Oxygen: Are We Peddling Poison?

During an acute exacerbation of congestive heart failure (CHF), the patient is often in a hypoxic state. The patient’s physiological response is to peripherally vasoconstrict and centralize blood flow, which increases the peripheral vascular resistance. At the same time, the pulmonary vascular bed vasoconstricts in an attempt to send blood to non-hypoxic areas of the lung, which increases the central vascular resistance [1]. In this acute state, the peripheral and central vascular resistance results in acute exacerbation of the CHF and represents a life threatening situation. A cycle of hypoxia and worsening heart failure is initiated that could result, if no intervention is taken, in a fatal outcome.

The Traditional Treatment
Oxygen is one of the most commonly used medications in the majority of cardiopulmonary disease patients admitted to the hospital, including those with CHF. [2] With the advent of pulse oximeters, the ability to measure oxygen saturation (SpO2) provides clinicians with the ability to detect hypoxemic states in a timely fashion and ensure that oxygen is delivered to achieve a non-hypoxic state. [3] Generally, with an acute exacerbation of congestive heart failure, the general clinical approach is to administer a maximal amount of oxygen to achieve saturation above 90%. This shortens the amount of time the patient is in a hypoxic state and reduces the negative effects of the physiologic compensation.

Initiation of high fractional inspired oxygen via an oxygen non-rebreathing mask provides an easy and rapid treatment modality in acute exacerbation of CHF. The goal is to treat the hypoxic state and return the patient to a normoxemic state. In a patient in acute distress, the goal is to ensure the SpO2 is above 90% in the shortest period of time, and applying near 100% O2 meets this criterion. As the patient’s level of distress is reduced, the oxygen is weaned to the physiological normal (>95%). [4] The patient is monitored during the treatment and recovery phase with the goal of adjusting oxygen as required, to ensure a normoxemic state (SpO2 95-98%).

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In CHF patients, oxygen has been used as part of the normal treatment regime to treat hypoxemia and to provide pulmonary vasodilatation effects. The accepted norm is that reducing pulmonary vasoconstriction reduces the workload imposed on the heart and speeds recovery during an exacerbation of CHF.

The Dangers of Administering Oxygen
But the truth is that, in acute exacerbation of moderate to severe CHF, oxygen concentrations above normal can have adverse effects. In effect, we are potentially peddling poison. Saadjian, Paganelli and Levy identified that increases in PaO2 result in a reduction of cardiac output due to decreases in heart rate. However, when the left ventricular function is very poor, the central chemo-mediated regulation is impaired, and the direct peripheral effect of oxygen on systemic circulation plays a leading part in cardiac impairment [5]. In fact, Mak et al. identified that “hyperoxia was associated with impairment of cardiac relaxation and increased left ventricular filling pressures in patients with and without CHF. Caution should be used in the administration of high FiO2, in the setting of CHF” [5]. Hague et al. demonstrated that in CHF “patients that inspire oxygen concentrations >21% elicited adverse hemodynamic changes in dose-dependent manner. It is associated with increased afterload in the left ventricle and significant impairment of diastolic events” [5].

In patients with acute exacerbation of CHF, the administration of high fractional inspired oxygen should be used with caution. [2, 3] The goal is to treat hypoxemia without incurring the negative effects demonstrated by high FiO2s. [1] In 2006, Thomson et al. identified that “hyperoxia-induced increases in vascular resistance and reductions in cardiac output may be detrimental in the context of critical illness” and “confirmed that hyperoxia, even after an episode of hypoxia, has significant effects on human circulation” [2].

Oxygen, like all drugs, has dose dependent effects. In fact, as clinicians we have become very complacent regarding the negative effects of hyperoxia. Concerns for interference with hypoxic drive in COPD seem to have overshadowed the effects of hyperoxia in CHF. With the common clinical practice of using pulse oximeters to monitor SpO2 as the fifth vital sign, there is no real reason for hyperoxia to exist. We have the potential to actually worsen the CHF in patients when we do not restrict oxygen saturations to a 90-92% range.

Dave Swift, RRT, is campus coordinator, professional practice respiratory therapy, at Ottawa Hospital – Civic Campus, Ottawa, Ontario, Canada. He is also respiratory therapy lead/subject matter expert, for the National Office of the Healthcare Emergency Response Team, Public Health Canada. If you’d like to submit a question about disaster response, email [email protected] or [email protected].


1. Hypoxic pulmonary vasoconstriction. R. Moudgil, E.D. Michelakis, S.l. Archer. Journal of Applied Physiology. Jan 1, 2005. 98(1); 390-403.

2. Hemodynamic effects of supplemental oxygen administration in CHF. W.A. Hague, J.Boehmer, B.S.Clemson,V.A.Levenberger, D.H.Silber, L.I.Sinoway. J. Of American college of Cardiology. Feb 1996;27(2);353-357.

3. Cardiovascular Effects of acute oxygen administration in healthy adults. W.S.Waring, A.J.Thomson, S.H.Adwani, A.J.russel, J.f.Potter, D.J.Webb, S.R.J.Maxwell. J. Cardiovasc. Pharmacology. 2003;42;245-250

4. Effects of short-term isocapnic hyperoxia and hypoxia on cardiovascular function. A.J.Thomson, G.B.Drummond,W.S.Waring, D.J.Webb, S.R.J.Maxwell. Journal of Applied Physiology. Sept 2006; 101(3);809-816

5. Effect of hyperoxia on left ventricular fuction and filling pressures in patients with and without congestive heart failure. S. Mak, E.R.Azevedo, P.P. Liu. Chest 2001;120(2);467-473

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