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01.Acid Base and ElectrolytesSecrets

How do you analyze arterial blood gas values? 1. pH- acidosis or alkalosis (primary), then the body compensates (secondary). 2. High CO2- respiratory acidosis (pH: < 7.4) or compensating for metabolic alkalosis (pH: > 7.4). Low CO2- respiratory alkalosis (pH: > 7.4) or compensating for metabolic acidosis (pH: < 7.4). 3. High bicarbonate- metabolic alkalosis (pH: > 7.4) or compensating for respiratory acidosis (pH: < 7.4). Low bicarbonate- metabolic acidosis (pH: < 7.4) or compensating for respiratory alkalosis (pH: > 7.4). Does the body compensate beyond a normal pH?Overcorrection does not occur. A patient with metabolic acidosis will eliminate CO2 to help restore a normal pH. However, if respiratory alkalosis is a compensatory mechanism (and not a rare, separate primary disturbance), the pH will not correct to > 7.4. Common causes of respiratory acidosis? COPD Asthma Drugs (opioids, benzodiazepines, barbiturates, alcohol, other respiratory depressants) Chest wall problems (paralysis, pain) Sleep apnea. Common causes of metabolic acidosis? Ethanol Diabetic ketoacidosis Uremia Lactic acidosis (e.g., sepsis, shock, bowel ischemia) Methanol/ethylene glycol, aspirin/salicylate overdose Diarrhea Carbonic anhydrase inhibitorsCommon causes of respiratory alkalosis? Anxiety/hyperventilation Aspirin/salicylate overdose.Common causes of metabolic alkalosis? Diuretics (except carbonic anhydrase inhibitors) Vomiting Volume contraction Antacid abuse/milk-alkali syndrome Hyperaldosteronism. What type of acid-base disturbance does aspirin overdose cause? Respiratory alkalosis and metabolic acidosis (two different primary disturbances). Look for coexisting tinnitus, hypoglycemia, vomiting, and a history of swallowing several pills. Alkalinization of the urine (with bicarbonate) speeds excretion. What happens to the blood gas of patients with chronic lung conditions? In certain people with chronic lung conditions (especially sleep apnea), pH may be alkaline during the day because they breathe better when awake. In addition, just after an episode of bronchitis or other respiratory disorder, the metabolic alkalosis that usually compensates for respiratory acidosis is no longer a compensatory mechanism and becomes the primary disturbance (elevated pH and bicarbonate). Remember sleep apnea, like other chronic lung diseases, can cause right-sided heart failure (cor pulmonale). Should you give bicarbonate to a patient with acidosis? For Step 2, almost never. First try intravenous fluids and correction of the underlying disorder. If all other measures fail and the pH remains < 7.0, bicarbonate may be given. The blood gas of a patient with asthma has changed from alkalotic to normal, and the patient seems to be sleeping. Is the patient ready to go home? For Step 2 purposes, the patient is probably crashing. The pH is initially high in patients with asthma because they are eliminating CO2. If the patient becomes tired and does not breathe appropriately, CO2 will begin to rise and pH will begin to normalize. Eventually the patient becomes acidotic and requires emergency intubation if appropriate measures are not taken. If this scenario is mentioned on boards, the appropriate response is to prepare for possible elective intubation and to continue aggressive medical treatment with beta 2 agonists, steroids, and oxygen. Fatigue secondary to work of breathing is an indication for intubation. Asthmatic patients are supposed to be slightly alkalotic during an asthma attack. If they are not, you should wonder why. Signs and symptoms of hyponatremia? Lethargy Seizures Mental status changes Confusion Cramps Anorexia ComaHow do you determine the cause of hyponatremia? The first step in determining the cause is to look at the volume status: Hypovolemic- Dehydration, diuretics, diabetes, Addison's disease/ hypoaldosteronism (low potassium) Euvolemic- SIADH, psychogenic polydipsia, oxytocin use Hypervolemic- Heart failure, nephrotic syndrome, cirrhosis, toxemia, renal failure How is hyponatremia treated? Hypovolemic hyponatremia- normal saline. Euvolemic and hypervolemic hyponatremia-water/fluid restriction: diuretics may be needed for hypervolemic hyponatremia. What medication is used to treat SIADH if water restriction fails? Demeclocycline- induces nephrogenic diabetes insipidus. What happens if hyponatremia is corrected too quickly? You may cause brainstem damage (central pontine myelinolysis). Hypertonic saline is used only when a patient has seizures from severe hyponatremia--and even then, only briefly and cautiously. Normal saline is a better choice 99% of the time for board purposes. What causes spurious (false) hyponatremia? Hyperglycemia (once glucose is > 200 mg/dl, sodium decreases by 1.6 mEq/L for each rise of 100 mg/dl in glucose) Hyperproteinemia HyperlipidemiaIn these instances, the lab value is low, but the total body sodium is normal. Do not give the patient extra salt or saline. What causes hyponatremia in postoperative patients? The most common cause is the combination of pain and narcotics (causing SIADH) with overaggressive administration of intravenous fluids. A rare cause that you may see is adrenal insufficiency (potassium is high and the blood pressure is low). What is the classic cause of hyponatremia in pregnant patients about to deliver? Oxytocin, which has an antidiuretic hormone-like effect. Signs and symptoms of hypernatremia? Same as the signs and symptoms of hyponatremia: Mental status changes/ confusion Hyperreflexia Seizures, and/or comaWhat causes hypernatremia? The most common cause is dehydration (free water loss) due to inadequate fluid intake relative to bodily needs. Watch for diuretics, diabetes insipidus, diarrhea, and renal disease as well as iatrogenic causes (administration of too much hypertonic intravenous fluid). Sickle cell disease, which may lead to renal damage and isosthenuria (inability to concentrate urine), is a rare cause of hypernatremia, as are hypokalemia and hypercalcemia, which also impair the kidney's concentrating ability. How is hypernatremia treated? Treatment involves water replacement, but the patient often is severely dehydrated; therefore, normal saline is used most frequently. Once the patient is hemodynamically stable, he or she often is switched to 1/2 normal saline. Five percent dextrose in water (D5W) should not be used for hypernatremia. What are the signs and symptoms of hypokalemia? Hypokalemia causes muscular weakness, which can lead to paralysis and ventilatory failure. When smooth muscles also are affected, patients may develop ileus and/or hypotension. Best known and best studied, however, is the effect of hypokalemia on the heart. EKG findings include loss of T wave or T-wave flattening, U waves, premature ventricular and atrial complexes, and ventricular and atrial tachyarrhythmias. What is the effect of pH on serum potassium? Changes in pH cause changes in serum potassium as a result of cellular shift. Alkalosis causes hypokalemia, whereas acidosis causes hyperkalemia. For this reason, bicarbonate is given to severely hyperkalemic patients. If the pH is deranged, normalization most likely will correct the potassium derangement automatically without the need to give or restrict potassium. Describe the interaction between digitalis and potassium. The heart is particularly sensitive to hypokalemia in patients taking digitalis. Potassium levels should be monitored carefully in all patients taking digitalis, especially if they are also taking diuretics (a common occurrence). How should potassium be replaced? Slowly- oral replacement is preferred, but if the potassium must be given intravenously for severe derangement, do not give more than 20 mEq/hr. Put the patient on an EKG monitor when giving IV potassium because potentially fatal arrhythmias may develop. When hypokalemia persists even after administration of significant amounts of potassium, what should you do? Check the magnesium level. When magnesium is low, the body cannot retain potassium effectively. Correction of a low magnesium level allows the potassium level to return to normal. What are the signs and symptoms of hyperkalemia? Weakness and paralysis may occur, but the cardiac effects are the best studied. EKG changes (in order of increasing potassium value) include tall, peaked T waves, widening of QRS, prolongation of the PR interval, loss of P waves, and a sine-wave pattern EKG. Arrhythmias include asystole and ventricular fibrillation. Tall, peaked T waves are commonly prominent in V2-V5. What causes hyperkalemia? Renal failure (acute or chronic) Severe tissue destruction (because potassium has a high intracellular concentration) Hypoaldosteronism (watch for hyporeninemic hypoaldosteronism in diabetes) Medications (stop potassium-sparing diuretics, beta blockers, nonsteroidal antiinflammatory drugs, and angiotensin-converting enzyme inhibitors) Adrenal insufficiency (also associated with low sodium and low blood pressure) What should you suspect if an asymptomatic patient has hyperkalemia? With hyperkalemia, the first consideration (especially if the patient is asymptomatic and the EKG is normal) is whether the lab specimen is hemolyzed. Hemolysis causes a false hyperkalemia due to high intracellular potassium concentrations. Repeat the test. The specimen was not hemolyzed. What is the first treatment? Get an EKG first to look for cardiotoxicity. In general, the best therapy for hyperkalemia is decreased potassium intake and administration of oral sodium polystyrene resin. But if the potassium level is > 6.5 and/or cardiac toxicity is apparent (more than peaked T waves), immediate intravenous therapy is needed. First give calcium gluconate (which is cardioprotective, although it does not change potassium levels); then give sodium bicarbonate (alkalosis causes potassium to shift inside cells) and glucose with insulin (insulin also forces potassium inside cells, and glucose prevents hypoglycemia). Beta 2 agonists also drive potassium into cells and can be given if the other choices are not listed on the test. If the patient has renal failure (high creatinine) or initial treatment is ineffective, prepare to institute dialysis emergently. What are the signs and symptoms of hypocalcemia?Hypocalcemia produces neurologic findings, the most tested of which is tetany. Tapping on the facial nerve at the angle of the jaw elicits contraction of the facial muscles (Chvostek sign), and inflation of a tourniquet or blood pressure cuff elicits hand muscle (carpopedal) spasms (Trousseau sign). Other signs and symptoms are depression, encephalopathy, dementia, laryngospasm, and convulsions/seizures. The classic EKG finding is QT-interval prolongation.What should you do if the calcium level is low? First, remember that hypoproteinemia (i.e., low albumin) of any etiology can cause hypocalcemia because the protein-bound fraction of calcium is decreased, in this instance, however, the patient is asymptomatic, because the ionized (unbound, physiologically active) fraction of calcium is unchanged. Thus, you should first check the albumin level and/or the ionized or free calcium level to make sure "true" hypocalcemia is present. Those of you who are mathematically inclined may want to know that for every 1 -gm/dl decrease in albumin below 4 gm/dl, you should correct the calcium by adding 0.8 mg/dl to the given calcium value. What causes hypocalcemia? DiGeorge's syndrome (tetany 24-48 hours after birth, absent thymic shadow on x-ray) Renal failure (remember the kidney's role in vitamin D metabolism) Hypoparathyroidism (watch for a postthyroidectomy patient; all four parathyroids may have been accidentally removed) Vitamin D deficiency Pseudohypoparathyroidism (short fingers, short stature, mental retardation, and normal levels of parathyroid hormone with end-organ unresponsiveness to parathyroid hormone) Acute pancreatitis Renal tubular acidosis Describe the relationship between low calcium and low magnesium. It is difficult to correct hypocalcemia until hypomagnesemia (of any cause) also is corrected. How does pH affect calcium levels? Alkalosis can cause symptoms similar to hypocalcemia through effects on the ionized fraction of calcium (alkalosis causes calcium to shift intracellularly). Clinically. this scenario is most common with hyperventilation/anxiety syndromes, in which the patient eliminates too much CO2, becomes alkalotic, and develops perioral and extremity tingling. Treat by correcting the pH. Reduce anxiety if hyperventilation is the cause. Describe the relationship between calcium and phosphorus. Phosphorus and calcium levels usually go in opposite directions (when one goes up. the other goes down), and derangements in one can cause problems with the other. This relationship becomes clinically important in patients with chronic renal failure, in whom you must not only try to raise calcium levels (with vitamin D and calcium supplements) but also restrict phosphorus. What are the signs and symptoms of hypercalcemia? Hypercalcemia is often asymptomatic and discovered by routine lab tests. When symptoms are present, recall the following rhyme: Bones (bone changes such as osteopenia and pathologic fractures) Stones (kidney stones and polyuria) Groans (abdominal pain (may be due to peptic ulcer disease and/or pancreatitis, both of which have an increased incidence with hypercalcemia), anorexia, constipation, ileus, nausea, vomiting) Psychiatric overtones (depression, psychosis, delirium/confusion) The EKG classically shows QT-interval shortening. What causes hypercalcemia? Hypercalcemia in outpatients most commonly is due to hyperparathyroidism. In inpatients, the most common cause is malignancy. Other causes include vitamin A or D intoxication, sarcoidosis, thiazide diuretics, familial hypocalciuric hypercalcemia (look for low urinary calcium, which is rare with hypercalcemia), and immobilization. Hyperproteinemia (e.g.. high albumin) of any etiology can cause hypercalcemia because of an increase in the protein-bound fraction of calcium, but the patient is asymptomatic because ionized (unbound) fraction is unchanged. Why is asymptomatic hypercalcemia usually treated? Prolonged hypercalcemia can cause nephrocalcinosis and renal failure due to calcium salt deposits in the kidney and may result in bone disease secondary to loss of calcium. How is hypercalcemia treated? First, give intravenous fluids. Then, once the patient is well hydrated, give furosemide (i.e. a loop diuretic) to cause calcium diuresis. Thiazides are contraindicated because they increase serum calcium levels. Other treatments include phosphorus administration (use oral phosphorus; intravenous administration can be dangerous), calcitonin, diphosphonates (e.g., etidronate, which often is used in Paget's disease), plicamycin, or prednisone (especially for malignancy-induced hypercalcemia). Correction of the underlying cause of hypercalcemia is the ultimate goal. The above measures are all temporary until definitive treatment can be given. For hyperparathyroidism, surgery is the treatment of choice. In what clinical scenario is hypomagnesemia usually seen? Alcoholism. Magnesium is wasted through the kidneys. What are the signs and symptoms of hypomagnesemia? Signs and symptoms are similar to those of hypocalcemia (prolonged QT interval on EKG and possibly tetany). In what clinical scenario is hypermagnesemia seen? Hypermagnesemla is classically iatrogenic in pregnant patients who are treated for preeclampsia with magnesium sulfate. It also commonly occurs in patients with renal failure. Patients who receive magnesium sulfate should be monitored carefully, because the physical findings of hypermagnesemia are progressive. The initial sign is a decrease in deep tendon reflexes; then hypotension and respiratory failure occur sequentially. How is hypermagnesemia treated? First, stop any magnesium infusion! Remember the ABCs, and intubate the patient if necessary. If the patient is stable, start intravenous fluids. Furosemide can be given next, if needed to cause a magnesium diuresis. The last resort is dialysis. In what clinical scenarios is hypophosphatemia seen? What are the signs and symptoms? Primarily in patients with uncontrolled diabetes (especially diabetic ketoacidosis) and alcoholics. Signs and symptoms of hypophosphatemia include neuromuscular disturbances (encephalopathy, weakness), rhabdomyolysis (especially in alcoholics), anemia, and white blood cell and platelet dysfunction. What is the intravenous fluid of choice in trauma patients? Ringer's lactate. The second choice is normal saline. What is the intravenous fluid of choice in nontrauma, hypovolemic patients? Normal saline or Ringer's lactate (regardless of other electrolyte problems). First fill the tank; then correct the imbalances that the kidney cannot sort out on its own. What is the maintenance fluid of choice for patients who are not eating? One-half normal saline with 5% dextrose in adults and one-fourth or one-third normal saline with 5% dextrose in children (because of renal differences). Should anything be added to the intravenous fluid for patients who are not eating? Usually potassium chloride, 10 or 20 mEq, is added to a liter of intravenous fluid each day to prevent hypokalemia (assuming that the baseline potassium level is normal).