Acid-Base Disorders Flashcards
Acid-Base Balance
- Normal blood pH: 7.4, range of 7.35-7.45
- Narrow range is necessary to maintain normal physiologic functions
- pH < 6.7 or >7.7 isn’t compatible with life
Acidosis Complications
- Depress myocardium
- Depress CNS/respiratory drive
- Decrease oxygen carrying capacity
- Decrease threshold for arrhythmia
- Increase serum potassium
- Decrease effect of catecholamines
Alkalosis Complications
- Decrease respiratory drive
- Impair oxygen delivery
- Increase potential for cardiac arrhythmia
- Decrease cerebral blood flow
- Decrease serum potassium
- Decrease ionized calcium
- Seizures
Normal Blood Gas Values
pH = 6.1 + log[HCO3/0.03 * pCO2]
- HCO3 typically ~24
- pCO2 typically ~40
pCO2
- Major acid in body
- In equilibrium with carbonic acid (H2CO3)
- Regulated by lungs (ventilation)
- Disturbances in pCO2 are referred to respiratory
HCO3-
- Serves as a buffer to acids in the body
- Major base in body
- Regulated by kidney
- Disturbances in HCO3 are referred to as metabolic
Component of Analysis
Arterial Blood Gas Analysis
- Measures pH, pCO2, pO2
- Calculate HCO3-, O2 saturation
Serum Electrolytes
- Total CO2 content - mainly HCO3, but also pCO2 and H2CO3
- Total CO2 content ~ HCO3 on ABGs
- Label vary with lab, some call carbon dioxide or bicarbonate
Compensation
- Non-involved system attempts to move pH back to normal
- Change in ventilation to compensate for metabolic disorders, occurs rapidly
- Changes in serum HCO3 to compensate for respiratory disorders, occurs slowly
- Compensation never completely corrects underlying disorder
- Amount of compensation is predictable and can be calculated
Metabolic Disorder Compensation
- Compensation by lungs
- CO2 retention to promote acidosis: hypoventilation, shallow breathing
- CO2 excretion to promote alkalosis: hyperventilation
- Effect on pH seen in minutes, 12-24 hours for max effects
- Expected Acidosis Compensation: pCO2 = (1.5(HCO3) + 8) +/-2
- Expected Alkalosis Compensation: pCO2 = Increases 0.6 mmHg for each mEq/L increase in HCO3
Respiratory Disorder Compensation
- Metabolic by kidneys
- Increases HCO3 reabsorption and production by kidney to promote alkalosis
- Increases HCO3 excretion to promote acidosis
- Effect takes 12-24 hours and day for max effects
- Expected Acute Acidosis Compensation: HCO3 - increase 1 mEq/L for every 10 mmHg INCREASE in pCO2
- Expected Chronic Acidosis Compensation: HCO3 - increase 3.5 mEq/L for every 10 mmHg INCREASE in pCO2
- Expected Acute Alkalosis Compensation: HCO3 - decrease 2 mEq/L for every 10 mmHg DECREASE in pCO2
- Expected Chronic Alkalosis Compensation: HCO3 - decrease 5 mEq/L for every 10 mmHg decrease in PCO2
Metabolic Acidosis
- Decrease in pH seen as a result of HCO3 decrease
- Loss of HCO3 either renally (renal tubular acidosis) or non-renally (diarrhea, intestinal drainage)
- Consumption from buffering: endogenous acids (lactic/keto) or exogenous acids (salicylates, chloride containing IVs, methanol)
Anion vs Non-Anion Gap
- Two categories of Metabolic Acidosis
- Anion gap is calculated to help determine etiology of acidosis
AG = Na - (Cl + Total CO2 content)
- Normal AG ~ 9
- Elevated AG >= 12, indicates presence of non-chloride containing anions
- Unmeasured anions include sulfates, phosphates, organic anions, and toxins
Anion Gap Metabolic Acidosis
-Due to presence of unmeasured anions
Causes
1. Accumulation of organic acids in renal insufficiency (amino acids, sulfates, phosphate)
2. Ingestion of acid or acid by-product (toxic ingestion, propylene glycol <= avoid in renal impaired/neonates)
EX: Metformin, especially in acutely ill patients
MUDPILES
Etiologies of Anion Gap Metabolic Acidosis M = Methanol U = Uremia D = Diabetic Ketoacidosis P = paraldehyde, Propylene Glycol I = Iron, Isoniazid (INH) L = Lactic Acid E = ethanol, ethylene glycol S = Salicylates
Non-Anion Gap Metabolic Acidosis
- Occurs when HCO3 deficit is replaced by chloride (to maintain electrical neutrality)
- Occurs via kidney reabsorption or exogenous sources of chloride (NS, Hypertonic saline, HCl)
Non-Anion Gap Endogenous Causes
- Renal tubular acidosis
- Diarrhea
- Intestinal fistula or drainage
- Carbonic anhydrase inhibitors
- Potassium-sparing diuretics
- Hypoaldosteronism
Non-Anion Gap Exogenous Causes
- HCl ingestions: bicarbonate buffers acid and Cl remain
- Use of large amounts of Cl containing fluids: usually mild and requires no treatment
Treating Acute/Severe Metabolic Acidosis
- pH < 7.2
- Treat underlying cause if possible
- Alkali therapy isn’t indicated usually, can be harmful
- If underlying cause can’t be removed/reversed, consider alkali therapy: IV sodium bicarbonate, tromethamine
Sodium Bicarbonate + Severe Metabolic Acidosis
- Unclear when beneficial, may have AE
- AE: promote intracellular acidosis, shift oxygen satuation to decrease delivery to tissues, hypervolemic hypernatremia, over correct
- HCO3 Dose = Vd HCO3 * BW (kg) * (Normal HCO3 - actual HCO3), administer 1/2 calculated dose of bicarbonate
- Vd HCO3 = 0.5
- Make sure patient is adequately ventilated, goal is to improve not correct to normal
Tromethamine + Severe Metabolic Acidosis
- THAM
- Sodium free organic amine
- Accepts protons
- May be able to correct intracellular pH
- Not shown to be more efficacious than sodium bicarboante
- Administer slowly
- AE: respiratory depression, chemical phlebitis, tissue damage
- Not available in US
Chronic Metabolic Acidosis Treatment
- Correct cause
- Gradual correction over days to weeks
- Oral admin of bicarbonate (NaHCO3)
- Oral admin of bicarbonate precursor (citrate, acetate)
Metabolic Alkalosis
- Increase pH and HCO3
- Loss of Cl-rich, bicarbonate poor fluid (loop/thiazide diuretics, emesis, nasogastric suctioning)
- Excessive bicarbonate intake
- Volume depletion: enhance reabsorption of bicarbonate
Metabolic Alkalosis Categories
- Based on response to saline volume expansion
- NaCl responsive: urine [Cl] < 10
- NaCl resistant: urine [Cl] > 20
NaCl Responsive Causes
- Vomiting, gastric drainage
- Some cases of secretory diarrhea that cause chloride loss without proportional bicarbonate loss
- Excessive diuretic use (loop/thiazide)
- Have signs of intravascular volume depletion usually
NaCl Resistant Causes
- Excess mineralcorticoid activity (Cushings, hyperaldosteroinism, corticosteroids) - increase Na reabsorption in distal tubule, K/H+ secretion into tubule lumen which promotes HCO3 generation/reclamation
- Alkali ingestion
- Significant potassium and magnesium deficiency
Metabolic Alkalosis Presentation
- No unique signs/symptoms with mild-moderate cases
- Severe (pH > 7.6): cardiac arrhythmia, neuromuscular irritability (tetany, hyperreflexia), mental confusion
Metabolic Alkalosis Treatment
- Correct cause/underlying condition
- Chloride usually responsive to NaCl volume expansion with NS: frequently need to replace with potassium chloride and magnesium too
- GI losses: antiemetics, H2 blockers, PPI
- Other treatments: HCl, ammonium chloride, arginine HCl
- Consider carbonic anhydrase inhibitors (acetazolamide) if not able to tolerate fluid
- Chloride resistant: correct cause, replace potassium/magnesium if in deficit, treat with spironolactone, amiloride, or triamterene
Respiratory Acidosis Causes
Acute
- Pulmonary emboli
- Severe pneumonia/bronchospasm
- Airway obstruction
- Trauma - crash, pneumothorax
- Narcotic/sedative overdose
- Increased CO2 production from excess glucose administration
Chronic
- Neuromuscular abnormalities (MS, polio)
- Pulmonary abnormalities (COPD)
Respiratory Acidosis Treatment
Acute: usually with concomitant hypoxia
- Treat underlying cause
- Maintain airway and improve oxygen status with supplemental oxygen
- Ventilation with or without intubation
Chronic
- Treat underlying disease/cause
- Cautious use of oxygen since may remove respiratory drive since its hypoxemic dependent
Respiratory Alkalosis Causes
Central stimulation of Respiration
- Anxiety, pain, fear
- Head trauma, brain tumors
- Pregnancy
- Progesterone
- Catecholamines, theophylline, nicotine, salicylates, analeptics
- Hypoxia
- Chronic liver disease
Peripheral Stimulation of Respiration
- Pulmonary emboli
- CHF, hypotension
- High altitude
Other Causes
- Excessive mechanical ventilation
- Voluntary hyperventilation
Respiratory Alkalosis Presentation
- CNS: light-headedness, confusion, syncope, seizures
- CV: arrhythmia
- GI: N/V
- Metabolic: hypocalcemia, hyperchloridemia, hypokalemia, hypophosphatemia
Respiratory Alkalosis Treatment
- Correct Cause: pain control, turn down ventilator, breathe into paper bad
- Oxygen therapy if hypoxemic
- If asymptomatic, treatment might not be required
Compensation Rules
- Primary disturbance always invokes a compensation response to try and normalize pH
- Never totally corrects pH
- Degree of compensation is predictable and a greater/lesser response represents a secondary/mixed disorder
Mixed Acid-Base Disorders
- Two of the above disorders occurring simultaneously
- Each have their own methods of how to treat and possible causes
R Acidosis + M Acidosis
Causes
- Cardiorespiratory arrest
- Lung disease patients who develop poor tissue perfussion (shock)
- Unable to compensate
- Treat both disorders: improve oxygen delivery and give alkali therapy
R Alkalosis + M Alkalosis
-Commonly occur together
Causes
-Over-aggressive mechanical ventilation and nasogastric sunctioning
-Hyperventilation from hepatic cirrhosis and use of loop diuretics
-Treat by administering NaCl or KCl and correct hyperventilation
R Alkalosis + M Acidosis
-pH closer to normal values than if either existed alone
Causes
-Salicylate intoxication
-Pulmonary renal syndromes
-Treat by correcting cause
