Acid-base Physiology
An outline of management is presented: this should be tailored to individual circumstances. Management of DKA has passed through 3 stages in the last 100 years: Stage 1: Preinsulin era (Feature: mortality of 100%) Stage 2: High dose insulin regime (Feature: mortality down to 10% but metabolic complications due to the treatment) Stage 3 (the present): Low dose insulin regime (Feature: low mortality) Mortality with the low dose insulin regime is down to about 2 to 5% overall. In older patients with DKA precipitated by a major medical illness (eg acute pancreatitis, myocardial infarction, septicaemia), the mortality rate is still high due to the severity of the precipitating problem. Restore normal carbohydrate and lipid metabolism Management can be considered in terms of emergency and routine components. Protect by intubation with a cuffed tube if patient is significantly obtunded. Consider placing a nasogastric tube in all patients. Intubation may be necessary for airway protection or ventilation (eg if aspiration, coma, pneumonia, pulmonary oedema, acute pancreatitis and ARDS) but this is not common. Maintain compensatory hyperventilation in intubated patients Patients with metabolic acidosis (eg severe DKA) have marked hyperventilation (ie respiratory compensation, Kussmaul respirations) and typically low arterial pCO2 levels. If intubated and ventilated, ventilatory parameters (tidal volume and rate) need to be set to continue a high minute ventilation. If this is not done and pCO2 is inappropriately high, a severe acidaemia and consequent severe cardiovascular collapse may occur This is a particular problem in all situations where a patient with a compensated metabolic acidosis is intubated and ventilated. The rule of thumb is to aim for a pCO2 level of 1.5 times th Continue reading >>
Arterial Blood Gases (blood Gases), Acidosis And Alkalosis
Sample The better choice is the Radial artery. The sample may be taken from the femoral artery or brachial. The tests are done immediately because oxygen and carbon dioxide are unstable. Arterial blood is better than the venous blood. For arterial blood don't use the tourniquet and no pull on the syringe plunger. For venous blood syringe or tubes are completely filled and apply a tourniquet for few seconds. Arterial VS Venous blood Arterial blood gives good mixture of blood from various areas of the body. Venous blood gives information of the local area from where the blood sample is taken. Metabolism of the extremity varies from area to area. Arterial blood measurement gives the better status of the lung oxygenating the blood. Arterial blood gives information about the ability of the lung to regulate the acid-base balance through retention or release of CO2. Precautions for the collection of blood Avoid pain and anxiety to the patient which will lead to hyperventilation. Hyperventilation due to any cause leads to decreased CO2 and increased pH. Keep blood cool during transit. Don't clench finger or fist. This will leads to lower CO2 and increased acid metabolites. pCO2 values are lower in the sitting or standing position in comparison with the supine position. Don't delay the performance of the test. Avoid air bubbles in the syringe. Excess of heparin decreases the pCO2 may be 40% less. Not proper mixing of the blood before running the test. Purpose of the test This test is done on the mostly hospitalized patient. Mostly the patients are on ventilator or unconscious. For patients in pulmonary distress. To assess the metabolic (renal) acid-base and electrolytes imbalance. Its primary use is to monitor arterial blood gases and pH of blood. Also used to monitor oxygenatio Continue reading >>
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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 >>
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 >>
Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State
Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>
5.5 Metabolic Acidosis - Compensation
Acid-Base Physiology 5.5.1 Hyperventilation Compensation for a metabolic acidosis is hyperventilation to decrease the arterial pCO2. This hyperventilation was first described by Kussmaul in patients with diabetic ketoacidosis in 1874. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The initial stimulation of the central chemoreceptors is due to small increases in brain ISF [H+]. The subsequent increase in ventilation causes a fall in arterial pCO2 which inhibits the ventilatory response. Maximal compensation takes 12 to 24 hours The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is �maximal� compensation rather than �full� compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is short-lived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. The expected pCO2 at maximal compensation can be calculated from a simple formula The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the Continue reading >>
Hyperventilation
You breathe in oxygen and breathe out carbon dioxide. Excessive breathing creates a low level of carbon dioxide in your blood. This causes many of the symptoms of hyperventilation. You may hyperventilate from an emotional cause such as during a panic attack. Or, it can be due to a medical problem, such as bleeding or infection. Your health care provider will determine the cause of your hyperventilation. Rapid breathing may be a medical emergency and you need to get treated, unless you have had this before and your provider has told you that you can treat it on your own. If you frequently overbreathe, you may have a medical problem called hyperventilation syndrome. When you're overbreathing, you might not be aware you're breathing fast and deep. But you'll likely be aware of the other symptoms, including: Feeling lightheaded, dizzy, weak, or not able to think straight Feeling as if you can't catch your breath Chest pain or fast and pounding heartbeat Belching or bloating Dry mouth Muscle spasms in the hands and feet Numbness and tingling in the arms or around the mouth Problems sleeping Continue reading >>
Diabetic Ketoacidosis: A Serious Complication
A balanced body chemistry is crucial for a healthy human body. A sudden drop in pH can cause significant damage to organ systems and even death. This lesson takes a closer look at a condition in which the pH of the body is severely compromised called diabetic ketoacidosis. Definition Diabetic ketoacidosis, sometimes abbreviated as DKA, is a condition in which a high amount of acid in the body is caused by a high concentration of ketone bodies. That definition might sound complicated, but it's really not. Acidosis itself is the state of too many hydrogen ions, and therefore too much acid, in the blood. A pH in the blood leaving the heart of 7.35 or less indicates acidosis. Ketones are the biochemicals produced when fat is broken down and used for energy. While a healthy body makes a very low level of ketones and is able to use them for energy, when ketone levels become too high, they make the body's fluids very acidic. Let's talk about the three Ws of ketoacidosis: who, when, and why. Type one diabetics are the group at the greatest risk for ketoacidosis, although the condition can occur in other groups of people, such as alcoholics. Ketoacidosis usually occurs in type one diabetics either before diagnosis or when they are subjected to a metabolic stress, such as a severe infection. Although it is possible for type two diabetics to develop ketoacidosis, it doesn't happen as frequently. To understand why diabetic ketoacidosis occurs, let's quickly review what causes diabetes. Diabetics suffer from a lack of insulin, the protein hormone responsible for enabling glucose to get into cells. This inability to get glucose into cells means that the body is forced to turn elsewhere to get energy, and that source is fat. As anyone who exercises or eats a low-calorie diet knows, fa Continue reading >>
Diabetic Ketoacidosis (dka)
Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>
Emergency Management Of Diabetic Ketoacidosis In Adults
Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] 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.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>
Severe Diabetic Ketoacidosis Complicated By Hypocapnic Seizure
Summary In clinical practice, seizures independent of hypoglycemia are observed in patients with type 1 diabetes mellitus (T1DM) more frequently than expected by chance, suggesting a link. However, seizures during management of diabetic ketoacidosis (DKA) have generally been considered a bad prognostic factor, and usually associated with well-known biochemical or neurological complications. We present the case of a 17-year-old girl with known T1DM managed for severe DKA complicated by hypocapnic seizure. We review the literature on this rare occurrence as well as outline other possible differentials to consider when faced with the alarming combination of DKA and seizure. Learning points: Seizures during DKA treatment require immediate management as well as evaluation to determine their underlying cause. Their etiology is varied, but a lowered seizure threshold, electrolyte disturbances and serious neurological complications of DKA such as cerebral edema must all be considered. Sudden severe hypocapnia may represent a rare contributor to seizure during the treatment of DKA. Background Diabetic ketoacidosis (DKA) is an endocrine emergency occurring in patients with both new-onset and established type 1 diabetes (T1DM). In brief, the diagnosis is based on clinical suspicion followed by fulfillment of biochemical criteria: Hyperglycemia (blood glucose level (BGL) >11 mmol/L); ketonuria and/or ketonemia and metabolic acidosis (pH <7.3, bicarbonate <15 mmol/L). It is a leading acute cause of diabetes-related morbidity and mortality, particularly in children (1), often due to well-described complications of treatment. The most common of these include cerebral edema, and electrolyte disturbances such as hypoglycemia and hypokalemia. Seizure activity occurring during treatment o 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 >>
Pediatric Diabetic Ketoacidosis
Practice Essentials Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Signs and symptoms Symptoms of acidosis and dehydration include the following: Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Patients with diabetic ketoacidosis may also have the following signs and symptoms: Cerebral edema Most cases of cerebral edema occur 4-12 hours after initiation of treatment. Diagnostic criteria of cerebral edema include the following: Major criteria include the following: Minor criteria include the following: See Clinical Presentation for more detail. Laboratory studies The following lab studies are indicated in patients with diabetic ketoacidosis: Imaging studies Head computed tomography (CT) scanning - If coma is present or develops Chest radiography - If clinically indicated Electrocardiography Electrocardiography (ECG) is a useful adjunct to monitor potassium status. Characteristic changes appear with extremes of potassium status. See the images below. Consciousness Check the patient’s consciousness level hourly for up to 12 hours, especially in a young child with a first presentation of diabetes. The Glasgow coma scale is recommended for this purpose. See Workup for more detail. Management Replacement of the following is essential in the treatment of diabetic ketoacidosis: Insulin - Continuous, low-dose, intravenous (IV) insulin infusion is generally considered the safest and most effective insulin delivery method for diabetic ketoacidosis Potassium - After initial resuscitatio Continue reading >>
Hyperventilation In Severe Diabetic Ketoacidosis*
Abstract 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. Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967. 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. 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. 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. 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. ) “iso-acidity” lines. A, changes in the index case: point 1, at presentation; point 2, 15 mins ABG 7.09 ⫾0.04 14.0 ⫾1.0 5.0 ⫾1.0 Ohman et al. (9) CSF 7.35 ⫾0.03 23.0 ⫾2.0 12.0 ⫾2.0 ABG 7.15 ⫾0.06 19.9 ⫾2.5 7.6 ⫾1.6 Marks et al. (10) CSF 7.22 ⫾0.03 25.0 ⫾2.7 10.2 ⫾1.7 ABG Continue reading >>
