Metabolic Acidosis And Alkalosis
Page Index Metabolic Acidosis. Metabolic Alkalosis Emergency Therapy Treating Metabolic Acidosis Calculating the Dose Use Half the Calculated Dose Reasons to Limit the Bicarbonate Dose: Injected into Plasma Volume Fizzes with Acid Causes Respiratory Acidosis Raises Intracellular PCO2 Subsequent Residual Changes Metabolic Acidosis. The following is a brief summary. For additional information visit: E-Medicine (Christie Thomas) or Wikepedia Etiology: There are many causes of primary metabolic acidosis and they are commonly classified by the anion gap: Metabolic Acidosis with a Normal Anion Gap: Longstanding diarrhea (bicarbonate loss) Uretero-sigmoidostomy Pancreatic fistula Renal Tubular Acidosis Intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants Renal failure Metabolic Acidosis with an Elevated Anion Gap: lactic acidosis ketoacidosis chronic renal failure (accumulation of sulfates, phosphates, uric acid) intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene, sulfates, metformin. rhabdomyolysis For further details visit: E-Medicine (Christie Thomas). Treating Severe Metabolic Acidosis. The ideal treatment for metabolic acidosis is correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO2. If it is decided to administer bicarbonate, the SBE and the size of the treatable space are used to calculate the dose required: Metabolic Alkalosis Etiology: Primary Metabolic alkalosis may occur from various causes including: Loss of acid via the urine, stools, or vomiting Transfer of Continue reading >>
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Acidosis Vs. Alkalosis
In this lesson, we're going to learn about acidosis and alkalosis. We'll take a look at the causes, signs, and symptoms that are associated with each condition. Balanced Blood We are constantly having to find balance in our lives. From balancing work and play time to saving and spending money, sleep and awake time. Well, ideally at least. We do this because we know that we function best when we're balanced. There are many similar balances that are going on inside of our bodies. An important balance that must be maintained to allow us to function properly is the balance between acids and bases in our bodies. When these are balanced, the acids pair up with the bases, and our blood is close to neutral. If too much acid is in the blood, then we experience acidosis. If too much base is in the blood, we experience alkalosis. Acidosis and alkalosis are caused by different conditions in our bodies, and they can cause different problems to occur. Acidosis Acidosis results from the build-up of acids in the blood or from the loss of base in the blood. Acids are put into our bloodstream through two systems in the body: the digestive system and the respiratory system. Acidosis that occurs from the digestive system is referred to as metabolic acidosis. In this instance, acids accumulate in the blood due to consumption of acidic foods or foods that are broken down into acids, excess acids being produced during metabolism, kidneys not properly removing acid from the bloodstream during filtration, or production of acid by the body due to other medical conditions, such as diabetes. The other possible way to develop acidosis is by the malfunctioning of the respiratory system, which we refer to as respiratory acidosis. This can happen if breathing is extremely slow or shallow, the lungs do Continue reading >>
Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Buffering and the Henderson-Hasselbalch Equation By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with arterial blood gas and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate (HCO3) accumulation due to Intracellular shift of hydrogen ion (H+as occurs in hypokalemia ) Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. The most common causes of metabolic alkalosis are Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) Among other causes (see Table: Causes of Metabolic Alkalosis ) are disorders that cause Continue reading >>
Unraveling Metabolic Alkalosis: A Complex Case History
Metabolic alkalosis, a disturbance of acid-base homeostasis, with many possible causes, is characterized by a primary increase in blood pH and bicarbonate (HCO3). Hypoventilation is the compensatory respiratory response to metabolic alkalosis that results in increased pCO2. The often complex nature of the etiology of metabolic alkalosis is nicely conveyed by a recently published case study report of severe metabolic alkalosis. This concerns a 64-year-old man who was brought to the emergency department of his local hospital by his sister after a 3-week history of worsening confusion, difficulty walking, lack of food intake, and vomiting. The patient has a long-term history of alcohol abuse, post-traumatic stress disorder, and gastroesophageal reflux disease. His sister reported that he had become more withdrawn over the past few weeks during which time his diet comprised only Pepsi and alcohol. Initial assessment revealed: acute kidney injury (serum creatinine 9.28 mg/dL (820 mmol/L) but within normal range a few months previously); hypokalemia (potassium 3.0 mmol/L); hypocalcemia (ionized calcium 0.75 mmol/L); severe hypochloremia (chloride 59 mmol/L). Blood gas results (pH 7.64, HCO3 62 mmol/L, pCO2 58 mmHg (7.7 kPa)) confirmed partially compensated severe metabolic alkalosis. This was complicated by a superimposed high-anion-gap metabolic acidosis secondary to acute renal failure and lactic acidosis. Much of this case study report is taken over to a helpful general discussion of the mechanisms that give rise to metabolic alkalosis and the diagnoses to be considered in assessing the patient who presents with metabolic alkalosis. The authors explain how this knowledge was applied in the assessment and care of their patient. In this case, hypovolemia, secondary to vomiti Continue reading >>
Simple Method Of Acid Base Balance Interpretation
A FOUR STEP METHOD FOR INTERPRETATION OF ABGS Usefulness This method is simple, easy and can be used for the majority of ABGs. It only addresses acid-base balance and considers just 3 values. pH, PaCO2 HCO3- Step 1. Use pH to determine Acidosis or Alkalosis. ph < 7.35 7.35-7.45 > 7.45 Acidosis Normal or Compensated Alkalosis Step 2. Use PaCO2 to determine respiratory effect. PaCO2 < 35 35 -45 > 45 Tends toward alkalosis Causes high pH Neutralizes low pH Normal or Compensated Tends toward acidosis Causes low pH Neutralizes high pH Step 3. Assume metabolic cause when respiratory is ruled out. You'll be right most of the time if you remember this simple table: High pH Low pH Alkalosis Acidosis High PaCO2 Low PaCO2 High PaCO2 Low PaCO2 Metabolic Respiratory Respiratory Metabolic If PaCO2 is abnormal and pH is normal, it indicates compensation. pH > 7.4 would be a compensated alkalosis. pH < 7.4 would be a compensated acidosis. These steps will make more sense if we apply them to actual ABG values. Click here to interpret some ABG values using these steps. You may want to refer back to these steps (click on "linked" steps or use "BACK" button on your browser) or print out this page for reference. Step 4. Use HC03 to verify metabolic effect Normal HCO3- is 22-26 Please note: Remember, the first three steps apply to the majority of cases, but do not take into account: the possibility of complete compensation, but those cases are usually less serious, and instances of combined respiratory and metabolic imbalance, but those cases are pretty rare. "Combined" disturbance means HCO3- alters the pH in the same direction as the PaCO2. High PaCO2 and low HCO3- (acidosis) or Low PaCO2 and high HCO3- (alkalosis). Continue reading >>
Acid Base Disorders
Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese Continue reading >>
Metabolic Alkalosis
Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. Terminology[edit] Alkalosis refers to a process by which the pH is increased. Alkalemia refers to a pH which is higher than normal, specifically in the blood. Causes[edit] The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels.[1] Chloride-responsive (Urine chloride < 10 mEq/L)[edit] Loss of hydrogen ions - Most often occurs via two mechanisms, either vomiting or via the kidney. Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. In the hospital setting this can commonly occur from nasogastric suction tubes. Severe vomiting also causes loss of potassium (hypokalaemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis.[2] Congenital chloride diarrhea - rare for being a diarrhea that causes alkalosis instead of acidosis.[3] Contraction alkalosis - This results from a loss of water in the extracellular space, such as from dehydration. Decreased extracellular volume triggers the renin-angiotensin-aldosterone system, and aldosterone subsequently stimulates reabsorption of sodium (and thus water) within the nephron of the kidney. However, a second action of aldosterone is to stimulate renal excretion of hydrogen ions (while retaining bicarbonate), and it is this loss of hydrogen ions that raises Continue reading >>
Acidosis And Alkalosis | Harrison's Principles Of Internal Medicine, 19e | Accessmedicine | Mcgraw-hill Medical
Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory system and the control of plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent derangements of neural respiratory control or are due to compensatory changes in response to a primary alteration in the plasma [HCO3]. DIAGNOSIS OF GENERAL TYPES OF DISTURBANCES The most common clinical disturbances are simple acid-base disorders; i.e., metabolic acidosis or alkalosis or respiratory acidosis or alkalosis. Primary respiratory disturbances (primary changes in Paco2) invoke compensatory metabolic responses (secondary changes in [HCO3]), and primary metabolic disturbances elicit predictable compensatory respiratory responses (secondary changes in Paco2). Physiologic compensation can be predicted from the relationships displayed in Table 66-1 . In general, with one exception, compensatory res Continue reading >>
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[acid-base Homeostasis: Metabolic Acidosis And Metabolic Alkalosis].
Nephrol Ther. 2014 Jul;10(4):246-57. doi: 10.1016/j.nephro.2014.05.004. Epub 2014 Jun 30. [Acid-base homeostasis: metabolic acidosis and metabolic alkalosis]. Centre de nphrologie et de transplantation rnale, hpital de la Conception, 147, boulevard Baille, 13385 Marseille cedex 05, France. Electronic address: [email protected]. Acid-base homeostasis ensured by the kidneys, which maintain the equilibrium between proton generation by cellular metabolism and proton excretion in urine. This requirement is lifesaving because of the protons' ability to bind to anionic proteins in the extracellular space, modifying their structure and functions. The kidneys also regenerate bicarbonates. The kidney is not the sole organ in charge of maintaining blood pH in a very narrow range; lungs are also involved since they allow a large amount of volatile acid generated by cellular respiration to be eliminated. Acid-base homeostasis; Acidit titrable; Acidose mtabolique; Alcalose mtabolique; Ammonium; Bicarbonate; Buffers; Ions ammoniums; Metabolic acidosis; Metabolic alkalosis; Proton; Protons; Tampons; Titratable acid; quilibre acide-base Continue reading >>
Alkalosis
The kidneys and lungs maintain the proper balance (proper pH level) of chemicals called acids and bases in the body. Decreased carbon dioxide (an acid) level or increased bicarbonate (a base) level makes the body too alkaline, a condition called alkalosis. There are different types of alkalosis. These are described below. Respiratory alkalosis is caused by a low carbon dioxide level in the blood. This can be due to: Fever Being at a high altitude Lack of oxygen Liver disease Metabolic alkalosis is caused by too much bicarbonate in the blood. It can also occur due to certain kidney diseases. Hypochloremic alkalosis is caused by an extreme lack or loss of chloride, such as from prolonged vomiting. Hypokalemic alkalosis is caused by the kidneys' response to an extreme lack or loss of potassium. This can occur from taking certain water pills (diuretics). Compensated alkalosis occurs when the body returns the acid-base balance to normal in cases of alkalosis, but bicarbonate and carbon dioxide levels remain abnormal. Continue reading >>
Abg: Respiratory Acidosis/metabolic Alkalosis
Home / ABA Keyword Categories / A / ABG: Respiratory acidosis/metabolic alkalosis ABG: Respiratory acidosis/metabolic alkalosis A combined respiratory acidosis / metabolic alkalosis will result in elevated PaCO2 and serum bicarbonate. Which process is the primary disorder (e.g. primary respiratory acidosis with metabolic compensation versus primary metabolic alkalosis with respiratory compensation) is dependent on the pH in an acidotic patient, the acidosis is primary (and the alkalosis is compensatory) and vice versa. Compensation behaves in accordance with the following rules: Metabolic Acidosis: As bicarbonate goes from 10 to 5, pCO2 will bottom out at 15. pCO2 = 1.5 x [HCO3-] + 8 (or pCO2 = 1.25 x [HCO3-]) Metabolic Alkalosis: compensation here is less because CO2 is driving force for respiration. pCO2 = 0.7 x [HCO3-] + 21 (or pCO2 = 0.75 x [HCO3-]) Acutely: [HCO3-] = 0.1 x pCO2 or pH = 0.008 x pCO2 Chronically: [HCO3-] = 0.4 x pCO2 or pH = 0.003 x pCO2 Respiratory Alkalosis: Metabolic compensation will automatically be retention of chloride (i.e., hyperchloremic, usually referred to as loss of bicarb although it is the strong ion difference that matters). If you have an anion gap, then youve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process. Acutely: [HCO3-] = 0.2 x pCO2 (or pH = 0.008 x pCO2) Chronically: [HCO3-] = 0.4 x pCO2 (or pH = 0.017 x pCO2) Continue reading >>
Alkalosis
Your blood is made up of acids and bases. The amount of acids and bases in your blood can be measured on a pH scale. It’s important to maintain the correct balance between acids and bases. Even a slight change can cause health problems. Normally, your blood should have a slightly higher amount of bases than acids. Alkalosis occurs when your body has too many bases. It can occur due to decreased blood levels of carbon dioxide, which is an acid. It can also occur due to increased blood levels of bicarbonate, which is a base. This condition may also be related to other underlying health issues such as low potassium, or hypokalemia. The earlier it’s detected and treated, the better the outcome is. Acid-base balance » There are five main types of alkalosis. Respiratory alkalosis Respiratory alkalosis occurs when there isn’t enough carbon dioxide in your bloodstream. It’s often caused by: hyperventilation, which commonly occurs with anxiety high fever lack of oxygen salicylate poisoning being in high altitudes Metabolic alkalosis Metabolic alkalosis develops when your body loses too much acid or gains too much base. This can be attributed to: excess vomiting, which causes electrolyte loss overuse of diuretics a large loss of potassium or sodium in a short amount of time antacids accidental ingestion of bicarbonate, which can be found in baking soda laxatives alcohol abuse Hypochloremic alkalosis Hypochloremic alkalosis occurs when there’s a significant decline of chloride in your body. This can be due to prolonged vomiting or sweating. Chloride is an important chemical needed to maintain balance in bodily fluids, and it’s an essential part of your body’s digestive fluids. Hypokalemic alkalosis Hypokalemic alkalosis occurs when your body lacks the normal amount Continue reading >>
Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3) that typically produce abnormal arterial pH values. Acidosis refers to physiologic processes that cause acid accumulation or alkali loss. Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss. Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present. Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO3 or in Pco2. Metabolic acidosis is serum HCO3< 24 mEq/L. Causes are Metabolic alkalosis is serum HCO3> 24 mEq/L. Causes are Respiratory acidosis is Pco2> 40 mm Hg (hypercapnia). Cause is Decrease in minute ventilation (hypoventilation) Respiratory alkalosis is Pco2< 40 mm Hg (hypocapnia). Cause is Increase in minute ventilation (hyperventilation) Compensatory mechanisms begin to correct the pH (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders ) whenever an acid-base disorder is present. Compensation cannot return pH completely to normal and never overshoots. A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response. Mixed acid-base disorders comprise 2 primary disturbances. Compensatory mechanisms for acid-base disturbances cannot return pH completely to normal and never overshoot. Primary Changes and Compensations in Simple Acid-Base Disorders 1.2 mm Hg decrease in Pco2 for every 1 mmol/L decrease in HC Continue reading >>
Metabolic Alkalosis: Practice Essentials, Pathophysiology, Etiology
Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Metabolic alkalosis is a primary increase in serum bicarbonate (HCO3-) concentration. This occurs as a consequence of a loss of H+ from the body or a gain in HCO3-. In its pure form, it manifests as alkalemia (pH >7.40). As a compensatory mechanism, metabolic alkalosis leads to alveolar hypoventilation with a rise in arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that would otherwise occur. Normally, arterial PaCO2 increases by 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration, a compensatory response that is very quick. If the change in PaCO2 is not within this range, then a mixed acid-base disturbance occurs. For example, if the increase in PaCO2 is more than 0.7 times the increase in bicarbonate, then metabolic alkalosis coexists with primary respiratory acidosis. Likewise, if the increase in PaCO2 is less than the expected change, then a primary respiratory alkalosis is also present. The first clue to metabolic alkalosis is often an elevated bicarbonate concentration that is observed when serum electrolyte measurements are obtained. Remember that an elevated serum bicarbonate concentration may also be observed as a compensatory response to primary respiratory acidosis. However, a bicarbonate concentration greater than 35 mEq/L is almost always caused by metabolic alkalosis. Metabolic alkalosis is diagnosed by measuring serum electrolytes and arterial blood gases . If the etiology of metabolic alkalosis is not clear from the clinical history and physical examination, including drug use and the presence of hypertension, then a urine chloride ion concentration can be obtained. Calculation of the serum anion gap may al Continue reading >>
Disorders Of Acid-base Balance
Module 10: Fluid, Electrolyte, and Acid-Base Balance By the end of this section, you will be able to: Identify the three blood variables considered when making a diagnosis of acidosis or alkalosis Identify the source of compensation for blood pH problems of a respiratory origin Identify the source of compensation for blood pH problems of a metabolic/renal origin Normal arterial blood pH is restricted to a very narrow range of 7.35 to 7.45. A person who has a blood pH below 7.35 is considered to be in acidosis (actually, physiological acidosis, because blood is not truly acidic until its pH drops below 7), and a continuous blood pH below 7.0 can be fatal. Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued. A person who has a blood pH above 7.45 is considered to be in alkalosis, and a pH above 7.8 is fatal. Some symptoms of alkalosis include cognitive impairment (which can progress to unconsciousness), tingling or numbness in the extremities, muscle twitching and spasm, and nausea and vomiting. Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders. As discussed earlier in this chapter, the concentration of carbonic acid in the blood is dependent on the level of CO2 in the body and the amount of CO2 gas exhaled through the lungs. Thus, the respiratory contribution to acid-base balance is usually discussed in terms of CO2 (rather than of carbonic acid). Remember that a molecule of carbonic acid is lost for every molecule of CO2 exhaled, and a molecule of carbonic acid is formed for every molecule of CO2 retained. Figure 1. Symptoms of acidosis affect several organ systems. Both acidosis and alkalosis can be diagnosed using a blood test. Metabolic Acidosis: Primary Bic Continue reading >>
