Critical Care and Clinical Skills Flashcards

Question

J\,Iatch the following shock syndromes with the appropriate Swan-Ganz catheter measurements/vital signs, using each answer once, more than once, or not at all. NoteCVP- central venous pressure (mm Hg), PCWP- pulmonary capillary wedge pressure (m111 I-Ig) , CI- cardiac index (L1mirlim2), SVR- systemic vascular resistance (dynes/cm2 ) CVP 16, PCWP 20, CI 1.2, SVR 1250 A. Hypovolemic shock B. Cardiogenic shock C. Septic shock

Answer 1

A. Hypovolemic shock **B. Cardiogenic shock ** C. Septic shock ## Footnote Hypovolemic shock is characterized by decreased central venous and intracardiac pressures, decreased cardiac output, elevated SVR (> 1200 dynes/cm2 ), and concomitant hypotension and tachycardia, with a dampened Swan-Ganz catheter waveform. Cardiogenic shock is characterized by a decreased cardiac index (less than 1.8 L/min/m2), elevated PCWP (> 18 mm Hg) and CVP, elevated SVR, and decreased systolic blood pressure « 100 mm Hg). Septic shock is characterized by low filling pressures, decreased SVR (although early septic shock can exhibit an elevated SVR) , and normal or increased cardiac output. Normal Swan-Ganz catheter parameters are as follows: CVP 1 to 6 mm Hg, PCWP 6 to 12 mm Hg, CI 2.4 to 4.0 Limin/nl, SVR 900 to 1200 dynes/cm2 (Marino, pp. 164, 505-509).

Answer 2

A. Hypovolemic shock B. Cardiogenic shock **C. Septic shock** ## Footnote Hypovolemic shock is characterized by decreased central venous and intracardiac pressures, decreased cardiac output, elevated SVR (> 1200 dynes/cm2 ), and concomitant hypotension and tachycardia, with a dampened Swan-Ganz catheter waveform. Cardiogenic shock is characterized by a decreased cardiac index (less than 1.8 L/min/m2), elevated PCWP (> 18 mm Hg) and CVP, elevated SVR, and decreased systolic blood pressure « 100 mm Hg). Septic shock is characterized by low filling pressures, decreased SVR (although early septic shock can exhibit an elevated SVR) , and normal or increased cardiac output. Normal Swan-Ganz catheter parameters are as follows: CVP 1 to 6 mm Hg, PCWP 6 to 12 mm Hg, CI 2.4 to 4.0 Limin/nl, SVR 900 to 1200 dynes/cm2 (Marino, pp. 164, 505-509).

Answer 3

**A. Hypovolemic shock ** B. Cardiogenic shock C. Septic shock ## Footnote Hypovolemic shock is characterized by decreased central venous and intracardiac pressures, decreased cardiac output, elevated SVR (> 1200 dynes/cm2 ), and concomitant hypotension and tachycardia, with a dampened Swan-Ganz catheter waveform. Cardiogenic shock is characterized by a decreased cardiac index (less than 1.8 L/min/m2), elevated PCWP (> 18 mm Hg) and CVP, elevated SVR, and decreased systolic blood pressure « 100 mm Hg). Septic shock is characterized by low filling pressures, decreased SVR (although early septic shock can exhibit an elevated SVR) , and normal or increased cardiac output. Normal Swan-Ganz catheter parameters are as follows: CVP 1 to 6 mm Hg, PCWP 6 to 12 mm Hg, CI 2.4 to 4.0 Limin/nl, SVR 900 to 1200 dynes/cm2 (Marino, pp. 164, 505-509).

Answer 4

A. Autosomal dominant inheritance B. Pheochromocytomas **C. Pituitary adenomas ** D. Medullary thyroid carcinoma E. Parathyroid hyperplasia ## Footnote j'vlultiple endocrine neoplasia (MEN) type 2 (Sipple syndrome) is an autosomal dominant disorder that localizes to chromosome 10 and is characterized by the development pheochromocytomas and medullary thyroid carcinoma . MEN-2 can be further subdivided into a type A (associated with parathyroid hyperplasia or adenomas) and type B (associated with multiple mucosal neuromas). Pituitary adenomas are associa ted with~lEN type 1 (Cecil, p. 1254).

Answer 5

**A. 1, 2, and3 are correct ** B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct E. All of the above are correct ## Footnote Intraoperative venous air embolism (VAE) has a high incidence during procedures performed in the sitting position (up to 25 to 45% of all cases). VAE is characterized by the development of bronchoconstriction, hypoxia , hypercarbia, hypotension, shock, cardiac arrhythmias, increased airway pressures, and decreased end-tidal CO2 (secondary to increased dead space). Transesophageal echocardiography is the most sensitive diagnostic modality for VAE, detecting volumes as small as 0.02 mLlI\g of air entering the venous system. The immediate treatment of suspected VAE entails rapid hemostasis with concomitant irrigation of the surgical field, lowering of the patient's head with left lateral decubitus positioning, increasing the Fi02 to 100%, stopping any concomitant nitrous oxide administration, manual occlusion of the jugular veins, and aspiration of air from a multi orifice CVP catheter (Greenberg, p. 602; Youmans, pp. 614- 615; Wilkins, pp. 409-410).

Answer 6

**A. Cerebral salt wasting** B. SIADH C. Both of the above D. None of the above ## Footnote Cerebral salt wasting (CS,V) is characterized by hyponatremia « 135) and hypovolemia secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine osmolality, decreased PCWP and CVP (hypovolemia), and normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion . SIADH is associated with a deCi'eased serum osmolality « 280), i11creases in urine sodium and osmolality levels (greater than plasma osmolality), elevated PCWP and CVP (hypervolemia), and normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be observed in a delayed fashion with SlADH. The treatment of SlADH is free water restriction, whereas the treatment of CSW is volume and salt replacement. CSW can accompany aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population , especially in the presence of vasospasm, to prevent the delayed development of ischemic deficits (Youmans, pp. 1829- 1830; Greenberg, pp. 17- 19).

Answer 7

A. Cerebral salt wasting **B. SIADH ** C. Both of the above D. None of the above ## Footnote Cerebral salt wasting (CS,V) is characterized by hyponatremia « 135) and hypovolemia secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine osmolality, decreased PCWP and CVP (hypovolemia), and normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion . SIADH is associated with a deCi'eased serum osmolality « 280), i11creases in urine sodium and osmolality levels (greater than plasma osmolality), elevated PCWP and CVP (hypervolemia), and normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be observed in a delayed fashion with SlADH. The treatment of SlADH is free water restriction, whereas the treatment of CSW is volume and salt replacement. CSW can accompany aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population , especially in the presence of vasospasm, to prevent the delayed development of ischemic deficits (Youmans, pp. 1829- 1830; Greenberg, pp. 17- 19).

Answer 8

A. Cerebral salt wasting B. SIADH C. Both of the above **D. None of the above** ## Footnote Cerebral salt wasting (CS,V) is characterized by hyponatremia « 135) and hypovolemia secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine osmolality, decreased PCWP and CVP (hypovolemia), and normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion . SIADH is associated with a deCi'eased serum osmolality « 280), i11creases in urine sodium and osmolality levels (greater than plasma osmolality), elevated PCWP and CVP (hypervolemia), and normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be observed in a delayed fashion with SlADH. The treatment of SlADH is free water restriction, whereas the treatment of CSW is volume and salt replacement. CSW can accompany aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population , especially in the presence of vasospasm, to prevent the delayed development of ischemic deficits (Youmans, pp. 1829- 1830; Greenberg, pp. 17- 19).

Answer 9

A. Cerebral salt wasting **B. SIADH** C. Both of the above D. None of the above ## Footnote Cerebral salt wasting (CS,V) is characterized by hyponatremia « 135) and hypovolemia secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine osmolality, decreased PCWP and CVP (hypovolemia), and normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion . SIADH is associated with a deCi'eased serum osmolality « 280), i11creases in urine sodium and osmolality levels (greater than plasma osmolality), elevated PCWP and CVP (hypervolemia), and normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be observed in a delayed fashion with SlADH. The treatment of SlADH is free water restriction, whereas the treatment of CSW is volume and salt replacement. CSW can accompany aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population , especially in the presence of vasospasm, to prevent the delayed development of ischemic deficits (Youmans, pp. 1829- 1830; Greenberg, pp. 17- 19).

Answer 10

A. Cerebral salt wasting **B. SIADH** C. Both of the above D. None of the above ## Footnote Cerebral salt wasting (CS,V) is characterized by hyponatremia « 135) and hypovolemia secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine osmolality, decreased PCWP and CVP (hypovolemia), and normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion . SIADH is associated with a deCi'eased serum osmolality « 280), i11creases in urine sodium and osmolality levels (greater than plasma osmolality), elevated PCWP and CVP (hypervolemia), and normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be observed in a delayed fashion with SlADH. The treatment of SlADH is free water restriction, whereas the treatment of CSW is volume and salt replacement. CSW can accompany aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population , especially in the presence of vasospasm, to prevent the delayed development of ischemic deficits (Youmans, pp. 1829- 1830; Greenberg, pp. 17- 19).

Answer 11

A. Propofol B. Isoflurane C. Etomidate **D. Nitrous oxide** E. Lorazepam ## Footnote Nitrous oxide increases cerebral blood flow and thus intracranial pressure when intracranial compliance is altered. Nitrous oxide can also diffuse into intracranial air faster than nitrogen can escape, which can contribute to the development of tension pneumocephalus (Greenberg, p. 2; Youmans, p. 1508; Wilkins, p. 405).

Answer 12

A. Dose-dependent EEG burst suppression B. Associated with decreases in cerebral blood flow C. Effects a re terminated primarily by redistribution **D. Can result in prominent peripheral vasoconstriction ** E. Dose-dependent myocardial suppression ## Footnote Barbiturates are anticonvulsants that result in prominent decreases in CBF and CMR02, dose-dependent EEG burst suppression, dose-dependent myocardial suppression, and peripheral vasodilation. Barbiturates are lipid-soluble and their CNS effects are primarily terminated by redistribution. At higher dosages, barbiturates can actually result in decreases in cerebral perfusion pressure if decreases in mean arterial pressure exceed the decrease in intracranial pressure (Katzung, p. 410; Youmans, pp. 1508, 1521; Greenberg, pp. 2, 776- 777; Will~ins, p. 404).

Answer 13

**A. Dobutamine** B. Dopamine C. Epinephrine D. Phenylephrine E. Isoproterenol ## Footnote See Table 7.37A. Dobutamine is relatively selective for PI receptors, which makes it the agent of choice in the treatment of severe systolic heart failure. Isoproterenol is also a p-selective agent but has clinically insignificant actions on (XI and (X2 receptors as well (Katzung, p. 128; Marino, pp. 278-298; Greenberg, pp. 7- 9).

Answer 14

A. Arsenic poisoning **B. Lead pOisoning ** C. Mercury poisoning D. Iron poisoning E. Succimer (DMSA) F. Penicillamine G. Thallium H. Deferoxamine I. Manganese poisoning J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 15

A. Arsenic poisoning B. Lead pOisoning **C. Mercury poisoning** D. Iron poisoning E. Succimer (DMSA) F. Penicillamine G. Thallium H. Deferoxamine I. Manganese poisoning J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 16

A. Arsenic poisoning B. Lead pOisoning C. Mercury poisoning D. Iron poisoning E. Succimer (DMSA) F. Penicillamine G. Thallium **H. Deferoxamine ** I. Manganese poisoning J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 17

A. Arsenic poisoning B. Lead pOisoning C. Mercury poisoning D. Iron poisoning **E. Succimer (DMSA) ** F. Penicillamine G. Thallium H. Deferoxamine I. Manganese poisoning J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 18

**A. Arsenic poisoning ** B. Lead pOisoning C. Mercury poisoning D. Iron poisoning E. Succimer (DMSA) F. Penicillamine G. Thallium H. Deferoxamine I. Manganese poisoning J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 19

A. Arsenic poisoning B. Lead pOisoning C. Mercury poisoning D. Iron poisoning E. Succimer (DMSA) **F. Penicillamine ** G. Thallium H. Deferoxamine I. Manganese poisoning J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 20

A. Arsenic poisoning B. Lead pOisoning C. Mercury poisoning D. Iron poisoning E. Succimer (DMSA) F. Penicillamine G. Thallium H. Deferoxamine **I. Manganese poisoning ** J. None of the above ## Footnote Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute pOisoning, the onset of symptoms usually takes 4 to 8 weeks to develop, but the evolution of polyneuropathy is slower in chronic

Answer 21

A. 4 B. 8 **C. 12** D. 16 E. 20 ## Footnote Symptomatic hyponatremia (generally < 125 mEq/L) should be corrected at a Imudmal rate of 0.5 mEq/L/h (thus 12 mEq/L/24 h) to avoid central pontine myelinolysis (Marino, p. 644; Greenberg, pp. 15- 16).

Answer 22

A. Two days B. Two weeks **C. Two months ** D. Two yea rs E. None of the above ## Footnote Wound healing occurs in primarily three phases: the inflammatory, the proliferative, and the remodeling phases. The inflammatory phase occurs during the first week and is characterized by hemostasis as well as neutrophil and macrophage infiltration. The proliferative phase occurs from approximately 5 days to 3 weeks and consists of neovascularization, wound contraction (myofibroblasts), extracellular matri'i: synthesis (fibroblasts), and cellular migration (epithelializa tion). The third phase (remodeling) occurs from approximately 4 weeks to 2 years and consists of the aggregation and alignment of collagen fibers, with a progressive increase in wound tensile strength for the first 6 to 8 months until it plateaus. The wound contains the maximuIll collagen content approximately 2 to 3 months after injury, during the early portion of the proliferative phase (Robbins, pp. 74-76; Will~ins, pp. 519- 520; Youmans, pp. 564-565).

Answer 23

A. 1,2, and3 are correct **B. 1 and3 are correct** C. 2 and 4 are correct D. Only 4 is correct E. All of the above are correct ## Footnote Entlurane is an inhaled general anesthetic. that actually lowers seizure threshold; methohexital is a barbiturate that also lowers seizure threshold. This property renders these two agents unsuitable for most neurosurgical procedures (Greenberg, pp. 2, 47; Katzung, p. 417; Youmans, pp. 1508- 1512).

Answer 24

A. Stalk effect B. The macroadenoma no longer synthesizes prolactin **C. Hooll effect ** D. Prior bromocriptine therapy favored the growth of non-hormone-producing neoplastic pituitary cells (null-cell adenoma) E. None of the above ## Footnote The 1-1001, effect results in false-negative lab assays for prolactin in the presence of extremely high prolactin levels. This is secondary to inhibition of formation of the normal prolactin-antibody complexes due to the presence of extremely high prolactin levels. In these cases, a 1:100 prolactin dilution should be obtained to effectively rule out a prolactinoma. Stalk effect results from compression of the adjacent hypothalamus or pituitary stalk by nonprolactin-secreting m 200 ng/mL (Greenberg, pp. 420- 426; Kaye and Laws, pp. 206- 210).

Answer 25

A. Distinguishes Cushing's disease from cortisol-producing adrenal adenomas B. Urine free cortisol levels will exhibit 90% suppression of baseline wi th Cushing's disease C. 17 -Ilydroxysteroids are suppressed to < 50% of baseline with Cushing's disease **D. Adrenal adenomas exhibit 25 to 50% suppression of urine free cortisol baseline levels ** E. None of the above ## Footnote The high-dose dexamethasone suppression test helps distinguish Cushing's disease (ACTH-secreting pituitary adenoma) from ectopic sources of ACTH and cortisolproducing adrenal adenomas. Pituitary adenomas will exhibit suppression with this test, with concomitant deCI'eases in 17 -hydroxysteroids to < 50% of baseline and urine free cortisol levels to < 90% of baseline. Adrenal adenomas are ACTI-I-independent and thus do not respond to the high-dose dexamethasone suppression test (Cecil, p.1217; Youmans, pp. 1196-1197).

Answer 26

A. 1,2, and 3 are correct B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct **E. All of the above are correct ** ## Footnote High-dose barbiturates uncouple cerebral blood flow and cerebral metabolism, thus resulting in decreases in CMROz and increases in CBF. Burst suppression on EEG results in maximal reductions in CMROz with continuous barbiturate infusions. JIigh-dose barbiturate therapy is associated with myocardial depression and hypotension, and patients often require concomitant vasopressor therapy to maintain an adequate mean arterial pressure during barbiturate infusions. Other effects of high-dose barbiturat infusion include inmmnosuppression, impaired gastric motility, increased lysosomal stability, and improved freeradical scavenging. Global cerebral perfusion is improved with barbiturate infusions, and it is thought that blood is "shunted" from normal brain regions to damaged (ischemic) regions. Although barbiturate infusions can lower ICP, improvements in overall outcomes in patients with closed head injuries undergoing high-dose barbiturate therapy is controversial (Greenberg, pp. 653- 654; Will~ins, p. 353).

Answer 27

A. 1,2, and 3 are correct B. 1 and 3 are correct **C. 2 and 4 are correct ** D. Only 4 is correct E. All of the above are correct ## Footnote Von \Villebrand's disease (VWD) results in prolongation of the partial thromboplastin time (PTT) and bleeding time. Coagulopathy resulting from VWD is typically treated with cryoprecipitate, which is rich in both factor VIII and von Willebrand factor as well as desmopressin (DDAVP), which facilitates the release of von Willebrand factor from epithelial cells (Ceci l, p. 994)

Answer 28

A. Patients with severe closed head injuries B. Patients with> 30% body surface area burns C. Hypotensive shock **D. Early postoperative enteral feeds** E. Incidence is deCl'eased with utilization of H2 blockers and sucralfate ## Footnote Superficial stress ulcers in the gastric/duodenal mucosa are a result of regional decreases in blood flow and are exacerbated by the presence 0fI-1+. Patients in the highest risk category for GI hemorrhages are those with severe closed head injuries (Cushing's ulcer) and those with burns over> 30% body surface area (Curling's ulcer). Superficial stress ulcers can lead to nosocomial sepsis and occult GI bleeding, although overt hemorrhage occurs in only 5% of all cases of stress ulcers. The risk of perioperative GI bleeding can be decreased with the administration of H2 blockers and sucralfate, maintenance of adequate systemic blood pressure and oxygen transport, and initiation of early enteral feedings (Marino, pp. 94- 101).

Answer 29

**A. 1,2, and 3 are correct ** B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct E. All of the above ## Footnote Acute-phase reactants are a group of proteins that are largely synthesized by the liver. Synthesis of the acutephase reactants is altered during periods of systemic inflammation, which results in prominent increases in several plasma proteins including C-reactive protein, serum amyloid A, fibrinogen, von Willebrand factor, ai-antitrypsin, haptoglobin, ceruloplasmin, and several complement proteins. Serum plasma levels of albumin and transferrin are typically decreased during periods of acute inflammation (Cecil, pp. 1535-1537).

Answer 30

A. 1, 2, and 3 are correct B. 1 and3 are correct C. 2 and 4 are correct D. Only 4 is correct **E. All of the above** ## Footnote There are several different proteins that act at the anterior hypothalamus to induce a systemic fever (pyrogens), including interleukin-l, interleukin-6, tumor necrosis factor, interferon-a, and some bacterial toxins. All of these substances induce local increases in prostaglandin E2 levels in the anterior hypothalamus to increase the temperature set point (Ceci l, pp. 1533-1535).

Answer 31

A. Systolic blood pressure B. Urine output C. Heart rate **D. Gastrointestinal pH ** E. Oxygen saturation ## Footnote In shock states, blood is selectively shunted away from the GI tract, which results in decreases in the local gastric pH. GI pH normalizes after adequate resuscitation and is thus an excellent indicator of regional perfusion. Normal systolic blood pressure, heart rate , and even urine output can all be observed in inadequately resuscitated patients who are in states of compensated shock (Marino, pp. 198-200; Brown et aI., pp. 569- 585).

Answer 32

A. ,tl'lelltal status changes **B. Respiratory acidosis ** C. Hyperglycemia D. Increased pulse pressure E. Elevated white blood cell count ## Footnote Septic shock is usually a result of bacteremia with gram-positive or gram-negative organisms, although it can also occur with fungal and anaerobic infections. Septic shock often exhibits fever, mental status changes, tachypnea, tachycardia, an increased pulse pressure, hyperglycemia, and an elevated white blood cell count. Septic shock results in tachypnea and a concomitant respiratory alkalosis early in the disease course, although late in the disease course a concomitant metabolic acidosis can occur from lactate accumulation (hypoperfusion). Septic shock is also accompanied by tachycardia and an increased cardiac output initially, although cardiac output and stroke volume are often decreased in the later stages of septic shock. i\·lost patients with sepsis exhibit an elevated white blood cell count and hyperglycemia (glucocorticoid release), although marked decreases in the white blood cell count and hypoglycemia (with prominent bacteremia) are also occasionally observed (Marino, pp. 505- 510).

Answer 33

A. Hyperglycemia B. Essential fatty acid deficiency **C. Metabolic alkalosis ** D. Hypophosphatemia E. Hepatic cholestasis ## Footnote Metabolic complications of total parentej'al nutrition (TPN) include volume overload, hyperglycemia, hypophosphatemia, hyperchloremic metabolic acidosis, hypomagnesemia, hypokalemia, trace element defiCiency, and essential fatty acid defiCiency. Patients on long-term TPN are also at risk to develop hepatic cholestasis and vitamin deficiencies. Other complications of TPN include complications related to central line placement (e.g., pneumothorax, hemothorax) and the presence of an indwelling central catheter (e.g. , venous thrombosis mid sepsis) (Marino, pp. 759- 763).

Answer 34

**A. 1, 2, a nd 3 are correct ** B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct E. All of the above ## Footnote Pseudomembranous colitis (PMC) is a relatively common cause of severe diarrhea and colitis in the ICU population and results from toxins produced by ClostricUu'/1l di((icile. PMC is usually associated with prior exposure to third-generation cephalosporins, clindamycin, or one of the penicillins, although many different antibiotics have been implicated in the development of this disorder. C. di/ficile produces two different toxins (tOxin A and toxin B) that ultimately result in disruption of colonic mucosal integrity, with subsequent fluid secretion, inflammation, and edema. Findings of PMC include fever, leukocytosis, watery diarrhea , abdominal pain/cramping, dehydration, hypoalbuminemia, and even the development of sepsis and toxic megacolon (with colonic perforations). The "gold standard" laboratory study for the diagnosis of PMC is direct cytotoxic assay of stool filtrate for C. dij]icile toxin. ELISA tests for C. ditficile toxin are also available; however, they exhibit low sensitivity. Direct culture of the bacterium is the most sensitive laboratory assay, but it is rarely performed due to time and cost constraints and the inability to differentiate between normal and toxic strains of c. ditncile. The treatment of PMC includes discontinuation of causative antibiotics, fluid and electrolyte repletion, aod the admiJlistration of oral metronidazole (Flagyl) (Marino, pp. 534-537).

Answer 35

**A. Pulmonary angiogram ** B. High resolution helical computed tomographic angiography C. Nuclear scintigraphic ventilation-perfusion lung scan D. Venous duplex ultrasound E. None of the above ## Footnote Pulmonary angiography continues to be the gold standard in the diagnosis of acute pulmonary embolism (PE), with close to a 100% positive predictive value and 90% negative predictive value. High-resolution helical CT angiography is evolving as a more accurate diagnostic modality for acute pulmonary embolism, although its sensitivity and specificity are not as well defined. Nuclear scintigraphic ventilationperfusion (V/Q) lung scan is often the initial diagnostic study of choice in patients with small pulmonary emboli, although approximately 40% of all patients with an acute PE will exhibit a nondiagnostic (indeterminate) V/Q scan. Lower extremity duplex ultrasound can often confirm the source of a PE, although a negative result does not significantly reduce the likelihood of a PE (Marino, pp. 112-115).

Answer 36

A. 1,2, and 3 are correct B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct **E. All of the above ** ## Footnote Warfarin (Coumadin) inhibits the synthesis of the vitamin K-dependent clotting factors (factors II, VII, L,{, X) and the anticoagulant proteins C and S (Katzung, p. 552).

Answer 37

A. 1, 2, and 3 are correct **B. 1 and 3 are correct ** C. 2 and 4 are correct D. Only 4 is correct E. All of the above ## Footnote Barbiturates, rifampin, and cholestyramine admirlistration can all result in decreased levels of warfarin (and thus decreases in u\TR). Cimetidine, metronidazole, trimethoprim-sulfamethoxazole, fluconazole, amiodarone, and disulfiram all result in increased levels of coumadin (and thus increases in INR) (Katzung, p. 554).

Answer 38

A. Hypertension **B. Hyperkalemia ** C. Low plasma renin activity D. Metabolic alkalosis E. IIypomagnesemia ## Footnote Primary aldosteronism (Conn's syndrome) is characterized by hypertension , hypernatremia, hypokalemia, metabolic alkalosis, and low plasma renin activity. Excessive aldosterone levels promote retention of sodium, water, and bicarbonate in the distal renal tubules, with concomitant losses of potassium and magnesium. The majority of cases of Conn's syndrome result from excessive production of aldosterone by an adrenal adenoma (Cecil , p. 1249).

Answer 39

**A. Emergent needle thoracocentesis ** B. Placement of a thoracostomy tube C. Portable chest x-ray D. Obtain an arterial blood gas E. CT scan of the chest ## Footnote Tension pneumothorax is a life-threatening condition tha t often exhibits tracheal deviation to the side opposite the pneumothorax. The marked increases in intrathoracic pressure that accompany tension pneumothorax can result in prominent decreases in venous blood return to the heart, with concomitant hypotension and shock, as in this case. ATLS guidelines recolllmend immediate empiric treatment of suspected tension pneumothorax with needle thoracocentesis, followed by placement of a definitive thoracostomy tube (American College of Surgeons Committee on Trauma, pp. 128-129).

Answer 40

A. STAT portable chest x-ray **B. Immediate cessation of inhala tional anesthetics ** C. Heparin anticoagulation D. Increase in ventilatory rate E. None of the above ## Footnote lvIalignant hyperthermia is a heritable disorder that is characterized by skeletal muscle hype tabolism secondary to decreased calcium sequestration in the sarcoplasmic reticulum. Malignant hyperthermia is associated with the administration of SUCCinylcholine and some inhalational anesthetics (e.g. , halothane, cyclopropane). This disorder is characterized by the acute onset of an increase in end-tidal CO2 , tachycardia, muscle rigidity, and an elevated temperature. With disease progression, arrhythmias, hypoxia , metabolic acidoSiS, pulmonary edema, disseminated intravascular coagulation, rhabdomyolysis, hypotension, and even cardiac arrest can occur. The mortality of malignant hyperthermia is as high as 30%. Suspected cases should be treated initially by the immediate cessation of the suspected offending agent, followed by the administration of IV dantrolene until symptoms cease (Greenberg, pp.4- 5).

Answer 41

A. 1,2, and 3 are correct B. 1 and 3 are correct C. 2 and4 are correct D. Only 4 is correct **E. All of the above are correct ** ## Footnote lvIalignant hyperthermia is a heritable disorder that is characterized by skeletal muscle hype tabolism secondary to decreased calcium sequestration in the sarcoplasmic reticulum. Malignant hyperthermia is associated with the administration of SUCCinylcholine and some inhalational anesthetics (e.g. , halothane, cyclopropane). This disorder is characterized by the acute onset of an increase in end-tidal CO2 , tachycardia, muscle rigidity, and an elevated temperature. With disease progression, arrhythmias, hypoxia , metabolic acidoSiS, pulmonary edema, disseminated intravascular coagulation, rhabdomyolysis, hypotension, and even cardiac arrest can occur. The mortality of malignant hyperthermia is as high as 30%. Suspected cases should be treated initially by the immediate cessation of the suspected offending agent, followed by the administration of IV dantrolene until symptoms cease (Greenberg, pp.4- 5).

Answer 42

A. Propofol B. Etomidate C. Lorazepam **D. Dantrolene ** E. Heparin ## Footnote lvIalignant hyperthermia is a heritable disorder that is characterized by skeletal muscle hype tabolism secondary to decreased calcium sequestration in the sarcoplasmic reticulum. Malignant hyperthermia is associated with the administration of SUCCinylcholine and some inhalational anesthetics (e.g. , halothane, cyclopropane). This disorder is characterized by the acute onset of an increase in end-tidal CO2 , tachycardia, muscle rigidity, and an elevated temperature. With disease progression, arrhythmias, hypoxia , metabolic acidoSiS, pulmonary edema, disseminated intravascular coagulation, rhabdomyolysis, hypotension, and even cardiac arrest can occur. The mortality of malignant hyperthermia is as high as 30%. Suspected cases should be treated initially by the immediate cessation of the suspected offending agent, followed by the administration of IV dantrolene until symptoms cease (Greenberg, pp.4- 5).

Answer 43

A. 1,2, and 3 are correct B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct **E. All of the above are correct ** ## Footnote Hypercalcemia is quite rare in the ICU setting and is usually secondary to the presence of hyperparathyroidism, thyrotoxicosis, or malignancy. Medications that are effective in the treatment of hypercalcemia include furosemide (promotes urinary excretion), isotonic saline (corrects hypovolemia and promotes calcium excretion), calcitonin (inhibits bone resorption), hydrocortisone, bisphosphonates (e.g., pamidronate), and plicamycin (mithramycin). Hemodialysis is also an effective treatment for hypercalcemia (Marino, pp. 679- 681).

Answer 44

**A. 1,2, and3 are correct ** B. 1 and3 are correct C. 2 and 4 are correct D. Only 4 is correct E. All of the above ## Footnote Fat embolism is characterized by pulmonary, cerebral, hepatic, and renal involvement. Cerebral symptoms are usually global, and pulmonary symptoms usually dominate the clinical presentation. Occasionally petechiae of the chest and conjunctivae are observed . Treatment entails aggressive oxygenation with positive-pressure ventilation, volume resuscitation, and the administration of corticosteroids (Robbins, pp. 110-111; Will~ins, pp. 2704-2705).

Answer 45

A. Staph. alirellS, Staph. epidennidis B. Staph. epidermiclis, Strep. pnewllonia **C. Staph. epidernl'idis, Staph. epidennidis ** D. Staph. epidennidis, P. acnes E. Staph. epidenniciis, Staph. [t.ltreliS ## Footnote Staphylococclls epiden11'idis is the most com111on pathogen to result in shunt infections in both an early and late fashion (Greenberg, p. 214).

Answer 46

A. Etomidate B. Propofol C. Lorazepam D. Halothane E. Isoflurane **F. Nitrous oxide** G. Fentanyl H. Pentobarbital I. None of the above ## Footnote Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and ICP. Etomidate can also suppress cortisol synthesis with prolonged infusions. IIalothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation, all of which can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CEF. Barbiturates also exhibit minimal effects upon evoked potentials (Greenberg, pp. 1-3; Katzung, pp. 417, 420-422).

Answer 47

A. Etomidate B. Propofol C. Lorazepam **D. Halothane ** E. Isoflurane F. Nitrous oxide G. Fentanyl H. Pentobarbital I. None of the above ## Footnote Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and ICP. Etomidate can also suppress cortisol synthesis with prolonged infusions. IIalothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation, all of which can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CEF. Barbiturates also exhibit minimal effects upon evoked potentials (Greenberg, pp. 1-3; Katzung, pp. 417, 420-422).

Answer 48

A. Etomidate B. Propofol C. Lorazepam D. Halothane E. Isoflurane F. Nitrous oxide **G. Fentanyl ** H. Pentobarbital I. None of the above ## Footnote Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and ICP. Etomidate can also suppress cortisol synthesis with prolonged infusions. IIalothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation, all of which can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CEF. Barbiturates also exhibit minimal effects upon evoked potentials (Greenberg, pp. 1-3; Katzung, pp. 417, 420-422).

Answer 49

**A. Etomidate ** B. Propofol C. Lorazepam D. Halothane E. Isoflurane F. Nitrous oxide G. Fentanyl H. Pentobarbital I. None of the above ## Footnote Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and ICP. Etomidate can also suppress cortisol synthesis with prolonged infusions. IIalothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation, all of which can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CEF. Barbiturates also exhibit minimal effects upon evoked potentials (Greenberg, pp. 1-3; Katzung, pp. 417, 420-422).

Answer 50

A. Etomidate B. Propofol C. Lorazepam D. Halothane E. Isoflurane F. Nitrous oxide G. Fentanyl **H. Pentobarbital ** I. None of the above ## Footnote Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and ICP. Etomidate can also suppress cortisol synthesis with prolonged infusions. IIalothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation, all of which can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CEF. Barbiturates also exhibit minimal effects upon evoked potentials (Greenberg, pp. 1-3; Katzung, pp. 417, 420-422).

Answer 51

A. Haemophihls'i11flllenzae B. Mora ~e lla catarrhaNs **C. Strep. ]Jneumoniae** D. ]({ebsiella pneumonia E. Staph. epidennidis ## Footnote Streptococcus pllewl10niCle is associated with approximately SO to 70% of all cases of meningitis occurring after traumatic skull fractures. lVter the appropriate antibiotics are administered and the patient recovers from meningitis, a thorough evaluation for the presence of a CSF fistula, with possible surgical repair, should be entertained (Will

Answer 52

A. Interstitial pneumonitis B. Hepatitis C. Bone marrow suppression D. Nausea **E. Hemorrhagic cystitis** ## Footnote BCl\TU is associated with alopecia, bone marrow suppression, dysphagia, encephalopathy, nausea, diarrhea, hepatitis, and renal failure. Some of the most important side effects of BCl\TU are dose-dependent pulmonary complications, including interstitial pneumonitis and pulmonary fibrosis (Katzung, pp. 888-889).

Answer 53

A. Oxybutynin **B. Bethanecol ** C. Imipramine D. Atropine E. Methacholine ## Footnote Bethanechol is a muscarinic agonist that facilitates detrusor contraction and inhibits contraction of the bladder sphincter and trigone, thus effectively treating urinary retention . Methacholine is also a muscarinic agonist, however, it is typically used to facilitate the diagnosis of hyperactive airway disease (e.g. , asthma) due to its potent bronchoconstrictive effects (Greenberg, p. 116; Katzung, pp. 94, 96, 100).

Answer 54

A. Gram-positive cocci B. Gram-positive rods C. Gram-negative cocci **D. Gram-negative rods ** E. None of the above ## Footnote While gram-positive cocci (e.g., Streptococcus plleu.- moniC/e) account for the majority of cases of coml11unityacquired pneumonias, gram-negative rods account for the majority of cases of nosocomial pneumonia. Gram-negative rods account for 46% of all cases of nosocomial pneumonia in ward patients and 83% of all patients on mechanical ventilation. PseudomollCls species are the most common bacteria to account for ventilator-associated nosocomial pneumonia (30% of all cases) (Marino, pp. 516-517).

Answer 55

**A. 1, 2, and 3 are correct ** B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct E. All of the above ## Footnote DIC is often a result of sepsis and severe systemic trauma, which results in endothelial cell damage and release of tissue factor. The presence of large amounts of tissue factor can result in the diffuse activation of both the fibrinolytic and coagulation pathways. Clinically, DIC is characterized by diffuse microvascular thrombosis, thrombocytopenia, and hemorrhage (especially GI bleeding). As DIC progresses, oliguric renal failure, ARDS, and even death from multiple organ failure can ensue. DIC often exhibits elevations of fibrin split products (D-dimer), decreases in fibrinogen, prolongations of the PT and PTT, and thrombocytopenia. Although not contraindicated, heparin is often ineffective in controlling the diffuse microvascular thrombosis that is inherent to DIC because antithrombin III levels are concomitantly decreased (Marino, pp. 712-713).

Answer 56

**A. Iodinated radiographic contrast dye ** B. Propylthiouracil C. Hydrocortisone D. Propranolol E. None of the above ## Footnote The 10dbasedow effect refers to the precipitation of thyrotoxicosis in patients with toxic nodular goiter (or occasionally Graves' disease) who are exposed to large levels of iodine acutely. Common precipitating agents include iodinated radiographic contrast dye and amiodarone (Cecil, pp.1235- 1236).

Answer 57

A. Rocuronium B. Vecuronium C. Pancuronium **D. Succinylcholine** E. None of the above ## Footnote Succinylcholine usually results in mild elevations in serum potassium levels and is rarely associated with severe hyperkalemia (Greenberg, p. 49; Katzung, p. 444).

Answer 58

A. Thiamine B. Vitamin K **C. Pyridoxine ** D. Vitamin B12 E. Vitamin D ## Footnote Isoniazid is associated with the development of peripheral neuropathy that occurs secondary to a relative pyridoxine defiCiency (excessive excretion). Administration of pyridoxine during isoniazid therapy is effective in preventing the development of peripheral neuropathy (Katzung, p. 773).

Answer 59

A. Mydriasis B. Xerostomia C. Delirium **D. Bradycardia ** E. Cutaneous flushing ## Footnote Atropine is an antimuscarinic agent that blocks almost all parasympathetic effects at high concentrations. Symptoms of atropine toxicity include delirium, mydriasis, cycloplegia , xerostomia, tachycardia , cutaneous flushing, and fever. Treatment of atropine toxicity involves the judicious use of physostigmine (Katzung, pp. 113-114).

Answer 60

A. 1,2, and 3 are correct **B. 1 and 3 are correct** C. 2 and 4 are correct D. Only 4 is correct E. All of the above ## Footnote Morphine, nitroglycerin, aspirin, oxygen, and b blockers are often administered in the setting of an acute myocardial infarction (Nfl). The administration of thrombolytics have been shown to improve outcome in patients with acute MI who exhibit chest pain (for> 30 minutes and < 12 hours), ST elevation of at least 0.1 mm in two contiguous leads, or new left bundle branch block and no evidence of heart failure or hypotension. Although the patient meets the criteria for the administration of t-PA, the recent surgical procedure makes this option less appealing due to the associated bleeding risk. Additionally, aspirin is universally recommended for the treatment of acute MI and would not be contraindicated approximately 48 hours after a simple microdiscectomy. The use of ~ blockers in this patient is contraindicated because the patienfs pulse is less than SO (Marino, pp. 304-305, 309- 310).

Answer 61

A. Isoproterenol B. Dopamine **C. Dobutamine ** D. Epinephrine E. Norepinephrine F. None of the above ## Footnote Isoproterenol is a potent ~ agonist that results in prominent increases in cardiac output and deCl'eases in diastolic blood pressure (peripheral vasodilation, )' Isoproterenol promotes both positive inotropic and chronotropic actions. Dopamine primarily activates dopaminergic receptors in the renal, mesenteric, and cerebral vasculature at low dosages, augmenting flow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, activating peripheral (J. receptors. Dobutamine is primarily a ~l agonist that is the inotropic agent of choice in acute, severe systolic heart failure. Epinephrine stimulates both (J. and ~ receptors. At low dosages, epinephrine stimulates primarily ~ receptors; at high dosages, (J. receptors are primarily stimulated. As opposed to dopamine, however, epinephrine is a potent renal vasoconstrictor, even at low dosages. Norepinephrine is an 226 Intensive Neurosurgery Board Review Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Answer 62

A. Isoproterenol B. Dopamine C. Dobutamine D. Epinephrine **E. Norepinephrine ** F. None of the above ## Footnote Isoproterenol is a potent ~ agonist that results in prominent increases in cardiac output and deCl'eases in diastolic blood pressure (peripheral vasodilation, )' Isoproterenol promotes both positive inotropic and chronotropic actions. Dopamine primarily activates dopaminergic receptors in the renal, mesenteric, and cerebral vasculature at low dosages, augmenting flow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, activating peripheral (J. receptors. Dobutamine is primarily a ~l agonist that is the inotropic agent of choice in acute, severe systolic heart failure. Epinephrine stimulates both (J. and ~ receptors. At low dosages, epinephrine stimulates primarily ~ receptors; at high dosages, (J. receptors are primarily stimulated. As opposed to dopamine, however, epinephrine is a potent renal vasoconstrictor, even at low dosages. Norepinephrine is an 226 Intensive Neurosurgery Board Review Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Answer 63

A. Isoproterenol **B. Dopamine ** C. Dobutamine D. Epinephrine E. Norepinephrine F. None of the above ## Footnote Isoproterenol is a potent ~ agonist that results in prominent increases in cardiac output and deCl'eases in diastolic blood pressure (peripheral vasodilation, )' Isoproterenol promotes both positive inotropic and chronotropic actions. Dopamine primarily activates dopaminergic receptors in the renal, mesenteric, and cerebral vasculature at low dosages, augmenting flow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, activating peripheral (J. receptors. Dobutamine is primarily a ~l agonist that is the inotropic agent of choice in acute, severe systolic heart failure. Epinephrine stimulates both (J. and ~ receptors. At low dosages, epinephrine stimulates primarily ~ receptors; at high dosages, (J. receptors are primarily stimulated. As opposed to dopamine, however, epinephrine is a potent renal vasoconstrictor, even at low dosages. Norepinephrine is an 226 Intensive Neurosurgery Board Review Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Answer 64

A. Isoproterenol B. Dopamine C. Dobutamine D. Epinephrine E. Norepinephrine **F. None of the above** ## Footnote Isoproterenol is a potent ~ agonist that results in prominent increases in cardiac output and deCl'eases in diastolic blood pressure (peripheral vasodilation, )' Isoproterenol promotes both positive inotropic and chronotropic actions. Dopamine primarily activates dopaminergic receptors in the renal, mesenteric, and cerebral vasculature at low dosages, augmenting flow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, activating peripheral (J. receptors. Dobutamine is primarily a ~l agonist that is the inotropic agent of choice in acute, severe systolic heart failure. Epinephrine stimulates both (J. and ~ receptors. At low dosages, epinephrine stimulates primarily ~ receptors; at high dosages, (J. receptors are primarily stimulated. As opposed to dopamine, however, epinephrine is a potent renal vasoconstrictor, even at low dosages. Norepinephrine is an 226 Intensive Neurosurgery Board Review Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Answer 65

**A. Isoproterenol ** B. Dopamine C. Dobutamine D. Epinephrine E. Norepinephrine F. None of the above ## Footnote Isoproterenol is a potent ~ agonist that results in prominent increases in cardiac output and deCl'eases in diastolic blood pressure (peripheral vasodilation, )' Isoproterenol promotes both positive inotropic and chronotropic actions. Dopamine primarily activates dopaminergic receptors in the renal, mesenteric, and cerebral vasculature at low dosages, augmenting flow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, activating peripheral (J. receptors. Dobutamine is primarily a ~l agonist that is the inotropic agent of choice in acute, severe systolic heart failure. Epinephrine stimulates both (J. and ~ receptors. At low dosages, epinephrine stimulates primarily ~ receptors; at high dosages, (J. receptors are primarily stimulated. As opposed to dopamine, however, epinephrine is a potent renal vasoconstrictor, even at low dosages. Norepinephrine is an 226 Intensive Neurosurgery Board Review Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Answer 66

A. Obtain an arterial blood gas B. Obtain a serum sodium level C. Administration of IV lorazepam **D. Administration of IV methylene blue ** E. Administration of IV hematin ## Footnote Prolonged nitroprusside infusions are associated with the accumulation of cyanide, which grad ually exhausts thiosulfate and methemoglobin reserves and can result in cyanide toxicity. Cyanide accumulation can result in delirium, ataxia, tinnitus, abdominal pain, blurry vision, muscle spasms, nausea, emesis, and dyspnea. \Vithout treatment, cyanide toxicity can progress to metabolic acidosis, hypotension, coma , and death. Treatment of nitroprusside-induced cyanide toxicity includes cessation of the medication and IV methylene blue. Sodium nitrite , sodium thiosulfate , and hemodialysis are also effective therapies (Marino, pp. 838- 841).

Answer 67

A. 1,2, and 3 are correct B. 1 and 3 are correct C. 2 and 4 are correct D. Only 4 is correct **E. All of the above** ## Footnote First-line therapy for asymptomatic patients with hyponatremia secondary to SIADI-I entails fluid restriction. The treatment of severe, symptomatic hyponatremia (typically Na < 120 mEq/L) secondary to SIADI-I involves more aggressive correction with 3% saline infusions, which are generally discontinued when the patient's symptoms resolve or the serum sodium reaches 128 to 130 mEq/L. The treatment of chronic SIADH often involves demeclocycline; the treatment of SIADH in association with congestive heart failure or renal fail ure often involves hemodialysis (Greenberg, pp.17- 19;Marino,p.643).

Answer 68

A. l.4 L **B. 2.7 L ** C. 3.5 L D. 4.8 L E. 6.0 L ## Footnote To calculate free water deficit, total body water (TEW) must be calculated initially. TEW is 0.5 times lean body mass (in kilograms) for a female and 0.6 times lean body mass for a male. Free water deficit is then calculated by multiplying TEW by (S1',,-140)/140. Thus, the free water deficit in this patient is 2.7 L (Greenberg, p. 19).

Answer 69

A. Vitamin D B. Thiamine C. Vitamin B12 **D. Vitamin C ** E. Pyridoxine ## Footnote Vitamin C is a necessary cofactor in the synthesis of collagen. Vitamin C is important in the intracellular hydroxylation of proline and lysine residues in the procollagen molecule (Robbins, pp. 456- 459; Wilkins, pp. 519-520).

Answer 70

**A. Vitamin A ** B. Vital'llin D C. Vitamin E D. Thiamine E. Folate ## Footnote Acute vitamin A toxicity can result in symptoms of elevated intracranial pressure (headache, nausea, emesis, blurry vision, papilledema), hepatomegaly, and ascites. These symptoms are usually transient and typically resolve after discontinuing the excessive intake of vitamin A; however, severely symptomatic patients occasionally require serial lumbar punctures (to treat the elevated intracranial pressure) and restoration of any underlying electrolyte abnormalities (e.g. , hypercalcemia) (Robbins, p. 441).

Answer 71

A. J'I'Iuscle wealmess B. Plethora C. Loss of diurnal rhythm of cortisol secretion **D. High serum ACTI-I level ** E. Solitary adrenal adenoma ## Footnote Cushing's syndrome usually results from iatrogenic steroid administration or adrena l adenomas. Under these circumstances, the diurnal rhythm of cortisol secretion is lost and serul11 ACTH levels are markedly depressed. Rarely, ectopic ACTH production by a malignant tumor occurs (e.g., oat cell carcinoma of the lung); tills can result in Cushing's syndrome with concomitant high serum ACTH levels. Cushing's disease results from an ACTH-producing pituitary adenoma. The clinical symptomatology of Cushing's syndrome and Cushing's disease is similar and consist of truncal obeSity, abdominal striae, acne, muscle weakness, hirsuitism, depression, lethargy, "moon faCies," and plethora (Greenberg, pp. 420-421).

Answer 72

**A. Respiratory acidosis ** B. Respiratory alkalosis C. J'I'Ietabolic acidosis D. Metabolic alkalosis E. Combined respiratory acidosis and metabolic acidosis F. Combined respiratory alkalosis and metabolic alkalosis ## Footnote The normal range for pH is 7.36 to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to 26 mEq/L. The initial step in the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory or metabolic. With primary metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction. \Vith primary respiratory disorders, the changes in pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the pH are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected compensatory change in PC02 for metabolic acidosis is 1.5 I-ICOJ + (8 ± 2). The expected compensatory change in PC02 for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pH is 0.008 X (PC02 - 40). With acute respiratory alkalosis, the expected change in pH is 0.008 x (40 - PC02). If the change in pH exceeds 0.008 times the change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated) respiratory disorders, the change in pH is 0.003 times the change in PC02 . In question 96, the values are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fully compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 100 is combined respiratory and metabolic acidosis (Marino, pp. 581- 586).

Answer 73

A. Respiratory acidosis B. Respiratory alkalosis C. J'I'Ietabolic acidosis **D. Metabolic alkalosis ** E. Combined respiratory acidosis and metabolic acidosis F. Combined respiratory alkalosis and metabolic alkalosis ## Footnote The normal range for pH is 7.36 to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to 26 mEq/L. The initial step in the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory or metabolic. With primary metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction. \Vith primary respiratory disorders, the changes in pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the pH are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected compensatory change in PC02 for metabolic acidosis is 1.5 I-ICOJ + (8 ± 2). The expected compensatory change in PC02 for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pH is 0.008 X (PC02 - 40). With acute respiratory alkalosis, the expected change in pH is 0.008 x (40 - PC02). If the change in pH exceeds 0.008 times the change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated) respiratory disorders, the change in pH is 0.003 times the change in PC02 . In question 96, the values are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fully compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 100 is combined respiratory and metabolic acidosis (Marino, pp. 581- 586).

Answer 74

**A. Respiratory acidosis ** B. Respiratory alkalosis C. J'I'Ietabolic acidosis D. Metabolic alkalosis E. Combined respiratory acidosis and metabolic acidosis F. Combined respiratory alkalosis and metabolic alkalosis ## Footnote The normal range for pH is 7.36 to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to 26 mEq/L. The initial step in the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory or metabolic. With primary metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction. \Vith primary respiratory disorders, the changes in pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the pH are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected compensatory change in PC02 for metabolic acidosis is 1.5 I-ICOJ + (8 ± 2). The expected compensatory change in PC02 for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pH is 0.008 X (PC02 - 40). With acute respiratory alkalosis, the expected change in pH is 0.008 x (40 - PC02). If the change in pH exceeds 0.008 times the change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated) respiratory disorders, the change in pH is 0.003 times the change in PC02 . In question 96, the values are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fully compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 100 is combined respiratory and metabolic acidosis (Marino, pp. 581- 586).

Answer 75

A. Respiratory acidosis B. Respiratory alkalosis **C. J'I'Ietabolic acidosis ** D. Metabolic alkalosis E. Combined respiratory acidosis and metabolic acidosis F. Combined respiratory alkalosis and metabolic alkalosis ## Footnote The normal range for pH is 7.36 to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to 26 mEq/L. The initial step in the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory or metabolic. With primary metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction. \Vith primary respiratory disorders, the changes in pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the pH are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected compensatory change in PC02 for metabolic acidosis is 1.5 I-ICOJ + (8 ± 2). The expected compensatory change in PC02 for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pH is 0.008 X (PC02 - 40). With acute respiratory alkalosis, the expected change in pH is 0.008 x (40 - PC02). If the change in pH exceeds 0.008 times the change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated) respiratory disorders, the change in pH is 0.003 times the change in PC02 . In question 96, the values are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fully compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 100 is combined respiratory and metabolic acidosis (Marino, pp. 581- 586).

Answer 76

A. Respiratory acidosis B. Respiratory alkalosis C. J'I'Ietabolic acidosis D. Metabolic alkalosis **E. Combined respiratory acidosis and metabolic acidosis ** F. Combined respiratory alkalosis and metabolic alkalosis ## Footnote The normal range for pH is 7.36 to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to 26 mEq/L. The initial step in the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory or metabolic. With primary metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction. \Vith primary respiratory disorders, the changes in pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the pH are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected compensatory change in PC02 for metabolic acidosis is 1.5 I-ICOJ + (8 ± 2). The expected compensatory change in PC02 for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pH is 0.008 X (PC02 - 40). With acute respiratory alkalosis, the expected change in pH is 0.008 x (40 - PC02). If the change in pH exceeds 0.008 times the change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated) respiratory disorders, the change in pH is 0.003 times the change in PC02 . In question 96, the values are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fully compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 100 is combined respiratory and metabolic acidosis (Marino, pp. 581- 586).

Critical Care and Clinical Skills Flashcards

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