It can also be caused by kidney or liver failure, some cancers, or the ingestion of toxins. Agonal breathing may be a sign of stroke or cardiac arrest. It requires immediate medical assistance. When blood sugar levels…. Multiple tests can analyze metabolism.
Most need blood drawn, but some can be ordered online and done at home. Here are 2. This simple, at-home test can introduce you to your metabolic hormones. Health Conditions Discover Plan Connect. Medically reviewed by Angela M. Causes Symptoms Treatment Prevention Vs. Cheyne-Stokes breathing Bottom line Kussmaul breathing is characterized by deep, rapid, and labored breathing.
What causes Kussmaul breathing? Initially, patients will develop tachypnea, which is increased respiratory rate, leading to decrease in CO 2 concentration.
Depth of breaths. Mechanical ventilation in these patients is particularly delicate, since a lung protective strategy, with low tidal volumes and controlled transpulmonary pressures, should be maintained, while attempting to increase minute-ventilation until metabolic acidosis is completely corrected[ 42 , 43 ]. There are two types of pulmonary edema that have been described in patients with DKA: One associated with elevated pulmonary venous pressure and another associated with increased pulmonary capillary permeability.
The diagnosis is made based on clinical findings of dyspnea, an A-a gradient on arterial blood gas and chest image showing bilateral pulmonary infiltrates.
Also known as hydrostatic pulmonary edema, it is usually existent at presentation of DKA, is corrected during the treatment of DKA and is more common in patients with concomitant renal failure[ 44 - 47 ]. The occurrence of circulatory overload and pulmonary edema with elevated pulmonary venous pressure is a result of the acute shift of an abundant volume of fluid into the extracellular compartment. This fluid shift happens as a consequence of solute accumulation in the extracellular compartment secondary to hyperglycemia[ 44 ].
Therefore, correction of hyperglycemia shifts fluid back into cells, also correcting hydrostatic pulmonary edema. However, some patients might require hemodialysis and mechanical ventilation. The degree of fluid shift and, consequently, the likelihood of developing hydrostatic pulmonary edema during a DKA episode are determined by the severity of hyperglycemia and by the volume status prior to the development of DKA[ 47 ].
The amount of fluid transferred from the cells into the extracellular space is directly proportional to the changes in serum glucose concentration[ 48 ]. Even though hydrostatic pulmonary edema has been described more commonly in patients with advanced renal disease, there are several cases reported in patients with DKA who developed pulmonary edema without having renal dysfunction.
Several cases have been reported of takotsubo cardiomyopathy happening in the setting of DKA and causing pulmonary edema[ 50 , 51 ]. There are also reports of myocardial dysfunction secondary to severe acidosis and electrolyte abnormalities[ 52 ].
Also known as non-hydrostatic pulmonary edema, this type of pulmonary edema is caused by changes at the histological level of the alveolar epithelium. In diabetic patients, there is thickening of the alveolar epithelium and pulmonary capillary basal membrane, corroborating the presence of pulmonary microangiopathy[ 53 , 54 ]. ARDS can develop during the course of DKA or during its treatment[ 3 ], and it is more frequent and severe than hydrostatic pulmonary edema[ 54 , 55 ].
The most accepted explanation is activation of lymphocytes and release of cytokines, especially interleukin-1, which serum levels are much higher during treatment of DKA[ 56 - 58 ]. The treatment of non-hydrostatic pulmonary edema in DKA is supportive. Focus should be on treating DKA and its exacerbating factor, early intubation and protective lung ventilation. In DKA, respiratory failure is caused by several electrolytes, metabolic and cardiac and lung end-organ damage.
Developing respiratory failure during DKA onset or treatment is associated with high mortality. Early recognition and treatment of the risk factors for the development of respiratory failure have the potential to decrease morbi-mortality of patients with DKA.
Conflict-of-interest statement: None of the authors have any conflict of interest or financial disclosures. Manuscript source: Invited manuscript. Peer-review started: August 24, First decision: October 5, Article in press: December 13, Specialty type: Endocrinology and metabolism. Country of origin: United States.
Peer-review report classification. Grade A Excellent : 0. Grade B Very good : B, B. National Center for Biotechnology Information , U. Journal List World J Diabetes v.
World J Diabetes. Published online Jan Alice Gallo de Moraes and Salim Surani. Author information Article notes Copyright and License information Disclaimer.
Author contributions: All authors have contributed to the conception, design and review of the manuscript; Gallo de Moraes A has been also involved in literature review and drafting of the manuscript.
Published by Baishideng Publishing Group Inc. All rights reserved. This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. This article has been cited by other articles in PMC.
Abstract Diabetes affects approximately 30 million persons in the United States. Keywords: Diabetes ketoacidosis, Respiratory physiology, Mechanical ventilation, metabolic acidosis, Hyperventilation, Kussmaul breathing, Respiratory failure.
Potassium Patients being admitted for DKA usually have a total body potassium deficit that averages to mEq[ 8 ]. Magnesium At presentation of DKA, the levels of serum magnesium are usually normal. Phosphorous Acidosis causes potassium shifts into the ECF and hyperglycemia causes phosphaturia by osmotic diuresis, which will ultimately lead to hypophosphatemia.
Open in a separate window. Figure 1. Pulmonary edema due to elevated pulmonary venous pressure Also known as hydrostatic pulmonary edema, it is usually existent at presentation of DKA, is corrected during the treatment of DKA and is more common in patients with concomitant renal failure[ 44 - 47 ]. Pulmonary edema due to increased pulmonary capillary permeability Also known as non-hydrostatic pulmonary edema, this type of pulmonary edema is caused by changes at the histological level of the alveolar epithelium.
Apart from its effect on blood glucose concentration, insulin has an important effect on fat metabolism in that it inhibits the enzyme lipase, an enzyme essential for the breakdown of triglyceride stored fat to its constituent fatty acids, a step necessary for the potential energy in fat to be realized. The negative effect of insulin on fat metabolism is appropriate because glucose is available as an energy source.
In periods of fasting or starvation when blood glucose is low and insulin production is consequently switched off, fat is metabolized as an alternative energy source. There are several hormones, the so-called counterregulatory hormones, which oppose the action of insulin; the most important of these is glucagon also produced within the pancreas but, by contrast to insulin, in response to a falling blood glucose.
Glucagon increases blood glucose by promoting the liver production of glucose from non-carbohydrate sources and stored glycogen. Other hormones which oppose the action of insulin include the stress hormones produced by the adrenal glands cortisol and catecholamines growth hormone and estrogen. By integration of the combined action of insulin and the counterregulatory hormones, blood glucose is maintained within narrow limits and cells continue to be supplied with a sufficient source of potential energy to function normally.
In the absence of insulin, glucose in blood cannot enter tissue cells where it is needed to provide energy, and the liver inappropriately continues to release glucose produced from non-carbohydrate sources and breakdown of glycogen to the blood.
The inevitable consequence is a rising blood glucose concentration. Most of the clinical signs and symptoms which characterize DKA can be attributed to either raised blood glucose hyperglycemia or lack of glucose within cells. The abnormalities in results of blood gas analysis stem mainly from lack of glucose within cells but first, for completeness, the consequences of hyperglycemia will be addressed.
Since glucose is an osmotically active substance, this loss of glucose in urine is associated with an osmotic diuresis and resulting dehydration, as an increasing volume of water is lost from the body in urine. Rising plasma osmolarity due to dehydration invokes the thirst response to correct the water deficit. The water deficit reduces blood volume, thereby decreasing blood pressure, so that hypotension is a presenting feature of DKA.
Osmotic diuresis is associated with large losses of electrolytes in urine, so that patients with DKA typically have a whole-body sodium and potassium deficit of mmol and mmol, respectively. If the fluid losses remain uncorrected, reduced renal blood flow consequent on reduced blood volume threatens renal function.
This in turn reduces renal excretion of glucose, thereby exacerbating hyperglycemia and all its deleterious consequences. In extreme cases, patients may present in acute renal failure. In summary, hyperglycemia in DKA causes an osmotic diuresis, which results in severe fluid and electrolyte deficit. FIG 2. Osmotic diuresis in DKA causes polyuria, glycosuria and electrolyte depletion.
These metabolic changes are an extension of the normal physiological response to starvation, when glucose is also in short supply, in this case not because of insulin deficiency, but because dietary carbohydrate, from which glucose is derived, is restricted. When glucose is in short supply, an alternative energy source is provided for in stored fat, and it is this switch to fat metabolism which lies at the root of the disturbance of acid-base balance in patients with DKA.
Fat is stored as triglycerides in adipocytes, the specialized cells of which adipose fat tissue is composed. The mobilization of fat as an alternative energy source begins with the breakdown lipolysis of triglycerides to its constituent free fatty acids and glycerol by the hormone-sensitive enzyme, lipase.
Insulin inhibits lipolysis, whilst the counterregulatory hormones promote lipolysis. In patients with DKA, therefore, lipolysis and the resulting production of free fatty acids proceed relatively unhindered. Free fatty acids are transported, bound to albumin, from adipocytes to tissues around the body where they are oxidized in cell mitochondria to acetyl CoA, providing much needed energy in the form of adenosine triphosphate ATP in the process.
Acetyl CoA is further metabolized to carbon dioxide and water in the citric acid cycle, yielding more energy-rich ATP. The liver provides an alternative fate for acetyl CoA if, as is the case in severe insulin deficiency, its production exceeds the metabolic capacity of the citric acid cycle. In this case, the liver converts some of the acetyl CoA derived from oxidation of fatty acids to the ketoacid, acetoacetic acid. As a type of hyperventilation, some people describe Kussmaul breathing as panicked breathing, where someone appears to be gasping for breath.
The deep, powerful breathing associated with Kussmaul breathing often causes inhalation and exhalation to become more evident and loud. Before the deep and labored patterns of Kussmaul breathing kicks in, those with metabolic acidosis typically have rapid and shallow breathing patterns. As acidosis progresses and becomes severe, Kussmaul breathing takes over. While the signs of Kussmaul breathing are obvious, the symptoms associated with metabolic acidosis, in general, are less evident.
Severe acidosis can cause organ failure, coma , and eventually death. It anyone suspects they may have Kussmaul breathing or acidosis, they must seek immediate medical attention. Though diabetes is a primary cause of the condition, anything that causes an acidic blood pH can result in Kussmaul breathing.
Known causes include:. When the body fails to produce enough insulin , is not processing enough glucose, and becomes extremely dehydrated, it begins to enter into survival mode, relying on fats, rather than carbohydrates , for fuel.
When fats are broken down, they release ketones that accumulate and raise blood acidity. Ketoacidosis is a serious condition most often associated with uncontrolled, or newly diagnosed diabetes.
Starvation, alcoholism , and extremely poor nutrition , however, can also cause ketoacidosis. Obesity and diets high in fats and extremely low in other nutrients, especially carbohydrates, may be a risk factor for ketoacidosis.
A range of factors can cause tissues to become oxygen starved and lactic acid to buildup in the blood. Conditions such as infection, diarrhea , bowel disorders, and chronic malnutrition can lead to a loss or lack of the chemical compounds that bind to and help manage hydrogen ions.
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