Synthesizing admission to high dependency units (Austin et

Synthesizing literature is an essential aptitude health
care professionals must execute to ensure evidence-based practice is continuing
to be implemented in their performance, with confidence. The research question the
writer chose to explore is, “Does giving high flow oxygen to patients with Chronic
Obstructive Pulmonary Disease (COPD) cause harm?” This is a very relevant issue
that is important to explore further, as the potential health outcomes from
misuse of oxygen with COPD patients can be life threatening. In this paper, the
writer will be synthesizing five different articles and will include relevant
recommendations based on the research evidence for clinical practice.

Synthesis

The overarching theme amongst four of the research articles
were that high flow oxygen administration amongst COPD patients does indeed cause
negative health outcomes (Austin, Wills, Walters, & Wood-Baker, 2010; Kent,
Mitchell, & McNicholas, 2011; Wijesinghe et al., 2011; Cameron, Pilcher,
Weatherall, Beasley, & Perrin, 2012). Makic, Martin, Burns, Philbrick, and
Rauen (2013) does not necessarily discuss high flow oxygen therapy in
particular, but does include similar side effects when examining supplemental
oxygen therapy in COPD patients (p. 33); as well, Cameron et al. agreed that
oxygen therapy in COPD patients can lead to hypercapnia (higher than normal
carbon dioxide levels) (p. 33). Further negative effects of high flow oxygen
administration include: acidosis, lengthened hospital stay, admission to high
dependency units (Austin et al., 2010, p. 2), increased mortality or risk of
death (Austin et al.; Wijesinghe et al.), respiratory acidosis (Austin et al.;
Cameron et al.), respiratory failure (Wijesinghe et al.; Cameron et al.; Makic
et al.), depressed ventilation, ventilation-perfusion mismatch (Austin et al.;
Kent et al.), need for assisted ventilation (Austin et al.; Wijesinghe et al.; Cameron
et al.), and poor adverse health outcomes (Wijesinghe et al.; Cameron et al.;
Makic et al.). For the most part, at least two articles mentioned a similar
effect of high flow oxygen therapy; this demonstrates durable and convincing
validity. Of note, there was no mention of positive effects or benefits to high
flow oxygen administration in any of the five articles; this debunks the belief
that oxygen is an effective therapy for acute exacerbation of COPD (AECOPD)
(Makic et al., 2013, p. 32).

The secondary theme to support the main issue includes
modified or controlled oxygen therapies that were consistently discussed
throughout the literature. (Austin et al., 2010; Kent et al., 2011) discussed
treatment using venturi masks for oxygen administration, the remaining articles
did not specifically discuss the particular method of administration for oxygen
therapy. Controlled/titrated oxygen therapies were recommended for COPD
patients to maintain oxygen saturation levels between 88%-92% (Austin, Wills,
Walters, & Wood-Baker, 2010; Wijesinghe et al., 2011; Cameron, Pilcher,
Weatherall, Beasley, & Perrin, 2012; Makic, Martin, Burns, Philbrick, &
Rauen, 2013). This relieves hypoxemia while also preventing hyperoxemia (Cameron
et al., p. 687).; Kent et al. recommends maintaining the oxygen saturation
levels between 90%-92% to prevent the risk of hypercapnia. Oxygen should be
administered if oxygen saturations are below 88% to relieve hypoxemia and its associated
risks (Wijesinghe et al.; Makic et al.). The positive effects of
controlled/titrated oxygen therapy include reduced: acidosis (Austin et al., p.

2)., need for assisted ventilation (Austin et al.; Wijensinghe et al.; Cameron
et al.)., mortality rate (Austin et al.; Cameron et al.)., risk for developing hypercapnia
(Kent, Mitchell, & McNicholas, 2011, p. 205)., risk of respiratory failure
(Wijesinghe et al.)., and risk for adverse/poor health outcomes (Wijesinghe et
al.; Cameron et al.; Makic et al.).

Through synthesizing the literature that focused on
oxygen administration related to COPD, the writer feels confident in the
ability to make and perform recommendations within clinical practice. Primarily,
prior to any oxygen therapy, ensure that the patients oxygen saturation has
been measured and that the measured number is appropriate for oxygen
administration, such as below 88%. If oxygen therapy is deemed appropriate,
ensure that high flow oxygen administration is only utilized when the patients’
condition, such as low saturation levels, is found. Lastly, it would be
important to monitor the patients’ oxygen saturation levels closely in order to
maintain the targeted range between 88%-92%. This is a knowledge the writer
believes can be advocated for through clinical practice. Weatherall, Perrin,
and Beasley were involved in publishing articles in both 2011 and 2012; the
writers were able to expand from the previous research knowledge to further
explore this issue. Their multiple published efforts signify the complexity of
the issue, but the writer believes the message was portrayed effectively,
providing clear recommendations for clinical practice.  The articles used for this paper were strong
research studies and the systematic review used a substantial amount of
references, further increasing the evidence and validity of the material.

Overall, the writer is knowledgeable in the research topic and is confident in
the recommendations to perform in the clinical setting.

Conclusion

In this paper, the writer was able to synthesize five
different research articles and was able to include relevant recommendations
for clinical practice based on the strong research evidence provided. The
research question, “Does giving high flow oxygen to patients with COPD cause
harm?” was answered effectively with repeated statements and themes made
throughout the articles. High flow oxygen therapy does indeed cause harm and a
variety of adverse health outcomes in COPD patients. The evidence supported
through the articles remained to be valid with numerous references and methods
to investing the issue making the answer to the research problem confident.

References

Austin, M., Wills, K.,
Blizzard, L., Walters, E., & Wood-Baker, R. (2010). Effect of high flow
oxygen on mortality in chronic obstructive pulmonary disease patients in
prehospital setting: randomized controlled trial. BMJ: British Medical Journal (Oversease & Retired Doctors Edition),
341(7779), 1-8. http://dx.doi.org/10.1136/bmj.c5462

Cameron, L., Pilcher, J.,
Weatherall, M., Beasley, R., & Perrin, K. (2012). The risk of serious adverse
outcomes associated with hypoxeaemia and hyperoxaemia in acute exacerbations of
COPD. Postgraduate Medical Journal, 88(1046),
684-689. http://dx.doi.org/10.1136 /postgradmedj-2012-130809

Kent, B. D., Mitchell, P. D.,
& McNicholas, W. T. (2011). Hypoxemia in patients with COPD: cause,
effects, and disease progression. International
Journal of Chronic Obstructive Pulmonary Disease, 6, 199-208.

http://dx.doi.org/10.2147/COPD.S10611

Makic, M. B., Martin, S. A.,
Burns, S., Philbrick, D., & Rauen, C. (2013). Putting evidence into nursing
practice: Four traditional practices not supported by the evidence. Critical Care Nurse, 33(2), 28-42. http://dx.doi.org/10.4037/ccn2013787

Wijesinghe, M., Perrin, K.,
Healy, B., Hart, K., Clay, J., Weatherall, M., & Beasley, R. (2011).

Pre-hospital oxygen therapy in acute exacerbations of chronic obstructive
pulmonary disease. Internal Medecine Jounral, 41(8), 618-622. http://dx.doi.org/10.1111/j.1445

-5994.2010.02207.x

 

 

 

 

Appendix

Research
Question: Does giving high flow oxygen to
patients with COPD cause harm?

 

 

Source #1
Austin, Wills, Walters & Wood-Baker, 2010

Source #2
Kent, Mitchell & McNicholas, 2011

Source #3
Wijesinghe, Perrin, Healy, Hart, Clay, Weatherall & Beasley,
2011

Source #4
Cameron, Pilcher, Weatherall, Beasley & Perrin, 2012

Source #5
Makic, Martin, Burns, Philbrick & Rauen, 2013

Main Idea
A:
The effects of high flow oxygen on COPD
patients.

 

-Decreased minute ventilation and an
increase CO2; this is observed through depressed ventilation or further
declining ventilation-perfusion mismatch from
inadequately ventilated alveoli and pulmonary capillaries, from hypoxic
pulmonary vasoconstriction causing the release of sequestered CO2 (p. 2)
-During AECOPD it’s associated with
increased: mortality, lengthened hospital stay, need for ventilation, and
admission to high dependency units (para 2). It can also cause acidosis (but
some of these patients were able to correct pH once inspired O2 was reduced)
-Mortality rate of 9% (p. 4).

-More likely to have respiratory
acidosis, with significantly higher arterial CO2 pressure (p. 5).
 

-Greater than normal doses of O2 therapy administration
increases risk for: reduced ventilator drive, increased ventilation-perfusion
mismatch, and resulting hypercapnia (p. 205).
 

-Risk for hypercapnia and respiratory
failure from AECOPD patients from high O2 administration.
-Increased oxygen flow and increasing
PaO2 were both related to increased death risk, assisted ventilation, or
respiratory failure (p. 620).

-Risk of poor health outcomes progresses
as the flow rate of oxygen continues to increase (para 8).

– Patients at risk for poor health
outcomes that received high flow oxygen therapy, 75% resulted in oxygen
saturation beyond the targeted range (p. 621).
-Association was found to be
statistically significant between increased flow rates and poor health
outcomes (para 2).

-Hyperoxemia post-ED occurred in ¼ of
AECOPD patients that were delivered via the ambulance; they were associated
with an increased risk for adverse health outcomes (p. 687).

-Hypercapnic respiratory failure as well
as assisted ventilation are associated with hyperoxemia (para 5).
-High association between both
hyperoxemia and poor health outcomes, but the study was unable to demonstrate
causality of this from reduced documentation (para 6).

-Longer ambulance transport to hospital,
the more exposure to hyperoxemia and adverse health outcomes (para 6).
 
 

-NOT PARTICULARLY HIGH FLOW (O2 IN
GENERAL): Delivering oxygen for COPD patients can lead to hypercapnia, apnea,
and other adverse health outcomes (p. 33).

-Providing more O2 further increases
plasma CO2 levels; as patients cannot blow off CO2 the CO2 levels rise
causing respiratory acidosis (p. 33).
-Increased O2 causes dead-space ventilation
which increases CO2 levels further (para 5).

 

Main Idea
B:
Modifications made in oxygen
administration for COPD patients.

 
 

-Campbell established clinical practice
involving titrating O2 treatment via venturi masks. This resulted in reports
indicating COPD mortality rates are associated with increased chronic stable
levels of arterial CO2 pressure (not absolute level of hypercapnia) (p. 2).

-“Oxygen should be administered only at
concentrations sufficient to maintain adequate O2 saturations.” (p. 7).

 

-Controlled O2 therapy (p. 205).

-Numerous Guidelines the writers provide,
state oxygen should only be administered to AECOPD patients if their oxygen
saturations are less than 88%; their oxygen therapy should be altered to
maintain their oxygen saturations between 88%-92% (p. 618).

-These guidelines/ recommendations are
important for the Ambulance Services to practice through their management
during transfer to the hospital; transfers can take time and administrating
very high concentrations can cause worsening health outcomes (para 1)
-Another recommended strategy is for
patients with a previous hypercapnic respiratory failure episode to issue a
24% or 28% venturi mask with an oxygen alert card, to further reduce the risk
of respiratory failure (p. 622).

-Guidelines recommending oxygen should be
titrated in order to maintain/achieve oxygen saturations 88%-92% (p. 684).
-Therefore, the target range of 88%-92%
continues to be the best standard of control; this is supported by level 1
verification (para 1).
 
 

-Failure in administering O2 in order to
treat hypoxemia places the patient at a larger risk than high CO2 levels
would (p. 34).

-Must monitor acid-base balance to
prevent apnea (para 2).

-O2 should be administered if O2
saturations are 88% or less or with PaO2 levels of 55mmHg (para 4).

Main Idea
C:
The effects of modified or controlled
oxygen therapy for COPD patients.
 
 
 
 

-Use of titrated O2 therapy is associated
with: less acidosis, decreased need for assisted ventilation, and reduced
mortality rate (p. 2).
-Less likely to have respiratory acidosis
due to hypercapnia (p. 5).
-Achieving O2 sats between 88-92% reduces
risk of death from respiratory failure vs. high flow patients (para 3).

-Less likely to have hypercapnia (para
4).

-Mortality rate of 2% (p. 4).

-Titrated therapy pre-hospital = 78%
decrease towards risk of in-hospital respiratory failure and resulting
mortality (p. 7).
 

-Controlled O2 therapy with a targeted O2
saturation between 90%-92% unlikely results in significant hypercapnia (p.

205).

-Reduces risk of respiratory failure (p.

622).
 

-From previous review: Higher oxygen
saturations at ambulance pickup are correlated with better health outcomes;
higher PaO2 post-ED was correlated with worsening health outcomes (p. 684).
-Associated findings between hyperoxemia
and adverse health outcomes delivers support for guidelines suggesting to
titrate O2 therapy for AECOPD patients (p. 687). Increased risks were found
to be <88% and >96% vs the recommended target range of 88%-92% (p. 688).

-Relieves hypoxemia without causing
hyperoxemia (para 3).

-Lower death rate than higher oxygen
concentration administration (para 3).
–p.687

-OXYGEN ADMINISTRATION (NOT MODIFIED OR
CONTROLLED THERAPY IN PARTICULAR):
-A guideline states that for chronic and
stable COPD patients with chronic hypoxemia and hypercarbia, O2 therapy for
15 hours or more per day can improve survival for those suffering with
chronic respiratory failure (p. 34).
-Increase of CO2 from O2 therapy is not
due to eliminating hypoxic drive (it is due to Haldane effect, hypoxic
vasoconstriction, and decreased minute ventilation) (para 6).
-Prevents organ failure (para 6).

-Improves well-being and prolongs the
patients’ lives (para 6).

Main Idea
D:
Concerns/challenges to promoting modified
O2 therapy/modifying practice.

-Lack of clear evidence showing benefits
to titrated O2 therapy responsible for lack of widespread cultural change (p.

2).
-Lack of equipment that is capable of
delivering a controlled amount of O2 concurrently with the ability to
administer nebulized drugs in ambulances.
-“More is better” oxygen culture that may
ignore potential dangers of high oxygen administration; will be needing
aggressive campaigning of education.

-O2 administrations, along with nebulized
bronchodilators (which need to be administered with 6-8L/min of O2), are
standard pre-hospital management practices for AECOPD patients (p. 1).
 
 

 

 

-High concentration oxygen given for
AECOPD while transferring to hospital occurs even though there’s evidence
that it causes poor outcomes; this may be due to: belief that hypoxemia must
be avoided entirely, wanting to relieve breathlessness, difficulties in
recognizing/ differentiating COPD from other conditions, and deficiency in
identifying hypoxemia risks (p. 684).
 

-Barriers to practicing best evidence:
perceived colleague status quo “We’ve always done it this way.” (p. 29).
-Statements: “if you give oxygen, you
will wipe out their drive to breathe and their carbon dioxide will increase”,
“it is ok for the COPD patient to have a high PaCO2 and a low PaO2, they live
there” (p. 32).

-Practice involving suppression the use
of oxygen in order to prevent adverse health outcomes in COPD patients is
dangerous and unjustified in most incidences. (p. 33).

-Belief that O2 therapy eliminates
hypoxic drive, resulting in: hypercarbia, acidosis and death (p. 34).
 

 

 

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