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Dka Lab Values Co2

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Tips From Other Journals

Diabetic ketoacidosis consists of elevated blood glucose, measurable ketone bodies and metabolic acidosis. Arterial blood gas determination is considered essential in the initial evaluation of patients with suspected diabetic ketoacidosis. Arterial blood sampling is painful, may be technically difficult and must be done in addition to venous sampling when testing for electrolytes and other values. The general correlation between arterial and venous pH measurements is well established, although this correlation has not been studied in patients with diabetic ketoacidosis. Brandenburg and Dire prospectively studied the relationship between arterial and venous blood gas values in the initial evaluation of patients with suspected diabetic ketoacidosis. Thirty-eight patients with 44 episodes of diabetic ketoacidosis who presented to an emergency department with blood glucose levels greater than 250 mg per dL (13.9 mmol per L), urine dipstick results positive for ketones and clinical suspicion of diabetic ketoacidosis were included in the study. Arterial and venous samples were obtained as temporally close to each other as possible for blood gas analysis. The mean difference between arterial and venous pH values was 0.03 (range: 0 to 0.11). Arterial and venous pH results, arterial and venous bicarbonate measurements and arterial bicarbonate and serum carbon dioxide results were also closely correlated. The authors conclude that the peripheral venous pH measurement is a valid and reliable substitute for arterial pH in patients with diabetic ketoacidosis. A potential disadvantage of using venous determinations to determine the presence of diabetic ketoacidosis is that it may be more difficult to detect when mixed acid-base disturbances are present, since venous blood values may Continue reading >>

Common Laboratory (lab) Values - Abgs

Common Laboratory (lab) Values - Abgs

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z Laboratory VALUES Home Page Arterial Blood Gases Arterial blood gas analysis provides information on the following: 1] Oxygenation of blood through gas exchange in the lungs. 2] Carbon dioxide (CO2) elimination through respiration. 3] Acid-base balance or imbalance in extra-cellular fluid (ECF). Normal Blood Gases Arterial Venous pH 7.35 - 7.45 7.32 - 7.42 Not a gas, but a measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The pH of a solution is equal to the negative log of the hydrogen ion concentration in that solution: pH = - log [H+]. PaO2 80 to 100 mm Hg. 28 - 48 mm Hg The partial pressure of oxygen that is dissolved in arterial blood. New Born – Acceptable range 40-70 mm Hg. Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg level for every year over 60 years of age: 80 - (age- 60) (Note: up to age 90) HCO3 22 to 26 mEq/liter (21–28 mEq/L) 19 to 25 mEq/liter The calculated value of the amount of bicarbonate in the bloodstream. Not a blood gas but the anion of carbonic acid. PaCO2 35-45 mm Hg 38-52 mm Hg The amount of carbon dioxide dissolved in arterial blood. Measured. Partial pressure of arterial CO2. (Note: Large A= alveolor CO2). CO2 is called a “volatile acid” because it can combine reversibly with H2O to yield a strongly acidic H+ ion and a weak basic bicarbonate ion (HCO3 -) according to the following equation: CO2 + H2O <--- --> H+ + HCO3 B.E. –2 to +2 mEq/liter Other sources: normal reference range is between -5 to +3. The base excess indicates the amount of excess or insufficient level of bicarbonate in the system. (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess. A value outside of the normal r Continue reading >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co 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 >>

Co2 Blood Test

Co2 Blood Test

What is a CO2 blood test? A CO2 blood test measures the amount of carbon dioxide (CO2) in the blood serum, which is the liquid part of blood. A CO2 test may also be called: a carbon dioxide test a TCO2 test a total CO2 test bicarbonate test an HCO3 test a CO2 test-serum You may receive a CO2 test as a part of a metabolic panel. A metabolic panel is a group of tests that measures electrolytes and blood gases. The body contains two major forms of CO2: HCO3 (bicarbonate, the main form of CO2 in the body) PCO2 (carbon dioxide) Your doctor can use this test to determine if there’s an imbalance between the oxygen and carbon dioxide in your blood or a pH imbalance in your blood. These imbalances can be signs of a kidney, respiratory, or metabolic disorder. Blood gas test » Your doctor will order a CO2 blood test based on your symptoms. Signs of an imbalance of oxygen and carbon dioxide or a pH imbalance include: shortness of breath other breathing difficulties nausea vomiting These symptoms may point to lung dysfunction involving the exchange between oxygen and carbon dioxide. You will need to have your blood’s oxygen and carbon dioxide levels measured frequently if you’re on oxygen therapy or having certain surgeries. Blood samples for a CO2 blood test may be taken from either a vein or an artery. Venipuncture blood sample Venipuncture is the term used to describe a basic blood sample taken from a vein. Your doctor will order a simple venipuncture blood sample if they only want to measure HCO3. To get a venipuncture blood sample, a healthcare provider: cleans the site (often the inside of the elbow) with a germ-killing antiseptic wraps an elastic band around your upper arm to cause the vein to swell with blood gently inserts a needle into the vein and collect blood in 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 >>

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 >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). 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. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Base Excess

Base Excess

In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L, with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.[1] Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid-base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined, under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40. The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions. Definition[edit] Pathophysiology sample values BMP/ELECTROLYTES: Na+ = 140 Cl− = 100 BUN = 20 / Glu = 150 K+ = 4 CO2 = 22 PCr = 1.0 \ ARTERIAL BLOOD GAS: HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40 ALVEOLAR GAS: pACO2 = 36 pAO2 = 105 A-a g = 10 OTHER: Ca = 9.5 Mg2+ = 2.0 PO4 = 1 CK = 55 BE = −0.36 AG = 16 SERUM OSMOLARITY/RENAL: PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20 URINALYSIS: UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95 UK+ = 25 USG = 1.01 UCr = 60 UO = 800 PROTEIN/GI/LIVER FUNCTION TESTS: LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7 ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5 AST/ALT = 0.6 BU = 0.2 AF alb = 3.0 SAAG = 1.0 SOG = 60 CSF: CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4 Base excess Continue reading >>

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

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 >>

End-tidal Capnography Can Be Useful For Detecting Diabetic Ketoacidosis, Monitoring Copd

End-tidal Capnography Can Be Useful For Detecting Diabetic Ketoacidosis, Monitoring Copd

End-Tidal Capnography Can be Useful for Detecting Diabetic Ketoacidosis, Monitoring COPD by Katrina DAmore, DO, MPH, Justin McNamee, DO, and Terrance McGovern, DO, MPH End-tidal capnography has gained momentum over the years as a standard for monitoring patients undergoing procedural sedation in the emergency department, with a level B recommendation coming out of ACEPs clinical policy regarding procedural sedation in 2014.1 It can identify hypoventilation earlier than other monitoring tools we have at our disposal in the emergency department, but its utility doesnt end there. It can quickly and efficiently answer clinical questions beyond that of sufficient ventilation. Are the chest compressions being performed on your cardiac arrest inadequate? Should you stop resuscitation efforts? Is your hyperglycemic diabetic in diabetic ketoacidosis (DKA)? Is that nasogastric tube in the stomach? End-tidal capnography can lend insight to these questions that emergency physicians encounter on a daily basis. End-tidal carbon dioxide (EtCO2) sensibly correlates with the pathophysiology of those and many other disease processes and can help guide decision making on your next shift. Capnography offers an indirect method to detect metabolic acidosis. EtCO2 measurements have been shown to closely estimate arterial partial pressure of carbon dioxide (pCO2) in healthy patients and also in the presence of metabolic derangements such as acidosis. The end-tidal capnogram is separated into four separate phases (see Figure 1). Phase 0 begins during the inhalation phase of the respiratory cycle and the capnogram drops precipitously from its peak level at the end of expiration. Once the patient begins to exhale (phase I), the initial expired air is predominantly dead space with little expired Continue reading >>

How To Read A Venous Blood Gas (vbg) - Top 5 Tips

How To Read A Venous Blood Gas (vbg) - Top 5 Tips

Share on Facebook Share on Twitter Arterial blood gas analysers are designed to measure multiple components in the arterial blood. The readout from the machine quotes normal values based on the assumption that the sample analysed is arterial (an ABG). There is currently a plague of ‘venous’ blood gases (VBG) in clinical practice. A VBG is obtained by placing a venous sample in the arterial blood gas analyser. VBGs are popular as it is far less painful for the patient to obtain a venous sample compared to an arterial sample. In addition, obtaining ABGs carries well known risks. VBGs are useful if you know how to interpret them and have a knowledge of their limitations. An ABG has a number of uses, the VBG can be substituted for some of these uses but not for others. 1) Assessment of oxygenation status The pO2 on a VBG bears no relationship to the paO2. The VBG is of no value in assessing oxygenation status. 2) Assessment of hypercarbia In patients with COPD we need to detect the presence of CO2 retention. This has an important impact on treatment. If the pCO2 on the VBG is above the normal arterial range (ie >45 mmHg, >6 kPa) the patient has CO2 retention. (100% sensitivity reported, so, at least in studies, it does not appear to miss any cases) However, the absolute value of pCO2 on the VBG above this range correlates poorly with the paCO2 and cannot be used to monitor the response to treatment in a CO2 retainer. 3) Assessment of pH status This is probably where the VBG is of most use but there are still limitations. The venous pH correlates well with the arterial pH. The venous pH tends to be more acidic than the arterial pH. Add 0.035 to the venous pH to estimate the arterial pH. In conditions such as DKA, it is probably reasonable to follow the pH response to tre Continue reading >>

Abg’s—it’s All In The Family

Abg’s—it’s All In The Family

By Cyndi Cramer, BA, RN, OCN, PCRN RealNurseEd.com 3.0 Contact Hour Self Learning Module Objectives: Identify the components of the ABG and their normal ranges Interpret ABG values and determine the acid base abnormality given Identify the major causes of acid base abnormalities Describe symptoms associated with acid base abnormalities Describe interventions to correct acid base abnormalities Identify the acceptable O2 level per ABG and Pulse Oximetry Identify four causes of low PaO2 The Respiratory System (Acid); CO2 is a volatile acid If you increase your respiratory rate (hyperventilation) you "blow off" CO2 (acid) therefore decreasing your CO2 acid—giving you ALKLAOSIS If you decrease your respiratory rate (hypoventilation) you retain CO2 (acid) therefore increasing your CO2 (acid)—giving you ACIDOSIS The Renal System (Base); the kidneys rid the body of the nonvolatile acids H+ (hydrogen ions) and maintain a constant bicarb (HCO3). Bicarbonate is the body’s base You have Acidosis when you have excess H+ and decreased HCO3- causing a decrease in pH. The Kidneys try to adjust for this by excreting H+ and retaining HCO3- base. The Respiratory System will try to compensate by increasing ventilation to blow off CO2 (acid) and therefore decrease the Acidosis. You have Alkalosis when H+ decreases and you have excess (or increased) HCO3- base. The kidneys excrete HCO3- (base) and retain H+ to compensate. The respiratory system tries to compensate with hypoventilation to retain CO2 (acid) To decrease the alkalosis Compensation The respiratory system can effect a change in 15-30 minutes The renal system takes several hours to days to have an effect. RESPIRATORY ACIDOSIS: pH < 7.35 (Normal: 7.35 - 7.45) CO2 > 45 (Normal: 35 – 45) 1. Causes: Hypoventilation a. Depressio Continue reading >>

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