Chapter
Renal Anatomy and Physiology
35 Ryan Barnette and Michael D. Lazar
Water: Distribution, Balance, Compartments
Body Fluid
• Body compartments: 60-40-20 rule
• Total body water (TBW): 60 percent of body weight
• Intracellular fluid (ICF): 40 percent of body weight
• Extracellular fluid (ECF): 20 percent of body weight
• TBW percent: ↑ in babies and ↓ in elderly and obesity
• TBW 40 L, 60 percent body weight
• Average adult male
• Extracellular fluid volume 15 L = 20 percent of body
weight (Table 35.1)
• Plasma osmolality: 285–95 mosm/kg = 2 (plasma Na+) +
glucose/18 + BUN/2.8
*Glucose and BUN contributions are minimal and thus osmo-
lality can be approximated by serum Na+
• Osmoreceptors: In the hypothalamus respond to changes
in the tonicity of body fluid
• Baroreceptors: In the right atria and great veins respond
to changes in intravascular volume. These receptors
prompt the inhibition or stimulation of antidiuretic
hormone (ADH or vasopressin) release from the posterior
pituitary. ADH acts at V1 receptors on vascular smooth
muscle resulting in vasoconstriction and V2 receptors on
the renal collecting tubule cells to increase aquaporin chan-
nels and the reabsorption of H2O.
• Strong ion difference (SID): Used to assist in categorizing
disorders of acid–base balance. Cations predominate in
plasma resulting in net positive +40 charge.1
SID = [strong cations] – [strong anions] = [Na+ + K+ +
Ca2+ + Mg2+] – [Cl− + lactate−]
• Decrease SID → acidosis
• Free water excess secondary to hyponatremia
• Diarrhea
• Increase in anions such as lactic acid or ketoacids
Table 35.1  Breakdown of Total Body Water
Intracellular fluid (ICF) Interstitial fluid Plasma
volume 80 percent of ECF 20 percent of ECF
40 percent of body weight
ICF: cations = K , Mg anions = phosphates, proteins; ECF: cation = Na ,
+ 2+
anions = Cl−, bicarbonate.
• Increase SID → alkalosis
• Dehydration resulting in contraction alkalosis
• Anion loss (i.e., chloride ions via emesis)
• SID of normal saline (NS) = 0 → resuscitation with NS can
cause hyperchloremic metabolic acidosis
Electrolytes
Sodium
• Hyponatremia (Na < 135 mEq/L)
• Symptoms: Neurologic symptoms due to cerebral
swelling such as headache, vomiting, gait disturbance,
seizures
• Causes: Evaluation begins with assessment of TBW
■■ Hypovolemic hyponatremia → renal versus extra-
renal losses
■■ Euvolemic hyponatremia → adrenal/thyroid insuf-
ficiency, SIADH, medications
■■ Hypervolemic hyponatremia → congestive heart
failure, liver cirrhosis, renal failure, nephrotic
syndrome
• Treatment: Typically asymptomatic when Na+ > 125
mEq/L. Conservative correction indicated with nor-
mal saline, salt tabs, fluid restriction. If associated with
seizures or severe neurologic symptoms correction can
be made with hypertonic saline.
• Goal correction: 4–6 mEq/L increase over 24 hours,
not to exceed 8–9 mEq/L in 24-hour period;
more rapid correction results in risk of osmotic
demyelination
• Hypernatremia (Na > 145 mEq/L)
• Symptoms: Lethargy, seizures, coma
• Causes: Pure water loss, hypotonic fluid loss (water
loss exceeds Na+ loss)
• Treatment: Begin by calculating water deficit.
■■ Acute hypernatremia can be corrected at
1 mEq/L/h for the first 6–8 hours to prevent the
potential cerebral dehydration and demyelination.
■■ Chronic hypernatremia can be corrected by
8 mEq/L/day.2
 Serum Na + 
Water deficit = Total body water[L] × −1
+
 140 
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 Chapter 35: Renal Anatomy and Physiology
Potassium
• Hypokalemia (<3.5 mEq/L)
• Signs/symptoms: Severe muscle weakness, flattened
T-waves/U-waves on ECG
• Causes: Medications (aminoglycosides, thiazide/loop
diuretics, laxative abuse), GI losses (diarrhea, suction-
ing), renal tubular acidosis, magnesium deficiency
• Treatment: Potassium chloride – maximum of 60
mEq/L infused through peripheral vein. Up to 200
mEq/L through central veins in critical care setting.3
• Hyperkalemia (>5.1 mEq/L)
• Signs/symptoms: May manifest as muscle weakness
and paralysis
■■ 6–7 mEq/L → peaked T-waves
■■ 10–12 mEq/L → prolonged PR, widening QRS,
Vfib, and asystole.4
• Causes: Most K+ exists intracellularly, therefore
increases are likely due to transcellular shifts such that
occur in acidotic states. Other causes include aldos-
terone antagonism, reperfusion of ischemic vascular
beds, and renal failure.
• Treatment: (1) Stabilize cardiac membranes with
calcium; (2) promote intracellular shift of potassium
with alkalosis (i.e., hyperventilation, bicarbonate),
insulin with glucose, and beta-agonism; (3) promote
K+ excretion with loop diuretics, resin exchange;
(4) hemodialysis
Calcium
• Hypocalcemia (total serum calcium < 8.5 mg/dL, ionized
calcium < 4.6 mg/dL)
• 40 percent serum calcium is ionized → metabolically
active
• 60 percent serum calcium is complexed with albumin
• Signs/symptoms: Paresthesias, muscle spasms, cardiac
dysrhythmias, seizures, QT prolongation on ECG
• Chvostek’s sign – Tapping facial nerve elicits facial
muscle contraction
• Trousseau’s sign – Carpal spasm
• Causes: Vitamin D deficiency, hypoparathyroidism,
chronic renal failure
• Treatment: Calcium gluconate/chloride5
• Hypercalcemia (total serum calcium > 14 mg/dL, ionized
Ca > 5.8 mg/dL)
• Signs/symptoms: Lethargy, weakness, nausea, vomit-
ing, abdominal pain, urinary stones, QT shortening,
hypertension, psychiatric symptoms, polyuria
• Causes: Most common are malignancy or hyperpar-
athyroidism. Others include medications such as
diuretics and lithium
• Treatment: Intravenous fluids, loop diuretics, and
bisphosphonates
Magnesium
• Hypomagnesemia (serum magnesium < 1.7 mg/dL) –
May cause concomitant hypokalemia, hypocalcemia
176
• Causes: Poor intake (i.e., chronic alcoholics, malnutri-
tion), medication-induced (i.e., diuretics, laxatives),
hypercalcemia
• Signs/symptoms: Fatigue, cardiac arrhythmia, nystag-
mus, athetosis, muscle weakness/cramps, confusion,
nervous system irritability
• Treatment: Raise serum levels > 2 mg/dL, also replace
potassium and calcium
• Hypermagnesemia (serum magnesium > 2.3 mg/dL)
• Causes: Intake (i.e., diuretics, laxatives), renal insuf-
ficiency, magnesium administration, rhabdomyolysis,
lithium toxicity, adrenal insufficiency
• Signs/symptoms: Hyporeflexia, weakness, vomiting,
flushing, urinary retention, respiratory and myocardial
depression (>10 mEq/L), heart block, potentiation of
neuromuscular blocker by impaired release of acetyl-
choline at neuromuscular junction
• Treatment: Stop intake, calcium to antagonize action,
loop diuretic
Phosphorus
• Hypophosphatemia (serum phosphate < 2.5 mg/dL)
• Causes: Chronic alcoholism, intravenous hyperali-
mentation (TPN), urinary phosphate wasting (i.e.,
Fanconi syndrome), chronic antacid use
• Signs/symptoms: Metabolic encephalopathy, delirium,
seizures, cardiac arrhythmias, respiratory weak-
ness due to diaphragm weakness, dysphagia, ileus,
decreased red- and white-blood cell function
• Energy source for ATP; therefore, hypophosphatemia
results in muscle weakness, leftward shift of the
oxyhemoglobin curve (due to decrease in 2,3-DPG
(diphosphoglycerate) levels
• Hyperphosphatemia (serum phosphate > 4.5 mg/dL)
• Causes: Excessive intake, tumor lysis syndrome, rhab-
domyolysis, acute/chronic kidney disease, hypopar-
athyroidism, acromegaly, bisphosphonates, vitamin D
toxicity
• Signs/symptoms: Also causes hypocalcemia; therefore,
similar signs and symptoms as hypocalcemia such as
cardiac arrhythmias, muscle spasms, acute renal failure
• Acute severe hyperphosphatemia associated with
symptomatic hypocalcemia can be life threatening
• Treatment:
■■ Acute: Normal saline (although may worsen
hypocalcemia), hemodialysis
■■ Chronic: Low phosphate diet, phosphate binders
Anatomy of the Kidney
• The kidneys are located in the retroperitoneum and are
made up of three regions. The outer cortex, the inner
medulla, and the innermost papilla, which empties into
calyces that forms the ureter.
• The functional unit of the kidney is the nephron, which
is made up of the glomerulus and the renal tubule.

The glomerulus contains a group of capillaries intimately
involved with the Bowman’s capsule and is the site of plasma
filtration. The renal tubule is made up of Bowman’s capsule,
proximal convoluted tubule, descending and ascending loop
of Henle, distal convoluted tubule, and the collecting ducts.
Renal Cortex
1. Receives the majority of blood flow
2. Shorter loops of Henle
3. Most specialized for filtration
Renal Medulla
1. Low flow
2. Longer loops of Henle associated with powerful concen-
tration gradient for optimal reabsorption and secretion
3. Most susceptible to ischemia
Renal Physiology
Renal blood flow (RBF) ≈ 20 percent of cardiac output. O2 con-
sumption is dependent on perfusion.
Right and left renal arteries → interlobar a. → arcuate
a. → interlobular a. → afferent arteriole enters the glomeru-
lus where ultrafiltrate is formed → exit the glomerulus as the
efferent arteriole which contributes a network of capillaries
that surround the tubule throughout its length allowing for the
continued secretion and reabsorption of substances based on a
variety of direct and indirect influences.
Renal plasma flow (RPF) = RBF × (1 – Hct)
Filtration fraction = the percentage of filtrate in the
Bowman’s space relative to the renal plasma flow = GFR/RPF ×
100 ≃ 20 percent
• Afferent arteriole: Dilated by prostaglandins, so increases
RPF and GFR
• Efferent arteriole: Constricted by angiotensin, so decreases
RPF but increases GFR
• Catecholamines increase FF by constricting afferent and
efferent arterioles
GFR is directly proportional to RPF and dependent on the
glomerular filtration pressure. As RPF decreases below a criti-
cal point GFR decreases substantially, thus the relationship is
not linear.
Control of RBF
1. Autoregulation occurs between MAPs 80 and 180 mmHg.
MAPs < 50 mmHg result in sharp decline in GFR.
2. Tubuloglomerular feedback: Macula densa cells sense
decreased [Cl−] at distal tubule, low BP, or sympathetic
stimulation of B1 receptors → secrete renin
3. Cardiac atria cells sense increased volume → secrete atrial
natriuretic peptide (ANP) → relaxes smooth muscle in the
afferent arteriole → ↑GFR
4. Angiotensin II, prostaglandins, and catecholamines affect
GFR
5. Neuronal and paracrine regulation via sympathetics from
levels T4–L1 and dopamine
Chapter 35: Renal Anatomy and Physiology
GFR is a reflection of overall renal function. Through the
passive ultrafiltration of plasma across the glomerular mem-
brane, the kidney is able to regulate total body salt and water
content, electrolyte composition, and eliminate waste products
of protein metabolism. Alterations in GFR can occur either with
changes to any aspect of the Starling forces or through a change
in RPF. The forces responsible for glomerular filtration are simi-
lar to the forces that operate in systemic capillaries – the Starling
forces. GFR can be calculated by inulin clearance (completely
filtered and not secreted or reabsorbed). However, in clinical
practice creatinine clearance is measured as an estimate of GFR.
Starling Equation
GFR = K f [(PGC − PBS ) −πGC ]
Net filtration = K f ([Pc − Pi ] − σ[πc − πi ])
Kf = filtration coefficient
PGC = hydrostatic pressure in glomerular capillary
PBS = hydrostatic pressure in Bowman’s space
πGC = oncotic pressure in glomerular capillary
Pc = capillary hydrostatic pressure
Pi = interstitial hydrostatic pressure
σ = reflection coefficient
πc = capillary oncotic pressure
πi = interstitial oncotic pressure
Tubular Resorption
• Proximal tubule
• 65–75 percent Na+, water, and Cl− are reabsorbed
• Secretion of hydrogen and reabsorption of bicarbonate
ions
• Secretes organic cations like creatinine
• As glucose clearance exceeds >160–200 mg/dL exceeds
proximal tubules ability/threshold for reabsorption
resulting in glucosuria
• Drugs: Carbonic anhydrase inhibitors (i.e.,
acetazolamide)
• Loop of Henle (LOH)
• 25–35 percent ultrafiltrate makes its way to the LOH
• 15–20 percent Na+, Ca2+, and Mg2+ reabsorbed
• Drugs: Loop diuretics
• Distal tubule
• PTH regulated Ca2+ reabsorption
• Aldosterone mediated Na+ reabsorption
• Drugs: Thiazides and thiazide-like diuretics (i.e.,
hydrochlorothiazide, metolazone)
• Collecting duct
• Site of sodium and H2O reabsorption mediated by
aldosterone
• Drugs: potassium sparing diuretics (i.e., spironolac-
tone, amiloride)
*Vasopressin receptor inhibitors (i.e., conivaptan) work at both
distal tubule and collecting duct
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 Chapter 35: Renal Anatomy and Physiology
Figure 35.1  Nephron system
The kidneys secrete the following hormones:
• Erythropoietin (EPO)
• Renin
• Prostaglandins
• 1,25-OH2 Vitamin D (Figure 35.1)
Renin–Angiotensin–Aldosterone
System (RAAS)
Release of renin depends on beta-adrenergic stimulation,
changes in afferent arteriolar wall pressure, and changes in
Cl− flow past the macula densa. Renin acts on angiotensinogen
(made in the liver) to form angiotensin I (ATI) (in the lungs).
Angiotensin converting enzyme (ACE) acts on AT-I to form
angiotensin-II (AT-II), which is responsible for blood pressure
regulation and aldosterone secretion.
ADH – produced in hypothalamus → transported to poste-
rior pituitary for release in response to increased serum osmo-
larity → increases water resorption via aquaporin channel
insertion in cells of the collecting tubule.6
• Diabetes insipidis:
• Central – decreased secretion of ADH
• Nephrogenic – kidneys unresponsive to ADH
178
■■ Associated with chronic renal disease, lithium
toxicity, hypercalcemia, hypokalemia7
• SIADH (syndrome of inappropriate ADH): Excessive
ADH secretion by the posterior pituitary
• Euvolemic hyponatremia – Increased diuresis second-
ary to atrial natriuretic peptide, inhibition of RAAS
• Urine Na > 20 mEq/L, low serum uric acid
Drug Clearance
Three mechanisms
• Glomerular filtration
• Active secretion by the renal tubules
• Passive reabsorption by the tubules
Drugs may be metabolized by the liver into water-soluble
molecules for excretion by the kidney. Alkalinization or acidifi-
cation of urine can ionize and trap molecules within the tubule
for excretion.
• Weak bases → trapped in acidic environments
• Treatment: ammonium chloride
• Weak acids (e.g., aspirin) → trapped in basic
environments
• Treatment: bicarbonate
 Chapter 35: Renal Anatomy and Physiology

Renal Function Tests Table 35.2 

Test of Normal values Causes of

BUN (Blood–Urea–Nitrogen) glomerular pathology
Protein digestion in the liver produces urea, which aids in the function
excretion of nitrogenous waste products such as ammonia in BUN 8–20 mg/dL Dehydration, protein
the kidneys. It is a surrogate of renal health and is partially intake, GI bleeding,
catabolism
reabsorbed at the proximal tubule. When flow to the kidneys is
Serum creatinine 0.5–1.2 mg/dL Age, muscle mass,
reduced in conditions, such as hypovolemia, the reabsorption catabolism
is increased and BUN levels rise. Besides intravascular volume
Creatinine clearance 120 mL/minute Age, medications
status, the BUN levels are altered with nutritional status, preg-
nancy, hepatic disease, GI hemorrhage, among others.
Azotemia = increased BUN and creatinine

Creatinine Clearance Table 35.3 

Cockcroft–Gault equation Test Postrenal Renal Prerenal

(140 − age) × wt (kg) BUN:creatinine <15 <15 >20
= × (× 0.85 for women)
Serum × creatinine(mg/dL) × 72 FENa >4% >1% <1%
Urine Na >40 >20 <20
Creatinine is secreted by the renal tubules. Therefore,
Creatinine clearance is an overestimation of GFR. Urine osmolality <350 <350 >500

Urinalysis
1. RBC – indicates glomerular filtration dysregulation (e.g.,
trauma, infections, tumors)
2. WBC – infection
3. Proteinuria – parenchymal disease
4. Fatty casts – nephrotic syndrome
5. Ketones – DKA, starvation
6. Urine specific gravity: (range: 1.003–1.03) indirect meas-
ure of hydration
7. Urine osmolality: (350–500 mOsm) indirect measure of
hydration
8. Urine sodium: (20–40 mEq) indirect measure of sodium
excretion
Oliguria = urine output < 0.5 mL/kg/hour
Anuria = UOP < 100 mL/day (Table 35.2)
Fractional excretion of sodium (FENa+): Utilized to assist
in differentiating pre-renal, intrarenal, and post-renal etiolo-
gies of acute renal failure.
FENa+ = Naurine × creatinineplasma × 100
Naplasma × creatinineurinary
<1% = prerenal
>1% = intrarenal or postrenal
Renal Pathology
Acute kidney injury = Abrupt loss of kidney function resulting
in retention of urea and other nitrogenous waste products and
in the dysregulation of extracellular volume and electrolytes.
AKI defined according to KDIGO (kidney disease improv-
ing global outcomes)
• Increase in serum creatinine by >0.3 mg/dL within 48
hours;
• Increase in serum creatinine to >1.5× baseline which is
known to have occurred within the prior 7 days; or
• Urine volume <0.5 mL/kg/hour for 6 hours (Table 35.3)
Pre-renal kidney injury occurs with decreased perfusion to
the kidneys, which may occur due to hypotension, blood loss,
heart failure, and liver disease.
Contrast-Induced Nephropathy (CIN)
• Injury to the kidneys is multifactorial
• Risk factors: diabetes mellitus, chronic kidney failure, con-
comitant exposure to other nephrotoxic agents, dehydra-
tion, advanced age
• Prevention: normal saline infusion 100 mL/hour ×
12 hours prior to exposure is the only intervention sup-
ported by most literature. The literature is inconclusive on
the effectiveness of N-acetylcysteine and bicarbonate.
Chronic Kidney Disease (CKD)
CKD is divided into different stages of disease according to the
GFR and the presence of albuminuria:
1. Stage 1 disease is defined by a normal GFR (>90 mL/min-
ute/1.73 m2) and persistent albuminuria
2. Stage 2 disease is a GFR between 60 and 89 mL/min-
ute/1.73 m2 and persistent albuminuria
3. Stage 3 disease is a GFR between 30 and 59 mL/min-
ute/1.73 m2
4. Stage 4 disease is a GFR between 15 and 29 mL/min-
ute/1.73 m2
5. Stage 5 disease is a GFR of <15 mL/minute/1.73 m2or
ESRD8
• Causes: diabetes mellitus, chronic hypertension, glo-
merulonephritis, obstructive, toxicity, hepatitis B/C,
and HIV
179
 Chapter 35: Renal Anatomy and Physiology
• Signs and symptoms of chronic kidney insufficiency
typically manifest when GFR < 15 mL/minute, and
when present may indicate end-stage renal disease
(ESRD)
End-Stage Renal Disease
Hyperkalemia, hypocalcemia, metabolic acidosis, uremia (a
cause of platelet dysfunction), hyperphosphatemia, anemia
(decreased erythropoietin and iron deficiency)
• Treatment → dialysis versus continuous veno-venous
hemofiltration (CVVH)
• Indications (AEIOU)
Acidosis (pH < 7.1)
Electrolyte abnormalities (Hyperkalemia > 6.5)
Ingestion of toxic substance that can be dialyzed
Overload (volume)
Symptomatic Uremia (>30 mg/dL)
• CVVH: Convection and ultrafiltration, reserved for criti-
cally ill patients that would not tolerate cardiovascular
stress associated with dialysis. Greater overall clearance
and volume removal compared to hemodialysis (24-hour
removal compared to 3–4 hours)
• Hemodialysis – Diffusion of substances across a semiper-
meable membrane
• Adverse effects: Hypotension (too much fluid
removed), “dialysis disequilibrium” (rapid fluid and
urea shifts resulting in cerebral edema, headache,
coma), hypocalcemia, fever, hypokalemia-induced
arrhythmias, bleeding (due to heparinization)9
• Electrolyte disturbances: Hypokalemia/magnesemia/
calcemia, increased pH due to bicarbonate infusion,
hyper or hyponatremia9
Acid–Base Balance and the Kidney
The kidneys are essential in the management of acid–base bal-
ance in the body through the reabsorption of HCO3− and the
excretion of H+ (or NH4+).
HCO3− reabsorption (primarily at the proximal tubule)
• Na+/H+ exchanger at the luminal membrane of cells pumps
H+ ions into the lumen → combines with filtered HCO3− →
forms H2CO3− → breaks down into CO2 and H2O which are
reabsorbed into the cell where they are converted via car-
bonic anhydrase back to HCO3− and H+. The bicarbonate is
reclaimed and the H+ is used to repeat the cycle.
• Contraction alkalosis – activation of renin–angiotensin
system results in angiotensin-II-mediated stimulation of the
Na+/H+ exchanger → increase reabsorption of HCO3−.10
• Seen with diuretic use and as a complication of
vomiting
H Excretion (primarily at the distal tubule and collecting
+ ingestion symptoms include altered mentation,
duct) hydrogen combines with HPO42−, NH3, and Cl−.
• H+ ATPase – stimulated by aldosterone
• H+/K+ ATPase
180
Respiratory Alkalosis
• Initial change: ↓PCO2 due to increased alveolar ventilation
• Compensatory response: ↓HCO3
• Acute → intracellular buffering, for every 10 mmHg
change in PCO2 bicarbonate will fall 2 mEq/L
• Chronic → decreased renal reabsorption of bicarb, for
every 10 mmHg change in PCO2 bicarb will fall 5 mEq/L
• Causes: Hyperventilation secondary to pneumonia, pul-
monary edema, PE, salicylates, pregnancy, sepsis, anxiety
Respiratory Acidosis
• Initial change: ↑PCO2
• Compensatory response: ↑HCO3−
• Acute → intracellular buffering, 1 mEq/L ↑HCO3− for
every 10 mmHg change in PCO2
• Chronic → generation of new bicarb due to the
excretion of ammonium, 4 mEq/L ↑HCO3− for every
10 mmHg change in PCO2
• Causes: Hypoventilation secondary to sedatives, neuro-
muscular pathology, airway obstruction, COPD/asthma
Note: “1-2-4-5” rule: change of 1, 2, 4, 5 mEq/L for acute
acidosis, acute alkalosis, chronic acidosis, chronic alkalosis,
respectively
Metabolic Alkalosis
• Initial change: ↑HCO3−
• Compensatory response: ↑ PCO2 via decreased ventilation
• Causes: GI suctioning, vomiting, loop/thiazide diuretics,
primary aldosteronism
Metabolic Acidosis
• Initial change: ↓HCO3−
• Compensatory response: ↓PCO2 via increased ven-
tilation, PCO2 = (1.5 × [HCO3−]) + 8 ± 2 = expected
compensation
• Causes: “MUDPILES” and “HARDUPS”
• Causes of anion gap metabolic acidosis (MUDPILES):
methanol, uremia, diabetic ketoacidosis, propylene
glycol, infection/isoniazid, lactic acid, ethylene glycol,
salicylates11
• Causes of non-anion gap metabolic acidosis
(HARDUPS):hyperalimentation (TPN), acetazolamide/
topiramate, renal tubular acidosis/CKD, diarrhea,
ureterosigmoid conduit, pancreatico-enteric fistula,
saline11
• Treatment: Alkalinize urine to trap ionic species for excre-
tion, correct acidemia, hemodialysis in critical cases
• Salicylate poisoning: Tinnitus, tachypnea (CNS
stimulation → respiratory alkalosis), tachycardia,
sweating, nausea/vomiting, hyperthermia, altered
mentation
• Ethylene glycol poisoning: Ingredient in antifreeze,
seizures, pulmonary edema, kidney failure associated
with calcium oxalate crystals. Metabolism by alcohol
dehydrogenase generates toxic formic acid
 Chapter 35: Renal Anatomy and Physiology

• Methanol: Metabolized by alcohol dehydrogenase into
toxic formaldehyde resulting in symptoms that include
nausea/vomiting
■■ Treatment: EtOH and fomepizole compete for
alcohol dehydrogenase limiting metabolism of
methanol and ethylene glycol
Acid–Base Tips
• Henderson–Hasselbach equation pH = pKa + log [A−]/
[HA]
• Winters formula PCO2 = 1.5 (HCO3−) + 8 ± 2
• Estimates expected change in CO2 in metabolic
acidosis.
• Anion gap (AG) = Na+ – (Cl− + HCO3−) = 10–15 (normal
value)
Acidemia = pH < 7.36
Alkalemia = pH > 7.44
Acid–base disorder workup? Obtain pH, PCO2, HCO3
• First, determine primary disorder
• Second, calculate anion gap
• Third, determine whether compensation is expected
The respiratory system compensates for acid–base distur-
bances rather quickly, whereas the renal systems response is
delayed.

References
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