PNBschool

PNBschool specializes in providing onsite ultrasound guided peripheral nerve block training to practicing anesthesia personnel.

Our focus is on ultrasound guided techniques, current trends in postoperative pain relief and new technology.

04/07/2026

Most people pick their local anesthetic out of habit… not strategy.

But here’s the truth 👇

Ropivacaine and bupivacaine both deliver excellent regional anesthesia — the difference is how they fail, how long they last, and who they’re safest for.

🔹 Need a safer profile with less cardiac/CNS toxicity? → Ropi
🔹 Need longer, denser analgesia for bigger cases? → Bupi

That choice matters more than most people think — especially when you’re balancing block quality vs. patient risk.

The best clinicians aren’t just placing blocks… they’re choosing drugs intentionally.

What’s your go-to — and why?

04/06/2026

Most people are missing THIS step in ultrasound-guided IV placement…

If you’re struggling with small veins or inconsistent success, your approach might be the problem—not your skill.

This is my go-to technique:

• Start out-of-plane → track the needle tip precisely into the vessel
• Confirm flash in the catheter hub → you’re in
• Then rotate in-plane → visualize and guide the needle further within the vein
• Advance with confidence → thread the catheter smoothly

This hybrid approach gives you maximum information at every step—and is a game changer for accessing smaller or deeper veins.

It’s not about guessing.
It’s about seeing everything.

Save this for your next difficult IV—and share it with someone who needs this technique.

Follow for more high-yield anesthesia content.

04/03/2026

A quick update: I have still never used Vasopressin🤷🏻‍♂️

Vasopressin remains one of the most targeted tools for vasoplegic, catecholamine-resistant hypotension.
Pure V₁ effect, minimal chronotropy, and useful when norepinephrine isn’t enough — especially in RAAS blockade or post-CPB physiology.

Please share in the comments, when is Vasopressin your drug of choice? How often do you use it? What dose do you use? Please share this post with anyone who uses it Vasopressin.

04/02/2026

Hypotension is the most common problem we manage in the OR—yet treatment often becomes reflexive.

Choosing the right vasopressor should be guided by physiology, not habit. Heart rate, vascular tone, cardiac output, and anesthetic depth all matter when deciding what to give and when to escalate.

Treat the cause first, then match the drug to the physiology.

04/01/2026

Hypertrophic cardiomyopathy (HCM) requires precise hemodynamic control.

Maintain preload and afterload, avoid tachycardia and increased contractility, and treat hypotension with vasoconstrictors rather than inotropes. Even small shifts in volume or SVR can precipitate dynamic LVOT obstruction and cardiovascular collapse.

A slow, controlled approach to induction and vigilant intraoperative management are essential.

03/31/2026

“The Popliteal Sciatic Block…Great analgesia… but at what cost?”

The popliteal sciatic nerve block delivers excellent analgesia (5/5 for a reason), but it comes with a tradeoff—this nerve is critical for motor function of the foot and ankle.

When you block it, you’re not just treating pain—you’re temporarily disabling plantarflexion, dorsiflexion, and proprioception.

That means:
• Foot drop risk
• Impaired balance
• Fall risk if not managed properly

So the question isn’t just “Does the patient need pain control?” It’s “Can they safely ambulate afterward?”

Clinical takeaway:
Use it intentionally.
Counsel clearly.
Protect your patient post-op (immobilization, assistive devices, fall precautions).

Great block. High yield.
But not benign.

Are you modifying your approach based on ambulation goals—or just looking at analgesia?

03/30/2026

Yes, Severe Mitral Stenosis scares me.

You don’t get into trouble slowly — you fall off a cliff with the wrong move.

Key principle:
Cardiac output is fixed → your job is to protect diastolic filling at all costs

⸻

High-yield management:
• Avoid tachycardia → this is the #1 trigger for decompensation
• Maintain sinus rhythm → AF = loss of atrial kick = rapid collapse
• Preserve preload, but don’t overload → tight balance
• Keep SVR stable → avoid sudden drops (and avoid reflex tachycardia)

⸻

Where people get burned:
• “It’s hypotensive → give ephedrine” → ❌ tachycardia worsens filling
• “Give fluids” → ❌ pulmonary edema
• Ignoring brief tachycardia → ❌ flash pulmonary edema can happen fast

⸻

Anesthesia implications:
• Smooth, controlled induction is everything
• Phenylephrine > ephedrine for hypotension
• Slow, titrated neuraxial if used
• Regional techniques are your friend when appropriate

⸻

Bottom line:
If you remember one thing —
👉 Heart rate control = survival in mitral stenosis

⸻

What’s your go-to strategy when the HR starts creeping up in the OR?

⸻

crna

03/27/2026

“Why does your ‘low-risk’ patient still puke?”

The Apfel PONV Risk Score keeps it simple:

1 point each:
• Female
• Non-smoker
• Hx of PONV / motion sickness
• Post-op opioids

0 → ~10%
4 → ~80%

Most patients aren’t “low risk”… they’re just under-treated.

Are you still giving the same antiemetic to everyone, or actually matching prophylaxis to risk?

03/26/2026

Most TKA blocks fail in one place… the posterior knee.

That’s where patients still hurt — and where the IPACK makes the difference.

The IPACK targets the posterior capsule, giving you a critical layer of analgesia that anterior blocks miss. Add posterior coverage and you give your patient the best chance at meaningful postoperative pain control without motor weakness.

But IPACK alone isn’t enough.

For more complete coverage, combine it with:
• Femoral Triangle Block (or ACB) → anterior knee + saphenous distribution

This is how you build a true, balanced block strategy:
👉 Anterior + Posterior coverage

Clinical takeaway:
If your patient still has posterior pain… it’s not a failed block — it’s a coverage gap.

Close the gap.

03/25/2026

This is one of the few true “never events” in anesthesia.

Unrecognized esophageal intubation doesn’t happen often—
but when it does, the outcome can be catastrophic.

And the pattern is always the same:

“Routine intubation → everything seems fine → it’s not.”

That’s the trap.

Chest rise.
Fogging.
Pulse ox looks okay… at first.

None of these confirm tube placement.

Only one thing matters: continuous waveform capnography.

No sustained ETCO₂ waveform?
→ You are NOT in the trachea until proven otherwise.

The most dangerous mistake isn’t the intubation—
it’s hesitating when something feels off.

If there is any doubt:
Take it out. Reintubate. Immediately.

You will never harm a patient by reintubating early.
You can absolutely harm them by waiting.

⸻

What’s your personal rule when ETCO₂ is questionable?

03/24/2026

Magnet or no magnet? For the life of me sometimes I’m still confused on this!

You’re not alone—this is one of the most commonly confused topics in anesthesia.

And the problem is…
pacemakers and ICDs do NOT respond to magnets the same way.

Here’s the part that actually matters:

• Magnet on a pacemaker → usually forces asynchronous pacing (VOO/DOO)
• Magnet on an ICD → turns OFF shocks/ATP but does NOT change pacing

That difference is everything.

Because in the OR with electrocautery:
→ Pacemakers can be inhibited → bradycardia/asystole
→ ICDs can misinterpret EMI → inappropriate shocks

So the real question isn’t:
“Do I use a magnet?”

It’s:
What device is this… and what am I trying to prevent?

Practical approach:
• Identify device type before the case
• Determine if the patient is pacemaker dependent
• Use magnet intentionally—not reflexively
• Always have external pacing and defibrillation available

Most mistakes here aren’t knowledge gaps—
they’re mixing up pacemaker vs ICD behavior under pressure.

⸻

What’s your approach?
Magnet routinely? ICD only? Case-by-case?

⸻

Reference:
Crossley GH, Poole JE, Rozner MA, et al. HRS/ASA expert consensus statement on the perioperative management of patients with cardiac implantable electronic devices. Heart Rhythm. 2011;8(7):1114–1154.

03/23/2026

Are we overusing sugammadex… or finally using the right drug?

Sugammadex changed the game for neuromuscular reversal—rapid, predictable, and not dependent on acetylcholinesterase inhibition. But the real question in 2026 isn’t how it works… it’s when should you actually choose it over neostigmine?

⸻

Sugammadex vs Neostigmine — what actually matters clinically

Sugammadex
• Directly encapsulates rocuronium/vecuronium → true reversal
• Works in deep blockade (PTC 1–2)
• Faster, more reliable recovery
• Minimal hemodynamic effects
• Higher cost

Neostigmine
• Indirect reversal via acetylcholinesterase inhibition
• Requires partial recovery (TOF ≥2–4)
• Slower, less predictable
• Muscarinic side effects → requires glycopyrrolate
• Much lower cost

⸻

The Controversy

This is where anesthesia gets divided:
• Some argue sugammadex should be standard → improved safety, less residual paralysis, smoother emergence
• Others push back → cost vs benefit, especially in routine cases where neostigmine performs adequately

Key issue:
Are we preventing complications—or just buying convenience?

⸻

What the evidence suggests
• Sugammadex reduces residual neuromuscular blockade compared to neostigmine
• Faster extubation times and more predictable recovery
• But no consistent mortality benefit, and cost remains a major barrier

⸻

Clinical Bottom Line

Use sugammadex when it changes outcomes:
• Deep blockade
• High-risk airway or pulmonary patients
• Need for rapid, reliable reversal

Neostigmine still has a role:
• Routine cases
• Adequate spontaneous recovery already present
• Cost-sensitive environments

⸻

Reference:
Brull SJ, Kopman AF. Current Status of Neuromuscular Reversal and Monitoring. Anesthesiology. 2017;126(1):173–190.

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18697 Bagley Road
Middleburg Heights, OH
44130

Website

http://PNBschool.com/

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