A 40-year-old previously healthy 90-kg man (ideal body weight of 80 kg) walks into the Emergency Department (ED) complaining of 5 days of myalgias, fevers, rhinorrhea, and dry cough. Over the last day, he has become short of breath walking across the room. In the ED, he is febrile, hypotensive requiring vasopressors, with a respiratory rate of 30 and SpO2 88% on a non-rebreather face mask. He receives 30 mL/kg crystalloid and develops worsening work of breathing requiring endotracheal intubation 2 hours after arrival in ED. Endotracheal tube placement is confirmed by end-tidal CO2 and bilateral breath sounds. His SpO2 nadir is 75% but despite 5 minutes of bagging his SpO2 remains in the mid-80s. His chest X-ray is shown below:
Which of the following statements is true?
Correct Answer: D
The ARMA trial randomly assigned 861 patients with ARDS to low tidal volume ventilation (6 mL/kg predicted body weight) or 12 mL/kg PBW. The 6 mL/kg group had a lower risk of 28-day mortality (RR 0.74, CI 0.61-0.88). A subsequent meta-analysis found similar results. Importantly, the ARMA protocol targeted both a tidal volume of 6 mL/kg and plateau pressure <30 cm H2O. Because this patient had a plateau pressure of 35 cm H2O on 6 mL/kg PBW, the protocol would advise further reductions in tidal volume to a minimum of 4 mL/kg PBW.
The fluid and catheter treatment trial randomized 1,000 patients with acute lung injury to management with a central venous catheter or PA catheter, finding no difference in 60-day survival. Furthermore, there was no evident benefit of the PAC in the duration of shock, ventilator-free days, fluid balance, or measures of lung or kidney function. The PAC group had significantly more catheter-related complications, mostly arrhythmias (and some cases of conduction block).
Lungs afflicted with diffuse injury are edematous and have poor compliance. The multicenter ART trial randomized 1,010 patients with moderate to severe ARDS to low tidal volume ventilation using a low-PEEP FIO2 /PEEP grid (as in ARMA) or a recruitment maneuver/decremental PEEP strategy: following neuromuscular blockade and using pressure control ventilation, PEEP raised from 25 to 35 and then 45 cm H2O for 2 minutes, and then dropped to 23 cm H2O and reduced 3 cm H2O at a time down to a minimum of 11 cm H2O with static compliance measured at each step, settling on 2 cm H2O above the PEEP yielding the highest compliance. The recruitment maneuver group suffered a higher 28-day mortality (HR 1.20, CI 1.01-1.42), reduced ventilator-free days, and increased risk of barotrauma including pneumothorax-requiring drainage.
Inhaled nitric oxide has long-been known to improve oxygenation by selectively improving blood flow to aerated regions of lungs, improving ventilation-perfusion matching, which is frequently impaired during critical illness. Indeed, in a meta-analysis of 12 randomized trials, iNO was found to increase the PaO2 /FiO2 ratio. However, this same meta-analysis showed that patients receiving iNO had a trend toward higher mortality (RR 1.10, CI 0.94-1.30) and significantly increased renal dysfunction (RR 1.50, CI 1.11-2.02).
The PROSEVA study randomized 455 patients with severe ARDS and intubated <36 hours to undergo prone-positioning of at least 16 hours daily or be left in the supine position. Prone positioning was associated with a dramatic improvement in 28-day mortality (HR 0.39, CI 0.25-0.63). Notably, prone positioning is occasionally utilized during the management of refractory hypoxemia in patients who have been intubated for many days. The PROSEVA study, by contrast, proned patients early in the course of their illness. The mechanism of benefit is not known with certainty, but speculated to be related to a reduction in ventilator injury owing to more even distribution of strain (because the proned ARDS lung has more uniform mechanical characteristics than the supine ARDS lung.)
A 52-year-old woman with a history of DVT on warfarin and active smoker develops several days of epigastric pain and melena and presents to the ED with a hemoglobin of 5.5 and tachycardia without hypotension, INR of 3.9, and a platelet count of 215,000/ µL. Following transfusion of 2 units PRBCs and 2 units FFP, she develops rapidly progressive acute hypoxemic respiratory failure and increased work of breathing requiring intubation, with CXR new confirming bilateral infiltrates.
Which of the following statements is true of the most likely etiology for her respiratory decompensation?
Correct Answer: C
TRALI is defined as new ARDS occurring within 6 hours of blood product administration, and in the absence of other risk factors for ARDS (such as aspiration, trauma, pneumonia). The incidence of TRALI declined dramatically in the last decade following a reduction in the use of plasma from multiparous female donors (which includes anti-HLA antibodies proportional to the number of pregnancies). Recipient risk factors include alcohol abuse, shock, and smoking. Although TRALI can occur after the transfusion of any blood product, high plasma components such as plasma, apheresis platelets, and whole blood have the highest risk per transfusion. TRALI most often occurs when passively transferred HLA and human neutrophil antigen antibodies activate neutrophils that have been sequestered in the lung microvasculature.
A 53-year-old man with a history of mild asthma and alcoholic cirrhosis complicated by ascites (controlled with diuretics) presents to the ED with shoulder pain after a mechanical fall. Musculoskeletal examination and plain films yield a diagnosis of an acute acromioclavicular joint injury. Vitals obtained in the ED are notable for SpO2 of 91% on RA. He uses albuterol MDI about once a week, denies dyspnea, and has no new pulmonary symptom. His lung examination is notable for subtle prolongation of the expiratory phase without wheezes and chest X-ray is clear.
Which is true of the likely etiology for hypoxemia?
This patient has a history of mild asthma and no active wheezing— hypoxemia is typically seen only in very severe life-threatening asthma attacks or with superimposed respiratory disease such as pneumonia. This patient likely has hepatopulmonary syndrome, defined as arterial hypoxemia in the setting of intrapulmonary vascular dilatations associated with liver disease and portal hypertension. Hepatopulmonary syndrome tends to be progressive, and when very severe can be an indication for liver transplantation. Diagnosis involves confirming arterial hypoxemia with an ABG and venous contrast-enhanced transthoracic echocardiography (“bubble study”), which visualizes contrast in the left side of the heart within 3 to 8 heart beats (more rapidly than normal, but less rapidly than with intracardiac shunting). Spider nevi are predictive of higher A-a oxygen gradients in patients with cirrhosis. Orthodeoxia (a decrease in PaO2 or SpO2 when the patient moves from supine to upright) is common in hepatopulmonary syndrome and is due to the redistribution of blood flow to lung zones with more intrapulmonary vascular dilatations.
A 65-year-old man diagnosed with idiopathic pulmonary fibrosis a year ago not on supplemental oxygen therapy presents to the ED with a week and a half of worsening exercise tolerance, increased dry cough, myalgias, and subjective fevers. Over the last day he has been unable to walk across the room without resting. Physical examination is remarkable for SpO2 of 85% on 6 L NC with tachypnea and increased work of breathing, bibasilar crackles. Laboratory test results reveal WBC 10,000/ µL (slightly increased absolute neutrophil count), normal metabolic panel and liver function tests, troponin of 0.1 ng/mL, and BNP of 120 pg/mL. Rapid flu is negative, and PCR panel is pending. CXR shows worsening bilateral opacities, and results of CT scan are shown in the figure below:
The patient is admitted to the ICU and placed on high flow nasal cannula at 40 LPM flow. Overnight FiO2 has ranged between 0.7 and 0.9 to maintain SpO2 in the low 90s, and he was unable to sleep because of dyspnea. On examination he appears to be tiring.
Correct Answer: A
This patient is experiencing an acute exacerbation of IPF (AE-IPF). In 2016, an International Working Group Report defined AE-IPF as “an acute, clinically significant respiratory deterioration characterized by evidence of new widespread alveolar abnormality” with the following diagnostic criteria:
This report recommended that AE-IPF be subcategorized as “Triggered Acute Exacerbation” and “Idiopathic Acute Exacerbation.” Thus the detection of a respiratory pathogen does not exclude the diagnosis but rather clarifies it as triggered. International guidelines make a weak recommendation against mechanical ventilation to treat acute respiratory failure in IPF because of estimated in-hospital mortality of nearly 90%. Although corticosteroids are commonly given during AE-IPF, no highquality trial data support this practice, which is driven by anecdotal reports of benefit. Risk factors for AE-IPF include higher BMI. In autopsy series of patients with AE-IPF, the most common acute pathologic finding is diffuse alveolar damage.
A 60-year-old thin female smoker presents to the ED with several days of worsening dyspnea, productive cough, and high fevers. She remains hypotensive despite fluid resuscitation and develops worsening hypoxemia/ARDS requiring intubation and mechanical ventilation. A central line is placed in the right internal jugular vein for vasopressor administration, and she is admitted to the ICU and placed on low tidal volume ventilation protocol using the high PEEP/FiO2 grid studied in the ALVEOLI trial. Twenty-four hours later admission blood cultures are positive for Streptococcus pneumonia and her respiratory status has continued to deteriorate, now on 6 mL/kg IBW with FIO2 of 0.8 and PEEP of 20 cm H2O with plateau pressure of 29 cm H2O. ScVO2 is 75% while on moderate dose of norepinephrine and ABG is 7.32/40/65. Using volumetric capnography you measure dead space to be 75%. Several hours later she desaturates, and the FiO2 is raised to 1.0 with PEEP 24 cm H2O. Because making the ventilator change she has worsening hypotension and SpO2 remains in the low 90s. SCVO2 is remeasured at 55% and repeat ABG is 7.24/48/59 with no change in minute ventilation from the prior ABG. In another 10 minutes, SpO2 drops to the low 80s and you are adding a second vasopressor.
Which of the following should you do next?
Correct Answer: E
High levels of PEEP can lead to increased Zone 1 conditions in the lung while simultaneously reducing cardiac output (by reducing venous return into the heart and increasing pulmonary vascular resistance). This can be life threatening if presence of this positive feedback loop is not quickly recognized.
The only option that is absolutely incorrect in this setting is (A). The intensivist should recognize this scenario and that the deteriorating hemodynamics is likely to produce cardiovascular collapse if quick action is not taken. Thus (C) and (D) would be wasting precious time. Nitric oxide may marginally improve V/Q matching and oxygenation but will not help with the hemodynamics, if the primary problem is reduced venous return. The intensivist must maintain a high index of suspicion for presence of this feedback loop and recognize that sometimes decreasing the PEEP will improve systemic oxygenation in addition to improving dead space and cardiac output. Intravascular volume expansion may also improve the above physiology but may not be necessary if hemodynamics rapidly improve with reduced airway pressure. Transient disconnection from ventilator and resuming ventilation at a lower PEEP would be the most appropriate intervention.
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