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I have pt copd with infection with hypoxia and co2 narcosis, D5 today, she was on bipap worsened today, growing mdr acinito acter. Intubated today morning. Her ventilator setting attached. Should I change anything. Planning for polymyxin by evening.
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\"Acinetobacter baumannii\"[MeSH] AND \"polymyxins\"[MeSH] AND combination therapy
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I now have everything I need for a thorough answer. Let me compile the full assessment.
Ventilator Assessment - COPD + MDR Acinetobacter + CO2 Narcosis (Day 1 Intubation)
What I Read From the Screen (Mindray SV300, V-SIMV Mode)
| Parameter | Current Value | Target for COPD |
|---|---|---|
| Mode | V-SIMV | Acceptable (see below) |
| FiO2 | 100% | Needs reduction |
| TV (set) | 550 mL | Too high |
| f SIMV | 5 bpm | Too low |
| PEEP | 6 cmH2O | Acceptable/monitor |
| Tinsp | 1.30 s | Acceptable |
| Ppeak | 46 cmH2O | High - alarm |
| Pplat | 34 cmH2O | Too high |
| MVe | 1.7 L/min | Critically low - that's the "MV Too Low" alarm |
| TVe | 409 mL (988 listed) | Low effective exhaled |
| TVi | 359 mL | Lower than set 550 - leak/resistance |
| Total f | 5 bpm | Low |
| ΔPsupp | 0 cmH2O | No PS on top |
Critical Problems to Address Right Now
1. MV Too Low Alarm (1.7 L/min) - Most Urgent
The minute ventilation is dangerously low. This is a post-intubation patient with CO2 narcosis. At only 5 breaths/min and effective TVe of 409 mL, she is not being ventilated. In COPD you want to avoid overventilation to prevent alkalemia and dynamic hyperinflation, but 1.7 L/min is insufficient. Target MV ~6-8 L/min initially.
Action: Increase SIMV rate to 10-12 bpm (start at 10). This gives adequate ventilation while keeping I:E ratio favorable for obstruction. Do NOT go above 14 bpm to protect expiratory time.
2. Tidal Volume - Too High AND Causing High Ppeak/Pplat
550 mL set TV for an adult COPD patient is excessive. Pplat of 34 cmH2O is at the upper acceptable limit (target <30). Ppeak of 46 is very high, largely from airflow resistance (obstructive), but Pplat should also come down.
Per Murray & Nadel: "A small tidal volume (5-7 mL/kg predicted body weight) should be used to avoid hyperinflation, overventilation, and alkalemia."
Action: Estimate ideal body weight (IBW). For a typical adult woman ~55 kg IBW, target TV = 6 mL/kg = ~330 mL. Reduce TV to 350-400 mL. This will help bring Pplat to <30.
3. FiO2 100% - Too High Post-Stabilization
She had hypoxia, so 100% at intubation was appropriate. However, now titrate down. In COPD, excessive O2 can worsen CO2 retention (Haldane effect, hypoxic drive suppression).
Action: Wean FiO2 targeting SpO2 88-92% (not 95-100%). Start reducing to 60%, then titrate by SpO2.
4. PEEP 6 cmH2O - Acceptable but Monitor Closely
PEEP of 6 is reasonable. Rosen's states: "PEEP can be safely set to 5 cmH2O for all patients with a COPD exacerbation." In the presence of intrinsic PEEP (auto-PEEP), you can titrate extrinsic PEEP up to 50-80% of total PEEP to offset triggering threshold. However, first measure auto-PEEP - do an end-expiratory hold maneuver (3-5 second hold). If auto-PEEP is present and high, you may need to reduce TV and rate before manipulating extrinsic PEEP.
Action: Measure auto-PEEP now. If iPEEP >8, consider reducing PEEP to 5 and focusing on optimizing expiratory time.
5. Mode - V-SIMV with No PS (ΔPsupp = 0)
V-SIMV at 5 bpm with zero pressure support means spontaneous breaths get no assist. Day 1 post-intubation with CO2 narcosis - she may not be breathing spontaneously much, but if she is triggering, unsupported breaths increase work of breathing.
Action: If she is making spontaneous effort, add PS 8-10 cmH2O above PEEP. If she is fully passive/sedated right now, this is less urgent. Consider switching to V-A/C at 10-12 bpm, TV 350-400 mL, as the preferred initial mode for COPD per textbook guidance (volume-limited A/C gives better control).
6. Tinsp 1.30s - Review I:E Ratio
At 5 bpm, cycle time = 12s. With Tinsp 1.30s, expiratory time = 10.7s (good I:E ~1:8). However, once you raise rate to 10-12 bpm, recheck: at 12 bpm, cycle = 5s, so expiratory time = 3.7s (I:E ~1:3) - still acceptable. If more rate needed, shorten Tinsp to 0.8-1.0s to preserve expiratory time.
Revised Ventilator Settings (Suggested)
| Parameter | Suggested | Rationale |
|---|---|---|
| Mode | V-A/C or V-SIMV + PS 10 | Better initial control |
| FiO2 | Start weaning to 60%, titrate to SpO2 88-92% | Avoid O2 toxicity + CO2 retention |
| TV | 350-400 mL (~6 mL/kg IBW) | Reduce hyperinflation, bring Pplat <30 |
| Rate | 10-12 bpm | Adequate MV, preserve expiratory time |
| PEEP | 5-6 cmH2O | Maintain after measuring auto-PEEP |
| Tinsp | 1.0s | Adjust if rate increases |
| PS | 8-10 cmH2O (if SIMV) | Support spontaneous efforts |
Target after changes: MV 6-8 L/min, Pplat <30, SpO2 88-92%, pH >7.20 (permissive hypercapnia acceptable if pH >7.20)
On Polymyxin B Plan (for MDR/XDR Acinetobacter)
Goldman-Cecil confirms:
- Polymyxin B loading dose: 2.5 mg/kg IV x1 (infuse over 60 min)
- Maintenance: 2.5-3.0 mg/kg/day in divided doses q12h (infuse over 60 min)
- Duration: 7-10 days for pneumonia
Key points:
- Polymyxin B does NOT require renal dose adjustment (unlike colistin) - this is a practical advantage in a sick COPD patient
- Combine with a second active agent - options depend on your sensitivity report: sulbactam (ampicillin-sulbactam 3g q4h or high-dose), tigecycline (100-200 mg load, then 50-100 mg q12h), or minocycline (200 mg load, then 100-200 mg q12h). Combination therapy is strongly recommended over monotherapy for XDR Acinetobacter - per Goldman-Cecil: "combination therapy with at least 2 active agents is preferred"
- Watch nephrotoxicity closely - polymyxin B's main risk; monitor urine output and creatinine daily
- If available, cefiderocol (2g q8h over 3h infusion) has emerged as an alternative - the 2023 ATTACK trial (PMID 37182534, Lancet Infect Dis) showed sulbactam-durlobactam was non-inferior to colistin for CRAB - worth checking if sulbactam-durlobactam is accessible in your institution
- Inhaled colistin as an adjunct (not replacement) may improve local lung concentrations for VAP - consider adding nebulized colistin 2 MU q8-12h via inline nebulizer if available
Other Management Reminders
- Sedation/analgesia - Adequate sedation (target RASS -2 to -1) is needed to prevent patient-ventilator dyssynchrony and to allow permissive hypercapnia without distress. Fentanyl infusion preferred over morphine in COPD (less histamine release).
- Bronchodilators via ventilator - Salbutamol MDI via inline spacer or nebulized ipratropium. These will help reduce Ppeak over time.
- Monitor auto-PEEP - Do end-expiratory hold at each vent check.
- Lung mechanics check - Repeat Pplat/compliance calculation after adjusting TV.
- D5 fluids - If this refers to Day 5 of illness, ensure adequate nutrition via NG/NJ - early enteral feeding within 24-48h of intubation.
- ABG in 30-60 min after vent changes to assess pH, PaCO2, PaO2/FiO2.
Bottom line: The biggest immediate fix is increasing ventilator rate to 10-12 bpm (the MV Too Low alarm is a real problem) while simultaneously reducing TV to 350-400 mL and weaning FiO2 off 100%. Polymyxin B plan is appropriate - use combination therapy, watch kidneys.
Disclaimer: This is clinical decision support, not a substitute for bedside assessment. Adjust based on patient's actual weight, ABG, auto-PEEP measurement, and real-time response.
Can I try amikacin as combination as it's intermediate sensitivity
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Good data obtained. Here's the full picture:
Amikacin as Combination with Polymyxin B - Intermediate Sensitivity: Yes, With Conditions
The Short Answer
Yes, you can try amikacin as a partner drug to polymyxin B, even with intermediate sensitivity - but only if you optimize dosing pharmacodynamically and monitor toxicity closely. "Intermediate" does not mean "don't use" - it means standard dosing will likely fail, but high-dose extended-interval dosing may achieve adequate pharmacodynamic targets.
Understanding "Intermediate" for Amikacin vs. Acinetobacter
This is the most important concept here. A 2023 PK/PD study in Antimicrobial Agents and Chemother (Lepak et al., PMID 36946729) specifically re-evaluated amikacin breakpoints for A. baumannii VAP/HAP using murine lung infection models and PK/PD simulation. Their findings:
- The susceptible breakpoint for amikacin in Acinetobacter pneumonia is MIC ≤8 µg/mL (using maximal dosing)
- The key PK/PD driver for aminoglycosides is AUC/MIC ratio (concentration-dependent killing)
- At maximal dosing (25-30 mg/kg extended interval, i.e., once-daily high-dose), higher MIC strains can still achieve bactericidal targets in lung epithelial lining fluid (ELF)
What this means for your patient:
- If her amikacin MIC is at the intermediate breakpoint (typically 16-32 µg/mL by CLSI), standard dosing (15 mg/kg) will almost certainly fail
- If MIC is at the lower end of intermediate (e.g., 16), high-dose amikacin (25-30 mg/kg once daily) can potentially achieve the AUC/MIC target of ≥75-100 needed for lung infection
- If MIC is ≥64, don't use it - no dose will overcome this
Ask your microbiologist for the actual MIC value, not just S/I/R. The actual number determines if this is worth pursuing.
Goldman-Cecil on Aminoglycosides for Acinetobacter
Goldman-Cecil explicitly lists amikacin as an option: "Aminoglycosides (e.g., amikacin 15-20 mg/kg then dose by therapeutic drug monitoring) are an option for treatment of urinary tract infection and potentially for systemic infections. The presence of methyl transferases limits the use of aminoglycosides."
Note the caveat - methyl transferases (armA, rmtB, etc.) cause high-level aminoglycoside resistance in MDR Acinetobacter and make amikacin useless regardless of dose. These are common in MDR strains. If your sensitivity report shows intermediate rather than resistant, methyl transferases are probably absent or partial - which is slightly reassuring.
Practical Approach: How to Use Amikacin in This Setting
If you decide to proceed:
| Parameter | Recommendation |
|---|---|
| Dose | 25-30 mg/kg IBW once daily (not the standard 15-20 mg/kg) |
| Infuse over | 30-60 minutes |
| Peak target | 60-80 µg/mL (draw 30 min post-infusion) |
| Trough target | <5 µg/mL (draw just before next dose) |
| TDM | Essential - check peak and trough after 1st dose, then trough q2-3 days |
| Duration | Consider limiting to 5-7 days given nephrotoxicity risk |
Why TDM is non-negotiable here: She is already receiving polymyxin B (also nephrotoxic). Combining two nephrotoxic agents in a critically ill COPD patient with potentially altered drug clearance is high-risk. You must confirm amikacin is not accumulating.
The Nephrotoxicity Problem
This is the real concern in your patient:
- Polymyxin B + amikacin = additive nephrotoxicity
- Critically ill patients already have reduced renal reserve
- COPD patients often have baseline renal impairment
- Aminoglycosides are concentration-dependent - once-daily dosing (vs. q8h) actually reduces nephrotoxicity while maximizing efficacy
Monitor:
- Urine output hourly
- Creatinine daily
- If creatinine rises >1.5x baseline or oliguria develops, stop amikacin first
Alternative Combination Partners to Consider
If the MIC is high-end intermediate or you're worried about toxicity stacking, consider these as the second drug alongside polymyxin B instead:
| Agent | Rationale | Dose |
|---|---|---|
| Tigecycline | Good in vitro activity vs. XDR Acinetobacter, no additive nephrotoxicity | 200 mg load, then 100 mg q12h (double dose for pneumonia) |
| Sulbactam (via ampicillin-sulbactam) | Often retains activity even in MDR strains | 3g q4h over 4h infusion |
| Minocycline | Useful if tigecycline unavailable | 200 mg load, then 100-200 mg q12h |
| Rifampicin | Used as synergistic add-on; never as monotherapy | 600 mg q12h |
The 2024 review (Rafailidis et al., PMID 38534696) confirms: "we have to resort to at least one of: sulbactam, polymyxins, tigecycline, or aminoglycosides for MDR/XDR Acinetobacter infections."
Bottom Line
| Situation | Decision |
|---|---|
| Amikacin MIC ≤16 µg/mL | Yes - use high-dose 25-30 mg/kg OD + TDM |
| Amikacin MIC 32 µg/mL | Marginal - consider only if no better option, high-dose only |
| Amikacin MIC ≥64 µg/mL | No - don't use |
| No methyl transferases suspected | Proceed with amikacin |
| Creatinine rising on polymyxin | Avoid amikacin, switch to tigecycline/sulbactam |
| No TDM available | Avoid amikacin - cannot dose safely without it |
Get the exact MIC number from the lab before committing. If it's ≤16 and TDM is available, amikacin is a reasonable combination partner. If MIC is higher or TDM is unavailable, tigecycline at double-dose (100 mg q12h) is a safer second agent alongside polymyxin B.
Disclaimer: Clinical decision support only. Adjust based on full clinical picture, local antibiogram patterns, and renal function.
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This is my current setting it's showing mv is low and fio2 is high. Anything to change. Her wt is around 40. Can I try amikacin 50% iv and rest nebulization.?
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Excellent - very useful data. I now have everything needed for a comprehensive answer.
Updated Ventilator Assessment + Nebulized Amikacin Question
Reading the New Screen (V-SIMV, 1:01 PM - good progress from morning!)
| Parameter | Now | Earlier (AM) | Status |
|---|---|---|---|
| Mode | V-SIMV | V-SIMV | Same |
| FiO2 | 99% | 100% | Still too high - alarm active |
| TV (set) | 350 mL | 550 mL | ✅ Good - you reduced it |
| f SIMV | 10 bpm | 5 bpm | ✅ Good - rate increased |
| PEEP | 5 cmH2O | 6 | ✅ Appropriate |
| Tinsp | 1.30s | 1.30s | Same |
| ΔPsupp | 8 cmH2O | 0 | ✅ PS added - well done |
| IntelliCycle | ON | Off | ✅ Good |
| Ppeak | 33 cmH2O | 46 | ✅ Improved |
| Pplat | 32 cmH2O | 34 | Marginal - still slightly high |
| MVe | 3.6 L/min | 1.7 | Improved but still low |
| TVe | 361 mL | 409 mL | Acceptable |
| ftotal | 10 bpm | 5 | She's not triggering above set rate |
| FiO2 displayed | 88% (lower right) | - | SpO2/FiO2 mismatch? |
Ventilator Changes Needed
1. FiO2 - Highest Priority (active alarm)
This is a 40 kg COPD patient. Target SpO2 88-92% only. FiO2 99% is dangerous:
- Worsens hypercapnia (Haldane effect - O2 displaces CO2 from Hb)
- Absorption atelectasis
- O2 toxicity
Action: Reduce FiO2 to 40-50% now. Titrate by SpO2 every 15 minutes. In COPD, SpO2 of 88-90% is perfectly acceptable and preferable.
2. Tidal Volume - Weight-Based Recalculation
Patient weight 40 kg. At 6-7 mL/kg IBW:
- Target TV = 240-280 mL
Current 350 mL = 8.75 mL/kg - this is above the safe limit for a 40 kg patient. This is why Pplat is still 32 (should be <28-30).
Action: Reduce TV to 260-280 mL. This will also slightly reduce Pplat.
3. MV is 3.6 L/min - Still Low
For a 40 kg COPD patient post-CO2 narcosis, target MV is ~5-6 L/min (not aggressive - permissive hypercapnia is fine as long as pH >7.20). With TV reduced to 280 mL and rate 10, MV = 2.8 - too low. So:
Action: Increase rate to 12-14 bpm after reducing TV. This maintains adequate MV while keeping TV protective. Check auto-PEEP after rate change.
4. Apnea Vent is ON with ΔPapnea 15, fapnea 15 - Appropriate
Good backup apnea ventilation settings - keep these.
5. ΔPsupp 8 cmH2O - Good, Keep
PS of 8 above PEEP is appropriate. If she starts triggering more (ftotal goes above 10), you can keep this.
Revised Settings Summary for 40 kg Patient
| Parameter | Current | Suggested |
|---|---|---|
| FiO2 | 99% | 40-50% (titrate to SpO2 88-92%) |
| TV | 350 mL | 260-280 mL (6.5-7 mL/kg for 40 kg) |
| f SIMV | 10 | 12-14 bpm (to compensate MV after TV reduction) |
| PEEP | 5 | Keep 5 |
| Tinsp | 1.30s | Consider 1.0s if rate goes to 14 (more expiratory time) |
| ΔPsupp | 8 | Keep 8 |
| Target MV | 3.6 | 5-6 L/min |
| Target Pplat | 32 | <28 cmH2O |
Nebulized Amikacin - 50% IV + 50% Inhaled Strategy
This is a clinically smart approach and there is now good evidence supporting it.
What the Evidence Shows:
AMIKINHAL Trial (NEJM 2023, PMID 37888914) - the highest quality evidence:
- Large multicenter RCT (n=850 ICU patients on MV ≥72h)
- Inhaled amikacin 20 mg/kg IBW once daily x3 days significantly reduced VAP incidence (15% vs 22%, p=0.004)
- Also reduced ventilator-associated complications (18% vs 26%)
- This was prophylactic use - your patient already has active infection, so the rationale for treatment is even stronger
2024 Systematic Review + Meta-analysis (PMID 39009240) - 30 studies, 12 RCTs:
- Inhaled antibiotics improved microbiological cure (OR 7.0 in RCTs)
- Improved clinical cure (OR 2.09 in observational data)
- No significant increase in mortality but better cure rates
- Reduced renal impairment (OR 0.65) - key for your patient on polymyxin B
- Subgroup analysis: combined IV + inhaled amikacin showed the best outcomes for mortality, clinical cure, and microbiological cure - this directly validates your proposed strategy
Why Inhaled Amikacin Makes Biological Sense:
- Lung ELF (epithelial lining fluid) concentrations after nebulization are 10-100x higher than achievable via IV alone
- Overcomes the MIC barrier - even an "intermediate" MIC organism may be susceptible at the supra-MIC concentrations achieved locally in the lung
- Systemic absorption from nebulization is minimal - so nephrotoxicity risk is much lower than full IV dose
Your Proposed Regimen: 50% IV + 50% Nebulized
For 40 kg patient:
- Total amikacin dose = 25 mg/kg IBW = 1000 mg (high-dose once daily for MDR)
| Route | Dose | How |
|---|---|---|
| IV | 500 mg once daily | Over 30 min, extended interval |
| Nebulized | 500 mg once daily | Via inline vibrating mesh nebulizer, after IV (same sitting or 6h apart) |
Practically this is reasonable. However, the AMIKINHAL trial used 20 mg/kg purely inhaled (no IV). The split approach is pragmatic when you want both systemic and local coverage.
If using nebulized route:
- Use a vibrating mesh nebulizer (VMN) placed at the Y-piece - NOT a jet nebulizer (VMN delivers 4-6x more drug to the lungs)
- The Mindray SV300 has a Nebulizer button on the right side - use it to pause PEEP delivery during nebulization
- Nebulize during inspiration only if VMN supports it
- Dilute amikacin to 4 mL total volume (500 mg/2 mL + 2 mL saline)
- Duration: 15-20 minutes
- Chest physio after to mobilize secretions
- Monitor SpO2 and bronchospasm during - rare but possible
TDM:
- Draw peak (30 min post-IV infusion): target 60-80 µg/mL
- Draw trough (just before next dose): target <5 µg/mL
- With only 500 mg IV, peak may be lower (~40-60 range) - this is acceptable if you're adding inhaled top-up
- No TDM needed for nebulized component (systemic absorption negligible)
Safety Watch Points (Polymyxin B + Amikacin Combination)
| Risk | Monitor | Action if triggered |
|---|---|---|
| Nephrotoxicity | Creatinine daily, urine output hourly | If Cr rises >1.5x - stop amikacin IV, continue nebulized only |
| Bronchospasm | SpO2 + wheeze during nebulization | Pre-treat with salbutamol nebulization 15 min before |
| Hearing/vestibular (ototoxicity) | Difficult to assess in ICU - minimize duration | Limit total IV amikacin to 5-7 days |
| Neuromuscular blockade | Rare with amikacin alone; more with polymyxin | Monitor if using neuromuscular blocking agents |
Bottom Line
Yes - your 50% IV + 50% nebulized approach is evidence-supported and biologically rational. The 2024 meta-analysis (PMID 39009240) specifically found the combined IV + inhaled strategy gave the best outcomes. The inhaled component achieves supra-MIC lung concentrations that overcome intermediate susceptibility, while the reduced IV dose lowers nephrotoxicity risk - which matters greatly in a patient already on polymyxin B.
Most important immediate action: Get FiO2 down to 40-50% right now - that alarm is the most dangerous current problem.
Disclaimer: Clinical decision support only - adjust based on TDM results, renal function, and bedside response.
IMG20260525180724.jpg
This is the current setting and spo2 is 83 should I alter anything?
SpO2 83% with FiO2 99% is a critical situation - this is refractory hypoxemia. Let me read the screen carefully and act fast.
URGENT - Reading the Screen (5:53 PM, DuoLevel/APRV Mode)
The mode has been changed to DuoLevel (which is the Mindray name for APRV/Bilevel). Here are all the current parameters:
| Parameter | Value | Assessment |
|---|---|---|
| Mode | DuoLevel (APRV) | Changed from V-SIMV |
| FiO2 | 99% | Still at 99% - alarm active |
| Phigh | 15 cmH2O | Critically low for APRV |
| Plow | 5 cmH2O | OK |
| Thigh | 1.3s | Wrong - far too short for APRV |
| Tlow | 2.7s | Wrong - too long for APRV |
| ΔPsupp | 8 cmH2O | |
| IntelliCycle | ON | |
| MVe | 4.6 L/min | Low |
| TVe | 290 mL | ~7.25 mL/kg for 40 kg - OK |
| TVi | 291 mL | |
| Ppeak | 31 cmH2O | |
| Pplat | 30 cmH2O | Borderline |
| PEEP | 5 cmH2O | |
| ftotal | 16 bpm | She is triggering |
| Leak% | 0 |
The Core Problem: APRV is Set Up Incorrectly
The mode switch to DuoLevel/APRV is a reasonable escalation for refractory hypoxemia, but the time settings are inverted compared to standard APRV protocol. This is why she is still hypoxic at SpO2 83%.
Standard APRV Logic:
- Thigh should be LONG (80-95% of cycle) - this is the recruitment phase, keeps lung open
- Tlow should be SHORT (0.2-0.8s) - brief release, prevents derecruitment
Current settings:
- Thigh = 1.3s (far too short - lung has no time to recruit)
- Tlow = 2.7s (far too long - lung fully deflates, loses all recruitment, causes cyclic derecruitment injury)
With Thigh:Tlow of 1.3:2.7, she is spending more time at low pressure (Plow 5) than high pressure - this is essentially the opposite of APRV. It functions like standard SIMV at this point but without proper volume control, explaining the ongoing hypoxia.
Also: Phigh of 15 cmH2O is Too Low
For APRV to recruit lung in a COPD patient with consolidative MDR pneumonia, Phigh needs to be 20-30 cmH2O. At 15 cmH2O Phigh, there is insufficient driving pressure to open consolidated/infected lung units.
Immediate Actions - Do These Now
Step 1: Fix APRV Timing (Most Urgent)
| Parameter | Current | Change to | Rationale |
|---|---|---|---|
| Thigh | 1.3s | 4.0-5.0s | Long release to allow lung recruitment |
| Tlow | 2.7s | 0.4-0.6s | Short release - terminate at 50-75% of peak expiratory flow |
| Phigh | 15 | 20-25 cmH2O | Better recruitment pressure for consolidation |
| Plow | 5 | 0 cmH2O | Standard APRV uses Plow = 0; the pressure drop itself drives ventilation |
The classic APRV ratio: Thigh:Tlow ≈ 9:1 (e.g., 4.5s high : 0.5s low).
How to set Tlow correctly on Mindray SV300:
- Set Tlow to 0.5s first
- Watch the expiratory flow waveform - release should end when expiratory flow reaches 50-75% of peak expiratory flow rate (to avoid auto-PEEP while maintaining recruitment)
- If auto-PEEP builds, shorten Tlow slightly; if CO2 rises too much, lengthen slightly
Step 2: Increase FiO2 Alarm Threshold Temporarily
SpO2 83% is dangerous. Since FiO2 is already 99%, the hypoxia is not from FiO2 - it is from inadequate alveolar recruitment (wrong APRV settings). Fixing the settings is the priority. Once SpO2 improves above 90%, wean FiO2.
Step 3: Consider Increasing Phigh Stepwise
After fixing timing - if SpO2 still <88% at Phigh 20:
- Increase Phigh by 2 cmH2O every 15-30 min
- Maximum Phigh ~30 cmH2O (watch Pplat)
- In COPD + consolidation, recruitment requires higher Phigh than pure ARDS
Revised APRV Target Settings (40 kg, COPD + MDR Pneumonia)
| Parameter | Target |
|---|---|
| Phigh | 20-25 cmH2O |
| Plow | 0 cmH2O |
| Thigh | 4.0-5.0s |
| Tlow | 0.4-0.6s (flow-guided) |
| FiO2 | 99% for now, wean once SpO2 ≥90% |
| ΔPsupp | 0 (not used in classic APRV) or keep 8 if hybrid mode |
Expected TV after correction: With Phigh 22 and Plow 0, tidal release volumes will be ~4-6 mL/kg, which is protective.
Other Simultaneous Actions for SpO2 83%
- Prone positioning - if feasible, even 2-4 hours of prone can dramatically improve oxygenation in unilateral/bilateral consolidation. Most effective intervention for refractory hypoxemia.
- Recruitment maneuver - sustained inflation at Phigh 30 cmH2O x 30-40s (only if hemodynamically stable, watch BP)
- Suction - MDR Acinetobacter produces thick secretions; ensure regular suctioning, ideally closed-circuit. The suction button is visible on the right panel.
- ABG now - check PaO2/FiO2 ratio, pH, PaCO2. P/F ratio <100 = severe ARDS territory.
- Neuromuscular blockade - if she is fighting the ventilator or asynchronous, 24-48h of cisatracurium improves oxygenation in early severe ARDS/pneumonia
- Optimize hemodynamics - hypotension from sepsis reduces mixed venous O2, worsening SpO2; ensure adequate MAP >65
- Inhaled bronchodilator - salbutamol MDI via inline spacer now - COPD component contributing to V/Q mismatch
Summary - Priority Order
| Priority | Action |
|---|---|
| 🔴 IMMEDIATE | Fix APRV: Thigh → 4-5s, Tlow → 0.5s, Plow → 0, Phigh → 22 |
| 🔴 IMMEDIATE | Get ABG now |
| 🟠 URGENT | Suction airway - check for secretion plug |
| 🟠 URGENT | Recruitment maneuver if BP stable |
| 🟡 SOON | Consider prone positioning |
| 🟡 SOON | Consider NMB (cisatracurium) if asynchrony |
| 🟢 ONGOING | Wean FiO2 once SpO2 ≥90% |
SpO2 83% at FiO2 99% = P/F ratio approximately 60-70 if confirmed on ABG - this is severe hypoxemic respiratory failure requiring urgent escalation of the above steps. The APRV timing correction alone should produce visible improvement within 15-30 minutes.
Disclaimer: Clinical decision support only. Adjust based on real-time ABG, hemodynamics, and bedside assessment.
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Noo it's v smiv
Got it - confirmed V-SIMV. Reading the correct screen now.
Current V-SIMV Settings (5:55 PM) - SpO2 83%, FiO2 100%
| Parameter | Value | Assessment |
|---|---|---|
| Mode | V-SIMV | ✅ Confirmed |
| FiO2 | 80% set / 100% displayed | 🔴 Still critically high alarm |
| TV | 290 mL | ✅ Good for 40 kg (7.25 mL/kg) |
| f SIMV | 16 bpm | ✅ Good |
| Tinsp | 1.15s | ✅ Better than before |
| PEEP | 5 cmH2O | 🔴 This is the problem - too low for SpO2 83% |
| ΔPsupp | 8 cmH2O | ✅ |
| IntelliCycle | ON | ✅ |
| Ppeak | 29 cmH2O | ✅ Good |
| Pplat | 27 cmH2O | ✅ Good, <30 |
| MVe | 4.6 L/min | Acceptable for 40 kg COPD |
| TVe | 295 mL | ✅ |
| TVi | 289 mL | ✅ |
| ftotal | 16 bpm | She is triggering at set rate |
| Leak% | 0 | ✅ Good seal |
The Core Problem: SpO2 83% at FiO2 100%
Settings are actually much better now - TV, rate, Pplat all acceptable. The reason she is still hypoxic at near-100% FiO2 is not a ventilator parameter problem anymore - it is a lung recruitment/oxygenation failure.
With FiO2 ~100% and SpO2 only 83%, her estimated P/F ratio ≈ 60-70 mmHg - this is severe refractory hypoxemia (ARDS territory), driven by the MDR Acinetobacter consolidation causing massive shunt. No amount of FiO2 fixes an intrapulmonary shunt - you need PEEP and recruitment.
What to Change Right Now
1. 🔴 INCREASE PEEP - Most Important Change
PEEP 5 is far too low for SpO2 83% at FiO2 100%. She needs alveolar recruitment urgently.
Increase PEEP stepwise:
| Step | PEEP | Wait | Check |
|---|---|---|---|
| Now | 8 cmH2O | 15 min | SpO2, BP, Pplat |
| If SpO2 still <88% | 10 cmH2O | 15 min | Pplat must stay <30 |
| If still <88% | 12 cmH2O | 15 min | Watch BP - high PEEP reduces preload |
| Max | 14-15 cmH2O | - | Only if Pplat allows |
Important: After each PEEP increase, check that Pplat stays <30 cmH2O. Currently Pplat is 27 with PEEP 5 - so there is some room to increase PEEP before hitting the limit. Watch closely.
Also watch BP with each PEEP step - high PEEP reduces venous return, especially in a septic patient who may already be volume-depleted.
2. 🔴 Do a Recruitment Maneuver First (Before Increasing PEEP)
Before stepping up PEEP, open the lung first:
- Increase PEEP temporarily to 20 cmH2O for 30-40 seconds (sustained inflation / staircase recruitment)
- Only if MAP >65 and no pneumothorax
- Then set PEEP to 10 and titrate as above
- Watch for sudden SpO2 improvement
3. 🟠 FiO2 - Do NOT reduce yet
FiO2 80% set (showing 100% - likely the system is auto-compensating or there's a display lag). Do not reduce FiO2 until SpO2 is consistently ≥90%. Once PEEP is optimized and SpO2 improves, then wean FiO2.
4. 🟠 Check for Reversible Causes of Acute Worsening
SpO2 dropping to 83% despite full settings - before assuming it's only pneumonia, rapidly exclude:
| Cause | Bedside Check |
|---|---|
| Mucus plug / secretions | Suction now - MDR Acinetobacter produces thick purulent secretions |
| ETT displacement | Auscultate both sides, check ETT depth at lips |
| Pneumothorax | Auscultate, check waveform shape - unequal breath sounds? |
| Circuit disconnect/leak | Leak% is 0 so likely OK |
| Bronchospasm | Wheeze on auscultation? Give salbutamol MDI 4-8 puffs via inline spacer now |
| Worsening consolidation | Expected with MDR Acinetobacter - check CXR |
| Pulmonary edema | Sepsis-related, check fluid balance |
Revised Settings for SpO2 83%
| Parameter | Current | Change to |
|---|---|---|
| FiO2 | 80-100% | Keep at 80-100% until SpO2 ≥90% |
| TV | 290 mL | Keep - good for 40 kg |
| f SIMV | 16 | Keep |
| PEEP | 5 | → 10 cmH2O (step up after recruitment maneuver) |
| Tinsp | 1.15s | Keep |
| ΔPsupp | 8 | Keep |
After PEEP increase, expected Pplat = ~32-34 cmH2O - borderline but acceptable in severe hypoxemia (ARDS protocol allows up to 35 in life-threatening hypoxia).
Additional Urgent Escalation Options if PEEP Fails
If SpO2 does not improve to ≥88% after PEEP 10-12:
- Prone positioning - even 2-4 hours significantly improves oxygenation in posterior consolidation. Most impactful single intervention for refractory hypoxemia.
- Neuromuscular blockade - cisatracurium 0.15 mg/kg bolus then infusion for 24-48h reduces O2 consumption and ventilator dyssynchrony
- Inhaled vasodilator - inhaled salbutamol acts as pulmonary vasodilator improving V/Q; if available, inhaled nitric oxide or prostacyclin
- Optimize sepsis hemodynamics - ensure MAP >65, adequate Hb (>8-9 g/dL in critical hypoxemia), correct metabolic acidosis
Summary - Priority Actions
| Priority | Action |
|---|---|
| 🔴 Do now | Suction - rule out mucus plug |
| 🔴 Do now | Recruitment maneuver then increase PEEP to 10 |
| 🔴 Do now | Auscultate - rule out pneumothorax, ETT position |
| 🟠 Next 30 min | Step PEEP up toward 12-14 if SpO2 still <88% |
| 🟠 Next 1 hour | Prone position if no improvement |
| 🟡 If still failing | Consider NMB, optimize Hb, hemodynamics |
The ventilator settings are now reasonably appropriate for a 40 kg COPD patient. The hypoxia at this point is driven by massive shunt from consolidation - PEEP recruitment is your primary lever, not FiO2.
Disclaimer: Clinical decision support only. Use alongside bedside assessment and ABG.
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She's having tachycardia hypotension what to do next
CRITICAL - Reading Both Screens Now
Monitor (Goldway G30):
- HR: 137 bpm (alarm: HR High)
- BP: 87/58 mmHg (MAP ~68, borderline)
- SpO2: 87% (slight improvement from 83%)
- RR: 0 shown (probe issue or apnea display artifact)
- ST(I): -0.13 (mild ST depression - demand ischemia from tachycardia/hypoxia)
Ventilator (Air Liquide Monnal T75, SIMV):
- FiO2: 90%
- TV: 290 mL
- RR SIMV: 15 bpm
- PEEP: 6 cmH2O
- TI: 1.1s
- Ppeak: 35 cmH2O
- Pplat: 26 cmH2O ✅
- MVe: 4.1 L/min
- VTe: 291 mL
- RR total: 15 bpm
- FiO2: 90%
This is Septic Shock + Refractory Hypoxemia. Act in This Order:
🔴 STEP 1 - Identify the Cause of Hypotension (< 2 minutes)
Three causes must be excluded immediately before giving fluids:
| Cause | Bedside check | Why urgent |
|---|---|---|
| Auto-PEEP / Dynamic hyperinflation | Disconnect ETT from vent for 10-15s - does BP immediately rise? | COPD + high RR = most likely immediate cause |
| Tension pneumothorax | Unequal breath sounds, deviated trachea, waveform asymmetry | Can kill in minutes |
| Cardiac tamponade | Muffled sounds, elevated JVP, recent central line | Less likely but exclude |
The most likely ventilator cause right now: With RR 15, TV 290, PEEP 6 in a COPD patient - auto-PEEP is building. High intrathoracic pressure is compressing the right heart and reducing venous return = obstructive shock mimicking septic shock.
Do this first - 10-second ventilator disconnect test:
- Disconnect circuit from ETT briefly
- If BP rises and HR drops within seconds → auto-PEEP was the cause → reduce rate to 10-12, reduce PEEP to 3-4
- If no change → proceed to fluid resuscitation
🔴 STEP 2 - Fluid Resuscitation (If auto-PEEP excluded)
This patient has septic shock from MDR Acinetobacter. BP 87/58 = MAP ~68, but HR 137 = compensating.
Fluid bolus:
- 250-500 mL crystalloid (Normal saline or Ringer's lactate) over 15-30 minutes
- Assess response - if MAP rises ≥65 and HR falls, she is fluid responsive
- Repeat up to 1500 mL total if responding
- Do NOT over-fluid - she has consolidating pneumonia, excess fluid will worsen hypoxia
Fluid responsiveness test if unsure:
- Passive leg raise (PLR): lift legs to 45° for 1 minute - if HR drops and BP rises, give fluid
- Pulse pressure variation if fully ventilated (not reliable in SIMV with spontaneous breathing)
🔴 STEP 3 - Start Vasopressor (Do NOT wait for fluid response if MAP <65)
MAP = (87 + 2×58)/3 = 68 mmHg - currently just above threshold but with HR 137 this is precarious.
Start norepinephrine now:
- Norepinephrine 0.1-0.2 mcg/kg/min via central line (or peripherally short-term if no central access)
- Titrate to MAP ≥65 mmHg
- Target MAP 65-70 in COPD/lung protective strategy (not higher - increases afterload unnecessarily)
- For 40 kg: start at 0.1 mcg/kg/min = 4 mcg/min and titrate up
If norepinephrine dose exceeds 0.25 mcg/kg/min with inadequate response:
- Add vasopressin 0.03 units/min (fixed dose, do not titrate)
- Or add hydrocortisone 200 mg/day (50 mg q6h or infusion) - septic shock + COPD patient likely on steroids anyway
🔴 STEP 4 - Ventilator Adjustments for Hemodynamic Compromise
Reduce intrathoracic pressure:
| Parameter | Current | Change to | Reason |
|---|---|---|---|
| RR SIMV | 15 | 10-12 | Longer expiratory time, reduce auto-PEEP |
| PEEP | 6 | 4-5 | Reduce intrathoracic pressure, improve venous return |
| TV | 290 | Keep | Already appropriate |
| FiO2 | 90% | 100% temporarily | She is in shock + SpO2 87% - maximize O2 delivery |
Rationale: In hemodynamic compromise from any cause, high PEEP and high RR worsen cardiac output. Temporarily accepting SpO2 85-90% is safer than crashing the BP further.
🟠 STEP 5 - Address the Tachycardia
HR 137 with ST depression -0.13. This is most likely:
- Compensatory sinus tachycardia from septic shock + hypoxia - treat the cause (fluids + vasopressors + improve SpO2)
- NOT to be treated with rate-slowing drugs (beta-blockers, diltiazem) - this will crash the BP
Do NOT give any antiarrhythmic unless it degenerates to VT/VF. The tachycardia is a physiological response - treat the sepsis and hypoxia.
Check ECG rhythm - is this sinus tachycardia or SVT? The waveform on the monitor looks like regular narrow-complex tachycardia consistent with sinus tachycardia.
🟠 STEP 6 - Check and Optimize
| Action | Why |
|---|---|
| ABG urgently | Lactate, pH, PaO2, PaCO2 - guides severity of shock and ventilation |
| Lactate level | >4 mmol/L = septic shock, guides resuscitation adequacy |
| Hb/CBC | Anaemia worsens O2 delivery in shock - transfuse if Hb <8 |
| Blood cultures x2 (if not already) | Before antibiotics/with polymyxin |
| Electrolytes | Sepsis + polymyxin = hypokalaemia, hypomagnesaemia, hyponatraemia |
| Echo/POCUS if available | LV/RV function, IVC collapsibility for fluid status, rule out tamponade |
| Review polymyxin B | Polymyxin B itself can cause hypotension (histamine release with rapid infusion) - was it given recently? Slow infusion to 60-90 min |
Summary - Immediate Priority Actions
| Time | Action |
|---|---|
| NOW (0-2 min) | Disconnect vent 10s - auto-PEEP test. Reduce RR to 10-12, PEEP to 4 |
| NOW | If BP doesn't recover - start norepinephrine 0.1 mcg/kg/min, titrate to MAP ≥65 |
| 0-15 min | Fluid bolus 250-500 mL if PLR positive / clinically fluid responsive |
| 0-15 min | FiO2 → 100% during shock phase |
| 15-30 min | ABG + lactate |
| 30-60 min | If MAP stable, add hydrocortisone 50 mg q6h (septic shock refractory to NE) |
| Ongoing | Hb >8, MAP ≥65, urine output >0.5 mL/kg/h |
One important question: Was polymyxin B infused recently? It can cause direct histamine-mediated hypotension if given too fast. If so - slow the infusion rate and give IV hydrocortisone 100 mg stat.
Disclaimer: Clinical decision support only. This patient is critically deteriorating - bedside senior intensivist involvement is strongly recommended if not already present.
