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Pco2 In Dka

Vbg Versus Abg

Vbg Versus Abg

OVERVIEW Venous blood gases (VBG) are widely used in the emergency setting in preference to arterial blood gases (ABG) as a result of research published since 2001 The weight of data suggests that venous pH has sufficient agreement with arterial pH for it to be an acceptable alternative in clinical practice for most patients Nevertheless acceptance of this strategy has been limited by some specialties and maybe inappropriate in some settings; for instance there is no data to confirm that this level of agreement is maintained in shock states or mixed acid-base disturbances Clinically acceptable limits of agreement for blood gas parameters remains poorly defined ARTERIAL BLOOD GAS PROS AND CONS Advantages gold standard test for determining the arterial metabolic millieu (pH, PaCO2, HCO3) can determine PaO2 Disadvantages pH, PCO2 (if normocapnic), HCO3 and base excess from a VBG are usually adequate for clinical decision making SpO2 is usually sufficient for clinical decision making unless pulse oximetry is unreliable for other reasons (e.g. shock state, poor pick up) painful (should be performed with local anaesthetic in conscious patients) increased risk of bleeding and hematoma risk of pseudo aneurysm and AV fistula infection nerve injury digital ischemia injury to staff delays in care serial exams may be needed venous sampling may better represent the tissue milieu CORRELATION BETWEEN VBG AND ABG pH Good correlation pooled mean difference: +0.035 pH units pCO2 good correlation in normocapnia non-correlative in severe shock 100% sensitive in detecting arterial hypercarbia in COPD exacerbations using cutoff of PaCO2 45 mmHg and laboratory based testing (McCanny et al, 2012), i.e. if VBG PCO2 is normal then hypercapnia ruled out (PaCO2 will be normal), though this conflic Continue reading >>

Management Of Diabetic Ketoacidosis In Extreme Insulin Resistance

Management Of Diabetic Ketoacidosis In Extreme Insulin Resistance

Abstract: Background: Management of diabetic ketoacidosis (DKA) in extreme insulin resistance (IR) is not well-described in the literature. Clinical case: The patient is an 18-year old young man with extreme IR due to Rabson-Mendenhall Syndrome (mutation of the insulin receptor). Two weeks prior to a routine visit at the National Institutes of Health (NIH), he underwent a root canal for an abscessed tooth, and did not take prescribed antibiotics. At NIH, labs showed A1c 14%, bicarbonate 26-30, and chronic glucosuria and ketonuria. He continued his home insulin regimen of 1500 units/day of U-500. Antibiotics were initiated; he was discharged in hemodynamically stable condition. Two days later, he was admitted to another hospital with DKA, pH 7.08, pCO2 27, bicarbonate 8, and worsened jaw pain. Insulin drip was started at 100 U/hr, increased on day 1 to 1000 U/hr, and 2000 U/hr on day 2 without resolution of acidosis. CT showed a dental abscess extending to adjacent soft tissue, the likely trigger for DKA. Due to lack of improvement despite IV antibiotics, bicarbonate was given, and dental extraction was performed, after which the patient developed septic shock requiring pressor support for 24 hrs. He improved thereafter, and was transitioned back to subcutaneous insulin. Conclusion: This case demonstrates the complexity of managing DKA in a patient with extreme IR. Routine diabetes care in extreme IR requires high-dose insulin, typically >200 U/day. Despite high-dose insulin, good glycemic control is often not achieved. DKA management in extreme IR is a major challenge due to the unusually high doses of insulin required, raising major safety concerns for providers not experienced with extreme IR. As seen in this case, insulin as high as 2000 U/hr can be safely administer Continue reading >>

Cerebral Edema In Children With Diabetic Ketoacidosis

Cerebral Edema In Children With Diabetic Ketoacidosis

Abstract Cerebral edema is the most frequent serious complication of diabetic ketoacidosis (DKA) in children, occurring in 1% to 5% of DKA episodes. The rates of mortality and permanent neurologic morbidity from this complication are high. The pathophysiologic mechanisms underlying DKA-related cerebral edema are unclear. A number of past and more recent studies have investigated biochemical and therapeutic risk factors for the development of cerebral edema. Recent studies have shown that a higher initial serum urea nitrogen concentration and lower initial partial pressure of carbon dioxide are associated with the development of cerebral edema. This and other information suggests that the pathophysiology of DKA-related cerebral edema may involve cerebral ischemia. Preview Unable to display preview. Download preview PDF. Continue reading >>

Beta-hydroxybutirate Levels As A Determinant For The Success Of Diabetic Ketoacidosis Management.

Beta-hydroxybutirate Levels As A Determinant For The Success Of Diabetic Ketoacidosis Management.

Abstract AIM: To obtain a greater understanding of the diagnosis and evaluation of success in diabetic ketoacidosis management. METHODS: A prospective observational study was performed on patients with diabetic ketoacidosis at the Emergency Unit of Cipto Mangunkusumo General Hospital. All patients that were admitted were had their blood glucose, beta-hydroxybutirate, acetoacetate, pH, pCO2, HCO3, anion gap and consciousness levels serially monitored on upon admittance (0 hour) and the 2nd, 6th, 12th, 18th and 24(th) hours. The correlation coefficient of each examination was also calculated. The benefit of serial examination of each variable was also determined for each ketoacidosis undergoing the study. RESULTS: Out of the 19 available samples, a strong negative correlation was found between beta-hydroxybutirate and pH with a value of r>0.5 (from -0.524 to -0.833 with p<0.05) for 24 hours, compared to acetoacetate with the lowest r of -0.515 to -0.731 lasting up to 12 hours. Blood glucose and pH is correlated only at 0 hour, the same with the correlation between beta-hydroxybutirate and HCO(3). pCO2 and anion gap is better compared to that of blood glucose and acetoacetate. There is no correlation between the three and the level of consciousness. Significant serial examinations to perform are blood glucose, beta-hydroxybutirate, and HCO(3). CONCLUSION: beta-Hydroxybutirate has a stronger correlation compared to blood glucose and or acetoacetate towards pH, pCO2, HCO(3), and anion gap. Patients with ketoacidosis are recommended to undergo blood beta-hydroxybutirate examination. Serial examination should be performed for blood glucose, beta-hydroxybutirate, and bicarbonate. Continue reading >>

Diabetic Ketoacidosis

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 >>

Alternative Management Of Diabetic Ketoacidosis In A Brazilian Pediatric Emergency Department

Alternative Management Of Diabetic Ketoacidosis In A Brazilian Pediatric Emergency Department

Go to: DKA is a severe metabolic derangement characterized by dehydration, loss of electrolytes, hyperglycemia, hyperketonemia, acidosis and progressive loss of consciousness that results from severe insulin deficiency combined with the effects of increased levels of counterregulatory hormones (catecholamines, glucagon, cortisol, growth hormone). The biochemical criteria for diagnosis are: blood glucose > 200 mg/dl, venous pH <7.3 or bicarbonate <15 mEq/L, ketonemia >3 mmol/L and presence of ketonuria. A patient with DKA must be managed in an emergency ward by an experienced staff or in an intensive care unit (ICU), in order to provide an intensive monitoring of the vital and neurological signs, and of the patient's clinical and biochemical response to treatment. DKA treatment guidelines include: restoration of circulating volume and electrolyte replacement; correction of insulin deficiency aiming at the resolution of metabolic acidosis and ketosis; reduction of risk of cerebral edema; avoidance of other complications of therapy (hypoglycemia, hypokalemia, hyperkalemia, hyperchloremic acidosis); identification and treatment of precipitating events. In Brazil, there are few pediatric ICU beds in public hospitals, so an alternative protocol was designed to abbreviate the time on intravenous infusion lines in order to facilitate DKA management in general emergency wards. The main differences between this protocol and the international guidelines are: intravenous fluid will be stopped when oral fluids are well tolerated and total deficit will be replaced orally; if potassium analysis still indicate need for replacement, it will be given orally; subcutaneous rapid-acting insulin analog is administered at 0.15 U/kg dose every 2-3 hours until resolution of metabolic acidosis; Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Is A Vbg Just As Good As An Abg?

Is A Vbg Just As Good As An Abg?

Faculty Peer Reviewed A rapid response is called overhead. As white-coated residents rush to the patient’s bedside, the medical consult starts to shout out orders to organize the chaos. “What’s the one-liner?” “Whose patient is this?” And of course, “Who’s drawing the labs?” Usually, at this point, the intern proceeds to collect the butterfly needle, assorted colored tubes, and the arterial blood gas (ABG) syringe. If lucky, there’s a strong pulse. The intern pauses, directs the needle, and hopes for that pulsatile jet of bright red blood to come through the clear tubing. If successful, a sigh of relief. If not, a wave of defeat and more butterfly needles are scattered across the bed as multiple residents attempt to get the elusive arterial blood. Obtaining the ABG is considered almost a rite of passage for the medicine intern. However in ill patients with thready pulses, it can be difficult to obtain. Also, getting the ABG is not without its complications. Significant pain, hematoma, aneurysm formation, thrombosis or embolization, and needlestick injuries are all risks [1]. Given these risks, the question is whether we are subjecting our patients to undue pain and potential complications when a venous blood gas (VBG) would suffice. An ABG provides important data including the pH, arterial oxygen tension (PaO2), carbon dioxide tension (PaCO2), arterial oxyhemoglobin saturation (SaO2), lactate, and electrolytes. In certain instances, an ABG is considered unequivocal. In order to calculate an A-a gradient, the ABG is necessary. To assess whether that HIV patient with PCP pneumonia needs steroids, we use the A-a gradient to help guide out treatment plan [2]. However, are there other patient populations in which the VBG is just as good as the ABG? Brande Continue reading >>

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Introduction Recently there have been numerous publications and discussions about whether VBGs can replace ABGs in DKA. The growing consensus is that VBGs are indeed adequate. Eliminating painful, time-consuming arterial blood draws is a huge step in the right direction. However, the ABG vs. VBG debate overlooks a larger point: neither ABG nor VBG measurements are usually helpful. It is widely recommended to routinely obtain an ABG or VBG, for example by both American and British guidelines. Why? Is it helping our patients, or is it something that we do out of a sense of habit or obligation? Diagnosis of DKA: Blood gas doesn’t help These are the diagnostic criteria for DKA from the America Diabetes Association. They utilize either pH or bicarbonate in a redundant fashion to quantify the severity of acidosis. It is unclear what independent information the pH adds beyond what is provided by the bicarbonate. Practically speaking, the blood gas doesn’t help diagnose DKA. This diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level). The addition of a blood gas to serum chemistries only adds information about the respiratory status, which does not help determine if the patient has ketoacidosis. Management: Does the pH help? It is debatable whether knowing or attempting to directly “treat” the pH is helpful. The pH will often be very low, usually lower than would be expected by looking at the patient. This may induce panic. However, it is actually a useful reminder that acidemia itself doesn't necessarily cause instability (e.g. healthy young rowers may experience lactic acidosis with a pH <7 during athletic exertion; Volianitis 2001). A question often arises regarding whether bicarbonate Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

About Diabetic ketoacidosis must be managed with a defined well documented and communicated plan It is seen in new presentations and Type 1 diabetics with intercurrent illness and poor control Patients need education on not to stop insulin when unwell and to seek medical help There is a severe deficit of Fluid, Insulin and Potassium Aetiology Glucose and K+ usually enter cells through the actions of Insulin In DKA the Insulin deficit leads to cell starvation and a switch to burning fatty acids The beta-oxidation of fats creates acid byproducts which lower the pH At the same time there is a profound osmotic diuresis due to the severe hyperglycaemia Vomiting can compound the fluid losses Clinical Recent thirst, polyuria and polydipsia, vomiting and breathlessness Severe hyperventilating Kussmaul's respiration to blow off CO2 Smell of acetone "nail varnish" on the breath (not all of us can smell it) Profound dehydration and volume loss from polyuria due to glycosuria Sunken eyes, reduced skin turgor, hypotensive, tachycardia, oliguric Possibly sepsis - chest and urine or elsewhere Investigations Ketonuria 3+ and glycosuria and Raised [glucose] There is a low bicarbonate < 15 mmols/l FBC - elevated WCC and CRP may suggest infection U&E - may show mild uraemia and hypernatraemia. Initially raised K+ due to acidosis but potassium levels fall with Insulin administration as it oves into the intracellular space so U&E needs repeated monitoring Glucose - high usually > 20 mmol/L Arterial Blood gas There is an increased Anion gap CXR if chest disease eg pneumonia suspected CT scan if comatose to exclude other diagnoses Management In a nutshell is careful replacement of Insulin, Fluid, Potassium. Involve Endocrinology and ITU support early. Ensure treatment plans well documented. E Continue reading >>

Respiratory Failure In Diabetic Ketoacidosis

Respiratory Failure In Diabetic Ketoacidosis

Go to: INTRODUCTION Ketoacidosis in subjects with type 1, or less frequently, type 2 diabetes mellitus remains a potentially life-threatening diabetic manifestation. The subject has justifiably attracted attention in the literature. Sequential reviews[1-9] have documented important changes in the clinical concepts that are related to diabetic ketoacidosis (DKA) and its management. A large number of case series of DKA have addressed various aspects of its clinical presentation and management. For this review, we selected representative studies focused on management, outcome, age differences, gender differences, associated morbid conditions, ethnicity and prominent clinical and laboratory features[10-35]. In recognition of the complexity of treatment, the recommendation to provide this care in intensive care units was made more than 50 years ago[36]. Severe DKA is treated in intensive care units today[31]. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe[39]. Losses of fluids and electrolytes, which are important causes of morbidity and mortality in DKA, vary greatly between patients. Quantitative methods estimating individual losses and guiding their replacement have also been reported[40,41]. The outcomes of DKA have improved with new methods of insulin administration[42] and adherence to guidelines[43-46]. The aim of treatment is to minimize mortality and prevent sequelae. One study documented that the target of zero mortality is feasible[42]. However, mortality from DKA, although reduced progressively in the early decades after the employment of insulin treatment[1], remains high. Up to fifty plus years ago, mortality from DKA was between 3% and 10%[1,16]. A recent review re Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

Can Venous Blood Gases Replace Arterial Blood Gases In Diabetic Ketoacidosis/renal Failure Induced Metabolic Acidosis?

Can Venous Blood Gases Replace Arterial Blood Gases In Diabetic Ketoacidosis/renal Failure Induced Metabolic Acidosis?

Universal Journal of Medical Science Vol. 3(3), pp. 65 - 69 DOI: 10.13189/ujmsj.2015.030303 Reprint (PDF) (646Kb) Naveen Mohan *, Gireesh Kumar K. P , Sreekrishnan T. P , Ajith Kumar. J , Ajith. V , Bharath Prasad. S , Krupanidhi Karunanithi , Arun Kumar. K Amrita Institute of Medical Sciences & Research Centre, India ABSTRACT The study aims to identify the correlation between arterial and venous blood gas variables, in patients with metabolic acidosis secondary to renal failure and/or diabetic ketoacidosis(DKA). Paired arterial and venous blood samples of 100 patients, with metabolic acidosis resultant to renal failure and/or diabetic ketoacidosis during 2009-2011, were analyzed and the correlation between the variables were assessed using SPSS software, applying Pearson's product moment correlation coefficient, Linear regression, Statistical parameter R2 and Chi-square test. Results: Mean ABG values for pH, HCO3, pCO2 and lactate were (7.29 +/- 0.448, 12.12 +/- 2.61, 25.2 +/- 4.0 and 5.39 +/-1.95 respectively) and mean VBG values for the same were (7.292 +/- 0.0451, 12,23 +/- 2.55, 27.8 +/- 3.9, and 5.19 +/- 1.81). Pearson product moment coefficient for pH, HCO3, pCO2 and lactate were 0.919, 0.967, 0.966 and 0.924 , with p <0.001 . Percentage variation in ABG as explained by VBG for pH = 84.4%, HCO3 =93.6%, pCO2 = 93.2% and lactate = 85.4%. Regression equations to predict arterial from venous values:-Arterial pH = 0.631 +0.913 x venous pH (R2=0.844), Arterial HCO3 = 0.990 x venous HCO3 (R2=0.936), Arterial pCO2 = -2.546 + 0.997 x venous pCO2 (R2=0.932), Arterial lactate = 0.993 x venous lactate (R2=0.854). Arterial and venous blood gas values showed significant correlation coefficient for pH, HCO3, pCO2 and lactate. Hence, VBG may be used as an alternative to ABG in t Continue reading >>

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Abg (arterial Blood Gas)

Abg (arterial Blood Gas)

Arterial Blood Gas analysis typically measures: And may include: These measurements are often used to evaluate oxygenation of the tissues and pulmonary function. pH is a measurement of the acidity of the blood, reflecting the number of hydrogen ions present. Lower numbers mean more acidity; higher number mean more alkalinity. pH is Elevated (more alkaline, higher pH) with: Hyperventilation Anxiety, pain Anemia Shock Some degrees of Pulmonary disease Some degrees of Congestive heart failure Myocardial infarction Hypokalemia (decreased potassium) Gastric suctioning or vomiting Antacid administration Aspirin intoxication pH is Decreased (more acid, lower pH) with: Strenuous physical exercise Obesity Starvation Diarrhea Ventilatory failure More severe degrees of Pulmonary Disease More severe degrees of Congestive Heart Failure Pulmonary edema Cardiac arrest Renal failure Lactic acidosis Ketoacidosis in diabetes pCO2 (Partial Pressure of Carbon Dioxide) reflects the the amount of carbon dioxide gas dissolved in the blood. Indirectly, the pCO2 reflects the exchange of this gas through the lungs to the outside air. Two factors each have a significant impact on the pCO2. The first is how rapidly and deeply the individual is breathing: Someone who is hyperventilating will "blow off" more CO2, leading to lower pCO2 levels Someone who is holding their breath will retain CO2, leading to increased pCO2 levels The second is the lungs capacity for freely exchanging CO2 across the alveolar membrane: With pulmonary edema, there is an extra layer of fluid in the alveoli that interferes with the lungs' ability to get rid of CO2. This leads to a rise in pCO2. With an acute asthmatic attack, even though the alveoli are functioning normally, there may be enough upper and middle airway obstru Continue reading >>

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