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Flashcards in Acid-Base & Electrolytes Deck (46):

How do you analyze arterial blood gas values?

3 basic points:

  1. pH tells you whether you are dealing with acidosis or alkalosis as the primary event. The body will compensate as much as it can (secondary event).
  2. Look at the carbon dioxide (CO2) value. If it is high, the patient either has respiratory acidosis (pH < 7.4) or is compensating for metabolic alkalosis (pH > 7.4). If CO2 is low, the patient either has respiratory alkalosis (pH > 7.4) or is compensating for metabolic acidosis (pH < 7.4).
  3. Look at the bicarbonate value. If it is high, the patient either has metabolic alkalosis (pH > 7.4) or is compensating for respiratory acidosis (pH < 7.4). If bicarbonate is low, the patient either has metabolic acidosis (pH < 7.4) or is compensating for respiratory alkalosis (pH > 7.4).


True or false: The body does not compensate beyond a normal pH.


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), then the pH will not correct to greater than 7.4. Overcorrection does not occur.


What are common causes of acidosis?

Respiratory acidosis: COPD, asthma, drugs that cause respiratory depression (opioids, benzodiazepines, barbiturates, alcohol), chest wall problems (paralysis, pain), and sleep apnea.

Metabolic acidosis: Ethanol, DKA, uremia, lactic acidosis (sepsis, shock, bowel ischemia), methanol/ethylene glycol, aspirin/salicylate overdose, diarrhea, and carbonic anhydrase inhibitors.


List the common causes of alkalosis.

Respiratory alkalosis: Anxiety/hyperventilation and aspirin/salicylate overdose.
Metabolic alkalosis: Diuretics (except carbonic anhydrase inhibitors), vomiting, volume contraction, antacid abuse/milk-alkali syndrome, and 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?

pH may be alkaline during the day because they breathe better when awake.

However, 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).

As a side note, remember that 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 purposes of the Step 2 boards, almost never.

First try IV fluids and correction of the underlying disorder. If all other measures fail and the pH remains less than 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, this scenario means that the patient is probably crashing.

Remember that 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 ß2 agonists, steroids, and O2. 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.


List the signs and symptoms of hyponatremia.

  • Lethargy
  • Seizures
  • Mental status changes or confusion
  • Cramps
  • Anorexia
  • Coma


How do you determine the cause of hyponatremia?

The first step in determining the cause is to look at the volume status:


How is hyponatremia treated?

Hypovolemic hyponatremia: normal saline.

Euvolemic and hypervolemic hyponatremia: water/fluid restriction

Hypervolemic hyponatremia: diuretics


 What medication is used to treat the syndrome of inappropriate antidiuretic hormone secretion (SIADH) if water restriction fails?

Demeclocycline, which induces nephrogenic diabetes insipidus

MoA: inhibits the renal action of ADH by interfering with the intracellular second messenger cascade (specifically, inhibiting adenylyl cyclaseactivation) after the hormone binds to vasopressin V2 receptors in the kidney. Exactly how demeclocycline does this has yet to be elucidated


What happens if hyponatremia is corrected too quickly?

How should it be managed?

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. In chronic severe symptomatic hyponatremia, the rate of correction should not exceed 0.5 to 1 mEq/L/hr.


What causes spurious (false) hyponatremia? 3

  • Hyperglycemia
    • (if >200 mg/dL, sodium decreases by 1.6 mEq/L for each rise of 100 mg/dL in glucose. Make sure you know how to make this correction.)
  • Hyperproteinemia
  • Hyperlipidemia

In these instances, the laboratory value is low, but the total body sodium is normal. Do not give the patient extra salt or saline.


How do you determine the actual sodium concentration in a patient with hyperglycemia?

(Once glucose is >200 mg/dL, sodium decreases by 1.6 mEq/L for each rise of 100 mg/dL in glucose.


What causes hyponatremia in postoperative patients?

Combination of pain + narcotics (causes SIADH) with overaggressive administration of IV fluids.

A rare cause that you may see on the USMLE is adrenal insufficiency; in this instance, 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 ADH-like effects


What are the signs and symptoms of hypernatremia?

Basically the same as the signs and symptoms of hyponatremia:

  • Mental status changes or confusion
  • Seizures
  • Hyperreflexia
  • Coma


What causes hypernatremia? 3 major ones

Most common cause: dehydration (free water loss) caused by inadequate fluid intake relative to bodily needs.

  • ddx: diuretics, diabetes insipidus, diarrhea, and renal disease, iatrogenic causes (administration of too much hypertonic IV fluid).

Sickle cell disease, which may lead to renal damage and isosthenuria (inability to concentrate urine), is a rare cause of hypernatremia

Hypokalemia and hypercalcemia, which also impair the kidney's concentrating ability.


How is hypernatremia treated?

Treatment involves water replacement, but the patient is often severely dehydrated; therefore normal saline is used most frequently.

Once the patient is hemodynamically stable, he or she is often 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?

  • muscular weakness; can lead to paralysis and ventilatory failure
  • ileus + hypotension when smooth muscles also are affected 
  • ECG: T wave or T-wave flattening, the presence of U waves, premature ventricular and atrial complexes, and ventricular and atrial tachyarrhythmias.


What is the effect of pH on serum potassium?

Alkalosis causes hypokalemia, whereas acidosis causes hyperkalemia.

Bicarbonate is given to severely hyperkalemic patients.

If the pH is deranged, normalization most likely will correct the K derangement automatically without the need to give or restrict K.


Describe the interaction between digoxin and potassium.

The heart is particularly sensitive to hypokalemia in patients taking digoxin. K levels should be monitored carefully in all patients taking digoxin, especially if they are also taking diuretics (a common occurrence).


How should potassium be replaced?

Like all electrolyte abnormalities, hypokalemia should be corrected slowly. Oral replacement is preferred, but if the K must be given intravenously for severe derangement, do not give more than 20 mEq/hr.

Put the patient on an ECG 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 Mg level - if low, the body cannot retain K effectively.


What are the signs and symptoms of hyperkalemia?

  • Weakness and paralysis may occur
  • ECG changes (in order of increasing K): tall peaked T waves, QRS widening, PR interval prolongation, loss of P waves, and a sine wave pattern. Arrhythmias include asystole and ventricular fibrillation


What causes hyperkalemia? 5 major categories

  • Renal failure (acute or chronic)
  • Severe tissue destruction (K has a high intracellular concentration)
  • Hypoaldosteronism (watch for hyporeninemic hypoaldosteronism in diabetes)
  • Medications (stop K-sparing diuretics, ß blockers, NSAIDs, ACEi, ARBs)
  • Adrenal insufficiency (also associated with low Na and low BP)


What should you suspect if an asymptomatic patient has hyperkalemia?

With hyperkalemia, the first consideration (especially if the patient is asymptomatic and the ECG is normal) is whether the laboratory specimen is hemolyzed. Hemolysis causes a false hyperkalemia result because of high intracellular potassium concentrations. Repeat the test.


What should you suspect if an asymptomatic patient has hyperkalemia, but the specimen was not hemolyzed. What should you do?

  1. Get an ECG first to look for cardiotoxicity
  2. Decreased K intake and administration of Kayexalate
  3. If the K level is > 6.5 or cardiac toxicity is apparent (more than peaked T waves), immediate IV calcium gluconate (which is cardioprotective, although it does not change potassium levels); then sodium bicarbonate (alkalosis causes K to shift into cells) and glucose with insulin (insulin also forces K into cells; glucose prevents hypoglycemia)
  4. ß2 agonists also drive K into cells and can be given if the other choices are not listed on the test.
  5. If the patient has renal failure (high creatinine) or initial treatment is ineffective, prepare to institute emergent dialysis.


What are the signs and symptoms of hypocalcemia?


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 ECG finding is QT-interval prolongation.


What should you do if the calcium level is low?

First, consider hypoproteinemia (i.e., low albumin) of any etiology, 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.

For every 1 g/dL decrease in albumin below 4 g/dL, correct the calcium by adding 0.8 mg/dL to the given calcium value.


What causes hypocalcemia?

  • DiGeorge syndrome (tetany 24–48 hr after birth, absent thymic shadow on x-ray)
  • Renal failure (remember the kidney’s role in vitamin D metabolism)
  • Hypoparathyroidism (s/p thyroidectomy)
  • 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) is also corrected.


How does pH affect calcium levels?

How do you manage these symptoms?

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, 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/reduce phosphorus.


What are the signs and symptoms of hypercalcemia?

often asymptomatic, but when present, can be:

  • Bones (osteopenia, pathologic fractures)
  • Stones (kidney stones, polyuria)
  • Groans (abdominal pain, anorexia, constipation, ileus, N/V)
    • Abdominal pain may also be caused by PUD and/or pancreatitis, both of which have an increased incidence with hypercalcemia
  • Psychiatric overtones (depression, psychosis, and delirium/confusion)
  • QT-interval shortening 


What causes hypercalcemia?

How do you differentiate between the etiologies?

  • hyperparathyroidism
  • malignancy 
  • Vitamin A/D intoxication
  • sarcoidosis 
  • thiazides
  • familial hypocalciuric hypercalcemia (low urinary Ca)
  • immobolization
  • Hyperproteinemia (high albumin, but asx because the ionized form is unchanged)

Check the parathyroid hormone level to differentiate hyperpara- thyroidism from other causes.


Why should you treat hypercalcemia, even if it's  asymptomatic?

Prolonged hypercalcemia can cause

  • nephrocalcinosis
  • urolithiasis
  • renal failure due to calcium salt deposits in the kidney
  • bone disease secondary to loss of calcium


How is hypercalcemia treated?

  1. give IV fluids
  2. give furosemide to cause Ca diuresis
    • do not give thiazides because they increase serum Ca
  3. give PO phosphorus, calcitonin, bisphosphonates, plicamycin, prednisone
  4. correct underlying cause of hypercalcemia
  5. surgery if hyperparathyroidism is the cause


In what clinical scenario is hypomagnesemia usually seen?

What are the signs and symptoms of hypomagnesemia?

Alcoholism - magnesium is wasted through the kidneys

Signs and symptoms are similar to those of hypocalcemia (prolonged QT interval, possibly tetany).


In what two clinical scenario is hypermagnesemia seen?

What are the signs and symptoms?

  1. iatrogenic - usually in pregnant women who are being treated with Mg sulfate for pre-eclampsia 
  2. patients with renal failure

The initial sign is a decrease in deep tendon reflexes, then hypotension and respiratory failure occur sequentially.


How is hypermagnesemia treated?

  • Stop magnesium infusion.
  • Assess ABCs (airway, breathing, circulation), and intubate the patient if necessary.
  • If the patient is stable, start IV fluids.
  • Furosemide can be given next, if needed, to cause a magnesium diuresis.
  • The last resort is dialysis.


In what two clinical scenarios is hypophosphatemia seen? What are the signs and symptoms?

Clinical Scenarios:

  1. uncontrolled diabetes, esp DKA
  2. alcoholics

Signs and Symptoms

  1. neuromuscular disturbances (encephalopathy, weakness)
  2. rhabdomyolysis (especially in alcoholic patients)
  3. anemia
  4. white blood cell and platelet dysfunction


What is the IV fluid of choice in hypovolemic patients?

NS or LR (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 adult patients who are not eating? children patients?

CHILDREN <10 kg: 1/4 NS D5W

CHILDREN >10 kg: 1/3 NS D5W



Should anything be added to the IV fluid for patients who are not eating?