Pulmonary and Critical Care Medicine In-Training Objectives

1. Diagnose abdominal compartment syndrome.

a. Intra-abdominal hypertension (IAH): intra-abdominal pressure (IAP) >12 mm Hg,
associated with at least one organ dysfunction.
b. Abdominal compartment syndrome = organ dysfunction+ sustained IAP >20
c. Diagnosis: measuring bladder pressures to confirm the high IAP
d. Caused by:
i. Reduced abdominal wall compliance (Abd sx, trauma, prone, rf, obesity)
ii. Increased intraluminal content (gastroparesis, ileus, bowel obstruction)
iii. increased intra-abdominal contents (hemoperitoneum, ascites),
iv. increased retroperitoneal contents (pancreatitis, retroperitoneal bleed)
v. capillary leak (massive fluid resuscitation, coagulopathy, sepsis, burns).
e. Oliguric AKI develops from renal vein and artery compression
f. Tx: Supportive Care, correction of positive fluid balance, and decompression

2. Diagnose asbestos-related pleural plaques.

• Asbestos is associated with multiple forms of pleural disease.
• Pleural plaques and diffuse pleural thickening are benign consequences asbestos
exposure.
• Characterized by:
o Smooth, white, raised, irregular lesions affecting predominantly the parietal
and, very rarely, the visceral pleura.
• Pleural plaques are asymptomatic in the absence of
parenchymal disease and are typically incidentally
identified on routine CXR.
• For the majority of patients, a confident clinical diagnosis of
asbestosis can be made on the basis of the exposure history
and the HRCT findings
3. Diagnose cystic fibrosis in an adult.
• Results from mutations in the CFTR gene
• Clinical features include respiratory symptoms and chronic airway infection with typical
cystic fibrosis pathogens: Pseudomonas aeruginosa and Staph aureus.
• Associated Conditions suggestive of CF : Recurrent pancreatitis, Chronic sinusitis
Male infertility (congenital bilateral absence of the vas deferens), Severe nasal
polyposis, Nontuberculous mycobacterial infection, Allergic bronchopulmonary
aspergillosis, Bronchiectasis.
• Lung disease is generally less severe in adults than in children
• Diagnosis is through:
o Elevated sweat chloride ≥60 mmol/L
o A family history of CF can be quite helpful in this regard. Sweat chloride testing
is the initial test for CF, although it is less sensitive in adults.
o Abnormal results on repeat testing are diagnostic of CF.
o DNA testing confirms the diagnosis and helps with prognosis. A negative sweat
chloride test in an adult patient does not rule out disease, repeat it.

4. Diagnose exercise-induced asthma.

- Exercise-induced bronchoconstriction describes the acute onset of bronchoconstriction

occurring during or immediately after exercise
- diagnosis of exercise-induced bronchoconstriction (EIB) is based on the combination of
compatible clinical symptoms (eg, exercise-related symptoms of dyspnea, cough, or
wheeze) and demonstration of reversible airflow limitation in response to exercise or a
surrogate challenge.
o Spirometry
▪ reduced FEV1/FVC ratio and its reversibility (with a 12% or greater
improvement in FEV1 after use of a bronchodilator)
o An exercise challenge test is the most direct and preferred way to establish a
diagnosis of EIB. Could use methacholine challange test
o Initial pharmacologic therapy for exercise-induced bronchospasm should consist
of administration of a short-acting β2-agonist 15 minutes before exercise.
5. Diagnose hypersensitivity pneumonitis.
• Repetitive inhalation of antigens in a sensitized patient can result in hypersensitivity
pneumonitis (HP), an immunologic response that results in noncaseating granulomas
and peribronchial mononuclear cell infiltration with giant cells.
• Results from an immunologic response to repetitive inhalation of antigens
 o Most common: thermophilic actinomycin, fungi, bird droppings, tree trimmings,
etc
• There are three forms of HP: acute, subacute and chronic
• Acute form of HP presents within 48 hours of a high-level
exposure to an inciting antigen and will often be associated with
fevers, flulike symptoms, cough, and SOB
• Chest imaging demonstrates bilateral hazy opacities, and HRCT
imaging reveals ground-glass opacities with centrilobular
nodules in a predominantly upper- and mid-lung distribution.
• Symptoms typically wane within 24 to 48 hours after removal
from the exposure.
• Subacute and chronic forms of HP likely occur after more
prolonged lower-level antigen exposure
• Steroids for patients with more severe symptoms, treatment is removal of exposure
to the offending antigen is essential.

6. Diagnose idiopathic pulmonary fibrosis.

• Classic Hx of 50-70 y/o who have a greater than 6-month duration of a dry cough and
dyspnea on exertion. PFTs show Normal FEV/FVC>70, DLCO <50%, TLC <80%
• Rare in those younger than 50 years of age
• Physical examination
o dry inspiratory crackles at the bases
o Nearly 50% of patients will have clubbing
• Pulmonary function testing show a restrictive abnormality with a reduced diffusing
capacity; however, an isolated reduction in diffusing capacity and normal pulmonary
function can also be seen.
• Chest CT: reticular opacities and honeycombing with a peripheral or basilar
predominance and minimal ground-glass opacification.
• Must r/out other causes of fibrotic lung disease
• The diagnosis of IPF/UIP can be made on the basis of a characteristic presentation (eg,
insidious onset of dyspnea) in combination with definite features of UIP on HRCT
o Diagnosis with lung biopsy — When performed, surgical lung biopsy results need
to be correlated with the HRCT findings
• Treatment:
o Optimun management of comorbidities as obesity, heart failure, deconditioning.
o Nintedanib: tyrosine kinase (-) moderates production of fibrogenic growth
factors,
o Pirfenidone: modulates production of fibrosis.
▪ Both agents slow the decline in PFTs but do not affect quality of life or
curative
 o Lung transplantation is a life-prolonging therapy

7. Diagnose pulmonary hypertension.

• Clinical Hx is a patient with PMHx of COPD/CHF who complains of Dyspnea on
exertion, fatigue, SOB at rest, Hypoxemia Sa02 88%.
• Defined as a resting mean pulmonary artery pressure of 25 mm Hg or greater
measured during right heart catheterization.
• Physical exam: prominent S2, and audible split eventually widens. A prominent
jugular venous a wave and a parasternal heave reflect RVH. As RV dilates,
holosystolic TR murmur may be detected. RV failure: JVD, hepatomegaly, ascites,
and peripheral edema, clear lungs.
• Chest X ray: Enlarged central pulmonary arteries with peripheral pruning, along with
prominent RV on lateral view.
• First Line: Echocardiography is a useful initial tool
i. Elevated right ventricular systolic pressure
• Definitive Diagnosis right heart catheterization
i. resting mean pulmonary artery pressure of 25 mm Hg or greater.

8. Diagnose respiratory failure in the setting of restrictive lung disease.

• No obvious clinical precipitant such as fluid overload, infection, left heart failure, or
pulmonary embolism
• Patients typically demonstrate impaired gas exchange, as evidenced by an arterial
oxygen tension to fraction of inspired oxygen ratio (PaO2/FiO2) of less than 225 mmHg
or a decrease in the PaO2 of 10 mmHg or more from baseline
• On HRCT reveals bilateral ground glass or consolidative opacities superimposed on a
background of typical HRCT features of IPF
• Restrictive Lung Diseases
o TLC < 80%
o Decrease DLCO Parenchymal Lung Disease, Heart Failure
▪ The predominant gas exchange abnormality in most patients with
underlying fibrotic lung disease and acute respiratory failure is
hypoxemia rather than hypercapnia.

o Normal DLCO: Pleural Disease, Chest Wall Disorder, Neuromuscular Dz

▪ Patients with kyphoscoliosis may develop slowly progressive ventilatory
failure and hypercapnia with secondary pulmonary hypertension
9. Diagnose right main-stem bronchus intubation.
• Manifestations include respiratory distress, tachypnea, hypoxemia, elevated peak
pressures, and unilateral breath sounds (Absent Breath Sound on Left lung)
• This leads to atelectasis of entire left lung and hyperinflation right lung
• If the tube is inserted deep into the right main bronchus, the right upper lobe bronchus
can be obstructed. This results in collapse of the left lung and the right upper lobe
• When suspected, a chest radiograph should be performed and once confirmed the ETT
can be moved caudally.
• Ultrasound
o Intubation of the right mainstem bronchus will result in the following findings
▪ suprasternal notch: may demonstrate dilation of tracheal mucosal-air
interface with posterior reverberation artifacts as the ETT cuff is inflated.
Absence of the "double trachea sign"
▪ right anterior lung field: presence of lung sliding
▪ left anterior lung field: absence of lung sliding with a lung pulse present
o Withdrawal of the endotracheal tube until lung sliding is reestablished bilaterally
ensures correct placement prior to the confirmatory radiograph

10. Manage an acute asthma exacerbation.

• Asthma exacerbation refers to an acute worsening in symptoms or lung function from
baseline that necessitates a step-up in therapy.
• Management:
o Monitoring of dyspnea, work of breathing, and vital signs
o Supplemental oxygen to maintain oxygen saturation above 93%.
o Frequent inhaled short-acting β2-agonist (SABA) administration (Albu/Leval -
buterol)
o Short-acting inhaled anticholinergics (Ipratropium) are less effective at relieving
acute bronchospasm, but useful as adjunctive therapy to SABA in the
management of acute exacerbations to reduce hospital admission rates.
o Prompt glucocorticoid therapy
o Magnesium sulfate may be used in addition to standard therapies to promote
further bronchodilation in severe asthma exacerbation.
o In asthmatic patients with acute respiratory failure, intubation is recommended
over NIPPV.
• For long term use following:
o Step 1 SABA PRN
o Step 2 Low Dose Inhaled Glucocorticoid
o Step 3: Low Dose Inhaled Glucocorticoid + LABA
o Step 4: High Dose Inhaled Glucocorticoid + LABA
• ALL PATIENTS AFTER ADMITTED DUE TO ASTHMA EXACERBATION SHOULD be

DISCHARGED WITH AN INHALED GLUCOCORTICOID AND SABA.

11. Manage Candida albicans in the sputum.

• Candida detected in the sputum of healthy
individuals usually reflect contamination
from the oral cavity during expectoration.
o NO antifungal therapy indicated.
• Candida Pneumonia occurs rarely and
generally only in severely
immunosuppressed patients.
o Treatment is not recommended
for Candida isolated from sputum or BAL specimens. Patients with disseminated
candidiasis who develop secondary Candida pneumonia should be treated for
disseminated disease.
▪ Most common antifungal agents used for disseminated disease are the
echinocandins (caspofungin, micafungin, anidulafungin) and fluconazole.

12. Manage delirium in the intensive care unit.

• Treatment involves identification and correction of the underlying cause, maintaining
adequate nutrition and hydration, and preventing complications.
• Measures to decrease the risk of delirium:
o providing patients with assistive visual and hearing devices, adequately
controlling pain, limiting psychoactive medications, frequent orientation,
encouraging mobility, and enabling uninterrupted sleep on a normal sleep-wake
cycle may help decrease the likelihood of developing delirium.
• Patients should be monitored regularly and assessed using scales such as the Confusion
Assessment Method-ICU (CAM-ICU)
• No medications are FDA approved for the treatment of delirium.
• Use of sedating medications, such as benzodiazepines and haloperidol, should be
avoided because they may cause or worsen delirium. Current evidence does not
support routine use of haloperidol or second-generation antipsychotic agents to treat
delirium in adult inpatients.
• Some evidence suggests that the melatonin receptor agonist ramelteon may be useful.
• Benzodiazepines can worsen delirium and are not recommended.
o Unless needed in patients with alcohol withdrawal or seizures.
13. Manage fluids in acute respiratory distress syndrome.
• Keep Lungs as dry as possible
• Conservative fluid management: CVP maintained <6mm/hg
o Limiting intravenous fluids and using diuretics to keep central venous pressures
at lower targets has been associated with a more rapid improvement in lung
function, shorter duration of mechanical ventilation, and shorter ICU length of
stay, but no effect on mortality.

14. Manage intrinsic positive end-expiratory pressure (auto-PEEP).

• Manifests as wheezing, marked expiratory prolongation, BP drop and patient restlessness

seen in ventilator if ventilator shows expiratory flow until the start of inspiratory flow
• Recognize auto-PEEP (manually) by performing an expiratory pause or “hold maneuver”:
Expiratory circuit occlusion for 3-5 seconds allow alveolar pressure to equilibrate with
airway pressure.
• Common causes of auto-PEEP (intrinsic PEEP) include COPD, asthma, ARDS, high minute
ventilation.
• Disconnect the ventilation circuit from the endotracheal tube and allow for a prolonged
exhalation to release auto-PEEP.
• Bronchodilators in the case of COPD/asthma (can also consider shortening inspiratory
time and prolonging expiratory time)
• Adjust ventilator settings for a more effective exhalation to avoid air trapping: lower RR,
decrease Vt, increase inspiratory flow, decrease I:E
• Treat reversible factors (bronchospasm, secretions, expiratory devices)

15. Prevent ventilator-associated pneumonia.

- Consider NIPPV when feasible
- Minimize sedation dosing
- Daily sedation holiday
- Elevate head of bed 30-45 degrees
- Daily oral care with chlorhexidine
- VAP bundles decrease VAP rates by 71%
▪ subglottic suctioning,
▪ GI and DVT prophylaxis,
▪ avoiding gastric overdistension
▪ Supine position
▪ Facilitate early mobility (speeds extubation)
 16. Treat a parapneumonic effusion.
• A pleural effusion associated with a bacterial pneumonia is a parapneumonic
effusion
• Classical Hx is a patient with a recently Diagnosed pneumonia who comes with a CC
of continued fatigue and cough. XRAY done remarkable for Left or Right Sided
Effusion.

➢ Uncomplicated
o Size <10mm on lateral decubitus: Antibiotics and serial follow .up to ensure
resulution
o Size >10mm, Pleural Fluid pH >7.2, Glucose >60: Thoracentesis and
Antibiotics
➢ Complicated
o Loculated, Pleural Fluid pH <7.2, Glucose <60: Abx + Thoracostomy Tube
Empyema: (+) Gram Stain or aspiration of pus, Fluid pH <7.0: Abx +
• Chest tube or catheter thoracostomy drainage is the least invasive option for
drainage of infected pleural fluid in patients with a complicated
parapneumonic effusion or empyema.
• Failure to improve after antibiotics and tube thoracostomy drainage (eg, the
effusion persists or worsens, fever persists or new fever develops, persistent or
worsening leukocytosis) may indicate that antibiotic coverage and/or that
drainage is inadequate.
o Some patients require surgical intervention (Video-assisted thoracic
surgery (VATS)
o Many patients may respond to intrapleural tissue plasminogen
activator (tPA) with /deoxyribonuclease (DNase) which decreases the
likelihood of intervention and shortens the duration of hospitalization

17. Treat a patient with COPD.

• You must first categorize patients into one of the following categories
• Categories are mainly base on exacerbations per year.

• Avoid using short acting and long acting anticholinergic agents together
 • Stage IV (very severe disease) with acute exacerbation (↑ sputum volume, change in
color and ↑ SOB) should be treated like CAP with ABX
• Roflumilast is a selective phosphodiesterase-4 inhibitor that is used to reduce chronic
symptoms and the frequency of exacerbations in patients with severe COPD
•

18. Treat a pleural effusion.

• First: Pleural effusion first question is to asses what is the posible etiology of effusion
o 2ary to Heart Failure, Cancer, Rheumatoid Arthritis, Pericarditis, Cirrhosis, Etc.
• Next Step: Thoracentesis (All Effusions >10mm in Lateral Decubitus)
o Question may provide Serum LDH, TP and Pleural Fluid LDH and TP
o In order to calculate Lights Criteria
o Lights Criteria (+) if: TPeff/TPserum >0.5, LDHeff/LDHserum>0.6
• Exudates = (+) Lights Criteria
o Lung Infections, Malignancy, Collagen Vascular Disease, Chylothorax, Etc..
• Transudates= (-) Lights Criteria
o CHF, Cirrhosis, Pericarditis, Nephrotic Syndrome

19. Treat anaphylactic shock.

• 1st Step: eliminating exposure to the inciting agent if known
• 2nd Step: Rapidly followed by epinephrine, either IM or IV.
• 3rd Step: ABCs if airway compromised intubation, IVF and Vasopressors if Hypotensive
• Refractory anaphylaxis with distributive and hypovolemic shock should be managed at ICU
as a SIRS case with additional non adrenergic vasopressors as vasopressin.
• Following recovery, patients should maintain home access to an epinephrine autoinjector
and may benefit from evaluation for anaphylactic triggers

20. Treat anaphylaxis.

• MC signs are cutaneous (sudden onset of generalized urticaria, angioedema, flusing,
purritus)
• Acute management → Epinephrine
• Removal of the inciting cause -> Activate emergency code -> IM injection of epinephrine
-> Supplemental oxygen -> Volume resuscitation with IV fluids -> Airway management.
• It is recommended in patients with mild symptoms (few hives, mild wheezing) as well
as for patients with moderate-to-severe symptoms.

21. Treat hypothermia-related bradycardia.

• Bradycardia may be physiologic in hypothermia. Cardiac pacing generally is not required
unless the bradycardia persists despite rewarming to 32 to 35°C (90 to 95°F).
• Transcutaneous > transvenous pacing recommended.
• In patients with severe hypothermia and hemodynamic instability, extracorporeal
support, including cardiopulmonary bypass, is recommended because it maximizes the
rewarming rate and can provide hemodynamic support

22. Treat intensive care unit–acquired weakness.

• ICU-acquired weakness includes:
o Critical illness polyneuropathy (with axonal nerve degeneration)
o Critical illness myopathy (with muscle myosin loss)
• ICU-acquired weakness is associated with long-term functional disability, prolonged
ventilation, and in-hospital mortality.
• Risk factors include hyperglycemia, sepsis, multiple organ dysfunction, and systemic
inflammatory response
• Strategies to limit or prevent ICU-acquired weakness include:
o Sedation limitation
o Early mobilization
23. Treat pulmonary edema.
• Heart failure is a common cause of hypoxemic respiratory failure.
• Pulmonary edema from heart failure is usually transudative fluid in the pulmonary
interstitium and alveolar spaces.
• Fluid can accumulate in the lungs as a result of acute or chronic impairment of either
systolic or diastolic heart function. It can interfere with gas exchange dramatically, but it
usually improves with noninvasive positive pressure ventilation and diuresis.
• Treatment consists of diuresis with goal of negative fluid balance. Initial dose should be
at least the same as prescribed at home, increasing it if poor or no response.

24. Treat respiratory failure due to COPD.

• Supplemental oxygen therapy should be provided to maintain an arterial PO2 greater
than 60 mm Hg (8.0 kPa) or an oxygen saturation of 88% to 92%.
• Short-acting β2-agonists and muscarinic antagonists result in similar bronchodilation,
and either can be used as monotherapy. However, dual treatment results in a greater
degree of bronchodilation and expiratory airflow, which may lead to symptom benefit in
select patients.
• In patients with impending respiratory failure, noninvasive mechanical ventilation may
be helpful in avoiding intubation.
o However, endotracheal intubation and mechanical ventilation are indicated in
patients experiencing life-threatening hypoxemia, progressive hypercapnia,
and/or severely altered mental status
• Glucocorticoids for acute exacerbations of COPD have been shown to reduce recovery
time, improve lung function and arterial hypoxemia, decrease risk of early relapse,
decrease treatment failure, and decrease length of hospital stay.
• Systemic glucocorticoids are recommended for short-duration treatment of acute
exacerbations of COPD.
• Macrolide antibiotics have inflammatory and antimicrobial effects. Long-term macrolide
therapy may reduce the frequency of exacerbations when prescribed to patients with
severe COPD and a history of frequent exacerbations.

25. Treat transfusion-related acute lung injury.

• defined as noncardiogenic pulmonary edema that occurs within 6 hours of transfusion.
• TRALI is mediated by initial priming of neutrophils in the recipient's lung parenchyma
(endothelial damage, for example) followed by their activation by anti-HLA and
antineutrophil antibodies present in donor plasma. The incidence of this complication
has been significantly reduced by screening donors for these antibodies.
• Signs and symptoms escalate quickly and include dyspnea, hypoxia, fever, chills, and
hypotension. Chest radiograph reveals diffuse bilateral pulmonary infiltrates.
• Management includes transfusion discontinuation and supportive care, supplemental
oxygen or mechanical ventilatory support as needed. This management is analogous to
that used for other causes of adult respiratory distress syndrome, which frequently
includes a brief course of mechanical ventilation.

26. Use D-dimer measurement to exclude pulmonary embolism.

• Patients with a Pulmonary Embolism Rule-Out Criteria score of zero do not require
further testing with D-dimer or imaging.
• Patients with a low probability Wells criteria score for DVT or PE should undergo D-
dimer testing; if the results are normal, no further imaging is necessary.
• Patients with moderate or high probability Wells criteria do not require D-dimer testing
but should undergo duplex imaging of the lower extremities for symptoms suggesting
deep venous thrombosis or CT angiography for symptoms suggesting pulmonary
embolism.
• Low d-dimer excludes pulmonary embolism.
Additional Objectives from Prior Years:

1. Evaluate pulmonary nodule.