Shivering in TTM-Treatment

Tier (progression)	Intervention(s) & Typical Dosing	Key Points / When to Move On
0 – Preventive non-sedating	• Skin counter-warming: forced-air blanket ≈ 43 °C • Acetaminophen 650–1000 mg IV/PO q4-6 h • Buspirone 30 mg PO/NG q8 h • Magnesium SO4 2 g IV load, then 0.5–1 g h-1 (goal Mg 3–4 mg/dL)	Start before cooling. Escalate if BSAS ≥ 2 despite these.
1 – Mild sedation single agent	Choose one: • Dexmedetomidine 0.2–1.5 µg kg-1 h-1 IV or • Opioid (e.g., Fentanyl 25–100 µg h-1 or Meperidine 25–50 mg IV q4-6 h / 12.5–35 mg h-1 infusion)	Re-score BSAS after titration; add second class if BSAS ≥ 2.
2 – Moderate sedation dual therapy	Dexmedetomidine plus opioid (Tier 1 doses) & continue Tier 0 measures.	Synergistic effect. Move to Tier 3 if shivering persists or deep sedation already needed.
3 – Deep sedation	• Propofol 50–75 µg kg-1 min-1 (up to 200 µg kg-1 min-1 if tolerated) • Continue earlier-tier agents as needed	Aim BSAS 0-1; watch for hypotension, hyper-triglyceridemia, PRIS.
4 – Neuromuscular blockade	Preferred Cisatracurium: 0.15 mg kg-1 bolus, then 1–3 µg kg-1 min-1 Alternate Vecuronium: 0.1 mg kg-1 bolus, then 0.8–1.2 µg kg-1 min-1	Use after adequate analgesia/sedation; reassess daily, monitor TOF 1–2/4.

Practical Tips & Adjuncts

• Sedation foundation: Most postarrest patients are intubated; pair this algorithm with baseline analgesia (e.g., fentanyl) and light sedation even at Tier 0.
• Adjunct/rescue agents (if limited by side-effects): low-dose ketamine 0.1–0.5 mg kg^-1 h^-1, clonidine 0.1–0.2 mg PO/NG, ondansetron 4 mg IV, or dantrolene 2.5 mg kg^-1 IV.
• Monitoring: Check BSAS hourly, core temperature continuously, and serum magnesium & triglycerides daily.
• Weaning sequence: During re-warming, stop NMB first, then propofol, then dexmedetomidine/opioids; keep Tier 0 measures until normothermia has been shiver-free for ≥ 4 h.

What Is the BSAS?

The Bedside Shivering Assessment Scale (BSAS) is a quick 4-point scale used at the bedside to grade the intensity of shivering during targeted-temperature management. The goal during TTM is a BSAS of 0–1.

Score	Shivering Description	Clinical Notes
0 (None)	No shivering detected on visual inspection or palpation of masseter, neck, or chest wall.	Target value during cooling; no metabolic penalty.
1 (Mild)	Shivering localized to the neck and/or thorax; may appear only as ECG artifact.	Begin Tier 0–1 measures if persistent.
2 (Moderate)	Intermittent shivering involving upper extremities ± thorax.	Escalate to dual therapy (Tier 2) if not already in use.
3 (Severe)	Generalized or sustained shivering involving the entire body.	Requires deep sedation or neuromuscular blockade (Tier 3–4).

Suggested assessment frequency: every 15–30 min during induction, hourly during maintenance, and every 30 min during re-warming.

Angioedema

ACE-Inhibitor–Induced Angioedema (ACEi-AE)

ACE-inhibitor–induced angioedema is bradykinin-mediated, so the traditional histamine-directed triad (epinephrine ± antihistamines ± glucocorticoids) offers little benefit. Management therefore hinges on early airway protection plus bradykinin-targeted therapy.

Key points for ACEi-AE at the bedside (“ABCs + B-kinin blockers”)

1. Airway first: Maintain a low threshold for awake fiber-optic or video-assisted intubation when voice change, tongue-base swelling, or rapid progression are present.
2. Stop the ACE inhibitor and list it as a permanent allergy.
3. Preferred pharmacologic options (start as soon as the airway is secure or judged stable):

Sequence	Drug (dose / route)	Rationale & evidence
1	Icatibant 30 mg SC (may repeat × 2 at ≥ 6 h intervals)	Bradykinin B2-receptor antagonist; RCT showed median symptom resolution 2 h vs 8 h with steroids/antihistamine.
2	C1-esterase inhibitor concentrate 20 IU kg⁻¹ IV	Replaces C1-INH, dampening kallikrein/FXII activity; supportive case series.
3	Fresh-frozen plasma (FFP) 1–2 units IV (up to 4 units)	Provides ACE and other kininases that degrade bradykinin; relief typically ≤ 4 h but includes transfusion risks.
4	Tranexamic acid 1 g IV push / 10 min	Antifibrinolytic that indirectly limits bradykinin generation; evidence limited but appears safe as rescue.

If you must combine therapies, give FFP before C1-INH to avoid neutralising the concentrate.

4. Adjuncts: Nebulised epinephrine for stridor while preparing the definitive airway. Use the histaminergic bundle (IM epinephrine, diphenhydramine, famotidine, methylprednisolone) only if an allergic trigger has not yet been ruled out.

Diagnostic work-up & differential diagnosis at presentation

Suspected type	Triggers & history	Typical distribution / onset	Urticaria?	Key labs / tests	Distinguishing points & first-line acute therapy
Histaminergic / anaphylactic	Food, stings, drugs, contrast	Seconds–minutes	Yes	Serum tryptase (peak ≈ 1–2 h)	Responds to IM epinephrine; usually resolves < 24 h.
ACE-inhibitor (bradykinin)	Any time during ACEi therapy (risk highest first 30 days)	Hours; tongue, lips, larynx	No	No confirmatory lab; consider C4 to exclude HAE	Does not respond to histamine-directed meds; treat as above.
Hereditary angioedema (C1-INH types I/II/III)	Family history; childhood onset; estrogen sensitivity	Skin, GI, airway; lasts 2–5 days	Usually no	Low C4 during attack; low or dysfunctional C1-INH	Responds to C1-INH, icatibant, ecallantide; TXA useful prophylaxis.
Acquired C1-INH deficiency	Age > 40; lymphoproliferative / autoimmune disease	Similar to HAE	No	Low C1-INH and low C1q	Treat underlying disorder + C1-INH or icatibant.
Other drug-related (ARB, tPA, DPP-4-i, NSAID)	Temporal link to drug	Similar to ACEi or histaminergic	Variable	Guided by mechanism (tryptase or complement)	Withdraw culprit; manage per bradykinin or histamine pathway.
Idiopathic non-histaminergic	Recurrent; no clear trigger	Face / extremities	No	Normal labs	Often steroid-resistant; consider bradykinin blockade if severe.

Treatment options by angioedema mechanism

Mechanism	First-line	Proven adjuncts	Second / rescue	Long-term prophylaxis
Histamine-mediated	IM epinephrine 0.3–0.5 mg q5 min prn	Diphenhydramine 25–50 mg; famotidine 20 mg; methylprednisolone 125 mg	Airway support	Allergen avoidance; omalizumab for chronic idiopathic.
Bradykinin-mediated (ACEi-AE)	Icatibant 30 mg SC	C1-INH 20 IU kg⁻¹ IV	FFP 1–2 U; TXA 1 g IV; ecallantide 30 mg SC	Avoid ACEi; avoid DPP-4-i or mTOR inhibitors if possible.
HAE (acute)	C1-INH, icatibant, ecallantide	FFP if above unavailable	TXA 1 g IV	Lanadelumab; berotralstat; C1-INH prophylaxis.
HAE / acquired (prophylaxis)	Lanadelumab 300 mg SC q2–4 wk	C1-INH 1,000 IU IV twice weekly	TXA 1 g PO bid	Treat lymphoid / autoimmune driver (acquired).

Practical take-aways

• Tranexamic acid 1 g IV and FFP 1–2 units are acceptable rescue therapies for ACEi-AE when icatibant or C1-INH is unavailable. Current data show safety but inconclusive efficacy for TXA, and only small case series for FFP—use when benefits outweigh risks.
• Always anticipate a difficult airway; progression can be deceptively rapid.
• Once the episode resolves, counsel the patient never to restart an ACE inhibitor and to carry documentation of the reaction.

*Lines marked with an asterisk indicate off-label or lower-quality evidence interventions.*

Chemical Cardioversion Success Rates for AFL/AFib

Pharmacologic Conversion – Non-Critically Ill Patients

Agent (route)	Atrial Flutter Conversion Rate	Atrial Fibrillation Conversion Rate	Pros / Cons & Key Contra-indications
Ibutilide (IV)	70 – 90 %	30 – 50 %	Pros: very rapid (≈30 min). Cons/CI: torsades (~4 %); continuous ECG; avoid if QT > 440 ms or severe hypokalaemia.
Flecainide (PO/IV)	≈ 34 %	60 – 70 %	Pros: “pill-in-the-pocket”. Cons/CI: QRS widening; risk of 1:1 flutter (co-give AV-nodal blocker); avoid if QRS > 120 ms or ≥2° AV-block.
Propafenone (PO/IV)	~ 33 %	60 – 70 %	Pros: rapid; mild β-block action. Cons/CI: metallic taste, bronchospasm; avoid in severe asthma, marked bradycardia, major hepatic impairment.
Vernakalant (IV)	≤ 10 % (not recommended)	50 – 70 %	Pros: atrial-selective; very fast. Cons/CI: dysgeusia, hypotension; avoid if SBP < 100 mm Hg, recent MI < 30 d, or severe aortic stenosis.
Amiodarone (IV/PO)	25 – 30 %	60 – 70 %	Pros: wide safety margin. Cons/CI: slower action; IV hypotension; long-term thyroid/lung/liver toxicity; avoid with severe iodine allergy.
Dofetilide (PO)	60 – 70 %	20 – 30 %	Pros: oral start; predictable kinetics. Cons/CI: telemetry admission; torsades risk; CI if CrCl < 20 mL/min or baseline QT > 440 ms.

Pharmacologic Conversion – Critically Ill / ICU Patients

Agent (route)	Atrial Flutter Conversion Rate	Atrial Fibrillation Conversion Rate	Pros / Cons & Key Contra-indications
Ibutilide (IV)	≈ 78 % (≤1 h)	≈ 80 % (≤1 h)	Pros: quickest; works in septic/ventilated pts. Cons/CI: torsades (~4 %); correct Mg⁺⁺/K⁺; avoid if QTc > 440 ms or recent class Ia/III drug.
Procainamide (IV)	≈ 70 % (≤12 h)	≈ 70 % (≤12 h)	Pros: efficacy similar to amiodarone; less hypotension than feared. Cons/CI: BP drop; QRS/QT widening; stop if SBP < 80 mm Hg, QRS > 160 ms, QTc > 500 ms.
Amiodarone (IV)	30 – 60 % (24 h)	60 – 80 % (24 h)	Pros: safe in low-EF or vasopressor pts; prevents relapse if continued. Cons/CI: slower; solvent hypotension; central line for ≥2 g; CI with high-grade AV-block or severe iodine allergy.
Vernakalant (IV)	— (not effective)	≈ 53 % (≤6 h, post-cardiac-surgery)	Pros: atrial-selective; rapid. Cons/CI: transient hypotension (34 %); use only if SBP ≥ 100 mm Hg, QTc < 440 ms; avoid recent MI < 30 d or severe AS.
Sotalol (IV loading)	~ 50 % (limited data)	65 – 70 %	Pros: β-block plus class III (rate + rhythm). Cons/CI: torsades risk (QT monitoring); negative inotrope—avoid if shock; CI if CrCl < 40 mL/min, QTc > 450 ms, HR < 50 bpm.

Device Directed Therapy for Pulmonary Embolus Therapy

Commercial Catheter Platforms for Large Pulmonary Embolism

Device (Manufacturer)	Mechanism / Category	Access size (Fr)	FDA PE Indication	Key Pros	Key Cons
FlowTriever® (Inari Medical)	Large-bore mechanical aspiration & nitinol disks	16 – 24 F	Yes	Removes bulk clot rapidly; often no lytics needed. Robust FLASH / FLAME data with low 30-day mortality and RV/LV improvement.	Very large sheath → bleeding / venotomy repair risk; blood loss (may need re-transfusion); limited reach into distal branches.
Indigo® Lightning 12 (Penumbra)	Computer-assisted vacuum aspiration	12 F	Yes	Smaller bore than FlowTriever; “Lightning” algorithm auto-stops suction when only blood detected → less blood loss; highly trackable catheter.	Requires 12 F venotomy; may need multiple passes; less real-world outcome data.
AlphaVac™ F1885 (AngioDynamics)	Directional aspiration with steerable funnel	18 F	Yes (2024)	Large funnel minimises clogging and limits blood loss; APEX-AV study showed marked RV/LV reduction.	Largest access of any PE device; limited post-market data; high capital cost.
AngioJet™ ZelanteDVT (Boston Scientific)	Rheolytic jet thrombectomy	8 F	Off-label	Widely available; can combine with “power-pulse” lytic; rapid debulking possible.	Black-box warning for bradyarrhythmia / hemolysis & AKI risk; off-label for PE; smaller lumen than other mechanical systems.
EKOSonic™ (Boston Scientific)	Ultrasound-assisted CDT (US-CDT)	5 – 6 F dual	Yes	Allows 50–70 % lower tPA dose vs standard CDT; RCTs (ULTIMA, SEATTLE II, OPTALYSE) show rapid RV recovery & low bleeding.	Requires 2–6 h thrombolytic infusion & ICU monitoring; no mechanical extraction for very large clot burden; higher disposable cost.
BASHIR™ (Thrombolex)	Expandable basket pharmacomechanical CDT	7 – 8 F	Yes	Basket re-establishes flow then bathes clot with low-dose lytic; smaller sheath; early BEC-PE / RESCUE data encouraging.	Lytic still required (bleeding risk); limited large-scale evidence; deployment learning curve.
Cragg-McNamara™ (Medtronic)	Multi-side-hole infusion catheter (standard CDT)	4 – 5 F	Off-label	Inexpensive; widely stocked; easy bilateral placement; minimal access size.	Requires 12–24 h lytic infusion → higher bleeding risk; passive lysis with slower RV recovery.
Uni-Fuse® (AngioDynamics)	Pressure-response-outlet infusion catheter	4 – 5 F	Off-label	Even drug dispersion; low cost; familiar workflow.	Same prolonged-infusion bleeding concerns; no mechanical component.
Fountain® (Merit Medical)	Gradient-hole infusion catheter	4 – 5 F	Off-label	Laser-drilled spiral holes give uniform dispersion (5–50 cm lengths); useful in distal branches or hybrid setups.	Needs prolonged lytic infusion; minimal data in massive clot; non-mechanical.

¹ “FDA PE indication” refers to explicit 510(k) clearance naming pulmonary embolism. Devices marked “Off-label” are cleared for peripheral use but commonly employed in PE at operator discretion.

How to use this chart

• Match patient & clot profile — Large-bore thrombectomy (FlowTriever, AlphaVac, Lightning 12) excels when a big, central clot must come out fast and bleeding risk is high.
• Balance bleeding vs access risk — Ultrasound- or basket-assisted CDT (EKOS, Bashir) lowers tPA dose but still requires several hours and systemic anticoagulation; standard infusion catheters are simplest but use full-dose lytic.
• Mind the sheath size — A 24 F FlowTriever or 18 F AlphaVac may not be tolerated in small femoral veins or severe RV failure; 5 F infusion catheters can be placed via a single 12 F dual-lumen sheath for bilateral therapy.
• Confirm indications & experience — Some devices (e.g. AngioJet, standard infusion catheters) are widely used in PE but technically off-label; follow institutional policy and your PERT algorithm.

Situations Where Catheter-Based PE Devices Outperform
Systemic Thrombolysis or Anticoagulation Alone

Clinical scenario	Why device therapy is preferred	Why thrombolytics / heparin fall short
Absolute / major relative contraindication to systemic lysis • Recent intracranial hemorrhage or neurosurgery • Intracranial mass / AVM • Major non-CNS surgery or trauma < 2 weeks • Active or high-risk bleeding diathesis	Mechanical or low-/no-lytic catheters debulk clot while avoiding systemic fibrinolytic exposure.	Systemic tPA forbidden or carries prohibitive ICH/GI-bleed risk; heparin alone cannot reverse shock or severe RV strain.
Massive (high-risk) PE with impending or ongoing hemodynamic collapse	Large-bore aspiration/thrombectomy provides immediate after-load relief and can be performed rapidly in the cath or IR suite.	Systemic tPA may require 30–120 min for effect and can worsen hypotension once given; anticoagulation alone is too slow.
Failure of systemic thrombolysis • Persistent shock / RV dysfunction ≥ 2 h after full-dose tPA	Serves as rescue strategy—mechanically removes residual clot, often restoring MAP and oxygenation within minutes.	Repeat lysis markedly increases ICH risk; further observation with heparin alone risks cardiac arrest.
Intermediate-high risk PE (RV/LV ≥ 1.0 plus elevated troponin) • Early clinical deterioration or escalating vasopressor/O2 needs • Moderate bleeding risk (e.g., age > 75, recent GI bleed)	Randomized and registry data (PEERLESS, FLASH) show rapid RV recovery, less ICU utilization, and fewer clinical deteriorations versus catheter-directed thrombolysis or AC alone.	Full-dose systemic tPA not guideline-endorsed in this group (bleeding vs. benefit); anticoagulation alone may not prevent progression.
Pregnancy / early postpartum with massive or intermediate-high risk PE	Mechanical thrombectomy or low-dose catheter lysis minimizes maternal & fetal hemorrhage risk while achieving reperfusion.	Systemic lytics carry up to 20 % maternal bleeding and fetal-loss risk; surgery poses greater anesthesia/uterine perfusion hazards; heparin alone insufficient when shock or severe RV strain present.
Very large proximal (saddle/main) clot with severe RV strain or refractory hypoxemia, but bleeding risk high	Registry (FLASH) shows > 20 % drop in mPAP and rapid RV/LV ratio normalization without systemic lytics.	Systemic tPA dose needed to clear massive burden raises major bleed risk; anticoagulation alone rarely reverses RV failure fast enough.

*Device therapy = mechanical thrombectomy, ultrasound-assisted catheter-directed thrombolysis (US-CDT), or low-dose pharmacomechanical CDT, selected per institutional protocol and operator expertise.*

How to apply this table

• Risk-stratify first — Use ESC/AHA classification, RV imaging, and biomarkers to identify high- and intermediate-high–risk patients.
• Screen for bleeding risk — Absolute or major relative thrombolytic contraindications immediately tilt the scale toward mechanical or low-dose catheter therapies.
• Engage your PERT early — Rapid multidisciplinary decision-making speeds access to the cath/IR suite and mechanical circulatory support if needed.
• Match device to anatomy & urgency — Large-bore aspiration (FlowTriever, AlphaVac) for central clot and shock; US-CDT (EKOS) or basket-assisted (BASHIR) when partial lytic use is acceptable.

Septic Pulmonary Emboli

 

CT Finding	Septic Pulmonary Emboli (SPE)	Hematogenous Metastases	Angio-invasive Fungal	Granulomatosis with Polyangiitis	Bland PE / Infarct
Typical distribution	Multiple bilateral peripheral nodules	Random; no pleural predilection	Peribronchovascular & random	Diffuse upper/lowero lbes	Wedge-shaped pleural-based opacity
Feeding-vessel sign	Common (≈60-80%)	Uncommon	Rare	Absent	Enlarged occluded artery (different appearance)
Cavitation	Frequent; thick-walled	Occasional; thin-walled	Very common → air-crescent sign	Common; irregular	Uncommon (late “gangrene”)
Halo sign	Possible	Rare	Classic early sign	May be present	Reverse-halo may evolve
Air-fluid level in nodule	Supports SPE	Rare	Possible (advanced)	Possible	Rare
Tree-in-bud pattern	Common	Rare	Possible	Possible	Absent
Pleural effusion / empyema	Up to 30 %; may be loculated	Rare	Possible	Occasional	Small effusion common
Vascular / cardiac clues	Central line, right-heart clot, septic thrombus	None	None	None	Pulmonary artery filling defect
Clinical context	Bacteremia, R-sided endocarditis, infected device	Known malignancy	Neutropenia, transplant, steroids	ENT/kidney disease, c-ANCA +	Recent DVT/PE, hypercoagulable
Evolution on follow-up CT	Rapid change ⇢ resolves on antibiotics	Slow response to oncologic Rx	Rapid progression if untreated	Slow improvement with immunosuppression	Opacity scars over weeks

How to Use This Table

• Step 1 — Scan for a feeding-vessel sign: a vessel entering a cavitating peripheral nodule strongly tips the balance toward SPE.
• Step 2 — Check distribution & ancillary signs: tree-in-bud plus cavitating nodules along the pleura + bacteremia = think SPE. A solitary wedge opacity without nodules leans toward bland infarct.
• Step 3 — Integrate clinical data: positive blood cultures or a known infected line shifts probability sharply toward SPE; a neutropenic host raises fungal concern; known cancer favors metastases.
• Step 4 — Plan targeted work-up: if SPE suspected, obtain blood cultures, transthoracic/TEE echo, and search for thrombophlebitis or infected devices while starting broad-spectrum antibiotics.

The pattern of multiple bilateral, predominantly peripheral nodules—several with central cavitation and a visible “feeding-vessel” sign—fits best with septic pulmonary emboli (often secondary to right-sided endocarditis, infected intravascular devices, or other deep sources of bacteremia). Other differentials (fungal nodules, vasculitis, hematogenous metastases) are possible, but the morphology and distribution here most strongly favor septic emboli.

How Good or Bad is AI in Reading an Abnormal CXR

Key Radiographic Features

Feature	Present?	Comment
Heart size / mediastinum	Yes (appears enlarged)	Cardiomegaly can be exaggerated on an AP portable view.
Cephalization (upper-lobe venous engorgement)	Yes	Upper-zone vessels as large as—or larger than—lower-zone vessels; suggests ↑ left-atrial pressure.
Interstitial edema	Yes	Coarse reticular pattern, possible Kerley lines and peribronchial cuffing.
Alveolar edema (“bat-wing” opacities)	Yes	Symmetric perihilar fluffy air-space opacities extending outward.
Pleural effusions	Probable small	Hazy or blunted costophrenic angles.
Lines / devices	Yes	ECG leads and pacing/monitor wires are visible.

Impression

The combination of vascular redistribution, interstitial thickening, symmetric perihilar air-space opacities, and probable small pleural effusions is most consistent with cardiogenic pulmonary edema / pulmonary vascular congestion due to acute de-compensated heart failure.

Caveats & Next Steps

• Always correlate clinically—BNP, bedside lung ultrasound (B-lines vs consolidation), echocardiography, or PA-catheter data help confirm elevated filling pressures.
• If shock, sepsis, or a normal heart size is present, keep ARDS and diffuse pneumonia in the differential.
• Repeat radiographs after aggressive diuresis/vasodilator therapy—rapid clearing within 24–48 hours favors a cardiogenic origin.