Overfeeding and CO2 Production of Critically Ill Respiratory Patients
Question
I have attached the instructions below. Just a heads up, I am a registered respiratory therapist and so is our instructor so an in depth explanation of things that are "common sense" or are the standard for our daily care does not have to be done. Please do not include anything about nursing in this essay.
Please include an abstract **it does not have to be on a separate page**
thank you
Instructions:
Module 7 Activity: Overfeeding & CO2 Production
Nutrition is required not only for the survival but also the well being of all living organisms. For patients in the intensive care unit, the concept of optimal nutrition has become incorporated into guidelines, standards, performance indicators and educational programs.
Indirect calorimetry measures respiratory gas exchange from which energy expenditure can be estimated. Oxygen consumption (VO2) and carbon dioxide (CO2) production occur during the oxidation of carbohydrate, protein, and fat. Heat production can be calculated from a measurement of VO2 and/or CO2.
From the reading and research evaluate the dangers of overfeeding and CO2 production of critically ill respiratory patient. Research the ingestion of carbohydrates and the elimination of CO2. Evaluate and critique the significance of overfeeding and CO2 production as a hindrance to recovery of the critically ill respiratory patient.
You will need to find and use at least 1 or 2 solid references in your research. Your paper will need to be in APA formatting including your cited references. This paper will be submitted
Solution
Abstract
Overfeeding critically ill respiratory individuals can result in significant and even deadly metabolic problems. The best way to provide nutrition care to patients is to evaluate their responses to food on a regular schedule. Nutritional supplements need to be adjusted over time to maintain metabolic stability and facilitate recovery. CO2 significantly impacts lung function, which could be clinically significant in critically ill patients, particularly those suffering from acute respiratory distress syndrome. In patients experiencing acute respiratory distress syndrome, hypercapnia may have positive advantages and the advantages of low-tidal volume breathing. The paper will discuss the hazards of overfeeding critically ill respiratory patients. It will also assess the importance of overfeeding and CO2 emissions. It will also explain how it is a stumbling block to recovery in critically ill individuals with respiratory failure.
Overfeeding and CO2 Production of Critically Ill Respiratory Patients
Dangers of Overfeeding and CO2 Production of Critically Ill Respiratory Patients
Critically sick patients require enough nutrition to meet their metabolic requirements. Adequate nutrition intake throughout critical illness enhances the effectiveness of weaning patients off mechanical breathing and shortens hospitalization (Franken field, 2019). Underfeeding reduces pulmonary epithelial development, promotes weakening of the respiratory muscle, and prolongs mechanical ventilation by failing to recover muscle mass and strength. On the other hand, overfeeding causes physiological stress and enhances mechanical ventilation by increasing carbon dioxide production, which boosts the required ventilation to maintain a constant level of arterial blood gases (Franken field, 2019). However, severe protein-calorie malnutrition continues to be a significant issue in many critically ill individuals.
Increased serum blood levels and hepatic steatosis also result from such modifications. Furthermore, excessive carbohydrate consumption combined with lipogenesis results in significant carbon dioxide production, as seen by a high respiratory quotient. Azotemia, hypertonic dehydration, and metabolic acidosis have resulted from overfeeding protein. Diabetes, triglyceride levels, and hepatic steatosis are associated with excessive carbohydrate infusion. Overfeeding can also result in hypercapnia and refeeding syndrome (Franken field, 2019). Finding patients at risk, offering proper assessment, coordinating multidisciplinary treatment plans, and ensuring appropriate and timely monitoring and management are all things that dietitians can do to avoid the respiratory problems of overfeeding.
Ingestion of Carbohydrates and the Elimination of CO2
In persons with severe pulmonary disease, a calorie-dense intake, mainly carbohydrates, increases carbon dioxide production and can lead to respiratory failure. Since fat energy produces less carbon dioxide, it can lower alveolar ventilation for any arterial blood carbon dioxide tension (Clark et al.,2019). Carbohydrate metabolism, which includes sugars, carbs, and fibers, generates the most carbon dioxide per unit of oxygen consumed. Since COPD patients have trouble exhaling carbon dioxide, a low-carbohydrate diet could make breathing easier (Clark et al.,2019). Even slight alterations in meals' carbohydrate and fat composition can significantly impact carbon dioxide, exercise capacity, and dyspnea in individuals with chronic obstructive pulmonary disease.
Significance of Overfeeding and CO2 Production as a Hindrance to Recovery of Critically Ill Respiratory Patients
Patients become overweight or obese as a result of overfeeding. Obesity also hurts respiratory performance by reducing lung capacity, especially forced expiratory volume and residual volume. In addition, it may compromise energy and resilience due to the inefficacy of the respiratory muscles (Franken field, 2019). These factors increase respirations, oxygen intake, and respiratory energy balance, resulting in respiratory muscles overload. It's vital to highlight that fatty tissue patterns significantly affect respiratory efficiency since fat develops in the chest and belly has the impact of a mechanical force. Obesity affects the respiratory system in various ways, including acute mechanical changes induced by fat deposition on the chest, belly, upper airway and increased inflammation. In addition, raising the neuronal respiratory rate and enhancing work for breathing produces respiratory sleeping problems and, as a result, the effect of rising respiratory failure.
Obese people produce more carbon dioxide due to oxidative metabolism than healthy people. The diaphragm contracts during normal breathing, moving the contents of the abdomen downward and forward. As a result, the external intercostal muscles contract and drive the ribs upward and onward simultaneously. The mechanism is compromised in obese people because excess body fat around the chest and abdomen hinders the action of the respiratory system (Franken field, 2019). Despite a link with a higher BMI, obesity does not affect airway function as evaluated by respiratory function unless in severely obese people. Increased obesity can compromise the performance of the respiratory muscles, presumably as a result of the diaphragm's increased stress. Some observed respiratory failure may be due to the increased resistance imposed by extra fatty tissue on the chest and abdomen, which creates a mechanical barrier for these muscles.
Conclusion
Obesity compresses the diaphragm, airways, and thoracic cavity, causing limiting respiratory symptoms. Excess fat also reduces the compatibility of the entire respiratory system, increases pulmonary tightness, and diminishes respiratory muscle strength. Obesity is on the rise worldwide, despite the evidence of increased health risks and lower quality of life. Although genetic vulnerability plays a role, it is possible to prevent and treat obesity to minimize the number of clinical and respiratory disorders.
References
Clark, I. E., Vanhatalo, A., Thompson, C., Joseph, C., Black, M. I., Blackwell, J. R., ... & Jones, A. M. (2019). Dynamics of the power-duration relationship during prolonged endurance exercise and influence of carbohydrate ingestion. Journal of Applied Physiology, 127(3), 726-736.
Franken field, D. C. (2019). Impact of feeding on resting metabolic rate and gas exchange in critically ill patients. Journal of Parenteral and Enteral Nutrition, 43(2), 226-233.
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