Fixed performance system = pt factors have no effect



Download 22.83 Kb.
Date30.06.2018
Size22.83 Kb.

NIV

B

VPS = variable performance system = FiO2 altered by IFR, MV, physical characterisitics of system; small reservoir with entrainment

FPS = fixed performance system = pt factors have no effect

100% O2 system = non-rebreathing circuits eg. Laerdal, Mapleson

Normal PIFR: 30-40L/min Normal MV: 4-8L (150ml/kg in children)
NPs: VPS; 1-4L; 24-40% (add on 4% per L); nasopharynx = reservoir 1=24 / 2=28 / 3=32 / 4=36

Variable conc depending on ventilatory pattern (eg. Insp flow rate, MV); no dead space  no rebreathing;

comfortable therefore patient compliance

Hudson mask: VPS; 6-15L; 35-60% (+5% per L); mask = reservoir 6=45 / 7=50 / 8=55 / 9=60 / 10=60-65

Rebreathing occurs <4L/min so min 6L/min; less comfy (heat build up, claustrophobia); incr dead space compare

to NP

Non-rebreather mask: 10-15L; 60-90%; bag = reservoir = 750-1000ml

Maintains higher FiO2 when PIFR > fresh gas flow by entraining from reservoir



Partial non-rebreather mask: 6-10L; 40-75%

Same as above but without valves


Venturi mask: FPS; >12L; 24-50% 4=24 / 12=24-50 / 15=60

More accurate FiO2, if total gas flow >60L/min / >30% higher than patient’s PIFR; less accurate FiO2 at higher

FiO2 or severe SOB; useful for COPD with type 2 resp failure

Clausen’s harness: FPS; near 100%

Little advantage over non-rebreather and less comfortable; good in those awaiting HBO / CO poisoning



ETT: FPS; 50-98% (50% without non-rebreather, 98% with)

T piece system: doubles O2 flow possible to decr entrainment
Complications: CO2 retention (when pO2 >80; carefully monitor FiO2 and RR after starting O2, use Venturi, aim SaO2 88-92%); diffusion atelectasis (in poorly ventilated lung, trapped gas reabsorbed; this usually limited by N2, but N2 washed out by high O2); ARDS (incr O2  decr macrophage activity, decr surfactant, incr pul cap perm); retrolental fibroplasia (esp in prems if pO2 >140); O2 toxicity (CNS, lung probs, bronchopul dysplasia); decr CO if severe CCF (due to incr vasc resistance)

NIV

Definition: PPV of spontaneously breathing patient without use of ETT

Pros: decr need for intubation in 25% overall; decr intubation-related complications; incr survival to discharge; decr ICU LOS; can treat patients not suitable for intubation; CPAP and BiPAP benefit in trt of resp failure caused by APO, COPD, immunosupp

Cons: less evidence in pneumonia, ARDS, asthma (uncertain, needs more trials), children; no significant benefit in ED without resp failure; BiPAP uncertain in APO (assoc with incr rate MI); not tolerated by 20-30% patients
Indications: type I resp failure with RR >30, type II resp failure with RR >24, abdominal breathing, TV <5ml/kg, VC <15ml/kg, PEFR <1.5ml/kg, paO2 <60 on 50% O2, pCO2 >60

+ awake, cooperative, breathing spontaneously, no XS secretions


CI’s: not above, maxfax #, BSF, upper airway obstruction, untreated pneumoT, marked CV instability

Complications: if no pul oedema, has little/no effect on SV and CI; facial skin necrosis, conjunctivitis, gastric dilation + abdo compartment syndrome; air trapping ( decr BP); aspiration; pneumoT; resp alkalosis; sinus pain; oronasal dryness; incr IOp and ICP

Failure = pt intolerance; pH <7.25; RR >35; decr LOC; poor clinical response

CPAP
FPS

Definition: spontaneous tidal breathing with fixed amount of airway p applied to airway throughout the ventilatory cycle; for improvement of hypoxaemia

Indications: COPD and bronchiectasis (pH <7.35 despite max medical trt), status asthmaticus (not recommended routinely), ARDS, APO, pneumonia (although ETT preferred), bronchiolitis, chest trauma (hypoxic despite regional wall analgesia), weaning from ventilator, acute resp failure, resp tract burns, acute on chronic resp failure with chest wall deformity/NM disease; OSA

Pros: may avoid intubation in 90% patients with APO; improves resp Fx by decr WOB / inflating collapsed alveoli / improving pul compliance / incr FRC; improves CV Fx by decr preload and afterload  incr CO; decr intrapul shunting, improved VQ

BiPAP
FPS

Provides IPAP and EPAP; preferred to CPAP in hypoventilatory resp failure

Indications: most benefit proven in severe COPD; for improvement of hypercarbia

Pathophysiology: IPAP  decr WOB, decr end-insp vol; EPAP  prevents alveolar collapse during expiration, extends time available for GE, incr arterial oxygenation and CO2 elimination, decr WOB as no need to re-open collapsed alveoli; decr afterload

Dose: titrate FiO2 to sats; in APO 10-15 : 8-12; in COPD 10:4; titrate IPAP to TV, pH, RR, PaCO2 (titrate up to 15-20 or max amount patient tolerates); titrate EPAP to FiO2, pO2, WOB to trigger

Pros: more rapid improvement in O2 and ventilation than CPAP; provides PEEP with added insp assistance

Notes from: Dunn




Mode

L/min

FiO2 %

Nasal prongs (VPS)

1

24

2

28

3

32

4

36-40

Hudson mask (VPS)

6

45

7

50

8

55

9

60

10-15

60-65

Non-rebreather (VPS)

8-12

60-80

Partial non-rebreather

6-10

40-70

Venturi (FPS)

4

24

12

24-50

15

60

ETT




50% without reservoir

98% with reservoir



Normal PiO2 = 20kPa (150mmHg)

Normal MV = 4-8L

Normal PIFR = 30-40L/min

Expected A-a gradient = (age/4) + 4

PAO2 (alveolar) = FiO2 X (p - 47) – (PaCO2 / 0.8)

O2-Hb Dissociation Curve


ppO2 (mmHg)

Hb SpO2 (%)

27

50

60

90

100

98

1g Hb contains 1.39ml O2 at 100%



Dissolved O2 = pO2 (mmHg) x 0.003ml/dL

Sats at end of pul capillary = 97%


Share with your friends:


The database is protected by copyright ©dentisty.org 2019
send message

    Main page