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. 2012 Dec;40(12):3135-9.
doi: 10.1097/CCM.0b013e3182656976.

Hyperoxia is associated with increased mortality in patients treated with mild therapeutic hypothermia after sudden cardiac arrest

David R Janz  1 , Ryan D Hollenbeck, Jeremy S Pollock, John A McPherson, Todd W Rice
Affiliations

Hyperoxia is associated with increased mortality in patients treated with mild therapeutic hypothermia after sudden cardiac arrest

David R Janz et al. Crit Care Med. 2012 Dec.

Abstract

Objective: To determine whether higher levels of PaO2 are associated with in-hospital mortality and poor neurological status at hospital discharge in patients treated with mild therapeutic hypothermia after sudden cardiac arrest.

Design: Retrospective analysis of a prospective cohort.

Patients: A total of 170 consecutive patients treated with therapeutic hypothermia in the cardiovascular care unit of an academic tertiary care hospital.

Interventions: None.

Measurements and main results: Of 170 patients, 77 (45.2%) survived to hospital discharge. Survivors had a significantly lower maximum PaO2 (198 mm Hg; interquartile range, 152.5-282) measured in the first 24 hrs following cardiac arrest compared to nonsurvivors (254 mm Hg; interquartile range, 172-363; p = .022). A multivariable analysis including age, time to return of spontaneous circulation, the presence of shock, bystander cardiopulmonary resuscitation, and initial rhythm revealed that higher levels of PaO2 were significantly associated with increased in-hospital mortality (odds ratio 1.439; 95% confidence interval 1.028-2.015; p = .034) and poor neurological status at hospital discharge (odds ratio 1.485; 95% confidence interval 1.032-2.136; p = .033).

Conclusions: Higher levels of the maximum measured PaO2 are associated with increased in-hospital mortality and poor neurological status on hospital discharge in patients treated with mild therapeutic hypothermia after sudden cardiac arrest.

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Conflict of interest statement

The authors have not disclosed any potential conflicts of interest

Conflict of Interest Statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
Figures 1a and 1b. Distribution and Cumulative Frequency Distribution Curves of Maximum PaO2 in the first 24 hours Following Sudden Cardiac Arrest.
Figure 1
Figure 1
Figures 1a and 1b. Distribution and Cumulative Frequency Distribution Curves of Maximum PaO2 in the first 24 hours Following Sudden Cardiac Arrest.
Figure 2
Figure 2. Maximum PaO2 and In-Hospital Mortality
Survivors had a significantly lower maximum PaO2 (198 mmHg) in the first 24 hours than non-survivors (254 mmHg)(p = 0·022)*. Values are medians (middle long horizontal line) and interquartile ranges (IQR: upper and lower caps).
Figure 3
Figure 3. Risk of In-Hospital Mortality associated with Maximum PaO2
Odds ratio adjusted for age, time to ROSC, shock, bystander CPR, and initial rhythm. The odds ratio for maximum PaO2 is for an increment of every 100mmHgabove 54 mmHg. Shock = requirement of vasoactive medications to maintain a mean arterial blood pressure greater than or equal to 65 mmHg.
Figure 4
Figure 4. Maximum PaO2 and Neurologic Status at Hospital Discharge
Patients with favorable neurological outcomes had significantly lower maximum PaO2 (197 mmHg) in the first 24 hours than patients with poor neurological outcomes (246·5 mmHg)(p = 0·026)* at hospital discharge. Values are medians (middle long horizontal line) and interquartile ranges (IQR: upper and lower caps).
Figure 5
Figure 5. CPC Score at Hospital Discharge by PaO2 Quartiles
There was no statistically significant association between increasing PaO2 and a change in CPC score (p = 0.08); however quartiles 1 and 2 had significantly better CPC scores at discharge than quartile 4 (p = 0·038* and 0·018**, respectively). Values are means (middle long horizontal line) and standard deviations (SD: upper and lower caps).
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