Acid Base 2
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| Can acidosis exist without acidemia? | Acedemia cannot exist without acidosis, but acidosis can exist at any blood pH if more than one disturbance is present; same thing for alkalosis/alkalemia
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| Metabolic disturbance | An acidosis or alkalosis resulting from a primary change in the
serum bicarbonate concentration
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| What is the difference between acidosis and acidemia? | Acidosis: pathophysiological process that tends to decrease blood pH; acidemia: arterial blood pH <7.36
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| What is the difference between alkalosis and alkalemia? | Alkalosis: pathophysiological process that tends to decrease blood pH; alkalemia: arterial blood pH <7.36
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| Respiratory disturbance | An acidosis or alkalosis resulting from a primary change in the
P CO2
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| Compensation | The physiologic metabolic (renal) and respiratory changes to
return the pH toward normal in response to a primary acidosis or
alkalosis.
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| Does compensation return pH to normal? | Not completely; time course varies: buffering (minutes to 6 hours), respiratory (minutes to 12 hours), metabolic (24-72 hours)
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| Simple disturbance | A single acid-base process (acidosis or alkalosis) and its expected
compensation are present
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| Mixed disturbance | two or more primary acid base disturbances are present. The
arterial blood pH will depend on the direction and magnitude of the
disturbances
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| What is the primary process and compensation in metabolic acidosis? | Primary process: decreased HCO3-; Compensation: decrease PCO2
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| What is the primary process and compensation in metabolic alkalosis? | Primary process: increased HCO3-; Compensation: increase PCO2
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| What is the primary process and compensation in respiratory acidosis? | Primary process: increased PCO2; Compensation: increase [HCO3-]
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| What is the primary process and compensation in respiratory alkalosis? | Primary process: decreased PCO2; Compensation: decreased [HCO3-]
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| Metabolic acidoses are categorized on the basis of ... | the anion that accumulates replacing the bicarbonate ion
into hyperchloremic metabolic acidosis and anion-gap metabolic acidosis.
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| anion gap (AG) | defined as the difference between the serum sodium concentration and the sum of the concentrations of the “measured” anions, chloride and bicarbonate.
Mathematically, this is represented as:
AG = [Na+] – [Cl-] – [HCO 3-]
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| What is a normal anion gap? | 10+/-2 mEq/L ; approximately 2/3 of normal anion gap accounted for by dissociated carboxyl groups on albumin, so adjust in setting of hypoalmbuminemia
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| Describe the changes seen in hypercholermic metabolic acidosis in terms of HCO3-, H+, and Cl- levels | serum bicarb reduced, chloride concentration increases-->NO NET CHANGE IN ANION GAP
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| Describe the changes seen in anion gap metabolic acidosis (aka "delta" acidosis) | decrease in bicarb due to addition of strong acid (e.g. lactic acid)-->AG >20 mEq/L ALWAYS represents a metabolic acidosis, regardless of pH or serum bicarb concentration
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| AG > 20 mEq/L | Always represent metabolic acidosis, regardless of pH or serum bicarbonate concentration
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| What is the easiest way to determine the etiology in a differential diagnosis of metabolic acidosis? | See anion gap; if AG is normal-->hypercholeremic; if AG is increased, High anion gap metabolic acidosis
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| In all the causes of high anion gap metabolic acidosis, you see an excessive production, inegestion, or retention of ____. | strong acid or a compount metabolized into a strong acid
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| What is the differential diagnosis for increased anion gap metabolic acidosis? | diabetic ketoacidosis, alcoholic ketolactic acidosis, lactic acidosis, renal failure, toxins (methanol, ethylene glycol, salicylate, paraldehyde)
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| What is the anion associated with diabetic ketoacidosis? What is the pathophysiology? | In diabetic ketoacidosis, insulin deficiency results in abnormal production of ketoacids: beta hydroxybutyrate, acetoacetate
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| What is the anion associated with alcoholic ketolactic acidosis? What is the pathophysiology? | Fasting after binge drinking leads to low glucose levels, suppressed insulin secretion and ketosis + tissue hypoperfusion and/or liver disease -->increased lactate: beta hydroxybutyrate, acetoacetate, lactate
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| What is the pathophysiology of lactic acidosis? | 1) Increased tissue lactate production (e.g., congenital enzymatic defects, tissue hypoperfusion or hypoxia, enhanced metabolic rate) or 2) decreased lactate utilization (e.g., hypoperfusion, liver disease, ethanol intoxication)
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| Hyperchloremic metabolic acidosis may result from ... | impaired acid excretion, increased
bicarbonate losses, or hydrogen ion gain, as outlined below
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| What can lead to impaired renal acid excretion? | Renal failure; distal renal tubular acidosis (classic/hypokalemic [type I], or hyperkalemic [type IV])
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| What can lead to renal bicarbonate loss? | Proximal renal tubular acidosis (type II), carbonic anhydrase inhibitors, therapy of diabetic ketoacidosis (due to urinary excretion of beta hydroxybutyrate and acetoacetate-->can't regenerate bicarbonate if ketogenesis suppressed)
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| What can lead to GI bicarb loss? | diarrhea, pancreatic drainage, urteral diversion
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| What can lead to acid gain? | Hyperalimentation solutions, ammonium chloride ingestion
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| Proximal renal tubular acidosis (Type II RTA) | characterized by impaired H+ secretion in proximal nephron-->lower bicarb reclaim--> bicarb wasting results when above threshold for reclamation; associated with hypokalemia due to increased distal K secretion (due to hyperaldeosteronism)
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| Proximal RTA in children vs. adults | children: usually due to congenital metabolic defects. adults: usually secondary to acquired proximal tubular damage (e.g. heavy metal exposure, multiple myeloma)
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| Proximal RTA is often accompanied by... | other proximal tubular transport defects including
renal glycosuria, phosphate wasting, aminoaciduria and hypouricemia (the Fanconi
syndrome).
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| Iatrogenic RTA | may result from therapy with carbonic anhydrase inhibitors (e.g. acetozolamide)
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| Classic distal renal tubular acidosis (Type I RTA) | either from defect in the distal nephron's proton pumps or from back leak of secreted hydrogen ion; urine pH cannot be reduced below 5.5 (daily acid load cannot be excreted)
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| What other electrolyte imbalances can you expect to see with Type I RTA? | may be associated with hypercalciuria and nephrocalcinosis; serum K+ usually low
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| What molecular defects can account for Type I RTA? | Impaired H + -ATPase function
Defective bicarbonate/chloride exchanger
Defective cytosolic carbonic anhydrase
Back-leak of H + ion
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| Hyperkalemic distal renal tubular acidosis (Type IV RTA) | characterized by hyperkalemia and hypercholermic metabolic acidosis, with 2 major patterns of disturbance: aldosterone deficiency/resistance and voltage dependent defect in H+ ion secretion
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| Type IV RTA secondary to aldosterone deficiency/resistance | hyperkalemia primary disturbance, suppressing proximal tubule ammoniagenesis-->metabolic acidosis; urinary acidification is intact; most have mild renal insufficiency
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| Type IV RTA secondary to voltage dependent defect in H+ ion secretion | Primary defect is collecting duct Na+ reabsorption-->decrease in voltage gradient favoring H+ ion secretion-->maximal urinary acidification impaired. Seen in variety of disorders
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| How does metabolic acidosis develop in kidney disease? | Early: patients develop hypercholeremic metabolic acidosis (due to reduced urinary buffers [NH3]); urinary acidification preserved; RAAS axis normal. Chronic: elevated AG due to retention of phosphates, sulfates, and organic anions
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| Urinary anion gap | The urine anion gap (UAG) is calculated as the difference between the measured cations in the urine (Na + and K + ) and urine Cl - : UAG = [Na+] + [K+] – [Cl-]
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| In diarrhea and other non-renal causes of hyperchloremic acidosis, the kidney should be attempting to compensate by increasing ___. The major mechanism for this increase is a marked increase in ___. | net acid excretion; urinary ammonium excretion
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| The UAG will be negative when ___. If there is little ammonium present, the UAG will be ___. | ammonium is present and balanced by negatively charged urinary chloride; zero or positive
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| ____ is the normal respiratory response to metabolic acidosis | Hyperventilation
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| respiratory compensation begins within ___ but takes ____ for maximal response. | minutes; 12-24 hours
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| Winter's formula | P CO2 = 1.5 x [HCO 3- ] + 8 ± 2
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| In patients with metabolic acidosis, what can you conclude if the PCO2 is greater than predicted with Winter's formula? Less? | Greater-->additional respiratory acidosis; less-->respiratory alkalosis
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| Why is respiratory compensation limited? | respiratory compensation is limited because the P CO2 cannot
be lowered much below 10 torr.
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| What is the treatment for metabolic acidosis? | remove underlying cause; alkali replacement required under certain circumstances (if pH less than 7.1 [respiratory compensation maxed and myocardial depression risk]), but only restore to safe range
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| If acute bicarb replacement is indicated, how can you estimate the amount to administer? | HCO 3
- dose (in mmol) = 0.5 x BW (kg) x{[HCO 3 ] desired - [HCO 3 ] actual }
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| How should you treat chronic metabolic acidosis? | Goal: prevent long term sequelae (e.g. bone disease, growth failure, nephrocalcinosis, nephrolithiasis; normalize serum bicarb concentration
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| What are the characteristics of metabolic alkalosis? | high blood pH due to primary elevation in bicarb; accompanied by compensatory increase in PCO2; generation of metabolic alkalosis due to gain of bicarb or loss of acid from body
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| The presence of a sustained metabolic alkalosis implies a defect in what process? | renal bicarbonate excretion; consider etiologies in both generation and maintenance of bicarb levels
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| How can the body lose acid in levels high enough to lead to metabolic alkalosis? | Renal acid loss (diuretic therapy, mineralcorticoid excess, cushing's syndrome, severe potassium depletion, bartter's and gitelman's syndrome, liddle's syndrome) and GI acid loss (gastric acid loss and chloride diarrhea)
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| How can the body gain alkali in levels high enough to lead to metabolic alkalosis? | bicarb administration, milk-alkali syndrome, infusion of organic anions (citrate, acetate, lactate), rapid correction of chronic hypercapnia
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| The maintenance of a metabolic alkalosis requires an impairment ___. | of renal bicarbonate
excretion.
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| What (3) things can lead to impaired renal bicarb excretion? | Decreased GFR (decreased effective arterial blood volume [pre-renal state], renal insufficiency), increased proximal tubular bicarb reclaim (pre-renal state, chloride depletion), and increased H+ excretion (mineralocorticoid excess, hypokalemia)
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| How is metabolic alkalosis diagnosed? | Urine chloride concentration (in absence of diuretic): < 20 mmol/L suggests volume depletion while >20 suggests excess mineralocorticoid or Bartter's syndrome. Urine Na+ increase (less reliable) due to increased bicarb loss
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| What is the respiratory compensation for metabolic alkalosis? | Hypoventilation; not as predictale as hyperventilation in metabolic acidosis; hypoventilation limited by hypoxemia, which is a strong respiratory stimulant
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| Saline responsive metabolic alkalosis: treatment | consists of volume expansion with isotonic saline; re-expansion + Cl- restoration-->decrease bicarb resorption distally, trigger bicarbonaturia and lower serum bicarb concentration; if hypokalemic, correct with KCl
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| Metabolic alkalosis due to gastric acid losses, diuretics, chloride depletion and the post-hypercapnic state: treatment | all respond to saline administration
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| Saline resistant metabolic alkalosis: treatment | Patients typically NOT volume or chloride depleted (check serum); may be complicated by mineralocorticoid excess (treat with MR inhibitor) or hypokalemia (give K+ and treat with K+ sparing diuretics if needed)
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| Respiratory acidosis: primary defect and possible causes | primary process is increase in arterial PCO2 due to abnormalities in respiratory function (impaired alveolar gas exchange, obstructive airway disease, disorders of respiratory muscles and chest wall, or CNS inhibition)
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| The renal compensation for respiratory disorders is ___; this is evidence by minimal changes in ___ | slow; minimal increase in serum bicarb
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| In chronic respiratory acidosis, hypercapnia stimulates ___ excretion and leads to an increase in the ___. | renal acid; serum bicarbonate concentration
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| The bicarbonate level generally increases by ___ mmol/L for each 10 torr increase in P CO2 , but rarely rises to greater than 35-40 mmol/L | 3.5 – 5.0
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| Maximal compensation typically requires ___ hours | (24-) 48
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| In chronic hypercapnia, what is the major stimulus for ventilation? What can you do this fix this? | hypoxemia; oxygen therapy may inhibit ventilation and worsen hypercapnia-->must be used with extreme caution if chronic respiratory acidosis
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| What are some of the symptoms of acute hypercapnia? | headache, asterixis, confusion, lethargy, obtundation
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| asterixis | flapping tremmor of the hand when it is dorsiflexed; also known as "liver flap"
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| obtundation | dulled or less sharp
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| Respiratory alkalosis: primary process | reduction in arterial PCO2 through hyperventilation
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| What are the most common etiologies for respiratory alkalosis? | hypoxemia, intrapulmonary disease, stimulation of the medullary respiratory center, and mechanical ventilation
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| How are bicarb levels in the serum affected by respiratory alkalosis? How effective is compensation? | Slow; in acute: small decrease in bicarb due to intracell buffering. Chronic: renal bicarb excretion increased and serum bicarb drops by ~5 mmol/L for each 10 torr fall in PCO2
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| What are signs and symptoms of respiratory alkalosis? | lightheadedness, parasthesias, cramps, carpopedal spasm, seizures (in extreme cases)
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| What is the treatment goal for respiratory alkalosis? | Treat underlying disorder; if related to anxiety, rebreathing into a paper bag may be effective
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| Mixed disturbances | More than one primary acid-base disturbance present (e.g. both metabolic acidosis from diabetic ketoacidosis and respiratory acidosis due to pneumonia); can even be antagonistic (m. acidosis + r. alkalosis)
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| To determine etiology of acid base disorder, what things should you pay attention in history? | Diuretics + vomiting (metabolic alkalosis); diarrhea, alcoholism, or diabetes mellitus (metabolic acidosis); chronic lung disease, CHF, or pneumonia (respiratory acidosis or alkalosis)
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| Kussmaul respirations | slow deep breaths seen as respiratory compensation for metabolic acidosis
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| Fruity oder | seen in ketosis
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| Stigmata of liver disease | respiratory alkalosis
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| volume contraction | metabolic alkalosis
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| CHF | respiratory alkalosis?
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| How do you measure tCO2? | [HCO3-] + [H2CO3] + CO2{serum}; usually, [HCO3-] ~= tCO2
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| Elevated serum creatinine or hyperglycemia may be associated with... | metabolic acidosis
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| What should you check when analyzing arterial blood gas? | check if pH, PCO2, and [HCO3-] fit simple disturbance; if acidosis, apply Winter's formula to see degree of respiratory compensation; normal pH, PCO2, and [HCO3-] do not exclude acid base disturbance-->check anion gap
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