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7 Hyponatremia, Sick Cell Syndrome, and Hypernatremia

7 Hyponatremia, Sick Cell Syndrome, and Hypernatremia

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due to kidney diseases (pyelonephritis, polycystic disease, interstitial

disease) or through the kidneys due to glycosuria or therapy with

diuretics or less retention of sodium by the kidney due to

adrenocortical insufficiency.

Dilutional hyponatremia (patient hypervolemic). This condition is

related to SIADH or conditions like congestive heart failure, renal failure,

nephrotic syndrome, and cirrhosis of the liver.

Pseudohyponatremia as seen in patients with hyperlipidemia and

hypergammaglobulinemia (also known as factitious hyponatremia).



Sick cell syndrome is defined as hyponatremia seen in individuals with acute

or chronic illness where cell membranes leak, allowing solutes normally inside

the cell to escape into extracellular fluid. Therefore, leaking of osmotically

active solutes causes water to move from intracellular fluid to extracellular

fluid, causing dilution of plasma sodium and consequently hyponatremia.

Sick cell hyponatremia also produces a positive osmolar gap. Sick patients

also produce high levels of ADH, which causes water retention, causing

hyponatremia.



CASE REPORT

A 36-year-old man was hospitalized with 3 days history of

malaise, drowsiness, and jaundice. He had a history of agoraphobia and alcohol abuse. On admission there was no meningismus, focal neurological signs, or liver failure. However,

later the patient became unconscious and developed hypotension and grand mal seizure and was transferred to the

ICU. His serum sodium level was 101 mEq/L and potassium

was 3.6 mmol/L, but all liver function tests were abnormally



high. His serum osmolality was 259 mOsm/kg, but calculated

osmolality was 214 mOsm/kg with an osmolar gap of

135 mOsm/kg. His serum albumin was 2.8 mg/dL. The

patient deteriorated despite aggressive therapy and later

died. The patient suffered from critical illness with multiorgan failure. Standard causes of hyponatremia were ruled

out, and he showed a markedly positive osmolar gap with

severe hyponatremia due to sick cell syndrome [8].



Hypernatremia is due to elevated serum sodium levels (above 150 mEq/L).

Symptoms of hypernatremia are usually neurological due to intraneuronal

loss of water to extracellular fluid. Patients exhibit features of lethargy, drowsiness, and eventually become comatose. Hypernatremia may be hypovolumic

or hypervolumic. The most common cause of hypovolemic hypernatremia is

dehydration, which may be due to decreased water intake or excessive water

loss through the skin (heavy sweating), kidney, or gastrointestinal tract (diarrhea). Patients usually present with concentrated urine (osmolality over

800 mOsm/kg) and low urinary sodium (,20 mmol/L). Hypervolemic

hypernatremia may be observed in hospitalized patients receiving sodium

bicarbonate or hypertonic saline. Hyperaldosteronism, Cushing’s syndrome,

and Conn’s disease may also cause hypervolemic hypernatremia.



5.8 Hypokalemia and Hyperkalemia



5.8 HYPOKALEMIA AND HYPERKALEMIA

Hypokalemia is defined as a serum potassium concentration ,3.5 mEq/L,

which may be caused by loss of potassium or redistribution of extracellular

potassium into the intracellular compartment. Hypokalemia may occur due

to the following:













Loss of potassium from the gastrointestinal tract due to vomiting,

diarrhea, and active secretion of potassium from villous adenoma of

rectum.

Loss of potassium from the kidneys due to diuretic therapy, and

glucocorticoid and mineralocorticoid excess. Increased levels of lysozyme

(seen in monocytic leukemia) may also cause renal loss of potassium.

Bartter’s, Liddle and Gitelman syndromes are rare inherited disorders due

to mutations in the ion transport proteins of the renal tubules that may

cause hypokalemia.

Intracellular shifts due to drug therapy with beta-2 agonists (salbutamol),

which drives potassium into the cell, or due to alkalosis (hydrogen ions

move out of the cell in exchange with potassium), or insulin therapy or

familial periodic paralysis and hypothermia.



Clinically, patients with hypokalemia present with muscle weakness, areflexia,

paralytic ileus, and cardiac arrhythmias. Electrocardiogram findings include

prolonged PR interval, flat T, and tall U.



CASE REPORT

A 69-year-old white man with a history of high-grade prostate carcinoma and widely metastatic adenocarcinoma presented to the hospital with metabolic alkalosis (arterial blood

pH of 7.61, pO2 of 45, and pCO2 of 48), hypokalemia (potassium 2.1 mEq/L), and hypertension secondary to ectopic

ACTH (adrenocorticotropic hormone) and CRH (corticotropin-releasing hormone) secretion. His serum cortisol was

also markedly elevated (135 µg/dL) along with ACTH

(1,387 pg/dL) and CRH (69 pg/dL). As expected, his urinary

cortisol was also elevated (16,267 µg/24 h). An abdominal CT



scan and MRI study showed multiple small liver lesions

and multiple thoracic and lumbar intensities consistent

with diffuse metastatic disease. The severe metabolic

alkalosis secondary to glucocorticoid-induced excessive

mineralocorticoid activity and hypokalemia were treated

with potassium supplements, spironolactone, and ketoconazole. This patient had Cushing’s syndrome, most likely

as a result of ectopic ACTH and CRH secretion from metastatic adenocarcinoma of the prostate gland [9].



Most of potassium of the body resides intracellularly. Hyperkalemia presents

as elevated serum or plasma potassium levels; a common cause is hemolysis

of blood, where potassium leaks from red blood cells into serum, thus artificially increasing potassium levels.



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Causes of hyperkalemia include:













Lysis of cells: in vivo hemolysis, rhabdomyolysis, and tumor lysis.

Intracellular shift. In acidosis, intracellular potassium is exchanged with

extracellular hydrogen ions, causing hyperkalemia. Thus hyperkalemia

typically accompanies metabolic acidosis. An exception is renal tubular

acidosis (RTA) types I and II where acidosis without hyperkalemia is

observed. Acute digitalis toxicity (therapy with digoxin or digitoxin)

may cause hyperkalemia (please note digitalis toxicity is precipitated in

the hypokalemic state).

Renal failure.

Pseudohyperkalemia. Although pseudohyperkalemia or artificial

hyperkalemia is most commonly seen secondary to red cell hemolysis,

it is also seen in patients with thrombocytosis and rarely in patients

with familial pseudohypokalemia. Patients with highly elevated white

blood cell counts, such as patients with chronic lymphocytic leukemia

(CLL), may also show pseudohyperkalemia. Diagnosis of

pseudohyperkalemia can be made from observation of higher serum

potassium than plasma potassium (serum potassium exceeds plasma

potassium by 0.4 mEq/L provided both specimens are collected

carefully and analyzed within 1 h), or measuring potassium in whole

blood (using a blood gas machine) where whole blood potassium is

within normal range.



Clinical features of hyperkalemia include muscle weakness, cardiac arrhythmias, and cardiac arrest. EKG findings include flattened P, prolonged PR

interval, wide QRS complex, and tall T waves. Drugs that may cause hyperkalemia are listed in Table 5.2.



Table 5.2 Drugs that may Cause Hyperkalemia

Potassium supplement and salt substitute

Beta-blockers

Digoxin and digitoxin (acute intoxication)

Potassium sparing diuretics (spironolactone and related drugs)

NSAIDs (non-steroidal antiinflammatory drugs)

ACE inhibitors

Angiotensin II-blockers

Trimethoprim/sulfamethoxazole combination (Bactrim)

Immunosuppressants (cyclosporine and tacrolimus)

Heparin



5.9 Introduction to AcidÀBase Balance



CASE REPORT

A 51-year-old male patient with CLL demonstrated high

plasma potassium of 6.8 mEq/L, but no abnormality was

observed in his electrocardiogram. He showed normal creatinine (1.1 mg/dL), low hemoglobin (7.3 g/dL), and high white

blood cell count (273.9 k/microliter). He was treated in the

emergency room with a presumed diagnosis of hyperkalemia

with calcium gluconate, sodium bicarbonate, albuterol



aerosol, glucose, insulin, and Kayexalate. His potassium

remained high for the next two days (in the range of low 6 s),

but his whole blood potassium was normal (2.7 mEq/L).

Based on these observations, diagnosis of pseudohyperkalemia was established. Interestingly, his plasma potassium was

increased to 9.0 mEq/L, but his whole blood potassium was

still 3.6 mEq/L [10].



5.9 INTRODUCTION TO ACIDÀBASE BALANCE

In general, an acid is defined as a compound that can donate hydrogen ions,

and a base is a compound that can accept hydrogen ions. In order to determine if a solution is acidic or basic, the pH scale is used, which is the abbreviation of the power of hydrogen ions; pH is equal to the negative log of

hydrogen ion concentration in solution. Neutral pH is 7.0. If a solution is

acidic, pH is below 7.0, and basic if above 7.0. Therefore, a physiological pH

of 7.4 is slightly basic. Concentration of hydrogen ions that are present in

both the extracellular and intracellular compartments of the human body are

tightly controlled. Although the normal human diet is almost at a neutral pH

and contains very low amounts of acid, the human body produces about

50À100 mEq of acid in a day, principally from the cellular metabolism of proteins, carbohydrates, and fats; this generates sulfuric acid, phosphoric acid,

and other acids. Although excess base is excreted in feces, excess acid generated

in the body must be neutralized or excreted in order to tightly control near

normal pH of the blood (arterial blood 7.35À7.45 and venous blood

7.32À7.48). Carbonic acid (H2CO3) is generated in the human body due to

dissolution of carbon dioxide in water present in the blood (Equation 5.5):

CO2 1 H2 O 5 H2 CO3 5 H1 1 HCO2

3



ð5:5Þ



The hydrogen ion concentration of human blood can be calculated from the

HendersonÀHasselbalch equation (Equation 5.6):

pH 5 pKa 1 logẵsalt=ẵacid



5:6ị



Here, salt is the concentration of bicarbonate [HCO32] and the concentration

of acid is the concentration of carbonic acid, which can be calculated from

the measured partial pressure of carbon dioxide. The value of pKa is 6.1,

which is the dissociation constant of carbonic acid at physiological temperature. The concentration of carbonic acid can be calculated by multiplying the



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partial pressure of carbon dioxide (pCO2) by 0.03. Therefore the

HendersonÀHasselbalch equation can be expressed as Equation 5.7:

pH 5 6:1 1 log



ẵHCO2

3

0:03 3 pCO2



5:7ị



The body has three mechanisms to maintain acidÀbase homeostasis:













A physiological buffer present in the body that consists of a

bicarbonateÀcarbonic acid buffer system, phosphate in the bone, and

intracellular proteins.

Respiratory compensation, where the lungs can excrete more carbon

dioxide or less depending on the acidÀbase status of the body.

The kidneys can also correct acidÀbase balance of the human body if

other mechanisms are ineffective.



Respiratory compensation to correct acidÀbase balance is the first compensatory mechanism. It is effective immediately, but it may take a longer time for

initiation of the renal compensatory mechanism. At the collecting duct,

sodium is retained in exchange for either potassium or hydrogen ions, and if

excess acid is present, more hydrogen ions should be excreted by the kidney

to balance acidÀbase homeostasis. In the presence of excess acid (acidosis),

kidneys excrete hydrogen ions and retain bicarbonate, while during alkalosis,

kidneys excrete bicarbonate and retain hydrogen ions. However, when there

is excess acid, hydrogen ions may also move into the cells in exchange for

potassium moving out of the cell. As a result, metabolic acidosis usually

causes hyperkalemia. Concurrently, the bicarbonate concentration is reduced

because hydrogen ions react with bicarbonate ions to produce carbonic acid.

The kidneys need to reabsorb more of the filtered bicarbonate, which takes

place at the proximal tubule.



5.10 DIAGNOSTIC APPROACH TO ACIDÀBASE

DISTURBANCE

Major acidÀbase disturbances can be divided into four categories: metabolic

acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis.

In general, metabolic acidosis or alkalosis is related to abnormalities in regulation of bicarbonate and other buffers in blood, while abnormal removal of

carbon dioxide may cause respiratory acidosis or alkalosis. Both states may

also co-exist. However, it is important to know normal values of certain parameters measured in blood for diagnosis of acidÀbase disturbances:







Normal pH of arterial blood is 7.35À7.45.

Normal pCO2 is 35À45 mmHg.



5.10 Diagnostic Approach to AcidÀBase Disturbance









Normal bicarbonate level is 23À25 mmol/L.

Normal chloride level is 95À105 mmol/L.



The first question is whether the pH value is higher or lower than normal. If the

pH is lower than normal, then it is acidosis, and if the pH is higher than normal,

the diagnosis of alkalosis can be made. If the diagnosis is acidosis, then the next

question to ask is whether the acidosis is metabolic or respiratory in nature.

Similarly, if the pH is above normal, the question is whether the alkalosis is metabolic or respiratory in nature. In general, if the direction of change from normal

pH is the same direction for change of pCO2 and bicarbonate, then the disturbance is metabolic in nature, and if the direction of change from normal pH is

in the opposite direction of change for pCO2 and bicarbonate, then the disturbance is respiratory. Therefore four different scenarios are possible:

















Metabolic acidosis, where the value of pH is decreased along with decreases

in the values of pCO2 and bicarbonate (both values below normal range).

Respiratory acidosis, where the value of pH is decreased but values of

both pCO2 and bicarbonate are increased from normal values.

Metabolic alkalosis, where the value of pH is increased along with values

of both pCO2 and bicarbonate (both values above reference range).

Respiratory alkalosis, where the value of pH is increased, but values of

both pCO2 and bicarbonate are decreased.



5.10.1 Metabolic acidosis

Metabolic acidosis may occur with an increased anion gap (high) or normal

anion gap. Anion gap is defined as the difference between measured cations

(sodium and potassium) and anions (chloride and bicarbonate) in serum.

Sometimes concentration of potassium is omitted because it is low compared

to sodium ion concentration in serum (Equation 5.8):

Anion gap 5 ẵsodium 2 ẵchloride 1 ẵbicarbonateị



5:8ị



The normal value is 812 mmol/L (mEq/L).

In metabolic acidosis bicarbonate should decrease, resulting in increased

anion gap metabolic acidosis. If the chloride level increases, then even with a

decline in bicarbonate, the anion gap may remain normal. This is normal

anion gap metabolic acidosis. Thus, normal anion gap metabolic acidosis is

also referred to as hyperchloremic metabolic acidosis. Causes of normal anion

gap metabolic acidosis include loss of bicarbonate buffer from the gastrointestinal tract (chronic diarrhea, pancreatic fistula, and sigmoidostomy), or renal

loss of bicarbonate due to kidney disorders such as renal tubular acidosis and

renal failure. Causes of increased anion gap metabolic acidosis can be remembered by the mnemonic MUDPILES (M for methanol, U for uremia, D for



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diabetic ketoacidosis, P for paraldehyde, I for isopropanol, L for lactic acidosis,

E for ethylene glycol and S for salicylate). In addition, alcohol abuse and other

toxins such as formaldehyde, toluene, and certain drug overdoses may also

cause metabolic acidosis with an increased anion gap.

In general, if any other metabolic disturbance co-exists with increased anion

gap metabolic acidosis, this can be diagnosed from the corrected bicarbonate

level (Equation 5.9):

Corrected bicarbonate 5 measured value of bicarbonate 1 ðanion gap 2 12Þ

ð5:9Þ

If corrected bicarbonate is less than 24 mmol/L, then there exists additional

metabolic acidosis, and if corrected bicarbonate is greater than 24 mmol/L,

then there exists additional metabolic alkalosis.

Winter’s formula is used to assess whether there exists adequate respiratory

compensation with metabolic disturbance (Equation 5.10):

Winter0 s formula: Expected pCO2 5 ẵ1:5 3 Bicarbonate 1 8 6 2ị



5:10ị



If pCO2 is as expected by Winter’s formula, then there is adequate respiratory

compensation, but if pCO2 is less than expected, then additional respiratory

alkalosis may be present. However, if pCO2 is more than expected, then there

is additional respiratory acidosis.



5.10.2 Metabolic alkalosis

Metabolic alkalosis is related to the loss of hydrogen ions or is due to the

gain of bicarbonate or alkali:













Loss of acid, from the gastrointestinal tract (GIT) (e.g. vomiting,

diarrhea).

Loss of acid from kidneys (e.g. glucocorticoid or mineralocorticoid

excess, diuretics).

Gain of alkali (e.g. “milk-alkali syndrome,” also called Burnett’s syndrome,

caused by excess intake of milk and alkali leading to hypercalcemia).



In general, the body attempts to compensate metabolic acidosis by using

respiratory compensation mechanisms where enhanced carbon dioxide elimination can be achieved by hyperventilation (Kussmaul respiration), but this

process may lead to respiratory alkalosis. In the case of metabolic alkalosis,

depression of the respiratory mechanism causes retention of carbon dioxide

to compensate for metabolic alkalosis. However, respiratory response to metabolic alkalosis may be erratic. In addition, during metabolic alkalosis, kidneys try to compensate increased pH by decreasing excretion of hydrogen ion



5.11 Short Cases: AcidÀBase Disturbances



and sodium ions. When an adequate compensation mechanism is absent,

mixed acidosis may occur.



5.10.3 Respiratory acidosis

Respiratory acidosis is due to carbon dioxide retention due to type II respiratory failure. Causes include:

















CNS disorders which damage or suppress the respiratory center

(e.g. stroke, tumor, drugs, alcohol).

Neuropathy or myopathy affecting muscles of ventilation (e.g.

GuillainÀBarré syndrome, myasthenia gravis).

Reduced movement of chest wall (e.g. flail chest, severe obesity

(Pickwickian syndrome)).

Airway obstruction (e.g. severe acute asthma).



5.10.4 Respiratory alkalosis

Major causes of respiratory alkalosis include:









CNS stimulation (e.g. drugs such as aspirin, ketamine).

Hysteria.

Bronchial asthma (early stage).



If the acidÀbase disturbance is related to respiratory disturbance, then it is

important to establish whether such disturbance is acute or chronic. In acute

respiratory disturbance, for any 10 mmHg pCO2 change (assuming a normal

value of 40 mmHg), the change in pH is 0.08 units. In chronic respiratory

disturbance, for any 10 mmHg pCO2 change, the change in pH is 0.03 units.



5.11 SHORT CASES: ACIDÀBASE DISTURBANCES



CASE 1

A patient overdosed on aspirin in an attempted suicide and

was brought to the ER. Her arterial blood pH was 7.57,

pCO2 was 20 mmHg, and bicarbonate was 22 mmol/L.

Because the pH was above the normal range, the patient

presented with alkalosis. In addition, both pCO2 and bicarbonate were also decreased, but these two values were

opposite in direction of pH (which was increased).

Therefore, the patient had respiratory alkalosis. In addition

to establishing the diagnosis of respiratory alkalosis, it was



also important to establish if this was an acute or chronic

respiratory disturbance. The decrease of pCO2 was 20 (normal value is 40 mmHg). Multiplying 20 by 0.08 (in acute

respiratory disturbance, for any 10 mmHg pCO2 change the

change in pH is 0.08 units) yields a value of 0.16. The

increase of pH was 0.18 (assuming a normal pH value of

7.4). This was comparable to 0.16, and the patient showed

acute respiratory alkalosis as expected with acute aspirin

overdose.



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CASE 2

A patient with myasthenia gravis admitted to the hospital

showed arterial blood gas pH of 7.13, pCO2 of 80 mmHg, and

bicarbonate of 26 mmol/L. Because blood pH was below the

reference range, the patient suffered from acidosis. Moreover,

both pCO2 and bicarbonate were increased, but pH was

decreased (change in opposite direction), indicating that the



patient had respiratory acidosis. Moreover, pCO2 was 80, and

assuming (for purposes of calculation) 40 was normal, the

change was 40, which when multiplied by 0.08 was equal to

0.32. The patient’s pH was 7.13, which was lower by 0.27

from a normal value of 7.4. Therefore, the patient had acute

respiratory disturbance (respiratory acidosis).



CASE 3

An adult pregnant female with persistent vomiting was

brought to the ER and her arterial blood pH was 7.62, pCO2

was 47 mmHg, and bicarbonate was 38 mmol/L. Because

pH was increased from the normal value, the patient presented with alkalosis. In addition, because both pCO2 and

bicarbonate were increased along with pH (all changes in

the same direction), the patient had metabolic alkalosis.



Using Winter’s formula, expected pCO2 should be 1.5 3

bicarbonate) 1 8 6 2 or 65 6 2 (i.e. between 63 and 67). If

pCO2 was as expected by Winter’s formula, then adequate

respiratory compensation was present, but this patient

showed a pCO2 of 47, indicating that in addition to metabolic alkalosis, additional respiratory alkalosis was also

present.



CASE 4

An adult male with insulin-dependent diabetes mellitus

(IDDM) was admitted with altered mental status and had the

following values: pH 7.22, pCO2 25 mmHg, bicarbonate

10 mmol/L, sodium 130 mmol/L, and chloride 80 mmol/L.

Because pH was lower than normal he had acidosis. In addition, all three parameters (pH, pCO2, and bicarbonate) were

decreased (changed in the same direction), establishing the

diagnosis as metabolic acidosis. The anion gap of the patient

was 40 (elevated). Therefore, the patient presented with metabolic acidosis with increased anion gap. The corrected

bicarbonate of the patient was 38 (using Equation 5.11):



Because the corrected bicarbonate was higher than 24, the

patient had additional metabolic alkalosis (corrected bicarbonate , 24 mmol/L, additional metabolic acidosis present;

corrected bicarbonate . 24 mmol/L, additional metabolic

alkalosis present). Moreover, using Winter’s formula, the

expected pCO2 was [1.5 3 Bicarbonate] 1 (8 6 2); the

expected pCO2 should be between 21 and 25. Because measured pCO2 was 25, adequate respiratory compensation was

present in the patient. In summary, this patient had increased

anion gap metabolic acidosis with additional metabolic alkalosis but adequate respiratory compensation.



Corrected bicarbonate 5 measured value of bicarbonate

1 ðanion gap 2 12Þ

ð5:11Þ



KEY POINTS





Plasma osmolality 5 2 3 [Sodium in mmol/L] 1 [Glucose mg/dL]/18 1 [BUN mg/

dL]/2.8 (BUN: blood urea nitrogen; Osmolar gap 5 Observed osmolality 2

Calculated osmolality).



Key Points











































Higher osmolar gap can be due to the presence of abnormal osmotically active

substances such as ethanol, methanol, and ethylene glycol (overdosed patients), or, if

fractional water content of plasma is reduced, can be due to hyperlipidemia or

paraproteinemia.

Diabetes insipidus is due to lack of secretion of ADH (cranial diabetes insipidus,

also known as central diabetes insipidus) or due to the inability of ADH to work at

the collecting duct of the kidney (nephrogenic diabetes insipidus).

The main clinical features of SIADH (syndrome of inappropriate antidiuretic

hormone secretion) include: hyponatremia (plasma sodium ,131 mmol/L),

decreased plasma osmolality (,275 mOsm/kg), urine osmolality .100 mOsm/kg,

and high urinary sodium ( .20 mmol/L) with no edema.

Major categories of hyponatremia include: absolute hyponatremia (patient is

hypovolemic) due to loss of sodium through gastrointestinal tract and kidneys, and

dilutional hyponatremia (patient hypervolemic) related to SIADH, volume overload

state, and pseudohyponatremia.

Hypokalemia may occur due to loss of potassium from the gastrointestinal tract

and intracellular shift.

Causes of hyperkalemia include: lysis of cells, intracellular shift, renal failure, or

pseudohyperkalemia.

Metabolic acidosis: The value of pH is decreased along with decreases in the values of

pCO2 and bicarbonate (both values below normal range). May be normal anion gap or

increased anion gap where anion gap 5 [sodium] 2 ([chloride] 1 [bicarbonate]) (normal

value is 8À12 mmol/L (mEq/L)). Causes of normal anion gap metabolic acidosis

include loss of bicarbonate buffer from the gastrointestinal tract (chronic diarrhea,

pancreatic fistula, and sigmoidostomy), or renal loss of bicarbonate due to kidney

disorders such as renal tubular acidosis and renal failure. Causes of increased anion

gap metabolic acidosis can be remembered by the mnemonic MUDPILES (M for

methanol, U for uremia, D for diabetic ketoacidosis, P for paraldehyde, I for isopropanol,

L for lactic acidosis, E for ethylene glycol, and S for salicylate).

Metabolic alkalosis: The pH value is increased along with values of both pCO2 and

bicarbonate (both values above reference range). Metabolic alkalosis is related to

loss of hydrogen ion or is due to gain of bicarbonate or alkali for any of the

following reasons: loss of acid from gastrointestinal tract issues (vomiting,

diarrhea), loss of acid from kidneys (glucocorticoid or mineralocorticoid excess,

diuretics), or gain of alkali (e.g. “milk-alkali syndrome,” also called Burnett’s

syndrome, caused by excess intake of milk and alkali leading to hypercalcemia).

Winter’s formula is used to assess whether there exists adequate respiratory

compensation with metabolic disturbance. Winter’s formula: expected pCO2 5 [1.5 3

Bicarbonate] 1 (8 6 2). If pCO2 is as expected by Winter’s formula, then there is

adequate respiratory compensation, but if pCO2 is less than expected, then additional

respiratory alkalosis may be present. However, if pCO2 is more than expected, then

there is additional respiratory acidosis.

Respiratory acidosis: The value of pH is decreased but values of both pCO2 and

bicarbonate are increased from normal values. Respiratory acidosis is due to carbon



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dioxide retention due to type II respiratory failure. Causes include: CNS disorders

that damage or suppress the respiratory center (e.g. stroke, tumor, drugs, alcohol,

neuropathy), or myopathy affecting muscles of ventilation (e.g. GuillainÀBarré

syndrome, myasthenia gravis), reduced movement of chest wall (e.g. flail chest,

severe obesity (Pickwickian syndrome)), or airway obstruction (e.g. severe acute

asthma).

Respiratory alkalosis: The value of pH is increased, but values of both pCO2 and

bicarbonate are decreased. Major causes of respiratory alkalosis include: CNS

stimulation due to drugs such as aspirin, ketamine, hysteria, or bronchial asthma

(early stage). If the acidÀbase disturbance is related to respiratory disturbance,

then it is important to establish whether such disturbance is acute or chronic. In

acute respiratory disturbance, for any 10 mmHg pCO2 change (assuming a normal

value of 40 mmHg), the change in pH is 0.08 units. In chronic respiratory

disturbance, for any 10 mmHg pCO2 change, the change in pH is 0.03 units.



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7 Hyponatremia, Sick Cell Syndrome, and Hypernatremia

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