101. Community-Acquired Pneumonia (CAP)
typical vs atypical · severity drives disposition (CURB-65/PSI, IDSA/ATS minor/major criteria) · empiric antibiotics by setting + risk · de-escalate by culture · Super Compact
Sx: cough (productive/purulent sputum), fever/chills, dyspnea, pleuritic chest pain, tachypnea/tachycardia, focal crackles/bronchial breath sounds/dullness · atypical: more gradual, dry cough, headache/myalgia · elderly: may present with confusion, falls, or decompensation without fever (severity, not the organism guess, drives admission)
Neg: denies orthopnea/PND/weight-based edema (argues against CHF as the infiltrate cause) · denies pleuritic pain with sudden dyspnea + hemoptysis + calf swelling (argues against PE) · denies large-volume aspiration event/witnessed choking (aspiration) · denies chronic cough with weight loss/night sweats/hemoptysis (TB, malignancy) · denies prior healthcare/abx exposure suggesting resistant organisms
SHx: smoking (pneumococcus, COPD overlap) · alcohol (Klebsiella, aspiration) · recent viral illness (post-influenza Staph) · exposures (birds — psittacosis, water/AC — Legionella) · vaccination status (pneumococcal, influenza, COVID)
Etiology: Streptococcus pneumoniae (most common typical) · Haemophilus influenzae, Moraxella (COPD) · atypicals — Mycoplasma, Chlamydophila, Legionella (severe, hyponatremia, GI/neuro) · respiratory viruses (influenza, RSV, COVID — often preceding/coexisting) · post-influenza Staph aureus (incl MRSA, necrotizing)
RF: age ≥65 · smoking/COPD · alcohol · immunocompromise · recent viral URI/influenza · chronic heart/liver/kidney disease · diabetes · aspiration risk
Data: CXR (lobar consolidation, infiltrate, air bronchograms; effusion — assess for parapneumonic) · CBC (leukocytosis ± left shift; leukopenia = severe) · BMP (hyponatremia — Legionella; renal — CURB-65 BUN, dosing) · lactate (sepsis) · blood cultures ×2 + sputum Gram stain/culture (before antibiotics, for severe/admitted) · respiratory viral PCR (influenza/COVID/RSV) · Legionella + pneumococcal urinary antigen (severe) · procalcitonin (adjunct, not gatekeeper to start) · SpO2/ABG · severity: CURB-65 (Confusion, Urea>19/BUN>19, RR≥30, BP<90/60, age≥65) + IDSA/ATS criteria
DDx: CHF/pulmonary edema (BNP, bilateral, cardiomegaly, response to diuresis) · PE (CTA, often clear CXR/hypoxia out of proportion) · aspiration pneumonia/pneumonitis (dependent segments, event) · TB/malignancy (chronicity, weight loss) · ILD (bilateral reticular, chronic) · COVID/viral (PCR, ground-glass)
Home Meds: reconcile inhalers/COPD regimen (continue/optimize) · hold nephrotoxins if AKI · review anticoagulation (procedures/effusion drainage) · ensure VTE prophylaxis · check drug interactions with macrolides/fluoroquinolones (QT)
Plan
CONSULT: Pulmonology (severe, non-resolving, complications) · Infectious Disease (resistant/atypical organisms, immunocompromise) · ICU/Critical care (septic shock, respiratory failure, IDSA major criteria)
– First, assess severity + disposition: CURB-65 / PSI + IDSA/ATS criteria → outpatient vs floor vs ICU; ICU for septic shock requiring vasopressors or respiratory failure requiring mechanical ventilation (major criteria), or ≥3 minor criteria
– Obtain cultures, then start empiric antibiotics promptly (do not delay in sepsis):
• Inpatient, non-severe (floor): beta-lactam + macrolide — e.g. ceftriaxone 1–2 g IV q24h + azithromycin 500 mg IV/PO q24h; OR respiratory fluoroquinolone monotherapy — levofloxacin 750 mg IV/PO q24h (or moxifloxacin 400 mg q24h)
• Inpatient, severe (ICU): beta-lactam + macrolide (ceftriaxone + azithromycin) OR beta-lactam + respiratory fluoroquinolone
• Add MRSA coverage (vancomycin 15–20 mg/kg IV q8–12h, target trough/AUC, OR linezolid 600 mg IV q12h) and/or antipseudomonal coverage (this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam; add metronidazole 500 mg IV q8h if anaerobic coverage needed) for risk factors (prior MRSA/Pseudomonas, recent hospitalization/IV antibiotics, structural lung disease) or per local validated risk + severity
• Influenza positive: add oseltamivir 75 mg PO BID; continue antibacterials if bacterial co-infection suspected
– Supportive care: supplemental O2 to SpO2 ≥92% (88–92% if CO2 retainer/COPD overlap); IV fluids for sepsis/hypoperfusion; antipyretics/analgesia; corticosteroids — consider in severe CAP (e.g. hydrocortisone) per current evidence, especially with septic shock
– Assess the effusion: if moderate/large or septic → diagnostic thoracentesis to exclude complicated parapneumonic effusion/empyema (pH <7.2, loculation → chest tube)
– De-escalate: tailor to culture/sensitivities at 48–72h; switch IV→PO when hemodynamically stable, improving, and able to take oral; duration usually 5 days (minimum) if afebrile 48–72h and clinically stable — longer for complications (empyema, abscess, Legionella, Pseudomonas/MRSA)
– Severity (CURB-65/PSI + IDSA minor/major), not your organism guess, sets the level of care; reserve broad MRSA/Pseudomonas coverage for genuine risk factors or severe disease, then de-escalate by culture.
– PT/OT: early mobilization; incentive spirometry; pulmonary hygiene
– Trend: SpO2/O2 requirement, RR/work of breathing, fever curve, WBC, lactate clearance, renal function (dosing), culture results, clinical response by 48–72h
– Escalation triggers: worsening hypoxemia/respiratory failure → HFNC/NIPPV/intubation + ICU; septic shock → vasopressors + ICU; non-resolving at 72h → reassess (resistant organism, empyema, wrong diagnosis — PE/CHF/malignancy, obstruction); new/enlarging effusion → drainage
– Discharge when: clinically stable (afebrile, stable vitals, SpO2 adequate on room air or baseline O2), tolerating oral antibiotics, mentation at baseline, safe to take PO; provide complete oral course + duration, follow-up CXR if indicated (age/smoker — exclude underlying malignancy), PCP/pulmonary follow-up, smoking cessation + vaccination counseling; return precautions (worsening dyspnea, fever, chest pain, confusion)
101. Community-Acquired Pneumonia (CAP)
complete reference · typical + atypical + viral · severity-based disposition · empiric therapy by setting and risk · de-escalation and duration · Full Card
Symptoms / Associated Sx
Cough productive of purulent sputum, fever and chills, dyspnea, and pleuritic chest pain, with tachypnea and tachycardia on exam
Focal findings — crackles, bronchial breath sounds, dullness to percussion, increased fremitus over the involved lobe
Atypical presentations are more gradual with a dry cough, headache, and myalgia; Legionella may bring prominent GI and neurologic symptoms
Older adults may present atypically with confusion, falls, decompensation of a chronic illness, or functional decline without a prominent fever
Neg
Pt denies orthopnea, paroxysmal nocturnal dyspnea, and progressive dependent edema — argues against heart failure as the cause of the infiltrate
Pt denies sudden pleuritic pain with acute dyspnea, hemoptysis, and calf swelling — argues against pulmonary embolism
Pt denies a witnessed choking or large-volume aspiration event — argues against aspiration as the precipitant
Pt denies a chronic cough with weight loss, night sweats, or hemoptysis — argues against tuberculosis or malignancy
Social History (SHx)
Smoking (pneumococcal disease, COPD overlap) and alcohol use (Klebsiella, aspiration risk)
Recent viral illness or influenza (predisposes to secondary bacterial, including post-influenza Staphylococcus aureus)
Exposures — birds (psittacosis), contaminated water or air-conditioning (Legionella), travel
Vaccination status for pneumococcus, influenza, and COVID-19
Main Etiology
Streptococcus pneumoniae — the most common typical bacterial cause
Haemophilus influenzae and Moraxella catarrhalis, particularly in COPD
Atypicals — Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella (associated with severe disease, hyponatremia, and GI or neurologic features)
Respiratory viruses (influenza, RSV, SARS-CoV-2) that often precede or coexist with bacterial infection
Staphylococcus aureus including MRSA — post-influenza and necrotizing pneumonia
RF
Modifiable: smoking, alcohol, vaccination gaps, and uncontrolled comorbidities
Non-modifiable: age 65 or older, COPD and structural lung disease, immunocompromise, and chronic heart, liver, or kidney disease
Data
Chest radiograph (lobar consolidation, infiltrate, air bronchograms; evaluate any effusion for a parapneumonic process)
CBC (leukocytosis with a left shift; leukopenia indicates severe disease) and BMP (hyponatremia suggests Legionella; BUN feeds CURB-65; renal function guides dosing)
Lactate (sepsis and hypoperfusion)
Blood cultures times two and a sputum Gram stain and culture (before antibiotics in severe or admitted disease; do not delay therapy to obtain them)
Respiratory viral PCR (influenza, SARS-CoV-2, RSV) and, in severe disease, Legionella and pneumococcal urinary antigens
Procalcitonin (an adjunct to support de-escalation; never a gatekeeper that delays empiric therapy)
Oximetry and ABG for gas exchange, and a severity score — CURB-65 (confusion, urea/BUN elevation, respiratory rate 30 or more, low blood pressure, age 65 or older) alongside the IDSA/ATS minor and major criteria
DDx
Heart failure / pulmonary edema (BNP, bilateral distribution, cardiomegaly, response to diuresis) · pulmonary embolism (CTA; often a clear CXR with hypoxia out of proportion) · aspiration pneumonia or pneumonitis (dependent segments, an aspiration event) · tuberculosis or malignancy (chronicity, weight loss, hemoptysis) · interstitial lung disease (chronic bilateral reticular changes) · COVID-19 or other viral pneumonia (PCR, ground-glass opacities)
Home Meds
Reconcile and continue or optimize the inhaler and COPD regimen
Hold nephrotoxins in the setting of acute kidney injury and renally dose-adjust antibiotics
Review anticoagulation around any planned thoracentesis or chest tube and ensure VTE prophylaxis
Watch QT-prolonging interactions with macrolides and fluoroquinolones
Plan
CONSULT: Pulmonology (severe, non-resolving, or complicated disease) · Infectious Disease (resistant or atypical organisms, immunocompromise) · ICU/Critical care (septic shock, respiratory failure, or IDSA major criteria)
Assess severity and disposition first: apply CURB-65 or PSI with the IDSA/ATS criteria to choose outpatient, floor, or ICU care; admit to the ICU for septic shock requiring vasopressors or respiratory failure requiring mechanical ventilation (major criteria), or when three or more minor criteria are met
Obtain cultures and then start empiric antibiotics promptly (do not delay in sepsis): for inpatient non-severe disease, a beta-lactam plus a macrolide — ceftriaxone 1–2 g IV q24h plus azithromycin 500 mg IV or PO q24h — or respiratory fluoroquinolone monotherapy with levofloxacin 750 mg IV/PO q24h (or moxifloxacin 400 mg q24h)
For severe (ICU) disease: a beta-lactam plus a macrolide (ceftriaxone plus azithromycin) or a beta-lactam plus a respiratory fluoroquinolone
Add MRSA coverage (vancomycin 15–20 mg/kg IV q8–12h dosed to target, or linezolid 600 mg IV q12h) and/or antipseudomonal coverage — this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam, adding metronidazole 500 mg IV q8h when anaerobic coverage is needed — for genuine risk factors (prior MRSA or Pseudomonas, recent hospitalization or IV antibiotics, structural lung disease) or per a validated local risk assessment with severity
If influenza is positive, add oseltamivir 75 mg PO BID and continue antibacterials when bacterial co-infection is suspected
Supportive care: supplemental oxygen to keep SpO2 92% or higher (88–92% in a CO2 retainer or COPD overlap), IV fluids for sepsis or hypoperfusion, antipyretics and analgesia, and consideration of corticosteroids in severe CAP per current evidence, particularly with septic shock
Evaluate any effusion: a moderate or large or septic-appearing effusion warrants a diagnostic thoracentesis to exclude a complicated parapneumonic effusion or empyema (a pH below 7.2 or loculation indicates the need for chest tube drainage)
De-escalate: tailor therapy to cultures and sensitivities at 48–72 hours, switch from IV to oral once hemodynamically stable and improving and able to take oral medication, and treat for a minimum of 5 days when afebrile for 48–72 hours and clinically stable — extending for complications such as empyema, abscess, Legionella, or Pseudomonas or MRSA infection
PT/OT: early mobilization, incentive spirometry, and pulmonary hygiene
Trend: oxygen requirement, respiratory rate and work of breathing, the fever curve, white count, lactate clearance, renal function for dosing, culture results, and the clinical response by 48–72 hours
Escalation triggers: worsening hypoxemia or respiratory failure → high-flow nasal cannula, NIPPV, or intubation with ICU transfer; septic shock → vasopressors and ICU; non-resolution at 72 hours → reassess for a resistant organism, empyema, or an alternative diagnosis (PE, heart failure, malignancy, or obstruction); a new or enlarging effusion → drainage
Discharge criteria: clinical stability (afebrile, stable vitals, adequate oxygenation on room air or baseline oxygen), tolerating oral antibiotics, and baseline mentation; provide the full oral course and duration, arrange a follow-up chest radiograph when indicated to exclude underlying malignancy (older smokers), and counsel on smoking cessation and vaccination with return precautions for worsening dyspnea, fever, chest pain, or confusion
Red Flags
Septic shock requiring vasopressors or respiratory failure requiring ventilation → ICU (IDSA major criteria)
Hypoxia out of proportion to the radiographic findings → reconsider pulmonary embolism
A complicated parapneumonic effusion (pH below 7.2, loculation) or frank pus → empyema requiring drainage
Post-influenza, rapidly cavitating, or necrotizing pneumonia → MRSA; add coverage and obtain ID input
Failure to improve by 72 hours → resistant organism, undrained collection, or a wrong diagnosis
Senior IM Resident Pearls
Severity sets the level of care. CURB-65 or PSI with the IDSA minor and major criteria decides floor versus ICU far better than how sick the film looks.
Don't broaden reflexively. Reserve MRSA and Pseudomonas coverage for real risk factors or severe disease, then de-escalate by culture.
Procalcitonin doesn't gate the first dose. Use it to help stop antibiotics, never to justify withholding them in a septic patient.
Hyponatremia and GI or neuro symptoms suggest Legionella. Send the urinary antigen and ensure atypical coverage in severe disease.
Five days is usually enough. If afebrile for 48–72 hours and stable, longer courses add toxicity without benefit outside complications.
Look behind the pneumonia in older smokers. A non-resolving infiltrate warrants follow-up imaging to exclude an obstructing malignancy.
Common mistake: anchoring on CAP and missing the coexisting effusion that became an empyema, or the PE or heart failure that the antibiotics will never treat.
Pulmonology — Pneumonia
102. Aspiration Pneumonia
distinguish aspiration pneumonitis (chemical, often self-limited) from aspiration pneumonia (bacterial) · dependent segments · address the dysphagia/risk · Super Compact
Sx: cough, dyspnea, fever developing over hours–days after an aspiration event or in a patient with chronic aspiration risk · sputum may be putrid (anaerobes/abscess) · crackles over dependent segments · witnessed choking/regurgitation may precede · in chronic aspirators: recurrent/indolent infiltrates, low-grade decline (separate the chemical pneumonitis that may resolve from established bacterial pneumonia)
Neg: denies orthopnea/PND/edema (CHF) · denies sudden pleuritic dyspnea + calf swelling (PE) · denies productive cough with classic lobar onset without aspiration risk (typical CAP) · denies weight loss/night sweats/hemoptysis over months (TB/malignancy/obstruction) · denies pure post-event transient symptoms that cleared quickly (suggests pneumonitis, not pneumonia)
SHx: alcohol/substance use (decreased consciousness) · smoking · institutionalization/tube feeds · prior stroke or neurodegenerative disease · recent procedure/sedation/intubation
Etiology: aspiration pneumonitis (Mendelson — sterile chemical injury from gastric acid, may resolve without antibiotics) vs aspiration pneumonia (bacterial — oropharyngeal flora; historically anaerobes, but typical aerobes — Strep, Staph, gram-negatives — predominate in most modern cases) · dependent segments (posterior upper lobes if recumbent, basal lower lobes if upright) · abscess/empyema if untreated
RF: dysphagia (stroke, dementia, neuromuscular, head & neck cancer) · impaired consciousness (alcohol, sedation, seizure) · GERD/reflux · tube feeding · poor dentition/oral hygiene · esophageal dysmotility/obstruction · supine positioning
Data: CXR/CT (infiltrate in dependent segments — posterior upper or basal lower lobes; cavitation/abscess; effusion → empyema) · CBC, BMP, lactate · blood + sputum cultures (before antibiotics; anaerobic yield limited) · SpO2/ABG · bedside swallow screen → formal swallow evaluation (speech-language pathology) ± video fluoroscopy/FEES (identify + grade dysphagia — central to management) · review meds for sedation/anticholinergic burden
DDx: aspiration pneumonitis (chemical, self-limited) (rapid onset post-event, may clear without antibiotics — avoid reflexive prolonged courses) · CAP (no aspiration risk, classic lobar) · CHF (BNP, bilateral) · PE (CTA) · post-obstructive pneumonia (mass — bronchoscopy) · TB (chronic, upper-lobe cavitary)
Home Meds: review/reduce sedatives, anticholinergics, and other deliriogenic/aspiration-promoting drugs · reconcile reflux therapy (PPI) · hold oral intake until swallow cleared (aspiration precautions) · ensure VTE prophylaxis · renally dose antibiotics
Plan
CONSULT: Speech-language pathology (swallow evaluation — essential) · Pulmonology (abscess, non-resolving, bronchoscopy) · Gastroenterology (refractory dysphagia, PEG decisions) · Infectious Disease (abscess/empyema, resistant organisms) · ICU (respiratory failure)
– First, distinguish pneumonitis from pneumonia: a witnessed aspiration with rapidly developing infiltrate/symptoms that improve over 24–48h may be chemical pneumonitis → supportive care, and antibiotics can often be withheld or stopped early if it resolves; persistent fever, leukocytosis, purulent sputum, or progression supports bacterial pneumonia
– Aspiration precautions immediately: NPO until a swallow screen/evaluation is done; elevate head of bed; suction as needed
– Empiric antibiotics (when bacterial pneumonia is established/likely): cover oropharyngeal flora and typical aerobes — ampicillin-sulbactam 3 g IV q6h, OR ceftriaxone 1–2 g IV q24h ± metronidazole 500 mg IV q8h (add anaerobic coverage for abscess, empyema, severe periodontal disease, or putrid sputum), OR a respiratory fluoroquinolone (levofloxacin 750 mg IV/PO q24h) · for healthcare-associated/severe or resistant risk, broaden per local antibiogram (this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam, + metronidazole 500 mg IV q8h for anaerobes)
– Routine broad anaerobic coverage is no longer recommended for uncomplicated aspiration pneumonia — reserve metronidazole/clindamycin-level anaerobic coverage for abscess, empyema, necrotizing disease, or severe periodontal disease
– Supportive care: O2 to SpO2 ≥92% (88–92% if COPD overlap); fluids for sepsis; chest physiotherapy/pulmonary hygiene
– Source/risk control (the key to preventing recurrence): formal swallow evaluation by speech-language pathology → diet texture modification, feeding strategies, positioning; treat reversible contributors (sedation, reflux, oral hygiene/dental care); discuss feeding-tube decisions thoughtfully in advanced dementia (tubes do not eliminate aspiration risk — goals-of-care conversation)
– Manage complications: lung abscess → prolonged antibiotics ± drainage; empyema → chest tube drainage + antibiotics (see the empyema card)
– Not every aspiration needs antibiotics — chemical pneumonitis can resolve on its own; reserve antibiotics for established bacterial pneumonia, and put the swallow evaluation and aspiration-risk reduction at the center of the plan to prevent the next episode.
– PT/OT + SLP: mobilization, swallow therapy, positioning
– Trend: O2 requirement, fever/WBC, sputum character, clinical course over 48–72h (distinguish resolving pneumonitis from progressive pneumonia), swallow status
– Escalation triggers: respiratory failure → NIPPV/intubation + ICU; non-resolving/cavitation → CT + bronchoscopy (exclude obstruction/abscess) + ID; new effusion → drainage
– Discharge when: clinically stable, oxygenation adequate, swallow plan established (diet/precautions or alternative feeding plan), antibiotic course defined; SLP/PCP/pulmonary follow-up, caregiver education on aspiration precautions; return precautions (recurrent fever/cough, worsening dyspnea, choking with meals)
102. Aspiration Pneumonia
complete reference · pneumonitis vs pneumonia · dependent-segment disease · targeted (not reflexive broad anaerobic) antibiotics · swallow evaluation central · Full Card
Symptoms / Associated Sx
Cough, dyspnea, and fever developing over hours to days after an aspiration event or in a patient with chronic aspiration risk
Sputum may be putrid when anaerobes or an abscess are involved, with crackles over the dependent lung segments
A witnessed choking or regurgitation event may precede the illness; chronic aspirators show recurrent or indolent infiltrates and gradual decline
Neg
Pt denies orthopnea, paroxysmal nocturnal dyspnea, and dependent edema — argues against heart failure
Pt denies sudden pleuritic dyspnea with calf swelling — argues against pulmonary embolism
Pt denies a chronic cough with months of weight loss, night sweats, or hemoptysis — argues against tuberculosis, malignancy, or an obstructing lesion
Pt denies transient post-event symptoms that cleared within a day or two — that pattern favors a chemical pneumonitis rather than bacterial pneumonia
Social History (SHx)
Alcohol or substance use producing decreased consciousness, and smoking
Institutionalization or tube feeding, and a history of stroke or neurodegenerative disease
Recent procedure, sedation, or intubation
Main Etiology
Aspiration pneumonitis (Mendelson syndrome) — a sterile chemical injury from aspirated gastric acid that may resolve without antibiotics
Aspiration pneumonia — bacterial infection from oropharyngeal flora; while anaerobes were historically emphasized, typical aerobes (streptococci, staphylococci, and gram-negatives) predominate in most modern cases
Disease localizes to dependent segments — the posterior segments of the upper lobes when recumbent, the basal segments of the lower lobes when upright
Untreated disease can progress to lung abscess or empyema
RF
Modifiable: sedating and anticholinergic medications, poor oral hygiene and dentition, reflux, and supine positioning
Non-modifiable: dysphagia from stroke, dementia, neuromuscular disease, or head and neck cancer, and impaired consciousness
Data
Chest radiograph or CT (an infiltrate in dependent segments; cavitation or abscess; an effusion suggesting empyema)
CBC, BMP, and lactate, with blood and sputum cultures before antibiotics (recognizing limited anaerobic yield)
Oximetry and ABG for gas exchange
A bedside swallow screen followed by a formal swallow evaluation by speech-language pathology, with video fluoroscopy or FEES when needed (identifying and grading the dysphagia is central to management)
Review of medications for sedation and anticholinergic burden
DDx
Aspiration pneumonitis (rapid onset after an event, may clear without antibiotics — avoid reflexive prolonged courses) · community-acquired pneumonia (no aspiration risk, classic lobar pattern) · heart failure (BNP, bilateral) · pulmonary embolism (CTA) · post-obstructive pneumonia (an obstructing mass — bronchoscopy) · tuberculosis (chronic upper-lobe cavitary disease)
Home Meds
Review and reduce sedatives, anticholinergics, and other aspiration-promoting or deliriogenic drugs
Reconcile reflux therapy and hold oral intake until the swallow is cleared (aspiration precautions)
Ensure VTE prophylaxis and renally dose antibiotics
Plan
CONSULT: Speech-language pathology (swallow evaluation — essential) · Pulmonology (abscess, non-resolving disease, bronchoscopy) · Gastroenterology (refractory dysphagia, feeding-tube decisions) · Infectious Disease (abscess or empyema, resistant organisms) · ICU (respiratory failure)
Distinguish pneumonitis from pneumonia first: a witnessed aspiration with a rapidly developing infiltrate and symptoms that improve over 24–48 hours may be a chemical pneumonitis warranting supportive care, with antibiotics withheld or stopped early; persistent fever, leukocytosis, purulent sputum, or progression supports bacterial pneumonia
Institute aspiration precautions immediately: NPO until a swallow screen or evaluation is completed, head-of-bed elevation, and suction as needed
Empiric antibiotics when bacterial pneumonia is established or likely: cover oropharyngeal flora and typical aerobes with ampicillin-sulbactam 3 g IV q6h, or ceftriaxone 1–2 g IV q24h with metronidazole 500 mg IV q8h added for anaerobic indications (abscess, empyema, severe periodontal disease, putrid sputum), or a respiratory fluoroquinolone (levofloxacin 750 mg IV/PO q24h); for healthcare-associated, severe, or resistant-risk disease, broaden per the local antibiogram (this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam, with metronidazole 500 mg IV q8h for anaerobes)
Routine broad anaerobic coverage is no longer recommended for uncomplicated aspiration pneumonia — reserve it for abscess, empyema, necrotizing disease, or severe periodontal disease
Supportive care: oxygen to keep SpO2 92% or higher (88–92% with COPD overlap), fluids for sepsis, and chest physiotherapy
Source and risk control, the key to preventing recurrence: a formal swallow evaluation guiding diet texture modification, feeding strategies, and positioning; treatment of reversible contributors (sedation, reflux, oral and dental care); and a thoughtful, goals-of-care-based discussion of feeding-tube decisions in advanced dementia, recognizing that tubes do not eliminate aspiration risk
Manage complications: a lung abscess with prolonged antibiotics and possible drainage; an empyema with chest tube drainage and antibiotics
PT/OT and SLP: mobilization, swallow therapy, and positioning
Trend: oxygen requirement, fever and white count, sputum character, and the 48–72 hour course to separate resolving pneumonitis from progressive pneumonia, along with swallow status
Escalation triggers: respiratory failure → NIPPV or intubation and ICU; non-resolution or cavitation → CT and bronchoscopy to exclude obstruction or abscess, with ID input; a new effusion → drainage
Discharge criteria: clinical stability with adequate oxygenation, an established swallow plan (diet and precautions or an alternative feeding plan), and a defined antibiotic course; arrange SLP, PCP, and pulmonary follow-up with caregiver education on aspiration precautions and return precautions for recurrent fever or cough, worsening dyspnea, or choking with meals
Red Flags
Putrid sputum, cavitation, or a necrotizing pattern → lung abscess or anaerobic infection requiring extended, sometimes drained, therapy
A loculated or purulent effusion → empyema requiring chest tube drainage
Recurrent aspiration pneumonias → an uncorrected dysphagia or obstructing lesion; pursue the swallow evaluation and bronchoscopy
Respiratory failure or septic shock → ICU
A non-resolving "aspiration" infiltrate in a smoker → exclude a post-obstructive malignancy
Senior IM Resident Pearls
Pneumonitis is not pneumonia. A chemical injury after a witnessed aspiration can resolve on its own — don't lock a well-appearing patient into a full antibiotic course reflexively.
Anaerobic coverage is no longer routine. Typical aerobes dominate modern aspiration pneumonia; reserve metronidazole-level coverage for abscess, empyema, or severe dental disease.
The swallow evaluation is the treatment. Antibiotics treat this episode; the SLP assessment and risk reduction prevent the next one.
Feeding tubes don't stop aspiration. In advanced dementia they're a goals-of-care decision, not an aspiration-prevention device.
Know the geography. Dependent segments — posterior upper lobes when recumbent, basal lower lobes when upright — tell you the mechanism.
Reduce the sedating burden. Trimming anticholinergics and sedatives lowers the aspiration risk more than any antibiotic.
Common mistake: treating every aspiration with prolonged broad-spectrum anaerobic antibiotics while never arranging the swallow evaluation that actually prevents recurrence.
Pulmonology — Pneumonia
103. Healthcare-Associated Pneumonia (HAP / VAP)
hospital-acquired (≥48h after admission) / ventilator-associated · cover MDR organisms (MRSA, Pseudomonas) empirically by risk · de-escalate aggressively by culture · Super Compact
Sx: new/worsening cough, purulent secretions, fever, dyspnea, hypoxemia, and a new/progressive infiltrate developing ≥48h after hospital admission (HAP) or >48h after intubation (VAP) · in ventilated patients: increased secretions, worsening oxygenation/ventilator requirements, fever/leukocytosis (the defining feature is the healthcare exposure that shifts the likely organisms toward resistant pathogens)
Neg: denies symptom onset before/at admission (would be CAP, not HAP) · denies orthopnea/PND/edema (CHF) · denies sudden pleuritic dyspnea (PE) · denies aspiration event as sole explanation · denies findings better explained by atelectasis/effusion alone without infection
SHx: recent/current hospitalization, ICU stay, mechanical ventilation · recent IV antibiotics (selects resistance) · prior MDR colonization/infection · immunosuppression · note the term "HCAP" has been retired — risk-stratify individually
Etiology: aerobic gram-negatives — Pseudomonas aeruginosa, Klebsiella, Enterobacter, Acinetobacter, E. coli · Staphylococcus aureus including MRSA · resistant organisms more likely with risk factors · polymicrobial common in VAP
RF for MDR organisms: IV antibiotics within 90 days · ≥5 days of hospitalization before onset (late-onset) · septic shock at onset · ARDS preceding · acute renal replacement therapy · prior MDR colonization · structural lung disease (Pseudomonas) · high local resistance rates
Data: CXR/CT (new/progressive infiltrate) · CBC, BMP, lactate · blood cultures ×2 + LOWER RESPIRATORY SECRETIONS for Gram stain/culture (sputum, or endotracheal aspirate/BAL in ventilated) (obtain before/with antibiotic start; guides essential de-escalation) · SpO2/ABG, P/F ratio · MRSA nares PCR (high negative predictive value — supports stopping vancomycin) · procalcitonin (de-escalation adjunct) · local antibiogram
DDx: CAP (onset before 48h) · aspiration (event, dependent segments) · CHF/volume overload (BNP, diuretic response) · PE (CTA) · ARDS (bilateral, P/F) · atelectasis (post-op, resolves with recruitment) · ventilator-associated tracheobronchitis (no new infiltrate)
Home Meds: reconcile recent antibiotic exposures (informs empiric choice — avoid the recently used class) · renally dose-adjust (vancomycin/aminoglycosides — levels) · ensure VTE + stress-ulcer prophylaxis · review for drug interactions
Plan
CONSULT: Infectious Disease (MDR organisms, treatment failure, de-escalation guidance) · Pulmonology/Critical care (VAP, bronchoscopy/BAL, respiratory failure) · ICU (septic shock, ventilation) · Pharmacy (PK/PD dosing of vancomycin/beta-lactams)
– First, obtain lower respiratory cultures and blood cultures, then start empiric antibiotics promptly (cultures are essential because de-escalation is the whole strategy)
– Empiric coverage by MDR risk + severity (per IDSA/ATS HAP/VAP guidance + local antibiogram):
• Antipseudomonal beta-lactam: this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam (alternatives: meropenem 1 g IV q8h); + metronidazole 500 mg IV q8h if anaerobic coverage is indicated
• MRSA coverage (if MRSA risk, high local MRSA prevalence, or severe): vancomycin 15–20 mg/kg IV q8–12h (target AUC/trough) OR linezolid 600 mg IV q12h
• Double antipseudomonal (second gram-negative agent — e.g. an aminoglycoside or antipseudomonal fluoroquinolone) only for high MDR risk / septic shock / high local resistance, then narrow to one once susceptibilities return
– Supportive care: O2/ventilatory support; fluids/vasopressors for sepsis; manage the ventilator (lung-protective settings if ARDS); VAP-prevention bundle (head-of-bed elevation, sedation interruption/spontaneous breathing trials, oral care, DVT/stress-ulcer prophylaxis)
– De-escalate aggressively at 48–72h: narrow to the cultured organism's susceptibilities; stop MRSA coverage if MRSA nares PCR negative and no MRSA isolated; stop the second gram-negative agent once one active drug is confirmed; use procalcitonin/clinical response to support stopping
– Duration usually 7 days for most HAP/VAP with good clinical response (longer for non-fermenting GNR like Pseudomonas, empyema, abscess, or slow response)
– The defining move in HAP/VAP is getting a good lower-respiratory culture up front so you can de-escalate — empiric breadth is justified, but staying broad blindly drives resistance, C. diff, and toxicity. MRSA-nares-negative is your permission slip to stop vancomycin.
– PT/OT: early mobilization (especially ventilated/ICU); prevent deconditioning
– Trend: O2/ventilator requirements, P/F ratio, fever/WBC, lactate, secretions, renal function + drug levels, culture/susceptibility results, response by 48–72h
– Escalation triggers: worsening respiratory failure → escalate support/intubation + ICU; septic shock → vasopressors + ICU; non-response at 72h → repeat imaging/cultures, consider resistant organism/empyema/abscess/wrong diagnosis, ID input
– Discharge when: clinically improved, off escalating support, afebrile/stable, able to complete therapy (IV→PO when an active oral agent exists and patient stable); define total duration, arrange follow-up, ID involvement for OPAT if prolonged IV needed; return precautions (recurrent fever, worsening dyspnea, new symptoms)
103. Healthcare-Associated Pneumonia (HAP / VAP)
complete reference · hospital-acquired and ventilator-associated · MDR-directed empiric therapy by individual risk · aggressive culture-based de-escalation · Full Card
Symptoms / Associated Sx
New or worsening cough, purulent secretions, fever, dyspnea, and hypoxemia with a new or progressive infiltrate, developing 48 hours or more after admission (HAP) or more than 48 hours after intubation (VAP)
In ventilated patients, increased secretions, worsening oxygenation or ventilator requirements, and fever or leukocytosis
The defining feature is the healthcare exposure that shifts the likely organisms toward resistant pathogens
Neg
Pt denies symptom onset before or at the time of admission — that would define community-acquired rather than hospital-acquired pneumonia
Pt denies orthopnea, paroxysmal nocturnal dyspnea, and edema — argues against heart failure
Pt denies sudden pleuritic dyspnea — argues against pulmonary embolism
Pt denies findings fully explained by atelectasis or an effusion alone without true infection
Social History (SHx)
Recent or current hospitalization, ICU stay, or mechanical ventilation
Recent IV antibiotics, which select for resistance, and any prior multidrug-resistant colonization or infection
Immunosuppression; note that the older "HCAP" category has been retired in favor of individual risk stratification
Main Etiology
Aerobic gram-negative bacilli — Pseudomonas aeruginosa, Klebsiella, Enterobacter, Acinetobacter, and E. coli
Staphylococcus aureus including MRSA
Resistant organisms are more likely with risk factors, and VAP is frequently polymicrobial
RF
Risk factors for MDR organisms: IV antibiotics within 90 days, five or more days of hospitalization before onset, septic shock at onset, preceding ARDS, acute renal replacement therapy, prior MDR colonization, structural lung disease, and high local resistance rates
Data
Chest radiograph or CT (a new or progressive infiltrate)
CBC, BMP, and lactate
Blood cultures times two and lower respiratory secretions for Gram stain and culture — sputum, or an endotracheal aspirate or BAL in ventilated patients (obtained before or with antibiotic initiation, since they guide the essential de-escalation)
Oximetry, ABG, and the P/F ratio
An MRSA nares PCR (its high negative predictive value supports stopping vancomycin), procalcitonin as a de-escalation adjunct, and the local antibiogram
DDx
Community-acquired pneumonia (onset before 48 hours) · aspiration (an event, dependent segments) · heart failure or volume overload (BNP, diuretic response) · pulmonary embolism (CTA) · ARDS (bilateral infiltrates, P/F ratio) · atelectasis (post-operative, resolves with recruitment) · ventilator-associated tracheobronchitis (no new infiltrate)
Home Meds
Reconcile recent antibiotic exposures to inform the empiric choice (avoid the recently used class)
Renally dose-adjust vancomycin and aminoglycosides with level monitoring
Ensure VTE and stress-ulcer prophylaxis and review for drug interactions
Plan
CONSULT: Infectious Disease (MDR organisms, treatment failure, de-escalation) · Pulmonology/Critical care (VAP, bronchoscopy and BAL, respiratory failure) · ICU (septic shock, ventilation) · Pharmacy (PK/PD dosing)
Obtain lower respiratory and blood cultures, then start empiric antibiotics promptly — cultures are essential because de-escalation is the entire strategy
Empiric coverage by MDR risk and severity (per IDSA/ATS HAP/VAP guidance and the local antibiogram): an antipseudomonal beta-lactam — this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam (alternative meropenem 1 g IV q8h), with metronidazole 500 mg IV q8h if anaerobic coverage is indicated
MRSA coverage for MRSA risk, high local prevalence, or severe disease: vancomycin 15–20 mg/kg IV q8–12h dosed to target, or linezolid 600 mg IV q12h
A second antipseudomonal gram-negative agent (an aminoglycoside or antipseudomonal fluoroquinolone) only for high MDR risk, septic shock, or high local resistance, then narrowed to one agent once susceptibilities return
Supportive care: oxygen and ventilatory support, fluids and vasopressors for sepsis, lung-protective ventilator settings if ARDS, and the VAP-prevention bundle (head-of-bed elevation, sedation interruption and spontaneous breathing trials, oral care, DVT and stress-ulcer prophylaxis)
De-escalate aggressively at 48–72 hours: narrow to the cultured organism's susceptibilities, stop MRSA coverage when the MRSA nares PCR is negative and no MRSA is isolated, drop the second gram-negative agent once one active drug is confirmed, and use procalcitonin and clinical response to support stopping
Duration is usually 7 days for most HAP/VAP with a good response, extended for non-fermenting gram-negatives such as Pseudomonas, empyema, abscess, or slow improvement
PT/OT: early mobilization, particularly in ventilated and ICU patients
Trend: oxygen and ventilator requirements, P/F ratio, fever and white count, lactate, secretions, renal function and drug levels, culture and susceptibility results, and the response by 48–72 hours
Escalation triggers: worsening respiratory failure → escalation of support or intubation and ICU; septic shock → vasopressors and ICU; non-response at 72 hours → repeat imaging and cultures, consider a resistant organism, empyema, abscess, or wrong diagnosis, with ID input
Discharge criteria: clinical improvement off escalating support, afebrile and stable, able to complete therapy (transitioning IV to oral when an active oral agent exists and the patient is stable); define the total duration, arrange follow-up, and involve ID for outpatient parenteral therapy when prolonged IV treatment is needed, with return precautions for recurrent fever, worsening dyspnea, or new symptoms
Red Flags
Septic shock or worsening respiratory failure → ICU and escalation of support
A non-fermenting gram-negative such as Pseudomonas or Acinetobacter → extended, sometimes combination, therapy and ID input
Failure to improve by 72 hours → resistant organism, an undrained empyema or abscess, or an incorrect diagnosis
Recurrent or relapsing VAP → inadequate source control or persistent colonization
Rising vancomycin levels with rising creatinine → nephrotoxicity; adjust and consider linezolid
Senior IM Resident Pearls
Culture before you broaden. A good lower-respiratory sample up front is what makes safe de-escalation possible — without it you're stuck broad.
MRSA-nares-negative means stop the vancomycin. The high negative predictive value is one of the most useful antibiotic-stewardship tools on the floor.
"HCAP" is gone. Risk-stratify each patient for MDR organisms rather than applying a blanket broad regimen to anyone with healthcare contact.
Seven days is usually enough. Most HAP/VAP with a good response needs no more, sparing toxicity and resistance.
Avoid repeating the recent class. If they had a cephalosporin last week, the resistant organism likely already survived it — pick a different mechanism.
The VAP bundle prevents the next case. Head-of-bed elevation, sedation holidays, and oral care are as important as the antibiotic.
Common mistake: starting broad empiric coverage without securing a culture, then having no way to de-escalate and leaving the patient on vancomycin and cefepime for a week unnecessarily.
Pulmonology — Pneumonia
104. COVID-19 / Viral Pneumonia
severity-based therapy: O2 need drives steroids + immunomodulation/antivirals · influenza/RSV/COVID · watch for bacterial co-infection + VTE · Super Compact
Sx: fever, dry or productive cough, dyspnea, myalgia, fatigue, sore throat, anosmia/ageusia (COVID); hypoxemia that can be out of proportion to symptoms ("silent hypoxia") · influenza: abrupt fever/myalgia; RSV: wheeze, esp elderly/immunocompromised · progressive hypoxemia over the first 1–2 weeks in COVID (the oxygen requirement, not the PCR alone, drives the treatment ladder)
Neg: denies orthopnea/PND/edema as the primary driver (CHF) · denies sudden unilateral pleuritic pain + calf swelling (PE — though viral illness is prothrombotic, keep PE on the radar) · denies purulent lobar consolidation suggesting primary bacterial CAP · denies chronic progressive dyspnea/reticular pattern (ILD)
SHx: vaccination status (COVID/influenza) · immunosuppression (severity, prolonged shedding) · exposures/outbreak/sick contacts · pregnancy (higher risk) · timing from symptom onset (antiviral windows)
Etiology: SARS-CoV-2 · influenza A/B · RSV · other respiratory viruses (parainfluenza, metapneumovirus, adenovirus) · bacterial co-infection/superinfection (esp Staph aureus post-influenza) · COVID pathophysiology: viral replication phase early, then host hyperinflammatory phase driving severe hypoxemia
RF for severe disease: age · obesity · diabetes · cardiovascular/pulmonary/kidney disease · immunocompromise · pregnancy · unvaccinated · (COVID) male sex
Data: respiratory viral PCR/antigen panel (COVID, influenza, RSV) · CXR/CT (bilateral peripheral ground-glass — COVID; viral interstitial pattern; assess for bacterial consolidation) · SpO2/ABG, P/F ratio · CBC (lymphopenia — COVID) · inflammatory markers (CRP, ferritin, D-dimer, LDH — trend severity) · BMP, LFTs, troponin/BNP if cardiac concern · blood/sputum cultures + procalcitonin if bacterial co-infection suspected · D-dimer (VTE risk)
DDx: bacterial CAP (lobar, purulent, procalcitonin) · CHF (BNP, response to diuresis) · PE (CTA — viral illness is prothrombotic) · ARDS from other cause (P/F, bilateral) · ILD (chronic) · drug/hypersensitivity pneumonitis
Home Meds: continue chronic cardiopulmonary meds unless contraindicated · review immunosuppressants (may need adjustment — ID/specialty input) · check interactions (e.g. nirmatrelvir-ritonavir has major drug interactions) · ensure VTE prophylaxis · reconcile inhalers
Plan
CONSULT: Infectious Disease (antiviral/immunomodulator selection, immunocompromised, severe) · Pulmonology/Critical care (respiratory failure, ARDS) · ICU (high-flow/NIV/intubation) · Pharmacy (drug interactions, dosing)
– First, grade severity by oxygenation (this drives the COVID treatment ladder): no O2 need vs low-flow O2 vs high-flow/NIV vs mechanical ventilation/ECMO
– COVID-19, severity-based (per current NIH/IDSA guidance — verify, as recommendations evolve):
• Hospitalized, on supplemental O2: dexamethasone 6 mg IV/PO daily (up to 10 days or until discharge)
• Antiviral (remdesivir) — consider in hospitalized patients, greatest benefit earlier and on low-flow O2; per current guidance
• Add immunomodulation (e.g. baricitinib or tocilizumab) for those with rapidly increasing O2 needs and systemic inflammation, on top of steroids, per current criteria
• Early/mild high-risk outpatients (context): nirmatrelvir-ritonavir within the window — note major drug interactions
– Influenza: oseltamivir 75 mg PO BID ×5 days (start empirically in hospitalized/severe regardless of duration of symptoms)
– Supportive care: oxygen — titrate; escalate through nasal cannula → high-flow nasal cannula → NIV → intubation; consider awake proning for hypoxemic non-intubated patients; conservative fluids
– Anticoagulation: VTE prophylaxis for all admitted patients (viral pneumonia, especially COVID, is prothrombotic); therapeutic anticoagulation only for confirmed/suspected VTE or per specific protocols
– Evaluate for bacterial co-infection: don't reflexively give antibiotics — true bacterial co-infection at presentation is relatively uncommon; use cultures/procalcitonin/clinical picture, treat if evidence (post-influenza Staph, focal consolidation)
– The oxygen requirement, not the positive PCR, drives therapy: steroids once they need oxygen, antivirals earlier, immunomodulators when inflammation is escalating. Resist starting antibiotics for every viral pneumonia — but keep PE and bacterial superinfection on the radar.
– PT/OT: mobilization as tolerated; proning support; rehab planning for prolonged courses
– Trend: O2 requirement/P-F ratio, work of breathing, inflammatory markers (CRP/ferritin/D-dimer), response to therapy, signs of secondary infection
– Escalation triggers: rising O2 needs/worsening P:F → high-flow/NIV/ICU; refractory hypoxemia → intubation/ARDS management/ECMO evaluation; deterioration → reassess for PE, bacterial superinfection, cardiac involvement
– Discharge when: stable oxygenation on room air or baseline O2 (or established home O2 plan), improving, able to manage at home; complete steroid course as indicated, arrange follow-up, isolation guidance, home O2 setup + pulmonary rehab referral if indicated; return precautions (worsening dyspnea, chest pain, low O2 saturations at home)
104. COVID-19 / Viral Pneumonia
complete reference · severity-driven steroids, antivirals, and immunomodulation · oxygen-escalation ladder · prothrombotic risk and bacterial co-infection · Full Card
Symptoms / Associated Sx
Fever, a dry or productive cough, dyspnea, myalgia, fatigue, sore throat, and anosmia or ageusia (COVID-19)
Hypoxemia that can be out of proportion to symptoms ("silent hypoxia"), with progressive hypoxemia over the first one to two weeks in COVID-19
Influenza presents with abrupt fever and myalgia; RSV often causes wheezing, especially in the elderly and immunocompromised
Neg
Pt denies orthopnea, paroxysmal nocturnal dyspnea, and edema as the primary driver — argues against heart failure
Pt denies sudden unilateral pleuritic pain with calf swelling — argues against pulmonary embolism, though viral illness is prothrombotic and PE stays on the radar
Pt denies purulent lobar consolidation suggesting a primary bacterial pneumonia
Pt denies a chronic progressive dyspnea with a reticular pattern — argues against interstitial lung disease
Social History (SHx)
Vaccination status for COVID-19 and influenza, and any immunosuppression (greater severity and prolonged shedding)
Exposures, outbreaks, or sick contacts, and pregnancy (higher risk)
Timing from symptom onset, which determines antiviral eligibility windows
Main Etiology
SARS-CoV-2, influenza A and B, and RSV, along with other respiratory viruses (parainfluenza, metapneumovirus, adenovirus)
Bacterial co-infection or superinfection, especially Staphylococcus aureus after influenza
COVID-19 pathophysiology evolves from an early viral replication phase to a host hyperinflammatory phase that drives severe hypoxemia
RF
Risk factors for severe disease: advanced age, obesity, diabetes, cardiovascular, pulmonary, and kidney disease, immunocompromise, pregnancy, and being unvaccinated
Data
A respiratory viral PCR or antigen panel (COVID-19, influenza, RSV)
Chest radiograph or CT (bilateral peripheral ground-glass opacities in COVID-19; a viral interstitial pattern; assess for bacterial consolidation)
Oximetry, ABG, and the P/F ratio, and CBC (lymphopenia in COVID-19)
Inflammatory markers (CRP, ferritin, D-dimer, LDH to trend severity), with BMP, LFTs, and troponin or BNP if there is cardiac concern
Blood and sputum cultures with procalcitonin if bacterial co-infection is suspected, and a D-dimer for VTE risk
DDx
Bacterial community-acquired pneumonia (lobar, purulent, elevated procalcitonin) · heart failure (BNP, response to diuresis) · pulmonary embolism (CTA — viral illness is prothrombotic) · ARDS from another cause (P/F ratio, bilateral infiltrates) · interstitial lung disease (chronic) · drug or hypersensitivity pneumonitis
Home Meds
Continue chronic cardiopulmonary medications unless contraindicated
Review immunosuppressants, which may need adjustment with ID or specialty input
Check drug interactions (nirmatrelvir-ritonavir has major interactions), ensure VTE prophylaxis, and reconcile inhalers
Plan
CONSULT: Infectious Disease (antiviral and immunomodulator selection, immunocompromised or severe disease) · Pulmonology/Critical care (respiratory failure, ARDS) · ICU (high-flow oxygen, NIV, intubation) · Pharmacy (drug interactions and dosing)
Grade severity by oxygenation first, since this drives the COVID-19 treatment ladder: no oxygen need, low-flow oxygen, high-flow or noninvasive ventilation, or mechanical ventilation and ECMO
COVID-19, severity-based (per current NIH and IDSA guidance, which should be verified as it evolves): for hospitalized patients on supplemental oxygen, dexamethasone 6 mg IV or PO daily for up to 10 days or until discharge
An antiviral (remdesivir) is considered in hospitalized patients, with greatest benefit earlier and on low-flow oxygen, per current guidance
Add immunomodulation (baricitinib or tocilizumab) on top of steroids for rapidly increasing oxygen needs and systemic inflammation, per current criteria; for early high-risk outpatients, nirmatrelvir-ritonavir within the window, noting major drug interactions
Influenza: oseltamivir 75 mg PO BID for 5 days, started empirically in hospitalized or severe cases regardless of symptom duration
Supportive care: titrate oxygen and escalate through nasal cannula, high-flow nasal cannula, noninvasive ventilation, and intubation; consider awake proning for hypoxemic non-intubated patients; and use conservative fluid management
Anticoagulation: VTE prophylaxis for all admitted patients, as viral pneumonia and especially COVID-19 are prothrombotic, with therapeutic anticoagulation reserved for confirmed or suspected VTE or specific protocols
Evaluate for bacterial co-infection rather than reflexively giving antibiotics — true co-infection at presentation is relatively uncommon; use cultures, procalcitonin, and the clinical picture, and treat when there is evidence such as post-influenza Staphylococcus or focal consolidation
PT/OT: mobilization as tolerated, proning support, and rehabilitation planning for prolonged courses
Trend: oxygen requirement and P/F ratio, work of breathing, inflammatory markers, response to therapy, and signs of secondary infection
Escalation triggers: rising oxygen needs or worsening P/F ratio → high-flow oxygen, NIV, and ICU; refractory hypoxemia → intubation, ARDS management, and ECMO evaluation; deterioration → reassess for PE, bacterial superinfection, and cardiac involvement
Discharge criteria: stable oxygenation on room air or baseline oxygen (or an established home oxygen plan), clinical improvement, and the ability to manage at home; complete the steroid course as indicated, arrange follow-up and isolation guidance, set up home oxygen and pulmonary rehabilitation when indicated, and give return precautions for worsening dyspnea, chest pain, or low home oxygen saturations
Red Flags
Rapidly rising oxygen needs with escalating inflammatory markers → the hyperinflammatory phase; escalate immunomodulation and level of care
Silent hypoxia — profound desaturation with minimal distress → can deteriorate quickly; monitor closely
Acute deterioration → reconsider pulmonary embolism, given the prothrombotic state
Refractory hypoxemia despite maximal support → ARDS; lung-protective ventilation and ECMO evaluation
New focal consolidation with purulent sputum after influenza → bacterial superinfection, often Staphylococcus
Senior IM Resident Pearls
Oxygen need drives the ladder. Steroids once they need oxygen, antivirals earlier, and immunomodulators when inflammation is climbing — the PCR alone doesn't set therapy.
Don't give steroids to the non-hypoxemic. Dexamethasone helps those on oxygen and may harm those who aren't — match the drug to the phase.
Resist reflexive antibiotics. Bacterial co-infection at presentation is uncommon; let cultures, procalcitonin, and the picture decide.
Viral pneumonia clots. Prophylactic anticoagulation for everyone admitted, and keep PE in mind when they deteriorate.
Awake proning can buy time. In the hypoxemic non-intubated patient it can improve oxygenation and delay or avoid intubation.
Mind the interactions. Nirmatrelvir-ritonavir interacts with a long list of common drugs — check before prescribing.
Common mistake: treating the test instead of the patient — starting antibiotics and steroids on a well-oxygenated viral pneumonia, or missing the PE behind a sudden decompensation.
Pulmonology — Obstructive Airway Disease
105. COPD Exacerbation
bronchodilators + systemic steroids + antibiotics (if increased purulence) · controlled O2 (88–92%) · NIV for hypercapnic failure · find the trigger · Super Compact
Sx: the cardinal triad — increased dyspnea, increased sputum volume, increased sputum purulence · increased cough/wheeze, chest tightness, prolonged expiration, accessory muscle use, pursed-lip breathing · severe: cyanosis, drowsiness (CO2 narcosis), hemodynamic compromise (define the exacerbation by the change from baseline, and always look for the precipitant)
Neg: denies orthopnea/PND/progressive edema (CHF, which coexists/mimics) · denies sudden unilateral pleuritic pain + calf swelling (PE — a common, easily missed trigger/mimic) · denies sudden severe dyspnea + chest pain (pneumothorax — secondary spontaneous risk) · denies fever + focal consolidation as primary (pneumonia) · denies chest pain + ECG changes (ACS)
SHx: smoking (pack-years, current status) · occupational/environmental exposures · home O2/NIV use · baseline functional status + prior exacerbations/hospitalizations/intubations (predicts severity) · vaccination status · medication adherence/inhaler technique
Etiology (triggers): respiratory infection (viral or bacterial — Haemophilus, pneumococcus, Moraxella; the most common trigger) · air pollution/environmental · medication noncompliance/poor inhaler technique · concurrent illness (PE, CHF, pneumonia, ACS) — exclude these mimics/co-triggers
RF: ongoing smoking · severe underlying COPD (low FEV1) · frequent prior exacerbations · comorbidities (CHF, PE risk) · poor adherence · winter/viral season
Data: ABG (define respiratory failure + hypercapnia + acidosis — pH guides NIV; compare to baseline CO2) · CXR (exclude pneumonia, pneumothorax, effusion, CHF) · ECG (arrhythmia, ischemia, cor pulmonale) · CBC, BMP · BNP (if CHF unclear) · D-dimer/CTA (if PE suspected — significant minority of "exacerbations" are PE) · sputum culture (if frequent exacerbations/severe/poor response) · respiratory viral PCR · SpO2/telemetry
DDx: CHF/pulmonary edema (BNP, orthopnea, response to diuresis) · PE (CTA — must exclude in unexplained/refractory) · pneumonia (consolidation, fever) · pneumothorax (CXR) · ACS (ECG, troponin) · asthma (reversibility, history)
Home Meds: continue/optimize maintenance inhalers (LABA/LAMA/ICS) · resume home O2/NIV with adjusted settings · reconcile cardiac meds · ensure VTE prophylaxis (immobility + COPD prothrombotic) · avoid excessive sedation (CO2 retention risk); careful with benzodiazepines/opioids
Plan
CONSULT: Pulmonology (severe, frequent exacerbations, NIV failure, chronic management) · ICU/Critical care (hypercapnic respiratory failure failing NIV, hemodynamic instability) · Respiratory therapy (nebs, NIV titration)
– Bronchodilators (cornerstone): short-acting beta-agonist + short-acting anticholinergic — albuterol 2.5 mg + ipratropium 0.5 mg nebulized q4–6h (or more frequently/continuous for severe); transition to/continue maintenance inhalers
– Systemic corticosteroids: prednisone 40 mg PO daily ×5 days (IV methylprednisolone if unable to take PO); shortens recovery and reduces relapse — 5 days is sufficient for most
– Antibiotics (when indicated): give for increased sputum purulence PLUS increased dyspnea or sputum volume, or if mechanically ventilated · azithromycin 500 mg daily, OR doxycycline, OR amoxicillin-clavulanate; escalate (e.g. respiratory fluoroquinolone, or antipseudomonal coverage — this institution uses cefepime in place of pip-tazo) for severe disease, frequent exacerbations, or Pseudomonas risk (bronchiectasis, prior isolation) · usually 5–7 days
– Controlled oxygen: target SpO2 88–92% — titrate carefully to avoid CO2 retention/narcosis (over-oxygenation suppresses hypoxic drive and worsens V/Q matching); use a Venturi mask for precise control if needed
– Noninvasive ventilation (NIV/BiPAP): for acute hypercapnic respiratory failure (pH <7.35 with PaCO2 >45) — the key intervention that reduces intubation and mortality; start early; monitor response (pH, CO2, work of breathing); intubate if NIV fails or contraindicated (decreased consciousness, hemodynamic instability, inability to protect airway)
– Identify + treat the trigger: evaluate for and exclude PE, CHF, pneumonia, ACS, pneumothorax (these masquerade as or coexist with exacerbations)
– Avoid respiratory depressants: minimize sedatives/opioids/benzodiazepines that worsen hypercapnia
– The combination that changes outcomes: bronchodilators + steroids + (selective) antibiotics + controlled O2 to 88–92% + early NIV for hypercapnic acidosis. And always ask what triggered it — a meaningful fraction of refractory "COPD exacerbations" are actually PE, CHF, or pneumonia.
– PT/OT + pulmonary rehab referral: mobilize; refer to pulmonary rehabilitation (reduces future exacerbations/readmissions)
– Trend: ABG/pH/CO2, SpO2, work of breathing, response to NIV, mental status, trigger workup results
– Escalation triggers: worsening acidosis/CO2 or failing NIV → intubation + ICU; declining mental status (CO2 narcosis) → ICU; hemodynamic instability → ICU; unexplained refractory course → re-evaluate for PE/other
– Discharge when: back near baseline, stable on room air or home O2, tolerating oral meds + maintenance inhalers (confirm technique); ensure 5-day steroid + antibiotic course defined, inhaler optimization, smoking cessation, vaccinations, pulmonary rehab referral, early follow-up (reduces readmission), action plan; return precautions (worsening dyspnea, purulent sputum, fever, drowsiness)
105. COPD Exacerbation
complete reference · bronchodilators, systemic steroids, selective antibiotics · controlled oxygen to 88–92% · early NIV for hypercapnic failure · trigger workup · Full Card
Symptoms / Associated Sx
The cardinal triad of increased dyspnea, increased sputum volume, and increased sputum purulence, defined by the change from the patient's baseline
Increased cough and wheeze, chest tightness, prolonged expiration, accessory muscle use, and pursed-lip breathing
Severe disease brings cyanosis, drowsiness from CO2 narcosis, and hemodynamic compromise
Neg
Pt denies orthopnea, paroxysmal nocturnal dyspnea, and progressive edema — argues against heart failure, which often coexists and mimics
Pt denies sudden unilateral pleuritic pain with calf swelling — argues against pulmonary embolism, a common and easily missed trigger or mimic
Pt denies sudden severe dyspnea with chest pain — argues against a secondary spontaneous pneumothorax
Pt denies fever with focal consolidation as the primary process and denies chest pain with ECG changes (acute coronary syndrome)
Social History (SHx)
Smoking history including pack-years and current status, and occupational or environmental exposures
Home oxygen or noninvasive ventilation use, and baseline functional status with prior exacerbations, hospitalizations, and intubations (which predict severity)
Vaccination status and medication adherence with inhaler technique
Main Etiology
Respiratory infection — viral or bacterial (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis), the most common trigger
Air pollution and environmental exposures
Medication noncompliance and poor inhaler technique
Concurrent illness — pulmonary embolism, heart failure, pneumonia, and acute coronary syndrome, which must be excluded as mimics or co-triggers
RF
Modifiable: ongoing smoking, poor adherence, and inhaler technique
Non-modifiable: severe underlying COPD with a low FEV1, frequent prior exacerbations, and comorbidities such as heart failure and PE risk
Data
ABG (defines respiratory failure, hypercapnia, and acidosis; the pH guides NIV; compare with the baseline CO2)
Chest radiograph (to exclude pneumonia, pneumothorax, effusion, and heart failure) and ECG (arrhythmia, ischemia, cor pulmonale)
CBC, BMP, and a BNP (when heart failure is unclear)
A D-dimer or CTA (when PE is suspected — a significant minority of apparent exacerbations are PE)
Sputum culture for frequent, severe, or poorly responding exacerbations, a respiratory viral PCR, and oximetry with telemetry
DDx
Heart failure or pulmonary edema (BNP, orthopnea, response to diuresis) · pulmonary embolism (CTA — must be excluded in unexplained or refractory cases) · pneumonia (consolidation, fever) · pneumothorax (CXR) · acute coronary syndrome (ECG, troponin) · asthma (reversibility, history)
Home Meds
Continue and optimize maintenance inhalers (LABA, LAMA, ICS) and resume home oxygen or NIV with adjusted settings
Reconcile cardiac medications and ensure VTE prophylaxis (immobility and COPD are prothrombotic)
Avoid excessive sedation given the CO2-retention risk, and use caution with benzodiazepines and opioids
Plan
CONSULT: Pulmonology (severe or frequent exacerbations, NIV failure, chronic management) · ICU/Critical care (hypercapnic respiratory failure failing NIV, hemodynamic instability) · Respiratory therapy (nebulizers, NIV titration)
Bronchodilators are the cornerstone: a short-acting beta-agonist plus a short-acting anticholinergic — albuterol 2.5 mg with ipratropium 0.5 mg nebulized every 4–6 hours, more frequently or continuously for severe disease — transitioning to or continuing maintenance inhalers
Systemic corticosteroids: prednisone 40 mg PO daily for 5 days (IV methylprednisolone if unable to take oral), which shortens recovery and reduces relapse, with 5 days sufficient for most
Antibiotics when indicated: for increased sputum purulence plus increased dyspnea or sputum volume, or if mechanically ventilated — azithromycin 500 mg daily, doxycycline, or amoxicillin-clavulanate; escalate (a respiratory fluoroquinolone, or antipseudomonal coverage with cefepime in place of piperacillin-tazobactam at this institution) for severe disease, frequent exacerbations, or Pseudomonas risk, usually for 5–7 days
Controlled oxygen: target SpO2 88–92%, titrated carefully to avoid CO2 retention and narcosis, since over-oxygenation suppresses the hypoxic drive and worsens V/Q matching; use a Venturi mask for precise control when needed
Noninvasive ventilation: for acute hypercapnic respiratory failure (pH below 7.35 with a PaCO2 above 45) — the key intervention that reduces intubation and mortality; start early and monitor the response, intubating if NIV fails or is contraindicated (decreased consciousness, hemodynamic instability, inability to protect the airway)
Identify and treat the trigger: evaluate for and exclude PE, heart failure, pneumonia, ACS, and pneumothorax
Avoid respiratory depressants that worsen hypercapnia
PT/OT and pulmonary rehabilitation: mobilize and refer to pulmonary rehabilitation, which reduces future exacerbations and readmissions
Trend: ABG with pH and CO2, oxygen saturation, work of breathing, the response to NIV, mental status, and the trigger workup
Escalation triggers: worsening acidosis or CO2 or failing NIV → intubation and ICU; declining mental status from CO2 narcosis → ICU; hemodynamic instability → ICU; an unexplained refractory course → re-evaluate for PE or another cause
Discharge criteria: a return near baseline, stable on room air or home oxygen, and tolerating oral medications and maintenance inhalers with confirmed technique; define the 5-day steroid and antibiotic courses, optimize inhalers, address smoking cessation and vaccinations, refer to pulmonary rehabilitation, arrange early follow-up (which reduces readmission), and provide an action plan with return precautions for worsening dyspnea, purulent sputum, fever, or drowsiness
Red Flags
A pH below 7.35 with hypercapnia → acute hypercapnic respiratory failure; start NIV early
Drowsiness or a declining mental status → CO2 narcosis; this is an ICU situation, not a reason for more oxygen
Refractory or unexplained exacerbation → exclude pulmonary embolism, which masquerades as a COPD flare
Sudden severe dyspnea with chest pain → secondary spontaneous pneumothorax
Falling oxygen saturation despite rising delivered oxygen, with rising CO2 → over-oxygenation suppressing the respiratory drive
Senior IM Resident Pearls
Target 88–92%, not higher. Over-oxygenating a COPD retainer raises CO2 and can tip them into narcosis — the saturation goal is deliberately modest.
NIV is the mortality intervention. Early BiPAP for hypercapnic acidosis prevents intubations and saves lives — start it before the patient tires.
Five days of steroids is enough. Longer courses add side effects without benefit for most exacerbations.
Antibiotics are selective. Increased purulence plus another cardinal symptom, or ventilation — not every flare needs them.
Always ask what triggered it. A meaningful fraction of refractory "exacerbations" are actually PE, heart failure, or pneumonia hiding in plain sight.
Pulmonary rehab and early follow-up reduce readmission. The discharge plan matters as much as the inpatient treatment.
Common mistake: cranking up the oxygen to "fix" the saturation in a retainer and precipitating CO2 narcosis, or never working up the PE behind a flare that won't improve.
Pulmonology — Obstructive Airway Disease
106. Asthma Exacerbation
SABA + ipratropium + early systemic steroids · magnesium for severe · the silent chest / rising CO2 / fatigue = impending failure → ICU · Super Compact
Sx: progressive dyspnea, wheeze, cough, chest tightness · tachypnea, prolonged expiration, accessory muscle use, inability to speak full sentences · severe/life-threatening: silent chest (no air movement), drowsiness/confusion, exhaustion, cyanosis, paradoxical breathing, normalizing or rising PaCO2 (a "normal" CO2 in a tiring asthmatic is ominous — they should be hyperventilating)
Neg: denies orthopnea/PND/edema (CHF — "cardiac asthma") · denies sudden pleuritic pain + calf swelling (PE) · denies sudden severe dyspnea + chest pain (pneumothorax — risk in severe asthma/barotrauma) · denies fever + focal consolidation (pneumonia trigger) · denies stridor/upper-airway obstruction (vocal cord dysfunction, anaphylaxis, foreign body)
SHx: asthma history + control (prior ICU/intubation = high risk) · triggers (allergens, viral URI, smoke, exercise, NSAIDs, beta-blockers) · adherence + inhaler technique · ICS use · smoking · recent oral steroid courses/ED visits
Etiology (triggers): viral respiratory infection (most common) · allergen exposure · poor controller adherence · irritants/smoke/pollution · medication (NSAIDs/aspirin in aspirin-sensitive, non-selective beta-blockers) · exercise/cold air · GERD
RF for fatal/near-fatal asthma: prior intubation/ICU admission · ≥2 hospitalizations or >3 ED visits in the past year · recent/frequent SABA use · poor adherence/perception of symptoms · psychosocial factors · food allergy
Data: peak expiratory flow (PEF) or FEV1 (grade severity + track response — % predicted/personal best) · SpO2 · ABG (if severe — a normal/rising PaCO2 signals fatigue/impending failure; early it's low from hyperventilation) · CXR (if atypical/severe — exclude pneumonia, pneumothorax) · CBC, BMP · consider trigger workup · continuous monitoring
DDx: COPD exacerbation (older, smoker, less reversible) · CHF/cardiac asthma (BNP, orthopnea) · PE (CTA) · pneumothorax (CXR) · anaphylaxis (urticaria, exposure, hypotension) · vocal cord dysfunction (inspiratory stridor, flat inspiratory loop) · upper airway obstruction/foreign body
Home Meds: continue/escalate inhaled controller (ICS or ICS-LABA) · avoid triggers (NSAIDs, non-selective beta-blockers) · ensure proper inhaler/spacer technique · reconcile and resume appropriate maintenance at discharge with step-up
Plan
CONSULT: Pulmonology (severe, refractory, recurrent, chronic management) · ICU/Critical care (impending respiratory failure, rising CO2, exhaustion) · Anesthesia (difficult intubation planning if deteriorating)
– Inhaled bronchodilators (first-line, immediately): short-acting beta-agonist — albuterol by nebulizer (2.5–5 mg) or MDI with spacer, frequent or continuous for severe; add ipratropium 0.5 mg nebulized (combined with albuterol) for moderate–severe exacerbations
– Systemic corticosteroids early (within the first hour): prednisone 40–60 mg PO daily (or IV methylprednisolone 40–125 mg if unable to take PO/severe); typical course 5–7 days, no taper needed for short courses
– Oxygen: titrate to SpO2 ≥93–95% (asthma, unlike COPD, generally targets normal saturation)
– Magnesium sulfate IV (severe/life-threatening): 2 g IV over 20 minutes for severe exacerbations not responding to initial therapy (bronchodilation, reduces admissions in severe cases)
– Reassess frequently with PEF + clinical status; escalate for poor response
– Severe/refractory adjuncts: consider IV magnesium (above), heliox, IV beta-agonist (specialist settings); watch for impending respiratory failure
– Impending respiratory failure (silent chest, exhaustion, drowsiness, rising/normalizing CO2): ICU; prepare for intubation — this is a high-risk intubation (use an experienced operator, ketamine for bronchodilation, anticipate dynamic hyperinflation/auto-PEEP → use low respiratory rate, prolonged expiratory time, permissive hypercapnia, watch for breath-stacking and barotrauma/pneumothorax); NIV is not a substitute for intubation when failing and is used cautiously
– Treat the trigger (viral, allergen, infection if present — antibiotics only if bacterial infection evidence)
– The danger sign is a tiring asthmatic whose CO2 is "normalizing" — early in an attack they hyperventilate (low CO2), so a rising or normal PaCO2 with fatigue and a quiet chest means impending arrest. Don't be reassured; escalate to ICU and prepare to intubate. Steroids go in within the first hour for everyone.
– PT/OT: mobilize once stable; education on technique
– Trend: PEF/FEV1, SpO2, work of breathing, mental status, ABG (CO2 trend) in severe, response to bronchodilators
– Escalation triggers: silent chest/rising CO2/exhaustion/drowsiness → ICU + intubation prep; poor PEF response → escalate therapy/admit; pneumothorax → decompression
– Discharge when: PEF improved (typically >70% predicted/personal best), stable on room air, good response sustained off frequent SABA, technique confirmed; provide oral steroid course, step up controller therapy (start/intensify ICS), inhaler/spacer technique teaching, written asthma action plan, trigger avoidance, early follow-up; return precautions (worsening dyspnea, poor SABA response, inability to speak, drowsiness)
106. Asthma Exacerbation
complete reference · SABA plus ipratropium, early systemic steroids, magnesium for severe · recognizing impending respiratory failure · high-risk intubation physiology · Full Card
Symptoms / Associated Sx
Progressive dyspnea, wheeze, cough, and chest tightness with tachypnea, prolonged expiration, accessory muscle use, and an inability to speak in full sentences
Severe or life-threatening features — a silent chest with no air movement, drowsiness or confusion, exhaustion, cyanosis, paradoxical breathing, and a normalizing or rising PaCO2
A "normal" CO2 in a tiring asthmatic is ominous, because they should be hyperventilating
Neg
Pt denies orthopnea, paroxysmal nocturnal dyspnea, and edema — argues against heart failure ("cardiac asthma")
Pt denies sudden pleuritic pain with calf swelling — argues against pulmonary embolism
Pt denies sudden severe dyspnea with chest pain — argues against a pneumothorax, a risk in severe asthma and from barotrauma
Pt denies inspiratory stridor or upper-airway symptoms — argues against vocal cord dysfunction, anaphylaxis, or a foreign body
Social History (SHx)
Asthma history and control, with prior ICU admission or intubation marking high risk
Triggers (allergens, viral URI, smoke, exercise, NSAIDs, beta-blockers), adherence, and inhaler technique
Inhaled corticosteroid use, smoking, and recent oral steroid courses or ED visits
Main Etiology
Viral respiratory infection, the most common trigger, and allergen exposure
Poor controller adherence and irritants such as smoke and pollution
Medications (NSAIDs or aspirin in aspirin-sensitive disease, non-selective beta-blockers), exercise and cold air, and GERD
RF
Risk factors for fatal or near-fatal asthma: prior intubation or ICU admission, two or more hospitalizations or more than three ED visits in the past year, recent or frequent SABA use, poor adherence or poor symptom perception, psychosocial factors, and food allergy
Data
Peak expiratory flow or FEV1 (to grade severity and track the response as a percentage of predicted or personal best)
Oximetry, and an ABG in severe disease (a normal or rising PaCO2 signals fatigue and impending failure; early in an attack it is low from hyperventilation)
A chest radiograph (in atypical or severe presentations, to exclude pneumonia and pneumothorax)
CBC and BMP, consideration of a trigger workup, and continuous monitoring
DDx
COPD exacerbation (older, smoker, less reversible) · heart failure or cardiac asthma (BNP, orthopnea) · pulmonary embolism (CTA) · pneumothorax (CXR) · anaphylaxis (urticaria, exposure, hypotension) · vocal cord dysfunction (inspiratory stridor, a flattened inspiratory loop) · upper airway obstruction or foreign body
Home Meds
Continue and escalate the inhaled controller (an inhaled corticosteroid or ICS-LABA combination)
Avoid triggers such as NSAIDs and non-selective beta-blockers, and ensure proper inhaler and spacer technique
Reconcile and resume appropriate maintenance therapy at discharge with a step-up
Plan
CONSULT: Pulmonology (severe, refractory, recurrent disease, chronic management) · ICU/Critical care (impending respiratory failure, rising CO2, exhaustion) · Anesthesia (difficult-intubation planning if deteriorating)
Inhaled bronchodilators are first-line and immediate: a short-acting beta-agonist (albuterol) by nebulizer (2.5–5 mg) or MDI with spacer, given frequently or continuously for severe disease, with ipratropium 0.5 mg nebulized added for moderate-to-severe exacerbations
Systemic corticosteroids early, within the first hour: prednisone 40–60 mg PO daily (or IV methylprednisolone 40–125 mg if unable to take oral or severe), typically for 5–7 days with no taper needed for short courses
Oxygen titrated to SpO2 93–95% — asthma, unlike COPD, generally targets a normal saturation
IV magnesium sulfate 2 g over 20 minutes for severe or life-threatening exacerbations not responding to initial therapy, which provides bronchodilation and reduces admissions in severe cases
Reassess frequently with peak flow and clinical status, escalating for a poor response
Severe or refractory adjuncts: IV magnesium as above, heliox, and IV beta-agonists in specialist settings, while watching for impending respiratory failure
Impending respiratory failure (silent chest, exhaustion, drowsiness, a rising or normalizing CO2) → ICU and preparation for a high-risk intubation: an experienced operator, ketamine for its bronchodilating effect, and anticipation of dynamic hyperinflation and auto-PEEP — managed with a low respiratory rate, prolonged expiratory time, and permissive hypercapnia, watching for breath-stacking, barotrauma, and pneumothorax; NIV is not a substitute for intubation when the patient is failing and is used cautiously
Treat the trigger (viral, allergen, or infection if present, with antibiotics only when there is evidence of bacterial infection)
PT/OT: mobilize once stable and reinforce inhaler technique
Trend: peak flow or FEV1, oxygen saturation, work of breathing, mental status, the ABG CO2 trend in severe disease, and the response to bronchodilators
Escalation triggers: a silent chest, rising CO2, exhaustion, or drowsiness → ICU and intubation preparation; a poor peak-flow response → escalate therapy and admit; a pneumothorax → decompression
Discharge criteria: an improved peak flow (typically above 70% of predicted or personal best), stable on room air, a sustained response off frequent SABA, and confirmed technique; provide the oral steroid course, step up controller therapy by starting or intensifying an inhaled corticosteroid, teach inhaler and spacer technique, give a written asthma action plan, address trigger avoidance, and arrange early follow-up, with return precautions for worsening dyspnea, a poor SABA response, inability to speak, or drowsiness
Red Flags
A silent chest with no air movement → severe obstruction with minimal ventilation; impending arrest
A normalizing or rising PaCO2 in a fatiguing patient → impending respiratory failure, not improvement
Drowsiness, confusion, or exhaustion → ICU and prepare to intubate
Sudden worsening with chest pain in severe asthma → pneumothorax from barotrauma
A prior intubation or ICU admission for asthma → a marker of near-fatal disease; treat aggressively early
Senior IM Resident Pearls
A normalizing CO2 is a warning, not relief. Early in an attack the asthmatic hyperventilates — a rising or "normal" CO2 with fatigue means they're tiring toward arrest.
Steroids in the first hour, for everyone. Early systemic steroids change the trajectory; don't wait to see if bronchodilators alone work.
Target normal saturation. Unlike COPD, asthma gets oxygen to 93–95% — there's no retainer physiology to protect.
Magnesium for the severe ones. IV magnesium adds bronchodilation and reduces admissions when initial therapy isn't enough.
Intubating asthma is dangerous. Anticipate auto-PEEP — low rate, long expiratory time, permissive hypercapnia, and vigilance for breath-stacking and pneumothorax.
Ask about prior intubations. A history of near-fatal asthma is the single best predictor of another one — escalate early in those patients.
Common mistake: being reassured by a "normal" blood gas in a tiring, quiet-chested asthmatic and missing the impending respiratory arrest.
Pulmonology — Respiratory Failure
107. Acute Hypoxemic Respiratory Failure
Type I failure (low PaO2) · support oxygenation while finding the cause · pneumonia · CHF · PE · ILD flare · ARDS · escalate O2 ladder, treat the driver · Super Compact
Sx: dyspnea, tachypnea, accessory muscle use, hypoxemia (SpO2 low, PaO2 <60 mmHg on room air) with a normal or low PaCO2 (Type I) · restlessness/agitation → drowsiness as it worsens · cyanosis · signs of the underlying cause (fever/crackles, JVD/edema, pleuritic pain, bilateral fine crackles) (stabilize oxygenation first, then rapidly identify which of the major causes is operating — they have very different treatments)
Neg: denies primary hypercapnia/CO2 narcosis as the main problem (that's Type II / acute-on-chronic — different card) · denies upper-airway obstruction/stridor · denies pure anxiety/hyperventilation without true hypoxemia · the Neg here is really excluding the WRONG cause within the differential (e.g. denies orthopnea/PND if not CHF; denies VTE risk/calf swelling if not PE)
SHx: cardiac history (CHF) · VTE risk/immobility/malignancy (PE) · known ILD/connective tissue disease · infection exposure (pneumonia/COVID) · aspiration risk · transfusions/sepsis/pancreatitis (ARDS precipitants)
Etiology (the differential to work through): pneumonia (consolidation, fever, infiltrate) · CHF/cardiogenic pulmonary edema (elevated filling pressures, BNP, bilateral, cardiomegaly) · PE (V/Q mismatch, clear CXR/hypoxia out of proportion) · ILD flare (chronic reticular + acute worsening) · ARDS (bilateral infiltrates, P/F <300, non-cardiogenic) · mechanisms: V/Q mismatch, shunt, diffusion limitation
RF: depends on cause — cardiac disease, VTE risk, infection, immunosuppression, known lung disease, sepsis/aspiration/pancreatitis/transfusion (ARDS)
Data: ABG (confirm hypoxemia, define Type I vs II, calculate A-a gradient + P/F ratio) · CXR (then CT as needed) (focal=pneumonia; bilateral perihilar/effusions/cardiomegaly=CHF; clear=PE; bilateral diffuse=ARDS/ILD) · ECG, troponin, BNP (cardiac) · D-dimer/CTA (PE) · bedside echo/POCUS (LV function, B-lines, RV strain) · CBC, BMP, lactate, cultures · respiratory viral PCR · P/F ratio drives ARDS classification
DDx (= the etiology to sort): pneumonia vs CHF vs PE vs ARDS vs ILD flare (CXR pattern + BNP/echo + CTA + clinical context discriminate) · combined/overlapping causes common · also: alveolar hemorrhage, atelectasis, pulmonary contusion
Home Meds: reconcile based on cause (diuretics for CHF, hold nephrotoxins, anticoagulation for PE) · ensure VTE prophylaxis · careful sedation (preserve respiratory drive unless intubated) · resume home O2 plan
Plan
CONSULT: Pulmonology/Critical care (cause workup, ventilatory management) · ICU (escalating O2 support, intubation) · Cardiology (cardiogenic edema) · cause-specific (ID, etc.)
– First, support oxygenation while diagnosing (parallel tracks):
• Oxygen escalation ladder: nasal cannula → high-flow nasal cannula (HFNC) → noninvasive ventilation (for selected causes, e.g. cardiogenic edema) → intubation/mechanical ventilation for refractory hypoxemia or failure; target SpO2 ≥92%
• consider awake proning in selected hypoxemic non-intubated patients (e.g. COVID/ARDS)
– Rapidly identify the cause with CXR/CT, ABG (A-a, P/F), BNP/troponin/echo, D-dimer/CTA, cultures — because the treatments diverge:
• Pneumonia → empiric antibiotics + cultures (see CAP/HAP cards)
• CHF/cardiogenic edema → IV diuresis (furosemide), preload/afterload reduction (nitroglycerin if hypertensive), NIV for flash edema
• PE → anticoagulation (or thrombolysis if massive); see PE card
• ARDS → treat the precipitant + lung-protective ventilation (low tidal volume 6 mL/kg IBW, plateau <30, PEEP titration, proning, conservative fluids); see ARDS card
• ILD flare → high-dose corticosteroids per pulmonology, treat triggers, supportive O2; see ILD card
– Treat reversible contributors (fluid overload, bronchospasm, secretions, anemia) and avoid over-sedation in non-intubated patients
– Two things happen at once: escalate oxygen support up the ladder to keep them alive, and quickly sort which of pneumonia/CHF/PE/ARDS/ILD is driving it — because diuresing a PE or anticoagulating pulmonary edema helps no one. POCUS at the bedside (B-lines, LV function, RV strain) is often the fastest discriminator.
– PT/OT: mobilize when stable; prevent ICU-acquired weakness
– Trend: SpO2/P-F ratio, work of breathing, ABG, response to cause-specific therapy, hemodynamics, mental status
– Escalation triggers: refractory hypoxemia/rising work of breathing → HFNC/NIV/intubation + ICU; failure of HFNC/NIV → intubation; shock → ICU; ARDS criteria → lung-protective ventilation + ICU
– Discharge when: underlying cause treated/improving, oxygenation stable on room air or established home O2, off escalating support; cause-specific follow-up + therapy; pulmonary rehab/home O2 as needed; return precautions (worsening dyspnea, low saturations, chest pain)
107. Acute Hypoxemic Respiratory Failure
complete reference · Type I failure · oxygen-escalation ladder while diagnosing · pneumonia vs CHF vs PE vs ARDS vs ILD flare · cause-directed therapy · Full Card
Symptoms / Associated Sx
Dyspnea, tachypnea, accessory muscle use, and hypoxemia (a low SpO2 and a PaO2 below 60 mmHg on room air) with a normal or low PaCO2 (Type I)
Restlessness and agitation progressing to drowsiness as hypoxemia worsens, with cyanosis
Signs of the underlying cause — fever and crackles, JVD and edema, pleuritic pain, or bilateral fine crackles
Neg
Pt denies primary hypercapnia or CO2 narcosis as the main problem — that defines Type II or acute-on-chronic failure, covered separately
Pt denies upper-airway obstruction or stridor
Pt denies pure anxiety or hyperventilation without true hypoxemia
The key negatives here exclude the wrong cause within the differential — for example, denying orthopnea and PND if heart failure is not the driver, or denying VTE risk and calf swelling if PE is not the driver
Social History (SHx)
Cardiac history (heart failure) and VTE risk from immobility or malignancy (pulmonary embolism)
Known interstitial lung disease or connective tissue disease, and infection exposure (pneumonia, COVID-19)
Aspiration risk and ARDS precipitants such as transfusion, sepsis, and pancreatitis
Main Etiology
Pneumonia (consolidation, fever, an infiltrate) and cardiogenic pulmonary edema from heart failure (elevated filling pressures, an elevated BNP, bilateral changes, cardiomegaly)
Pulmonary embolism (V/Q mismatch, often a clear CXR with hypoxia out of proportion)
An ILD flare (a chronic reticular pattern with acute worsening) and ARDS (bilateral infiltrates, a P/F ratio below 300, non-cardiogenic)
The underlying mechanisms are V/Q mismatch, shunt, and diffusion limitation
RF
Risk factors depend on the cause — cardiac disease, VTE risk, infection, immunosuppression, known lung disease, and sepsis, aspiration, pancreatitis, or transfusion for ARDS
Data
ABG (to confirm hypoxemia, define Type I versus II, and calculate the A-a gradient and P/F ratio)
Chest radiograph and then CT as needed (focal disease in pneumonia; bilateral perihilar changes, effusions, and cardiomegaly in heart failure; a clear film in PE; bilateral diffuse infiltrates in ARDS or ILD)
ECG, troponin, and BNP (cardiac causes), and a D-dimer or CTA (PE)
Bedside echo or POCUS (LV function, B-lines, RV strain)
CBC, BMP, lactate, cultures, and a respiratory viral PCR, with the P/F ratio driving ARDS classification
DDx
Pneumonia versus heart failure versus pulmonary embolism versus ARDS versus ILD flare (the CXR pattern, BNP and echo, CTA, and clinical context discriminate) · combined or overlapping causes are common · also alveolar hemorrhage, atelectasis, and pulmonary contusion
Home Meds
Reconcile based on the cause — diuretics for heart failure, holding nephrotoxins, anticoagulation for PE
Ensure VTE prophylaxis and use careful sedation to preserve respiratory drive unless intubated
Resume the home oxygen plan
Plan
CONSULT: Pulmonology/Critical care (cause workup and ventilatory management) · ICU (escalating oxygen support, intubation) · Cardiology (cardiogenic edema) · cause-specific services such as Infectious Disease
Support oxygenation while diagnosing, on parallel tracks. Use the oxygen-escalation ladder — nasal cannula, high-flow nasal cannula, noninvasive ventilation for selected causes such as cardiogenic edema, and intubation with mechanical ventilation for refractory hypoxemia or failure — targeting SpO2 92% or higher, and consider awake proning in selected hypoxemic non-intubated patients
Rapidly identify the cause with chest imaging, ABG (A-a gradient and P/F ratio), BNP, troponin, echo, D-dimer or CTA, and cultures, because the treatments diverge
Pneumonia → empiric antibiotics and cultures (see the CAP and HAP cards)
Cardiogenic edema → IV diuresis with furosemide, preload and afterload reduction (nitroglycerin if hypertensive), and NIV for flash pulmonary edema
Pulmonary embolism → anticoagulation, or thrombolysis if massive (see the PE card)
ARDS → treat the precipitant and apply lung-protective ventilation (a low tidal volume of 6 mL/kg ideal body weight, a plateau pressure below 30, PEEP titration, proning, and conservative fluids; see the ARDS card)
ILD flare → high-dose corticosteroids per pulmonology, treatment of triggers, and supportive oxygen (see the ILD card)
Treat reversible contributors such as fluid overload, bronchospasm, secretions, and anemia, and avoid over-sedation in non-intubated patients
PT/OT: mobilize when stable to prevent ICU-acquired weakness
Trend: oxygen saturation and P/F ratio, work of breathing, ABG, the response to cause-specific therapy, hemodynamics, and mental status
Escalation triggers: refractory hypoxemia or rising work of breathing → high-flow oxygen, NIV, or intubation and ICU; failure of high-flow oxygen or NIV → intubation; shock → ICU; ARDS criteria → lung-protective ventilation and ICU
Discharge criteria: the underlying cause treated or improving, stable oxygenation on room air or established home oxygen, and off escalating support; arrange cause-specific follow-up and therapy, pulmonary rehabilitation or home oxygen as needed, and return precautions for worsening dyspnea, low saturations, or chest pain
Red Flags
Refractory hypoxemia despite high-flow oxygen → impending need for intubation; escalate to ICU
Hypoxia out of proportion to a clear chest film → pulmonary embolism until excluded
Bilateral infiltrates with a P/F ratio below 300 and no cardiogenic explanation → ARDS
Rising work of breathing with falling saturations on maximal support → mechanical ventilation
Failure to improve despite treatment → reconsider the diagnosis or a second coexisting cause
Senior IM Resident Pearls
Two tracks at once. Escalate oxygen to keep them alive while you sort the cause — don't let the workup delay support, or support delay the workup.
POCUS is the fastest discriminator. B-lines, LV function, and RV strain at the bedside often separate edema, pneumonia, and PE before the formal studies return.
The treatments are opposites. Diuresing a PE or anticoagulating pulmonary edema helps no one — get the cause right before committing.
Hypoxia out of proportion is a PE. A profoundly hypoxemic patient with a clear film deserves a PE workup.
HFNC buys real time. High-flow nasal cannula can avert intubation in many hypoxemic patients — but recognize failure early.
Causes coexist. Pneumonia can precipitate heart failure, and a PE can complicate pneumonia — keep looking if one treatment doesn't fix it.
Common mistake: committing to a single diagnosis and its treatment before the bedside data are in, and treating the wrong mechanism.
Pulmonology — Respiratory Failure
108. Acute on Chronic Respiratory Failure
acute decompensation on chronic hypercapnia · COPD · OHS · neuromuscular disease · NIV is the cornerstone · know the baseline CO2/pH · find the trigger · Super Compact
Sx: worsening dyspnea on a background of chronic disease, drowsiness/confusion/headache (hypercapnia), asterixis, daytime somnolence, accessory muscle use · the picture is an acute rise in PaCO2 with acute-on-chronic respiratory acidosis (acutely low pH with an elevated bicarbonate reflecting chronic compensation) (the baseline blood gas is everything — distinguish the chronic compensated state from the acute decompensation superimposed on it)
Neg: denies a purely acute presentation without chronic disease (would be acute failure) · denies pure hypoxemic failure without CO2 retention (Type I) · denies an acute neurologic catastrophe as the cause of decreased drive (stroke) · the Neg often excludes the wrong chronic substrate (e.g. denies obesity/OSA symptoms if not OHS; denies progressive weakness if not neuromuscular)
SHx: known COPD (severity, home O2/NIV) · obesity + OSA symptoms (OHS) · neuromuscular disease (ALS, myasthenia, muscular dystrophy, prior polio) · chest wall disease (kyphoscoliosis) · sedative/opioid use · adherence to home NIV
Etiology (chronic substrate + acute trigger): chronic substrates: COPD, obesity hypoventilation syndrome (OHS), neuromuscular disease, chest wall disorders · acute triggers: infection/pneumonia, COPD exacerbation, sedatives/opioids, heart failure, PE, electrolyte disturbance, missed home NIV, oversedation/over-oxygenation
RF: severe underlying lung/neuromuscular/chest wall disease · obesity · sedative/opioid use · nonadherence to home NIV/O2 · recurrent infections · uncorrected hypothyroidism (contributes to OHS)
Data: ABG (acute-on-chronic respiratory acidosis — acutely ↓pH, ↑PaCO2 above the patient's chronic baseline, with a chronically elevated HCO3; compare to prior gases) · CXR (pneumonia, edema, atelectasis) · ECG, BNP (cardiac trigger/cor pulmonale) · CBC, BMP (electrolytes — hypophosphatemia/hypokalemia weaken respiratory muscles) · TSH (OHS) · D-dimer/CTA if PE suspected · drug levels/tox if oversedation · continuous monitoring + serial ABGs
DDx (chronic substrate + trigger): COPD exacerbation · OHS decompensation · neuromuscular weakness (myasthenic crisis, ALS progression) · chest-wall disease · with triggers: pneumonia, CHF, PE, oversedation, metabolic (serial ABG + cause workup sort these)
Home Meds: resume home NIV/CPAP/BiPAP with appropriate settings · reconcile + minimize sedatives/opioids/benzodiazepines (precipitate/worsen) · continue inhalers/diuretics as indicated · careful controlled O2 · correct electrolytes
Plan
CONSULT: Pulmonology (NIV management, chronic ventilatory failure, home setup) · ICU/Critical care (severe acidosis, NIV failure, intubation) · Neurology (neuromuscular cause — myasthenia, ALS) · Sleep medicine (OHS/OSA, home NIV titration)
– Noninvasive ventilation (cornerstone): BiPAP for acute hypercapnic respiratory acidosis (pH <7.35, ↑PaCO2) — supports ventilation, unloads respiratory muscles, reduces intubation and mortality; titrate IPAP/EPAP to improve pH/CO2 and work of breathing; start early
– Controlled oxygen: target SpO2 88–92% — avoid over-oxygenation which worsens hypercapnia by suppressing drive and worsening V/Q matching
– Identify + treat the acute trigger (essential): antibiotics for pneumonia, bronchodilators/steroids for COPD exacerbation, diuresis for CHF, anticoagulation for PE, reverse/stop sedatives or opioids (naloxone if opioid-induced), correct electrolytes (phosphate, potassium, magnesium — repletion improves respiratory muscle strength)
– Substrate-specific care: COPD (see COPD card); OHS (NIV/CPAP, weight management, treat OSA — see OHS card); neuromuscular (treat the specific disease — e.g. myasthenic crisis with IVIG/plasmapheresis + neurology; monitor with NIF/FVC, not just SpO2 — they fail abruptly)
– Know when NIV won't work / intubate: decreased consciousness with inability to protect airway, hemodynamic instability, copious secretions, NIV failure (no improvement in pH/CO2), or the neuromuscular patient with declining vital capacity → intubation + ICU
– The chronic baseline gas is the key: a CO2 of 70 with a near-normal pH is the compensated chronic state, while a CO2 of 70 with a pH of 7.25 is acute decompensation needing NIV now. Hunt the trigger relentlessly — infection, sedation, heart failure, PE, missed home NIV — because NIV buys time but the trigger is what's killing them. In neuromuscular disease, trend FVC/NIF; they crash without warning on pulse oximetry.
– PT/OT: mobilize when stable; respiratory muscle considerations
– Trend: serial ABG (pH/CO2 vs baseline), SpO2, mental status, work of breathing, response to NIV, trigger resolution; FVC/NIF in neuromuscular disease
– Escalation triggers: NIV failure/worsening acidosis → intubation + ICU; declining mental status/airway compromise → intubation; falling FVC/NIF (neuromuscular) → ICU + airway; hemodynamic instability → ICU
– Discharge when: back to chronic compensated baseline, trigger treated, stable on home NIV/O2 (confirm settings + adherence plan); pulmonary/sleep/neuro follow-up, home NIV optimization, address sedating meds, vaccination; return precautions (increasing drowsiness, worsening dyspnea, headache, confusion)
108. Acute on Chronic Respiratory Failure
complete reference · acute decompensation on chronic hypercapnia · COPD, OHS, neuromuscular, chest wall · NIV cornerstone · trigger-directed therapy · Full Card
Symptoms / Associated Sx
Worsening dyspnea on a background of chronic disease, with drowsiness, confusion, or headache from hypercapnia, asterixis, daytime somnolence, and accessory muscle use
The picture is an acute rise in PaCO2 producing an acute-on-chronic respiratory acidosis — an acutely low pH with an elevated bicarbonate reflecting chronic renal compensation
The baseline blood gas is everything — it distinguishes the chronic compensated state from the acute decompensation superimposed on it
Neg
Pt denies a purely acute presentation without underlying chronic disease — that would be acute respiratory failure
Pt denies pure hypoxemic failure without CO2 retention — that is Type I failure
Pt denies an acute neurologic catastrophe causing decreased respiratory drive, such as a stroke
The key negatives often exclude the wrong chronic substrate — for example, denying obesity and OSA symptoms if OHS is not the cause, or denying progressive weakness if a neuromuscular cause is not operating
Social History (SHx)
Known COPD with its severity and home oxygen or NIV use, and obesity with OSA symptoms (OHS)
Neuromuscular disease (ALS, myasthenia gravis, muscular dystrophy, prior polio) and chest wall disease such as kyphoscoliosis
Sedative or opioid use and adherence to home NIV
Main Etiology
Chronic substrates: COPD, obesity hypoventilation syndrome, neuromuscular disease, and chest wall disorders
Acute triggers: infection or pneumonia, a COPD exacerbation, sedatives or opioids, heart failure, pulmonary embolism, electrolyte disturbance, missed home NIV, and oversedation or over-oxygenation
RF
Modifiable: sedative and opioid use, nonadherence to home NIV or oxygen, and uncorrected hypothyroidism contributing to OHS
Non-modifiable: severe underlying lung, neuromuscular, or chest wall disease, obesity, and recurrent infections
Data
ABG (an acute-on-chronic respiratory acidosis — an acutely low pH with a PaCO2 above the patient's chronic baseline and a chronically elevated bicarbonate; compare with prior gases)
Chest radiograph (pneumonia, edema, atelectasis), with ECG and BNP (a cardiac trigger or cor pulmonale)
CBC and BMP (electrolytes — hypophosphatemia and hypokalemia weaken the respiratory muscles), and TSH (OHS)
A D-dimer or CTA if PE is suspected, drug levels or toxicology for oversedation, and continuous monitoring with serial ABGs
DDx
COPD exacerbation · OHS decompensation · neuromuscular weakness (myasthenic crisis, ALS progression) · chest-wall disease · with triggers such as pneumonia, heart failure, pulmonary embolism, oversedation, and metabolic derangement (serial ABGs and a cause workup sort these)
Home Meds
Resume home NIV, CPAP, or BiPAP with appropriate settings
Reconcile and minimize sedatives, opioids, and benzodiazepines that precipitate or worsen the decompensation
Continue inhalers and diuretics as indicated, use careful controlled oxygen, and correct electrolytes
Plan
CONSULT: Pulmonology (NIV management, chronic ventilatory failure, home setup) · ICU/Critical care (severe acidosis, NIV failure, intubation) · Neurology (neuromuscular causes — myasthenia, ALS) · Sleep medicine (OHS and OSA, home NIV titration)
Noninvasive ventilation is the cornerstone: BiPAP for acute hypercapnic respiratory acidosis (a pH below 7.35 with an elevated PaCO2) supports ventilation, unloads the respiratory muscles, and reduces intubation and mortality; titrate IPAP and EPAP to improve the pH, CO2, and work of breathing, and start early
Controlled oxygen targeting SpO2 88–92%, avoiding over-oxygenation that worsens hypercapnia by suppressing drive and worsening V/Q matching
Identify and treat the acute trigger, which is essential: antibiotics for pneumonia, bronchodilators and steroids for a COPD exacerbation, diuresis for heart failure, anticoagulation for PE, reversal or cessation of sedatives or opioids (naloxone for opioid-induced cases), and correction of electrolytes (phosphate, potassium, and magnesium repletion improves respiratory muscle strength)
Substrate-specific care: COPD per the COPD card; OHS with NIV or CPAP, weight management, and OSA treatment per the OHS card; and neuromuscular disease treated specifically (a myasthenic crisis with IVIG or plasmapheresis and neurology), monitored with NIF and FVC rather than oxygen saturation alone, since these patients fail abruptly
Recognize when NIV won't work and intubate: decreased consciousness with an inability to protect the airway, hemodynamic instability, copious secretions, NIV failure without improvement in pH or CO2, or a neuromuscular patient with a declining vital capacity → intubation and ICU
PT/OT: mobilize when stable with attention to respiratory muscle conditioning
Trend: serial ABG (pH and CO2 against baseline), oxygen saturation, mental status, work of breathing, the response to NIV, and trigger resolution, along with FVC and NIF in neuromuscular disease
Escalation triggers: NIV failure or worsening acidosis → intubation and ICU; declining mental status or airway compromise → intubation; a falling FVC or NIF in neuromuscular disease → ICU and airway management; hemodynamic instability → ICU
Discharge criteria: a return to the chronic compensated baseline, the trigger treated, and stability on home NIV or oxygen with confirmed settings and an adherence plan; arrange pulmonary, sleep, and neurology follow-up, optimize home NIV, address sedating medications, ensure vaccination, and give return precautions for increasing drowsiness, worsening dyspnea, headache, or confusion
Red Flags
An acutely low pH with a CO2 above the chronic baseline → acute decompensation requiring NIV now, not the compensated chronic state
Worsening drowsiness or confusion → CO2 narcosis and possible NIV failure; prepare for intubation
A falling FVC or NIF in a neuromuscular patient → impending abrupt collapse despite a reassuring oximetry reading
Over-oxygenation with a rising CO2 → suppressed respiratory drive worsening the hypercapnia
Opioid or sedative as the trigger → reverse it; a reversible precipitant is being missed
Senior IM Resident Pearls
The baseline gas defines the emergency. A CO2 of 70 with a near-normal pH is chronic and compensated; the same CO2 with a pH of 7.25 is an acute decompensation needing NIV immediately.
NIV buys time; the trigger is the disease. Hunt relentlessly for infection, sedation, heart failure, PE, or missed home NIV — those are what's actually decompensating the patient.
Target 88–92%, and beware over-oxygenation. As in COPD, too much oxygen suppresses drive and raises CO2.
Trend FVC and NIF in neuromuscular disease. These patients crash abruptly with a normal-looking pulse oximetry until the moment they don't.
Replete phosphate, potassium, and magnesium. Weak respiratory muscles from electrolyte depletion are a reversible contributor.
Reverse the sedation. An opioid or benzodiazepine precipitant is one of the most satisfying and rapidly reversible causes.
Common mistake: treating a chronically elevated CO2 as an emergency, or missing that an acutely acidotic gas means the patient needs NIV and a trigger search right now.
Pulmonology — Respiratory Failure
109. Obesity Hypoventilation Syndrome (OHS)
obesity + chronic daytime hypercapnia not otherwise explained · "Pickwickian" · overlaps OSA · PAP therapy + weight loss · diagnosis of exclusion · Super Compact
Sx: daytime hypersomnolence, morning headache, dyspnea on exertion, fatigue, loud snoring/witnessed apneas (overlapping OSA), poor concentration · signs: obesity, plethora, peripheral edema and signs of cor pulmonale/pulmonary HTN in advanced disease · may present acutely with worsening somnolence/confusion when decompensated (the core defect is chronic daytime hypoventilation in an obese patient, with a compensated respiratory acidosis found on the gas)
Neg: denies a chronic productive cough/extensive smoking history pointing to COPD as the cause of hypercapnia · denies progressive limb weakness/bulbar symptoms (neuromuscular disease) · denies acute onset without a chronic obese/sleep-disordered background · denies symptoms of hypothyroidism left untreated (a contributor to exclude)
SHx: obesity (often severe, BMI ≥30–40+) · known/suspected OSA, CPAP use + adherence · sedative/opioid use · alcohol · comorbid metabolic syndrome/diabetes/hypertension · prior episodes of hypercapnic decompensation
Etiology: obesity (BMI ≥30) + chronic daytime alveolar hypoventilation (PaCO2 ≥45 mmHg awake) not explained by another cause · mechanisms: increased work of breathing/reduced compliance from obesity, blunted ventilatory response to CO2, and overlapping OSA (present in ~90%) · "Pickwickian syndrome"
RF: severe obesity · obstructive sleep apnea · male sex · metabolic syndrome · untreated hypothyroidism (contributor) · sedative/opioid use
Data: ABG (daytime hypercapnia PaCO2 ≥45 with chronic compensated respiratory acidosis — elevated bicarbonate; awake, at baseline) · serum bicarbonate (elevated HCO3 is a useful screen for chronic hypercapnia) · sleep study/polysomnography (confirm + characterize OSA overlap) · TSH (exclude hypothyroidism) · PFTs/CXR (exclude COPD, ILD, chest-wall/neuromuscular causes) · ECG/echo (cor pulmonale, pulmonary hypertension, RV strain) · CBC (secondary polycythemia)
DDx: COPD (smoking, obstruction on PFTs) · OSA without hypoventilation (no daytime hypercapnia) · neuromuscular/chest-wall hypoventilation (weakness, restrictive PFTs, low NIF) · hypothyroidism (TSH) · central hypoventilation (rare) · medication-induced (sedatives/opioids)
Home Meds: resume/initiate PAP therapy (CPAP or BiPAP) with adherence support · minimize sedatives/opioids/benzodiazepines · careful controlled O2 (avoid suppressing drive) · treat hypothyroidism if present · optimize comorbidities (diabetes, hypertension, heart failure)
Plan
CONSULT: Sleep medicine (PAP titration, polysomnography, long-term management) · Pulmonology (chronic hypoventilation, cor pulmonale) · Bariatric/weight-management or surgery (definitive weight loss) · ICU (acute decompensation failing NIV)
– Positive airway pressure therapy (cornerstone): CPAP is often effective when OSA predominates and daytime hypercapnia is mild/corrects with apnea control; BiPAP (NIV) when hypercapnia persists despite CPAP or in more severe hypoventilation — titrated to correct nocturnal and ultimately daytime CO2; ensure adherence (the single most important chronic therapy)
– Controlled oxygen: target SpO2 88–92%; avoid over-oxygenation, which can worsen hypercapnia by suppressing the ventilatory drive (oxygen alone does not treat the hypoventilation — PAP does)
– Acute decompensation (acute-on-chronic hypercapnic failure): NIV/BiPAP urgently (see the acute-on-chronic respiratory failure card), identify + treat triggers (infection, heart failure, sedation, PE), correct electrolytes; intubate if NIV fails or airway/consciousness compromised
– Weight loss (definitive direction): structured weight-management program; bariatric surgery for appropriate candidates (can substantially improve or resolve OHS)
– Treat contributors + comorbidities: replace thyroid hormone if hypothyroid; minimize sedating medications; manage cor pulmonale/pulmonary hypertension and right heart failure (cautious diuresis); treat coexisting OSA
– Diagnosis of exclusion: confirm by excluding COPD, ILD, neuromuscular, chest-wall, and other causes of hypercapnia before attributing it to OHS
– OHS is obesity plus unexplained chronic daytime hypercapnia — an elevated bicarbonate on a routine panel in an obese, sleepy patient is the clue that should prompt an ABG and a sleep study. PAP therapy and weight loss are the treatment; supplemental oxygen alone is a trap because it doesn't fix the hypoventilation and can worsen the CO2.
– PT/OT: mobility, exercise as part of weight management
– Trend: ABG/CO2 (vs baseline), serum bicarbonate, SpO2, daytime symptoms, PAP adherence/efficacy, signs of right heart strain
– Escalation triggers: acute hypercapnic decompensation failing NIV → intubation + ICU; declining consciousness → ICU; progressive cor pulmonale/right heart failure → pulmonology/cardiology
– Discharge when: back to chronic compensated baseline, on effective PAP therapy with an adherence plan, triggers treated; sleep medicine + pulmonary follow-up, home PAP setup, weight-management/bariatric referral, address sedating meds, manage comorbidities; return precautions (worsening daytime sleepiness, morning headaches, increasing dyspnea/edema, confusion)
109. Obesity Hypoventilation Syndrome (OHS)
complete reference · obesity with chronic daytime hypercapnia · OSA overlap · PAP therapy and weight loss · diagnosis of exclusion · Full Card
Symptoms / Associated Sx
Daytime hypersomnolence, morning headache, exertional dyspnea, fatigue, loud snoring with witnessed apneas (overlapping OSA), and poor concentration
Signs of obesity, facial plethora, peripheral edema, and features of cor pulmonale and pulmonary hypertension in advanced disease
Patients may present acutely with worsening somnolence or confusion when decompensated; the core defect is chronic daytime hypoventilation in an obese patient with a compensated respiratory acidosis on the gas
Neg
Pt denies a chronic productive cough or an extensive smoking history pointing to COPD as the cause of hypercapnia
Pt denies progressive limb weakness or bulbar symptoms — argues against a neuromuscular cause
Pt denies an acute onset without a chronic obese, sleep-disordered background
Pt denies untreated hypothyroid symptoms — a contributor that should be excluded
Social History (SHx)
Obesity, often severe (BMI 30–40 or higher), and known or suspected OSA with CPAP use and adherence
Sedative or opioid use and alcohol
Comorbid metabolic syndrome, diabetes, and hypertension, with any prior hypercapnic decompensation
Main Etiology
Obesity (BMI 30 or higher) with chronic daytime alveolar hypoventilation (an awake PaCO2 of 45 mmHg or higher) not explained by another cause
The mechanisms are increased work of breathing and reduced compliance from obesity, a blunted ventilatory response to CO2, and overlapping OSA (present in roughly 90%)
Historically termed the "Pickwickian syndrome"
RF
Modifiable: severe obesity, untreated hypothyroidism, and sedative or opioid use
Non-modifiable: obstructive sleep apnea, male sex, and metabolic syndrome
Data
ABG (daytime hypercapnia with a PaCO2 of 45 or higher and a chronic compensated respiratory acidosis with an elevated bicarbonate, measured awake at baseline)
Serum bicarbonate (an elevated bicarbonate is a useful screen for chronic hypercapnia)
A sleep study (polysomnography) (to confirm and characterize the OSA overlap), and TSH to exclude hypothyroidism
PFTs and a chest radiograph (to exclude COPD, ILD, and chest-wall or neuromuscular causes)
ECG and echocardiography (cor pulmonale, pulmonary hypertension, RV strain), with a CBC for secondary polycythemia
DDx
COPD (smoking, obstruction on PFTs) · OSA without hypoventilation (no daytime hypercapnia) · neuromuscular or chest-wall hypoventilation (weakness, restrictive PFTs, a low NIF) · hypothyroidism (TSH) · central hypoventilation (rare) · medication-induced hypoventilation from sedatives or opioids
Home Meds
Resume or initiate PAP therapy (CPAP or BiPAP) with adherence support
Minimize sedatives, opioids, and benzodiazepines, and use careful controlled oxygen to avoid suppressing the drive
Treat hypothyroidism if present and optimize comorbidities such as diabetes, hypertension, and heart failure
Plan
CONSULT: Sleep medicine (PAP titration, polysomnography, long-term management) · Pulmonology (chronic hypoventilation, cor pulmonale) · Bariatric or weight-management services (definitive weight loss) · ICU (acute decompensation failing NIV)
Positive airway pressure therapy is the cornerstone: CPAP is often effective when OSA predominates and daytime hypercapnia is mild or corrects with apnea control, while BiPAP (NIV) is used when hypercapnia persists despite CPAP or in more severe hypoventilation, titrated to correct nocturnal and ultimately daytime CO2; adherence is the single most important chronic therapy
Controlled oxygen targeting SpO2 88–92%, avoiding over-oxygenation that worsens hypercapnia by suppressing the ventilatory drive — oxygen alone does not treat the hypoventilation, PAP does
Acute decompensation (acute-on-chronic hypercapnic failure) is managed with urgent NIV or BiPAP, identification and treatment of triggers (infection, heart failure, sedation, PE), and electrolyte correction, with intubation if NIV fails or the airway or consciousness is compromised
Weight loss is the definitive direction: a structured weight-management program, and bariatric surgery for appropriate candidates, which can substantially improve or resolve OHS
Treat contributors and comorbidities: replace thyroid hormone if hypothyroid, minimize sedating medications, manage cor pulmonale, pulmonary hypertension, and right heart failure with cautious diuresis, and treat coexisting OSA
Remember it is a diagnosis of exclusion: confirm by excluding COPD, ILD, neuromuscular, chest-wall, and other causes before attributing the hypercapnia to OHS
PT/OT: mobility and exercise as part of weight management
Trend: ABG and CO2 against baseline, serum bicarbonate, oxygen saturation, daytime symptoms, PAP adherence and efficacy, and signs of right heart strain
Escalation triggers: acute hypercapnic decompensation failing NIV → intubation and ICU; declining consciousness → ICU; progressive cor pulmonale or right heart failure → pulmonology and cardiology
Discharge criteria: a return to the chronic compensated baseline, effective PAP therapy with an adherence plan, and treated triggers; arrange sleep medicine and pulmonary follow-up, home PAP setup, weight-management or bariatric referral, attention to sedating medications, and comorbidity management, with return precautions for worsening daytime sleepiness, morning headaches, increasing dyspnea or edema, or confusion
Red Flags
Worsening somnolence or confusion → acute hypercapnic decompensation; start NIV and search for a trigger
An elevated bicarbonate on a routine panel in an obese, sleepy patient → unrecognized chronic hypercapnia; obtain an ABG
Edema, an elevated JVP, and RV strain → cor pulmonale from chronic hypoventilation and pulmonary hypertension
Over-oxygenation with a rising CO2 → suppressed drive; oxygen is not the treatment, PAP is
Sedative or opioid exposure → can precipitate decompensation; reduce or reverse it
Senior IM Resident Pearls
An elevated bicarbonate is the tell. In an obese, sleepy patient it signals chronic hypercapnia and should prompt an ABG and a sleep study.
PAP treats OHS; oxygen alone is a trap. Supplemental oxygen without ventilatory support doesn't fix the hypoventilation and can worsen the CO2.
It's a diagnosis of exclusion. Rule out COPD, neuromuscular, chest-wall disease, and hypothyroidism before settling on OHS.
OSA overlaps in nearly everyone. Around 90% have coexisting obstructive sleep apnea — characterize it with a sleep study.
Weight loss can cure it. Bariatric surgery in appropriate candidates can substantially improve or resolve the syndrome.
Target 88–92%. As with other chronic hypercapnic states, modest oxygen goals protect the respiratory drive.
Common mistake: treating the sleepy, hypercapnic obese patient with oxygen alone and never starting the PAP therapy that actually addresses the hypoventilation.
Pulmonology — Respiratory Failure
110. Acute Respiratory Distress Syndrome (ARDS)
Berlin definition · non-cardiogenic bilateral infiltrates, P/F ≤300 · lung-protective ventilation + proning + treat the precipitant · Super Compact
Sx: acute, rapidly progressive dyspnea and hypoxemia (typically within a week of an insult), tachypnea, diffuse crackles, increasing oxygen requirement refractory to supplemental O2 · usually in a critically ill patient with an identifiable precipitant (sepsis, pneumonia, aspiration, pancreatitis, trauma, transfusion) (the defining features are non-cardiogenic bilateral infiltrates with severe hypoxemia — confirm it's not just heart failure/overload, then ventilate to protect the lung)
Neg: denies a history pointing to cardiogenic pulmonary edema as the sole cause (orthopnea/PND/known heart failure — though ARDS can coexist) · denies a purely chronic dyspnea/known ILD as the explanation · denies findings fully explained by atelectasis or effusion · denies fluid overload alone accounting for the picture
SHx: precipitating illness/exposure (sepsis, severe pneumonia, aspiration event, acute pancreatitis, major trauma, recent transfusion, near-drowning, inhalational injury) · alcohol use (risk factor) · baseline pulmonary status
Etiology: direct lung injury — pneumonia, aspiration, inhalation injury, near-drowning, pulmonary contusion · indirect injury — sepsis (most common overall), severe trauma/shock, acute pancreatitis, massive transfusion (TRALI), burns · final common pathway: diffuse alveolar damage → increased capillary permeability → non-cardiogenic pulmonary edema
RF: sepsis · severe pneumonia · aspiration · pancreatitis · multiple transfusions · trauma/shock · chronic alcohol use · advanced age
Data: ABG + P/F ratio (Berlin severity: mild P/F 200–300, moderate 100–200, severe <100, on PEEP ≥5) · CXR/CT (bilateral opacities not fully explained by effusions/collapse/nodules) · BNP + echocardiography (exclude/quantify cardiogenic edema — ARDS is non-cardiogenic, though they can coexist) · CBC, BMP, lactate, cultures, lipase (identify the precipitant) · workup for the underlying cause
DDx: cardiogenic pulmonary edema/heart failure (BNP, echo, response to diuresis) · diffuse alveolar hemorrhage (dropping Hgb, bloody BAL) · acute interstitial pneumonia/ILD flare (chronicity, pattern) · diffuse pneumonia (infectious workup) · acute eosinophilic pneumonia (BAL eosinophils)
Home Meds: hold/adjust per critical illness · ensure VTE + stress-ulcer prophylaxis · careful sedation/analgesia for ventilation · vasoactive/fluid management per shock state · reconcile chronic meds when recovering
Plan
CONSULT: ICU/Critical care (mechanical ventilation — central) · Pulmonology · Infectious Disease (sepsis/pneumonia precipitant) · ECMO center referral (refractory severe ARDS) · cause-specific services
– Treat the precipitant aggressively: source control + antibiotics for sepsis/pneumonia, treat pancreatitis, etc. (ARDS resolves only when the driver is controlled)
– Lung-protective ventilation (the central evidence-based intervention): low tidal volume 6 mL/kg ideal body weight (4–8 mL/kg range), plateau pressure <30 cmH2O, permissive hypercapnia (tolerate higher CO2/lower pH to protect the lung), PEEP titration (higher PEEP for moderate–severe to recruit and improve oxygenation) — reduces mortality (ARDSNet)
– Prone positioning: for moderate–severe ARDS (P/F <150) — proning for ≥16 h/day improves survival (PROSEVA); institute early
– Conservative fluid strategy: after resuscitation/once hemodynamically stable, target net even-to-negative balance (improves ventilator-free days — FACTT)
– Neuromuscular blockade: consider early short-course paralysis in severe ARDS with ventilator dyssynchrony (per current evidence)
– Refractory hypoxemia: optimize PEEP/recruitment, ensure proning + paralysis tried; veno-venous ECMO for refractory severe ARDS at an experienced center (EOLIA/CESAR context)
– Corticosteroids: consider in selected ARDS per current evidence (e.g. dexamethasone) — discuss with critical care
– Avoid excessive sedation: use lightest effective sedation, daily awakening/spontaneous breathing trials when appropriate, to shorten ventilation
– The interventions that actually save lives in ARDS are mechanical, not pharmacologic: low-tidal-volume lung-protective ventilation, proning for the moderate-to-severe, conservative fluids, and treating the precipitant. Resist large tidal volumes even when the CO2 climbs — permissive hypercapnia is the price of protecting the lung.
– PT/OT: early mobilization when stable; prevent ICU-acquired weakness; rehab planning
– Trend: P/F ratio, plateau/driving pressure, oxygenation, ventilator settings, fluid balance, precipitant control, response to proning
– Escalation triggers: refractory hypoxemia despite lung-protective ventilation + proning + paralysis → ECMO evaluation; worsening shock/multiorgan failure → critical care escalation
– Discharge (survivors) when: liberated from ventilation, precipitant resolved, oxygenation stable; arrange pulmonary rehab, follow-up PFTs/imaging (ARDS survivors can have prolonged recovery + functional/cognitive impairment), post-ICU follow-up; return precautions per residual disease
110. Acute Respiratory Distress Syndrome (ARDS)
complete reference · Berlin definition and severity · lung-protective ventilation, proning, conservative fluids · precipitant-directed care · Full Card
Symptoms / Associated Sx
Acute, rapidly progressive dyspnea and hypoxemia, typically within a week of an insult, with tachypnea, diffuse crackles, and an increasing oxygen requirement refractory to supplemental oxygen
Usually occurring in a critically ill patient with an identifiable precipitant such as sepsis, pneumonia, aspiration, pancreatitis, trauma, or transfusion
The defining features are non-cardiogenic bilateral infiltrates with severe hypoxemia
Neg
Pt denies a history pointing to cardiogenic pulmonary edema as the sole cause (orthopnea, PND, known heart failure), though ARDS can coexist with cardiac disease
Pt denies a purely chronic dyspnea or known interstitial lung disease as the explanation
Pt denies findings fully explained by atelectasis or an effusion
Pt denies a picture accounted for by fluid overload alone
Social History (SHx)
A precipitating illness or exposure — sepsis, severe pneumonia, an aspiration event, acute pancreatitis, major trauma, recent transfusion, near-drowning, or inhalational injury
Alcohol use, which is a risk factor
Baseline pulmonary status
Main Etiology
Direct lung injury — pneumonia, aspiration, inhalation injury, near-drowning, and pulmonary contusion
Indirect injury — sepsis (the most common overall cause), severe trauma and shock, acute pancreatitis, massive transfusion (TRALI), and burns
The final common pathway is diffuse alveolar damage with increased capillary permeability producing non-cardiogenic pulmonary edema
RF
Modifiable: timely sepsis and aspiration management, transfusion stewardship, and chronic alcohol use
Non-modifiable: the severity of the precipitating illness, advanced age, and shock
Data
ABG and the P/F ratio (Berlin severity — mild with a P/F of 200–300, moderate 100–200, and severe below 100, all on a PEEP of at least 5)
Chest radiograph or CT (bilateral opacities not fully explained by effusions, collapse, or nodules)
BNP and echocardiography (to exclude or quantify cardiogenic edema, since ARDS is non-cardiogenic though the two can coexist)
CBC, BMP, lactate, cultures, and lipase (to identify the precipitant), with a directed workup for the underlying cause
DDx
Cardiogenic pulmonary edema or heart failure (BNP, echo, response to diuresis) · diffuse alveolar hemorrhage (a dropping hemoglobin, a progressively bloody BAL) · acute interstitial pneumonia or an ILD flare (chronicity, pattern) · diffuse pneumonia (infectious workup) · acute eosinophilic pneumonia (BAL eosinophilia)
Home Meds
Hold or adjust home medications per the critical illness and ensure VTE and stress-ulcer prophylaxis
Use careful sedation and analgesia for ventilation and manage vasoactive agents and fluids per the shock state
Reconcile chronic medications during recovery
Plan
CONSULT: ICU/Critical care (mechanical ventilation — central) · Pulmonology · Infectious Disease (a sepsis or pneumonia precipitant) · an ECMO center (refractory severe ARDS) · cause-specific services
Treat the precipitant aggressively: source control and antibiotics for sepsis or pneumonia, treatment of pancreatitis, and so on, since ARDS resolves only when the driver is controlled
Lung-protective ventilation is the central evidence-based intervention: a low tidal volume of 6 mL/kg ideal body weight (within a 4–8 mL/kg range), a plateau pressure below 30 cmH2O, permissive hypercapnia (tolerating a higher CO2 and lower pH to protect the lung), and PEEP titration with higher PEEP for moderate-to-severe disease to recruit lung and improve oxygenation — this reduces mortality (the ARDSNet trial)
Prone positioning for moderate-to-severe ARDS (a P/F below 150) for 16 or more hours per day improves survival (the PROSEVA trial); institute it early
A conservative fluid strategy after resuscitation and once hemodynamically stable, targeting a net even-to-negative balance, which improves ventilator-free days (the FACTT trial)
Neuromuscular blockade as an early short course in severe ARDS with ventilator dyssynchrony, per current evidence
Refractory hypoxemia: optimize PEEP and recruitment and ensure proning and paralysis have been tried, then consider veno-venous ECMO at an experienced center for refractory severe disease
Corticosteroids in selected ARDS per current evidence (such as dexamethasone), in discussion with critical care
Avoid excessive sedation: use the lightest effective sedation with daily awakening and spontaneous breathing trials when appropriate to shorten ventilation
PT/OT: early mobilization when stable to prevent ICU-acquired weakness, with rehabilitation planning
Trend: the P/F ratio, plateau and driving pressure, oxygenation, ventilator settings, fluid balance, precipitant control, and the response to proning
Escalation triggers: refractory hypoxemia despite lung-protective ventilation, proning, and paralysis → ECMO evaluation; worsening shock or multiorgan failure → critical care escalation
Discharge criteria (survivors): liberation from ventilation, a resolved precipitant, and stable oxygenation; arrange pulmonary rehabilitation, follow-up PFTs and imaging (ARDS survivors can have a prolonged recovery with functional and cognitive impairment), and post-ICU follow-up, with return precautions per any residual disease
Red Flags
A P/F ratio below 100 → severe ARDS; ensure proning, paralysis, and an ECMO referral pathway
Refractory hypoxemia despite maximal lung-protective ventilation → ECMO evaluation at an experienced center
A rising plateau or driving pressure → injurious mechanics; reduce tidal volume and reassess
A dropping hemoglobin with a bloody BAL → diffuse alveolar hemorrhage rather than ARDS
Failure to improve as the precipitant is treated → reconsider an uncontrolled source or an alternative diagnosis
Senior IM Resident Pearls
The lifesaving interventions are mechanical, not pharmacologic. Low-tidal-volume ventilation, proning, and conservative fluids change mortality; there is no magic drug.
Permissive hypercapnia is the price of protection. Resist the urge to raise tidal volumes when the CO2 climbs — protecting the lung matters more than a normal gas.
Prone the moderate-to-severe early. Sixteen-plus hours a day of proning improves survival in P/F below 150 — don't wait until it's a last resort.
Dry the lungs once they're stable. A conservative fluid strategy after resuscitation buys ventilator-free days.
It's a syndrome, not a diagnosis. Always hunt and treat the precipitant — ARDS resolves only when the driver is controlled.
Exclude the heart. Confirm the edema is non-cardiogenic, recognizing that ARDS and heart failure can coexist.
Common mistake: ventilating with large tidal volumes to normalize the CO2, which injures the lung and worsens outcomes.