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Learning Objectives

By the end of this episode, listeners should be able to:

• Explain sepsis from a cellular / metabolic standpoint (ATP production, aerobic → anaerobic shift, lactate).
  
  

• Recognize sepsis in the field using SIRS, qSOFA, shock index, and capnography trends.
  
  

• Identify high-risk patients and common infection sources that should trigger a “sepsis mindset.”
  
  

• Describe prehospital priorities: oxygenation, fluid resuscitation, access (IV/IO), and when to escalate to push-dose epinephrine.
  
  

• Understand how and why early sepsis alerts, aggressive fluids, and timely antibiotics in the ED impact mortality.
  
  

• Apply practical assessment pearls (hands-on exam, real respiratory counts, medication review) to avoid missing septic shock.
  
  

Dr. Garlisi’s Story: Why Sepsis Matters

• Personal story of his 1-year-old niece with unrecognized septic shock:
  
  

  • Presented with fever, vomiting, tachycardia, poor cap refill, mental status change.
    
    

  • No IV, no antibiotics, no pediatric consult, no transfer, minimal monitoring.
    
    

  • Progressed to seizures, CT showing “Swiss cheese” brain, now with severe, lifelong disability.
    
    

• Take-home:
  
  

  • Sepsis can devastate a previously healthy child in hours.
    
    

  • Under-recognition and delayed treatment = permanent damage.
    
    

  • Motivates his lifelong focus on early recognition and aggressive management.
    
    

Sepsis at the Cellular Level – Why ATP Is Everything

• Basic metabolic formula (memorize this!):
  
  

  • Glucose + O₂ → ATP + CO₂ + H₂O
    
    

  • 3 key processes:
    
    

    • Glycolysis (cytoplasm) – 2 ATP
      
      

    • Krebs cycle (mitochondria) – 2 ATP
      
      

    • Electron transport chain – ~34 ATP
      
      

  • Net: ~38 ATP / glucose – a huge “return on investment.”
    
    

• If ATP production fails:
  
  

  • Cells die → tissues die → organs fail → organ systems fail → patient dies.
    
    

• The body’s delivery system for glucose & O₂:
  
  

  • Pump: heart
    
    

  • Pipes: blood vessels/containers
    
    

  • Fluid: plasma/water to carry glucose & oxygen
    
    

  • RBCs/Hemoglobin: carry oxygen
    
    

  • Insulin: allows glucose to enter cells
    
    

• Sepsis disrupts this entire system via:
  
  

  • Vasodilation → blood pooling, poor circulation
    
    

  • Leaky capillaries → fluid shifts into interstitium
    
    

  • Microthrombi → blocked microcirculation
    
    

• Result:
  
  

  • Switch from aerobic to anaerobic metabolism, lactate rises, ATP production plummets → multi-organ dysfunction.

Pathophysiology: From Local Infection to Distributive Shock

• Typically focusing on bacterial sepsis:
  
  

  • Local infection (often pneumonia, UTI, skin, abdomen, lines/devices).
    
    

  • Body fails to contain infection → bacteria and toxins enter bloodstream.
    
    

• Exaggerated immune response:
  
  

  • Massive release of cytokines and other mediators.
    
    

  • Acts like a dysregulated autoimmune reaction against the host.
    
    

• Vascular consequences:
  
  

  • Distributive shock:
    
    

    • Vasodilation (“pipes too big for the volume”).
      
      

    • Leaky vessels → third-spacing.
      
      

    • Microvascular thrombosis → impaired perfusion.
      
      

• Clinical impact:
  
  

  • Decreased O₂ delivery + impaired CO₂ clearance.
    
    

  • Switch to anaerobic metabolism → lactate elevation.
    
    

  • Progressive organ failure: brain, heart, kidneys, lungs, gut, hypothalamus (→ hypothermia).
    
    

Recognizing Sepsis in the Field

The “Sepsis Mindset”

• Sepsis is:
  
  

  • Insidious, lethal, and a great masquerader.
    
    

  • The most frequently missed shock type across EMS → ICU.
    
    

• Think of sepsis as:
  
  

  • The “STEMI of infectious disease”.
    
    

  • Time-critical medicine, on par with trauma, STEMI, and stroke.
    
    

• High-performance paramedics:
  
  

  • Are good detectives: thorough H&P, risk factor assessment, physical exam.
    
    

  • Look for SIRS + suspected infection = sepsis.
    
    

  • Don’t wait for labs or imaging to act.
    
    

SIRS Criteria (Systemic Inflammatory Response Syndrome)

SIRS “checklist” highlights:

• Temperature:
  
  

  • > 100.9°F (38.3°C) or < 96.8°F (36°C)
    
    

  • Important: Septic patients can be cold – hypothermia is often worse.
    
    

• Heart rate:
  
  

  • > 90 bpm (not just “>100”).
    
    

• Respiratory rate:
  
  

  • > 20 breaths/min.
    
    

• Capnography:
  
  

  • ETCO₂ < 32 mmHg suggests hyperventilation & poor perfusion.
    
    

• Blood pressure:
  
  

  • SBP < 90 mmHg or MAP < 70 mmHg.
    
    

• Mental status:
  
  

  • Any altered mental status.
    
    

EMS equation:
SIRS + suspected infection → treat as sepsis.

qSOFA (Quick SOFA)

qSOFA = Quick Sequential Organ Failure Assessment
Triggers concern when ≥ 2:

• RR elevated (tachypnea).
  
  

• Altered mental status.
  
  

• Low systolic BP (hypotension).
  
  

Used more by in-hospital clinicians, but EMS can use it as a quick severity screen.

Shock Index

• Shock Index = HR / SBP
  
  

  • Values > 0.9 concerning for shock → aggressive fluids.
    
    

• Simple, quick bedside tool to justify:
  
  

  • More fluid resuscitation.
    
    

  • Earlier pressor consideration.
    
    

Capnography as a “Live Feed”

• ETCO₂ reflects perfusion and metabolism, not just ventilation.
  
  

• Sepsis / shock:
  
  

  • Poor perfusion → ↓ CO₂ delivery → low ETCO₂.
    
    

• Cardiac arrest example:
  
  

  • CPR: ETCO₂ often 10–12.
    
    

  • ROSC: ETCO₂ jumps up before pulse/BP.
    
    

• In sepsis:
  
  

  • ETCO₂ trend is a real-time severity marker and early deterioration signal.
    
    

Who Is at Risk? History, Risk Factors, and Hidden Sources

Key Sepsis Risk Factors

• Diabetes (“risk factor for everything”).
  
  

• Immunosuppressive meds:
  
  

  • Biologics: Humira, Stelara, Remicade, etc.
    
    

  • Chronic steroids.
    
    

• Cancer patients and chemotherapy.
  
  

• Renal dialysis patients (frequent access, lines, immunocompromise).
  
  

• Elderly, especially with polypharmacy and frailty.
  
  

• Extremes of age:
  
  

  • Neonates/young infants: immature immune systems, poor thermoregulation.
    
    

• Indwelling devices:
  
  

  • Foley catheters, central lines, dialysis catheters, ports.
    
    

  • Artificial joints, hardware, prosthetics.
    
    

• Recent surgery or hospitalization.
  
  

Medication Review Pearls

• Beta blockers (e.g., metoprolol):
  
  

  • May mask tachycardia → they “should” be tachycardic but aren’t.
    
    

  • Don’t be falsely reassured by a HR < 90 in a hypotensive patient on beta blockers.
    
    

• Immunosuppressants / biologics / steroids:
  
  

  • Reduce ability to mount a normal immune response.
    
    

• Antibiotics:
  
  

  • Long-term / recent antibiotics can change flora and risk.
    
    

Finding the Source – “Seek and You Will Find”

When you see SIRS or concerning qSOFA/shock index, actively hunt for infection:

• Respiratory / pneumonia:
  
  

  • Cough, fever/chills, dyspnea, hypoxia, tachypnea.
    
    

  • Auscultation: rales or focal findings.
    
    

• Urinary tract:
  
  

  • Frequency, urgency, dysuria, hematuria, suprapubic tenderness.
    
    

  • Catheters/Foleys: look for indwelling urinary devices.
    
    

• GI / abdominal:
  
  

  • Pain, vomiting, diarrhea.
    
    

  • Post-op abdomen, hernias, signs of intra-abdominal abscess.
    
    

  • Palpate the abdomen: RUQ (gallbladder, cholangitis), suprapubic (UTI).
    
    

• Skin / soft tissue:
  
  

  • Cellulitis, abscesses, wounds, decubitus ulcers.
    
    

  • Bedbound patients: check heels, sacrum, other pressure areas.
    
    

• Joints:
  
  

  • Warm, swollen, painful joints – suspect septic arthritis.
    
    

• Lines/devices:
  
  

  • Central lines, ports, dialysis access, hardware.
    
    

Big message: paramedics should be risk factor experts and thorough examiners, not just vital-sign collectors.

Field Lactate and Labs – Helpful but Not Everything

• Some EMS systems now checking point-of-care lactate:
  
  

  • Field values generally correlate well with hospital labs.
    
    

  • Helpful in supporting sepsis suspicion and tracking response.
    
    

• Caveats:
  
  

  • Elevated lactate = hypoperfusion, not necessarily infection.
    
    

  • High lactate alone doesn’t prove sepsis; interpret in context (SIRS, infection risk, exam).
    
    

  • Similarly, fever or high WBC alone do not prove bacterial infection.
    
    

Prehospital Management: BLS and ALS Priorities

BLS-Level Interventions

• Doorway assessment: “Sick or not sick?”
  
  

• Immediate basics:
  
  

  • Oxygen for hypoxia.
    
    

  • Positioning:
    
    

    • Lay patient flat, legs elevated to autotransfuse (basic “fluid bolus”).
      
      

  • Manual BP with a real cuff and stethoscope.
    
    

  • Count respirations accurately – not “16 or 18” by default.
    
    

• Use tools you do have:
  
  

  • Capnography when available.
    
    

  • EKG and blood glucose as rapid, point-of-care assessments.
    
    

• Frequent vitals:
  
  

  • Q5 minute vital signs for critically ill patients.
    
    

ALS-Level Interventions

IV/IO Access

• IV preferred (and supported by new AHA guidance), but don’t delay:
  
  

  • Large-bore IVs (18 or larger, bilateral AC if possible).
    
    

• If IV not quickly obtainable in a sick hypotensive patient:
  
  

  • IO early, not as a last resort.
    
    

  • Humeral head IO:
    
    

    • Higher flow rates (5–6 L/hr vs ~2–3 L/hr tibial).
      
      

    • Technique: thumbs from acromion toward mid-shaft, feel “golf tee” head, 45° angle.
      
      

    • Yellow needle, doesn’t always need to be fully buried, follow device markings.
      
      

  • Many medics underuse IO due to inexperience or lack of training → practice on mannequins.
    
    

Fluid Resuscitation

• Sepsis is primarily distributive shock – the “pipes” are too big:
  
  

  • Massive vasodilation, relative hypovolemia, leaky capillaries.
    
    

• Prehospital fluid:
  
  

  • Normal saline remains the most practical and safest default in EMS.
    
    

  • Hang large bags (1 L) for adult patients; aim toward guideline-driven ~30 mL/kg total (ideal body weight), counting EMS fluid in ED.
    
    

• Speed matters:
  
  

  • Pressure infusers or blood pressure cuff around the bag to “rain” fluid in.
    
    

  • You can push a liter in <10 minutes with pressure.
    
    

• Pediatric patients:
  
  

  • Use 20 mL/kg bolus; can use flushes for exact dosing or partial bags as needed.
    
    

Vasopressors – Push-Dose Epinephrine

• If hypotension persists after adequate fluid bolus:
  
  

  • Prepare push-dose epinephrine early.
    
    

• Local mixing example (per their protocol):
  
  

  • 100 mL D5 bag + 1 mg (1 mL) of epinephrine → 10 mcg/mL solution.
    
    

• Why epinephrine works well in septic shock:
  
  

  • β₁: ↑ HR, ↑ contractility.
    
    

  • α₁: vasoconstriction → improves systemic vascular resistance.
    
    

• Field strategy:
  
  

  • One provider boluses fluid while partner mixes push-dose Epi and stands ready.
    
    

  • If fluid isn’t enough, quickly escalate to Epi.
    
    

Respiratory Support

• Treat hypoxia aggressively (oxygen, airway maneuvers).
  
  

• Consider CPAP in appropriate pneumonia/respiratory distress with adequate BP:
  
  

  • Improves oxygenation and may help avoid intubation.
    
    

• Be cautious: low BP may limit CPAP use (it can reduce venous return).

ED Perspective: What Happens After the Sepsis Alert?

When EMS calls in a sepsis alert, the ED:

• Reserves/clears a resuscitation room.
  
  

• Preps to:
  
  

  • Obtain IV access (including central if needed).
    
    

  • Draw blood cultures before antibiotics when possible.
    
    

  • Continue aggressive fluid resuscitation (30 mL/kg).
    
    

  • Check lactate and other labs.
    
    

  • Get imaging (e.g., chest X-ray) quickly.
    
    

  • Start broad-spectrum antibiotics tailored to suspected source and patient history.
    
    

• Time targets:
  
  

  • Current standards: antibiotics within 3 hours of sepsis recognition.
    
    

  • Emerging goal: <1 hour from recognition for best outcomes.
    
    

• Pressors:
  
  

  • If fluids fail to restore pressure, start vasopressors (e.g., norepinephrine/Levophed).
    
    

  • Push-dose Epi often used as bridge while drips from pharmacy arrive.
    
    

Antibiotic Stewardship & Toxicity

• Not all sepsis patients need “the biggest gun” immediately:
  
  

  • Vancomycin, while great for MRSA, is nephrotoxic.
    
    

  • Many antibiotics can injure kidneys, liver, or hearing (ototoxicity).
    
    

  • Some can affect bone development in children.
    
    

• MRSA considerations:
  
  

  • Many healthcare workers likely colonized with MRSA.
    
    

  • Nares swabs may guide how long to stay on MRSA coverage.
    
    

• Ideally:
  
  

  • Cultures first, then empiric antibiotics.
    
    

  • De-escalate based on culture and sensitivity results.
    
    

Age, Mortality, and How Fast Things Go Bad

• Sepsis affects any age, from newborns to centenarians.
  
  

• Mortality climbs sharply with age:
  
  

  • 65–74 years: ~15%.
    
    

  • 75–84 years: ~38.7%.
    
    

  • ≥85 years: ~75%.
    
    

• Extremes of age are especially high risk:
  
  

  • Neonates/young infants:
    
    

    • Poor vascular response, immature immune systems, unable to thermoregulate.
      
      

    • Small changes can be profound; often need aggressive evaluation and early transfer to pediatric centers.
      
      

  • Elderly:
    
    

    • Polypharmacy, chronic diseases, blood thinners, beta blockers, frailty.
      
      

• Sepsis can deteriorate incredibly fast:
  
  

  • Example call: nursing facility patient, cold, tachypneic, unresponsive → sepsis recognized, fluids and push-dose Epi prepared, yet patient arrested rapidly despite appropriate care.

Assessment & Documentation Pearls

• Put hands on the patient:
  
  

  • Touch for temperature, perfusion, skin changes.
    
    

  • Palpate the abdomen in all quadrants.
    
    

• Manual BP first, especially if machine readings don’t make sense.
  
  

• Legitimately count respirations – don’t default to “16”.
  
  

• Use MAP (mean arterial pressure) as a more reliable perfusion marker:
  
  

  • Target MAP ≥ 65 mmHg.
    
    

  • It may be okay to tolerate lower systolic if MAP is adequate but still resuscitating.
    
    

• Continuous re-assessment:
  
  

  • Q5 minute vitals for critically ill.
    
    

  • Watch trends, not single data points.
    
    

• Differential diagnosis mindset:
  
  

  • Always ask: “What’s going to kill this patient first, and fastest?”
    
    

  • Focus early on threats like shock, hypoxia, hypoglycemia.
    
    

• Communicate clearly to ED:
  
  

  • “We’ve already given X liters; BP still 80 over palp; HR 120; MAP falling; ETCO₂ low; high suspicion for sepsis. Sepsis alert activated.”

Key Take-Home Messages for EMS

• Sepsis = STEMI of infectious disease – treat it as time-critical.
  
  

• Think at the cellular level: sepsis turns off ATP production and behaves like cyanide to the body.
  
  

• Use SIRS + suspected infection → sepsis, even without labs or imaging.
  
  

• Don’t be fooled: no fever doesn’t rule out sepsis; hypothermia can be worse.
  
  

• Capnography, shock index, and MAP are powerful, real-time tools.
  
  

• Fluids early and fast, then push-dose Epi if needed; don’t delay IO in sick hypotensive patients.
  
  

• Be a sepsis detective:
  
  

  • Identify risk factors, scrutinize meds, and search for pneumonia, UTI, abdominal, skin, joint, or device-related sources.
    
    

• Call sepsis alerts from the field – you set the tone for ED urgency.
  
  

• Basic or advanced, your assessment quality and early actions can make the difference between recovery, disability, and death.

From The Episode