Which of the following assessment date would make the nurse suspect of developing ARDS

Questions

Multiple Choice (choose the best answer)

I.1. A 60-year-old man recovered after receiving mechanical ventilator support for months because of a severe traumatic brain injury. He was intubated for several weeks, and tracheostomy was postponed because of diffuse intravascular coagulation. He has shortness of breath. His pulmonary function test results (Table I.Q1) and a flow volume loop (Figure I.Q1) are shown.

Table I.Q1

According to these results, which is the most likely explanation of the patient’s underlying condition?

a.

Unilateral mainstem bronchus obstruction

b.

Variable intrathoracic upper airway obstruction

c.

Variable extrathoracic upper airway obstruction

d.

Fixed upper airway obstruction

Figure I.Q1.

I.2. A 67-year-old man presented with a middle cerebral artery infarction. In the ED, he was intubated for mechanical ventilation. Figure I.Q2 shows the initial ventilator flow-time and pressure-time waveforms.

Figure I.Q2.

While he was being transported to the neurocritical care unit, however, he became progressively and profoundly hypotensive and had transient arrhythmias. The ventilator was set on volume assist-control mode, with a Vt of 500 mL and a constant inspiratory flow rate of 50 L/min. The patient had a history of hypertension, atrial fibrillation, diabetes mellitus, peripheral artery disease, and COPD. What is the most appropriate first treatment?

a.

Disconnect the ventilator for 30 seconds.

b.

Extubate the patient and administer O2 with a mask.

c.

Place a chest tube immediately.

d.

Transport the patient to the ED for chest radiography.

I.3. Which of the following will cause the end-tidal CO2 to increase quickly?

b.

Massive pulmonary embolism

c.

Cardiopulmonary arrest

I.4. A 63-year-old man presented with acute respiratory failure. He was intubated and given mechanical ventilation in the ED. The initial settings for the mechanical ventilator were Vt, 750 mL; respiratory rate, 10 breaths per minute; and PEEP, 5 cm H2O. The patient was transferred to the ICU. He was deeply sedated and paralyzed, and no spontaneous breathing effort was noted. An intern decreased the Vt to 500 mL and increased the respiratory rate to 15 breaths per minute. Which of the following changes would you expect to occur as a result of the intern’s intervention?

a.

Decreased airway resistance

c.

Increased dead space fraction

d.

Increased CO2 production

I.5. During mechanical ventilation, what primarily influences oxygenation?

I.6. What Vt range is appropriate for an adult male with an ideal body weight of 66 kg?

I.7. Lung-protective ventilation includes which of the following measures?

b.

Maintaining Pplat less than 30 cm H2O

c.

Using a Vt of 4 to 8 mL/kg ideal body weight

I.8. Which mode of ventilation provides full support for all breaths (timed and patient triggered)?

d.

Noninvasive ventilation

I.9. Which of the following describes the cardiopulmonary interaction during PPV?

a.

The pressure remaining in the alveoli at the end of inspiration can compress the adjacent pulmonary vasculature and impede pulmonary blood flow.

b.

The intrathoracic veins are compressed, and the central venous and right atrial pressures are elevated.

c.

The decrease in venous return to the right side of the heart causes increased right ventricular stroke volume, preload, and pulmonary blood flow.

I.10. What is the benefit in selecting a dual-control adaptive pressure ventilation mode?

a.

The patient must spontaneously trigger a breath.

b.

The ventilator delivers a target Vt while using the lowest driving pressure necessary.

c.

The ventilator delivers a target Vt while using the highest driving pressure necessary.

d.

The patient must be comatose.

I.11. Which of the following is not recommended for the management of ARDS?

a.

PEEP levels guided by esophageal balloon monitoring

d.

High-frequency oscillatory ventilation

I.12. For which patient population is the use of inhaled nitric oxide most established?

b.

Patients with right-sided heart failure

c.

Neonates with persistent pulmonary hypertension

d.

Recipients of transplanted lung

I.13. The application of high PEEP is often used for refractory hypoxemia in ARDS. Which of the following is not a potential consequence for patients with traumatic brain injury?

a.

Improved cardiac output and cerebral perfusion pressure

b.

Decreased cardiac output and cerebral perfusion pressure

c.

Increased intracranial pressure

d.

Decreased venous drainage from the brain to the heart

I.14. By which mechanism can hypercapnia increase intracranial pressure?

a.

Prolonged elevation of Paco2 produces arterial hypertension.

b.

Elevated Paco2 causes cerebrovascular vasodilatation.

c.

Elevated Paco2 decreases oxygenation of brain tissue.

d.

Elevated Paco2 decreases reabsorption of CSF.

I.15. A 60-year-old woman with a history of coronary artery disease and long-term use of β-blockers is transferred to the ICU from the ED with suspected abdominal sepsis due to cholangitis. While she is waiting for urgent surgical evaluation, she is in acute respiratory distress and needs emergency intubation. Immediately after she receives sedatives for tracheal intubation, refractory arterial hypotension develops (BP 70/30 mm Hg, HR stable at 70 bpm). The patient receives boluses of phenylephrine but remains hypotensive (BP 72/32 mm Hg, HR 68 bpm). Which of the following factors precipitated the arterial hypotension?

a.

Increased mean systemic BP

b.

Decreased isovolumetric contraction

c.

Decreased systemic vascular resistance

I.16. A 78-year-old man with a history of hypertension is admitted for an elective laparoscopic cholecystectomy. Vital signs include the following: BP 111/70 mm Hg, HR 76 bpm, respiratory rate 17 breaths per minute, and Spo2 92% with room air. He states that he has been taking his antihypertensive medication. During the preoperative evaluation, the anesthesiologist hears a 3/6 crescendo-decrescendo systolic ejection murmur that radiates to the carotids and is immediately preceded by a systolic click. According to this patient’s condition, which of the following changes would be observed in a volume-pressure curve?

a.

Increased left ventricular volume and pressure due to regurgitant flow

b.

Decreased left ventricular volume caused by decreased preload

c.

Increased left ventricular pressure and increased end-systolic volume

d.

Decreased stroke volume and decreased end-systolic volume

I.17. A 75-year-old man with a past medical history of uncontrolled hypertension and hyperlipidemia is admitted to the ED for worsening fatigue, dyspnea on exertion, and a 7-kg weight gain over the past 2 months. He is awake and alert but in moderate distress. He is using accessory respiratory muscles and says it is difficult to breathe. Vital signs include the following: BP 106/70 mm Hg, HR 106 bpm, respiratory rate 22 breaths per minute, and Spo2 89% with room air. The patient appears uncomfortable and can speak in only short sentences. On cardiac examination, he has a regular rate and rhythm, with the apex displaced laterally to the midaxillary line in the 6th intercostal space, and a third heart sound. On lung auscultation, he has diffuse bilateral rales in the lower lung fields and his extremities have ankle edema (2+) bilaterally. How does this patient’s clinical condition affect the Frank-Startling curve?

a.

The curve shifts up and to the right.

b.

The curve shifts down and to the left.

c.

The curve shifts up and to the left.

d.

The curve shifts down and to the right.

I.18. A 68-year-old man with a past medical history of uncontrolled type 2 diabetes mellitus, chronic renal insufficiency, hypertension, and hyperlipidemia is admitted to the ED with a 5-day history of productive cough with associated fevers, chills, and rigors. On examination, he is lethargic. Vital signs are HR 94 bpm, BP 80/40 mm Hg, respiratory rate 35 breaths per minute, Spo2 89% on 3 L O2 by nasal cannula, and temperature 39.5°C. On physical examination he has rhonchi appreciated on auscultation over the right side of his chest. Laboratory test results are as follows: white blood cell count 22×109/L, sodium 133 mmol/L, potassium 5.5 mmol/L, and glucose 192 mg/dL. Chest radiography shows consolidation of the right middle and lower lobe air space. Which statement is true?

a.

Systolic dysfunction is at least twice as common as diastolic dysfunction in patients with septic shock.

b.

Septic shock results exclusively in arterial dilatation as a result of failure of the vascular smooth muscle to vasoconstrict.

c.

Diastolic dysfunction is a poor prognostic marker in patients with sepsis.

d.

The adverse effects of fluid resuscitation when a patient is on the flat portion of the Frank-Starling curve is related to altered diastolic compliance at higher filling pressures.

I.19. A 65-year-old man who was admitted to the ICU with a diagnosis of septic shock and ARDS is receiving mechanical ventilator support. He appears to have increased work of breathing, and his vasopressor support has been increased for refractory shock. The intensivist wants to proceed with a fluid responsiveness test for this patient who has respiratory efforts. Which of the following would be the most reliable?

a.

Inferior vena cava distensibility index

b.

Inferior vena cava collapsibility index

c.

Left ventricular outflow tract peak velocity variability

d.

Left ventricular outflow tract area and passive leg raising

I.20. Which of the following hormones is not released into the systemic circulation by the kidneys?

d.

Antidiuretic hormone (vasopressin)

I.21. During urine acidification, which part of the renal tubular system generates most of the ammonia?

a.

Proximal convoluted tubules

b.

Distal convoluted tubules

c.

Thick ascending loop of Henle

I.22. What is the main factor responsible for regulation of the glomerular filtration rate?

a.

Glomerular plasma flow rate

b.

Glomerular capillary hydraulic pressure

c.

Tubuloglomerular feedback mechanisms

d.

Myogenic response of blood vessels

I.23. Diagnosis of AKI in critically ill patients is based on an increased serum creatinine level and decreased urine output. Which of the following statements is true?

a.

A small increase in creatinine (0.3 mg/dL) is associated with a poor short-term prognosis for hospitalized patients.

b.

AKI classification should be done only on the basis of serum creatinine because urinary volume measurement is cumbersome.

c.

Robust data are available for the use of biomarkers in the diagnosis and management of AKI.

d.

AKI is not associated with in-hospital mortality.

I.24. Which of the following conditions is not recommended for accurately conducting indirect calorimetry?

a.

The patient has been awake for at least 6 to 8 hours after anesthesia.

b.

The patient is receiving nothing by mouth, and enteral nutrition is withheld for 6 hours before testing.

c.

The test is conducted at least 4 hours after dialysis.

d.

The test is administered at least 30 minutes after administration of pain and sedation medications.

I.25. A 65-year-old woman with subarachnoid hemorrhage is admitted to the neurocritical care unit and intubated. The team will begin enteral nutrition with a nasoenteric tube. Her BMI is 28.9. What are her protein requirements?

a.

Based on actual body weight, 0.8 g/kg

b.

Based on actual body weight, 1.2 to 2.0 g/kg

c.

Based on ideal body weight, 2.0 g/kg

d.

Based on ideal body weight, 2.5 g/kg

I.26. An 85-year-old man was transferred to the ICU with respiratory failure and was immediately intubated. He was eating well but had minimal intake in the past 24 hours. The critical care team would like to initiate enteral nutrition. What type of tube is recommended?

I.27. On oral examination, a patient has spongy, bleeding gums. Which vitamin deficiency is most likely?

I.28. A 32-year-old man with a history of Crohn disease is admitted to the ICU with shortness of breath and recurrent small-bowel obstruction. He has lost 11.4 kg over the past 6 months and is moderately malnourished. His daily fluid limit is 1,500 mL. What form of nutrition support is recommended?

a.

Peripheral parenteral nutrition

b.

Central parenteral nutrition

c.

Infusion of dextrose and amino acids

d.

Infusion of 5% dextrose in 0.45% normal saline

I.1. Answer d.

Different patterns can appear on a flow-volume loop when patients have obstructive physiology. Variable intrathoracic obstruction (Figure I.A1A) is caused by lesions within the intrathoracic airways that obstruct the lumen of the airway but move in response to airway pressure changes during the respiratory cycle. An example is tracheobronchomalacia with a breakdown of the cartilaginous rings. Variable extrathoracic obstruction (Figure I.A1B) is caused by lesions within the extrathoracic airways that obstruct the lumen of the airway but move in response to airway pressure changes during the respiratory cycle. An example is a mobile thyroid mass compressing the trachea.

Figure I.A1.

The flow-volume loop in the question (Figure I.Q1) is the result of a fixed airway obstruction. This pattern is caused by either an intrathoracic or extrathoracic lesion that obstructs the airway lumen but does not move in response to airway pressure changes during the respiratory cycle. Examples are tracheal stenosis or bulky lymphadenopathy encasing the trachea.

Nussbaumer-Ochsner Y, Thurnheer R. Images in clinical medicine: subglottic stenosis. N Engl J Med. 2015 Jul 2;373(1):73.

I.2. Answer a.

In the patient’s flow-time curve, the flow at end-expiration is not zero before the patient receives the next breath. This signifies auto-PEEP, defined as the magnitude of the end-expiratory pressure in excess of the set extrinsic PEEP. High V˙ e and expiratory airflow obstruction are the most important risk factors for the development of auto-PEEP. Auto-PEEP decreases venous return by mechanical compression and obstruction of the intrathoracic portion of the superior vena cava. PEEP can also decrease left ventricular afterload. Lung hyperinflation may cause bradycardia and vasodilatation through autonomic reflexes. Excessive PEEP can cause acute right ventricular failure by hyperinflation of the lungs, and shock and cardiac arrest may occur. To minimize auto-PEEP, one should minimize V˙e and use small Vts with prolongation of the time available for exhalation. If the patient is in shock or cardiac arrest due to auto-PEEP, one should consider a brief trial of apnea or temporarily disconnect the endotracheal or tracheostomy tube from the ventilator circuit to allow complete exhalation.

Berlin D. Hemodynamic consequences of auto-PEEP. J Intensive Care Med. 2014 Mar-Apr;29(2):81–6. Epub 2012 May 15.

I.3. Answer d.

Mucous plugging can cause an increased end-tidal CO2 if it leads to decreased Vts and thus decreased ventilation. All the other choices (accidental extubation, massive pulmonary embolism, and cardiopulmonary arrest) lead to decreased end-tidal CO2 due to increased dead space ventilation (or lack of CO2 detection with accidental extubation).

Anderson CT, Breen PH. Carbon dioxide kinetics and capnography during critical care. Crit Care. 2000;4(4):207–15. Epub 2000 Jul 12.Close

I.4. Answer c.

When the intern decreased the Vt, the volume of the anatomical dead space remained the same. V ˙e was not changed (750 mL × 10 = 500 mL × 15). Therefore, the dead space fraction of the total ventilation increased. Paco2 increased because of the increased dead space fraction, while CO2 production and airway resistance did not change.

Robertson HT. Dead space: the physiology of wasted ventilation. Eur Respir J. 2015 Jun;45(6):1704–16. Epub 2014 Nov 13. Erratum in: Eur Respir J. 2015 Oct;46(4):1226.

I.5. Answer a.

Supplemental O2 supplies the lungs with supra-atmospheric levels of O2, increasing the Po2 in the alveoli. PEEP recruits collapsed alveoli and reduces alveolar collapse at the end of exhalation. V˙e and respiratory rate influence ventilation and CO2 removal.

Kacmarek RM, Stoller JK, Heuer AJ, editors. Egan’s fundamentals of respiratory care. 11th ed. St Louis (MO): Elsevier/Mosby; c2017. 1,392 p.

I.6. Answer b.

The appropriate Vt range for an adult patient is 6 to 8 mL/kg ideal body weight. Therefore, the range of safe Vt delivery is 350 to 550 mL.

Kacmarek RM, Stoller JK, Heuer AJ, editors. Egan’s fundamentals of respiratory care. 11th ed. St Louis (MO): Elsevier/Mosby; c2017. 1,392 p.

I.7. Answer d.

Lung-protective ventilation is widely defined as using Vt of 4 to 8 mL/kg ideal body weight and maintaining a Pplat less than 30 cm H2O. Lung-protective ventilation reduces mortality among patients with ARDS and improves outcomes for patients with ventilator-induced lung injury.

Kacmarek RM, Stoller JK, Heuer AJ, editors. Egan’s fundamentals of respiratory care. 11th ed. St Louis (MO): Elsevier/Mosby; c2017. 1,392 p.

I.8. Answer b.

In CMV (commonly referred to as assist control), regardless of trigger type (timed or patient), the ventilator delivers a breath with a set Vt or inspiratory pressure, inspiratory time or flow rate, PEEP, and Fio2. Each breath has the same characteristics. The patient-triggered breaths are assisted breaths, and the timed breaths are controlled breaths.

Kacmarek RM, Stoller JK, Heuer AJ, editors. Egan’s fundamentals of respiratory care. 11th ed. St Louis (MO): Elsevier/Mosby; c2017. 1,392 p.

I.9. Answer d.

PPV can have a profound effect on hemodynamic parameters, including cardiac output and BP. Positive intrathoracic pressure during inspiration elevates central venous pressure and right atrial pressure, resulting in a decrease in venous return to the right side of the heart, which decreases right ventricular stroke volume, preload, and pulmonary blood flow. Additionally, PEEP can compress the pulmonary vasculature. Since HR usually does not change with PEEP, the entire decrease in cardiac output is a consequence of decreased left ventricular stroke volume. Close monitoring of hemodynamics should be coupled with mechanical ventilation, particularly when titrating PEEP to a higher level.

Kacmarek RM, Stoller JK, Heuer AJ, editors. Egan’s fundamentals of respiratory care. 11th ed. St Louis (MO): Elsevier/Mosby; c2017. 1,392 p.

Luecke T, Pelosi P. Clinical review: positive end-expiratory pressure and cardiac output. Crit Care. 2005;9(6):607–21. Epub 2005 Oct 18.Close

I.10. Answer b.

The clinician sets the target Vt and the upper and lower limits for driving pressure. The ventilator delivers the Vt with the lowest pressure needed.

I.11. Answer d.

High-frequency oscillatory ventilation has not shown any positive effect on mortality and has harmed patients with ARDS.

Fan E, Del Sorbo L, Goligher EC, Hodgson CL, Munshi L, Walkey AJ, et al; American Thoracic Society, European Society of Intensive Care Medicine, and Society of Critical Care Medicine. An official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine Clinical Practice guideline: mechanical ventilation in adult patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. 2017 May 1;195(9):1253–63. Erratum in: Am J Respir Crit Care Med. 2017 Jun 1;195(11):1540.

I.12. Answer c.

The FDA has approved inhaled nitric oxide for use only in neonates with persistent pulmonary hypertension. However, inhaled nitric oxide is used in patients who have other conditions, including ARDS, right-sided heart failure, and adult pulmonary hypertension, and in patients who have received a transplanted heart or lung (or both). Refractory hypoxemia has been treated successfully, but inhaled nitric oxide has not been shown to decrease mortality in any patient population.

George I, Xydas S, Topkara VK, Ferdinando C, Barnwell EC, Gableman L, et al. Clinical indication for use and outcomes after inhaled nitric oxide therapy. Ann Thorac Surg. 2006 Dec;82(6):2161–9.Close

INOMAX (nitric oxide) for inhalation [Internet]. United Kingdom: Mallinckrodt Pharmaceuticals. c2017 [cited 2018 Jun 6]. Available from: http://inomax.com/about-inomax.

I.13. Answer a.

PEEP has the potential to decrease cardiac output and cerebral perfusion pressure, increase intracranial pressure, and decrease venous drainage.

Boone MD, Jinadasa SP, Mueller A, Shaefi S, Kasper EM, Hanafy KA, et al. The effect of positive end-expiratory pressure on intracranial pressure and cerebral hemodynamics. Neurocrit Care. 2017 Apr;26(2):174–81.

I.14. Answer b.

Hypercapnia directly and indirectly (through alteration of CSF pH) dilates the cerebral vasculature, and hypercapnia can cause intracranial hypertension.

Roberts BW, Karagiannis P, Coletta M, Kilgannon JH, Chansky ME, Trzeciak S. Effects of Paco2 derangements on clinical outcomes after cerebral injury: a systematic review. Resuscitation. 2015 Jun;91:32–41. Epub 2015 Mar 28.

I.15. Answer c.

Acute decrease in systemic vascular resistance and decreased venous return due to venodilatation are the most remarkable effects of induction of anesthesia with subsequent arterial hypotension before intubation in the ICU. At higher HRs, the relative amount of time in diastole is decreased; thus, acute myocardial ischemia can be present in patients with coronary artery disease. However, this patient’s HR remained essentially the same. In addition, initiation of mechanical circulatory support and use of PEEP can worsen arterial hypotension. For this patient with suspected abdominal sepsis, the initial management should be aggressive fluid resuscitation and use of vasopressors to offset the adverse effect of sedatives. Choice a is incorrect because the mean systemic pressure (the pressure measured when flow ceases within the circulatory system [10-15 mm Hg]) is lower than the systemic arterial pressure and is similar to the right atrial pressure. After administration of most sedatives, venodilatation leads to lower mean systemic pressure. Choice b is incorrect because isovolumetric contraction remains similar if not increased because of decreased left ventricular afterload. Choice d is incorrect because a slight decrease in HR within the normal range would not explain the severity of arterial hypotension.

Zanger DR, Solomon AJ, Gersh BJ. Contemporary management of angina: part II: medical management of chronic stable angina. Am Fam Physician. 2000 Jan 1;61(1):129–38.Close

I.16. Answer c.

Aortic stenosis, the most common valvular disease worldwide, usually results from valve leaflet calcification in the sixth or seven decade of life. On auscultation, an ejection click is typically heard before a crescendo-decrescendo systolic murmur. With an increased afterload, the left ventricular pressure and end-systolic volume are increased, and the stroke volume is decreased. When the heart can no longer compensate, angina develops with heart failure or syncope (or both).

Choice a is incorrect because the volume-pressure curve variations are consistent with aortic regurgitation and increased regurgitant flow into the left ventricle. Choice b is incorrect because the volume-pressure curve variations are consistent with mitral stenosis. Choice d is incorrect because it is inconsistent with aortic stenosis.

Argulian E, Windecker S, Messerli FH. Misconceptions and facts about aortic stenosis. Am J Med. 2017 Apr;130(4):398–402. Epub 2017 Jan 18.

I.17. Answer d.

The patient’s clinical presentation is consistent with acute decompensated congestive heart failure. Therefore, the Frank-Starling curve is shifted down and to the right. Option c is incorrect because it is consistent with increased cardiac contractility. Choices a and b are incorrect because they are inconsistent with congestive heart failure.

The Frank-Starling curve is affected by changes in cardiac determinants such as contractility, afterload, and preload. Modifications in preload result in changes along the same line of the Frank-Starling curve. However, changes in afterload and contractility result in a shift of the Frank-Starling curve, as follows:

An increase in contractility shifts the curve up and to the left as a result of increased cardiac output (eg, exercise).

A decrease in contractility shifts the curve down and to the right as a result of increased left ventricular end-diastolic volume and decreased cardiac output (eg, congestive heart failure).

A decrease in afterload shifts the curve up and to the left. Thus, for a given preload, the stroke volume and cardiac output are increased.

An increase in afterload shifts the curve down and to the right because of decreased stroke volume and cardiac output.

Sequeira V, van der Velden J. Historical perspective on heart function: the Frank-Starling Law. Biophys Rev. 2015 Dec;7(4):421–47. Epub 2015 Nov 19.

I.18. Answer d.

In the flat portion of the Frank-Starling curve, additional fluid administration results in increased pulmonary hydrostatic pressures and the release of atrial natriuretic peptides. The net effect is a fluid shift into the interstitial space with pulmonary and tissue edema as a result of altered O2 delivery and extraction, distortion of the tissue architecture, disturbance of cell-to-cell interaction, limited capillary blood flow, and altered lymphatic drainage.

Choice a is incorrect because diastolic dysfunction is more common than systolic dysfunction among patients with septic shock. Choice b is incorrect because septic shock results from not only arterial vasodilatation but also from profound venous dilatation, thus resulting in an increase in the unstressed blood volume, diminished venous return, and reduced cardiac output. Choice c is incorrect because diastolic dysfunction is considered a good prognostic marker among patients with septic shock.

Marik P, Bellomo R. A rational approach to fluid therapy in sepsis. Br J Anaesth. 2016 Mar;116(3):339–49. Epub 2015 Oct 27.

I.19. Answer d.

Patients who are receiving mechanical ventilator support with active rather than passive breathing should be tested with passive leg raising. The other tests were validated in patients receiving passive mechanical ventilation (no respiratory efforts). This patient had increased work of breathing and ventilator dyssynchrony.

Monnet X, Rienzo M, Osman D, Anguel N, Richard C, Pinsky MR, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. 2006 May;34(5):1402–7.Close

I.20. Answer d.

Renin, an important hormone for hemostatic stability, is secreted by juxtaglomerular cells located in the walls of afferent arterioles in the renal interstitium. Erythropoietin is responsible for production of red blood cells. In adults, about 90% of erythropoietin is produced by renal interstitial fibroblasts, and 10% is contributed by extrarenal sources, primarily liver cells. Serum phosphorus regulation by the kidneys involves production of FGF 23 in osteoblasts in response to increases in serum phosphate. FGF 23 requires a cofactor to exert its action on the renal proximal tubule. Klotho is produced in the kidney and activates FGF receptor.

Vasopressin is a potent endogenous peptide influencing many biologic functions, including regulation of water balance, BP, platelet function, and thermoregulation. It is synthesized as a prohormone in the posterior hypothalamus and is stored in the posterior pituitary. Vasopressin acts on V1, V2, V3, and oxytocin-type receptors. V1 receptors are located in the vasculature, myometrium, and platelets. V2 receptors are located along the distal tubule and collecting duct. V3 receptors are mainly found in the pituitary gland.

Schrier RW. Vasopressin and aquaporin 2 in clinical disorders of water homeostasis. Semin Nephrol. 2008 May;28(3):289–96.Close

I.21. Answer a.

Ammonia excretion is the major mechanism by which the kidneys excrete acid. Of the net acid excreted or new bicarbonate generated by the kidneys, approximately one-half to two-thirds (approximately 40-50 mmol daily) is from ammonia excretion in the urine. Most of the ammonia produced is excreted from the proximal convoluted tubules into the urine rather than added to the venous blood. Synthesis and excretion of ammonia increase greatly during acid loading, in contrast to the limited increase in titratable acidity. Transport of the produced ammonia along the nephron and into the urine is a complex process.

Hamm LL, Nakhoul N, Hering-Smith KS. Acid-base homeostasis. Clin J Am Soc Nephrol. 2015 Dec 7;10(12):2232–42. Epub 2015 Nov 23.

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I.22. Answer b.

The transcapillary movement of water across the glomerular capillaries is controlled by Starling forces (like in all capillary beds). Filtration results from an imbalance between the mean transcapillary hydraulic pressure gradient, which favors filtration, and the mean transcapillary oncotic pressure, which opposes filtration. The mediators of renal autoregulation are a myogenic response, which is intrinsic to the blood vessels, and a tubuloglomerular feedback mechanism by which chloride is taken up in the macula densa segment of the distal tubule. In addition, changes in the filtration fraction affect the oncotic pressure in peritubular capillaries and contribute to glomerular tubular balance.

Gong R, Dworkin LD, Brenner BM, Maddox DA. The renal circulations and glomerular ultrafiltration. In: Brenner BM, editor. Brenner & Rector’s the kidney. 8th ed. Vol. 1. Philadelphia (PA): Saunders/Elsevier; c2008. p. 91–129.

I.23. Answer a.

According to the latest KDIGO guidelines, 0.3 mg/dL is the minimum serum creatinine level elevation from baseline that is associated with increased hospital mortality for AKI patients. AKI is an independent predictor of hospital mortality and is a risk factor for future chronic kidney disease. Available biomarkers are limited by their performance characteristics, and the utility of biomarkers needs to be validated for clinical outcomes.

Maciel AT, Vitorio D. Urine biochemistry assessment in critically ill patients: controversies and future perspectives. J Clin Monit Comput. 2017 Jun;31(3):539–46. Epub 2016 Apr 1.

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I.24. Answer b.

In patients receiving continuous tube feeding, the rate and composition of nutrition infusion should remain constant for at least 12 hours before and during indirect calorimetry. If the patient is receiving intermittent feedings, measuring resting metabolic rate should be done 4 hours after the feeding.

Wooley JA, Frankenfield D. Energy. In: Mueller CM, editor. The A.S.P.E.N. adult nutrition support core curriculum. 2nd ed. Silver Spring (MD): American Society for Parenteral and Enteral Nutrition; c2012. p. 22–35.

Wooley JA, Sax HC. Indirect calorimetry: applications to practice. Nutr Clin Pract. 2003 Oct;18(5):434–9.

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I.25. Answer b.

The daily protein requirements for a critically ill patient are 1.2 to 2.0 g/kg based on actual body weight. Protein needs would be increased if the patient were receiving hemodialysis or CRRT. Actual body weight is used for calculations when BMI is less than 30. Ideal body weight is used for calculations when BMI is 30 or more.

McClave SA, Martindale RG, Rice TW, Heyland DK. Feeding the critically ill patient. Crit Care Med. 2014 Dec;42(12):2600–10.

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McClave SA, Martindale RG, Vanek VW, McCarthy M, Roberts P, Taylor B, et al; A.S.P.E.N. Board of Directors; American College of Critical Care Medicine; Society of Critical Care Medicine. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2009 May-Jun;33(3):277–316.

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I.26. Answer c.

Nasoenteric feeding is recommended for patients at high risk for aspiration. Risk factors for aspiration include mechanical ventilation, reduced level of consciousness, inability to protect airway, and age older than 70 years. At this time, a gastrostomy tube is not recommended because the expected duration of need is less than 4 weeks.

McClave SA, Martindale RG, Rice TW, Heyland DK. Feeding the critically ill patient. Crit Care Med. 2014 Dec;42(12):2600–10.

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McClave SA, Martindale RG, Vanek VW, McCarthy M, Roberts P, Taylor B, et al; A.S.P.E.N. Board of Directors; American College of Critical Care Medicine; Society of Critical Care Medicine. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2009 May-Jun;33(3):277–316.

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I.27. Answer d.

A vitamin C deficiency could result in spongy, bleeding gums and scurvy, petechiae, and poor wound healing.

Clark SF. Vitamins and trace elements. In: Mueller CM, editor. The A.S.P.E.N. adult nutrition support core curriculum. 2nd ed. Silver Spring (MD): American Society for Parenteral and Enteral Nutrition; c2012. p. 121–51.

Pogatshnik C, Hamilton C. Nutrition-focused physical examination: skin, nails, hair, eyes, and oral cavity. Support Line. 2011 Apr;33(2):7–13.

I.28. Answer b.

Indications for the appropriate use of parenteral nutrition include intestinal obstruction, distal high-output fistulas, severe gastrointestinal tract bleeding, or severe malabsorption. Parenteral nutrition should be initiated promptly after ICU admission for malnourished or nutritionally high-risk patients with a nonfunctioning gastrointestinal tract. Peripheral parenteral nutrition is hyperosmolar at 600 to 900 mOsm/L and requires larger fluid volume; therefore, it is not desirable for patients requiring fluid restriction.

McClave SA, Martindale RG, Vanek VW, McCarthy M, Roberts P, Taylor B, et al; A.S.P.E.N. Board of Directors; American College of Critical Care Medicine; Society of Critical Care Medicine. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2009 May-Jun;33(3):277–316.

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Mirtallo JM, Patel M. Overview of parenteral nutrition. In: Mueller CM, editor. The A.S.P.E.N. adult nutrition support core curriculum. 2nd ed. Silver Spring (MD): American Society for Parenteral and Enteral Nutrition; c2012. p. 234–44.

Which assessment data confirms the diagnosis of ARDS?

Which early clinical manifestation might indicate the development of ARDS?

Which assessment data indicate to the nurse the client diagnosed with ARDS has experienced a complication secondary to the ventilator *?

Which patient is at greatest risk of developing acute respiratory distress syndrome ARDS )?