An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
PE in Pregnancy
PE is a leading cause of maternal death, and pregnancy both increases thrombotic risk and degrades the usual clinical signal. Delayed diagnosis harms two patients; indiscriminate imaging and anticoagulation create their own risks.
A 29-year-old at 31 weeks’ gestation pauses halfway across the ED room, one hand braced against her sternum and the other over her abdomen. Her breathing is quick, her lips dry, and she says the pain began suddenly while folding laundry; the fetal movement she noticed earlier now feels less obvious. Her blood pressure is 104/68, heart rate 128, and oxygen saturation 92% on room air. The monitor continues to alarm as the next decision waits.
— What’s your move? Read on.
Before you read
How should pregnancy alter—not eliminate—the use of D-dimer, CTPA, and V/Q scanning?
What separates submassive from massive PE at the bedside?
When to Think of It
Think PE with unexplained dyspnea, pleuritic chest pain, syncope/presyncope, hemoptysis, tachycardia, hypoxemia, unilateral leg swelling, or sudden cardiopulmonary deterioration—especially with prior VTE, thrombophilia, cesarean delivery, immobility, obesity, or malignancy. Normal physiologic pregnancy dyspnea should not explain hypoxemia, syncope, unilateral findings, or abrupt onset.
Sick or Not Sick
The key fork is hemodynamic stability: hypotension, shock, cardiac arrest, or obstructive physiology means high-risk PE and immediate resuscitation/reperfusion planning; a normotensive patient can undergo expedited diagnostic evaluation. In stable patients, assess RV strain by echocardiography/CT, biomarkers, oxygenation, and clinical trajectory.
The First Fifteen Minutes
Place on monitors, obtain two IVs, left-lateral tilt when feasible, oxygen for maternal SpO₂ <95%, and call obstetrics, anesthesia, and pulmonary/critical care early.
High clinical suspicion or imaging delay, with no active bleeding or major anticoagulation contraindication → enoxaparin 1 mg/kg SC every 12 hours, because therapeutic factor Xa inhibition prevents clot extension; use IV unfractionated heparin instead if shock, likely procedure, severe renal failure, or rapid reversibility is needed.
If UFH is selected → 80 units/kg IV bolus, then 18 units/kg/hour infusion, titrated by institutional aPTT or anti-Xa protocol, because it reaches therapeutic effect immediately and can be stopped rapidly.
Persistent hypotension/shock from suspected massive PE → alteplase 100 mg IV over 2 hours after multidisciplinary risk-benefit discussion, because fibrinolysis can rapidly relieve pulmonary obstruction; pregnancy is not an absolute contraindication, but maternal rescue takes priority and bleeding/obstetric risk is substantial.
Cardiac arrest or peri-arrest → standard ACLS epinephrine 1 mg IV/IO every 3–5 minutes, because restoring maternal circulation is the fastest route to fetal perfusion; modify positioning and prioritize maternal resuscitation.
Definitive Care & Disposition
If DVT symptoms are present, compression ultrasound can establish VTE and justify treatment without chest imaging. In stable patients, obtain chest radiograph first; a normal radiograph often favors V/Q scanning, while an abnormal radiograph or significant alternative lung disease favors CTPA. Use a validated pregnancy-adapted pathway such as YEARS: with no YEARS criteria, D-dimer <1000 ng/mL may exclude PE; with ≥1 criterion, use <500 ng/mL—follow local assay units/protocol. Continue weight-adjusted LMWH through pregnancy and for at least 6 weeks postpartum, with at least 3 months total treatment. Massive or deteriorating PE requires ICU care, multidisciplinary thrombectomy/embolectomy or thrombolysis consideration, and continuous fetal assessment when viable.
How This One Kills
The lethal error is waiting for definitive imaging in a pregnant patient with shock or high clinical probability while withholding anticoagulation. The opposite error—calling every physiologic tachycardia “PE” and ordering imaging without structured assessment—creates diagnostic noise and delays recognition of hemorrhage, sepsis, or aortic catastrophe.
The Differential — What Else Looks Like This
Aortic dissection — tearing pain, pulse/BP asymmetry, neurologic deficit; anticoagulation can be catastrophic.
Peripartum cardiomyopathy — orthopnea, pulmonary edema, S3, reduced EF; treatment centers on heart failure rather than anticoagulation alone.
Amniotic fluid embolism — abrupt hypoxemia, hypotension, DIC during labor or shortly postpartum; thrombolysis may worsen hemorrhage.
Pneumonia/pneumothorax — fever/focal infiltrate or unilateral absent breath sounds; missing the lung process delays source-specific treatment.
The Second-Day Story
Pregnancy normally produces tachycardia, mild dyspnea, elevated D-dimer, and leg edema, so the classic signal is blunted. Older patients may present only with exertional intolerance, presyncope, abdominal discomfort, or reduced fetal movement. Preserve suspicion when symptoms are abrupt, disproportionate, associated with hypoxemia or syncope, or accompanied by unilateral leg findings; use a pregnancy-adapted diagnostic pathway rather than intuition alone.
Back to Our Patient
Back to the 29-year-old at 31 weeks: her abrupt dyspnea, pleuritic pain, tachycardia, and hypoxemia make PE a priority rather than normal pregnancy physiology. She is currently normotensive but concerning, so the team monitors her, obtains IV access and a chest radiograph, assesses for DVT, and uses a pregnancy-adapted diagnostic pathway; because her clinical suspicion remains high and imaging is delayed, therapeutic enoxaparin 1 mg/kg SC every 12 hours is started after bleeding review. CTPA demonstrates bilateral PE with RV strain but no shock, so she is admitted to a monitored setting with obstetric and critical-care involvement, continued anticoagulation, and fetal surveillance.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 29-year-old G3P2 at 31 weeks with sudden pleuritic chest pain, dyspnea, and decreased perceived fetal movement beginning today. She is tachycardic at 128, saturating 92% on room air, and normotensive at 104/68; she has no fever, cough, vaginal bleeding, unilateral leg pain, or focal neurologic symptoms. Exam shows tachypnea and mild right calf asymmetry without wheeze or pulmonary edema. ECG shows sinus tachycardia, and her chest radiograph is not diagnostic. My leading diagnosis is acute PE with intermediate risk based on RV strain but no shock; I’m placing her on oxygen and monitors, consulting OB and critical care, starting therapeutic LMWH while expediting CTPA, and will escalate to reperfusion planning if she becomes unstable.”
Study Directive
Draw the pregnancy-adapted YEARS algorithm from memory, including both D-dimer thresholds.
Practice choosing V/Q versus CTPA using three sample chest radiographs.
Memorize therapeutic LMWH and UFH dosing, then verify renal-adjustment details in Lexicomp or your institutional protocol.
Review one case of massive PE in pregnancy and state the trigger for anticoagulation, thrombolysis, and ICU consultation.
Hammache M, Simard C, Hamel S, et al. · Chest, 2025 · PMID 40404047 · cited 4×
A current reference for using pregnancy-adapted diagnostic algorithms, including D-dimer, compression ultrasonography, and selection of V/Q scanning versus CTPA, to evaluate suspected PE while limiting unnecessary imaging.
HEAR can rapidly identify patients with a low short-term risk of major cardiac events without initially using troponin. It is a risk-stratification tool—not...
A 47-year-old warehouse supervisor sits upright beneath the fluorescent lights, rubbing a pressure-like sensation from his chest toward his left shoulder. His skin is warm and dry, and he says the discomfort began while carrying a box but eased before arrival. The ECG is on the screen, the first troponin is still pending, and the question is whether his reassuring appearance is enough.
Before You Read
What does HEAR measure, and what important variable does it omit?
Which patients can safely enter a low-risk accelerated diagnostic pathway?
When does a low score become falsely reassuring?
Why It Matters
HEAR can rapidly identify patients with a low short-term risk of major cardiac events without initially using troponin. It is a risk-stratification tool—not a diagnosis, and not permission to ignore concerning symptoms or ECG changes.
When to Think of It
Use HEAR in adults with possible ACS who are clinically stable and have a nondiagnostic ECG: History, ECG, Age, and Risk factors, each scored 0–2, for a total of 0–8. It is most useful as the pre-troponin portion of a broader HEART or accelerated diagnostic pathway.
Sick or Not Sick
The key call is whether the patient is appropriate for a low-risk pathway at all. A HEAR score of 0–3 may identify a low-risk group in selected populations, but the decision still requires serial high-sensitivity troponin, clinical reassessment, and local pathway validation. STEMI, ischemic ECG changes, hemodynamic instability, ongoing severe pain, or a highly concerning story overrides a low numerical score.
The First Fifteen Minutes
Obtain a 12-lead ECG within 10 minutes, repeat it for ongoing symptoms, place the patient on monitoring, establish IV access, and send serial high-sensitivity troponins per local protocol.
Suspected ACS without active bleeding or true aspirin allergy → aspirin 324 mg PO, chewed once, because irreversible platelet inhibition reduces coronary thrombus propagation.
Ischemic discomfort with adequate blood pressure and no PDE-5 inhibitor use, RV infarct concern, or severe aortic stenosis → nitroglycerin 0.4 mg SL every 5 minutes for up to 3 doses, because venodilation lowers preload and myocardial oxygen demand; it is symptom therapy, not a rule-out test.
Do not give anticoagulants or P2Y12 inhibitors solely because of a HEAR score; add them only when ACS is diagnosed or strongly suspected and cardiology/local protocol directs it.
Definitive Care & Disposition
Complete the validated HEART pathway with serial hs-troponins and reassessment. Low-risk patients with nonischemic ECGs and negative serial troponins may be discharged with timely follow-up and clear return precautions; intermediate-risk patients generally need observation, further testing, or cardiology input. High-risk patients, dynamic ECG changes, significant troponin elevation, recurrent pain, or instability require ACS admission and urgent cardiology evaluation.
How This One Kills
The dangerous failure is using HEAR as a “negative troponin” and discharging a patient with an evolving MI, posterior infarction, left main ischemia, or an atypical but high-risk story. HEAR does not include troponin and is not validated to overrule an ischemic ECG or clinician concern.
The Atypical Presentation
Women, older adults, and patients with diabetes or CKD may report dyspnea, fatigue, nausea, epigastric discomfort, or isolated shoulder pain rather than chest pressure. Their “history” component can be deceptively low despite real ischemia. Ask what the patient was doing, what symptoms limit activity, and whether this differs from baseline; score the story, but do not let the score replace judgment.
Back to Our Patient
Back to the 47-year-old warehouse supervisor: his exertional pressure is concerning, but his stable appearance and currently nondiagnostic ECG permit structured risk assessment rather than immediate discharge. His HEAR score is 2—moderately suspicious history, normal ECG, age 47, and no major risk factors—so he enters a serial hs-troponin pathway after receiving aspirin 324 mg chewed; nitroglycerin is reserved for recurrent pain with safe blood pressure. Serial troponins remain negative, repeat ECGs show no dynamic changes, and he is discharged with prompt primary-care/cardiology follow-up and explicit return precautions rather than being labeled “no cardiac disease.”
Patient Presentation to Attending
“This is a 47-year-old man with exertional pressure-like chest discomfort radiating to the left shoulder that began carrying a box and resolved before arrival. He has no pleuritic pain, dyspnea, syncope, fever, vomiting, or tearing radiation, and he is currently pain-free, normotensive, and well appearing. His ECG is nonischemic without dynamic changes, and his initial hs-troponin is pending. His HEAR score is 2, placing him in a potentially low-risk group but not excluding ACS. I plan aspirin, serial ECGs and hs-troponins using our accelerated pathway, reassessment for recurrent symptoms, and discharge only if the complete pathway remains negative.”
Study Directive
Memorize the 0–2 scoring anchors for all four HEAR domains.
Score five real or simulated chest-pain cases before seeing the troponin results, then compare your disposition with the validated pathway.
Review your institution’s hs-troponin timing and discharge criteria.
Practice a one-sentence explanation to patients: “This score estimates risk; the serial ECG and troponin sequence completes the evaluation.”
Key Medications
Aspirin: 324 mg PO chewed once for suspected ACS; use 162–325 mg according to local protocol.
Nitroglycerin: 0.4 mg SL every 5 minutes for up to 3 doses if appropriate; avoid with hypotension, recent sildenafil/vardenafil use within 24 hours, tadalafil within 48 hours, or suspected RV infarction.
If definite high-risk ACS requires anticoagulation, UFH is commonly 60 units/kg IV bolus, maximum 4,000 units, then 12 units/kg/hour, maximum 1,000 units/hour, titrated by protocol; dosing varies by institution—verify in Lexicomp or the ACS protocol.
Pediatric HEAR/ACS pathways are not interchangeable with adult validation studies.
High-Yield Pearls
HEAR is a gateway to serial testing, not a replacement for serial testing.
The score is least trustworthy when the ECG is ischemic, symptoms are ongoing, or the clinical story is discordantly alarming.
A “low-risk” score predicts short-term event risk only within the population and pathway in which it was validated.
Acute pericarditis — positional pain, diffuse ST elevation/PR depression; treating as focal ACS may lead to unnecessary invasive therapy.
Esophageal rupture — severe vomiting followed by chest pain, subcutaneous emphysema, toxicity; antithrombotics can be disastrous.
Board Question
Which statement about the HEAR score is most accurate?
AIt includes high-sensitivity troponin as its fifth component
BA score of 0–3 alone rules out ACS in every patient
CIt uses history, ECG, age, and risk factors to identify patients for further low-risk evaluation
DIt should be used to discharge patients with STEMI if the score is low
Reveal answer
Correct: C
HEAR is the pre-troponin component of HEART: history, ECG, age, and risk factors. It supports selection for an accelerated pathway but does not independently rule out ACS or override an ischemic ECG.
Supports using the History, ECG, Age, and Risk Factors (HEAR) score to identify selected ED chest-pain patients at very low 30-day cardiac risk, potentially before troponin testing.
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Ventricular Septal Defect
A VSD is often acyanotic, but a large defect can produce severe pulmonary overcirculation and heart failure as pulmonary vascular resistance falls after...
A 6-week-old infant arrives wrapped in a pink blanket, breathing fast enough to tug the fabric at the ribs. The parents describe sweaty feeds, frequent pauses, and a diaper that has stayed nearly dry since morning; beneath the monitor, a harsh sound fills each heartbeat. The infant is pale but awake, and the room grows quiet as the team decides whether this is a feeding problem or something more dangerous.
Before You Read
Why can a VSD cause heart failure even when oxygen saturation is normal?
Which findings indicate pulmonary overcirculation and impending decompensation?
When is a murmur less reassuring than its disappearance?
Why It Matters
A VSD is often acyanotic, but a large defect can produce severe pulmonary overcirculation and heart failure as pulmonary vascular resistance falls after birth. A deteriorating infant may have a quieter murmur because flow across the defect has decreased—not because the lesion has improved.
When to Think of It
Enter VSD when an infant has a harsh holosystolic murmur at the lower left sternal border, poor feeding, diaphoresis with feeds, tachypnea, recurrent respiratory symptoms, poor weight gain, hepatomegaly, or signs of pulmonary edema. Large defects may have a softer murmur, a diastolic rumble at the apex, a hyperdynamic precordium, and a loud P2.
Sick or Not Sick
The key call is compensated versus decompensated heart failure/low systemic perfusion. Sick features include marked work of breathing, hypoxemia, exhaustion, altered mental status, hepatomegaly with poor perfusion, oliguria, acidosis, or shock. A well-appearing, feeding infant with stable oxygenation can undergo expedited cardiology evaluation; a toxic or failing infant needs resuscitation and PICU-level care.
The First Fifteen Minutes
Place on cardiorespiratory monitoring, obtain IV/IO access, check glucose and temperature, minimize feeding if respiratory distress is significant, and use oxygen only for hypoxemia; excessive oxygen can worsen pulmonary overcirculation.
Clinical pulmonary edema or significant congestive heart failure → furosemide 1 mg/kg IV, because loop diuresis rapidly reduces pulmonary venous congestion; a typical adult ED dose is 40 mg IV, but pediatric dosing and renal status govern.
Shock with suspected low cardiac output after specialist consultation → epinephrine infusion 0.05–0.5 mcg/kg/min IV, titrated to perfusion, because beta-1 stimulation supports contractility and alpha effects support vascular tone; use institutional pediatric vasoactive protocols.
Avoid empiric prostaglandin solely for an isolated VSD; cyanosis, shock, or ductal-dependent physiology → alprostadil 0.05–0.1 mcg/kg/min IV, because maintaining ductal patency can bridge an alternative critical congenital lesion while echocardiography is arranged. Dose varies and requires PICU/cardiology guidance.
Respiratory failure despite support → ketamine 1–2 mg/kg IV for induction and rocuronium 1.2 mg/kg IV for paralysis, because controlled airway management reduces oxygen consumption and work of breathing; involve pediatric anesthesia and anticipate hemodynamic collapse.
Definitive Care & Disposition
Obtain echocardiography to define defect size, shunt direction, pulmonary pressures, ventricular function, and associated lesions. Small restrictive VSDs often close spontaneously and need outpatient cardiology follow-up. Moderate or large defects with heart failure require pediatric cardiology management, commonly diuretics and nutritional support, with surgical or catheter closure if symptoms, growth failure, pulmonary hypertension, or ventricular enlargement persist. Admit infants with respiratory distress, poor perfusion, dehydration, significant feeding intolerance, or uncertain diagnosis; PICU for respiratory failure, shock, severe acidosis, or escalating vasoactive support.
How This One Kills
The specific danger is assuming that a quieter murmur means improvement. As pulmonary vascular resistance rises or the infant becomes low-flow, the pressure gradient across the VSD falls, the murmur softens, and the infant may deteriorate into pulmonary hypertension or Eisenmenger physiology.
The Atypical Presentation
The infant may not have a dramatic murmur, and oxygen saturation is often normal because the shunt is left-to-right. Instead, look for feeding that takes too long, sweating, tachypnea during sleep, recurrent “bronchiolitis,” falling weight percentile, hepatomegaly, and fewer wet diapers. In a sick infant, reassess perfusion and acid-base status rather than relying on the murmur’s intensity.
Back to Our Patient
Back to the 6-week-old with sweaty feeds and tachypnea: the trigger presentation suggests pulmonary overcirculation from a significant VSD, and the infant’s pallor, tachypnea, oliguria, and hepatomegaly make this decompensated heart failure rather than a simple feeding issue. The team monitors, obtains IV access, limits oral intake during distress, gives furosemide 1 mg/kg IV, and obtains urgent echocardiography; oxygen is used only if hypoxemic. Echo shows a large left-to-right VSD with pulmonary edema and preserved but strained ventricular function, so the infant is admitted to the PICU for cardiology-directed diuresis, nutritional support, and planning for definitive closure.
Patient Presentation to Attending
“This is a 6-week-old infant with two weeks of worsening tachypnea, diaphoresis and pauses during feeds, poor intake, and decreased urine output. The infant is awake but pale, tachypneic with retractions, has a harsh holosystolic murmur at the lower left sternal border, hepatomegaly, and no focal wheezing; oxygen saturation is 97% on room air. The combination of feeding intolerance, pulmonary findings, hepatomegaly, and oliguria is concerning for decompensated heart failure from a large VSD, although bronchiolitis and other congenital lesions remain possible. I’m placing the infant on continuous monitoring, obtaining IV access, giving furosemide 1 mg/kg IV, limiting feeds during respiratory distress, and arranging emergent echocardiography with PICU and cardiology admission.”
Study Directive
Draw the pressure and flow changes across a VSD from birth through the first 8 weeks.
Review an echocardiogram showing restrictive versus nonrestrictive VSD and identify shunt direction.
Memorize infant heart-failure findings: tachypnea, diaphoresis with feeds, hepatomegaly, growth failure, and oliguria.
Practice an initial stabilization plan for a distressed infant, including when to use diuresis, vasoactive support, alprostadil, and PICU consultation.
Key Medications
Furosemide: 1 mg/kg IV in infants; repeat/adjust based on response, renal function, and electrolytes. Adult ED starting dose is commonly 20–40 mg IV.
Epinephrine infusion for pediatric shock: 0.05–0.5 mcg/kg/min IV, titrated; dose is institution-dependent—check pediatric critical-care protocol.
Alprostadil: 0.05–0.1 mcg/kg/min IV when ductal-dependent disease is suspected; lower maintenance doses are often used after response—verify urgently with cardiology/PICU.
Ketamine: 1–2 mg/kg IV induction; rocuronium: 1.2 mg/kg IV for RSI. Pediatric airway dosing varies with physiology—verify local protocol.
Chronic captopril or digoxin therapy is specialist-directed, not an empiric ED intervention.
High-Yield Pearls
Normal oxygen saturation does not make a large VSD benign; left-to-right shunting causes pulmonary overcirculation without early cyanosis.
A large VSD may become clinically apparent weeks after birth as pulmonary vascular resistance falls.
Severe pulmonary hypertension can eventually reverse the shunt; late cyanosis is a warning of advanced vascular disease.
The Mimics
PDA — continuous “machinery” murmur and bounding pulses; confusing the lesions can misdirect assessment of shunt physiology.
AV septal defect — atrioventricular valve regurgitation, widely split S2, and often Down syndrome; closure strategy differs.
Tetralogy of Fallot — cyanosis and episodic hypercyanotic spells; treating it as isolated pulmonary overcirculation misses ductal dependence or dynamic obstruction.
Bronchiolitis — wheeze and respiratory distress without cardiomegaly/hepatomegaly; diuresis alone delays respiratory and infectious care.
Board Question
A 2-month-old with a large VSD develops worsening tachypnea and poor feeding. The murmur is now softer than at a prior visit, and the infant has hepatomegaly and poor perfusion. What best explains the quieter murmur?
ASpontaneous closure of the VSD
BIncreased left-to-right pressure gradient
CReduced flow across the defect from rising pulmonary vascular resistance or low cardiac output
DDevelopment of an atrial septal defect
Reveal answer
Correct: C
Murmur intensity depends on flow and the pressure gradient across the defect. As pulmonary vascular resistance rises or systemic output falls, the gradient and turbulent flow may decrease even while the infant worsens.
Provides a practical synthesis of neonatal VSD diagnosis, assessment of hemodynamic significance, and indications for medical management versus closure or specialist referral.
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Advanced Modes of Mechanical Ventilation
Advanced modes can improve synchrony, oxygenation, or work of breathing, but none rescues a poor assessment or injurious settings. The ventilator must be...
A 63-year-old man lies motionless beneath the ventilator’s blue LEDs, his chest rising unevenly as the machine clicks and hisses. The screen shows repeated high-pressure alarms, a climbing respiratory rate, and a plateau pressure that has crept upward despite acceptable oxygen saturation. The bedside nurse reports that the patient is “fighting the vent,” and the next adjustment has not yet been made.
Before You Read
When does an advanced mode solve a physiologic problem, and when does it merely hide one?
How should you distinguish high resistance from low compliance at the bedside?
What targets matter more than the mode name in ARDS?
Why It Matters
Advanced modes can improve synchrony, oxygenation, or work of breathing, but none rescues a poor assessment or injurious settings. The ventilator must be adjusted to the patient’s physiology, with lung-protective targets taking precedence over attractive labels.
When to Think of It
Consider advanced modes when conventional volume- or pressure-control ventilation produces refractory dyssynchrony, severe hypoxemia, high plateau pressures, variable mechanics, or a need to reduce spontaneous effort. Common options include pressure-regulated volume control, pressure control, pressure support, APRV, proportional assist modes, and—rarely in adults—high-frequency oscillatory ventilation.
Sick or Not Sick
The critical call is whether the problem is the patient or the ventilator circuit. Immediately assess disconnection, obstruction, secretions, bronchospasm, pneumothorax, tube migration, cuff leak, auto-PEEP, and acute worsening compliance before changing modes. If unstable, disconnect and manually ventilate with 100% oxygen while troubleshooting.
The First Fifteen Minutes
Call for help, assess the patient first, auscultate, inspect the tube/circuit, check peak and plateau pressures, and obtain an ABG/VBG and portable chest radiograph when indicated.
Severe dyssynchrony threatening ventilation despite analgesia → fentanyl 25–100 mcg IV boluses, then 25–200 mcg/hour infusion, because analgesia reduces pain-driven respiratory effort; titrate to the lightest effective sedation.
Need for ongoing sedation in a hemodynamically stable adult → propofol 5–50 mcg/kg/min IV infusion, because it provides rapidly titratable hypnosis; reduce or avoid it in hypotension, severe hypertriglyceridemia, or prolonged high-dose exposure.
Hemodynamic instability or need to preserve respiratory drive during induction → ketamine 1–2 mg/kg IV, because dissociative anesthesia often preserves sympathetic tone and bronchodilates.
Persistent dangerous dyssynchrony or severe ventilator-induced effort despite adequate analgesia/sedation → rocuronium 1.2 mg/kg IV for RSI or 0.6 mg/kg IV for paralysis, because neuromuscular blockade eliminates injurious patient effort; provide deep analgesia/sedation first and use only with a clear indication.
ARDS with SpO₂ below target despite lung-protective ventilation → increase PEEP in a stepwise protocol and consider prone positioning, because recruitment and improved V/Q—not simply a higher FiO₂—address shunt physiology. No medication is required for this ventilator adjustment.
Definitive Care & Disposition
Use volume assist-control or pressure control according to familiarity and mechanics; target tidal volume 6 mL/kg predicted body weight in ARDS, reducing to 4–5 mL/kg if plateau pressure remains >30 cm H₂O. Aim plateau pressure <30 cm H₂O, adequate pH rather than a normal PaCO₂, and individualized PEEP/FiO₂. PRVC adjusts pressure to achieve a set tidal volume but can deliver variable pressures and does not eliminate dyssynchrony. APRV may support recruitment in selected refractory hypoxemia but requires expertise and careful release-time management. For moderate-severe ARDS, prone at least 12–16 hours/day when appropriate; consider early neuromuscular blockade only for severe dyssynchrony or inability to achieve lung-protective ventilation. Admit to ICU; reassess daily for sedation reduction, spontaneous awakening/breathing trials, and liberation from ventilation.
How This One Kills
The fatal mistake is treating a high-pressure alarm by simply switching modes while missing an obstructed tube, tension pneumothorax, or severe bronchospasm. A second failure is normalizing oxygenation with excessive tidal volumes or plateau pressures, converting transient respiratory failure into ventilator-induced lung injury.
The Atypical Presentation
A patient may appear “comfortable” because sedation suppresses visible distress while ventilator waveforms reveal severe ineffective efforts or double-triggering. Conversely, a high peak pressure may be caused by airway resistance with a normal plateau, not stiff lungs. Examine waveforms, compare peak with plateau pressure, inspect expiratory flow, and briefly disconnect to manual ventilation when the patient is deteriorating.
Back to Our Patient
Back to the 63-year-old beneath the blue ventilator lights: the high-pressure alarms and rising plateau pressure indicate a compliance problem until proven otherwise, not simply a need for a more advanced mode. The team first disconnects him for manual ventilation, finds no obstruction, notes bilateral breath sounds, and sees expiratory flow returning to zero; bedside ultrasound shows no pneumothorax, while ARDS from pneumonia explains the reduced compliance. After analgesia with fentanyl and titratable propofol sedation, they use low tidal volume based on predicted body weight, adjust PEEP and FiO₂, and consider paralysis only if dyssynchrony prevents lung protection; he remains in the ICU for prone therapy and daily liberation assessment.
Patient Presentation to Attending
“This is a 63-year-old intubated man with pneumonia-associated ARDS who has developed rising peak and plateau pressures, repeated high-pressure alarms, and visible ventilator dyssynchrony. He is oxygenating acceptably but has worsening compliance; expiratory flow returns to zero, and there is no unilateral absent breath sound, circuit disconnection, or obvious tube obstruction. I’m treating this first as a patient-and-ventilator emergency by manually ventilating while checking the circuit, tube, chest, and waveforms. After confirming ARDS physiology, I’ll use 4–6 mL/kg predicted body weight, keep plateau pressure below 30, optimize PEEP and FiO₂, provide analgesia and lightest effective sedation, and use neuromuscular blockade only if severe dyssynchrony prevents lung-protective ventilation.”
Study Directive
Draw pressure-time and flow-time waveforms for high resistance, low compliance, auto-PEEP, double-triggering, and ineffective efforts.
Calculate predicted body weight and a 6 mL/kg tidal volume for five sample patients.
Practice a ventilator emergency sequence: patient, tube, circuit, chest, waveform, then settings.
Compare PRVC, pressure control, pressure support, APRV, and proportional assist in one sentence each, including the physiologic problem each is intended to solve.
Key Medications
Fentanyl: 25–100 mcg IV bolus, then 25–200 mcg/hour IV infusion, titrated; institutional ranges vary.
Propofol: 5–50 mcg/kg/min IV infusion; avoid rapid bolus in unstable patients and monitor triglycerides with prolonged use.
Ketamine: 1–2 mg/kg IV for induction; infusion dosing varies—check institutional protocol.
Rocuronium: 1.2 mg/kg IV for RSI or 0.6 mg/kg IV for routine paralysis; continuous infusion requires neuromuscular monitoring and deep sedation.
For severe asthma with bronchospasm, albuterol 2.5–5 mg nebulized may be used; ipratropium 0.5 mg nebulized can be added. Verify repeated-dose protocols.
Pediatric ventilation and sedation doses differ substantially; use a pediatric critical-care reference rather than adult defaults.
High-Yield Pearls
Peak pressure reflects resistance plus compliance; plateau pressure isolates the elastic load of the respiratory system.
If expiratory flow never reaches zero, increasing respiratory rate can worsen auto-PEEP and hypotension.
A new mode cannot correct a blocked tube, pneumothorax, or incorrect predicted-body-weight calculation.
The Mimics
Circuit obstruction or mucus plug — high peak pressure with abruptly reduced delivered volume; mode changes do not remove the obstruction.
Pneumothorax — sudden hypoxemia, hypotension, unilateral breath sounds, rising pressures; delay in decompression can cause arrest.
Auto-PEEP/dynamic hyperinflation — expiratory flow fails to reach zero and hypotension worsens; increasing rate or inspiratory time makes it worse.
Patient-ventilator dyssynchrony — waveform scooping, double-triggering, or missed efforts; indiscriminate paralysis can mask pain, seizures, or metabolic drive.
Board Question
A mechanically ventilated patient with ARDS has a tidal volume of 6 mL/kg predicted body weight, a plateau pressure of 34 cm H₂O, and acceptable oxygenation. What is the best next ventilator adjustment?
AIncrease tidal volume to reduce respiratory rate
BReduce tidal volume toward 4–5 mL/kg predicted body weight
CSwitch to APRV without changing any targets
DIncrease FiO₂ to 100% and leave the tidal volume unchanged
Reveal answer
Correct: B
Plateau pressure above 30 cm H₂O increases ventilator-induced lung injury risk. Reduce tidal volume, accepting permissive hypercapnia if necessary, while maintaining adequate pH and addressing oxygenation with PEEP/FiO₂ and adjuncts such as proning.
A practical reference for matching ventilator mode and settings to patient physiology while recognizing mode-specific risks and monitoring priorities at the bedside.
Yesterday’s Differential
The daily puzzle — from editions past
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
An 82-year-old woman on digoxin and a diuretic for atrial fibrillation is brought in with two days of nausea, vomiting, and vague visual disturbance — she keeps mentioning that lights look yellow. She is bradycardic at 44 and mildly confused. What’s the diagnosis, and the first move?
Check your answer
Digoxin Toxicity. Recognize the pattern, stop the digoxin, and check a level and potassium. Treat the toxic patient — significant dysrhythmia, hemodynamic compromise, or hyperkalemia — with digoxin-specific antibody fragments (Fab) rather than chasing individual rhythms.
From the July 23 edition
Today, three days ago: Nitroglycerin. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
SL: 0.4 mg q5 min up to 3 doses if BP allows. IV infusion: start 5–10 mcg/min and titrate; SCAPE protocols may use much higher early doses per institutional protocol. Recent PDE-5 inhibitor use, hypotension, RV infarct/preload-dependent states, severe aortic stenosis caution.
From the July 16 edition
A 64-year-old man has ongoing chest pressure and ST depression in V1–V3. The initial ECG is otherwise nondiagnostic. Which additional test most directly evaluates the suspected ischemic territory?
ARight-sided leads V3R–V6R
BPosterior leads V7–V9
CRepeat ECG in 24 hours
DExercise stress testing
Reveal answer
Correct · B
Posterior leads V7–V9. Horizontal ST depression in V1–V3 may represent posterior STEMI; posterior leads can reveal ST elevation and should prompt emergent reperfusion evaluation. Right-sided leads are most useful when inferior MI suggests RV involvement.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
A 35-year-old male presents with left eye pain and vision loss after an unwitnessed altercation. On exam, there is significant left periorbital edema and ecchymosis; the left eye appears mildly proptotic. He is unable to open the eye unassisted due to swelling and pain. His...
In this episode, Sam Ashoo, MD and Dr. T.R. Eckler, MD discuss the May 2026 Emergency Medicine Practice article, Emergency Department Evaluation and Management of Serious and High-Risk Infections in the Febrile Returning Traveler . 0:16 — Podcast Introduction 1:08 — Episode Introduction 7:30 — Malaria 13:55 — Dengue 17:33 — Enteric Fever...
July covers acute flank pain, spondylosis and spondylolisthesis, fingertip injuries, post menopausal bleeding, and pediatric migraine. 1. July Introduction: Acute Flank Pain 2. Spondylosis and Spondylolisthesis 3....
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
Advanced ventilator modes hinge on how spontaneous effort interacts with machine-delivered support—a key distinction when choosing assisted modes and avoiding patient–ventilator dyssynchrony.
Spontaneous breathing can occur without ventilatory support (unassisted spontaneous breathing) or be integrated with mechanical ventilation with assisted ventilation modes (assisted spontaneous breathing).
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Cephalexin
First-generation cephalosporin
Indication
Outpatient non-purulent cellulitis and other MSSA/streptococcal SSTI, streptococcal pharyngitis, uncomplicated cystitis, and impetigo. Not MRSA-active.
What’s your dose? — reveal dosing & cautions
ED Dose
500 mg PO q6h (q12h for milder infections). Cellulitis: 500 mg PO QID. Strep pharyngitis: 500 mg PO BID x10 days. Pediatric: 25–50 mg/kg/day divided q6–12h.
Renal Adjustment
Reduce dose/frequency in CrCl < 30 mL/min (e.g. extend interval). HD: dose after dialysis.
Contraindications
Cephalosporin hypersensitivity. Use caution with documented severe (anaphylactic) penicillin allergy, though cross-reactivity with first-generation cephalosporins is low.
Interactions
Probenecid increases levels; metformin concentrations may rise.
Monitoring
Clinical response, GI tolerance; renal function in CKD.
ED Pearl
Covers MSSA and strep but NOT MRSA — a purulent abscess or cellulitis needs MRSA coverage (TMP-SMX or doxycycline), not cephalexin alone.
Procedural sedation, post-intubation sedation, refractory status epilepticus infusion in ICU context, and induction alternative in selected hemodynamically stable patients.
What’s your dose? — reveal dosing & cautions
ED Dose
Procedural sedation: 0.5–1 mg/kg IV, then 0.25–0.5 mg/kg increments. Post-intubation sedation: commonly 5–50 mcg/kg/min infusion titrated to sedation/BP.
Renal Adjustment
No renal adjustment; context-sensitive accumulation with prolonged infusion.
Contraindications
Hemodynamic instability/shock relative, egg/soy allergy no longer absolute in many policies but check local guidance, hypersensitivity.
Interactions
Opioids/benzodiazepines/other sedatives increase respiratory and hemodynamic depression.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Misc
Benign Early Repolarization
Widespread concave ST elevation with J-point notching in a young, well patient is usually benign — but the same read in anyone over 50 should not be called BER.
The Tracing
A 24-year-old man is sent in from a walk-in clinic after an ECG done for palpitations showed 'ST elevation.' He feels well, has no chest pain, and his vitals are normal. On the tracing there is widespread concave ST elevation, most prominent across the mid-to-left precordial leads V2-5, with smaller elevation in the inferior limb leads. Look closely at V4 and there is a notch at the J point — a small hook where the QRS meets the ST segment. The T waves are tall, peaked and slightly asymmetrical, concordant with the QRS. In V6 the ST elevation is dwarfed by the T wave. There is no reciprocal ST depression anywhere.
Widespread concave ST elevation, most prominent in the mid-to-left precordial leads (V2-5)
Notching or slurring at the J point — the 'fish hook' pattern, best seen in V4
Prominent, slightly asymmetrical T waves concordant with the QRS
ST elevation to T wave height ratio in V6 < 0.25
No reciprocal ST depression to suggest occlusion MI
Pearls
The ST/T ratio in V6 does real work at the bedside: < 0.25 favors BER, > 0.25 favors pericarditis, since pericarditis raises the ST segment relative to a normal-amplitude T wave.
BER is dynamic with autonomic tone — the ST elevation and J-point notching become more prominent at slower heart rates and fade with tachycardia or exercise, which can be reassuring on a repeat tracing.
Up to 10-15% of ED chest-pain patients have BER, so this is a pattern you will meet constantly; the skill is separating it from the occlusion it mimics.
Pitfalls
Do not diagnose BER in patients over 50, especially with ischemic risk factors — ST elevation in that group is far more likely to be ischemia.
BER mimics both pericarditis and acute MI; the distinguishing features (ST/T ratio, fish hook, PR depression) have limited specificity and can coexist.
The label 'benign' is not absolute: global early repolarization patterns have been linked to idiopathic VF and, in inferior leads, to increased cardiac death in long-term follow-up.
At the Bedside
In a young, well patient whose morphology fits BER with no reciprocal change, you can avoid an unnecessary cath activation — but confirm with an old ECG and, when in doubt or the patient is older, treat the ST elevation as ischemia until serial ECGs and troponins prove otherwise.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · PE in Pregnancy
Self-Examination
Test Your Understanding
A 30-year-old at 28 weeks has sudden dyspnea and pleuritic chest pain. She has no hemoptysis, no clinical signs of DVT, and PE is not judged the most likely diagnosis. Her pregnancy-adapted YEARS D-dimer is 850 ng/mL. What is the best next step?
ADiagnose PE and give alteplase
BExclude PE without chest imaging
CProceed directly to CTPA in every case
DStart warfarin and arrange outpatient follow-up
Reveal answer
Correct answer · B
In pregnancy-adapted YEARS, a patient with zero YEARS criteria can have PE excluded when D-dimer is <1000 ng/mL. This applies only when the clinical pathway is followed appropriately and the patient is stable.
Study Pace4 topics today; Issue 12 of 94 — Cardiology / Pulmonary (Weeks 7-8 A)Deadline · June 1, 2026