How Does Diabetic Ketoacidosis Cause Vomiting?
DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body’s cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can’t get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn’t available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body’s metabolic processes aren’t able to function as well. A higher level of ketones also affects levels of sugar and electrolytes in the body. As ketones accumulate in the blood, more ketones will be passed in the urine, taking sodium and potassium salts out with them. Over time, levels of sodium and potassium salts in the body become depleted, which can cause nausea and vomiting. The result is a vicious cycle. The most important prevention strategies are to monitor blood glucose levels routinely, keep blood glucose levels controlled (e.g., Continue reading >>
Does Chronic Hyperventilation Cause Brain Damage?
“Does chronic hyperventilation cause brain damage?” “…since it causes cerebral hypoxia due to low CO2 level, can we deduce that it cause brain damage?” Voluntarily hyperventilating is unlikely to cause any problems. Your brain and body is generally too intelligent to allow you to damage yourself in such a manner. Low CO2 levels from Hyperventilation can cause cerebral vasoconstriction and ischemia. This usually is only a seen in settings of artificial respiration. Well it does not directly cause brain damage. However, you are correct that it can cause brain damage indirectly. When you hyper ventilate, your brain becomes depleted of oxygen. This is not good. Extened periods of lack of oxygen can cause cells (and neurons) to become damaged, or even die. This should not really be a problem unless it is a regular occurance. Hyperventilating for a few seconds every day wont do much, but if you are hyperventilating for very long periods of time multiple times daily, this could be a problem. I strongly suggest you speak to a doctor about this if you are concerned. If I can help, I suggest practising breathing excersises regularly. This will allow you over time to become more in control of your breathing, and thus be able to control your hyperventilating. It is as simple as breathing in slowly, holding your breath for a few seconds, and then exhaling slowly. Do this for a few minutes each day, it should help. Continue reading >>
Ap2 Respiratory System Lecture
Sort breathing rate increases above normal. PO2 increase, CO2 decreases in alveoli.The hemoglobin saturation is already at 98% so more O2 can't come into the blood, however additional CO2 leaves the blood. Low blood CO2 decreases blood H+, so pH rises (respiratory alkalosis) causes dizziness and fainting hyperventilating to slow or too shallow breathing caused by airway obstruction or brainstem injury; O2 decreases, CO2 increases in alveoli, both pressure gradients are affected so both O2 & CO2 can't leave blood and go to aveoli. Blood pH may fall (increase H+ from CO2) , blood becomes more acidic (respiratory acidosis) hypoventilating Continue reading >>
Hyperventilation In Severe Diabetic Ketoacidosis.
Abstract OBJECTIVE: To explore whether the carbon dioxide-bicarbonate (P(CO(2))-HCO(3)) buffering system in blood and cerebrospinal fluid (CSF) in diabetic ketoacidosis should influence the approach to ventilation in patients at risk of cerebral edema. DATA SOURCE: Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967. DESIGN: A clinical vignette is used--a child with severe diabetic ketoacidosis who presented with profound hypocapnia and then deteriorated--as a basis for discussion of integrative metabolic and vascular physiology. STUDY SELECTION: Studies included reports in diabetic ketoacidosis where arterial and CSF acid-base data have been presented. Studies where simultaneous acid-base, ventilation, respiratory quotient, and cerebral blood flow data are available. DATA EXTRACTION AND SYNTHESIS: We revisit a hypothesis and, by reassessing data, put forward an argument based on the significance of low [HCO(3)](CSF) and rising Pa(CO(2))- hyperventilation in diabetic ketoacidosis and the limit in biology of survival; repair of severe diabetic ketoacidosis and Pa(CO(2))-and mechanical ventilation. CONCLUSION: The review highlights a potential problem with mechanical ventilation in severe diabetic ketoacidosis and suggests that the P(CO(2))--HCO(3) hypothesis is consistent with data on cerebral edema in diabetic ketoacidosis. It also indicates that the recommendation to avoid induced hyperventilation early in the course of intensive care may be counter to the logic of adaptive physiology. Continue reading >>
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Dealing with Breathing Problems article more useful, or one of our other health articles. The term hyperventilation describes excessive ventilation of the lungs, beyond what is required to achieve normal arterial blood gases. Where hyperventilation occurs chronically or in recurrent episodes and is associated with somatic (respiratory, neurological, intestinal) or psychological (anxiety) symptoms, it is known as hyperventilation syndrome. About 5-10% of general medical outpatients are thought to have this syndrome and, because of the range of somatic symptoms, the risk of misdiagnosis is high. Pathogenesis Hyperventilation has little effect on arterial pO2 and almost no effect on oxygen saturation which is nearly 100% under normal circumstances. Its main effect is to lower pCO2 and produce a respiratory alkalosis. A secondary hypocalcaemia also occurs as calcium dissociation is shifted towards the unionised, bound form. There are many factors that influence the respiratory drive, including the elasticity of the lungs and the resistance in the airways but the most important factors are arterial pH, pCO2 and pO2. Of these, pCO2 is most important, although some people with chronic obstructive pulmonary disease (COPD) can depend on the hypoxic drive. Epidemiology It is quite common but precise prevalence is unknown. A postal survey indicated that 8% of adults without asthma have functional breathing problems (of which symptomatic hyperventilation is the most common). Hyperventilation syndrome is more common in people with asthma and also more common i Continue reading >>
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>