Professor David Tuxen talks about mechanical ventilation pitfalls in asthma management. Topics include appropriate mechanical ventilation settings and their pathophysiological basis, as well as important complications such as dynamic hyperinflation and pneumothorax. The target audience is intensive care registrars.
2. he "passed away from an asthma attack" on Monday after
paramedics worked to revive him for 50 minutes
Thunderstorm Asthma
1. Jul 1983: Birmingham, England
2. Nov 1987: Melb, Australia
3. Nov 1989: Melb, Australia
4. Jul 1994: London, England
5. Oct 1997: Wagga Wagga, Australia
6. Jun 2004: Naples, Italy
7. Nov 2010: Melb, Australia
8. Nov 2013: Ahvaz, Iran
9. Nov 2016: Melb, Australia
10.Dec 2016: Kuwait
Nov 2016: Melb, Australia
>8500 ED presents
9 deaths – HC F 20 31 min
OM M 18 15
died in amb
MP M 35
CL M - 70
SL M 49
3. PITFALL 1
Patient severe asthma required intubation and mech vent
(FIO2 0.5, RR 18, Vt 700 ml, PaO2 105, PaCO2 55, pH 7.23, Bic 22)
→ BP↓ 80 (CVP 16) → Fluid fill → BP↓ 95 (CVP 18) → Inotropes
What is the problem?
1.Hypovolaemia
2.Pneumothorax
3.Respiratory tamponade
4.LRTI with septic shock
5.Unsuspected cardiac disease
10. EFFECTS
of VE,
VT & R
Tuxen & Lane.
Am Rev Respir Dis
1987; 136: 872-879
(cm H2O)
10 16 26
0
1
2
3
4
V T
V EE
VEI
PIP
Pplat
LUNG
VOL
(L)
FRC
0
20
40
60
80
100
VT
VE
VI
0.6 1.0
100
1.6 0.6 1.0
100
1.6 0.6 1.0
100
1.6
11. ACUTE SEVERE ASTHMA
Ve REQUIRED
for normal PaCO2/pH:
10-25 L/min
Ve SAFE
for VEI < 20ml/kg:
115 ml/kg/min
(8 L/min)
HYPOTENSION in most
PNEUMOTHORAX in some
>1/3 of MV MORTALITY
HYPOTENSION in most
PNEUMOTHORAX in some
>1/3 of MV MORTALITY
PaCO2 50-90 , pH 7.0-7.3
BUT NO HYPOTENSION
PNEUMOTHORAX
MORTALITY
PaCO2 50-90 , pH 7.0-7.3
BUT NO HYPOTENSION
PNEUMOTHORAX
MORTALITY
12. ASTHMA - VENTILATOR Mx
1. SEDATE & minimal PARALYSE (NMBA)
2. HYPOVENTILATE: VE 115 ml/min/kg, VT <8 ml/kg, R 10-12
VI 80-100 L/min or Te ≥ 4 sec
3. ASSESS DHI (VEI, Pplat, PEEPi ), BP in apnea, blood gases
4. ADJUST VENTILATION BASED ON DHI (not PaCO2 / pH)
(DHI↑ → reduce rate, DHI↓ → increase R)
Tuxen. ARRD1992;146 (5): 1136
13.
14.
15.
16.
17.
18.
19. Same patient, severe asthma, heavy sedation, and ventilated
FIO2 0.4, RR 12, VT 600 ml, VI 80 L/min PaO2 90, PaCO2 60, pH 7.23, Bic 24
BP 110, HR 95, CVP 8, Pplat 25, PEEPi 10
Nursing complain - repeated high pressure alarm (P limit 50 cmH20)
RMO - good air entry both sides, transient P limit ↑ → PIP 58 cmH20
RMO reduces VI to 40 L/min → PIP↓ 40 cmH20 → alarm stops. Calls you.
What should you do 1. Well done! (back to sleep)
2. CXR
3. VI back to 80 & ↑ PIP limit
4. Restore VI to 80 & ↓ RR
5. Other
PITFALL 2
20. EFFECTSEFFECTS
of Vof VEE &V&VII
Tuxen & Lane
ARRD1987; 136: 872
0
20
40
60
80
PIP
(cm H2O)
Pplat
LUNG
VOL
(L)
0
1
2
3
4
VT
VEE
VEI
FRC
V I
V E
100 70
10
40 100 70
16
40 100 70
26
40
21. PITFALL 3
28 yo ♀ admit severe asthma - 2/7 slow improve on neb salbut & IV H’cort
Then deteriorates with increasing dyspnoea & wheeze
RR↑ 28 → 40, PEF↓ 120 → 80, PaO2 75, PaCO2 40, pH 7.42, Bic 25
Rx - contin neb salbut, aminophylline bolus+ 40 mg/hr,
IV salbutamol 12 mcg/min, & Tx to ICU.
4 hrs - increasing dyspnoea & distress,
RR↑ 50, PEF 200, Chest - minimal wheeze
Gases: FIO2 0.4, PaO2 85, PaCO2 30, pH 7.36, Bic 16
What is going on?
22. LACTIC ACIDOSIS
Asthma + IV Salbutamol → LACTIC ACID IN 70 %
Se Lact 5.5 ± 2.5 (2-12)
2 Patterns Ambulance Salb. Bolus (500-750mcg /15-30min)
Hospital Salb. Infus (5-20 mcg/min)
Management Bolus <500 mcg, infus <10 mcg/min
Measure lactate if Bic <22 or decrease >2
Reduce or cease IV Salb. if lact too high
23. PITFALL 4
A 56 yo female with severe acute on chronic asthma required prolonged
MV including high dose asthma Rx and 4 days paralysis.
After 10 days MV, airflow improved considerably
BUT patient incapable of weaning - tachypnea & hypercapnia.
O/E: Severe limb weakness, hyporeflexia, sensation intact
What has happened??
27. Adrenaline
Ventolin (ETT)
Pancuronium
Adrenaline x 2
Bicarb (25 meq)
Ca Gluconate
PITFALL 5
36 yo F - rapid asthma deterioration - emergency intubation & ventilation
Vt 600 ml, R 12-14 /min
5 min - P 113, BP unrecordable, ECM commenced
15 min - pH 7.08, PCO2 96, PO2 36, Sat 46%, Bic 27
ECG 60 SR, pulseless, cyanosed, FD pupils,
neck veins distended
Pericardial tap unrewarding, CXR - no pneumo
25 min - ECM ceased
30 min - HR 120, BP 110, neck viens down
33 min - Re-ventilated : Vt 600 ml, R6-8 /min
pH 7.04, PCO2 91, PO2 396, Sat 100%, Bic 27
Pupils reacting, BP maintained. Rosengarten, Tuxen. Anaes & Int Care 1990;19:118
28. SEVERE HYPOTENSION /
EMD
Almost always due to excessive dynamic hyperinflation
(May have secondary tension pneumothoraces)
Best management
1. Apnea test
2. Profound hypoventilation (RR 4-6)
3. Colloid fluid loading
29. MOST DIFFICULT MECH VENT
Eg Hypotension,high PIP despite RR<6, PaCO2 >100, pH <7.00
1. Adenaline, Mg, Ketamine
2. Bicarb, fluid load & more hypoventilation
3. Heliox (50:50)
4. Inhalational anaesthetic (halothane or isofluorane)
5. ECMO (should not be needed)
30. PITFALL 6
33 yo, 67 kg female with severe asthma – sedated, paralysed & MV
RR 12, VT 600 ml, VI 80 L/min
FIO2 0.4, PaO2 90, PaCO2 60, pH 7.23, Bic 24
MV stable then: PIP/Pplat↑ 35/20 → 48/33, BP↓105 → 90 , HR↑ 100 → 140
O/E Reduced air entry on left, trachea ? shifted to right
What is the most appropriate 1st action (1 only)
1. Reduce RR 2. Urgent CXR
3. Inotropes 4. Blind ICC(s)
5. Colloid fluid loading 6. IC Jelco
32. PNEUMOTHORAX
CAUSES - DHI, CVC, Jelco’s (spontaneous is rare)
EFFECTS - PROPENSITY FOR TENSION due to AO
→ Ipsilateral VE↓ → Contralateral VE↑
→ Contralateral DHI↑ → RISK B/L PNEUM ↑
MANAGEMENT – Suspected → Reduce RR + urgent CXR
Severe BP↓ → BLIND ICC
ALL ICC’s - BLUNT INSERTION
33. PNEUMOTHORA
X
Most commonly due to excessive dynamic hyperinflation or CVC
Best management when clinically suspected
1. Reduce RR (protect 2nd
lung)
2. No intercostal needles (unless in extremis)
3. Urgent CXR
4. Intercostal catheter with blunt dissection
Severe hypotension – urgent ICC (with blunt dissection)