ACID-BASE- THERAPY

TREATMENT OF METABOLIC ACIDOSIS

• Correct underlying problems
• Give bicarbonate IV based on base deficit (BD)
– LD {Base deficit(mEq)} = 0.5L/kg x Wt x (desired HCO₃⁻ - actual HCO₃⁻)
– LD = 0.5 L x60kg x (24mEq/L-15mEq/L)= 270mEq/L
– Give 1/3 to ½ of calculated base deficit (dose of bicarb) over 30 minutes to several
hours
– Check ABGs (30 minutes after the end of infusion)
– Check blood chemistry panel, especially potassium (K)
– Give supplemental replacement for ongoing losses (2mEq/kg/day). Up to 10
mEq/Kg/day in severe losses. Patients with RTA may require maintenance doses up
to 15 mEq/Kg/day
– Replace other electrolytes (K, Mg, etc.)
• IV bicarb therapy can lead to paradoxical acidosis. Therefore intent of treatment is to
increase pH up to 7.2 and bicarb 8-10 mEq/L but not to normalize bicarb level or pH
• Bicarb causes alkalosis and leads the oxy-HgB curve to shift to the left leading to less
oxygen delivery to tissues
• Fluid and Na overload can lead to pulmonary congestion and hypernatremia, hypokalemia,
hypomagnesemia, hypocalcemia, etc.
• The American Heart Assoc. ACLS states that bicarb should not be given to patients with
hypoxia and cardiac arrest. No significant benefits over general supportive care in reducing
mortality.
• See table 52-9 for patients that can benefit or be harmed by alkali replacement therapy
• Dichloroacetate (DCA) is investigational, increases pH by stimulating the effect of lactate
dehydrogenase. SE: Peripheral neuropathy (PN). Give thiamine to prevent PN.
• Tromethamine (THAM) is a 0.3N alkaline solution that combines with hydrogen to form
bicarb and a cationic buffer. It is a carbon dioxide consuming agent that buffers both
respiratory and metabolic acids
– Give THAM LD=1.1 mmol/kg X base deficit
– As it causes osmotic diuresis, THAM increases urine flow and pH, and excretion of
CO2 and electrolytes.
– THAM can cause alkalosis if administered too quickly. Give slowly 1-5mmol/Kg
over 1 hour and monitor ABGs
– THAM has not been proven to be more efficacious than NaHCO3

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 For oral therapy for ambulatory patients with Metabolic Acidosis (See the following table
below)
• Correct underlying problems
• Shohl’s Solution – provides 1mEq of Na and 1mEq of Bicarb. Contains 334mg of citric
acid and 500mg of sodium citrate per each 5 ml.
• Give treatment according to base deficit (BD)
• LD {Base deficit(mEq)} = 0.5L/kg x Wt x (desired HCO₃⁻ - actual HCO₃⁻)
– Give 60-70 mEq TID for 3-5 days
– Give supplemental doses (40mEq TID) for ongoing losses in addition to the LD.
– Check blood chemistry panel, especially potassium (K)

Milliequivalents of
Generic Name Trade Name(s) Dosage Form(s) Comment
Alkali
Shohl’s solution Bicitra (Willen) 1 mEq Na/mL; Solution (500 mg Na Citrate preparations
(sodium citrate/citric equivalent to 1 mEq citrate, 334 mg citric increase absorption
acid) bicarbonate acid/5 mL) of aluminum
Sodium bicarbonate Various 3.9mEq 325 mg tablet Bicarbonate preparations
(eg, Sodamint) bicarbonate/tablet (325 can cause bloating
mg) because of CO2 productio
7.8 mEq 650 mg tablet
bicarbonate/tablet (650
mg)
Baking soda 60 mEq bicarbonate/tsp Powder
(various) (5 g/tsp)
Potassium citrate Urocit-K (Mission) 5 mEq citrate/tablet 5 mEq tablet See above
Potassium K-Lyte (Bristol) 25 mEq 25 mEq tablet
bicarbonate/potassium bicarbonate/tablet (effervescent)
citrate K-Lyte DS 50 mEq 50 mEq tablet See above
(Bristol) bicarbonate/tablet (effervescent)
(double strength)
Potassium Polycitra-K 2 mEq K/mL; equivalent Solution (1,100 mg K See above
citrate/citric acid (Willen) to 2 mEq bicarbonate citrate, 334 mg citric
acid/5 mL)
30 mEq bicarbonate/unit Crystals for
dose packet reconstitution (3,300
mg K citrate, 1,002 mg
citric acid/unit dose
packet)
Sodium Polycitra (Willen) 1 mEq K, 1 mEq Na/mL; Syrup (Polycitra) See above
citrate/potassium Polycitra-LC equivalent to 2 mEq solution (Polycitra-LC)
citrate/citric acid (Willen) bicarbonate (Both contain 550 mg K
citrate, 500 mg Na

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 citrate, 334 mg citric
acid/5 mL)
TREATMENT OF METABOLIC ALKALOSIS

 Correct underlying causes

 Administration of sodium and potassium chloride if responsive

 Administration of HCl if unresponsive to sodium and/or potassium replacement therapy.

Dose of HCl (mEq) (Chloride Deficit) = 0.2 x BW(Kg) x (103 - observed Cl-)

0.2 x BW represents the estimated Cl- space

Administer IV (via central venous catheter to reduce phlebitis) as 0.1N (100mEq HCl/L)
HCl solution in D5W or normal saline at 100-125ml/Hr (10-15mEq/Hr)

Monitor blood gases every 4 hours during infusion

 Ammonium Chloride IV infusion - 20gm (400mEq) or less/day

 Arginine hydrochloride 10% solution IV at a rate of 10gm/hr

Contains 475 mEq/L of chloride
Causes hyperkalemia. Therefore, monitor potassium

 Spironolactone or amiloride if due to hyperaldosteronism

 Acetazolamide 250-500mg IV to increase renal excretion of bicarb

TREATMENT OF RESPIRATORY ACIDOSIS

• Dependent on the chronicity of the respiratory acidosis

• Goal is to Improve ventilation
• Treat underlying problems
– Beta-adrenergic agents
– Antibiotics
– Steroids
– Narcotic analgesic blockers in narcotic overdose
– Avoid sedatives and tranquilizers
– Aggressive pulmonary toilet to clear airway in order to improve gas exchange
– Hydration to decrease viscosity of secretion
• Administration of supplemental oxygen
• Mechanical Ventilation/Endotracheal intubation
– Use oxygen with care – may suppress hypoxic drive
• Administration of respiratory stimulants
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 – Doxapram (Dopram) is used to acutely lower PaCO2 and lessen respiratory
acidosis)
– Provera appears to be effective in chronic respiratory acidosis caused by CNS-
mediated hypoventilation
– THAM and Bicarb can restore responsiveness to beta-agonists and be beneficial in
severe bronchospasm
• Do not use bicarb (rarely use in resp. acidosis)
– Bicarb should not be given to a patient with pure respiratory acidosis because it can
lead to paradoxical respiratory acidosis by increasing the CO₂ load
– Rapid correction can eliminate patient’s drive to breathe and cause metabolic
alkalosis
• Monitor ABGs
• Do not give Oxygen when PO2 = 50mmHg in patients with chronic respiratory acidosis. If
Po2 is less than 50mmHg give oxygen very carefully in a controlled flow of oxygen
• If pCO2 increases while patient is on oxygen, it is a sign of carbon dioxide narcosis and
oxygen should be discontinued

TREATMENT OF RESPIRATORY ALKALOSIS

 Identify and correct underlying problems

• Correct hypovolemia, relieve pain, treat salicylate overdose
• Rebreathing expired air in a paper bag to treat psychogenic hyperventilation
• Treatment of Respiratory Alkalosis is usually not necessary
• Oxygen therapy should be initiated in patients with hypoxemia

TREATMENT OF MIXED ACID-BASE DISORDER

• Thorough History and Physical Exam
• Correction or removal of underlying cause (s)
• Dependent on acid-base abnormalities diagnosed
• Volume repletion
• Antibiotics
• Mechanical ventilation (use capnography and/or spirometry where necessary to help mech.
vent. settings)
• Analgesia/sedation

REFERENCES

• Dipiro’s Pharmacotherapy. 10th Ed. Chapter 52.

• Lee, M. Basic skills in understanding Laboratory data. 6th Ed. ASHP publications.
• Broughton JO. Understanding Blood gases.
• Kellum, J, Puyana J. Acid-Base Disorders. ACS Surgery online
• Kim Lyerly. The handbook of Surgical Intensive Care: Practices of the Surgical residents at
the Duke University Medical Center. 2nd Ed. 1989.
• The Washington’s Manual of Medical Therapeutics. 35th Ed. 2016.
• www.medscape.com/criticalcare. Accessed on 3/24/18.
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Margareth Larose-Pierre, Pharm.D., Associate Dean and Director of Pharmacy Practice Division - Crestview
Associate Professor of Pharmacy Practice – FAMU-COPPS