General Surgery (Board Review Series) 1st Edition

7

Fluids, Electrolytes, and Critical Care

James F. Calland

1. Fluids
2. Water
3. Estimation of total body water

• is based on the “rule of thirds.”

1. Total body waterequals two thirds of total body weight.
2. Intracellular wateris approximately two thirds of total body water.
3. Extracellular wateris approximately one third of total body water.
4. One third of extracellular water is intravascular.
5. Two thirds of extracellular water is interstitial.
6. Third space fluidscollect outside of the functional or “exchangeable” extracellular space (e.g., pleural effusions, ascites).
7. Large amounts of fluid may be unavailable to the circulation in third spaces.
8. The abdominal peritoneumcan hold up to 18 L of third space fluids in the presence of an inflammatory process (e.g., peritonitis, postoperatively).
9. Circulating blood volumeis 7% of body weight in adults.
10. Alterations in water balance

• are common in surgical patients.

1. Hypovolemia
2. Causes of hypovolemia

• include hemorrhage, gastrointestinal losses[e.g., diarrhea, fistula, nasogastric (NG) tube drainage], third space losses, insensible losses, and inadequate intake.

2. Early signs

P.136

• include decreased urine output, thirst, and poor skin turgor.

3. Late signs

• include tachycardia, confusion, and alterations in body temperature.

4. Laboratory values

• may include an elevated blood urea nitrogen (BUN), BUN/creatinine (Cr) > 20, high urine specific gravity (> 1.020), osmolarity (> 500 mOsm/L), and low urine Na¹.

1. Hypervolemia
2. Causes of hypervolemia

• include heart, renal, and liver failure and depleted serum albumin.

2. Characteristics

• include peripheral edema, dyspnea, pulmonary edema, and jugular venous distention.
• Excessive intravenous (IV) fluid administration or excess salt intakecan exacerbate these conditions.

3. Measuring daily weight changes

• is an accurate method for monitoring potential hypervolemia.

1. IV fluids

Table 7-1. Electrolyte Concentration of Common Intravenous (IV) Solutions

IV Solutions Na+* Cl-* HCO3-* K+* Ca2+* Glucose (g/L) 0.9% NaCl (normal saline) 154 154 — — — — 0.45% NaCl (½ normal saline) 77 77 — — — — Lactated Ringer's 130 109 28† 4 2.7 — 5% dextrose in H2O — — — — — 50 3% NaCl (hypertonic saline) 513 513 — — — — *These electrolytes are measured in mEq/L. †Lactate in solution is metabolized in HCO3-.

1. Crystalloid versus colloid solutions
2. Crystalloid solutionsuse ions in the form of salts (e.g., NaCl) as osmotically active particles (Table 7-1).
3. Colloid solutionsuse proteins, polysaccharides, and other macromolecules as osmotically active particles.
4. Hetastarch

• is a synthetic solution containing polysaccharides.

2. Albumin solutions (5% or 25%)

• are made from human plasma.
• are commonly used in the management of hypoalbuminemia and hypovolemia despite a lack of evidence supporting their use versus crystalloid.
• Use of albumin solutions is also questioned because of their high cost and short half-life (< 24 hours).

3. Fresh frozen plasma (FFP)

P.137

• from human donors is a colloid solution frequently used for repletion of clotting factorsduring resuscitation.

1. The use of colloid solutions for volume resuscitation has not been shown to provide additional benefit versus crystalloid solutions.
2. Maintenance fluids

• provide the minimal requirements for daily water and electrolyte balance.

1. Obligatory urine productionnecessary for excretion of the daily solute load varies by a patient's age and size (500–1000 mL/24 hr for a 70-kg patient).
2. Insensible lossesaccount for about 500 mL/day for an average 70-kg patient.
3. Evaporative skin losses

• During fever, patients lose an extra 500 mL for each degree C above 37.

2. Respiratory lossesare increased in patients with tachypnea or a tracheostomy.

• Humidified oxygen reduces these losses.

3. Losses in stoolaccount for 250 mL/day in normal patients.
4. Estimations for maintenance IV fluids
5. For the first 10 kg of body weight

• give 100 mL/kg divided over 24 hours.

2. For the second 10 kg of body weight

• administer 50 mL/kg.

3. All weight thereafter requires 20 mL/kg divided over 24 hours.
4. Alternatively, the “4–2–1 rule” uses

• 4 mL/kg/hr for the first 10 kg
• 2 mL/kg/hr for the second 10 kg
• 1 mL/kg/hr for the remaining weight.

3. Maintenance electrolyte replacement

• also depends on body weight.

1. Na⁺requirements are highly variable.

• Administration of 1–2 mEq/kg/24 hr is generally sufficient.

1. K⁺average 0.5–1.0 mEq/kg/day with care to avoid hyperkalemia.
2. Replacement of additional fluid losses

• should approximate in volume and electrolyte concentration the fluid that is being lost (Table 7-2).

1. Blood losses

• should be replaced 1:3 with normal saline or lactated Ringer's solution because of redistribution of crystalloid solutions into the extravascular space.

1. NG tube losses

• are most appropriately replaced with K⁺in excess of that found in the NG tube aspirate.

1. K⁺and H⁺ losses from NG tube drainage can result in metabolic alkalosis with paradoxic aciduria.

P.138

2. Paradoxic aciduriaresults from an aldosterone-mediated compensatory renal loss of H⁺ in an effort to resorb K⁺ in the distal tubules.
3. Diarrhea losses

• should be replaced with HCO₃– and K⁺-rich fluids if necessary.

1. Before replacing fluid losses

• assess the patient's respiratory status, cardiac status, and overall fluid balance.

Table 7-2. Composition of Gastrointestinal Secretions

Source Volume (mL/24 hr) Na+ (mEq/L) K+ (mEq/L) HCO3- (mEq/L) Stomach 1000–2000 60–100 10–20 — Small intestine 2000–4000 120–140 5–10 30–40 Pancreas 300–800 135–145 5–10 95–120 Bile 300–600 135–145 5–10 30–40

1. Blood products
2. Transfusion of blood

• is used in patients when a critical reduction in red blood cell (RBC) mass results in tissue ischemia(e.g., severe hemorrhage or anemia).

1. Hematocrit (Hct) levels

• Specific indications vary greatly depending on the patient's overall condition; however, a Hct < 30 [hemoglobin (Hgb) < 10] is a relative indication for transfusion.

1. A type and cross-match of the recipient's bloodshould be attempted before transfusion.
2. Blood typing

• identifies the patient's specific ABO and Rh antigentypes (5–10 minutes).

2. A “screen”

• tests the recipient's serum for antibodiesto antigens other than ABO (45 minutes).

3. A cross-match

• tests the compatibilityof the donor's RBCs and the recipient's serum (45–60 minutes).

1. Whole bloodis sometimes used in severe hemorrhage.

• Transfusion of concentrated packed red blood cells (PRBCs)is generally preferred.

1. Stored blood is often deficientin platelets, factor V, factor VIII, and calcium.
2. Administration of 1 unit of PRBCs usually results in a 3–4-point increase in the Hct.
3. In an emergency, transfusion of type-specific bloodor O^- blood (universal donor) may be required.

P.139

1. For elective surgery, patients may donate their own blood before surgery should it be needed for transfusion.
2. FFP (human)

• is used primarily as a replacement for depleted clotting factors, and is sometimes used as a volume expander.

3. Cryoprecipitate

• is used for replacement of von Willebrand factor, factor VIII, and fibrinogen.

4. Other blood components

• such as factor VIII concentrate and factor IX concentrateare used to correct specific coagulation defects (see Chapter 2).

5. Complications of transfusion

• are outlined in Table 7-3.

1. A febrile response

• may frequently result due to a reaction between the recipient's cells and the donor's leukocytes.

1. This may be prevented by administration of leukocyte-depleted blood.
2. Treatment generally consists of antipyretic therapy.

Table 7-3. Complications of Transfusion of Blood Products

Reaction Cause Characteristics Treatment Hemolytic ABO incompatibility (often due to clerical error) Fever, chills, back pain, abdominal pain, shock, spontaneous bleeding, hemoglobinuria Stop transfusion, IV fluids, mannitol Febrile Reaction with donor leukocytes Fever, chills Antipyretics, leukocyte depleted PRBCs Anaphylactic Recipient antibodies against donor serum proteins Itching, urticaria, broncospasm Severe: stop transfusion, antihistamines, Viral transmission Hepatitis C (< 1/30,000); HIV (< 1/300,000) Hepatitis, cirrhosis, AIDS Prevention, pharmaco-therapy (see Chapter 4) Fluid overload Rapid administration of blood products (especially in the elderly) Dyspnea, pulmonary edema Diuretics, slow rate of administration Bacterial contamination Introduction of skin flora (Staphylococcusand Streptococcus sp.) Bacteremia, sepsis Treat infection (i.e., with antibiotics)

1. Anaphylaxis

• may occur with itching, rash, dyspnea, and even shock.

1. Mild symptomsmay be treated with antihistamines and observation.

P.140

2. Advanced symptomsrequire immediate cessation of transfusion, proper airway control, fluid resuscitation, bronchodilators, and steroids.
3. ABO incompatibility

• Although rare, it is a life-threatening condition.

1. Characteristics

• include fever, chills, back pain, abdominal pain, shock, spontaneous bleeding, hemoglobinuria, and oliguria.

2. Intraoperative excessive bleeding

• may be an early sign of a severe reaction.

3. Renal failure

• is a frequent complication.

4. Treatmentinvolves

• immediate cessation of the transfusion.
• aggressive fluid resuscitation.
• administration of mannitol.

1. Shock

• is defined as inadequate perfusion of vital tissues.

1. Hypovolemic shock

is the result of inadequate circulating blood volume.

1. Causes

• include hemorrhage, gastrointestinal losses, dehydration, and burn injury.

2. Early signs

• include tachycardia, diaphoresis, and apprehension.
• More progressive shock may be associated with orthostatic hypotension, thirst, and oliguria.

3. Late signs

• include decreased mental status, agitation, and tachypnea.

4. Physiologic signs

• include high systemic vascular resistance (SVR), low central venous pressure (CVP), and decreased cardiac output.

5. Managementinvolves

• treatment of the underlying causeof fluid loss.
• aggressive resuscitationwith fluid administration.
• Continuous monitoringof vital signs, CVP, and urine output are useful for measuring adequacy of resuscitation.
• During the initial resuscitation, hypovolemic patients generally respond to rapid infusion of 2 L of fluid with some clinical improvement.
• Failure to respondto this initial bolus may be a marker of severe ongoing blood loss, requiring early transfusion, early operative intervention, or both.

P.141

1. Septic shock

results from the systemic effects of infection (e.g., abscess, pneumonia).

1. Potential mediators

• include bacterial products such as lipopolysaccharideand inflammatory mediators such as interleukin-1 and tumor-necrosis factor-α.

2. Manifestations

• include confusion, fever, flushed skin, tachycardia, and hypotension.

3. Unlike hypovolemic shock, septic shock is associated with

• a decrease in SVR.
• an increase in cardiac output.
• low central venous pressure.

4. Managementinvolves

• effective treatment of the underlying infectious source.
• administration of antibiotics.
• volume resuscitation.

1. Cardiogenic shock

is defined as an inability of the heart to meet the perfusion needs of vital tissues and may be due to intrinsic or extrinsic causes.

1. Intrinsic causes

• include ischemic heart disease(e.g., infarction), valvular heart disease, arrhythmias, and myocardial contusion.

2. Extrinsic causes

• include cardiac tamponade and tension pneumothorax.

3. Manifestations

• include cool, diaphoretic skin; jugular venous distention; peripheral edema; and anxiety.

4. High adrenergic tone

• results in an elevated SVR, high CVP, and low cardiac output.

5. Managementinvolves

• optimizing preload(left-ventricular filling pressure).
• pharmacologic inotropic(contractility) support.
• afterload reduction.

1. Preload

• is measured indirectly by CVP monitoring or by Swan-Ganz catheterization.

2. If preload is low, administer fluids.
3. If preload is high, diuresis may be necessary.
4. Inotropic support

• involves the use of pharmacologic agents (e.g., dobutamine, milrinone) that increase contractility and cardiac output.

1. Afterload reduction

P.142

• is most commonly achieved with pharmacologic agents such as hydralazine, nitroglycerin, and nitric oxide.

1. Cardiac tamponadeand tension pneumothorax require immediate decompression of the pericardial or pleural space, respectively.
2. Neurogenic shock

results from injury to the brain or spinal cord, anaphylaxis, or fainting (psychogenic shock).

1. In surgical patients, neurogenic shock generally presents as hypotensionin the setting of paralysis or spinal cord injury.
2. An aggressive search for other causes of hypotension(e.g., hemorrhage) should be performed before a diagnosis of neurogenic shock is made.
3. Patients are normovolemicbut lack vascular tone resulting in decreased CVP, tachycardia, and low SVR.
4. Managementinvolves

• optimizing preload.
• increasing afterload with phenylephrine or norepinephrine.
• treating neurologic dysfunction.

III. Electrolytes

1. Disorders of Na⁺balance
2. Hyponatremiais defined as a serum Na⁺ < 130 mEq/L.

• Hyponatremia can occur when total body Na⁺is normal, elevated, or depleted.
• Hyponatremia occurring when serum osmolality is normal(280–295 mOsm/kg) suggests that total body Na⁺ is normal or elevated (pseudohyponatremia).

1. Causes of pseudohyponatremia

• may include hyperglycemia, uremia, or hyperlipidemia.

1. Symptoms

• may include irritability, hyperactive deep tendon reflexes, and seizures when serum Na⁺is < 120 mEq/L.

1. The etiology and management of hyponatremia

• depends on the volume status of the patient (hypovolemic, euvolemic, hypervolemic) as outlined in Table 7-4.

1. Symptomatic hyponatremia

• should be corrected at a rate no greater than 0.5–2.0 mEq/hr because of the risk of central pontine myelinosis.
• Correction with normal salineis appropriate although hypertonic saline may be used on rare occasions.

2. Hypernatremiais defined as a serum Na⁺ > 145 mEq/L.

. Causes

• include inadequate free water replacement (most common), IV administration

P.143

of saline solutions, and excess free water loss (e.g., in diabetes insipidus).

1. Characteristics

• are those of dehydration.
• include orthostatic hypotension, poor skin turgor, dry mucous membranes, and lethargy.

1. Treatment

• is based on the underlying defect.

2. Stop ongoing administration of Na⁺-rich fluidsand administer free water according to the free water deficit.
3. Desmopressin (DDAVP)may be administered in the setting of diabetes insipidus.

Table 7-4. Characteristics of Hyponatremia

Imbalance Causes Management Hyponatremia with euvolemia Excess ADH (e.g., postoperatively, SIADH), psychogenic polydipsia, excessive infusion of hypotonic fluids, escess hyperosmotic solute in the blood (pseudohypernatremia) Restrict intake of hypotonic fluids (free water restriction) Hyponatremia with hypervolemia Congestive heart failure, renal failure, liver failure, ascites, excessive fluid resuscitation Fluid restriction Hyponatremia with hypovolemia Inadequate volume resuscitation with hypotonic fluids, hypovolemia with excessive ADH secretion (e.g., postoperatively, closed head injury) Oral salts, resuscitation with normal saline (0.9%) ADH = antidiuretic hormone; SIADH = syndrome of inappropriate antidiuretic hormone.

1. Disorders of K⁺balance (Table 7-5)
2. Hypokalemiais generally defined as a serum K⁺ < 3 mEq/L.
3. Potential causes in surgery patientsinclude

• gastrointestinal losses(e.g., diarrhea, fistula, NG tube losses).
• renal losses(e.g., diuretics, hypomagnesemia, hyperaldosteronemia).
• inadequate intake(e.g., inadequate K⁺ in postoperative fluids).
• third space losses(e.g., peritonitis, small bowel obstruction).
• intracellular shift of K⁺(e.g., insulin overdose, severe metabolic alkalosis).

1. Signs and symptoms

• include muscle weakness, paresthesias, paralytic ileus, and arrhythmias (e.g., ventricular fibrillation).

1. Characteristic electrocardiogram (ECG) changes

• include T wave flattening, U waves, ST depression, and PR and QT widening.

1. Treatmentinvolves

P.144

P.145

• oral or IV replacement with K⁺salts (e.g., KCl).

Table 7-5. Disorders of Potassium Balance

Disorder Causes Characteristics ECG Findings Management Hypokalemia (< 3 mEq/L) Diuretics, GI losses (e.g., diarrhea, NG tube, fistulae), severe metabolic alkalosis, hypomag-nesemia, hyperal-dosteronemia Muscle weakness, ileus, arrhythmias (e.g., ventricular fibrillation), hypotension, digitalis toxicity Flat T waves, U waves, ST depression, PR and QT widening IV or oral replacement with K+solutions (e.g., KCl, KPO4) Hyperkalemia (> 6 mEq/L) Renal failure, excess administration, cell death and intracellular release of K+(e.g., crush injuries, reperfusion of ischemic tissue) Paresthesias, severe muscle weakness, cardiac irritability and arrhythmias Peaked T waves, flat P waves, QRS prolongation, deep S waves, sine wave appearance of QRS complex Mild: saline, kayexalate glucose, insulin, HCO3- Severe (ectopy): emergent IV Ca2+, hemodialysis, in addition to treatment measures for mild hyperkalemia ECG = electrocardiogram; GI = gastrointestinal; IV = intravenous; NG = nasogastric.

2. Hyperkalemiais generally defined as a serum K⁺ > 6 mEq/L.
3. Potential causesinclude

• renal failure.
• unchecked K⁺administration.
• drugs(e.g., K⁺ penicillin, digitalis, succinylcholine).
• tissue necrosiswith cellular release (e.g., crush injuries, compartment syndrome, major burns, rewarming after hypothermia).
• adrenal insufficiency(e.g., low aldosterone state).
• inappropriately obtained blood sample(e.g., hemolysis of sample).

1. Signs and symptoms

• include paresthesias, severe muscle weakness, and arrhythmias, including ventricular fibrillation.

1. ECG changes

• include peaked T waves, flattened P waves, prolonged QRS complex, and disappearance of the QRS complex into a sine wave.

1. Treatment
2. Hemodialysisis the most effective treatment of hyperkalemia.
3. Sodium polystyrene sulfonate (Kayexalate)given orally or rectally prevents resorption of K⁺ in the stool.
4. Insulin (+ glucose) and HCO₃^-cause an intracellular shift of K⁺.
5. IV calcium gluconate or CaCl₂should be given in cases of severe hyperkalemia (i.e., marked ECG changes, arrhythmias, K⁺ > 7.5 mEq/L).

• Without lowering K⁺, Ca⁺protects against hyperkalemia by decreasing the excitability of the myocardium.

5. With severe hyperkalemia, all of these therapies should be initiated [see III B 2 d (1)–(4)].
6. Disorders of Ca²⁺balance
7. Hypocalcemia(Table 7-6) is defined as a serum Ca²⁺ < 8 mg/dL or an ionized Ca²⁺ < 2.5 mEq/L.
8. Serum Ca²⁺values are falsely elevated in hypoalbuminemic states.

• True calcium = observed calcium – (3.5 – serum albumin) × 0.8.

1. Significant risk factorsfor hypocalcemia include

• elective parathyroidectomy.
• inadvertent parathyroidectomy during thyroid surgery.

1. Signs and symptoms

• include muscle cramps, perioral tingling, spasm, seizures, and laryngeal stridor.

1. ECG changes

• include prolonged PR interval.

1. Treatmentinvolves

P.146

• oral or IV Ca²⁺replacement.
• vitamin D replacement.
• IV calcium gluconate for severe hypocalcemia.

Table 7-6. Characteristics of Hypocalcemia

Causes Characteristics Treatment Vitamin D deficiency Muscle cramps Mild to moderate: Vitamin D and oral Ca2+ Chronic renal failure Perioral tingling replacement Inadequate intake Paresthesias Severe: IV replacement with calcium Postparathyroidectomy Hyperactive deep tendon reflexes gluconate Excessive administration of Ca2+ (poor fluids) Laryngeal stridor Seizures Massive transfusion (i.e., citrate binding of Ca2+) Carpopedal spasm (Trousseau's sign) Facial twitching with palpation (Chvostek's sign) IV = intravenous.

2. Hypercalcemiais defined as a serum Ca²⁺ > 10.5 mg/dL or an ionized Ca²⁺ > 4.5 mEq/L.
3. Most frequent causes in surgery

• include hyperparathyroidismand malignant metastases to bone.

1. Signs and symptoms

• include weakness, nausea, vomiting, abdominal and musculoskeletal pain, nephrolithiasis, and neuropsychiatric symptoms.

1. ECG changes

• include short QT interval and prolonged PR interval.

1. Initial treatmentinvolves

• restriction of Ca²⁺intake.
• rehydration with crystalloid.

1. Other therapiesinclude

• furosemide, which may also be used to promote urinary Ca²⁺excretion.
• steroids.
• phosphate.
• biphosphonates (e.g., etidronate).
• calcitonin.
• mithramycin.
• surgical resection of the parathyroids(see Chapter 19).

1. Disorders of Mg²⁺balance (Table 7-7)

P.147

1. Hypomagnesemiais defined as Mg²⁺ < 1.5 mEq/L and is common in surgical patients secondary to inadequate provision of Mg²⁺ postoperatively.
2. Presentationis similar to that of hypocalcemia.

• Severe refractory arrhythmias (e.g., torsade de pointes) may occur.

1. Treatmentinvolves

• oral or IV replacement with Mg²⁺salts.

Table 7-7. Characteristics of Magnesium Disorders

Disorders Causes Characteristics Treatment Hypomagnesemia Inadequate intake, malabsorption, medications (cyclosporine, tacrolimus, amphotericin) Anorexia, nausea, vomiting, weakness, increased deep tendon reflexes, asterixis/tremor, hypokalemia, ECG changes (torsades de pointes) Oral salts or IV replacement with magnesium solutions (MgSo4), potassium replacement Hypermagnesemia Excessive administration (i.e., to treat eclampsia), renal failure, adrenal insufficiency Sedation/obtundation, decreased deep tendon reflexes, weakness, bradycardia/hypotension, respiratory paralysis IV calcium salts ECG = electrocardiogram; IV = intravenous.

2. Hypermagnesemiais defined as Mg²⁺ > 4 mEq/L and is frequently caused by renal failure.
3. Symptoms of hypermagnesemia

• rarely occur with Mg²⁺< 8 mEq/L.
• may include weakness, fatigue, somnolence, bradycardia, hypotension, and respiratory paralysis.

1. Treatment involves

• hydration.
• administration of Ca²⁺salts.
• hemodialysis to remove Mg²⁺from the serum (rare).

1. Acid–Base Disorders
2. Primary and compensatory mechanisms of acid–base disorders (Table 7-8)
3. Acidosis
4. Respiratory acidosis

• is caused by alveolar hypoventilation.
• is compensated by retention of HCO₃^-in the proximal tubules of the kidneys.

1. Criteria for diagnosis

• is hypercarbiain the setting of acidosis.

P.148

1. Acute respiratory acidosis is often causedby suppression of respiratory drive either by drugs or injuries to the central nervous system or chest.
2. Treatment of acute respiratory acidosisincludes

• correcting the underlying disorder.
• increasing ventilation.

3. Ventilated patients unable to compensate by increasing their ventilation may benefit from increases in the ventilatory rate or tidal volume.
4. For acute rises in PaCO₂of 10 mm Hg, there is a decrease in pH of 0.08.
5. Chronic respiratory acidosis

• is often found in patients with chronic obstructive pulmonary disease (COPD), pneumonia, and pulmonary defects such as shunting.

1. These patients

• frequently have a high baseline PCO₂.
• may decompensate rapidly under stress (e.g., infection, surgery).

2. Management involves

• treating the underlying disorder.
• appropriate ventilatory support if acute decompensation occurs.

Table 7-8. Primary and Compensatory Mechanisms of Acid–Base Disorders

Abnormality Primary Change Compensatory Change Metabolic acidosis ↓[HCO3-] ↓PaCO2: 1.2 mm Hg ↓ in PaCO2 for every 1 mEq/L ↓ in [HCO3 -] Metabolic alkalosis ↑[HCO3-] ↑PaCO2: 0.7 mm Hg ↑ in PaCO2 for every 1 mEq/L ↑ in [HCO3-↑] Respiratory acidosis ↑PaCO2 ↑HCO3- Acute: 1 mEq/L ↑ in [HCO3-] for every 10 mm Hg ↑ in PaCO2 Chronic: 3.5 mEq/L ↑ in [HCO3 -] for every 10 mm Hg ↑ in PaCO2 Respiratory alkalosis ↓PaCO2 ↓HCO3- Acute: 2 mEq/L ↓ in [HCO3-] for every 10 mm Hg ↓ in PaCO2 Chronic: 4 mEq/L ↓ in [HCO3-] for every 10 mm Hg ↓ in PaCO2.

2. Metabolic acidosis

. Causes of metabolic acidosis (Table 7-9)

• are differentiated based on the presence or absence of an anion gap.

1. Anion gap = Na⁺– (Cl^- + HCO₃^-); normal range = 5–12.
2. An elevatedanion gap indicates

• the loss of HCO₃^-.
• replacement with an unmeasured base (e.g., lactate, α-ketoglutarate).

P.149

• In surgery patients, the most common cause of metabolic acidosis is poor tissue perfusion from hypovolemia or inadequate cardiac output.

1. Treatment(see Table 7-9)
2. Hyperventilation with subsequent respiratory alkalosis is a compensatory mechanismfor metabolic acidosis.

Table 7-9. Treatment of Common Causes of Metabolic Acidosis

Classification Causes Treatment High anion gap (>12) Lactic acidosis (e.g., shock) Diabetic ketoacidosis Uremia (renal failure) Ingestions: Alcohol Methanol Ethylene glycol Salicylates Paraformaldehyde Volume resuscitation, optimize cardiac output Hydration, insulin, electrolyte replacement Hemodialysis, NaHCO3, electrolyte replacement Glucose administration (starvation-like state) Ethanol, hemodialysis, IV folate Ethanol, hemodialysis Hemodialysis, alkalinize urine Water, milk, ammonium salts, NaHCO3, dialysis Normal anion gap (hyperchloremic) (5–12) GI losses (e.g., diarrhea, fistulae) Renal tubular acidosis Carbonic anhydrase inhibitors (e.g., acetazolamide) Excessive Cl- administration (i.e., TPN solutions) Appropriate volume and electrolyte replacement Discontinue medication Adjustment of fluid electrolyte concentrations

1. Alkalosis
2. Respiratory alkalosisresults from elevated alveolar minute ventilation (hyperventilation).
3. Causes mayinclude

• anxiety-pain or apprehension associated with a procedure.
• fever.
• iatrogenic-tidal volume or respiratory rate set too high on the ventilator.

4. Hypoxia-hyperventilation may be an early sign of pulmonary embolus.
5. Liver failure-high ammonia levels can stimulate ventilation.
6. Respiratory alkalosis can cause

• hypokalemia, hypocalcemia, hypomagnesemia, decreased O₂release from Hgb, and cerebral hypoperfusion secondary to vasoconstriction.

1. Treatment

• focuses on identification and treatment of the underlying cause.

P.150

2. Metabolic alkalosisis generally caused by depletion of acids associated with fluid losses.

• Excessive administration of citrate found in transfused blood may be converted to HCO₃–, which causes metabolic alkalosis, although this occurs infrequently.

1. Causes

• include gastrointestinal losses (e.g., prolonged NG suctioning), diuretic therapy, hyperaldosteronism, and corticosteroid excess (e.g., iatrogenic, Cushing's syndrome).

1. Treatmentinvolves

• replacement of fluid losses.
• correction of the underlying cause.

1. Principles of Critical Care
2. The initial assessment of critically ill patients

focuses on their pulmonary, cardiovascular, and neurologic condition.

• Airway, breathing, and circulation (ABCs) are the primary focus of the initial assessment.

1. Pulmonary assessment evaluates

• the Airway, or work of breathing.
• the adequacy of oxygenation and ventilation (Breathing).

1. The initial pulmonary assessment includes

• evaluation of the patient's general appearance.
• auscultatory examination.
• chest radiograph.
• arterial blood gases.

1. General indications for intubationinclude

• impending respiratory failure.
• inability to protect the airway(i.e., risk of aspiration in obtunded patient).
• hypoventilation (PCO₂> 70 mm Hg).
• hypoxemia (Po₂< 50 mm Hg).
• extreme respiratory fatigue.

1. Potential causesof respiratory failure

• include pneumonia, acute respiratory distress syndrome, sepsis, congestive heart failure, aspiration, lung and chest trauma (e.g., contusion, multiple rib fractures), pulmonary embolus, and neurologic injury (e.g., trauma, pharmacologic).

1. Acute respiratory distress syndrome

• is a syndrome of diffuse respiratory failure seen frequently in critically ill patients.
• may be associated with sepsis, severe infection, shock, severe trauma or burn injury, aspiration, inhalation injury, and pancreatitis.

P.151

• Treatment involves mechanical ventilation when necessary and treatment of the underlying illness.

1. Summary of common ventilator settings(Table 7-10)

Table 7-10. Common Ventilator Settings

Ventilator Mode Mechanism Clinical Utility SIMV Provides a minimum number of breaths/min at a set tidal volume. Synchronized with patient breaths, if present. Work of spontaneous breaths done by patient. Useful in most settings, especially ventilator weaning. ACMV Provides a minimum number of breaths/min. Allows for complete mechanical control of the pressure and/or volume of each breath delivered. Frequently used in patients with altered lung compliance. Pressure control Type of ACMV. Delivers variable tidal volume with each breath at a preset pressure to protect the lungs from barotrauma (pneumothorax). Used in the setting of decreased lung compliance (i.e., large↑ in pressure resulting from small ↑ in volume). PS Provides positive pressure during voluntary inspiration to improve tidal volume with each breath the patient takes. Especially useful for patients weaning from the ventilator. CPAP Supplies a continuous airway pressure that traps gas in the lungs and increases expiratory reserve volume and functional residual capacity. Often used during ventilator weaning. PEEP Provides positive pressure during expiration to prevent airway collapse. “Physiologic PEEP” normally caused by partially closed glottis with expiration about 5 cm H2O. Can be used with most ventilator settings. ↑ PEEP may improve oxygenation. ACMV = assist controlled mechanical ventilation; CPAP = continuous positive airway pressure; PEEP = positive end-expiratory pressure; PS = pressure support; SIMV = synchronized intermittent mandatory ventilation.

2. Cardiovascular assessment (Circulation)

• evaluates volume status, vascular tone, and myocardial function.

1. Useful initial tests

• include evaluation of vital signs, heart rhythm, chest radiograph, weight, and urine output.

1. Hemodynamically unstable patients(e.g., patients with hypotension)

• may benefit from invasive monitoring when the cause is unclear (i.e., hypovolemia versus heart failure).

2. A pulmonary artery catheter (Swan-Ganz)

• allows for indirect measurement of cardiac output and SVR.

3. The pulmonary arterial wedge pressure (PAWP)

P.152

• is an indirect measure of left ventricular end-diastolic pressure.
• is useful for optimizing preload and cardiac function.

4. Complications of pulmonary artery catheters

• may include infection, arrhythmia, pneumothorax, and pulmonary artery or cardiac rupture.

1. Hypovolemiais a frequent cause of cardiovascular instability.

• Treatment involves adequate volume resuscitation.

1. Pharmacologic agents

• may be used to optimize cardiac output, SVR, and ultimately tissue perfusion(BP = CO × SVR).

1. Inotropic drugs

• include dopamine, dobutamine, and epinephrine.

2. Vasoconstrictors

• include norepinephrine and phenylephrine.

3. Vasodilators

• include hydralazine, nitrates, nitric oxide, and angiotensin-converting enzyme (ACE) inhibitors.

3. Neurologic assessment

• is an essential part of the initial evaluation of the critically ill patient.

1. The Glasgow Coma Scale (GCS)

• helps to standardize the patient's response in three basic neurologic categories:

1. Verbalization
2. Motor response
3. Eye opening
4. Standard tests

• are also useful for evaluating mentation, strength, and sensory function.

1. Useful tests for patients with known or suspected brain injury

• include computed tomography (CT) scans, electroencephalogram (EEG), and intracranial pressure monitoring (see BRS Surgical Specialties, Chapter 7).

4. Further assessment

• should include evaluation for potential infection and abnormalities of other organ systems (e.g., renal, hepatic, gastrointestinal, skin).

5. The patient's immune reaction to stresses(i.e. trauma, surgery, infection)

• may also cause physiologic abnormalities.

1. The systemic inflammatory response syndrome (SIRS) is characterized by

• temperature > 38°C or < 36°C.
• heart rate > 90 beats/minute.
• respiratory rate > 20 breaths/minute or PaCO₂< 32 mm Hg.
• white blood cell count > 12,000 or < 4000 cells/mm³.

1. Sepsismay be used to describe SIRS as a result of infection.
2. Septic shockis refractory hypotension resulting from sepsis.
3. Multiple system organ failure

• is a late manifestation of SIRS associated with a very high mortality.

1. Severe failure

• of the respiratory, cardiovascular, renal, and hepatic systems may be present.

2. Causes

• may include infection, severe trauma, and massive burn injuries.

P.153

P.154

Review Test

Directions: Each of the numbered items or incomplete statements in this section is followed by answers or by completions of the statement. Select the ONE lettered answer or completion that is BEST in each case.

1. A 5-year-old, 25-kg boy is now postoperative day 1 from an open appendectomy for nonperforated appendicitis. He is still experiencing some nausea and has minimal bowel sounds upon physical examination. The patient is afebrile and is otherwise healthy. Which of the following electrolyte solutions and rate of administration would be most appropriate for providing maintenance postoperative hydration in this patient?

(A) 5% dextrose in 3/4 normal saline at 65 mL/hr

(B) 5% dextrose in normal saline at 85 mL/hr

(C) Normal saline (0.9%) at 65 mL/hr

(D) 5% dextrose in 1/4 normal saline at 85 mL/hr

(E) 5% dextrose in 1/4 normal saline at 65 mL/hr

1–E. The standard formulas for determining the rate of administration of maintenance fluids are as follows:

[(100 mL/kg × 10 kg) + (50 mL/kg × 10 kg) + (20 mL/kg × 5 kg)]/24 hr

or

(4 mL/kg/hr × 10 kg) + (2 mL/kg/hr × 10 kg) + (1 mL/kg/hr × 5 kg)

Using these formulas, a 25-kg patient would require a rate of approximately 65 mL/hr over 24 hours. In addition, 1/4 normal saline (38.5 mEq/L of Na⁺) would most appropriately provide the daily maintenance sodium requirements of 1–2 mEq/kg/day (25–50 mEq/day) in this patient, whereas administration of normal saline (145 mEq/L Na⁺) would give well in excess of normal daily maintenance requirements. It is important to remember, however, that these formulas serve only as guidelines. Clinical assessment of the patient's condition and fluid status are the most important components of determining the rate and type of fluid administered.

2. A 64-year-old man undergoes upper endoscopy for chronic gastrointestinal bleeding that reveals mild gastritis but no evidence of ulceration or active bleeding. Rectal examination is heme-positive but without gross blood. Immediately after starting a blood transfusion for symptomatic anemia, the patient becomes confused. His blood pressure is 70/30 mm Hg, his heart rate is 145 beats/min, and his temperature is 39°C (102.2°F). Which of the following is the most appropriate next step in the management of this patient?

(A) Slow the rate of infusion of blood and give diphenhydramine

(B) Discontinue blood transfusion and give intravenous (IV) antibiotics

(C) Increase rate of infusion of blood and perform immediate upper endoscopy

(D) Discontinue blood transfusion and administer a bolus of crystalloid solution

(E) Discontinue blood transfusion and administer calcium gluconate intravenously

2–D. This patient is showing signs of rapid clinical deterioration secondary to ABO incompatibility. In this setting, immediate steps include discontinuing the transfusion and administering crystalloid solution. These steps, in association with appropriate management of the respiratory system [airway, breathing, and circulation (ABCs)], are crucial in the treatment of these patients. Administration of antibiotics or calcium gluconate would not treat the primary origin of the problem, nor would they provide significant benefit in the volume resuscitation of a hemodynamically unstable patient in this situation. Although one should always be concerned about acute massive gastrointestinal bleeding in patients that deteriorate so rapidly, the absence of significant pathology on recent endoscopy and the temporal relationship to the blood transfusion make a transfusion reaction more likely, thus negating the need for immediate upper endoscopy at this point in the evaluation.

3. A 53-year-old woman is undergoing an elective sigmoid resection for recurrent diverticulitis. Intraoperatively, the patient requires transfusion of 2 units of packed red blood cells (PRBCs) for significant blood loss early in the case. After starting the transfusion, the anesthesiologist notes that the patient's blood pressure is now 70/40 mm Hg, having dropped from 120/80 mm Hg. There is no intra-abdominal bleeding noted, however her urine has suddenly become very dark. Electrocardiogram (ECG) reveals sinus tachycardia without evidence of myocardial ischemia. Which of the following is the most frequent cause of this patient's current condition?

(A) Primary bacterial contamination of donor blood

(B) Clerical errors in matching donor blood to recipient

(C) Inadequate screening of donor blood for leukocytes

(D) Recipient antibody formation to minor antigens on donor blood cells

(E) Binding of serum calcium by citrate present in donor blood

3–B. This patient is having a severe transfusion reaction secondary to ABO incompatibility. The cardiovascular instability and hemoglobinuria are temporally related to transfusion without other obvious causes for the clinical scenario. The most common cause of a transfusion reaction occurring secondary to ABO incompatibility is a clerical error in matching the appropriate donor blood to the recipient. Although this occurs rarely, it can result from errors in the blood bank or with the medical personnel administering the blood. Thus, great care should be taken to assure appropriate matching occurs at all levels. Recipient antibody formation to antigens other than ABO system may rarely cause mild immune reactions, although this occurs infrequently. Binding of serum calcium and primary bacterial contamination of donor blood is rare. Screening of donor blood for leukocytes is not routinely performed or required.

4. A 19-year-old man sustains orthopedic injuries after a motor vehicle accident. During evaluation and treatment, he receives 4 units of packed red blood cells (PRBCs) for significant blood loss. His family asks about the risk of his contracting human immunodeficiency virus (HIV) from blood transfusion. Which of the following is the approximate risk of transmission of HIV from each unit of PRBCs?

(A) 1/300

(B) 1/3000

(C) 1/50,000

(D) 1/300,000

(E) 1/1,000,000

4–D. Although viral transmission with blood transfusion is rare, it can still occur and must be considered when transfusions are performed. The reported risk of transmission of human immunodeficiency virus (HIV) per unit of blood transfused is estimated to be approximately 1/300,000. Donated blood is routinely screened for HIV contamination; however, despite an excellent sensitivity of these tests, they do not identify absolutely all HIV-contaminated blood samples.

5. A 62-year-old, 90-kg woman undergoes exploratory laparotomy and resection of an obstructing sigmoid colon cancer. Postoperatively, the patient is transferred to the surgical floor where she receives normal saline at 100 mL/hr. The next morning she is tachycardic with a heart rate of 120 beats/min and a blood pressure of 95/60 mm Hg. Her urine output is diminished to 20 mL/hr. Her physical examination is remarkable for a distended abdomen without bowel sounds and with mild tenderness. Her hematocrit is now 36% (it was 33% the night before). Abdominal radiograph shows a gasless abdomen, and a chest radiograph is read as “normal.” Which of the following is the most likely source for her hypotension in the intensive care unit the day after surgery?

(A) Renewed bleeding within the abdominal cavity

(B) Gastrointestinal bleeding from stress ulceration

(C) Acute gastric dilation with a vasovagal response

(D) Third space losses within the peritoneum

(E) Septic shock from gram-negative organisms

5–D. The most likely cause of volume loss and hypotension in this patient is inadequate provision of fluid in the setting of significant third space losses after major intra-abdominal surgery. The peritoneum and the intestinal lumen can accommodate a large amount (approximately 18 L) of third space fluid, which can occur in the setting of intra-abdominal infections, intestinal obstruction, and even postoperatively. The increase in the hematocrit may be secondary to volume loss (i.e., plasma loss) with hemoconcentration of the red blood cells (RBCs). This also makes massive bleeding unlikely in this setting. Acute gastric dilation can result in hypotension, although this would have been noted on the abdominal radiograph. Septic shock occurring this early in the postoperative course for elective surgery is unlikely unless perforation has occurred. However, perforation is frequently associated with other signs and symptoms, such as peritoneal signs (e.g., guarding, rebound pain) and identification of free peritoneal air on radiograph evaluation.

6. A 26-year-old man sustains multiple injuries in a motor vehicle accident, including multiple rib fractures, a pulmonary contusion, pelvic fracture, and a left femur fracture. On hospital day 2 the patient is on the ventilator in synchronized intermittent mandatory ventilation (SIMV) mode set at a rate of 14. FIO₂is 50%, tidal volume is set at 800 ml, and positive end-expiratory pressure (PEEP) is 2 cm H₂O. An arterial blood gas reveals a pH of 7.38, PaCO₂ of 38 mm Hg, PaO₂ of 60 mm Hg, and a HCO₃^- of 22 mEq/L. Which of the following ventilatory changes would be most appropriate for improving this patient's oxygenation?

(A) Increase the PEEP from 2 to 8 cm H₂0

(B) Increase the respiratory rate from 14/min to 18/min

(C) Increase the tidal volume from 800 ml to 1000 ml

(D) Increase the FIO₂ to 75%

(E) Change from SIMV mode to pressure-control mode

6–A. The most appropriate measure to manage this patient's hypoxia is to increase the positive end-expiratory pressure (PEEP) from 2 cm H₂O to 8 cm H₂O. This helps to improve ventilation of collapsed alveoli and the ventilation/perfusion mismatch resulting from this collapse. Increasing the FIO₂ would also help to improve oxygenation but is also associated with other complications if used chronically (e.g., direct pulmonary toxicity). Excessive PEEP may also be associated with complications such as pneumothorax, although this rarely occurs with low levels of PEEP (i.e., 2 cm H₂O to 8 cm H₂O). Increasing the respiratory rate and increasing the tidal volume would improve ventilation (i.e., PaCO₂) but would not specifically address the issue of oxygenation. Altering the mode of ventilation is not necessary in this situation because simpler measures are available to address the hypoxia.

7. A 32-year-old man sustained a left femur fracture after a steel beam fell on his legs and trapped him underneath. It was approximately 2 hours before coworkers were able to locate him and remove the beam. On admission, the patient received 2 units of packed red blood cells (PRBCs) for hypotension and had significant blood loss from the femur fracture. On hospital day 2, the patient is noted to have frequent runs of ectopy on the electrocardiogram (ECG) monitor. Widened QRS complexes are also noted. His urine is dark red, but microscopic examination of the urine reveals no red blood cells (RBCs). Which of the following events is most likely responsible for this patient's current findings?

(A) Hemolysis secondary to the blood transfusion

(B) Acute tubular necrosis secondary to hypovolemia

(C) An unrecognized kidney laceration

(D) Fat embolus syndrome

(E) Rhabdomyolysis

7–E. The most likely cause of the findings in this patient is hyperkalemia associated with rhabdomyolysis. Extensive necrosis of muscle tissue can occur after crush injuries without visible signs of necrosis noted at the level of the skin. Necrosis of muscle cells with subsequent lysis can lead to release of large amounts of K⁺ from the cytoplasm of these cells, resulting in the widened QRS complex and ectopy seen on the ECG. Hemolysis related to blood transfusion would generally not result in severe hyperkalemia unless it was associated with ABO incompatibility, which occurs within minutes to hours of transfusion. Acute tubular necrosis may occur after periods of hypovolemia and may lead to renal failure and hyperkalemia; however, this generally does not present acutely, as in this patient. Unilateral kidney injuries can occur in the absence of hematuria, although in an otherwise healthy individual this would not affect renal function. Hyperkalemia is not a typical characteristic of fat embolus syndrome.

8. A 65-year-old man with non–insulin-dependent diabetes mellitus (NIDDM) is postoperative day 2 after undergoing an elective colon resection for adenocarcinoma. The patient is poorly responsive. On examination, the patient is obtunded, his pupils are pinpoint, his heart rate is 130 beats/min, and his blood pressure is 70/50 mm Hg. A patient care assistant states that the patient was awake 1 hour before, but somewhat confused. Arterial blood gas reveals a pH of 7.29, PaCO₂of 75 mm Hg, PaO₂ of 70 mm Hg, and a HCO₃⁺ of 23 mEq/L. Which of the following is the most appropriate initial step in the management of this patient?

(A) Administer an insulin bolus immediately

(B) Obtain a chest radiograph immediately

(C) Administer naloxone and control the airway

(D) Administer sodium bicarbonate

(E) Obtain a ventilation-perfusion (V/Q) scan to rule out pulmonary embolus

8–C. This patient has a severe acute respiratory acidosis with a pH of 7.29 and a PaCO₂ of 75 mm Hg with minimal compensatory changes in HCO₃^- levels. In a postoperative patient with acute respiratory acidosis and pinpoint pupils, one should be concerned about overdose with narcotic analgesics. Initial treatment of this patient should involve appropriate management of the airway, with intubation if necessary, and administration of naloxone, an antagonist to narcotic analgesics. Hyperglycemia in a patient with non-insulin-dependent diabetes mellitus (NIDDM) is unlikely to present with a severe respiratory acidosis, as opposed to metabolic acidosis and so the insulin bolus is not useful. NaHCO₃ does not treat the primary cause of acidosis in this situation and would not be indicated. A chest radiograph may play a role in the evaluation of this patient, but not in the immediate management of acute severe respiratory acidosis. Acute pulmonary embolus is unlikely to be associated with an isolated respiratory acidosis; however, if it is suspected, appropriate diagnostic evaluation and treatment should be initiated after initial resuscitative measures are taken.

9. A 55-year-old woman underwent a Whipple procedure for pancreatic adenocarcinoma. Postoperatively, she develops a pancreaticocutaneous fistula, which drains approximately 400 mL/day. On evaluation, the patient is noted to be tachycardic with a heart rate of 115 beats/min and a blood pressure of 100/80 mm Hg. Her skin is noted to be dry, and her urine output has decreased significantly over the past 2–3 days. Labs reveal a Na⁺of 140 mEq/L, Cl^-of 120 mEq/L, and HCO₃^- of 15 mEq/L. To resuscitate this patient, which of the following is the most appropriate fluid?

(A) 5% dextrose in normal saline (0.9%)

(B) 5% dextrose in ½ normal saline (0.45%)

(C) 5% albumin solution

(D) Lactated Ringer's solution

(E) 5% dextrose in water + insulin bolus

9–D. Pancreatic fistulae are frequently associated with a significant loss of HCO₃^-, leading to a metabolic acidosis. This patient's low HCO₃^- level in the absence of a significant anion gap {Na⁺ (140)–[Cl^- (120) + HCO₃^-(15)] = 5} in the setting of a pancreatic fistula and dehydration suggests a significant loss of fluid and HCO₃^- from this source. Appropriate resuscitation with a crystalloid solution that resembles the fluid being lost is necessary. Lactated Ringer's solution contains 28 mEq/L of lactate, which is quickly metabolized to HCO₃^-by the liver. Other saline and albumin solutions do not contain HCO₃^- and, although they are appropriate solutions in most situations, would not be the best choice for this patient. Insulin should be given when one expects severe hyperglycemia as the primary problem, although the acidosis associated with severe hyperglycemia is generally associated with a large anion gap (> 12).

Directions: Each set of matching questions in this section consists of a list of four to twenty-six lettered options followed by several numbered items. For each numbered item, select the appropriate lettered option(s). Each lettered option may be selected once, more than once, or not at all.

Questions 10–16

1. Cardiogenic shock due to extrinsic causes
2. Cardiogenic shock due to intrinsic causes
3. Hypovolemic shock secondary to blood loss
4. Hypovolemic shock secondary to third space losses
5. Hypovolemic shock secondary to insensible losses
6. Septic shock
7. Neurogenic shock

For each patient description, select the associated type(s) of shock.

10. A 65-year-old, otherwise healthy man underwent laparoscopic cholecystectomy 3 weeks ago for acute cholecystitis and cholelithiasis. Now he presents with fever, chills, and right upper quadrant (RUQ) pain, and a new onset of confusion, according to his wife. He is tachycardic (130 beats/min), he appears flushed, and his skin is warm. (SELECT 1 TYPE OF SHOCK)

10–F. Septic shock is associated with severe peripheral vasodilation with increased cardiac output. This leads to flushing and warm skin to palpation, in contrast to hypovolemic shock, which results in peripheral vasoconstriction. Other signs and symptoms are related to the primary infection, such as fever, chills, and leukocytosis. This patient is experiencing symptoms suggestive of cholangitis or a peritoneal infection related to the recent surgery.

11. A 19-year-old man presents to the emergency department by ambulance with a stab wound adjacent to the left nipple region. His blood pressure is 50/30 mm Hg and he is unresponsive. (SELECT 2 TYPES OF SHOCK)

11–A, C. Hypovolemia secondary to blood loss is an obvious cause of shock after a stab wound to the chest either from injury to major blood vessels or direct injury to the heart. However, this injury can also result in cardiogenic shock due to extrinsic causes such as cardiac tamponade from injury to the pericardium and tension pneumothorax from lung injury. Theoretically, direct injury to a major coronary vessel can result in a myocardial infarction, even in a young patient. However, consideration of the previous potential causes of shock should be considered first and foremost.

12. A 23-year-old medical student suddenly becomes faint and dizzy while observing a right inguinal hernia repair in the operating room. The student collapses and during evaluation is noted to have a blood pressure of 85/50 mm Hg. (SELECT 1 TYPE OF SHOCK)

12–G. This is a classic vasovagal response resulting in acute transient peripheral dilation with subsequent hypotension and syncope. This response is a form of neurogenic shock, although different from the typical description of patients with a spinal injury.

13. A 42-year-old, obese woman presents with a 2–3 day history of persistent nausea and vomiting. Her blood pressure is 80/50 mm Hg with a heart rate of 140 beats/min. She is noted to have an unreducible umbilical hernia on examination. Abdominal radiograph reveals a high-grade small bowel obstruction. During operative repair of the incarcerated hernia, there is no evidence of strangulation. (SELECT 1 TYPE OF SHOCK)

13–D. This patient's hypotension is secondary to hypovolemia from third space losses as well as dehydration from frank gastrointestinal losses associated with vomiting. Several liters of fluid can be sequestered (“third spaced”) in the intestine when bowel obstruction occurs. If this fluid is not replaced or is combined with other losses from the gastrointestinal tract, it can result in hypotension and even hypovolemic shock.

14. A 25-year-old man is admitted to the neurosurgery intensive care unit after a motor vehicle accident. On admission the patient is noted to have a blood pressure of 120/80 mm Hg with a heart rate of 105 beats/min. Upon evaluation he is found to have a complete spinal cord injury at the sixth cervical vertebrae, as well as a bruise on his abdomen in the distribution of his seatbelt and a bruise on his chest from hitting the steering wheel. Six hours after admission the patient's blood pressure gradually falls to 60/40 mm Hg and the patient becomes unresponsive. (SELECT 4 TYPES OF SHOCK)

14–A, B, C, G. Although the spinal injury can result in neurogenic shock in this patient, one must consider several causes of shock, particularly in a patient with traumatic injuries sustained from blunt trauma. The bruise on the abdomen can be a harbinger of intra-abdominal injuries (e.g., splenic or liver trauma), which can result in immediate or delayed hypovolemic shock secondary to blood loss. Blunt trauma to the chest can result in a myocardial contusion, which can infrequently result in impaired cardiac function and intrinsic cardiogenic shock. Blunt chest trauma can also result in a tension pneumothorax or cardiac tamponade (extrinsic cardiogenic shock) by various mechanisms.

15. A 35-year-old man sustains a 50% full-thickness burn injury to his torso and lower extremities during a house fire. Over the next 2 days, the patient develops a worsening paralytic ileus and a gradual decrease in his blood pressure to 80/60 mm Hg despite following the Parkland formula for determining the amount of fluid to give after a burn injury. (SELECT 2 TYPES OF SHOCK)

15–D, E. Burn injuries can be associated with large amounts of insensible fluid losses from evaporation of fluid directly from the exposed wounds. These patients require large amounts of fluid for maintenance and resuscitation because of these losses. In addition, this patient's paralytic ileus can result in significant third spacing of fluid, also contributing to hypovolemia.

16. During placement of a triple lumen catheter in a 72-year-old woman, the patient suddenly becomes hypotensive with a blood pressure of 60/30 mm Hg during advancement of the guidewire. (SELECT 3 TYPES OF SHOCK)

16–A, B, C. Placement of any central venous catheter can cause multiple injuries, resulting in hypotension and shock. Lung injury with tension pneumothorax can result from such placement. In addition, advancement of the guidewire or the catheter itself can perforate the major blood vessels involved and the myocardium, resulting in severe blood loss or cardiac tamponade (extrinsic cardiogenic shock). Advancement of catheters or guidewires through the heart can also incite various arrhythmias, resulting in cardiac failure and intrinsic cardiogenic shock.