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Internal Medicine > Fluids, Electrolytes, and Acid Base Disorders > Flashcards

Fluids, Electrolytes, and Acid Base Disorders Flashcards

1
Q

Where does the majority of Na+ reabsorption occur?

A

The proximal tubule

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2
Q

MOA of furosemide

A

Inhibition of the Na+/K+/Cl- cotransporter in the thick ascending limb of the loop of Henle

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3
Q

MOA of Thiazide diuretics

A

Inhibition of Na+/Cl- cotransporter at the early distal tubule

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4
Q

How does aldosterone affect Na+ and K+?

A

Aldosterone increases the absorption of Na+ and the secretion of K+ in the late distal tubules.

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5
Q

_______ increases Na+ reabsorption. _______ increases water reabsorption.

A

Aldosterone; ADH

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6
Q

Describe water homeostasis.

A

As the plasma osmolarity increases, the osmoreceptors signal to the posterior pituitary and cause the release of ADH which result in more water reabsorption and thus a decrease in serum osmolarity. As the osmolarity decreases, the osmoreceptors shrink and stop signaling for the pituitary to release ADH.

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7
Q

In a hyponatremic patient, at what point do symptoms begin to develop?

A

When the Na+ level is <120.

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8
Q

In patients with intracranial problems, why is it important to keep the serum sodium slightly high or at least definitely not low?

A

Because as serum sodium decreases and the plasma osmolarity decreases, water will shift from the ECF into brain cells and cause a further increase in ICP.

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9
Q

In hypovolemic hypotonic hyponatremia, what does a low urine sodium mean?

A

If there is a low urine sodium <10 mEq/L, it implies increased sodium retention by the kidneys to compensate for extra renal losses which could occur in the form of diarrhea, vomiting, NG suction, diaphoresis, third spacing, burns, or pancreatitis (of sodium containing fluid).

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10
Q

In hypovolemic hypotonic hyponatremia, what does a high urine sodium mean?

A

If there is a high urine sodium >20 mEq/L renal salt loss is likely, for example diuretic use, decreased aldosterone (due to ACE inhibitors) ATN

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11
Q

What are some causes of euvolemic hypotonic hyponatremia?

A
  • SIADH
  • Psychogenic polydipsia
  • Hypothyroidism
  • Postop Hyponatremia
  • Oxytocin use
  • Administration or intake of relative excess of free water
  • Drugs: haldol, cyclophosphamide, certain antineoplastics
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12
Q

What are some causes of hypervolemic hypotonic hyponatremia?

A
  • CHF
  • Nephrotic syndrome
  • Liver disease
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13
Q

What is isotonic hyponatremia?

A

AKA pseudohyponatremia. This can be caused by any condition that leads to elevated proteins or lipids. An increase in plasma solids lowers the plasma sodium concentration but the amount of sodium in the plasma is normal.

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14
Q

What are some substances that cause a hypertonic hyponatremia?

A
  • Glucose
  • Sorbitol, mannitol, glycerol, maltose
  • Radiocontrast agents
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15
Q

Explain hypertonic hyponatremia.

A

This occurs when there is the presence of an osmotic substance that causes an osmotic shift of water out of the cells. These substances cannot cross the cell membrane and therefore cause water to shift out of cells.

For example: Hyperglycemia increases osmotic pressure and water shifts from cells into the ECF leading to a dilutional hyponatremia. The actual sodium content in the ECF is unchanged.

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16
Q

What are some of the clinical features of hyponatremia?

A
  • Neurologic symptoms: cerebral edema/swelling, HA, delirium, irritability, muscle twitching, weakness, hyperctive DTRs,
  • Increased ICP, seizures, coma
  • GI: N/V/ ileus, watery diarrhea
  • CV: HTN due to increased ICP
  • increased salivation and lacrimation
  • Oliguria progressing to anuria which may not be reversible if therapy is delayed
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17
Q

In a patient with hyponatremia, what does it mean if the urine osmolality is low?

A

It means that the kidneys are responding appropriately by diluting the urine. For ex: primary polydipsia.

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18
Q

In a patient with hypernatremia, what does it mean if the urine osmolality is high?

A

It means there are increased levels of ADH and the kidney is not excreting free water. Ex: CHF, SIADH, hypothyroidism.

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19
Q

What should the urine Na+ be in a patient with hyponatremia?

A

It should be low.

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20
Q

In a patient with hyponatremia, if the urine Na+ is high, what could be causing that?

A
  • Renal salt wasting nephropathy
  • Hypoaldosteronism
  • Diuretics
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21
Q

In a patient with hyponatremia, and the urine Na+ is low, what is that consistent with?

A

SIADH

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22
Q

How do you treat isotonic and hypertonic hyponatremias?

A

Diagnose and treat the underlying disorder.

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23
Q

How do you treat hypotonic hyponatremia?

A

Mild (120-130): free water restriction

Moderate (110-120): loop diuretics

Severe (<110) hypertonic saline, increased by 1-2 mEq/hr

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24
Q

Hypovolemic hypernatremia occurs when there is more water loss than sodium loss. What can cause this?

A
  • Diuretics, osmotic diuresis, renal failure

- Diarrhea, diaphoresis, respiratory losses

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25
Q

Isovolemic hypernatremia occurs when sodium stores are normal but there has been loss of water. What causes this?

A
  • Diabetes insipidus

- Insensible respiratory losses (tachypnea)

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26
Q

Hypervolemic hypernatremia occurs when there is gain of Na+ and water but more Na+ than water. What causes this?

A
  • TPN
  • NaHCO3- therapy
  • Exogenous glucocorticoids/Cushing’s Syndrome
  • Saltwater drowning
  • Primary hyperaldosteronism
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27
Q

Excessively rapid correction of hypernatremia can cause?

A

Cerebral edema. Rate of correction should not exceed 12 mEq/L/day and no more than 8 mEq/L in the first 24 hours.

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28
Q

Clinical Features of Hypernatremia

A
  • Mostly neurologic: AMS, restlessness, weakness, FND, confusion, seizures, coma
  • Decreased salivation, tissues and mucous membranes are dry
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29
Q

In a patient with hypernatremia, what should the urine volume be? What should the urine osm be?

A

The urine volume should be low and the urine Osm should be high, >800.

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30
Q

How do you treat hypotonic hypernatremia?

A

-Give isotonic NaCl to restore hemodynamics

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31
Q

How do you treat Isovolemic hypernatremia?

A

Patients with DI require vasopressin, others you can prescribe oral fluids or D5W

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32
Q

How do you treat hypervolemic hypernatremia?

A

Give diuretics (like furosemide) and D5W to remove excess sodium. Dialyze patients with renal failure.

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33
Q

Which is the physiologically active form of Ca2+?

A

The free ionized form. It is under tight hormonal control by PTH and is independent of albumin levels.

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34
Q

How are calcium levels affected in hypoalbuminemia?

A

In hypoalbuminemia, total calcium is low but ionized calcium is normal.

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35
Q

What is the formula for estimating ionized calcium in hypoalbuminemia?

A

Total calcium - (serum albumin*0.8)

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36
Q

How does pH alter the ratio of calcium binding?

A

An increase in pH (alkalosis) increases the binding of calcium to albumin. Therefore in alkalemic states (especially acute respiratory alkalosis) total calcium is normal but ionized calcium is low and the patient frequently manifests the signs and symptoms of hypocalcemia.

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37
Q

What are some causes of hypocalcemia?

A
  1. ) Hypoparathyroidism
  2. ) Acute pancreatitis
  3. ) Renal insufficiency
  4. ) Hyperphosphatemia
  5. ) Pseudohypoparathyroidism
  6. ) Hypomagnesemia
  7. ) Vitamin D deficiency
  8. ) Malabsorption
  9. ) blood transfusion
  10. ) Osteoblastic mets
  11. ) Hypoalbuminemia
  12. ) DiGeorge Syndrome
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38
Q

What is pseudohypoparathyroidism?

A

Autosomal recessive disease causing congenital end organ resistance to PTH so PTH levels are actually high. Also characterized by mental retardation and short metacarpal bones.

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39
Q

How does hypomagnesemia cause hypocalcemia?

A

Hypomagnesemia causes decreased PTH secretion

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40
Q

Symptoms of hypocalcemia?

A
  • Rickets and osteomalacia
  • Increased NM irritability: numbness and tingling (circumoral), tetany, hyperactive DTRs, Chvostek, Trousseau signs, Seizures
  • Basal ganglia calcifications
  • CV: arrhythmias, prolonged QT interval
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41
Q

What lab tests would you want in a workup of hypocalcemia?

A
  • BUN, Cr
  • Magnesium
  • Albumin
  • Ionized calcium
  • Amylase, lipase, and possibly LFTs
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42
Q

How do you treat hypocalcemia?

A

If symptomatic provide emergent tx w/ IV calcium gluconate. For long term management use oral calcium supplements (calcium carbonate) and vitamin D

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43
Q

How do you treat PTH deficiency?

A
  • Replace vitamin D and give calcitriol

- Also give a thiazide to prevent nephrolithiasis

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44
Q

What are the “endocrinopathis” that can cause hypercalcemia?

A
  • Hyperparathyroidism
  • Renal failure (secondary hyperparathyroidism)
  • Paget Disease of Bone
  • Acromegaly, Addison’s Disease
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45
Q

What are the malignancies that can cause hypercalcemia?

A
  • Multiple myeloma
  • Bone mets that cause osteoclastic activity to increase
  • Paraneoplastic syndromes that release PTHrp
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46
Q

What are some pharmacologic causes of hypercalcemia?

A
  • Vitamin D intoxication
  • Milk Alkali syndrome
  • Drugs: thiazides, lithium
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47
Q

What are 2 “other” causes of hypercalcemia?

A
  • Sarcoidosis

- Familial hypercalciuric hypercalcemia

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48
Q

Clinical features of hypercalcemia

A
  • Bones
  • -Bone aches and pains
  • -Brown Tumors (osteitis fibrosa cystica)
  • Stones
  • -Nephrolithiasis
  • -Nephrocalcinosis
  • Groans
  • -MSK pain and weakness
  • -Pancreatitis
  • -PUD
  • -Gout
  • -Constipation
  • Psychiatric overtones
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49
Q

How do you treat hypercalcemia?

A
  • IV FLUIDS
  • Furosemide to further inhibit Ca2+ reabsorption
  • Bisphosphonates
  • Calcitonin
  • Hemodialysis in renal failure pts
  • Glucocorticoids in vitamin D related mechanisms and multiple myeloma
50
Q

How do alkalosis and insulin levels affect K+?

A

Alkalosis and insulin administration may cause hypokalemia because they cause a shift of potassium into cells.

51
Q

How does acidosis and cell lysis affect K+?

A

Acidosis and anything resulting in cell lysis increases serum K+ because both of these mechanisms force K+ out of cells into the ECF.

52
Q

What are some GI losses that can cause hypokalemia?

A
  • Vomiting
  • NG suctioning
  • Diarrhea
  • Laxatives and Enemas
  • Intestinal fistulas
  • Malabsorption
53
Q

What are some renal losses that can cause hypokalemia?

A
  • Diuretics
  • RTA or parenchymal disease
  • Primary and secondary hyperaldosteronism
  • Excessive glucocorticoids
  • Magnesium Deficiency
  • Bartter Syndrome
54
Q

What is Bartter Syndrome?

A

An autosomal recessive defect in salt reabsorption in the TAL which leads to hyperplasia of the JGA which leads to increases renin levels and secondary aldosterone elevations.

55
Q

What are a couple of other causes of hypokalemia?

A
  • Deficient intake
  • Insulin administration
  • Abx: Bactrim and Ampho B
  • Profuse Sweating
  • Epinephrine (beta-2 agonists)
56
Q

With GI loss of K+, will urine K+ be high or low?

A

Low

57
Q

With renal losses of K+, will urine K+ be high or low?

A

High

58
Q

What is a common cause of both hypokalemia and a NAGMA?

A

Diarrhea

59
Q

What is the most dangerous complication of hypokalemia?

A

Cardiac arrhythmias. T waves flatten out, then invert, then U waves appear

60
Q

Why should you always monitor K+ in patients taking Digoxin?

A

Because hypokalemia predisposes to digoxin toxicity!

61
Q

What are the clinical features of hypokalemia?

A
  • Cardiac arrhythmias
  • Ileus
  • Muscular weakness, fatigue, paralysis, and muscle cramps
  • Decreased DTRs
  • Polyuria and polydipsia
  • N/V
  • Digitalis toxicity
  • Flattening of T waves, U waves on EKG
62
Q

How do you treat hypokalemia?

A
  1. ) Identify and treat the underlying cause
  2. ) Discontinue any meds that can aggravate hypokalemia
  3. ) Oral KCl (10 mEq of KCl increases K+ level by 0.1 mEq/L
  4. ) IV KCl if K+ <2.5 or if there is an arrhythmias
63
Q

What are 3 broad categories of hyperkalemia?

A
  • Increased total body potassium
  • Redistribution
  • Pseudohyperkalemia
64
Q

What are the causes of increased total body potassium that lead to hyperkalemia?

A
  • Renal failure
  • Addison’s disease
  • Potassium sparing diuretics (spironolactone)
  • ACE-inhibitors
  • Iatrogenic overdose
  • Blood transfusion
65
Q

What are the redistribution causes of hyperkalemia?

A
  • This occurs due to the translocation of potassium ions from the intracellular space to the extracellular space
  • Acidosis
  • Tissue/cell breakdown (rhabdo, burns, hemolysis)
  • GI Bleeding
  • Insulin deficiency
  • Rapid administration of a beta-blocker
66
Q

How does hyperkalemia lead to an acidosis?

A

-Hyperkalemia inhibits renal ammonia synthesis. Therefore net acid excretion is impaired and it results in a metabolic acidosis which further exacerbates the hyperkalemia.

67
Q

What are the clinical features of hyperkalemia?

A
  • Arrhythmias
  • Muscle weakness and rarely flaccid paralysis
  • Decreased DTRs
  • Respiratory failure
  • N/V intestinal colic, diarrhea
68
Q

What are the EKG changes seen in hyperkalemia

A
  • Peaked T waves
  • PR prolongation
  • Widened QRS
  • can lead to a sine-wave pattern and eventually death
69
Q

How do you treat hyperkalemia?

A
  • If there are EKG changes or hyperkalemia is severe, give IV calcium which will stabilize the RMP of the myocardium and decrease myocardial excitability
  • *be careful giving Ca2+ to patients on digoxin because hypercalcemia predisposes to digoxin toxicity just as hypokalemia does.
  • Glucose and insulin which will shift K+ into the intracellular compartment.
  • NaHCO3- which causes an alkalosis and shifts K+ into cells. Only given in an emergency or severe hyperkalemia.
  • Kayexalate: GI potassium exchange resin that absorbs K+ in the colon and prevents reabsorption
  • Hemodialysis: most rapid and effective way of lowering K+ but reserved for intractable hyperkalemia and those with renal failure
  • Furosemide diuretics
70
Q

What are normal magnesium levels?

A

1.8-2.5

71
Q

Where is magnesium mostly located within the body?

A

2/3 of it is in the bone. The other 1/3 is intracellular

72
Q

What are 4 broad categories of causes of hypomagnesemia?

A
  1. GI Losses
  2. Alcoholism
  3. Renal causes
  4. Other: postparathyroidectomy, DKA, thyrotoxicosis, lactation, burns, pancreatitis, cisplatin
73
Q

What GI losses can lead to hypomagnesemia?

A
  • Malabsorption, steatorrheic states
  • Prolonged fasting
  • Fistulas
  • Pts receiving TPN w/o mag supplements
74
Q

What are some renal causes of hypomagnesemia

A
  • SIADH
  • Diuretics
  • Bartter Syndrome
  • Drugs: Gentamicin, ampho B, cisplatin
  • Renal transplant
75
Q

Clinical features of hypomagnesemia:

A
  1. ) Neuromuscular and CNS hyperirritability
  2. ) Coexisting hypocalcemia
  3. ) Coexisting hypokalemia
  4. ) EKG changes
76
Q

What EKG changes are see in hypomagnesemia?

A
  • Prolonged QT
  • T-wave flattening
  • Torsades de Pointes
77
Q

What neuromuscular/CNS problems are seen in hypomagnesemia?

A
  • Muscle twitching, weakness, tremors
  • Hyperreflexia, seizures
  • Mental status changes
78
Q

How does hypomagnesemia relate to hypocalcemia?

A

-When mag is low, there is decreased release of PTH and bone resistance to PTH therefore hypocalcemia develops.

79
Q

How does hypomagnesemia relate to hypokalemia?

A

In the muscle and myocardium, when either intracellular Mag or K+ decreases, a corresponding decrease in the other takes place.

80
Q

How do you treat hypomagnesemia?

A
  • Mild: give oral Mg2+ (mag oxide)

- Severe: parenteral Mg2+ (mag sulfate)

81
Q

What are some causes of hypermagnesemia?

A
  1. Renal failure
  2. Early stage burns, massive trauma or surgical stress, volume deficit, severe acidosis
  3. Excessive intake of magnesium containing laxatives or antacids combined with renal insufficiency
  4. Adrenal insufficiency
  5. Rhabdomyolysis
  6. Iatrogenic - eclampsia or preeclampsia treated with Mag Sulfate
82
Q

Clinical features of hypermagnesemia?

A
  • Nausea, weakness
  • Facial paresthesias
  • Progressive loss of DTRs
  • EKG changes: prolonged PR, widened QRS, elevated T waves
  • Somnolence–> coma–> muscular paralysis
  • Death caused by respiratory failure or cardiac arrest
83
Q

Treatment of hypermagnesemia?

A
  • Withhold exogenously administered magnesium
  • Prescribe IV calcium gluconate for emergent symptoms (cardioprotection )
  • Administer saline and furosemide
  • Order dialysis in renal failure patients
  • Prepare to intubate if respiratory depression is severe
84
Q

What are normal levels of phosphate?

A

3-4.5

85
Q

Where is most phosphate found in the body?

A

Bones. The remainder is intracellular in soft tissues.

86
Q

What controls phosphate absorption?

A

Vitamin D controls phosphate absorption in the gut

87
Q

What controls phosphate excretion?

A

PTH controls phosphorus excretion by the kidneys.

88
Q

What are some reasons for decreased intestinal absorption of phosphate?

A
  • Alcohol abuse
  • Vitamin D deficiency
  • Malabsorption
  • Excessive use of phosphate binding antacids
  • Hyperalimentation (TPN)
  • Starvation
89
Q

What are some causes of increased renal excretion of phosphate?

A

-Excess PTH (vitamin D deficiency, hyperparathyroidism)
-Hyperglycemia
-ATN
RTA
-Hypokalemia or hypomagnesemia

90
Q

What are some other causes of decreased phosphate?

A
  • Respiratory alkalosis
  • Anabolic steroids
  • Severe hyperthermia
  • DKA
  • Hungry bone syndrome
  • refeeding syndrome?
91
Q

What are symptoms of severe hypophosphatemia?

A
  • Neuro: encephalopath, confusion, seizures, numbness, paresthesias
  • MSK: muscular weakness, myalgias, bone pain, rickets/osteomalacia.
  • Heme: hemolysis, RBC and WBC and platelet dysfunction
  • Cardiac: cardiomyopathy and myocardial depression secondary to low ATP–> cardiac arrest
  • Rhabdomyolysis
  • Anorexia
  • Difficulty in ventilator weaning
92
Q

What are the 2 most common causes of severe hypophosphatemia?

A

Alcohol abuse

DKA

93
Q

Treatment for mild hypophosphatemia?

A

-Oral supplementation

94
Q

Treatment for severe hypophosphatemia?

A

Parenteral supplementation (or if patient is NPO also)

95
Q

Causes of hyperphosphatemia

A
  • Decreased renal excretion due to renal insufficiency, bisphosphonates, hypoparathyroidism, vitamin D intoxication, and/or tumor calcinosis
  • Increased phosphate administration
  • Rhabdo, cell lysis, or acidosis (which releases PO34- into the ECF).
96
Q

What are the clinical features of hyperphosphatemia?

A

-Metastatic calcifications and soft tissue calcifications. The associated hypocalemia symptoms occur and can lead to neurologic changes (tetany, neuromuscular irritability)

97
Q

Treatment of hyperphosphatemia?

A
  • Phosphate binding antacids containing aluminum hydroxide or carbonate
  • Hemodialysis if the patient has renal failure
98
Q

Causes of an AGMA?

A
  • Ketoacidosis
  • -Starvation
  • -Alcoholic
  • -Diabetic
  • Lactic acidosis
  • -Decreased tissue perfusion
  • -Shock states
  • -Excessive expenditure of energy (seizures)
  • Renal failure
  • Intoxication
  • -Salicylates
  • -Methanol
  • -Ethylene Glycol
99
Q

What acid base disturbance(s) does salicylate ingestion cause?

A

-Primary respiratory alkalosis and primary metabolic acidosis

100
Q

What are 2 general causes of a non-anion gap metabolic acidosis?

A
  • Renal loss of bicarb

- GI loss of bicarb

101
Q

What are the causes of renal loss of bicarb which would lead to a NAGMA?

A
  • Proximal RTA: decreased HCO3- reabsorption caused by MM, cystinosis, and Wilson’s disease
  • Distal RTA: inability to make HCO3- caused by SLE, sjogren syndrome and ampho B
  • Carbonic Anhydrase inhibition (acetazolamide)
102
Q

What are the causes of GI loss of bicarb which would lead to a NAGMA?

A
  • Diarrhea: loss of HCO3- in the diarrhea
  • Pancreatic fistulas: pancreatic secretions contain high levels of HCO3-
  • Small bowel fistula
  • Utereterosigmoidostomy: colon secretes HCO3- in urine in exchange for Cl-
103
Q

Clinical Features of Metabolic Acidosis

A
  1. Hyperventilation-Kussmaul respiration. Less prominent when chronic. Compensatory mechanism
  2. Decreased CO and decreased tissue perfusion.
104
Q

What is Winter’s Formula?

A

Expected PaCO2 = 1.5 (serum bicarb) + 8 +/-2

105
Q

When calculating winter’s formula in an AGMA, what does it mean if the actual PaCO2 is higher than expected?

A

That means that there is a metabolic acidosis with a respiratory acidosis. This is a serious finding because this failure of compensation can be a sign of impending respiratory failure. The classic example is an asthmatic child who has a PaCO2 that goes from abnormal to normal with no treatment. This is a bad sign and it probably means the child will need emergent intubation shortly.

106
Q

When calculating winter’s formula in an AGMA what does it mean if the actual PaCO2 is lower than expected?

A

That means the patient has a metabolic acidosis with a respiratory alkalosis.

107
Q

What are the 2 types of metabolic alkalosis?

A
  1. ) Saline sensitive metabolic alkalosis (urine chloride <10 mEq/L) characterized by ECF contraction and hypokalemia
  2. ) Saline resistant metabolic alkalosis (urine chloride >20 mEq/L) characterized by ECF expansion and hypertension due to increased mineralocorticoids.
108
Q

What are some causes of saline sensitive metabolic alkalosis?

A
  1. Vomiting or NG suction
  2. Diuretics
  3. Villous adenoma of the colon, diarrhea with a high chloride content.
109
Q

What are some causes of saline resistant metabolic alkalosis?

A
  • Adrenal disorders: primary hyperaldosteronism.
  • Cushing Syndrome
  • Severe hypokalemia
  • Bartter Syndrome
  • Diuretic abuse

Primary hyperaldosteronism: leads to increased tubular reabsorption of Na+ and HCO3- and an excessive loss of Cl- in the urine. The result is a metabolic alkalosis and expansion of the ECF compartment because of Na+ reabsorption.

110
Q

How soon does renal compensation (increased bicarb reabsorption) begin after respiratory acidosis?

A

12-24 hours and it can take up for 5 days or so to complete.

111
Q

How do you tell if renal compensation is acute for respiratory acidosis?

A

For every 10 mmHg increase in PaCo2 there is a 1 mmol/L increase in HCO3-

112
Q

How do you tell if renal compensation if chronic for respiratory acidosis?

A

For every 10 mmHg increase in PaCO2 there is a 4 mmol/L increase in HCO3-

113
Q

In what population do you commonly see respiratory acidosis with chronic renal compensation?

A

Those with underlying lung disease (COPD)

114
Q

Causes of respiratory acidosis

A

ALVEOLAR HYPOVENTILATION

  1. Primary pulmonary disease: COPD, airway obstruction
  2. neuromuscular disease (Myasthenia gravis)
  3. CNS malfunction (brainstem injury)
  4. Drug induced hypoventilation (opioids, sedatives, narcotic overdose)
  5. Respiratory muscle fatigue
115
Q

Clinical features of respiratory acidosis

A
  • Somnolence, confusion, myoclonus

- Headaches, confusion, papilledema

116
Q

How does PaCO2 affect CNS activity?

A

Increased PaCO2 –> increased CBF –> increased CSF pressure which results in generalized CNS depression

117
Q

In a patient with respiratory acidosis, what conditions are indications for intubation?

A
  • Severe acidosis
  • PaCO2 >60 or inability to increase PaO2 with supplemental Oxygen
  • If patient is obtunded or shows deterioration in mental status
  • Impending respiratory fatigue (ensues with prolonged labored breathing)
118
Q

In a patient with respiratory alkalosis, how do you tell if renal compensation is acute?

A

For every 10 mmHg decrease in PaCO2, the plasma HCO3- decreases by 2mEq/L

119
Q

In a patient with respiratory alkalosis, how do you tell if renal compensation is chronic?

A

For every 10 mmHg decrease in PaCO2, the plasma HCO3- decreases by 5-6 mEq/L

120
Q

Causes of respiratory alkalosis?

A

ALVEOLAR HYPERVENTILATION

  1. Anxiety
  2. PE, pneumonia, asthma
  3. Sepsis
  4. Hypoxia-leads to increased RR
  5. Mechanical ventilation
  6. Pregnancy-increased serum progesterone levels cause hyperventilation
  7. Liver disease (cirrhosis)
  8. Medication (salicylate toxicity)
  9. Hyperventilation syndrome
121
Q

Clinical features of respiratory alkalosis?

A
  • Sx related to decreased cerebral blood flow 2/2 vasoconstriction: lightheadedness, dizziness, anxiety, paresthesias, and perioral numbness
  • Tetany (indistinguishable from hypocalcemia)
  • Arrhythmias (in severe cases)

Internal Medicine (6 decks)

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