Core EM - Emergency Medicine Podcast

We discuss this ominous complication of providing local anesthesia.

Hosts:

Elaine Jonas, MD

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3





Download


Leave a Comment





Tags: Critical Care, Toxicology





Show Notes

I. Pathophysiology & Mechanisms

Definition: Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption.

Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue.

Agent Profile: Bupivacaine (High Risk)

Highly lipophilic with high protein binding.

“Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole.

Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility.

Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin).

Contributing Factors:

Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity.

Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold.

II. Risk Assessment & Prevention

Patient-Specific Risk Factors

Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance).

Body Composition: Low muscle mass/frailty (decreased volume of distribution).

Organ Dysfunction:

Hepatic: Reduced metabolism of amide LAs.

Renal: Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold.

Cardiac: Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade.

Pregnancy: Increased sensitivity to cardiotoxicity.

Procedural Risk Factors

Vascularity of Site (Highest to Lowest Risk):

Intercostal blocks (highest absorption rate).

Caudal/Epidural.

Interfascial plane blocks (e.g., TAP block).

Psoas compartment/Sciatic.

Brachial plexus.

Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection.

Prevention Mandates

Weight-Based Dosing:

Lidocaine (Plain): Max 4.5 mg/kg.

Lidocaine (with Epi): Max 7 mg/kg.

Bupivacaine: Max 2.5–3 mg/kg.

Incremental Injection: 3–5 mL aliquots with frequent aspiration.

Intravascular Marker: Use Epinephrine (1:200,000) to detect accidental IV placement (HR increase >10 bpmor SBP increase >15 mmHg).

III. Clinical Presentation

Neurologic Phase (Early to Late)

Subjective: Metallic taste, tinnitus, circumoral numbness/tingling.

Objective: Visual disturbances, agitation, confusion, tremors.

Critical: Generalized tonic-clonic seizures, rapid progression to CNS depression, coma, and apnea.

Note: Early phases are often masked in patients receiving midazolam or propofol.

Cardiovascular Phase

Initial: Hypertension and tachycardia (if epi used) or transient stimulatory phase.

Conduction Defects: PR prolongation, QRS widening (classic sign), bundle branch blocks.

Dysrhythmias: Bradycardia (most common), VT/VF, PEA, asystole.

Contractility: Profound, refractory hypotension and cardiogenic shock.

IV. Immediate Management Algorithm

Goal: Prevent hypoxia/acidosis and sequester the toxin.

1. Initial Actions

Stop Injection: Immediately halt all LA administration.

Call for Help: Specify “LAST Protocol” and “Intralipid Kit.”

Airway Management:

100% O2​.

Hyperventilate slightly if needed to counter respiratory acidosis.

Low threshold for intubation (hypoxia/acidosis rapidly worsen LAST).

2. Seizure Control

First-line: Benzodiazepines (e.g., Midazolam).

Avoid: Propofol if hemodynamically unstable (exacerbates cardiac depression).

Neuromuscular Blockers: May be needed for ventilation, but remember they do not stop CNS seizure activity.

3. Lipid Emulsion Therapy 20%

Indications: Start at first sign of serious toxicity (airway compromise, seizures, or CV instability).

Bolus: 1.5 mL/kg IV over 1 minute.

Infusion: 0.25 mL/kg/min immediately following bolus.

If Instability Persists:

Repeat bolus (up to 2 times).

Increase infusion to 0.5 mL/kg/min.

Upper Limit: ≈12 mL/kg total dose.

4. Modified ACLS

Epinephrine: Use low doses (<1 mcg/kg) to avoid worsening arrhythmias and interfering with lipid rescue.

Antiarrhythmics: Amiodarone is preferred.

CONTRAINDICATED:

Lidocaine: (Class Ib antiarrhythmic—will worsen toxicity).

Vasopressin: Associated with poor outcomes in animal LAST models.

Calcium Channel Blockers / Beta Blockers: Exacerbate myocardial depression.

Refractory Arrest: Early consultation for ECMO or Cardiopulmonary Bypass (CPB).

V. Differential Diagnosis for the Peri-Procedural Patient

High Spinal: Ascending sensory/motor block, profound sympathectomy (hypotension/bradycardia).

Anaphylaxis: Urticaria, wheezing (rare with amides, more common with esters).

Air/Gas Embolism: Sudden dyspnea, “mill-wheel” murmur, acute right heart strain.

Vasovagal Syncope: Bradycardia/hypotension, usually lacks the QRS widening or seizure activity.

VI. Post-Resuscitation & Complications

Observation:

At least 2 hours after a CNS-only event.

At least 4–6 hours after a CV event.

Lipid Complications:

Lab Interference: Lipemia interferes with hemoglobin, creatinine, and electrolyte measurements (draw labs before ILE if possible).

Pancreatitis: Rare, delayed complication of high-dose ILE.

Fat Embolism/Overload: Rare pulmonary complications.

VII. Clinical “Red Flags” for Toxicity

Unexpected Agitation: In a patient who just received a block, don’t assume “anxiety.”

Wide QRS: Any widening of the QRS complex post-injection is LAST until proven otherwise.

Refractory Arrest: Standard ACLS failing in a patient who received LA. Lipid must be given.

Critical Note: LAST is a clinical diagnosis. Do not wait for serum lidocaine levels or laboratory confirmation to initiate Lipid Emulsion Therapy. Immediate correction of pH and PaCO2​ is as vital as the lipid itself.





Read More

We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure.

Hosts:

Nicolas Gonzalez, MD

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3





Download


Leave a Comment





Tags: Cardiology





Show Notes

Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. 

Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

1. Core Definition & Hemodynamic Profile

Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.

Hemodynamic Criteria:

Cardiac Index (CI): >4.0 L/min/m2.

Cardiac Output (CO): >8 L/min.

Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state).

The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses.

2. Pathophysiology: The Hemodynamic Paradox

Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

Effective Arterial Blood Volume: Paradoxically low despite high total CO.

Neurohormonal Cascade:

Activation of Renin-Angiotensin-Aldosterone System (RAAS).

Increased Sympathetic Nervous System tone.

Increased Antidiuretic Hormone (ADH) secretion.

Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion.

Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy.

3. Differential Diagnosis: Etiological “Buckets”

Category A: Increased Metabolic Demand (Systemic)

Hyperthyroidism/Thyrotoxicosis:

Direct T3 effects: increased chronotropy/inotropy.

Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation.

Myeloproliferative Disorders:

High cell turnover and increased oxygen consumption drive compensatory CO increase.

Sepsis (Hyperdynamic Phase):

Cytokine-mediated global vasodilation.

Note: Often transient; may transition to sepsis-induced myocardial depression.

Category B: Peripheral Vascular Effects (Shunting/Vasodilation)

Arteriovenous Fistulas (AVF) / Malformations (AVM):

Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population).

Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation.

Chronic Liver Disease (Cirrhosis):

Formation of “spider angiomata” and internal AV shunts.

Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide).

Thiamine Deficiency (Wet Beriberi):

Accumulation of pyruvate/lactate → systemic vasodilation.

Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema.

Chronic Lung Disease:

Hypoxia/Hypercapnia-driven systemic vasodilation.

Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output.

Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma.

4. Special Focus: Hemodialysis Access-Induced HOHF

Physiologic Phases of AVF Creation:

Acute Phase:

Immediate ↓ SVR.

↑ Stroke volume and Heart Rate (SNS-mediated).

Endothelial shear stress → Nitric Oxide release → further arterial dilation.

Subacute Phase (Days to 2 Weeks):

RAAS-driven volume expansion.

↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).

Natriuretic peptide surge (BNP/ANP) peaks around Day 10.

Chronic Phase (Weeks to Months):

Adaptive hypertrophy.

Decompensation occurs when dilation exceeds contractility limits.

5. Point-of-Care Physical Exam & Maneuvers

Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF):

Maneuver: Manually compress the AVF (or inflate cuff to >50 mmHg above SBP) for 30 seconds.

Positive Result: Reflexive bradycardia or a transient rise in systemic BP.

Significance: Confirms the shunt is a major contributor to the cardiac workload.

Peripheral Pulse Assessment:

Water Hammer Pulses: Rapid upstroke and collapse.

Quincke’s Pulse: Visible capillary pulsations in the nail beds.

Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries.

Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs).

6. Diagnostic Workup (Technical Targets)

POCUS / Echocardiography:

Left Ventricle: Hyperdynamic function; EF typically >60%.

Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2).

IVC: Plethoric with minimal respiratory variation.

Doppler: High flow velocities across the AV access if applicable.

Laboratory Evaluation:

BNP/NT-proBNP: Often markedly elevated (e.g., >70,000 in severe cases), though mean values in literature hover around 700–800 pg/mL.

Hematology: CBC to evaluate for severe anemia (trigger for HOHF if Hgb<7–8 g/dL) or myeloproliferative markers.

Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis).

7. Management Strategy: A Stepwise Approach

Phase 1: Immediate Stabilization (Volume Offloading)

Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide).

Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion.

Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially.

Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse.

Phase 2: Targeted Therapy (Etiology Specific)

Anemia: Transfuse to goal Hgb>7–8 g/dL to reduce demand.

Beriberi: High-dose IV Thiamine (100–500 mg).

Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole).

Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases)

Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites.

Flow Reduction (Banding): Surgical narrowing of the fistula to target flow <600 mL/min.

RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery).

Ligation: Complete closure of the AVF.

Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas).

8. Key Clinical Takeaways

The “Normal EF” Trap: Do not be reassured by an EF of 55–65%; in the context of pulmonary edema and high CO, this is potentially HOHF.

Pulse Pressure: Look for a wide pulse pressure (e.g., 180/60) as a marker of low SVR.

ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid.





Read More

We explore how to refine and optimize care in the vital minutes following ROSC.

Hosts:

Jonathan Elmer, MD, MS

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC_care.mp3





Download


Leave a Comment






Show Notes

Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. 

Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

I. Phase 1: Stabilization (Minutes 0–10)

The “Rearrest” Window & Pathophysiology

High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC.

Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside.

Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse.

Secondary Injuries: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations).

Immediate Resuscitative Actions

Vascular Access:

Transition rapidly from IO to reliable IV access within 1–2 minutes.

Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes.

Vasoactive “Bridge”:

Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration.

Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing).

Physician-Specific Task: Arterial Line:

Goal: Placement within 5 minutes of ROSC.

Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a <2-minute procedure.

Utility: Immediate detection of rearrest and beat-to-beat titration of vasopressors.

II. Phase 2: Diagnostic Workup (Minutes 10–40)

Etiology Epidemiology

ACS Shift: Acute Coronary Syndrome (ACS) is the cause in only 6–10% of resuscitated survivors (lower than historical estimates).

Common Etiologies:

Respiratory: COPD, pneumonia, mucus plugging.

Cardiac: Arrhythmia (cardiomyopathy/scar), RV failure (PE), or LV failure.

Neurological: Intracranial hemorrhage (SAH/ICH), status epilepticus (4–5%).

Metabolic: Dialysis-related disarray/hyperkalemia.

Toxicology: Overdose accounts for ~10% of cases in urban centers.

The “Broad Net” Strategy

“Rainbow Labs”: Comprehensive panel including toxicology and serial biomarkers.

Pan-Scan Protocol:

Components: CT/CTA Head/Neck, Contrast CT Chest/Abdomen/Pelvis.

Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest).

Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility.

Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence of the global arrest-induced ischemia.

III. Hemodynamic & Respiratory Targets

Mean Arterial Pressure (MAP)

Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion.

Clinical Target: Aim for MAP >80 mmHg.

The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence.

Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow.

Ventilation and Oxygenation

PaCO2 Management:

Target: High-normal to slightly hypercarbic (45–55 mmHg).

Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%.

PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral.

IV. Neurological Prognostication & Communication

The “Stunned” Brain

Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail.

Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury.

Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours.

Family Engagement

Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation.

Psychological Impact: Significantly reduces PTSD, anxiety, and depression in survivors’ families.

Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome.

Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization).





Read More

We review diagnosing and managing bacterial meningitis in the ED.

Hosts:

Sarah Fetterolf, MD

Avir Mitra, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/Meningitis_2_0.mp3





Download


Leave a Comment





Tags: CNS Infections, Infectious Diseases, Neurology





Show Notes

Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. 

Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

Patient Presentation & Workup

Patient: 36-year-old male, currently shelter-domiciled, presenting with 3 weeks of generalized weakness, fevers, weight loss, and headaches.

Vitals (Initial): BP 147/98, HR 150s, Temp 100.2°F, RR 18, O2 99% RA.

Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F.

Physical Exam Findings:

Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion).

Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°).

Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache).

Imaging:

Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax.

CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy).

Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement.

CSF Analysis & Microbiology

Bacterial Meningitis

Opening Pressure: Elevated (Normal is <170 mm H2​O).

Color: Cloudy or turbid.

Gram Stain: Positive in 60%–80% of cases before antibiotics; drops to 7%–41% after antibiotics.

Cell Count: Very high (>1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN).

Glucose: Low (<40 mg/dL); CSF/blood glucose ratio is <0.3–0.4.

Protein: High (>200 mg/dL).

Cytology: Negative.

Viral Meningitis

Opening Pressure: Normal.

Color: Clear or bloody.

Gram Stain: Negative.

Cell Count: Slightly elevated (<300/mm3 WBC); dominated by lymphocytes (<20% PMN).

Glucose: Normal.

Protein: Moderately elevated (<200 mg/dL).

Cytology: Negative.

Fungal Meningitis

Opening Pressure: Normal to elevated.

Color: Clear or cloudy.

Gram Stain: Negative.

Cell Count: Elevated (<500/mm3 WBC).

Glucose: Normal to slightly low.

Protein: High (>200 mg/dL).

Cytology: Negative.

Neoplastic (Cancer-related) Meningitis

Opening Pressure: Normal.

Color: Clear or cloudy.

Gram Stain: Negative.

Cell Count: Elevated (<300/mm3 WBC).

Glucose: Normal to slightly low.

Protein: High (>200 mg/dL).

Cytology: Positive (this is the key differentiator).

Management Protocol

Immediate Treatment: Early administration of antibiotics/antivirals is critical to reduce mortality.

Antibiotics: Ceftriaxone 2g IV q12h + Vancomycin (or Rifampin in cephalosporin-resistant areas).

Listeria Coverage: Add Ampicillin for patients > 50 years old.

Antivirals: Acyclovir 10 mg/kg q8h.

Steroids: Dexamethasone 10 mg IV q6h for 4 days (proven to reduce mortality and improve outcomes).

Surgical Intervention: Neurosurgery performed an emergent EVD in the ED to relieve pressure from obstructive hydrocephalus.

Post-Exposure Prophylaxis: Indicated only for N. meningitidis (not S. pneumoniae) for contacts < 24 hours from diagnosis.

Regimens: Rifampin for 2 days, single-dose Ciprofloxacin, or IM Ceftriaxone (if pregnant).

Stats & Clinical Pearls: Austrian Syndrome

The Triad: Concurrent pneumonia, endocarditis, and meningitis caused by Streptococcus pneumoniae.

Risk Factors: Asplenia (due to the spleen’s role in filtering encapsulated bacteria), alcohol use disorder, and immunosuppression.

Mortality Rate: Extremely high at 28%; mortality is highest when there is CNS involvement.

Incidence: Worldwide, S. pneumoniae is the leading cause of bacterial meningitis, accounting for 3,000–6,000 cases annually.





Read More

We discuss the diagnosis and management of SCAPE in the ED.

Hosts:

Naz Sarpoulaki, MD, MPH

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/SCAPEv2.mp3





Download


Leave a Comment





Tags: Acute Pulmonary Edema, Critical Care





Show Notes

Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. 

Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

The Clinical Case

Presentation: 60-year-old male with a history of HTN and asthma.

EMS Findings: Severe respiratory distress, SpO₂ in the 60s on NRB, HR 120, BP 230/180.

Exam: Diaphoretic, diffuse crackles, warm extremities, pitting edema, and significant fatigue/work of breathing.

Pre-hospital meds: NRB, Duonebs, Dexamethasone, and IM Epinephrine (under the assumption of severe asthma/anaphylaxis).

Differential Diagnosis for the Hypoxic/Tachypneic Patient

Pulmonary: Asthma/COPD, Pneumonia, ARDS, PE, Pneumothorax, Pulmonary Edema, ILD, Anaphylaxis.

Cardiac: CHF, ACS, Tamponade.

Systemic: Anemia, Acidosis.

Neuro: Neuromuscular weakness.

What is SCAPE?

Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload.

Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload.

Bedside Diagnosis: POCUS vs. CXR

POCUS is the gold standard for rapid bedside diagnosis.

Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones).

Cardiac: Assess LV function and check for pericardial effusion.

Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR.

Management Strategy

1. NIPPV (CPAP or BiPAP)

Start NIPPV immediately to reduce preload/afterload and recruit alveoli.

Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation.

Evidence: NIPPV reduces mortality (NNT 17) and intubation rates (NNT 13).

2. High-Dose Nitroglycerin

The goal is to drop SBP to < 140–160 mmHg within minutes.

No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously.

IV Bolus: 500–1000 mcg over 2 minutes.

IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required).

Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues.

3. Refractory Hypertension

If SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator:

Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid).

Nicardipine: Effective alternative for rapid BP control.

Enalaprilat: Consider if the above are unavailable.

Troubleshooting & Pitfalls

The “Mask Intolerant” Patient

Hypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV).

AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam).

The Role of Diuretics

In SCAPE, diuretics are not first-line.

The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient.

Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed.

Disposition

Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions.

Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered.

Take-Home Points

Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR.

NIPPV Immediately: Don’t wait. It saves lives and prevents tubes.

High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose.

Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask.

Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase.





Read More