Which of the following is not true of mortality in ARDS?
Correct Answer: D
Mortality in ARDS has declined substantially over the last 20 years, likely in large part due to improved supportive care, including the use of lung protective ventilation, and improved approaches to fluid management, transfusions, and sedation. In a study of 179 patients with ARDS, low PaO2 /FIO2 ratio, low static respiratory compliance, oxygenation index, use of vasopressors, and dead space were all associated with increased mortality. Older patients are at an increased risk of death.
A 45-year-old man with morbid obesity (BMI 55) presents to the ED at 6 am with right leg pain, and cellulitis that has kept him awake all night. He is admitted to the ward and his fevers and skin examination are improved with antibiotics during the first 16 hours of hospitalization. At 2 am you are called to evaluate the patient for ICU admission because of somnolence and hypoxemia (SpO2 falling to high 70s on 2LNC). The rapid response team had difficulty waking the patient and ABG was performed before your arrival in the patient’s room: 7.29/74/52. Following arterial puncture, the patient woke up and by your arrival he is able to converse but remains sleepy with eyes closed, denying dyspnea, with SpO2 now 92% on 2LNC, and normal work of breathing. Medication history was reviewed and no opiates have been administered. The ward team is requesting ICU transfer because of acute hypercarbic respiratory failure and initiation of BiPAP. You review recent laboratory test results and note that serum bicarbonate has been 38 to 40 over the last 6 months.
Which of the following statements is true:
OHS is defined as alveolar hypoventilation in the awake state in a patient with BMI of 30 or higher without other cause. It likely results from the effects of obesity on multiple physiologic pathways including sleepdisordered breathing such as OSA, restrictive pulmonary mechanics, and altered ventilatory control. During sleep all patients experience reduced ventilatory responses to hypoxemia and hypercapnia, and this appears to be true to a greater extent in patients with OHS. In this patient, it is important to distinguish chronic versus acute pathology. The higher serum bicarbonate reflects a renal compensation to chronic hypercapnia, which is likely from OHS, especially in the absence of neuromuscular weakness or obstructive lung disease. In a patient with OHS in a deep sleep, an arterial pH of 7.29 with PaCO2 of 74 is likely to be near the patient’s baseline physiology.
OSA is common but not universal among patients with OHS. Acute hypercapnia may cause somnolence in eucapnic patients once PaCO2 rises to greater than 75 mm Hg. However, patients with chronically elevated PaCO2 are typically resistant to CO2 narcosis until PaCO2 rises to 90 to 100 mm Hg. Acetazolamide will cause the kidney to waste bicarbonate and may increase alveolar ventilation. However, in doing so it reduces the buffer against acute increases in PaCO2 and may result in electrolyte abnormalities and other side effects and is not recommended as first line therapy for this disorder. OHS rises in prevalence with BMI and is present in up to 50% of patients with BMI >50. Narcan could be tried in this scenario but is very unlikely to be effective and may precipitate nausea. First line therapy for patients with OHS is CPAP, given that up to 90% of patients with OHS have coexisting OSA, though Bi-PAP may be used in patients who fail CPAP. Many hospitals have policies regarding new initiation of CPAP that would govern the decision on ICU admission. However, a strong argument could be made in this case that if the patient is otherwise ready for discharge the next day, an expedited outpatient sleep study might serve him better than a night in the ICU.
A 24-year-old man with a history of severe asthma with multiple intubations presents to the ED with several days of worsening dyspnea despite the frequent use of albuterol nebs. The same morning, he visited a friend who has a cat and his dyspnea rapidly worsened. CXR shows hyperinflation and the ED physician gives solumedrol, continuous albuterol nebs, and initiates critical care consultation because of persistent accessory muscle use after an hour of care in the ED.
Which of the following statements about severe asthma exacerbations is correct?
Correct Answer: E
Severe hypoxemia is unusual in asthma and suggests the presence of pneumonia or extensive mucous plugging. Reduced PEF generally predicts hypercapnia rather than hypoxemia. PEF below 50% of baseline suggests a severe exacerbation, but notably hypercapnia is rare until PEF falls to less than 25% of baseline. Asthmatic patients in exacerbation have high respiratory drive, and the presence of elevated PaCO2 is a concerning sign that often heralds the imminent need for intubation and mechanical ventilation. Magnesium sulfate is generally recommended for asthma exacerbation when severe airflow limitation persists despite initial therapy with bronchodilators. Heliox has a lower density than air and thus reduces resistance to airflow. However, clinical trials have yielded conflicting results and its use limits the maximum FiO2 to approximately 0.8 and requires the use of correction factors for ventilator gas flow. Survival in patients requiring mechanical ventilation for asthma exacerbations improved markedly following implementation of permissive hypercapnia ventilatory strategies. Dynamic hyperinflation creates intrinsic PEEP (air trapping), which can reduce venous return, place strain on the right ventricle, and may precipitate cardiovascular collapse. Ventilator adjustments that may be helpful include reducing the tidal volume (shorter inspiratory time and less volume to exhale), decreasing the rate, and optimizing triggering. Intrinsic PEEP can be measured during an expiratory pause although neuromuscular blockade may be necessary to obtain reliable measurements. Setting the extrinsic (applied) PEEP to up to 80% of the intrinsic PEEP can reduce the inspiratory effort required to trigger the ventilator without substantially increasing the risk of barotrauma. Notably patients with the most severe exacerbations may require paralysis that would obviate any benefit to improved triggering, and so this strategy is most useful during the ventilator weaning phase.
A 60-year-old man with very severe emphysema who is noncompliant with prescribed home oxygen therapy presents to the ED with a bleeding traumatic laceration on his foot. Triage vitals reveal T 36 C, HR 90, BP 120/50, RR 18, SpO2 71% RA. On further questioning he complains of chronic dyspnea on exertion but does not feel any worse than normal. Laboratory test results are notable for a hematocrit of 60%. Supplemental oxygen with a nonrebreathing mask is administered with O2 sat quickly rising to 100%. Given the high acuity and census in the ED he is placed in the hallway to await physician evaluation and suturing. Thirty minutes later the patient is noted by the nurse to be unarousable, ABG 7.05/130/140 with bicarb 45.
Which of the following statements is true?
Correct Answer: C
This patient suffers from chronic hypercarbic hypoxemic respiratory failure (with secondary polycythemia) as a result of very advanced emphysema. Hypercapnia results from an increase in CO2 production and/or a decrease in alveolar ventilation (which may be due to either decreased minute ventilation or increased dead space fraction). Acutely, increased PaCO2 leads to increased brain blood flow and ICP but decreased level of consciousness. The mechanism of reduced LOC is not well established but probably involves global increases in inhibitory neurotransmitters. Narcan may be tried but can be expected to have minimal effect.
Patients with emphysema have major disruptions in v/q matching and increased dead space. They breathe with a lower tidal volume and higher respiratory rate to compensate, typically reaching a minute ventilation that is higher than normal. They variably develop chronic hypercapnia with compensatory metabolic alkalosis via renal compensation (increased serum bicarbonate). When severe hypoxemia accompanies advanced lung disease, compensatory polycythemia allows some improvement in oxygen delivery.
Most patients with COPD and chronic hypercapnia have at most a mild increase in PaCO2 with oxygen therapy. However, excessive supplemental oxygen administration in a very small subset of patients with advanced chronic hypercarbic hypoxemic respiratory failure can lead to a vicious cycle of increased PaCO2 and somnolence. The mechanisms by which this occurs remain somewhat controversial. The best study on this phenomenon dates to the early 1980s, in which Aubier and colleagues studied 22 patients with advanced COPD with mean age of 65 years, mean PaO2 of 38, and mean PaCO2 of 65. They were studied first on room air and then asked to breathe pure oxygen for 15 minutes. The mean increase in PaCO2 in these patients at the end of the test period was 23 mm Hg, and although minute ventilation declined initially, by the end of the 15-minute period it had risen back to 93% of baseline. Furthermore, there was no correlation between the change in minute ventilation and the increase in PaCO2 across the 22 patients. Subsequent analysis revealed that the majority of the increase in PaCO2 was due to a combination of the Haldane effect (rightward displacement of the CO2 -Hb dissociation curve, causing the considerable red cell mass to liberate CO2 in the presence of an acute increase in oxyhemoglobin) and an increase in dead space fraction, likely due to worsening V/Q mismatch in the setting of impaired hypoxic pulmonary vasoconstriction. Patients at highest risk for this phenomenon are those with advanced lung disease and a very low initial PaO2 who have high levels of supplemental oxygen applied abruptly.
Acetazolamide may increase respiratory drive somewhat but can be dangerous by reducing the buffer against acute increases in PaCO2 . Nocturnal noninvasive ventilation may be considered but is best initiated in a sleep laboratory in patients who are likely to be compliant with close follow-up.
The is intubated, quickly regains his baseline level of alertness, and is extubated 4 hours later. He is alarmed by his need for mechanical ventilation and before discharge he asks you about his life expectancy.
Which of the following measures is the best predictor of survival in COPD?
Correct Answer: B
Postbronchodilator FEV1 (percent predicted) does have some predictive power for survival but is limited by high variability across patients. More recently the BODE index was developed: BMI, Obstruction (FEV1), Dyspnea, and Exercise capacity (6-minute walk distance). Initially described in 2004, the BODE index is superior to FEV1 in predicting survival in patients with COPD.
© 2010-2030 Your Doctor - Dr.Khalil Al-Yousifi - Kuwait - Contact Us