Respiratory
Acute respiratory distress syndrome: CCS-style ventilator management
— Onset within 1 week of a known clinical insult or new/worsening respiratory symptoms
— Bilateral opacities on chest imaging not fully explained by effusions, lobar collapse, or nodules
— Respiratory failure not fully explained by cardiac failure or fluid overload (objective assessment — echo if no risk factor)
— Impaired oxygenation graded by PaO₂/FiO₂ on PEEP ≥5 cm H₂O: mild 200–300, moderate 100–200, severe ≤100
— Pulmonary insults: pneumonia (most common), aspiration, inhalation injury, near-drowning, pulmonary contusion
— Extrapulmonary insults: sepsis, pancreatitis, massive transfusion (TRALI), trauma, burns, DKA, drug overdose
— Move location to ICU
— Order echocardiogram to exclude cardiogenic edema (or measure BNP)
— Begin lung-protective ventilation before the case clock advances further
CCS pearl: Do not wait for the formal Berlin label. Once you see "bilateral infiltrates" + worsening hypoxemia + a precipitant on the CCS stem, advance the clock by intubating early and writing for low-tidal-volume ventilation — late escalation is penalized.

— Patient on 6 L NC → escalated to NRB → still SpO₂ 85% = classic shunt physiology
— Sepsis source: fevers, UTI symptoms, recent line, abdominal pain (pancreatitis), cellulitis
— Aspiration risk: witnessed event, altered mental status, dysphagia, recent extubation, GI bleed
— Transfusion history: ARDS within 6 hours of blood product = TRALI
— Trauma: chest wall injury, long-bone fracture (fat embolism), massive resuscitation
— Drugs/toxins: amiodarone, bleomycin, nitrofurantoin, salicylate OD, opioid OD, e-cigarette/vaping (EVALI)
— Travel/exposure: influenza, COVID-19, hantavirus, legionella
— Pancreatitis: epigastric pain radiating to back, alcohol use, gallstones
— Chronic alcohol use doubles ARDS risk after sepsis
— Smoking and obesity increase risk; obesity paradoxically improves survival
— Prior chemotherapy/radiation → consider drug-induced pneumonitis differential
Board pearl: A patient transfused 4 units PRBC for GI bleed who develops bilateral infiltrates and hypoxemia within 6 hours → TRALI (a form of ARDS); stop the transfusion, report to blood bank, and the donor (often multiparous female with anti-HLA antibodies) should be deferred from future donation.
Key distinction: TACO (transfusion-associated circulatory overload) presents with elevated BNP, JVD, HTN, and responds to diuresis; TRALI has normal-to-low CVP and does not respond to diuretics — supportive ventilation is the answer.

— RR >30, SpO₂ low despite high FiO₂
— Tachycardia from hypoxia and underlying sepsis
— BP variable — hypotension suggests concurrent septic shock
— Fever if infectious driver
— Diffuse bilateral crackles ("velcro" quality), often more prominent in dependent zones
— No focal consolidation typically; dullness if effusion
— Wheezing rare — if present, reconsider asthma/COPD/CHF
— No S3 gallop, no JVD, no peripheral edema typically in pure ARDS
— If present → suspect cardiogenic component or fluid overload
— Bedside echo is the modern standard — assess LV function, RV size, IVC, B-lines
— PCWP historically ≤18 mm Hg (Swan-Ganz no longer routine; pulmonary artery catheters did not improve outcomes — ARDSNet FACTT trial)
— BNP: <100 supports non-cardiogenic; >500 favors cardiac, but overlap exists in critical illness
Step 3 management: When the CCS stem says "bilateral crackles, no JVD, no S3, recent pancreatitis" — do not order furosemide. Order echocardiogram to confirm preserved EF, then proceed with lung-protective ventilation and source control. Diuresis is reserved for the conservative fluid strategy phase after shock has resolved (FACTT trial: conservative fluids → more ventilator-free days, no mortality change).
Board pearl: Petechiae + hypoxemia + altered mental status 24–72 hours after long-bone fracture = fat embolism syndrome — manage as ARDS with lung-protective ventilation; early fracture fixation is preventive.

— Early: respiratory alkalosis with hypoxemia (compensatory hyperventilation)
— Late: respiratory acidosis as fatigue sets in or with permissive hypercapnia on the vent
— Calculate PaO₂/FiO₂ ratio — defines severity and PEEP/prone decisions
— A-a gradient widened (shunt physiology)
— Bilateral patchy alveolar/interstitial opacities sparing costophrenic angles early
— No cardiomegaly, no Kerley B lines, no cephalization (helps distinguish from CHF)
— Progresses to diffuse "whiteout" in severe disease
— Heterogeneous dependent consolidation with anterior sparing ("baby lung")
— Useful to rule out PE, abscess, empyema, lobar pneumonia
— Blood cultures ×2, sputum Gram stain/culture, urinalysis/UA culture
— Respiratory viral PCR (influenza, RSV, SARS-CoV-2)
— Procalcitonin, lactate
— Legionella and pneumococcal urinary antigens for severe CAP
— BNP/NT-proBNP, troponin, ECG
— Bedside echocardiogram — single most useful test to exclude cardiogenic edema
— CBC (leukocytosis, thrombocytopenia in sepsis), CMP, lipase if pancreatitis suspected
— Coags + fibrinogen (DIC common in sepsis-driven ARDS)
— LDH (often elevated; nonspecific)
CCS pearl: On the CCS interface, an efficient opening order set for suspected ARDS reads: ABG, CXR portable, CBC, BMP, lactate, blood cultures ×2, urinalysis, sputum culture, BNP, troponin, ECG, bedside echo. Then advance the clock 30 minutes to receive results and pivot.
Key distinction: Cardiogenic edema = cardiomegaly, vascular cephalization, Kerley B lines, pleural effusions, ↑BNP, ↓EF. ARDS = patchy peripheral opacities, normal heart size, ↔BNP, preserved EF.

— Excludes LV systolic/diastolic dysfunction as primary cause
— Assesses RV function — ARDS frequently induces acute cor pulmonale (20–25%), worsening prognosis
— Evaluates IVC for volume status guidance
— Indicated when etiology unclear or immunocompromised host
— Sends for bacterial, fungal, PCP, viral, AFB, cytology
— Distinguishes diffuse alveolar hemorrhage (progressively bloodier returns) from pure ARDS
— Diffuse B-lines with spared areas, subpleural consolidations, irregular pleural line favor ARDS
— Smooth pleural line + symmetric B-lines + bilateral effusions favor cardiogenic edema
— When PE is on differential (sudden hypoxemia, RV strain, no clear infiltrate driver)
— ANA, ANCA, anti-GBM, anti-Jo-1 → diffuse alveolar hemorrhage, vasculitis, antisynthetase syndrome
— IgE, eosinophils → acute eosinophilic pneumonia (steroid-responsive)
— Drug-induced pneumonitis screen (amiodarone, nitrofurantoin, methotrexate, immune checkpoint inhibitors)
Board pearl: Acute eosinophilic pneumonia mimics ARDS in a young smoker with peripheral eosinophilia on BAL — responds dramatically to corticosteroids, unlike most ARDS phenotypes. Don't miss it.
Step 3 management: In refractory ARDS without a clear precipitant, escalate to bronchoscopy with BAL before empiric immunosuppression. The exam rewards making a diagnosis, not blind steroid use.
Key distinction: Diffuse alveolar hemorrhage — hemoptysis (only ⅓ of patients), dropping Hgb, progressively bloody BAL returns; requires immunosuppression, not just ventilatory support.

— Mild (P/F 200–300): trial HFNC or NIV in select patients (no shock, alert, cooperative)
— Moderate (P/F 100–200): intubate, lung-protective ventilation, higher PEEP, consider prone
— Severe (P/F <100): intubate, prone positioning ≥16 h/day, consider neuromuscular blockade, ECMO referral
— HFNC (FLORALI trial) reasonable in non-hypercapnic hypoxemic respiratory failure
— NIV higher failure rate in moderate–severe ARDS; reserve for immunocompromised, COPD overlap, or cardiogenic component
— Intubate early if: P/F <150, shock, altered mental status, accessory muscle use after 1 hour of HFNC, rising RR
— ROX index (SpO₂/FiO₂ ÷ RR) <4.88 at 12 h on HFNC predicts intubation
— Tidal volume 6 mL/kg ideal body weight (calculated by height/sex, not actual weight)
— Plateau pressure ≤30 cm H₂O
— Driving pressure (Pplat − PEEP) <15 cm H₂O — strongest predictor of mortality
— PEEP titrated per FiO₂ using ARDSNet table; higher PEEP for moderate–severe
— SpO₂ goal 88–95%, PaO₂ 55–80
— pH ≥7.20 (permissive hypercapnia accepted)
CCS pearl: A first-pass CCS vent order should read: "Intubate, mechanical ventilation: AC/VC, TV 6 mL/kg IBW, RR 18, FiO₂ 1.0, PEEP 10, titrate to SpO₂ 88–95% and Pplat ≤30." Then advance the clock 1 hour and recheck ABG and plateau pressure.
Board pearl: Driving pressure (ΔP = Pplat − PEEP) is the single most important modifiable mechanical variable; keep <15.

— Fentanyl infusion for analgesia (first-line per PADIS guidelines)
— Propofol or dexmedetomidine for sedation; avoid benzodiazepines (delirium, longer vent days)
— Target RASS −2 to 0; perform daily spontaneous awakening trials
— Cisatracurium ×48 hours for severe ARDS (P/F <150) with ventilator dyssynchrony despite deep sedation
— ACURASYS showed benefit; ROSE trial neutral — current use is selective, not routine
— Always pair with deep sedation; monitor train-of-four
— Dexamethasone 20 mg IV daily ×5 days, then 10 mg ×5 days (DEXA-ARDS) — moderate–severe ARDS within 30 days of onset
— Dexamethasone 6 mg ×10 days for COVID-19 ARDS requiring O₂ (RECOVERY)
— Avoid in unresolved infection without source control; screen for strongyloides in endemic populations
— Empiric broad-spectrum within 1 hour if sepsis/pneumonia suspected (vanc + pip-tazo or cefepime; add oseltamivir during flu season)
— De-escalate based on cultures
— Conservative strategy (FACTT) once shock resolved: net even-to-negative balance with diuretics → more ventilator-free days
— Inhaled nitric oxide or epoprostenol — rescue for refractory hypoxemia or RV failure; improves oxygenation transiently, no mortality benefit
Step 3 management: Stress ulcer prophylaxis (PPI/H2 blocker) and VTE prophylaxis (LMWH or heparin SC) are required orders on every ventilated patient — these are CCS checkbox items.
Board pearl: Daily SAT + SBT (ABCDEF bundle) reduces vent days and ICU mortality — don't forget the A2F bundle orders.

— Volume-control AC, TV 6 mL/kg IBW (start 8, reduce over 2 h to 6, can go to 4 if Pplat high)
— PEEP/FiO₂ tables — low or high PEEP strategies; higher PEEP for moderate–severe per LOVS/ExPress meta-analysis
— Pplat ≤30, ΔP <15, pH ≥7.20 (RR up to 35 allowed for permissive hypercapnia)
— Severe ARDS, P/F <150 on FiO₂ ≥0.6, PEEP ≥5
— ≥16 hours/day (PROSEVA trial — absolute mortality reduction ~16%)
— Continue until P/F >150 in supine for 4 hours
— Risks: pressure injuries, ETT displacement, line dislodgement, facial edema
— Refractory hypoxemia despite optimized vent, prone, and NMB
— P/F <50 for >3 h, P/F <80 for >6 h, or uncompensated hypercapnia with pH <7.25 (EOLIA criteria)
— Best at high-volume ECMO centers — early transfer improves outcomes
— Contraindications: irreversible underlying disease, severe comorbidity, prolonged high-pressure ventilation >7 days (relative)
— Consider at day 10–14 if prolonged ventilation anticipated; no mortality benefit to early trach but improves comfort/weaning
CCS pearl: Refractory hypoxemia escalation order on CCS: deepen sedation → neuromuscular blockade → prone → inhaled vasodilator → ECMO referral. Each step should be tried before the next; the exam rewards a stepwise, evidence-based ladder.
Board pearl: PROSEVA proning works because it improves V/Q matching, reduces overdistension of nondependent lung, and reduces ventilator-induced lung injury.

— Higher baseline mortality; frailty score predicts outcomes better than age alone
— Reduced respiratory reserve, sarcopenia → harder weaning, longer ventilator days
— Goals-of-care discussion early — clarify code status, intubation preferences, advance directives before crisis escalation
— Delirium risk high: avoid benzodiazepines, prioritize dexmedetomidine, early mobilization
— Sedation pharmacokinetics altered: lower propofol doses; monitor for hypotension and hypertriglyceridemia
— AKI develops in ~40% of ARDS patients — synergistic mortality
— Conservative fluids especially important; avoid nephrotoxins (aminoglycosides, IV contrast when possible)
— CRRT (continuous renal replacement) preferred over intermittent HD in hemodynamically unstable ARDS — better fluid removal tolerance
— Dose-adjust meds: cefepime (neurotoxicity risk), piperacillin-tazobactam, vancomycin (trough/AUC monitoring)
— Cisatracurium preferred NMB in renal failure (Hofmann elimination, no active metabolites)
— Higher ARDS mortality; hepatopulmonary syndrome can confound oxygenation assessment
— Coagulopathy increases procedural bleeding risk (central lines, bronchoscopy)
— Avoid acetaminophen >2 g/day, benzodiazepines (encephalopathy), nephrotoxic NSAIDs
— Propofol dose reduction; fentanyl preferred over morphine (no active metabolites)
— Watch for hepatorenal syndrome with aggressive diuresis
— Use ideal body weight for TV calculation, not actual
— Higher PEEP often needed (chest wall stiffness, atelectasis)
— Reverse Trendelenburg improves mechanics
— Paradoxical survival advantage ("obesity paradox") in ARDS
Step 3 management: Before escalating to ECMO or prolonged ventilation in an elderly patient with limited functional baseline, document a goals-of-care conversation with surrogate — the exam rewards proactive communication.
Board pearl: Cisatracurium is the NMB of choice in renal/hepatic failure due to organ-independent Hofmann elimination.

— Physiologic changes: ↑minute ventilation, ↓FRC, baseline respiratory alkalosis (pH ~7.42, PaCO₂ ~30)
— Target PaO₂ ≥70 and SpO₂ ≥95% — fetal oxygenation depends on maternal PaO₂
— Permissive hypercapnia limited — fetal acidosis risk; keep PaCO₂ <60 if possible
— Left lateral tilt to relieve aortocaval compression after 20 weeks
— Common precipitants: influenza, COVID-19, pyelonephritis, amniotic fluid embolism, preeclampsia/pulmonary edema
— Delivery considerations: if maternal status worsening near term, delivery may improve respiratory mechanics
— Multidisciplinary team: OB, MFM, neonatology, ICU
— Uses oxygenation index (OI = FiO₂ × MAP × 100 / PaO₂) instead of P/F ratio
— Mild OI 4–8, moderate 8–16, severe ≥16
— Same lung-protective principles; TV 5–8 mL/kg IBW
— Surfactant not routinely beneficial in pediatric ARDS (unlike neonatal RDS)
— Broader infectious differential: PCP, CMV, invasive aspergillus, mucormycosis, nocardia
— Early bronchoscopy with BAL strongly indicated
— Add empiric TMP-SMX (PCP), voriconazole (aspergillus) until cultures back
— NIV may be reasonable trial in selected immunocompromised patients (avoid VAP risk) — but don't delay intubation if failing
— Adjust immunosuppression in consultation with primary service
Board pearl: ARDS in pregnancy + influenza season → start oseltamivir empirically without waiting for testing; maternal influenza mortality is high and treatment is time-sensitive.
Key distinction: Amniotic fluid embolism — sudden hypoxemia, hypotension, DIC, and altered mental status during labor/delivery; supportive management with lung-protective ventilation, blood products, and uterotonic support; mortality very high.

— Volutrauma (overdistension), barotrauma (high pressures), atelectrauma (cyclic opening/closing), biotrauma (cytokine release)
— Prevented by lung-protective ventilation — the entire rationale
— Sudden ↓SpO₂, ↑peak pressure, ↓BP, unilateral absent breath sounds → needle decompression then chest tube
— Develops >48 h after intubation
— Prevent with HOB elevation 30–45°, oral chlorhexidine, daily SAT/SBT, subglottic suction ETT, DVT and PUD prophylaxis (the VAP bundle)
— Treat with broad-spectrum coverage including MRSA and pseudomonas; de-escalate per cultures
— From high PEEP, hypoxic vasoconstriction, hypercapnia
— Manage: minimize Pplat, ΔP; optimize oxygenation; consider iNO; prone
— Risk factors: prolonged NMB, corticosteroids, hyperglycemia, immobility
— Causes prolonged ventilator weaning; early mobilization helps
— Persistent dyspnea, reduced DLCO (often normalizes by 1 year)
— Cognitive impairment (40–50% at 1 year)
— PTSD, depression, anxiety
— Functional disability — many do not return to baseline employment
Step 3 management: When peak pressure rises suddenly on a stable vent — first disconnect from vent and bag manually, then assess for DOPE: Displacement (ETT), Obstruction (mucus, kink), Pneumothorax, Equipment failure. CCS rewards systematic troubleshooting.
Board pearl: Survivors of ARDS need pulmonary rehab, mental health screening, and cognitive assessment — refer at discharge.

— P/F <150 despite optimized PEEP/FiO₂ → consider prone positioning and NMB
— P/F <80 despite proning → consult ECMO center early
— Worsening RV failure on echo → reduce Pplat, add iNO, consider VV-ECMO
— Severe hypoxemia (P/F <50 ×3 h, or <80 ×6 h)
— Uncompensated hypercapnia (pH <7.25 with PaCO₂ ≥60 ×6 h despite RR 35)
— Refractory to standard rescue therapies
— Earlier is better — transfer before catastrophic deterioration; >7 days of high-pressure ventilation is a relative contraindication
— Pulmonary/critical care: primary management
— Infectious disease: for unusual organisms, immunocompromised hosts, persistent fever
— Cardiology: if cardiogenic component suspected or RV failure
— Nephrology: for CRRT in concurrent AKI
— Palliative care: early integration for symptom management and goals-of-care
— Nutrition: enteral feeding within 24–48 h (trophic feeds adequate first week)
— Stabilize first: secure airway, adequate sedation, vasopressors as needed
— Communicate vent settings, ABG, hemodynamics, medications in handoff
— Use specialized transport teams for ECMO candidates
CCS pearl: On CCS, when the case escalates beyond your current facility's capability, the correct order is "Transfer to tertiary care center with ECMO capability" — and continue stabilizing in transit (don't drop sedation or vasopressors).
Step 3 management: Early palliative care consultation (within 72 h of ICU admission for ARDS) is associated with better goals-concordant care without increasing mortality — a high-yield Step 3 systems-based answer.

— JVD, S3, peripheral edema, ↑BNP, cardiomegaly, cephalization, Kerley B lines on CXR
— Echo shows ↓EF or diastolic dysfunction
— Responds to diuresis, afterload reduction, NIV (BiPAP)
— Can cause ARDS but typically starts focal before bilateral
— Productive cough, focal consolidation, positive cultures/antigens
— Note: severe pneumonia is an ARDS trigger when bilateral involvement develops
— Witnessed aspiration → chemical injury → bilateral infiltrates within hours
— Often involves right lower lobe and posterior segments
— Supportive care; antibiotics only if pneumonia develops (>48–72 h fever, leukocytosis)
— Sudden hypoxemia, clear CXR or oligemia, RV strain on echo/ECG
— CTPA confirms; treat with anticoagulation ± thrombolysis
— Hemoptysis (variable), dropping Hgb, progressively bloody BAL
— Causes: ANCA vasculitis, anti-GBM, SLE, drugs
— Treat with high-dose steroids + immunosuppression ± plasmapheresis
— Idiopathic, rapidly progressive; histologically identical to ARDS
— Diagnosis of exclusion after BAL/biopsy; high mortality
— Young smokers, peripheral eosinophilia, steroid-responsive within hours
— Exposure history (birds, molds, hot tubs); resolves with avoidance + steroids
Key distinction: ARDS vs. cardiogenic edema is the single most tested distinction — anchor on history (precipitant), echo (EF), BNP, and exam (JVD/S3). When in doubt, get an echocardiogram.
Board pearl: Severe CAP that progresses to bilateral infiltrates and refractory hypoxemia is ARDS — both diagnoses coexist; treat the pneumonia AND apply lung-protective ventilation.

— Within 6 hours of transfusion; donor anti-HLA/anti-neutrophil antibodies
— Stop transfusion, report to blood bank; supportive ventilation
— Volume overload from transfusion; ↑BNP, ↑BP, JVD; responds to diuretics
— Amiodarone, bleomycin, methotrexate, nitrofurantoin, immune checkpoint inhibitors, gemcitabine
— Insidious in chronic exposure; acute with high-dose chemo
— Stop drug; corticosteroids; permanent pulmonary fibrosis risk with amiodarone/bleomycin
— Chronic dyspnea, "crazy paving" on CT, milky BAL — whole-lung lavage treatment
— Rapid ascent >2500 m, exertion; descent + supplemental O₂ + nifedipine
— Post-seizure, severe TBI, SAH; massive sympathetic surge
— Supportive; resolves with treatment of underlying neuro insult
— After rapid drainage of large pneumothorax or pleural effusion (>1.5 L)
— Prevented by limiting initial drainage
— Tinnitus, mixed acid-base disturbance, non-cardiogenic edema; treat with alkalinization, dialysis
— Young adult, vaping (especially THC + vitamin E acetate), bilateral infiltrates, GI symptoms
— Stop vaping; corticosteroids; diagnosis of exclusion (rule out infection)
— Specific therapies: dexamethasone, remdesivir, tocilizumab/baricitinib for severe; same lung-protective principles
Step 3 management: New ARDS in a patient on amiodarone for >2 months → suspect amiodarone pulmonary toxicity; check DLCO if stable, get CT (often basilar/peripheral fibrosis), stop amiodarone, start steroids, and switch antiarrhythmic.
Board pearl: Vaping + bilateral infiltrates + GI symptoms in young adult = EVALI until proven otherwise.

— Once P/F >300, hemodynamically stable, RSBI <105, passing SBTs on minimal support → extubate
— Step-down to floor when off vasopressors, stable on ≤4 L NC, mentation clear
— Stable oxygenation on room air or low-flow O₂ with home setup arranged
— Tolerating diet, ambulating with PT clearance
— Wound/line care addressed; central lines removed
— Medication reconciliation — particularly important after ICU stays (chronic meds often held)
— Follow-up appointments scheduled before discharge
— Resting SpO₂ ≤88% or PaO₂ ≤55 on room air → qualifies for continuous O₂
— SpO₂ 89% with cor pulmonale, polycythemia, or HF → also qualifies
— Reassess in 60–90 days; many ARDS survivors no longer need O₂
— Influenza (annual), pneumococcal (PCV20 or PCV15+PPSV23), COVID-19, RSV (≥60), Tdap update
— Sepsis → complete antibiotic course, source control verified
— Pancreatitis → address etiology (cholecystectomy for gallstones, alcohol cessation)
— Aspiration → swallow evaluation, dysphagia management, GERD treatment
— Resume chronic outpatient meds (statin, ACE inhibitor, beta-blocker, inhalers) — frequently held during ICU stay
— Avoid amiodarone, nitrofurantoin in ARDS survivors when alternatives exist
Step 3 management: Discharge ARDS survivors with scheduled pulmonologist follow-up within 4–6 weeks, PCP within 1–2 weeks, and a post-ICU recovery clinic referral if available — this reduces readmission and addresses post-ICU syndrome.
Board pearl: Medication reconciliation errors are the #1 source of post-ICU adverse drug events — explicitly review pre-admission med list against discharge list.

— Pulmonary function tests (spirometry, lung volumes, DLCO) — DLCO often reduced but improves over 6–12 months
— Repeat chest imaging to assess for residual fibrosis (CT if persistent abnormalities)
— 6-minute walk test for functional assessment
— Oxygen reassessment — wean home O₂ if SpO₂ adequate
— Med reconciliation, BP, glucose, weight
— Screen for post-ICU syndrome: cognitive, psychiatric, functional
— Referral for any survivor with persistent dyspnea, exercise limitation, or deconditioning
— Evidence-based: improves dyspnea, exercise capacity, QoL
— PHQ-9 (depression), GAD-7 (anxiety), screen for PTSD symptoms (nightmares, flashbacks of ICU)
— ~40% of ARDS survivors meet criteria for at least one psychiatric condition at 1 year
— Refer to therapy, consider SSRIs
— MoCA at follow-up; if impaired, refer to neuropsychology and consider occupational therapy
— Cognitive deficits in 40–50% at 1 year, equivalent to mild dementia in some
— Physical therapy, occupational therapy
— Return-to-work counseling — half of working-age survivors do not return to prior employment at 1 year
— Up to ⅓ of family members develop PTSD or depression after a loved one's ICU stay
— Provide resources, support groups (e.g., THRIVE peer support)
Step 3 management: A patient 2 months post-ARDS discharge with persistent fatigue, difficulty returning to work, and intrusive memories → screen for post-ICU syndrome, refer to post-ICU recovery clinic, and address mental health with therapy ± pharmacotherapy.
Board pearl: DLCO is the most sensitive PFT abnormality in ARDS survivors — typically improves but may never fully normalize.

— When patient is hypoxic and altered → emergency exception applies; intubate to save life
— If patient is alert and refusing → assess decision-making capacity, document, respect autonomy if capacity intact
— Obtain surrogate consent when patient lacks capacity per state hierarchy (spouse → adult children → parents → siblings)
— Review POLST/MOLST on arrival; verify with family
— A "DNR" does NOT mean "do not intubate" — clarify each component separately
— Re-address goals of care if trajectory worsens (P/F dropping, multiorgan failure)
— Use REMAP framework: Reframe, Expect emotion, Map values, Align, Plan
— Time-limited trials (e.g., "3 days of aggressive support, then reassess") are ethically appropriate and exam-favored
— Document conversations clearly
— Ethically and legally equivalent to withholding
— Continue comfort care: opioids, benzodiazepines for dyspnea/anxiety; the doctrine of double effect permits this even if it hastens death
— Extubation to comfort care is appropriate when consistent with patient values
— Suspected abuse, occupational lung injury (some states), reportable infections (TB, novel respiratory pathogens, COVID-19)
— Handoff from ICU to floor is a high-risk transition: use structured tools (I-PASS, SBAR)
— Medication reconciliation at every transition
— Verify follow-up appointments scheduled BEFORE discharge — unfilled follow-ups predict readmission
— Mandatory report to blood bank so donor can be deferred — patient safety obligation
— During pandemic-level surge, triage protocols based on SOFA scores, prognosis; institutional/state guidance applies; never base solely on age or disability
Step 3 management: A family member of an intubated ARDS patient asks "Should we keep going?" — propose a time-limited trial with explicit endpoints and a follow-up family meeting in 48–72 hours. This balances hope, realism, and ethics.
Board pearl: Comfort-directed opioids at the end of life are ethically permitted under the doctrine of double effect — relieving suffering is the intent, even if respiratory depression occurs.

Board pearl: If forced to pick one intervention that saves lives in ARDS — 6 mL/kg IBW tidal volume. Everything else builds on that foundation.

— Distractor: TACO would show ↑BNP, ↑BP, JVD.
— Distractor: 8–10 mL/kg (incorrect — VILI).
Step 3 management: When the question gives you a hemodynamically stable ARDS patient with worsening oxygenation, the answer ladder is almost always: optimize PEEP/FiO₂ per ARDSNet → NMB → prone → iNO → ECMO. Memorize this order.

ARDS is acute hypoxemic respiratory failure with bilateral non-cardiogenic infiltrates and P/F ≤300 on PEEP ≥5, and the cornerstone of management is lung-protective ventilation (6 mL/kg IBW, Pplat ≤30, ΔP <15) layered with prone positioning, NMB, conservative fluids, and ECMO escalation for refractory cases.
CCS pearl: On the CCS interface, the winning ARDS sequence is ICU transfer → ABG/CXR/echo/cultures → intubate with 6 mL/kg IBW + PEEP per ARDSNet → broad-spectrum antibiotics + source control → sedation/analgesia + DVT/PPI prophylaxis + HOB 30° → reassess at 6h and 24h with proning/NMB/ECMO escalation as needed → daily SAT/SBT → extubate when ready → schedule pulm and PCP follow-up before discharge. Get the order and the timing right, and you score.
Board pearl: Of every intervention you can offer, low tidal volume ventilation saves the most lives — never let an ARDS patient leave your CCS case on 10 mL/kg.

