Introduction:
Permissive hypoxemia is a lung-protective approach to offer a patient with severe acute respiratory distress syndrome (ARDS) adequate oxygen delivery (DO2) while minimizing the negative effects of the frequently toxic ventilatory support necessary to preserve normal arterial oxygenation. However, in many patients with severe ARDS, striking an acceptable compromise between sustaining adequate tissue oxygenation and preventing ventilator-induced lung damage (VILI) can be difficult.
What Exactly Is Acute Respiratory Distress Syndrome (ARDS)?
Fluid accumulation in the lungs' tiny air sacs, known as alveoli, causes an inflammation-related lung injury known as acute respiratory distress syndrome, or ARDS. ARDS refrains the lungs from inflating with air, resulting in critically low blood oxygen levels (hypoxemia). Other organs, including the brain, heart, kidneys, and stomach, are deprived of oxygen. ARDS is harmful and can cause a variety of significant and fatal complications.
What Is Hypoxemia?
Hypoxemia is described as a lack of oxygen in the blood circulation at a level lower than normal. Oxygen partial pressure (PaO2) or oxygen hemoglobin saturation (SaO2) generated from arterial blood gas samples are routinely used to describe oxygen levels. The latter, known as peripheral oxygen saturation (SpO2), can also be evaluated via pulse oximetry. The PaO2 or SaO2 at which clinicians consider hypoxemia severe and a patient's subsequent response varies greatly.
Hypoxaemia is prevalent in critically unwell patients and is usually treated using ventilatory and non-ventilatory techniques. The goal is to return arterial oxygenation to normal levels, reducing hypoxia-related morbidity and death. However, measures used to treat hypoxaemic critically ill individuals have been linked to harm, which may exceed the benefit of increased arterial oxygenation. For example, ventilator-induced lung damage and oxygen toxicity caused by excessive inspired oxygen concentrations (FiO2) are known to cause harm, which may offset the advantageous effects of normalizing oxygen saturation (PaO2 and SaO2).
What Is Permissive Hypoxemia?
Permissive hypoxemia is a concept in which a lower degree of arterial oxygenation (PaO2) is tolerated to avoid the negative consequences of high fractional inspired oxygen and invasive mechanical ventilation. However, no exact threshold for permissive hypoxemia is known now, and its use in adults is formally unproven.
How Permissive Hypoxemia Might Work?
Accepting lower levels of arterial oxygenation may eliminate the need to use treatments that, while effective in raising PaO2, have little or no effect on mortality and morbidity. Furthermore, in light of recent studies, reducing arterial oxygenation may provide an additional benefit. It has been established that avoiding hypoxemia improves outcomes in patients with myocardial infarction, stroke, or cardiac arrest.
Permissive hypoxemia is a lung-protective technique that aims to reduce VILI. If no steps are taken to increase oxygen delivery(DO2) and decrease oxygen uptake (VO2), this method will inevitably result in tissue hypoxia. A potential management strategy for patients with ARDS whose permissive hypoxia has been problematic by tissue hypoxia requires the objective influence of cardiac output and hemoglobin concentration (if necessary) to account for hypoxemia and maintain a standard (but not supranormal) level of tissue DO2.
In the clinical setting of ARDS, particularly when managed by permissive hypoxemia, increasing cardiac output can enhance tissue oxygenation, limit tissue hypoxia, and permit lower ventilator settings to lessen the risk of VILI. A combination strategy of permissive hypoxia and supranormal cardiac output may thus accomplish the final objective of preserving tissue oxygenation and eliminating tissue hypoxia while avoiding the clinical cost of increasing PaO2.
Is Permissive Hypoxia Tolerated Equally by Diverse Organ Systems?
Different organ systems may be more or less tolerant of hypoxemia. For example, as long as cerebral perfusion is maintained, a healthy brain can tolerate hypoxemia better than other organ systems. It should be highlighted, however, that hypoxemia can cause long-term cognitive deficits and structural brain damage, as shown at extremely high altitudes and in some ARDS survivors. Furthermore, because the wounded brain is very vulnerable to hypoxemia, a permissive hypoxemia strategy may not be appropriate for individuals with traumatic or ischemic brain injury.
Furthermore, permissive hypoxia can raise the pressure in the pulmonary arteries and promote right-ventricular dysfunction, which can have a negative impact on the clinical outcome of ARDS. While potentially minimizing mechanical ventilation's adverse hemodynamic, mechanical, and biochemical effects, permissive hypoxemia may increase renal vascular resistance, resulting in renal hypoperfusion and decreased glomerular filtration rate.
On the other hand, the ultimate goal of permissive hypoxemia is to diminish VILI and its accompanying biotrauma. This pulmonary inflammatory reaction can harm the kidneys and other tissues and organs through the systemic production of inflammatory cytokines. As a result, the consequences of permissive hypoxia on renal functions are unknown and may vary. Clinical trials are required to assess the security and efficacy of permissive hypoxemia as a viable therapy for VILI prevention.
How Does Supranormal Cardiac Output Work as a Physiologic Response to Low Oxygen Content?
The three major components of DO2, cardiac output, SaO2, and hemoglobin concentration, are physiologically interconnected, and an increase in one another can compensate for a reduction in one. As a result, if cardiac output is sufficiently raised during hypoxemia or anemia, hypoxia of the tissues may not occur. This hypothesis's physiologic rationale depends on the observation that cardiac output increases in the aftermath of acute hypoxemia and acute isovolemic anemia. In this event, supranormal cardiac output could act as a physiologically responsive mechanism to avoid tissue hypoxia by keeping the oxygen supply in equilibrium with the oxygen demand.
Supranormal cardiac output is an essential counterproductive mechanism for delivering adequate oxygen to tissues during hypoxemia or anemia. If oxygenation to the tissues is preserved appropriately, critically ill patients may be able to tolerate mild to moderate hypoxemia or anemia. This should cause researchers to focus on the sufficiency of DO2 instead of the numerical values of its constituents, such as SaO2 and hemoglobin concentration. Recognizing the significance of supranormal cardiac output as a physiologic response to low CaO2 levels may benefit hypoxic individuals, especially those with severe ARDS.
Conclusion:
To summarize, clinical evidence supporting permissive hypoxemia is currently lacking, and it will be critical to carefully weigh the risks and advantages of permissive hypoxemia before moving forward with efficacy and effectiveness trials. Researchers believe that future investigations of permissive hypoxia should concentrate on severe ARDS patients with high FiO2 rather than severely sick individuals on regular mechanical breathing.
