High Fidelity Human Based Simulation of Patient with Reduced Baroreceptor

Importance of Topic & Reason of Choosing

The use of simulators gives the basis for potential research in safe environments based on facts but is currently being underused according to articles mentioning the following “it remains underused in hospitals and other healthcare settings” or “despite the intuitive appeal of simulation as a learning tool, especially for procedural competence, there have been small gains to date”. If the drug/treatment-based simulation works, the potential for real-life success is augmented.

The objectives are to reduce the baroreceptor reflex of the patient, followed by an abnormal reduction in heart rate via propranolol intake, and finally, show the temporary restoration of heart rate homeostasis via atropine application. The main aim is to use a High Fidelity Based Simulation Mannequin to mimic low baroreceptor reflex in, the scenario of propranolol intake and to show that the application of atropine temporarily stabilizes heart rate homeostasis.

Search terms used for the following experiment where done by searching keywords like “Pleomorphic” or “Laryngectomy” on search engines such as “PubMed”. Inclusion criteria involved searching terms in English, fully accessible, and where possible more recent research studies to ensure up-to-date knowledge; further exclusion criteria excluded out of topic based on a general reading of the abstract and results.

Case and Results

The topic being explored involved is a male patient in his early 20s with a Pleomorphic Adenoma (benign salivary gland neoplasm) leading to partial blockage of both glossopharyngeal and vagus nerves, which both behave as baroreceptors transmitters for the homeostasis of mean arterial blood pressure within the body. Note: the patient mentions the medication (propranolol) acquired via “a friend” to reduce anxiety and not another doctor. The simulator is being used to understand situations where the baroreceptor complex for controlling heart rate and contractility has been compromised due to the previously mentioned situation. This experiment covers diagnosis and temporary/permanent treatment for the patient.

Pleomorphic Adenoma leads to partial blockage of both glossopharyngeal and vagal Nerves which behave as baroreceptor transmitters for the regulation of heart rate. Pleomorphic Adenoma is the most common salivary gland neoplasm. Epidemiological studies show 84% presence in parotid glands, 8% in submandibular glands, and 6.5% in minor salivary glands; these benign tumors align with the paths of both the vagus and glossopharyngeal nerves, hence partially obstructing signaling and function. This reduced baroreceptor activity leads to reduced heart rate in patients due to deficient baroreceptor reflex and propranolol (beta-blockers) intake.

To understand how the patient’s sinus bradycardia surged from a normal propranolol overdose we must first understand the mechanism behind the reflex. Blockage of the vagus and pharyngeal nerves lead to reduced activity on the Nucleus Tractus solitarius which lowers the activity of the ventral lateral medulla and overall leads to a fall in sympathetic stimulation of the post-ganglionic sympathetic fibres in the thoracic and cervical para-vertebral ganglia. This lowers noradrenaline in cardiac plexus acting on G-coupled receptors, which overall reduces activation of adenylyl cyclase and prevents its formation of cAMP for preventing activation of pyruvate kinase A which can’t phosphorylate DHP Receptors not releasing Ca2+ which in turn cannot act on ryanodine receptors to release Ca2+ and act on troponin and initiate contractions. Results are negative chronotropic and inotropy which lead to sinus bradycardia caused by propranolol and worsened by reduced reflexes.

The diagnosis will involve blood pressure monitoring detecting possible hypotensive states, followed by a type II electrocardiogram measuring the electric activity of the heart, and finally, blood test involving full blood count (normal). Urea and electrolytes should show decreased levels of creatinine in the blood due to possible decreased mean arterial pressure resulting in lower hydrostatic pressure followed by reduced glomerular filtration rate.

The final test will be a full-body computerized tomography which shows the outcome of Pleomorphic Adenoma. Short-term treatments should involve different doses of 5mg of Atropine every 6 minutes at the start and then periodically at intervals of heart rates below 55bpm until the patient has been stabilized. Fine needle aspiration of the of the tumor will be performed for further confirmation of non-malignancy and pleomorphic adenoma diagnosis which can finally be followed by local surgical resection as a possible final treatment.

The heart rate factor of the patient was initially set to 1 (normal), baroreceptor gain set to 100 (overall), cardiac baroreceptor gain set to 10, and peripheral baroreceptor gain set to 10; all demonstrating stabilized individual with a heart rate of 72bpm. This was followed by the application of 2mg of propranolol 30 seconds after the start of the simulation which lead to a peak reduced heart rate 58bpm 5.5 minutes after the start of stimulation; this was done as means to show the effect of propranolol on an individual consisting of normal baroreceptor reflex.

Reduced baroreceptor reflex simulation included a reduction in baroreceptor gain to 40, cardiac baroreceptor gain to 4, and peripheral cardiac receptor gain to 4; this state was set at 6 minutes after the start of the simulation. This was followed by a rapid drop in heart rate which reached 41bpm; the application of 5mg of atropine re-stabilized the heart rate to 68bpm; initially, this application was every 6 minutes but was changed to a periodical basis of when heart rate was minimal below 55bpm, which was done until patient returned to stability.

Discussion

Effectiveness of Atropine: The addition of Atropine showed to be effective in combating reduced heart in patients with reduced baroreceptor reflex and normal doses of propranolol intake caused by uncontrolled anxiety. This propranolol combating effect can be backed by “Part 7.3: Management of Symptomatic Bradycardia and Tachycardia”. Now although it’s proven to be effective in combating propranolol, it can be argued to be ineffective in specific individuals even in altered states; backed by “Atropine”: “If there is no improvement in the clinical state after repeat doses of atropine, additional treatments with atropine are unlikely to be effective”. Also backed by the “Effectiveness study of atropine for progressive myopia in Europeans” which states: “Moreover, some studies have suggested that atropine is less effective in persons of non-Asian descent.”

Effectiveness of Simulators in Teaching & Research: The use of simulators gives the basis for potential research and teaching for students and healthcare professionals in safe environments according to “Training and simulation for patient safety” which mentions that “Simulation-based medical education enables knowledge, skills, and attitudes to be acquired for all healthcare professionals in a safe, educationally orientated and efficient manner”. Although proven effective for research and training, these simulators are currently being underused for the same cohort according to the same article which mentions that “simulators remain underused in hospitals and other healthcare settings” or “despite the intuitive appeal of simulation as a learning tool, especially for procedural competence, there have been small gains to date”. Possible factors for underuse could include lack of publication to cohort, the difficulty of use, or but mostly fear of use due to the uncertainty present in humans which simulators possibly lack, which leads us to the next point.

Effectiveness of Simulators in Treating & Risks: High fidelity human-based simulators can be effective in treating patients by first “without risk to the patient” simulating the drug and if successful, moved on to human trials as mentioned by the “Improving Patient Safety through Simulation Training in Anaesthesiology: Where Are We?” which states that “If the drug/treatment-based simulation works, the potential for a real-life success is augmented.”

Contrastingly we can argue that because these high fidelity human-based simulators aren’t based on tables of acquired data but on equations working on a single flow, consisting of resistors and capacitors augmented by constants, that the potential for simulating human-based risk factors is low. This is backed by the article: “High-fidelity is not superior to low-fidelity simulation but leads to overconfidence in medical students” which stated that “The use of high-fidelity simulation led to equal or even worse performance and growth in knowledge as compared to low-fidelity simulation, while also inducing undesirable effects such as overconfidence.”

Conclusion

In conclusion, the baroreceptor reflex of the high fidelity human-based simulator was reduced to 40% which lead to sinus bradycardia during propranolol intake in individuals with reduced baroreceptor reflex caused by the vagus and glossopharyngeal nerve obstructions. The addition of 5mg of atropine proved to restore homeostasis temporarily in individuals with a chronic baroreceptor complex deficiency. Although simulations can be very useful for later testing in real-life circumstances, they do not provide proof of demonstrating the concept in an actual human where many factors could wrong. Nevertheless, the use of High Fidelity Human-Based Mannequins is still a great tool for learning, and testing and could be used in the simulation of multiple physiological scenarios.

Reflections

Operating a High Fidelity Based Simulation Mannequin was a skill I did not yet possess, changing the homeostatic conditions, application of medications, and setting different conditions were skills in simulation I learned and improved with practice, to the point I started to predict the effects of certain simulations, examples included “predicting the effect of propranolol applications higher than 5mg lead to bradycardia in individuals with the normal function” which was tested and proofed.

I think the work has been very valuable in terms of creating a new scenario that future candidates can use to simulate and solve rare cases in clinical scenarios. Now, even though simulations are performed on high-fidelity mannequins, the mannequins are still not human, so we don’t have proof of demonstrating the concept in that area. In terms of changing variables in the experiment, I would have done a higher number of repeats with a wider range of baroreceptor reflex functions and added different scenarios for treating propranolol dependency an effect which would possibly still be present in the patient.

Some minor deficiencies in the experiment included starting off with too high amounts of the atropine (10mg) which caused a significant increase in the heart rate (tachycardia) due to dose surpassing dysfunction of the baroreceptor, this was initially counteracted with 80mg of propranolol but changed to simply adding a reduced 5mg of atropine, a finer solution to stability.

I see myself using these High Fidelity Based Human Simulators before treating patients, I see it as a research tool to counteract the uncertainty acquired from reading articles, books, and the media. Overall, I have been inspired to use these high-fidelity simulators to simulate drug-based trials for conditions dealing with cardiorespiratory dysfunction; such as hypercapnia, hypoxemia, hypertension, hypoventilation, tachycardia, and bradycardia. I now imagine the many different combinations of drugs and treatments which can be created to counteract such desired conditions.