Abd2009

Disturbance Of Acid-Base Regulation Dr. Matongjun Emergency Department of Tianjin General Hospital

ABG pH 7.35 – 7.45 P CO2 35 – 45 mmHg P O2 75 – 100 mmHg HCO 3 - 22 – 26 mmol/L

Acid-base homeostasis Buffer system Carbonic acid / Bicarbonate Organ regulation Lungs Characteristic: Sensitive, quickly, but tired easily so can not continue long term Kidneys Characteristic: powerful but slower (hours to days)

Henderson-Hasselbalch equation pH=pKa+lg [HCO 3 － ] [H 2 CO 3 ]

Category SABD pH: acidosis, alkalosis Etiology: respiratory, metabolic MABD Two or three SABD are taking place simultaneously

Definition HCO 3 － ↓ , H + ↑ pH   HCO 3 -  * compensation process P CO 2  *

manifestation Kussmaul’s respiration Nausea ， vomiting and abdominal pain Tachycardia, cardiac output decrease and hypotension Headache, weakness, lethargy and confusion, the level of consciousness is depressed, the deep tendon reflex decrease. Alter plasma potassium and Calcium concentration

Category Increased anion gap and normal anion gap Anion Gap [Na + ] - ( [Cl - ] + [HCO 3 - ] ) Normal range 8~16 mmol/L unmeasured anions, consist of proteins (primarily albumin), sulfates, phosphates, and organic acids

Anion Gap All anions and cations in Serum TOTAL 151 TOTAL 151 Sulfates 1 Phosphates 2 Magnesium 1.5 Organic acids 5 Potassium 4.5 Proteins 15 Calcium 5 Bicarbonate 24 Sodium 140 Chloride 104 CATIONS ANIONS

Category Increased AG HCO 3 - decreases and replaced by other anions Normal AG (hyperchloremic) HCO 3 - decreases and replaced by Cl -

Elevated AG Metabolic Acidosis Lactic acidosis L Unmeasured osmoles , Ethylene glycol, Aldehydes , Paraldehydes U Alcoholic lactic acidosis A Methanol ingestion M Starvation ketosis S Salicylate intoxication S Uremia U Diabetic ketoacidosis K Etiology

increased serum chloride concentrations generally due to gastrointestinal or renal bicarbonate wasting Ingestion of chloride salts or chloride-containing anion exchange resins Normal AG Metabolic Acidosis

Treatment Remove the Cause alkali therapy Benefit: decrease the risk of cardiovascular compromise Risk: 5%NaHCO 3 is hyperosmotic, hypernatremia, hypercapnia, cerebrospinal fluid acidosis, and overshoot alkalosis Indication: renal failure; arterial blood pH below 7.20 or HCO 3 - concentration below 10 mmol/L Goal: Maintain the blood pH > 7.20 and plasma HCO 3 - concentration > 10 mmol/L

definition plasma HCO 3 － concentration >27 mmol  L arterial blood pH>7.40 Compensation PaCO 2 ↑

Etiology loss of acid from GI tract or urine, loss fluid with a chloride HCO 3 - concentration ratio that is higher than plasma loss of gastric contents, Vomiting or nasogastric suctioning. Diuretics (Cl lost ) Hyperaldosteronism (H + and Cl - lost ) alkaline drugs ingestion Antacid overuse (HCO 3 - ) Blood transfusions (citrate )

Diagnosis History Symptoms Irritability and Possible tetany, tingling , facial twitching, muscle tremors volume depletion ： weakness, postural dizziness hypokalemia ： muscle weakness, paresthesias physical examination respiratory rate BP(hypertension+Hypokalemia+metabolic alkalosis suggest primary mineralocorticoid-induced disease)

Treatment stopping the intake of soda bicarbonate Saline-responsive Correct volume deficits potassium supplementation ： 4.5-5.5 mmol/L H 2 R antagonists ： ranitidine, cimetidine, diminish H + secretion; pump inhibiter, Omeprarole Saline-unresponsive remove the mineralocorticoid source or block with spironolactone

Definition Lungs fail to eliminate CO 2 so PaCO 2 is elevated Compensation HCO 3 － ↑

Etiology inhibition of the respiratory center: head trauma, Neurological disorders, anesthesia disorders of respiratory muscle: Chest trauma upper airway obstruction disorders affecting gas exchange across pulmonary capillaries: COPD, pneumonia, acute or chronic respiratory failure , cardiac arrest

Signs and Symptoms respiratory distress, dyspnea level of consciousness  If severe, patients may complain of headaches or show signs of increased intracranial pressure due to the vasodilatory properties of C0 2 , increase cerebral blood flow

Pathophysiology Acute Compensation l mmol/L increase in HCO 3 - for each 10mmHg in PCO 2 The HCO 3 - rarely rises above 30mmol/L Chronic Compensation Over the next 2-3 d the kidneys increase H + secretion leading to an elevation of serum HCO 3 - by 3~4mmol/L for each 10mmHg increase in PaCO 2

Treatment improving ventilation HCO 3 - should not be given Oxygen should also be used with care Diet: Low carbohydrate, high fat

Definition decrease in blood PaCO 2 compensatory decrease in HCO 3 － .

Causes of Respiratory Alkalosis Increased CNS drive for respiration Anxiety CNS infection/infarction/trauma Drugs - salicylates/nicotine/aminophylline Fever/sepsis - especially Gram-negative sepsis Pregnancy/progesterone Anemia, Pulmonary edema/pneumonia , Pulmonary emboli Carbon monoxide toxicity Reduced inspired 0 2 tension - high altitude Increased mechanical ventilation

Signs and Symptoms hyperventilation: rapid, deep respirations perioral and extremity paresthesias, muscle cramps, seizures cardiac arrhythmias  K + ,  Ca +

Pathophysiology Acute Compensation extra-and intra-cellular buffering ， l~2mmol/L fall in HCO 3 － for every 10mmHg decrease in PaCO 2 The HCO3- rarely goes below 18mmol/L. Chronic Compensation kidneys decrease the secretion of H + ， serum HCO 3 － decreases 4~5mmol/L for every 10mmHg decrease in PaCO 2 .

Treatment correcting the underlying disorder In ICU, hypoxemia and improper ventilatory settings are the most common cause Rebreathing in a paper bag can help the patient with psychogenic hyperventilation Treatment of the alkalosis is usually not necessary Antianxiety medications, diazepam

Diagnosis The proper evaluation of patients with suspected acid-base disorders requires consideration of The clinical picture Blood Gas Results Serum electrolytes

Diagnosis metabolic or respiratory determined by the primary change, in HCO 3 - or PCO 2 acute or chronic An acute process is measured in minutes to hours a chronic process is measured in days to weeks or longer simple or mixed The primary change of simple disorder is in only one parameter The primary change of mixed disorder is in both

ABG The simplest approach to the evaluation of blood gases is to consider pH. Pco 2 and HCO 3 - separately and then combine the information

ABG Interpretation Identify whether pH, pCO 2 , and HCO 3 are abnormal pH 7.30 pCO2 55 HCO3 26 Match like disorders pH and pCO 2 are both the two matching values tell what the problem is – Acidosis or Alkalosis

ABG Interpretation Determine if abnormality is due to the kidneys (metabolic ) or the lungs (respiratory) pH 7.30 pCO2 55 HCO3 26 Match the like abnormalities Respiratory (lung problem) and Acidosis = Respiratory Acidosis Acid Acid = LUNGS Normal = Kidneys

MABD The compensation can be expected. If the compensation is outside the expected range, it is a MABD Two methods to diagnose MABD Method I A rigorous method which involves calculation of the expected compensations Method II Look on a nomogram If Pco 2 and HCO 3 - change in opposite direction consider a MABD

Method I Metabolic Acidosis: Expected pCO 2 = 1.5 x [HCO 3 - ] + 8 ± 2 Alkalosis: Expected pCO 2 =↑6 mmHg per 10 mEq/L ↑ in HCO 3 -

Method I Respiratory Acidosis Acute Expected ↑ HCO 3 - = ↑ 1mEq/L for each 10 mm ↑ PCO 2 Chronic: Expected ↑ HCO 3 - = ↑ 3.5mEq/L for each 10 mmHg PCO 2 Alkalosis Acute Expected ↓ HCO 3 - = ↓ 2mEq/L for each 10 mm Hg ↓ PCO 2 Chronic Expected ↓ HCO 3 - = ↓ 5 mEq/L for each 10 mmHg ↓ PCO 2

Example 1 pH=7.08, pCO 2 =14, HCO 3 - =4, Na=140, Cl=104 The pH is low indicating the primary disorder is acidosis. The anion gap is 140 - (104 + 4) = 32, thus elevated The pCO 2 is low, the expected compensation The predicted pCO 2 by the above equation is 1.5×4+8 = 14 ， This is the observed pCO 2 simple increased anion gap metabolic acidosis pH=7.08, pCO2=14, HCO3-=4, Na=140, Cl=124 ？

Example 2 pH 7.37, pCO 2 =18, HCO 3 - =10, Na=140, Cl=114 the pH to be normal The anion gap is 16, thus increased Expected pCO 2 is 1.5×10+8 = 23 (21 at minimum), there must be an element of respiratory alkalosis a combination of increased anion gap metabolic acidosis and a respiratory acidosis

Example 3 In a patient with severe COPD, and who is diuretics, the pH=7.42, pCO 2 = 65, HCO 3 - =41, Na 143, K 3.1, Cl 88 Start with a metabolic alkalosis, why? pCO 2 should be 50.2 mmHg 6 mmHg CO 2 for each 10 mEq/L HCO 3 - ， 41-24 = 17; 1.7×6 + 40 = 50.2 mmHg pCO 2 is measured at 65, there is a respiratory acidosis

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