Pulmonary Disorders II

Streptococcus pneumoniae is the most common bacterial cause of adult community-acquired pneumonia, although its incidence has declined with the use of pneumococcal vaccines in adults and pneumococcal conjugate vaccines in children (Inocencio & Fellin, 2021, p. 420). Choice a is wrong because Pseudomonas aeruginosa is the most common cause of ventilator-acquired pneumonia, not community-acquired pneumonia (Inocencio & Fellin, 2021, p. 422). Choice b is wrong because Staphylococcus aureus is among the most common causes of hospital-acquired pneumonia, which occurs 48 hours or more after admission (Inocencio & Fellin, 2021, p. 422). Choice d is wrong because Mycoplasma pneumoniae is an atypical pathogen rather than the most common bacterial cause of community-acquired pneumonia (Inocencio & Fellin, 2021, p. 420).

Ventilator-acquired pneumonia arises more than 48 to 72 hours after endotracheal intubation, and Pseudomonas is the most common causative organism (Inocencio & Fellin, 2021, p. 422). Choices a and b are wrong because Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae are the most common organisms in hospital-acquired pneumonia generally, but this patient is specifically intubated, which makes Pseudomonas the better answer (Inocencio & Fellin, 2021, p. 422). Choice d is wrong because Mycoplasma pneumoniae is an atypical community-acquired pathogen (Inocencio & Fellin, 2021, p. 420).

The findings with the highest specificity for pneumonia include asymmetric breath sounds, pleural rubs, egophony, and increased tactile fremitus (Inocencio & Fellin, 2021, p. 423). Choices a, b, and c are wrong because fever with chills, pleuritic chest pain, productive cough, dyspnea, and tachypnea are the findings with the highest sensitivity for pneumonia, but they are less specific (Inocencio & Fellin, 2021, p. 423).

Right-heart catheterization is the gold standard for the diagnosis of PH; it measures the pulmonary artery pressure (greater than 25 mm Hg) and the left atrial pressure (less than 18 mm Hg indicates World Health Organization [WHO] group 1) (Lakin, Hoy, & Fellin, 2021, p. 443). Choice a is wrong because echocardiography with a bubble study is a cardiac assessment used to evaluate PH, but it does not confirm the diagnosis (Lakin, Hoy, & Fellin, 2021, p. 443). Choice c is wrong because chest X-ray may show increased size of the proximal pulmonary arteries but is not diagnostic (Lakin, Hoy, & Fellin, 2021, p. 443). Choice d is wrong because BNP is used to assess strain on the heart and monitor therapy, not to confirm PH (Lakin, Hoy, & Fellin, 2021, p. 443).

Physical findings of PH include splitting of the second heart sound with an increased pulmonic component (P2), peripheral edema related to right ventricular failure, ascites, a right ventricular heave, a holosystolic murmur, and elevated jugular venous pressure (Lakin, Hoy, & Fellin, 2021, p. 442). Choice b is wrong because fixed splitting of S2 is associated with an atrial septal defect, not PH (Lakin, Hoy, & Fellin, 2021, p. 442). Choice c is wrong because a low-pitched diastolic rumble at the apex suggests mitral stenosis, which is a cause of PH rather than a finding of PH itself (Lakin, Hoy, & Fellin, 2021, p. 442). Choice d is wrong because an S3 gallop reflects left ventricular volume overload, such as heart failure, rather than right ventricular strain (Lakin, Hoy, & Fellin, 2021, p. 442).

A trial of calcium channel blockers is recommended only for patients with a positive response to vasoreactivity testing, and calcium channel blocker therapy can lose effectiveness over time (Lakin, Hoy, & Fellin, 2021, p. 445). Choice a is wrong because advanced functional class alone does not justify a calcium channel blocker (Lakin, Hoy, & Fellin, 2021, p. 445). Choice c is wrong because endothelin receptor antagonists are a separate drug class and are not a prerequisite for calcium channel blocker therapy (Lakin, Hoy, & Fellin, 2021, p. 445). Choice d is wrong because an elevated pulmonary artery pressure confirms PH but does not by itself predict a response to calcium channel blockers (Lakin, Hoy, & Fellin, 2021, pp. 443, 445).

These findings indicate a tension pneumothorax, which is a medical emergency. The first action is immediate decompression with a 14- to 16-gauge needle into the second intercostal space, midclavicular line of the affected side, followed by insertion of a chest tube at the fourth or fifth intercostal space, midaxillary line (Akintade, 2021, p. 473). Choice a is wrong because obtaining a chest X-ray delays life-saving treatment of a tension pneumothorax (Akintade, 2021, p. 473). Choice c is wrong because chest tube insertion follows needle decompression rather than replacing it as the first step (Akintade, 2021, p. 473). Choice d is wrong because intubation is not the initial intervention for tension pneumothorax and does not relieve the pleural pressure (Akintade, 2021, p. 473).

A pneumothorax produces decreased breath sounds and fremitus along with a hyperresonant percussion note over the affected area (Akintade, 2021, p. 472). Choice b is wrong because dullness with increased fremitus suggests consolidation or effusion, not air in the pleural space (Akintade, 2021, p. 472). Choice c is wrong because bronchial breath sounds and egophony suggest pneumonia with consolidation (Akintade, 2021, p. 472). Choice d is wrong because a pleural friction rub suggests pleuritis rather than pneumothorax (Akintade, 2021, p. 472).

In a tension pneumothorax, air enters the pleural space but is unable to exit. As pressure rises, the lung collapses, the mediastinum shifts to the opposite side, and venous return to the right heart is impaired, resulting in decreased cardiac output and hypotension (Akintade, 2021, p. 471). Choice a is wrong because free movement of air in and out describes an open pneumothorax, which lowers the likelihood of mediastinal tension and shift (Akintade, 2021, p. 471). Choice c is wrong because blood in the pleural space is a hemothorax, not a pneumothorax (Akintade, 2021, p. 471). Choice d is wrong because the hypotension of tension pneumothorax is mechanical, from impaired venous return, not from inflammatory vasodilation (Akintade, 2021, p. 471).

A hemothorax is blood in the pleural space (Coates, 2021, p. 460). Choice a is wrong because air in the pleural space is a pneumothorax (Coates, 2021, p. 460). Choice c is wrong because pus in the pleural space is an empyema (Coates, 2021, p. 460). Choice d is wrong because chyle in the pleural space is a chylothorax, caused by injury of the thoracic ducts (Coates, 2021, p. 460).

If pleural fluid is bloody, insertion of a chest tube is often required (Coates, 2021, p. 462). Choice a is wrong because observation with serial chest X-rays is used for an asymptomatic small effusion, not a bloody effusion (Coates, 2021, pp. 460, 462). Choice b is wrong because diuresis is used for an effusion likely due to congestive heart failure, not for a traumatic hemothorax (Coates, 2021, p. 461). Choice d is wrong because pleurodesis with a sclerosing agent is used to prevent recurrence of malignant effusions, not for a hemothorax (Coates, 2021, p. 462).

A hemothorax is blood in the pleural space and typically results from chest trauma; the associated blood loss can produce hypotension (Coates, 2021, pp. 460, 462). Choice b is wrong because bilateral effusions with jugular venous distention and an S3 suggest congestive heart failure with transudative effusions (Coates, 2021, p. 460). Choice c is wrong because cirrhosis and hypoalbuminemia cause transudative effusions through increased hydrostatic or decreased oncotic pressure (Coates, 2021, p. 460). Choice d is wrong because dyspnea, pleuritic chest pain, and fever suggest an infected or parapneumonic effusion, not a hemothorax (Coates, 2021, p. 460).

According to Light's criteria, an exudative pleural effusion has one or more of the following: a ratio of pleural fluid protein to serum protein greater than 0.5, a ratio of pleural fluid LDH to serum LDH greater than 0.6, or a pleural fluid LDH more than two-thirds the upper limit of normal serum LDH (Coates, 2021, p. 461). This fluid meets all three criteria, so it is exudative. Choice a is wrong because a transudate would not meet Light's criteria, and a transudative effusion typically has a serum glucose equal to the pleural fluid glucose and a pH between 7.40 and 7.55 (Coates, 2021, p. 461). Choice c is wrong because an empyema is infection with pus in the pleural space, not merely an exudate (Coates, 2021, p. 460). Choice d is wrong because a chylothorax is accumulation of chyle from injury of the thoracic ducts (Coates, 2021, p. 460).

If the risk of infection is small and the effusion is likely due to congestive heart failure, the response may be assessed by initiating diuresis and following the effusion with serial chest X-rays to assess for resolution (Coates, 2021, p. 461). Choice a is wrong because chest tube insertion is reserved for empyema or bloody fluid, not an uncomplicated heart failure effusion (Coates, 2021, p. 462). Choice b is wrong because pleurodesis is used to prevent recurrence of malignant effusions (Coates, 2021, p. 462). Choice d is wrong because repeated thoracentesis is used for reaccumulating malignant effusions that need infrequent drainage, not for a heart failure effusion (Coates, 2021, p. 462).

On a lateral decubitus chest X-ray, amounts as small as 5 ml may blunt the costophrenic angle (Coates, 2021, p. 460). Choice a is wrong because the lateral chest X-ray requires at least 75 ml of pleural fluid, and the posteroanterior chest X-ray requires at least 200 ml (Coates, 2021, p. 460). Choice b is wrong for the same reason: the lateral view requires at least 75 ml, not 200 ml (Coates, 2021, p. 460). Choice d is wrong because the meniscus pattern describes pleural fluid climbing along the ribs, not air (Coates, 2021, p. 460).

Dyspnea, insidious or sudden in onset, is the most common symptom of pulmonary embolism (Lakin, Hoy, & Fellin, 2021, p. 447). Choice a is wrong because hemoptysis occurs with pulmonary infarction, not with every embolus (Lakin, Hoy, & Fellin, 2021, p. 447). Choice b is wrong because syncope may occur but is not the most common symptom (Lakin, Hoy, & Fellin, 2021, p. 447). Choice d is wrong because pleuritic pain occurs with pulmonary embolism with infarction, not with every embolus (Lakin, Hoy, & Fellin, 2021, p. 447).

Venous stasis is a component of Virchow's triad; deep venous thrombosis in the lower extremities and pelvis leads to 70% of pulmonary emboli, and prolonged immobility or surgery involving general anesthesia longer than 30 minutes contributes to venous stasis (Lakin, Hoy, & Fellin, 2021, p. 447). Choice a is wrong because vessel wall injury (such as surgery or a fractured hip or pelvis) is a separate Virchow component and is not the primary factor described here (Lakin, Hoy, & Fellin, 2021, p. 447). Choice c is wrong because hypercoagulability relates to factors such as estrogen supplies or malignancy, neither of which is described (Lakin, Hoy, & Fellin, 2021, p. 447). Choice d is wrong because genetic predisposition is a less immediate explanation than the venous stasis of recent surgery and immobility (Lakin, Hoy, & Fellin, 2021, p. 447).

Fibrinolytic treatment (for example, alteplase 100 mg IV infused over 2 hours) may be appropriate for massive proximal pulmonary embolism associated with persistent systemic hypotension and signs of right heart strain (Lakin, Hoy, & Fellin, 2021, p. 450). Choice a is wrong because surgical embolectomy is reserved for patients with massive emboli in the central pulmonary arteries causing hypotension and shock, and it is not required as the sole first therapy here (Lakin, Hoy, & Fellin, 2021, p. 451). Choice b is wrong because an inferior vena cava filter prevents further emboli and is indicated when the risk of further emboli is high or anticoagulation is contraindicated, not as the primary treatment (Lakin, Hoy, & Fellin, 2021, p. 451). Choice d is wrong because observation with oxygen alone is inadequate for a massive embolus with hypotension (Lakin, Hoy, & Fellin, 2021, p. 450).

The chest X-ray in cardiogenic pulmonary edema shows vascular redistribution to the upper lung fields, interstitial edema, Kerley B lines, pleural effusions (usually bilateral or on the right), and cardiomegaly (Inocencio & Fellin, 2021, p. 436). Choice b is wrong because a wedge-shaped peripheral infiltrate suggests pulmonary infarction from an embolus, not edema (Inocencio & Fellin, 2021, p. 436). Choice c is wrong because a cavity in the upper lobe suggests tuberculosis or abscess, not pulmonary edema (Inocencio & Fellin, 2021, p. 436). Choice d is wrong because a visceral pleural line with increased translucency indicates a pneumothorax (Inocencio & Fellin, 2021, p. 436).

In an acute episode of heart failure, noninvasive positive pressure ventilation via continuous positive airway pressure (CPAP) should be attempted before intubation. It redistributes edema out of the lungs and back into the vascular space and offloads the work of breathing (Inocencio & Fellin, 2021, p. 438). Choice a is wrong because bilevel positive airway pressure is chosen when carbon dioxide retention is present, which is not the primary problem described here (Inocencio & Fellin, 2021, p. 438). Choice c is wrong because high-flow nasal oxygen provides oxygen but does not offload the work of breathing the way CPAP does (Inocencio & Fellin, 2021, p. 438). Choice d is wrong because incentive spirometry is used to prevent atelectasis, not to manage acute cardiogenic pulmonary edema (Inocencio & Fellin, 2021, p. 438).

NYHA class II is described as slight limitation with moderate exertion, with the patient comfortable at rest (Inocencio & Fellin, 2021, p. 436). Choice a is wrong because class I means no limitation from ordinary activities (Inocencio & Fellin, 2021, p. 436). Choice c is wrong because class III means marked limitation with activity and comfort only at rest (Inocencio & Fellin, 2021, p. 436). Choice d is wrong because class IV means symptoms with any activity and occasionally at rest (Inocencio & Fellin, 2021, p. 436).

Four-drug therapy for suspected or active tuberculosis includes isoniazid, rifampin, ethambutol, and pyrazinamide (Inocencio & Fellin, 2021, p. 426). Choice b is wrong because streptomycin and ciprofloxacin are not part of the standard first-line four-drug regimen (Inocencio & Fellin, 2021, p. 426). Choice c is wrong because vancomycin is not a first-line antituberculosis drug (Inocencio & Fellin, 2021, p. 426). Choice d is wrong because azithromycin is not part of the standard first-line four-drug regimen (Inocencio & Fellin, 2021, p. 426).

A PPD of 10 mm or greater is positive in health care workers, HIV-negative injection drug users, residents of nursing homes and homeless shelters, and recent immigrants (Inocencio & Fellin, 2021, p. 425). Choice a is wrong because 5 mm or greater is positive in an HIV-infected patient, a recent contact, an immunocompromised patient, or a patient with a chest film typical of tuberculosis (Inocencio & Fellin, 2021, p. 425). Choice c is wrong because 15 mm or greater is positive in any person (Inocencio & Fellin, 2021, p. 425). Choice d is wrong because the test is read by measuring the largest diameter of the indurated area, not the erythematous area (Inocencio & Fellin, 2021, p. 425).

The standard regimen for latent tuberculosis consists of isoniazid 300 mg orally daily for a duration of 9 months, which is also the preferred duration for HIV-positive patients and pregnant women (Inocencio & Fellin, 2021, p. 427). Choice b is wrong because 9 months, not 6 weeks, is the standard duration (Inocencio & Fellin, 2021, p. 427). Choice c is wrong because pyridoxine 25 to 50 mg orally daily may be given during isoniazid therapy to prevent neuropathy (Inocencio & Fellin, 2021, p. 427). Choice d is wrong because isoniazid is effective as single-agent prophylaxis for latent tuberculosis (Inocencio & Fellin, 2021, p. 427). ---