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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 

Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland

Monday, June 27, 2016

Salbutamol induced hyperlactaemia


24/F with a history of Asthma presented to the ED complaining of shortness of breath that progressively got worse over the past couple of days in-spite-of increased use of inhalers. She has been intubated twice before due to asthma exacerbations. She never smoked and denied having any pets. 

In the ED, she received prednisone and multiple doses of albuterol nebulizations. Physical exam showed mild distress, BP 110/70, PR 110/min RR 28/min. She was able to talk in full sentences and was saturating 100% on 2 liters. Her best peak flow was reportedly 400, and she only did 150. She had bilaterally decreased air entry and significant expiratory wheezing. 

ABG on arrival showed a lactate level of 3 with a peak flow of 220. With treatment, in spite of an improvement in her peak flow to 300, she looked more tachypneic and lactate level increased to 5.5. Rest of the labs and CXR were normal.


Salbutamol/ Albuterol is a β2 agonist used for bronchodilation in asthma. Salbutamol causes lactic acidosis by a combination of factors, but the exact etiology remains unclear. It is probably due to its metabolic effects. By creating a hyperadrenergic state it enhances glycogenolysis and gluconeogenesis, leading to more glucose, enhanced glycolysis, and pyruvate production. At the same time, enhanced lipolysis and increased free fatty acids inhibit pyruvate dehydrogenase enzyme, preventing pyruvate from entering the Krebs cycle. This causes pyruvate reduction to lactate.

Reports of lactic acidosis induced by high dose beta agonists used for tocolysis and bronchodilation have been described in obstetric and asthmatic patients. 

What are the types of Lactic Acidosis?

Type A Lactic Acidosis occurs when oxygen delivery to the tissues is compromised. 

Type B Lactic Acidosis occurs when either lactate production is increased or lactate removal is decreased without obvious oxygen delivery problems. It occurs due to increase in both endogenous and exogenous catecholamines. Enhanced β2 receptor activation leads to increased glycogenolysis, gluconeogenesis, lipolysis and ultimately to increased conversion of pyruvate to lactic acid. Concurrent corticosteroid use may enhance the beta receptor sensitivity further potentiating the lactic acidosis. 

Conditions associated with type B lactic acidosis include inborn errors of metabolism (pyruvate dehydrogenase deficiency), systemic disorders (liver failure), and medications (ethanol, metformin, and corticoids). It has also been postulated that endogenous (distress) or exogenous (drugs) adrenergic stimulation may be associated with increased conversion of pyruvate to lactate. 

What are the common blood gas findings in Acute Asthma?
The common metabolic disturbances seen during an acute attack are respiratory alkalosis, followed by respiratory acidosis as patients get tired of breathing.

What are the possible causes of lactic acidosis in Asthma?
1. Pulsus paradoxus and intrinsic PEEP decrease cardiac output and venous return
2. Production of lactate by overworked respiratory muscles
3. Hyperadrenergic State (Beta 2 agonist-induced)

Why is it important for us to know about this?
Albuterol induced lactic acidosis creates a paradoxical situation where there is enhanced bronchodilation but worsening tachypnea as a result of compensation for metabolic acidosis. Acidosis results in hyperventilation which could be mistaken for poor response to treatment. Physicians might misinterpret this situation as worsening respiratory failure and give more albuterol, creating a vicious cycle and ultimately leading to respiratory failure. 

Serial peak flow measurements and examination is the ideal way to identify this situation.

Take Home:
While treating asthmatic patients for severe bronchospasm, when lungs sound clear following treatment but tachypnea persists, suspect albuterol-induced hyperlactatemia. 


  1. Dodda, Venkata R., and Peter Spiro. "Can albuterol be blamed for lactic acidosis?." Respiratory care 57.12 (2012): 2115-2118.
  2. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C. Transient lactic acidosis as a side effect of inhaled salbutamol. Chest. 2002 Jul;122(1):385-6
  3. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C: Transient lactic acidosis as a side effect of inhaled salbutamol. Chest 2002; 122: 385–6Stratakos, G Kalomenidis, J Routsi, C Papiris, S Roussos, C 
  4. Prakash S, Mehta S: Lactic acidosis in asthma: Report of two cases and review of the literature. Can Respir J 2002; 9: 203–8Prakash, S Mehta, S 


     Lakshay Chanana


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