A 79-year-old male with a history of hypertension, dyslipidemia, and type-2 diabetes mellitus presents to the emergency department complaining of increasing shortness of breath, over the past 4 hours. Arterial blood gas (ABG) analysis at room air shows:
Upon admission, the patient is administered oxygen via a face mask with oxygen reservoir at 15 L/min. The SpO2 raises from 87% to 99%. Thirty minutes later, the patient is still dyspneic (respiratory rate: 32 breaths/min). Noninvasive blood pressure is 180/85 mm Hg, heart rate is 100 bpm. ABG now shows:
Chest auscultation reveals mild bilateral crackles at the bases of the lungs and mild wheezing.
What is the MOST likely diagnosis?
Correct Answer: B
Cardiogenic pulmonary edema triggers dyspnea through various mechanisms. In this scenario, acidosis and hypercapnia are absent. Here, the correction of hypoxia does not reduce the respiratory drive. No major alteration in respiratory mechanics is seen, except the increased respiratory rate. These observations indicate interstitial congestion as a potential trigger for the respiratory failure. The patient’s past medical history of various cardiovascular risk factors pointing to congestive heart failure as a potential etiology. Nonetheless, no options can be safely excluded without the execution of primary diagnostic tests (ECG and chest x-ray). Bilateral wheezing is a sign of bronchial constriction. It may be caused by the irritation due to an underlying infectious disease (pneumonia), particularly in a context of chronic self-triggering inflammation, like that associated with a chronic obstructive pulmonary disease (COPD). Bronchospasm may be associated to pulmonary vascular congestion as well. The absence of a raised white blood cell count makes pneumonia and COPD exacerbation unlikely. The absence of signs of impaired respiratory mechanics such as the use of abdominal wall muscles to counteract outflow obstruction does not support this hypothesis either. Pulmonary embolism fits with the described scenario in which minute ventilation cannot be reduced without sedating the patient. Wheezing, however, is uncommon and a depressed PO2 /FiO2 of less than 210 mm Hg in the setting of pulmonary embolism indicates a significant shunt and is usually accompanied by right heart failure and some degree of hemodynamic instability.
A 70-year-old male patient with a history of pulmonary hypertension and smoking has been admitted to the neurocritical care unit because of a Hunt and Hess Grade 4 subarachnoid hemorrhage (SAH) caused by a ruptured aneurysm of the anterior communicating artery (ACA). Successful endovascular clot retrieval was performed on day 1. On day 4, his hypoxemia worsened, reaching a ratio of PaO2 to inspired oxygen (FiO2 ) of less than 200 mm Hg at a FiO2 of 0.6. The chest x-ray shows bilateral diffuse infiltrates suggestive of pulmonary edema.
Which among the following is the best test to identify the cause of pulmonary edema?
Correct Answer: A
Neurogenic pulmonary edema typically occurs within 72 hours after the onset of neurologic injury, but can occur later as well. It results in a combination of cardiogenic and noncardiogenic pulmonary edema and occurs as a result of a large sympathetic stimulus causing hydrostatic as well as permeability pulmonary edema. In this patient, identifying the degree of contribution to lung edema from hydrostatic versus permeability will help guide therapy. Transpulmonary thermodilution technique allows the calculation cardiac index, extravascular lung water index (ELWI), and pulmonary vascular permeability index, which will help differentiate between purely hydrostatic (cardiogenic) pulmonary edema from that occurring due to increased capillary pulmonary permeability.
Although, CT scan might give information on type of lung pathology, it would not differentiate between cardiogenic and noncardiogenic pulmonary edema. Similarly, lung ultrasound will not differentiate between types of pulmonary edema but is most effective in monitoring effect of treatment on pulmonary interstitial fluid. Measuring circulating levels of catecholamines is reasonable as well, but it only allows to identify a specific subset of patients who may benefit of alfa-adrenergic blockade.
A 20-year-old male patient with no medical history is admitted in the operating room for emergent decompressive craniotomy after a motorbike accident causing a posterior cranial fossa epidural hematoma (diagnosed on CT scan). The neurosurgeon accesses the posterior fossa and relieves an opening pressure of 40 cm H2O. Very quickly, the patient develops severe hypotension with a blood pressure of 50/30 mm Hg, for which high-dose norepinephrine is started. He also develops hypoxemia with an alveolar-arterial gradient of more than 100 mm Hg. In addition, the end-tidal CO2 concentration drops by 10 mm Hg. With a high-dose noradrenaline infusion, the BP returns to normal, but hypoxia remains.
Which among the following is most likely to be present in this patient?
The fulminant form of neurogenic pulmonary edema (NPE) develops between 30 and 60 minutes following neurologic injury and has been characterized by hypoxemia with an alveolar-arterial gradient of more than 100 mm Hg, a chest x-ray showing extensive pulmonary edema, the presence of a preserved cardiac output, and the absence of ischemic sign on the electrocardiogram. Typically, these patients have pink frothy fluid on tracheal aspiration or sputum if endotracheal intubation has not been performed yet. Cardiogenic pulmonary edema (CPE) is the main differential diagnosis and may be present at the same time as NPE. In this scenario, though, hypotension occurs specifically at posterior fossa decompression, which can be explained by waning of the Cushing reflex causing a drop in adrenal release of catecholamines. A persisting low end-tidal CO2 concentration would indicate air embolism which typically occurs as a result of air entering a cerebral vein, especially when the patient is in a sitting position. In this case, the pressure of the posterior cranic fossa is positive making this unlikely.
A 31-year-old primiparous female gave birth 10 hours ago after preterm labor. The delivery was vaginal and proceeded without complications under epidural analgesia. The baby is a 25-week gestational age female and weighs 1780 g. Terbutaline administration failed in delaying the delivery. The mother has a history of anaphylaxis triggered by NSAIDs, past history of deep venous thrombosis, hypertension, and hypothyroidism. She has had a dry cough with mild fever and malaise for the past 10 days treated with amoxicillin. The patient now develops acute onset dyspnea and cannot speak in full sentences. She denies pain. Vitals are:
Bilateral rales and wheezing at the left base is heard on auscultation, cardiac sounds are normal, no jugular distension is observed, the skin is warm and well perfused. Blood gas analysis:
What is the MOST likely cause of the patient’s respiratory failure?
Correct Answer: C
Although infrequent, tocolytic pulmonary edema is triggered by drugs such as beta-agonists and calcium antagonists, with symptoms occurring within 12 hours after delivery. It is a purely hydrostatic edema occurring in the presence of normal cardiac function and results in a marked increase in the arterial-alveolar gradient and a hypoxic-nonhypercapnic respiratory failure. Pulmonary embolism (PE) is an important differential, especially with high alveolar-arterial gradient and history of deep venous thrombosis. However, PE with this degree of shunt would typically be accompanied by some degree of right heart failure. This patient does not have clinical signs of right cardiac failure (no gallop, jugular distension, or hypotension). The acuity of presentation makes pneumonia a less likely diagnosis. Peripartum cardiomyopathy and heart failure is another important differential. Although the respiratory signs and symptoms are compatible with cardiac failure, stable hemodynamics and adequate peripheral perfusion poorly fit with that clinical scenario.
A 5-year-old female patient has fallen from the balcony of her apartment located on a third floor. Impact on various branches of a tree before hitting the soil has dampened the velocity of the impact. Trauma burden includes two broken ribs on the right hemithorax, lung contusion, and a suspicion of spinal cord injury at the level of T1. She has to be sedated for a magnetic resonance imaging session.
Which strategy could BETTER diminish the incidence of postprocedure atelectasis?
Correct Answer: D
Breathing an unnecessarily high FiO2 leads to alveolar collapse (hyperoxic atelectasis) and, in addition, increases alveolar permeability, decreases surfactant production, and induces inflammatory mediators (thereby ventilation-induced lung injury). There is not an easy predictable PEEP value that protects all patients from atelectasis, although any value has been shown to be more protective than a PEEP of 0 cm H2O. It has been shown that patients who are sedated and spontaneously breathing without invasive ventilation or PEEP have a lower risk for atelectasis when compared to those who were sedated and mechanically ventilated. Available physiological evidence suggests that breathing a lower FiO2 was protective against atelectasis.
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