Sleep, Respiratory, and Critical Care Medicine Practice Flashcards

Vocabulary-style study cards covering pulmonary and critical care topics including OSA, COPD, Asthma, ARDS, and critical care management guidelines.

Distinction between OSA and OHS

OSA causes intermittent nocturnal upper-airway obstruction, while daytime breathing is normal. OHS causes persistent daytime hypoventilation due to obesity and reduced respiratory drive.

Obesity Hypoventilation Syndrome (OHS)

Obesity associated with awake daytime alveolar hypoventilation and hypercapnia after excluding other causes.

Relationship between OSA and OHS

Nearly all patients with OHS have OSA, but only a small proportion of patients with OSA develop OHS.

Evaluation of Sleep-Disordered Breathing

Polysomnography to confirm sleep-disordered breathing, calculate the apnea–hypopnea index, and titrate positive-airway-pressure therapy.

First-line Positive-Airway-Pressure Therapy

CPAP for OSA; CPAP or BiPAP may be used for OHS, particularly when ventilatory support is needed to improve $CO_2$ clearance.

Recommended Lifestyle Measures in OSA/OHS

Weight loss and avoidance of CNS depressants such as alcohol and sedatives.

Next Diagnostic Step for Suspected OHS

Obtain an awake room-air ABG. PaCO_2 \bge 45 mmHg supports OHS; normal daytime $PaCO_2$ favors isolated OSA.

Common Symptoms of OSA

Snoring, excessive fatigue, and daytime somnolence.

Cardiovascular Disorder Associated with OSA

Atrial fibrillation and other cardiovascular complications. CPAP improves symptoms, although cardiovascular benefits vary by outcome and adherence.

Diagnosis Criteria for OSA

Overnight polysomnography. OSA is generally diagnosed with \bge 15 obstructive events/hour without symptoms or \bge 5 events/hour with compatible symptoms or comorbidities.

Treatment of Symptomatic OSA

Positive-airway-pressure therapy, weight loss when appropriate, and selected oral appliances that advance the mandible.

Pregnancy Complications Associated with OSA

Gestational hypertension, preeclampsia, and gestational diabetes.

Main Clinical Features of OHS

Obesity, daytime hypercapnia, sleepiness, dyspnea, fatigue, hypoxemia, elevated bicarbonate, and possible pulmonary hypertension or cor pulmonale.

Laboratory Findings in Chronic OHS

Elevated serum bicarbonate from chronic hypercapnia and possible secondary erythrocytosis from chronic hypoxemia.

Unilateral Diaphragmatic Paralysis Presentation

Dyspnea—especially when supine—an elevated hemidiaphragm, restrictive spirometry, and an exaggerated fall in supine $FVC$. Fluoroscopic sniff testing demonstrates paradoxical upward movement of the affected side.

Manifestations of narcolepsy

Excessive daytime sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations, and low CSF hypocretin-$1$ in type $1$ narcolepsy.

Narcolepsy Diagnosis and Treatment

Overnight polysomnography followed by a multiple sleep latency test showing short sleep latency and sleep-onset REM periods. Modafinil treats daytime sleepiness; REM-suppressing drugs can treat cataplexy.

REM Sleep Behavior Disorder

Dream-enactment behavior caused by loss of normal REM atonia. It is diagnosed by polysomnography, may precede synucleinopathies, and is commonly treated with melatonin.

Findings Suggesting Methemoglobinemia

Cyanosis after oxidant exposure, poor response to oxygen, normal $PaO_2$ on ABG, an oxygen-saturation gap, and pulse oximetry tending toward approximately $85\%$.

Methemoglobinemia Confirmation and Treatment

Confirm with co-oximetry. Treat significant symptomatic disease with methylene blue, unless contraindicated—for example, use caution in G6PD deficiency.

Spirometric distinction between Asthma and COPD

Reversibility of airflow obstruction following bronchodilator administration.

Bronchodilator Response Criteria for Asthma

A significant increase in $FEV_1$ or $FVC$ after bronchodilator administration; traditional criteria use an increase of $>12\%$ and $>200\,mL$.

Normalization of Airflow after Bronchodilator

Suggests asthma rather than fixed COPD.

COPD Bronchodilator Responsiveness

Yes. Some patients with COPD demonstrate improvement, so reversibility alone does not completely exclude COPD.

DLCO in Uncomplicated Asthma

$DLCO$ is usually normal or increased because the alveolar-capillary surface remains intact.

Reduced DLCO with Airflow Obstruction

Suggests emphysema. $DLCO$ is generally normal in isolated chronic bronchitis.

Pulmonary Vascular Disease PFT Findings

It reduces $DLCO$ by decreasing perfused pulmonary capillary volume, while spirometry may remain normal.

Pulmonary Compliance

The ease of lung expansion.

Flow–Volume Loop Orientation

Expiration appears above the horizontal axis and inspiration below it. The loop progresses from TLC toward RV during expiration.

Obstructive Flow–Volume Loop Pattern

Reduced peak expiratory flow with a concave or “scooped-out” expiratory limb. Air trapping may increase RV and TLC.

Post-bronchodilator Asthma vs. COPD Loops

Asthma commonly demonstrates substantial improvement or normalization, whereas COPD usually shows persistent airflow obstruction.

Restrictive Flow–Volume Loop Pattern

A small, narrow loop with reduced lung volumes. The overall contour may be preserved, and $FEV_1/FVC$ is normal or increased.

Causes of Restrictive Lung Disease

Intrinsic causes include IPF, sarcoidosis, and asbestosis. Extrinsic causes include obesity, kyphoscoliosis, neuromuscular disease, and pleural disease.

Fixed Upper-Airway Obstruction Flow Pattern

Flattening of both the inspiratory and expiratory limbs because airflow is limited during both phases.

Causes of Fixed Upper-Airway Obstruction

Tracheal stenosis, a fixed laryngeal or tracheal tumor, and extrinsic compression such as a large substernal goiter.

Variable Extrathoracic Obstruction Mechanics

Negative pressure during inspiration narrows the extrathoracic airway, while expiration tends to open it.

Variable Extrathoracic Obstruction Flow Pattern

Flattened inspiratory limb with a relatively preserved expiratory limb.

Examples of Variable Extrathoracic Obstruction

Vocal-cord dysfunction, laryngomalacia, and extrathoracic tracheomalacia.

Variable Intrathoracic Obstruction Mechanics

Positive intrathoracic pressure during expiration compresses the involved airway, while inspiration tends to hold it open.

Effect of Inspiration on Variable Intrathoracic Obstruction

Negative intrathoracic pressure expands the intrathoracic airway and reduces dynamic collapse.

Variable Intrathoracic Obstruction Flow Pattern

Flattened expiratory limb with a relatively preserved inspiratory limb.

Causes of Variable Intrathoracic Obstruction

Intrathoracic tracheomalacia and tumors involving the lower trachea or main bronchi.

Most Common Cause of Recurrent Wheezing

Obstructive airway diseases, particularly asthma and COPD.

Investigation of Unexplained Recurrent Wheezing

Spirometry with bronchodilator testing before committing the patient to long-term therapy.

Long-Term Asthma Management Principles

Avoid triggers, administer indicated vaccines, ensure correct inhaler technique and adherence, use an ICS-containing regimen, step treatment up when uncontrolled, and step down after sustained control.

Biologic Therapies for Severe Asthma

Dupilumab targets IL-$4$/IL-$13$ signaling; mepolizumab targets IL-$5$; benralizumab targets the IL-$5$ receptor; omalizumab targets IgE; tezepelumab targets TSLP.

Assessment of Severe Acute Asthma Exacerbation

Review baseline lung function, previous ICU admission or intubation, current symptoms and triggers, accessory-muscle use, pulsus paradoxus, mental status, peak flow, oxygenation, and $PaCO_2$.

Impending Respiratory Failure Signs in Asthma

Silent chest, exhaustion, altered mental status, worsening hypoxemia, and normal or elevated $PaCO_2$ despite respiratory distress.

Initial Treatment for Moderate-to-Severe Asthma

Controlled oxygen, repeated inhaled SABA, inhaled ipratropium for severe attacks, early systemic glucocorticoids, and IV magnesium sulfate for severe refractory bronchospasm.

Indications for Glucocorticoids in Asthma Exacerbation

For moderate or severe exacerbations and for mild exacerbations that do not respond adequately to initial inhaled bronchodilator therapy.

Outpatient Glucocorticoid Dose (Post-Asthma Attack)

Prednisone $40-60\,mg$ daily, usually for approximately $5-7$ days in adults.

Importance of Glucocorticoids in Asthma Exacerbations

They reduce hospitalization, accelerate recovery, decrease treatment failure, and reduce early relapse.

Antibiotic Indications in Asthma Treatment

Not routinely. Use them only when bacterial infection is suspected, such as pneumonia or bacterial sinusitis.

Relapse Prevention Post-Asthma Exacerbation

Ensure an ICS-containing controller regimen, provide a short systemic-steroid course when indicated, correct inhaler technique, address adherence and triggers, and arrange follow-up.

Therapy Intensification for As-Needed Budesonide–Formoterol

Budesonide–formoterol may be scheduled as maintenance and reliever therapy, with a short systemic-steroid course when indicated.

Asthma Treatment in Pregnancy

Use guideline-based stepwise therapy similar to that used outside pregnancy; maintaining adequate asthma control is safer than undertreating the disease.

Use of Formoterol in Asthma Relievers

Unlike most LABAs, it has a rapid onset of action—within several minutes—while retaining a long duration.

Escalation Checkpoints for Uncontrolled Asthma

Confirm the diagnosis, inhaler technique, adherence, trigger exposure, and relevant comorbidities.

Aspirin-Exacerbated Respiratory Disease Triad

Asthma, chronic rhinosinusitis with nasal polyps, and respiratory reactions to aspirin or other COX-$1$–inhibiting NSAIDs.

Mechanism and Therapy for AERD

COX-$1$ inhibition shifts arachidonic-acid metabolism toward excess leukotriene production. Leukotriene-modifying treatment such as montelukast may help.

Reactive Airways Dysfunction Syndrome

Nonimmune asthma-like airway hyperresponsiveness beginning after a single high-level irritant exposure. Spirometry may be normal or obstructive; methacholine testing can support the diagnosis.

Emphysema Pathologic Change

Elastase-mediated destruction of alveolar walls and the surrounding pulmonary capillary bed.

Dead-Space Ventilation in Emphysema

Alveolar-wall destruction produces ventilated airspaces with reduced perfusion and decreased gas-exchange surface area.

Elastic Recoil and Airflow Obstruction (Emphysema)

Loss of recoil causes air trapping and dynamic airway collapse during expiration, increases compliance and RV, and contributes to V/Q mismatch and increased physiologic dead space.

Definition of COPD

A heterogeneous chronic lung condition characterized by persistent respiratory symptoms and airflow obstruction resulting from airway and/or alveolar abnormalities, usually caused by exposure to noxious particles or gases.

Initial COPD Pharmacotherapy (GOLD Groups)

Group A: one bronchodilator. Group B: LABA + LAMA. Group E: LABA + LAMA; consider adding ICS when eosinophils are high, especially \bge 300/\mu L.

COPD Interventions Reducing Mortality

Smoking cessation, indicated vaccinations, and long-term oxygen therapy for qualifying severe resting hypoxemia.

Most Important Nonpharmacologic COPD Therapy

Smoking cessation.

Benefits of Pulmonary Rehabilitation in COPD

Improved exercise tolerance, dyspnea, functional status, and health-related quality of life.

Slowing COPD Progression and Improving Survival

Smoking cessation slows progression; long-term oxygen improves survival in qualifying severe resting hypoxemia.

LTOT Indication in Stable COPD

When severe resting hypoxemia persists despite optimal treatment.

Hypoxemia Thresholds for LTOT in COPD

PaO_2 \ble 55 mmHg or SaO_2 \ble 88\%, or $PaO_2 56-59 mmHg/SaO_2 89\%$ with cor pulmonale, pulmonary hypertension, or secondary erythrocytosis.

Cardinal Symptoms of COPD Exacerbation

Increased dyspnea, increased sputum volume, and increased sputum purulence.

Clinical Classification of COPD Exacerbations

Mild: SABA only. Moderate: antibiotics and/or systemic steroids. Severe: ED assessment or hospitalization.

Initial Bronchodilator Treatment (COPD Exacerbation)

Increase short-acting inhaled bronchodilation, usually SABA with or without SAMA.

Benefits of Systemic Glucocorticoids (COPD Exacerbation)

They improve lung function and hypoxemia, shorten recovery and hospitalization, and reduce early relapse and treatment failure.

Antibiotic Indications in COPD exacerbation

With sputum purulence plus another cardinal symptom, when all three cardinal symptoms are present, or when ventilatory support is required.

Indication for NIV in COPD Exacerbation

Acute hypercapnic respiratory failure with respiratory acidosis, generally $PaCO_2 > 45 mmHg$ and pH \ble 7.35.

Benefits of NIV (COPD Exacerbation)

Reduced acidosis, intubation, treatment failure, hospital stay, and mortality.

Predictors of NIV Success (COPD Exacerbation)

Moderate respiratory acidosis, preserved ability to follow commands, manageable secretions, and early physiologic improvement.

Findings Favoring Immediate Intubation over NIV

Respiratory arrest, inability to protect the airway or clear secretions, severe hemodynamic instability, severe encephalopathy, facial barriers, or NIV failure.

ICS Utility in COPD Patients

Frequent exacerbators despite adequate bronchodilation, especially with high blood eosinophils or concomitant asthma.

Primary Role of ICS in COPD

Reducing exacerbations in appropriately selected patients; it is not primarily used to relieve acute symptoms.

Adverse Effects of Inhaled Corticosteroids in COPD

Pneumonia, oral candidiasis, dysphonia, and skin bruising.

Treatment of Secondary Pulmonary Hypertension from COPD

Optimize COPD, correct hypoxemia with oxygen when indicated, encourage smoking cessation, and provide rehabilitation; PAH-specific drugs are not routinely used.

Manifestations of Significant PH in COPD

Disproportionate hypoxemia, peripheral edema, loud P$2$, tricuspid-regurgitation murmur, or right-heart dysfunction.

Alpha-$1$ Antitrypsin Deficiency Presentation

Early emphysema, minimal smoking exposure, basilar-predominant emphysema, unexplained liver disease, or panniculitis.

A1AT Deficiency Imaging and Skin Findings

Basilar-predominant emphysema and panniculitis.

Testing Candidates for A1AT Deficiency

All patients with COPD or otherwise unexplained persistent airflow obstruction should be tested at least once.

Palliative Care Consideration in COPD

In advanced disease with severe refractory symptoms, repeated hospitalizations, progressive functional decline, or when the patient’s goals favor comfort-focused care.

Opioid Use for Refractory Dyspnea (COPD)

Carefully titrated low-dose opioids can reduce refractory breathlessness as part of palliative care.

Acid–Base Pattern in Stable Chronic COPD Hypercapnia

Chronic respiratory acidosis with elevated $PaCO_2$, compensatory bicarbonate elevation, and a near-normal pH.

Acute-on-Chronic Hypercapnic Respiratory Failure Pattern

$PaCO_2$ rises above baseline with relatively little immediate bicarbonate change, causing a new fall in pH.

Most Common Acid–Base Disturbance in Cirrhosis

Chronic respiratory alkalosis due partly to hyperventilation.

Secondary Acid–Base Disturbances in Cirrhosis

Normal-anion-gap acidosis from diarrhea; hyperkalemic acidosis from spironolactone; metabolic alkalosis from loop diuretics.

Bronchiectasis Definition and Presentation

Permanent bronchial dilation causing chronic productive cough, recurrent respiratory infections, and sometimes hemoptysis.

Evaluation of Bronchiectasis

HRCT confirms bronchial dilation. Depending on context, investigate immunodeficiency, cystic fibrosis, ABPA, NTM/TB, aspiration, or autoimmune disease.

Lung Abscess Presentation and Treatment

Subacute fever, weight loss, foul sputum, and a cavity with an air–fluid level, often after aspiration. Treat with prolonged anaerobic-active antibiotics such as ampicillin–sulbactam.

Adult Presentation of Cystic Fibrosis

Bronchiectasis, chronic sinusitis, recurrent pancreatitis, pancreatic insufficiency, male infertility, or recurrent atypical infections.

Manifestations of Cystic Fibrosis (CF)

Chronic respiratory disease, upper-lobe bronchiectasis, sinusitis, pancreatic disease, malabsorption, male infertility, and recurrent bacterial or NTM infection.