinical Presentation Muscle cramps Weakness Hypoxia Arrhythmias

Slide 52:

Metabolic Alkalosis Saline responsive intravascular volume expansion with normal saline potassium repletion Ammonium chloride / Arginine chloride in resistant casessistant alkalosis gastric losses) Saline resistant potassium repletion mineralocorticoid antagonists acetazolamide Hemo or peritoneal dialysis : in severe alkaloses with hyperosmolar states

Mixed Acid – Base Disorders:

Mixed Acid – Base Disorders Respiratory Acidosis + Metabolic Acidosis Resp. Distress Syndrome Respiratory Acidosis + Metabolic Alkalosis Excessive diuretic therapy, Chronic respiratory acidosis with C.C.F. Metabolic Acidosis + Respiratory Acidosis Hepatic Failure Respiratory Alkalosis + Metabolic Acidosis Salicylate intoxication Gm – ve sepsis Compensatory adjustments fall outside the expected reange

When to suspect a mixed acid base disorder::

When to suspect a mixed acid base disorder: 1. The expected compensatory response does not occur 2. Compensatory response occurs, but level of compensation is inadequate or too extreme 3. Whenever the PCO 2 and [HCO 3 - ] becomes abnormal in the opposite direction. 4. pH is normal but PCO 2 or HCO 3 - is abnormal 5. In anion gap metabolic acidosis, if the change in bicarbonate level is not proportional to the change of the anion gap. 6. In simple acid base disorders, the compensatory response should never return the pH to normal. If that happens, suspect a mixed disorder.


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