Do Blood Thinners Affect Oxygen Levels

Do Blood Thinners Affect Oxygen Levels – Introduction

We use the term blood thinner to denominate a group of drugs that affect the coagulation cascade and platelet aggregation, both processes involved in physiological hemostasis.

We can further categorize this group of drugs by the mechanism in which each of them produces a pathophysiological effect: (1)

Antiplatelets: these are drugs that inhibit the process of platelet adhesion and or aggregation. The exact mechanism by which the effect is exerted differs among them.

  • Acetyl-salicylic acid (aspirin).
  • Clopidogrel, ticagrelor, prasugrel and ticlopidine.

Anticoagulants: this group pertains to drugs that exert an effect on different steps involved in the coagulation cascade.

  • Heparin and heparin-derived molecules.
  • Novel oral anticoagulant drugs, such as rivaroxaban, apixaban, betrixaban, edoxaban and dabigatran.
  • Direct thrombin inhibitors, argatroban, desirudin and bivalirudin are examples.
  • Vitamin K antagonists, warfarin, the prototypic drug.

Now let us assess this interesting question by looking at the literature. Is there any evidence that suggests that blood thinners diminish oxygen levels?

Do Blood Thinners Affect Oxygen Levels

Do Blood Thinners Affect Oxygen Levels

An observational FDA phase IV clinical trial on adverse drug reactions states that many users have reported decreased blood oxygen saturation while taking aspirin. (2) There were no reports found about the relationship between anticoagulants and oxygen levels.

Further, let’s analyze part of the existing literature on the relationship between oxygen levels and blood thinners and assess some facts about what was found.

First, let’s categorize “low oxygen levels”. We generally refer to this concept as the decrease in arterial blood oxygen pressure, but there are many other terms related to oxygen and its usage by our organism, such as oxygen saturation, referring to the amount of hemoglobin saturated with oxygen molecules measured as a percentage.

Next, arterial blood oxygen partial pressure refers to the amount of dissolved oxygen in the blood.

There are other terms that refer to the usage of oxygen by our cells and pertain to the realm of metabolic activities that take precedence at the cellular level, such as measuring tissue-specific metabolic oxygen consumption and other measurements that are under investigation. (3)

Having our terms defined, let’s dive into the literature.

The special case for aspirin

Since a study was published about this possible adverse effect of aspirin, we are to analyze this drug first.

Aspirin is known as the prototypic non-steroidal anti-inflammatory drug (NSAID). Aspirin exerts its effects by acetylating and, therefore, irreversibly blocking cyclooxygenase (COX) 1 and a dose-dependent reversible blockage of COX 2.

COX 1 is an enzyme that participates in the production of thromboxane (TX) A2, a molecule implicated in the aggregation of platelets. (1)

At toxic doses, it has been shown to alter normal pH levels, thus producing a shift in the hemoglobin saturation curve according to the acid-base disorder involved. (4)

For example, in the early stages of acute intoxication, there is an attempt by compensatory mechanisms to counteract the acidic environment that results from excess salicylates by augmenting the respiratory rate, thus producing respiratory alkalosis.

In this scenario, the hemoglobin saturation curve experiences a shift to the right, meaning a lower affinity to oxygen molecules to be carried to the tissues.

When acidity overcomes, the shift is produced to the left, increasing the affinity of hemoglobin for oxygen molecules in the lung tissue but impeding its release under peripheral tissue conditions. (5)

For sure, these processes occur under the conditions of acute toxicity, in which an inappropriate dose is taken accidentally or voluntarily. But the question is: does this effect occur at normal dosages?

The answer can be found in a study performed by Bridges et al., where blood samples analyzing hemoglobin saturation were performed on a group of subjects under a therapeutic aspirin dose and a control group who was not under treatment. No significant differences in oxygen saturation were found. (6)

Furthermore, aspirin produces acetylation of hundreds of molecules other than COX, including hemoglobin. But perhaps the most interesting finding is that neither this effect produces significant changes in hemoglobin saturation rates. (7)

Finally, aspirin has a decoupling effect by inhibiting mitochondrial enzymes involved in oxidative metabolism.

Again, aspirin did not show a significant effect on oxidative metabolism in vivo biological models at therapeutic doses. (8)

What about anticoagulants

To date, there was no evidence found of adverse reactions related to oxygen physiology for the anticoagulant group.

On the other hand, we should consider the evidence that favors the use of this group of drugs for ischemic conditions such as Acute Myocardial Infarction, Venous Thromboembolism and Peripheral Arterial Occlusion syndromes.

A whole body of evidence supports the use of this therapeutic approach to the treatment of such severe diseases.

What are other relationships between blood thinners and oxygen physiology

As mentioned in the previous section, it is relevant in this topic to address the value of blood thinners in the management of a wide spectrum of pathology, including but not limited to coronary artery disease, cerebral ischemic disease, peripheral artery disease and venous thromboembolism.

They not only exert a benefit by restoring perfusion to tissues in the acute setting but also have been shown to prevent atherothrombotic events.

Aspirin is a well-documented example of prevention when indicated to prevent atherothrombotic events, especially relevant in coronary artery disease and stroke prevention.

Anticoagulants serve the function of restoring tissue perfusion in determinate cases, such as pulmonary embolism or deep vein thrombosis, and play a role in the long prevention of relapse.

The effects exerted by these drugs under these pathological conditions range from restoration of blood flow to a definite organ and anti-inflammatory properties on the underlying etiological process.

For example, aspirin has been shown to improve inflammatory states associated with atherosclerosis at the endothelial and platelet levels. Acetylation of metabolic-related molecules such as Glucose 6- phosphatase may play a role in restoring metabolic processes under ischemic conditions. (7)

Furthermore, aspirin seems to improve mortality and morbidity in Chronic Obstructive Pulmonary Disease patients in several contexts. (9)


From our research, there seems not to be a negative relation between blood thinners and oxygen levels. So, let me reframe our original question: do blood thinners offer a benefit regarding oxygen physiology and tissue oxygenation under a definite context?

Certainly, yes, there are many instances in which this group of drugs imposes a benefit upon the risks involved in the pathological process.

The risk-benefit relation is an aspect we commonly assess in clinical practice and should always result from a contrast between evidence-based knowledge and the specific case that is being evaluated.

Lastly, there are many gaps in our knowledge about the possible benefit of these drugs in oxygen-related physiology and the possible effect of aspirin on hemoglobin saturation.

More research is needed to discover, if any, a causal relationship between the latter.

See Also

Heart Failure Patient Education

What is the Creatinine Level in Blood Tests

High Blood Pressure Patient Education

Current Version
August 29, 2022
Written By
Franco Cuevas, MD
  3. Hall, J. E. (2016). Guyton and hall textbook of medical physiology (13th ed.). W B Saunders.
  4. Tyler J. Runde; Thomas M. Nappe. Salicylates Toxicity. StatPearls [Internet]. July 2022.
  5. Baynes J. W. & Dominiczak M. H. (2019). Medical biochemistry (Fifth). Elsevier Health Sciences.
  6. Bridges, K & Schmidt, G & Jensen, M & Cerami, Anthony & Bunn, H. (1975). The acetylation of hemoglobin by aspirin. In vitro and in vivo. The Journal of clinical investigation. 56. 201-7. 10.1172/JCI108068.
  7. Ornelas, A., Zacharias-Millward, N., Menter, D.G. et al. Beyond COX-1: the effects of aspirin on platelet biology and potential mechanisms of chemoprevention. Cancer Metastasis Rev 36, 289–303 (2017).
  8. Ioan Petrescu, Corneliu Tarba. Uncoupling effects of diclofenac and aspirin in the perfused liver and isolated hepatic mitochondria of rat. Biochimica et Biophysica Acta (BBA) – Bioenergetics, Volume 1318, Issue 3, 1997, Pages 385-394.
  9. Fawzy A, Putcha N, Aaron CP, Bowler RP, Comellas AP, Cooper CB, Dransfield MT, Han MK, Hoffman EA, Kanner RE, Krishnan JA, Labaki WW, Paine R 3rd, Paulin LM, Peters SP, Wise R, Barr RG, Hansel NN; SPIROMICS Investigators. Aspirin Use and Respiratory Morbidity in COPD: A Propensity Score-Matched Analysis in Subpopulations and Intermediate Outcome Measures in COPD Study. Chest. 2019 Mar;155(3):519-527.

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