Commit e797597b authored by Jeff Webb's avatar Jeff Webb
Browse files

Various documentation cleanup.

Added hyperozemia event to Blood Chemistry Methodology.
parent 9120c4e0
{
"Name": "ImpairedAlveolarExchangeSurfaceArea",
"Description": "Cause Acute Respiratory Distress by generically reducing the alveolar surface area.",
"Name": "PulmonaryShunt",
"Description": "Test pulmonary shunt condition and exacerbation action.",
"StartType": {
"PatientConfiguration": {
"PatientFile": "StandardMale.json",
......
......@@ -9,59 +9,59 @@
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......@@ -316,7 +316,7 @@
<h6>Links</h6>
<hr>
<ul>
<li><a href="https://healtheng.illinois.edu/research/focus/simulation/training-simulator-for-extra-corporeal-membrane-oxygenation-in-adults/" target="_blank">ECMO Simulator Website</a></li>
<li><a href="https://healtheng.illinois.edu/collaboration/jump-osf/simulation-training-for-mechanical-circulatory-support-using-extra-corporeal-membrane-oxygenation-ecmo-in-adult-patients/" target="_blank">ECMO Simulator Website</a></li>
</ul>
</div>
</div>
......
......@@ -14,6 +14,8 @@ Authors Clipp, Webb, and Bray have transitioned to the Pulse team.
Pulse Publications:
- Jeffrey B. Webb, Aaron Bray, and Rachel B. Clipp. "Parameterization of Respiratory Physiology and Pathophysiology for Real-Time Simulation." 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC'20). 2020.
- Mrinali Kesavadas and Pavithra Rajeswaran, "Cyber Physical CPR Training System with Physiological Feedback." 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). 2019.
- Bray, Aaron, Jeffrey B. Webb, Andinet Enquobahrie, Jared Vicory, Jerry Heneghan, Robert Hubal, Stephanie TerMaath, Philip Asare, and Rachel B. Clipp. "Pulse Physiology Engine: an Open-Source Software Platform for Computational Modeling of Human Medical Simulation." SN Comprehensive Clinical Medicine. 2019.
- Gessa, Farooq M., "Testing and Validation Framework for Closed-Loop Physiology Management Systems for Critical and Perioperative Care" (2019). Master's Theses. 220. https://digitalcommons.bucknell.edu/masters_theses/220
- Rodriquez Jr, Dario, Thomas Blakeman, Dina Gomaa, and Richard Branson. Advancing Mechanical Ventilation Management through Simulation. No. AFRL-SA-WP-SR-2019-0006. USAFSAM/FHE Wright-Patterson AFB United States, 2019.
......
......@@ -173,6 +173,13 @@ The engine triggers the hypoxia event when the partial pressure of oxygen in the
If the partial pressure of oxygen in the blood falls below 15&nbsp; an irreversible state is triggered and it will be impossible to regain homeostasis.
### Hyperoxemia
Hyperoxemia occurs when the partial pressure of oxygen in the blood rises above 120 mmHg, usually due to excessive supplemental oxygen delivery. Hyperoxemia can induce cerebral vasoconstriction, neuronal cell death, and seizures. In addition, hyperoxemia reduces the cardiac index and heart rate while increasing peripheral vascular resistance @cite gershengorn2014hyperoxemia.
The engine triggers the moderate hyperoxemia event when the partial pressure of oxygen in the aorta rises above 120 mmHg. This is a reversible condition and is considered resolved when the partial pressure falls below 117 mmHg. This 3 mmHg window provides a buffer to account for normal fluctuations in the model.
If the partial pressure of oxygen in the blood rises to greater than 200 mmHg, the severe hyperoxemia event is triggered to flag the oxygen toxicity.
### Brain Oxygen Deficit
The brain is unable to complete any significant anaerobic metabolism. Therefore, without oxygen in the brain, unconsciousness results within five to ten seconds, and permanent damage can occur within five to ten minutes @cite guyton2006medical. Additionally, irreversible damage can occur if the oxygen tension in the brain is too low for a prolonged period of time @cite dhawan2011neurointensive.
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......@@ -4,7 +4,6 @@
@anchor patient-overview
Overview
========
========
Abstract
--------
......
......@@ -1079,17 +1079,17 @@ Disease states are applied to the simulated patient by modifying various paramet
Growth/increasing functions define a as 1 and b as the maximum multiplier, while decay/decreasing functions define b as 1 and a as the minimum multiplier. Therefore, a severity of 0 will not change the healthy value and allows for an intuitive continuous function without any discontinuities. The respiratory system also includes logic to combine effects for each parameter when multiple insults/interventions are applied.
When an artificial airway is applied (i.e., mechanical ventilator or anesthesia machine), there is a change in the respiratory circuit's resistance and compliance @cite arnal2018parameters. Intubated patients will have these modifiers stacked/combined with all other action/condition modifiers.
When positive pressure ventilation is applied (i.e., mechanical ventilator or anesthesia machine), there is a change in the respiratory circuit's resistance and compliance @cite arnal2018parameters. Intubated patients will have these modifiers stacked/combined with all other action/condition modifiers.
<center><br>
<i>Table 2. Property changes due to the application of respiratory diseases and an artificial airway. ARDS and COPD are applied by the user with a severity defined between 0 and 1 and mapped using with linear or exponential functions. Mild severity = 0.3, moderate severity = 0.6, severe severity = 0.9. The fatigue factor is a multiplier on the muscle pressure source target that effectively reduces the tidal volume due to the increased effort of breathing.</i>
<i>Table 2. Property changes due to the application of respiratory diseases and positive pressure ventilation. ARDS and COPD are applied by the user with a severity defined between 0 and 1 and mapped using with linear or exponential functions. Mild severity = 0.3, moderate severity = 0.6, severe severity = 0.9. The fatigue factor is a multiplier on the muscle pressure source target that effectively reduces the tidal volume due to the increased effort of breathing.</i>
</center>
<table>
<tr>
<th>Parameter</th>
<th>Standard Healthy</th>
<th>Artificial Airway</th>
<th>Positive Pressure Ventilation</th>
<th colspan="4">Restrictive (ARDS)</th>
<th colspan="4">Obstructive (COPD)</th>
</tr>
......@@ -1106,14 +1106,15 @@ When an artificial airway is applied (i.e., mechanical ventilator or anesthesia
<th>Moderate</th>
<th>Severe</th>
</tr>
<tr><td>Alveolar Dead Space (L)</td><td>0</td><td>0</td><td>N/A</td><td>0</td><td>0</td><td>0</td><td>Linear Growth</td><td>0.6</td><td>1.2</td><td>1.8</td></tr>
<tr><td>Airway Resistance (cmH20-s/L)</td><td>1.125</td><td>9</td><td>N/A</td><td>1.125</td><td>1.125</td><td>1.125</td><td>N/A</td><td>1.125</td><td>1.125</td><td>1.125</td></tr>
<tr><td>Bronchi Resistance (cmH20-s/L)</td><td>0.45</td><td>0.45</td><td>N/A</td><td>0.45</td><td>0.45</td><td>0.45</td><td>Exponential Growth</td><td>1.74</td><td>6.7</td><td>25.8</td></tr>
<tr><td>Lung Compliance (L/cmH2O)</td><td>0.1</td><td>0.04</td><td>Linear Decay</td><td>0.082</td><td>0.064</td><td>0.046</td><td>Linear Growth</td><td>0.13</td><td>0.16</td><td>0.19</td></tr>
<tr><td>Inspiratory-Expiratory Ratio</td><td>0.5</td><td>0.5</td><td>Exponential Growth</td><td>1.1</td><td>2.6</td><td>12.1</td><td>Linear Decay</td><td>0.3</td><td>0.15</td><td>0.03</td></tr>
<tr><td>Diffusion Surface Area (m^2)</td><td>68.3</td><td>68.3</td><td>Exponential Decay</td><td>34.3</td><td>17.2</td><td>8.6</td><td>Exponential Decay</td><td>34.3</td><td>17.2</td><td>8.6</td></tr>
<tr><td>Pulmonary Capilary Resistance (cmH20-s/L)</td><td>85.6</td><td>85.6</td><td>N/A</td><td>85.6</td><td>85.6</td><td>85.6</td><td>Linear Growth</td><td>128.4</td><td>171.2</td><td>214.0</td></tr>
<tr><td>Fatigue Factor</td><td>1</td><td>1</td><td>Linear Decay</td><td>0.76</td><td>0.52</td><td>0.28</td><td>Linear Decay</td><td>0.76</td><td>0.52</td><td>0.28</td></tr>
<tr><td>Alveolar Dead Space (L)</td><td>Respiratory</td><td>0</td><td>0</td><td>N/A</td><td>0</td><td>0</td><td>0</td><td>Linear Growth</td><td>0.6</td><td>1.2</td><td>1.8</td></tr>
<tr><td>Airway Resistance (cmH20-s/L)</td><td>Respiratory</td><td>1.125</td><td>9</td><td>N/A</td><td>1.125</td><td>1.125</td><td>1.125</td><td>N/A</td><td>1.125</td><td>1.125</td><td>1.125</td></tr>
<tr><td>Bronchi Resistance (cmH20-s/L)</td><td>Respiratory</td><td>0.45</td><td>0.45</td><td>N/A</td><td>0.45</td><td>0.45</td><td>0.45</td><td>Exponential Growth</td><td>1.74</td><td>6.7</td><td>25.8</td></tr>
<tr><td>Lung Compliance (L/cmH2O)</td><td>Respiratory</td><td>0.1</td><td>0.04</td><td>Linear Decay</td><td>0.082</td><td>0.064</td><td>0.046</td><td>Linear Growth</td><td>0.13</td><td>0.16</td><td>0.19</td></tr>
<tr><td>Inspiratory-Expiratory Ratio</td><td>Respiratory</td><td>0.5</td><td>0.5</td><td>Exponential Growth</td><td>1.1</td><td>2.6</td><td>12.1</td><td>Linear Decay</td><td>0.3</td><td>0.15</td><td>0.03</td></tr>
<tr><td>Diffusion Surface Area (m^2)</td><td>Respiratory</td><td>68.3</td><td>68.3</td><td>Exponential Decay</td><td>34.3</td><td>17.2</td><td>8.6</td><td>Exponential Decay</td><td>34.3</td><td>17.2</td><td>8.6</td></tr>
<tr><td>Pulmonary Capillary Resistance (mmHg-s/mL)</td><td>Cardiovascular</td><td>0.062</td><td>0.062</td><td>N/A</td><td>0.062</td><td>0.062</td><td>0.062</td><td>Linear Growth</td><td>0.094</td><td>0.126</td><td>0.157</td></tr>
<tr><td>Pulmonary Shunt Resistance (mmHg-s/mL)</td><td>Cardiovascular</td><td>8.9</td><td>8.9</td><td>Exponential Decay</td><td>2.23</td><td>0.56</td><td>0.14</td><td>N/A</td><td>8.9</td><td>8.9</td><td>8.9</td></tr>
<tr><td>Fatigue Factor</td><td>Respiratory</td><td>1</td><td>1</td><td>Linear Decay</td><td>0.76</td><td>0.52</td><td>0.28</td><td>Linear Decay</td><td>0.76</td><td>0.52</td><td>0.28</td></tr>
</table>
Modifications to respiratory circuit resistances and compliances can further be examined and validated through volume-flow curves, like those created during spirometry testing. Figure 17 shows results from a simulated pulmonary function test with the standard patient healthy and with moderate ARDS and COPD.
......@@ -1146,6 +1147,10 @@ The destruction of the alveolar membranes also destroys the pulmonary capillarie
Decreased Inspiration-Expiration (IE) ratio is another pathophysiologic feature of COPD. As with asthma, the normal IE ratio is scaled using a multiplier based on severity. Either chronic bronchitis severity or emphysema severity (whichever is higher) is used to determine the IE ratio scaling multiplier.
#### Acute Respiratory Distress Syndrome
#### Lobar Pneumonia
Lobar pneumonia is a form of pneumonia that affects one or more lobes of the lungs. Symptoms typically include increased respiration rate, decreased tidal volume, reduced oxygen saturation, decreased IE ratio, and increased body temperature @cite ebell2006outpatient . As fluid fills portions of the lung, it becomes more difficult to breathe. Fluid also reduces the effective gas diffusion surface area in the alveoli, reducing alveolar transfer of oxygen and carbon dioxide into and out of the bloodstream @cite guyton2006medical . The engine simulates lobar pneumonia by decreasing the alveoli compliance in the respiratory circuit, which models increased breathing difficulty due to fluid congestion in the alveoli. Similarly, gas diffusion surface area is reduced using the same function as for COPD. Decreased IE ratio is pathophysiologic feature of lobar pneumonia. Like COPD, the normal IE ratio is scaled using a multiplier based on severity.
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......@@ -7017,4 +7017,15 @@ on Severe Disability and Mortality After Head Injury},
pages={1},
year={2020},
publisher={Nature Publishing Group}
}
@article{gershengorn2014hyperoxemia,
title={Hyperoxemia--too much of a good thing?},
author={Gershengorn, Hayley},
journal={Critical Care},
volume={18},
number={5},
pages={556},
year={2014},
publisher={BioMed Central}
}
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