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Show Notes

Quick episode takeaway

This episode “caps the year” by translating prehospital ECG recognition → system destination decisions → cath lab findings → interventions → outcomes, including tricky mimics/edge cases (subtle STEMI, CTO vs acute occlusion, SCAD, CABG anatomy, shock + Impella).

Learning objectives

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

• Recognize classic and subtle STEMI patterns and understand why computer reads lag human interpretation
  
  

• Prioritize PCI-center destination decision-making (first medical contact → balloon time)
  
  

• Understand why early DAPT + anticoagulation matters (and what it looks like on angiography)
  
  

• Differentiate acute occlusion vs CTO features and how collateral flow can blunt ECG changes
  
  

• Identify SCAD as an important MI mechanism (especially in younger women/pregnancy) and why “less is more”
  
  

• Appreciate why aVR elevation + diffuse depression is a red-flag pattern (even if no longer “classic STEMI criteria”)
  
  

• Understand cardiogenic shock escalation and why support (Impella) may matter as much as opening the artery
  
  

Key EMS/prehospital pearls (repeated themes)

• Don’t outsource interpretation to the monitor. The computer read may hedge (“possible acute”) even when it’s a slam-dunk STEMI.
  
  

• Destination matters. When feasible and within your system, direct-to-PCI can save an hour+ and preserve myocardium.
  
  

• Think in “first contact to balloon,” not just “door-to-balloon.” The team cites phenomenal EMS-to-balloon times (even <40 minutes in some cases).
  
  

• Field therapy matters. Seeing the clot burden on cath reinforces why early aspirin + P2Y12 + anticoagulation can change outcomes.
  
  

CASE 1 — “STEMI 101” Inferior STEMI with massive RCA thrombus (Ashtabula → Geauga)

Presentation

• Male, late 70s, chest pain, rural-ish start point (Ashtabula County)
  
  

ECG highlights

• 2–3 mm ST elevation in II, III, aVF
  
  

• Reciprocal depression in anterior leads
  
  

• Computer interpretation: “inferior infarct, possibly acute” → but clinicians call it clearly STEMI
  
  

Systems win

• Crew sought permission for direct transport to PCI center (Geauga) instead of local non-PCI options → potentially saves 60–90 min.
  
  

Cath lab findings

• Normal left system
  
  

• Large thrombus burden in distal RCA (clot “hanging down”/extending)
  
  

Clinical twist

• By lab arrival, ST segments had resolved (reperfusion/partial flow) but clot still huge → reinforces early anticoagulation/antiplatelet rationale.
  
  

Intervention

• Aspiration thrombectomy (Penumbra) used because thrombus was extensive (not routine for all STEMIs)
  
  

• Then long stent placement + high-pressure post-dilation (they reference balloon atmospheres/time like “24 for 20”)
  
  

Outcome pearl

• Patient discharged ~48 hrs later with preserved EF → “saving myocytes” through speed + meds + flow restoration.
  
  

EMS takeaways

• Treat the ECG, not the computer.
  
  

• Direct-to-PCI when appropriate can be game-changing.
  
  

• Massive thrombus cases illustrate why early meds aren’t “checkboxes”—they can change perfusion before the lab.
  
  

CASE 2 — Subtle inferior changes masking a big problem: Acute RCA occlusion vs CTO question

Presentation

• Male, ~60, remote PCI 20 years ago, minimal follow-up
  
  

• Initially pain-free after meds; later pain returns
  
  

ECG evolution

• First ECG: “not STEMI” / subtle
  
  

• Later ECG: mild inferior STE (still not dramatic) → activation happens based on trend + story
  
  

Cath lab diagnostic dilemma

• Left system shows abnormal territory + collateral backfilling to RCA
  
  

• RCA appears totally occluded: Is it an acute event or a CTO?
  
  

How they reason it out

• Angio features: acute occlusion may show tapering/dye staining, vs CTO more abrupt/organized appearance
  
  

• Procedural clue: wire crosses relatively easily in fresh thrombus compared with calcified CTO (“pushing a wire through a brick”)
  
  

Intervention

• RCA opened with PCI; very long stent (48 mm Synergy)
  
  

• Other lesion evaluated—concern for possible second active rupture; turned out to be CTO → medical management rather than forcing high-risk intervention
  
  

CTO medical therapy discussion (practical)

• Antianginal “three-prong” approach:
  
  

  • Beta blocker
    
    

  • Calcium channel blocker
    
    

  • Nitrates
    
    

• Refractory symptoms → consider ranolazine and/or CTO PCI
  
  

EMS takeaways

• Small ST changes can hide large myocardium at risk, especially when collaterals exist.
  
  

• Serial ECGs + clinical changes matter.
  
  

• “Culprit vs bystander” lesions drive cath lab decisions—sometimes the win is treating the culprit and stopping.
  
  

CASE 3 — Anterior STEMI caused by SCAD (Spontaneous Coronary Artery Dissection)

Presentation

• Female, ~55, no major history, compelling chest pain story
  
  

ECG

• Early anterior STE in V2–V4 (not the most dramatic “textbook” pattern)
  
  

Cath findings

• RCA normal
  
  

• LAD distal segment looks “ratty”/irregular → consistent with SCAD
  
  

Management strategy: “Do less, harm less”

• Distal SCAD is often managed conservatively
  
  

• Avoid wiring/instrumentation if possible because of risk of entering false lumen and propagating dissection
  
  

Discharge meds nuance

• Acute presentation treated like STEMI initially (because you don’t know it’s SCAD in the field)
  
  

• Post-diagnosis:
  
  

  • Aspirin + P2Y12 often continued (expert consensus varies)
    
    

  • Beta blocker commonly used
    
    

  • Statins usually NOT unless indicated for standard lipid reasons
    
    

SCAD risk population pearl

• More common in women, including pregnancy-associated cases
  
  

• The group emphasizes maintaining suspicion when a young/pregnant patient has real cardiac symptoms.
  
  

EMS takeaways

• SCAD is a real MI mechanism—don’t dismiss chest pain in younger women/pregnant patients.
  
  

• “STEMI care” starts the same prehospital; downstream cath strategy may diverge.
  
  

CASE 4 — aVR elevation + diffuse depression: “Proximal LAD/left main pattern” complicated by prior CABG + subclavian stenosis

Presentation

• Female, ~70, chest pain
  
  

• History initially unclear (patient didn’t report CABG; chart suggested it; hadn’t had care in ~10 years)
  
  

• Reported progressive angina for ~3 years
  
  

ECG pattern discussed

• ST elevation in aVR and V1
  
  

• Diffuse ST depression across multiple leads
  
  

• Recognized as a high-risk pattern (classically “prox LAD / left main / severe ischemia” pattern)
  
  

• They note this pattern used to be treated as STEMI criteria in many systems, but criteria changed—symptoms drive urgency
  
  

Cath findings (complex)

• Prior CABG: LIMA→LAD + vein grafts to RCA and circumflex
  
  

• Native disease: circumflex occluded, severe ostial LAD stenosis, RCA CTO
  
  

• Vein grafts occluded
  
  

• Major kicker: severe subclavian stenosis compromising LIMA flow (and high risk of embolization if manipulated)
  
  

Decision: when “bailing out” is the best medicine

• Rather than push high-risk intervention locally, they stopped and transferred for subclavian intervention + higher-level revascularization planning
  
  

EMS/ED coordination takeaway

• The “hard questions” from cardiology aren’t gatekeeping—they’re risk management: are we helping or causing harm?
  
  

• Also: look for sternotomy wires—physical exam can reveal the missing history.
  
  

CASE 5 — Hemodynamic deterioration → cardiogenic shock pathway and Impella support

Presentation

• Male, ~70, chest pain; initial ECG not dramatic (possible confounders like LBBB)
  
  

• Blood pressure drifts from ~105 to ~90 systolic, symptoms recur → escalating concern
  
  

Cath findings

• Culprit: occluded ramus (often electrically “quiet” depending on territory)
  
  

• Severe LAD stenosis also present
  
  

• Both lesions treated (ramus + LAD stents), but patient remains hypotensive
  
  

Shock evaluation and escalation

• They emphasize: low BP alone isn’t enough (could be dehydration, RCA infarct, etc.)
  
  

• Use right heart cath to measure filling pressures, cardiac output/index, SVR
  
  

• Reference threshold concepts like cardiac index < 2.2 and other markers (e.g., power index) to decide on mechanical support
  
  

Impella discussion (practical + blunt)

• Impella = micro-axial LV pump via large-bore (often 14 Fr) femoral access
  
  

• Benefits: forward flow and ventricular unloading → lowers myocardial oxygen demand
  
  

• Tradeoffs: big access = bleeding/vascular risk; transport with large-bore device is non-trivial
  
  

System-of-care highlight

• “Shock team” model: interventionalist + heart failure + CT surgery to plan:
  
  

  • Support strategy (pressors/inotropes vs Impella vs escalation)
    
    

  • Transfer to tertiary center for advanced support (ECMO/transplant eval if needed)
    
    

• Jaga can manage balloon pumps; Impella typically transferred downtown for higher monitoring needs
  
  

EMS takeaways

• Watch for trends: softening pressures + recurrent pain = escalation.
  
  

• Early recognition + rapid cath + access to mechanical support can be lifesaving.
  
  

• Shock care is system care—destination planning doesn’t stop after PCI.
  
  

Practical “what to do Monday” EMS checklist

• ECG: trust your training; don’t let monitor wording de-escalate you.
  
  

• Serial 12-leads: subtle → evolving is still actionable.
  
  

• Destination: when policy allows, push early for PCI destination in clear STEMI/occlusion patterns.
  
  

• History clues: CABG scars/sternotomy wires matter when history is unreliable.
  
  

• Women/pregnancy: keep SCAD on the mental list—don’t dismiss.
  
  

• Shock: treat the trend, not just the number; hypotension + ischemia = time-sensitive.
  
  

Quotes/one-liners worth pulling for social clips

• “You’re saving millions of myocytes.”
  
  

• “Don’t rely on the computer interpretation.”
  
  

• “Interventional cardiology is all feel—never push against resistance.”
  
  

• “Sometimes the safest thing is to bail out.”
  
  

Suggested chapter markers (YouTube)

1. Intro + why this episode is best watched
   
   

2. Case 1: inferior STEMI + massive thrombus + aspiration thrombectomy
   
   

3. Case 2: subtle ECG → acute RCA vs CTO reasoning + long stent
   
   

4. Case 3: SCAD recognition and conservative management
   
   

5. Case 4: aVR pattern + CABG anatomy + subclavian stenosis (when not to rush)
   
   

6. Case 5: shock escalation + right heart cath metrics + Impella + shock team
   
   

7. Wrap-up and thanks
   
   

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The Protocols

From The Episode