The acidosis with elevated PCO2, hypoxemia and normal bicarbonate suggests an acute respiratory acidosis of rapid onset probably due to drug intoxication.

A 24-year-old woman is found lying in the street by passers-by. On arrival of the emergency team she was found with an oxygen saturation of 88% breathing room air and on examination with pinpoint pupils. She was transferred to the emergency room of the nearest hospital, where the baseline arterial blood gases showed: pH 7.25, PaC02 60 mmHg, Pa02 58 mmHg, bicarbonate 26 mEq/1 and base excess of -1. In blood sodium was 137 mEq/1 and chloride 100 mEq/1:

Respiratory alkalosis due to lack of chloride.

Arterial blood gas test

Respiratory alkalosis (Pa CO2 < 35 mmHg) occurs when there is too little carbon dioxide in the blood. This may be due to hyperventilation or else excessive breaths given via a mechanical ventilator in a critical care setting. The action to be taken is to calm the person and try to reduce the number of breaths being taken to normalize the pH. The respiratory pathway tries to compensate for the change in pH in a matter of 2–4 hours. If this is not enough, the metabolic pathway takes place. Under normal conditions, the Henderson–Hasselbalch equation will give the blood pH where: 6.1 is the acid dissociation constant (pKa) of carbonic acid () at normal body temperature [] is the concentration of bicarbonate in the blood in mEq/L PaCO2 is the partial pressure of carbon dioxide in the arterial blood in mmHg

Can Venous Blood Gas Be Used as an Alternative to Arterial Blood Gas in Intubated Patients at Admission to the Emergency Department? A Retrospective Study.

Blood gas analysis plays an important role in both diagnosis and subsequent treatment of critically ill patients in the emergency department and the ICU. Historically, arterial blood is predominantly used for blood gas analysis. The puncture is painful and complications may occur. The purpose of the present study was to evaluate the agreement between arterial and venous blood gas analysis and whether the sole use of venous blood gas analysis would have changed therapy. Adult patients who were intubated in the field and received an arterial and venous blood gas analysis within 15 mins after admission to the ED were eligible for inclusion. The values for pH, pCO<sub2</sub, HCO<sub3</sub-, base excess and lactate levels were collected retrospectively. Mean differences were calculated by subtracting venous from arterial values. The agreement between venous and arterial measurements was assessed using the method of Bland and Altman. Blood gases were assessed by two independent physicians using a standardized questionnaire to determine whether the use of venous blood gases would have led to a different interpretation of the situation (other diagnostic path) or a change of therapy (eg. respirator adjustment). Acceptable limits were defined before the collection of data started. Fifty patients (62% male, median age 63years) who were treated at the Emergency Department between June 1, 2014 and December 31, 2014 were included in the study. Following average differences and limits of agreement (LOA) were documented: pH 0.02312 with LOA from -0.048 to 0.094; pCO<sub2</sub -3.612 mmHg with LOA from -15 to 8.1 mmHg; BE -0.154 mmol/l with LOA from -3.7 to 3.4 mmol/l; HCO<sub3</sub-0.338 mmol/l with LOA from -2.27 to 2.9 mmol/l; Lactate -0.124 mg/dl with LOA from -2.28 to 2.03 mg/dl. Using venous blood gas results 100% of the patients with metabolic alkalosis were correctly diagnosed. Metabolic acidosis was detected with a high sensitivity (80.64%), specificity (89.47%) and positive predictive value (92.59%). The answers to lactate and acidosis due to AKI showed a specificity and positive predictive value of 100%. The respiratory adjustment showed a high sensitivity (91.89%) but a low specificity (38.46%). For pH, bicarbonate, BE and lactate venous blood gases can be used as surrogates for arterial measurements. Venous pCO<sub2</sub can be used for screening of hypercapnia and trending. Respirator adjustments may be done too often if the venous blood gas is used.

Respiratory acidosis

Diagnosis Diagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH <7.35 and a PaCO2 >45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH. Terminology Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36. See also Acidosis Alkalosis Arterial blood gas Chemical equilibrium pCO2 pH pKa Metabolic acidosis Metabolic alkalosis Respiratory alkalosis References External links Acid–base disturbances

Base excess

Interpretation Base excess beyond the reference range indicates metabolic alkalosis if too high (more than +2 mEq/L) metabolic acidosis if too low (less than −2 mEq/L) Blood pH is determined by both a metabolic component, measured by base excess, and a respiratory component, measured by PaCO2 (partial pressure of carbon dioxide). Often a disturbance in one triggers a partial compensation in the other. A secondary (compensatory) process can be readily identified because it opposes the observed deviation in blood pH. For example, inadequate ventilation, a respiratory problem, causes a buildup of CO2, hence respiratory acidosis; the kidneys then attempt to compensate for the low pH by raising blood bicarbonate. The kidneys only partially compensate, so the patient may still have a low blood pH, i.e. acidosis. In summary, the kidneys partially compensate for respiratory acidosis by raising blood bicarbonate.

Arterial blood gas test

In general, it is much easier to correct acute pH derangement by adjusting respiration. Metabolic compensations take place at a much later stage. However, in a critical setting, a person with a normal pH, a high CO2, and a high bicarbonate means that, although there is a high carbon dioxide level, there is metabolic compensation. As a result, one must be careful as to not artificially adjust breaths to lower the carbon dioxide. In such case, lowering the carbon dioxide abruptly means that the bicarbonate will be in excess and will cause a metabolic alkalosis. In such a case, carbon dioxide levels should be slowly diminished. See also Anion gap Radial artery puncture Chemical equilibrium Hemoximetry Arteriovenous oxygen difference References External links Online arterial blood gas calculator Diagnostic intensive care medicine Respiratory physiology Blood tests Respiratory therapy

PCO2

Medicine In medicine, the partial pressure of carbon dioxide in arterial blood is called or PaCO2. Measurement of in the systemic circulation indicates the effectiveness of ventilation at the lungs' alveoli, given the diffusing capacity of the gas. It is a good indicator of respiratory function and the closely related factor of acid–base homeostasis, reflecting the amount of acid in the blood (without lactic acid). Normal values for humans are in the range 35–45 mmHg. Values less than this may indicate hyperventilation and (if blood pH is greater than 7.45) respiratory alkalosis. Values greater than 45 mmHg may indicate hypoventilation, and (if blood pH is less than 7.35) respiratory acidosis. Aquatic Sciences

Arterial Blood Gas -- Results, Reporting, and Critical Findings

Example 1 [28] : ABG: pH = 7.39, PaCO 2 = 51 mm Hg, PaO 2 = 59 mm Hg, HCO 3 = 30 mEq/L and SaO 2 = 90%, on room air. pH is in the normal range, so use 7.40 as a cutoff point, in which case it is < 7.40, and acidosis is present. The elevated PaCO 2 indicates respiratory acidosis, and the elevated HCO 3 indicates a metabolic alkalosis. The value consistent with the pH is PaCO 2 . Therefore, this is a primary respiratory acidosis. The acid-base that is inconsistent with the pH is the elevated HCO3, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective. Last, the decreased PaO 2 indicates an abnormality with oxygenation. However, a history and physical will help delineate the severity and urgency of required interventions, if any. Example 2 [28] : ABG: pH = 7.45, PaCO 2 = 32 mm Hg, PaO 2 = 138 mm Hg, HCO 3 = 23 mEq/L, the base deficit = 1 mEq/L, and SaO 2 is 92%, on room air.

InternalMed_Harrison

The patient presented with a mixed acid-base disorder, with a significant metabolic alkalosis and a bicarbonate concentration of 44 meq/L. A venous blood gas was drawn soon after his presentation; venous and arterial blood gases demonstrate a high level of agreement in hemodynamically stable patients, allowing for the interpretation of acid-base disorders with venous blood gas results. In response to his metabolic alkalosis, the Pco2 should have increased by 0.75 mmHg for each 1-meq/L increase in bicarbonate; the expected Pco2 should have been ~55 mmHg. Given the Pco2 of 62 mmHg, he had an additional respiratory acidosis, likely caused by respiratory muscle weakness from his acute hypokalemia and subacute hypercortisolism.

Peripheral venous blood gases and pulse-oximetry in acute cardiogenic pulmonary oedema.

The role of venous blood gases as an alternative to arterial blood gases in patients with severe acute heart failure has not been established. To assess the correlation between arterial and peripheral venous blood gases together with pulse-oximetry (SpO2), as well as to estimate arterial values from venous samples in the first hours upon admission of patients with acute cardiogenic pulmonary oedema. Simultaneous venous and arterial blood samples were extracted on admission and over the next 1, 2, 3, 4, and 10 hours. SpO2 was also registered at the same intervals. A total of 178 pairs of samples were obtained from 34 consecutive patients with acute cardiogenic pulmonary oedema. Arterial and venous blood gases followed a parallel course in the first hours, showing high correlation rates at all time intervals. Venous samples underestimated pH (mean difference -0.028) and overestimated CO2 (+5.1 mmHg) and bicarbonate (+1 mEq/l). Conversely, SpO2 tended to underestimate SaO2 (mean±SD: 93.1±9.1 vs. 94.2±8.4). Applying simple mathematical formulae based on these differences, arterial values were empirically calculated from venous samples, showing acceptable agreement in the Bland-Altman test. Likewise, a venous pH <7.32, pCO2 >51.3 mmHg, and bicarbonate <22.8 mEq/l could fairly identify arterial acidosis, either respiratory or metabolic, with a test accuracy of 92, 68, and 91%, respectively. In patients with cardiogenic pulmonary oedema, arterial blood gas disturbances may be estimated from peripheral venous samples. By monitoring SpO2 simultaneously, arterial punctures could often be avoided.

Arterial blood gas test

Guidelines A 1 mmHg change in PaCO2 above or below 40 mmHg results in 0.008 unit change in pH in the opposite direction. The PaCO2 will decrease by about 1 mmHg for every 1 mEq/L reduction in [] below 24 mEq/L A change in [] of 10 mEq/L will result in a change in pH of approximately 0.15 pH units in the same direction. Assess relation of pCO2 with pH: If pCO2 & pH are moving in opposite directions i.e., pCO2 ↑ when pH is <7.4 or pCO2 ↓ when pH > 7.4, it is a primary respiratory disorder. If pCO2 & pH are moving in same direction i.e., pCO2 ↑when pH is >7.4 or pCO2 ↓ when pH < 7.4, it is a primary metabolic disorder. Parameters and reference ranges These are typical reference ranges, although various analysers and laboratories may employ different ranges.

Arterial blood gas test

The normal range for pH is 7.35–7.45. As the pH decreases (< 7.35), it implies acidosis, while if the pH increases (> 7.45) it implies alkalosis. In the context of arterial blood gases, the most common occurrence will be that of respiratory acidosis. Carbon dioxide is dissolved in the blood as carbonic acid, a weak acid; however, in large concentrations, it can affect the pH drastically. Whenever there is poor pulmonary ventilation, the carbon dioxide levels in the blood are expected to rise. This leads to a rise of carbonic acid, leading to a decrease in pH. The first buffer of pH will be the plasma proteins, since these can accept some H+ ions to try to maintain acid-base homeostasis. As carbon dioxide concentrations continue to increase (PaCO2 > 45 mmHg), a condition known as respiratory acidosis occurs. The body tries to maintain homeostasis by increasing the respiratory rate, a condition known as tachypnea. This allows much more carbon dioxide to escape the body through the

Partial Pressure of Carbon Dioxide -- Clinical Significance

There are differences in the acute and chronic stages of respiratory acidosis or alkalosis. Acute respiratory acidosis from increased PCO2 will result in immediate changes to serum bicarbonate levels due to the bicarbonate buffer system; however, this is limited in its ability to achieve homeostasis. The kidney will gradually increase the serum bicarbonate levels in chronic cases. Chronic respiratory acidosis is when the acidemia exists for 3 to 5 days, which is approximately how long it will take the kidney to buffer the acidemia. In acute respiratory acidosis, normally, the serum bicarbonate will increase by 1 mEq/L for every 10 mmHg increase in PCO2. For chronic respiratory acidosis, the serum bicarbonate will increase by 4 to 5 mEq/L for every 10 mmHg rise in PCO2. [6] [5] The result typically causes a mild chronic acidosis or low-normal pH near 7.35. [6] In regards to respiratory alkalosis, the same timeframe applies to acute versus chronic. In acute respiratory alkalosis, for every decrease in PCO2 by 10 mmHg, the serum bicarbonate will also decrease by 2 mEq/L. In chronic respiratory alkalosis, or alkalosis lasting 3 to 5 days, for every 10mmHg drop in PCO2, it is expected that serum bicarbonate will decrease by 4 to 5 mEq/L. [5] [6]

Blood gas test

A blood gas test or blood gas analysis tests blood to measure blood gas tension values, it also measures blood pH, and the level and base excess of bicarbonate. The source of the blood is reflected in the name of each test; arterial blood gases come from arteries, venous blood gases come from veins and capillary blood gases come from capillaries. The blood gas tension levels of partial pressures can be used as indicators of ventilation, respiration and oxygenation. Analysis of paired arterial and venous specimens can give insights into the aetiology of acidosis in the newborn. Values measured

Blood gas test

Blood gas tests also measure the levels of bicarbonate and of standard bicarbonate, of base excess, of oxygen saturation, and of pH. An arterial blood gas test is more often used. Clinical significance Blood gas tests can be used in the diagnosis of a number of acidosis conditions such as lactic, metabolic, and respiratory acidosis, diabetic ketoacidosis, and also of respiratory alkalosis. Particularly, umbilical cord blood gas analysis can give an indication of preceding fetal hypoxic stress. In combination with other clinical information, normal paired arterial and venous cord blood gas results can usually provide a robust defence against a suggestion that an infant had an intrapartum hypoxic‐ischaemic event.

Respiratory acidosis

Acute respiratory acidosis: HCO3− increases 1 mEq/L for each 10 mm Hg rise in PaCO2. Chronic respiratory acidosis: HCO3− rises 3.5 mEq/L for each 10 mm Hg rise in PaCO2. The expected change in pH with respiratory acidosis can be estimated with the following equations: Acute respiratory acidosis: Change in pH = 0.08 X ((40 − PaCO2)/10) Chronic respiratory acidosis: Change in pH = 0.03 X ((40 − PaCO2)/10) Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia. Diagnosis

The regulation of PCO2 is also involved in metabolic acidosis and alkalosis, as well. In metabolic acidosis, for every 1 mEq/L drop of bicarbonate, there will be a decrease in PCO2 by 1.2 mmHg. [5] For sudden drops in bicarbonate, it will take approximately 12 to 24 hours to reach full compensation; however, this process will start in as early as 30 minutes by chemoreceptor and CSF pH changes. [7] Another way to determine the expected PCO2 and compare the value obtained on blood gas analysis with metabolic acidosis is to utilize Winter’s equation. [8] If the measured PCO2 is higher or lower than the Winter’s equation PCO2, there may be a secondary respiratory acidosis or alkalosis, respectively. This situation may be the case in underlying lung pathology or neuromuscular pathology, such as an anoxic injury-causing minute ventilation control to become reduced. Also, in the presence of very severe metabolic acidosis, there is a limit to respiratory compensation with minute ventilation. The PCO2 typically cannot fall below 8 to 12 mmHg, and the sustained increase in minute ventilation to achieve this low PCO2 will usually cause rapid respiratory fatigue. In the case of metabolic alkalosis, the expected compensation of PCO2 is to increase by 0.7 mmHg for every 1 mEq/L increase in serum bicarbonate. [5]

[What you should know of the arterial blood gases during the watch].

Gasometry is the measurement of dissolved gases in the blood, by measuring pH, carbon dioxide pressure (pCO(2)), serum bicarbonate (HCO(3-)), and lactate and serum electrolytes: sodium, potassium and chlorine you can make a diagnosis, etiology and treatment in the critically ill patient. The aim is to provide five steps for the interpretation of blood gases by: 1. The definition of acidemia or acidosis, or alkalemia or alkalosis. 2. Defining the metabolic component or respiratory. 3. To determine the anion gap; levels above 15 ± 2 determine other likely causes of excess anions (methanol, uremia, diabetic ketoacidosis, paraldehyde, ionized, lactic acidosis, ethylene glycol and salicylates. 4. Compensation, using the Winter formula. 5. The delta gap, with the formula for determining intrinsic and metabolic alkalosis. When anion gap is normal, is calculated urinary anion gap; the value is negative if the loss is extrarenal, contrary to the positive result is renal etiology.

Hypercapnia

In many people a high causes a feeling of shortness of breath, but the lack of this symptom is no guarantee that the other effects are not occurring. A significant percentage of rebreather deaths have been associated with CO2 retention. The effects of high can take several minutes to hours to resolve once the cause has been removed. Diagnosis Blood gas tests may be performed, typically by radial artery puncture, in the setting of acute breathing problems or other acute medical illness. Hypercapnia is generally defined as an arterial blood carbon dioxide level over 45 mmHg (6 kPa). Since carbon dioxide is in equilibrium with carbonic acid in the blood, hypercapnia drives serum pH down, resulting in respiratory acidosis. Clinically, the effect of hypercapnia on pH is estimated using the ratio of the arterial pressure of carbon dioxide to the concentration of bicarbonate ion, . Tolerance

Pulmonary gas pressures

The alveolar pO2 is not routinely measured but is calculated from blood gas measurements by the alveolar gas equation. Partial pressure of carbon dioxide Pathology The partial pressure of carbon dioxide, along with the pH, can be used to differentiate between metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Hypoventilation exists when the ratio of carbon dioxide production to alveolar ventilation increases above normal values – greater than 45mmHg. If pH is also less than 7.35 this is respiratory acidosis. Hyperventilation exists when the same ratio decreases – less than 35mmHg. If the pH is also greater than 7.45 this is respiratory alkalosis. See also Alveolar-arterial gradient Diffusing capacity Pulmonary alveolus References Respiratory physiology

Metabolic alkalosis

To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used: pCO2 = 0.7 [HCO3] + 20 mmHg ± 5 pCO2 = 0.7 [HCO3] + 21 mmHg Treatment To effectively treat metabolic alkalosis, the underlying cause(s) must be corrected. A trial of intravenous chloride-rich fluid is warranted if there is a high index of suspicion for chloride-responsive metabolic alkalosis caused by loss of gastrointestinal fluid (e.g., due to vomiting). Terminology 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. See also Hypokalemia Metabolic acidosis Respiratory acidosis Respiratory alkalosis References External links Acid–base disturbances

Metabolic acidosis

Diagnostic approach and causes Metabolic Acidosis is defined as a reduced serum pH, and an abnormal serum bicarbonate concentration of <22 mEq/L, below the normal range of 22 to 29 mEq/L. However, if a patient has other coexisting acid-base disorders, the pH level may be low, normal or high in the setting of metabolic acidosis. In the absence of chronic respiratory alkalosis, metabolic acidosis can be clinically diagnosed by measuring serum bicarbonate levels in the blood, which is generally a standard component of blood panels. Imperatively, when weighing a metabolic acidosis diagnosis, the change in serum bicarbonate levels over time should be considered; if baseline bicarbonate results are unknown, a single set of values may be misinterpreted. Causes Generally, metabolic acidosis occurs when the body produces too much acid (e.g., lactic acidosis, see below section), there is a loss of bicarbonate from the blood, or when the kidneys are not removing enough acid from the body.

Respiratory acidosis

Types Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mEq/L). Causes Acute Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Respiratory failure

Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases (hypoxemia, hypercapnia, or both), and evidence of increased work of breathing. Respiratory failure causes an altered mental status due to ischemia in the brain. The typical partial pressure reference values are oxygen Pa O2 more than 80 mmHg (11 kPa) and carbon dioxide Pa CO2 less than 45 mmHg (6.0 kPa). Cause

Sepsis

More specific definitions of end-organ dysfunction exist for SIRS in pediatrics. Cardiovascular dysfunction (after fluid resuscitation with at least 40 ml/kg of crystalloid) hypotension with blood pressure < 5th percentile for age or systolic blood pressure < 2 standard deviations below normal for age, or vasopressor requirement, or two of the following criteria: unexplained metabolic acidosis with base deficit > 5 mEq/l lactic acidosis: serum lactate 2 times the upper limit of normal oliguria (urine output ) prolonged capillary refill > 5 seconds core to peripheral temperature difference Respiratory dysfunction (in the absence of a cyanotic heart defect or a known chronic respiratory disease) the ratio of the arterial partial-pressure of oxygen to the fraction of oxygen in the gases inspired (PaO2/FiO2) < 300 (the definition of acute lung injury), or

Respiratory alkalosis

Diagnosis The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual. The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentrations (and blood pH) after a respiratory or metabolic acid-base disturbance Classification There are two types of respiratory alkalosis: chronic and acute as a result of the 3–5 day delay in kidney compensation of the abnormality. Acute respiratory alkalosis occurs rapidly, have a high pH because the response of the kidneys is slow. Chronic respiratory alkalosis is a more long-standing condition, here one finds the kidneys have time to decrease the bicarbonate level. pH Alkalosis refers to the process due to which there is elevation of blood pH. Alkalemia refers to an arterial blood pH of greater than 7.45.

Acidosis

Mutations to the V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural deafness. Arterial blood gases will indicate low pH, low blood HCO3, and normal or low PaCO2. In addition to arterial blood gas, an anion gap can also differentiate between possible causes. The Henderson-Hasselbalch equation is useful for calculating blood pH, because blood is a buffer solution. In the clinical setting, this equation is usually used to calculate HCO3 from measurements of pH and PaCO2 in arterial blood gases. The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is lactic acid, which disappears as blood flow and oxygen debt are corrected. Treatment

Base excess

Base excess (or deficit) is one of several values typically reported with arterial blood gas analysis that is derived from other measured data. The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958. Estimation Base excess can be estimated from the bicarbonate concentration ([HCO3−]) and pH by the equation: with units of mEq/L. The same can be alternatively expressed as Calculations are based on the Henderson-Hasselbalch equation: Ultimately the end result is: Interpretation Base excess beyond the reference range indicates metabolic alkalosis if too high (more than +2 mEq/L) metabolic acidosis if too low (less than −2 mEq/L)

Winters' formula

Winters' formula, named for Dr. R.W. Winters, is a formula used to evaluate respiratory compensation when analyzing acid–base disorders and a metabolic acidosis is present. It can be given as , where HCO3− is given in units of mEq/L and pCO2 will be in units of mmHg. Winters' formula gives an expected value for the patient's PCO2; the patient's actual (measured) PCO2 is then compared to this: If the two values correspond, respiratory compensation is considered to be adequate. If the measured PCO2 is higher than the calculated value, there is also a secondary respiratory acidosis or mixed acid base disorder. If the measured PCO2 is lower than the calculated value, there is also a secondary respiratory alkalosis or mixed acid base disorder. References Respiratory therapy Mathematics in medicine

Respiratory alkalosis

pH Alkalosis refers to the process due to which there is elevation of blood pH. Alkalemia refers to an arterial blood pH of greater than 7.45. Treatment Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur. If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels. In popular culture In The Andromeda Strain, one of the characters is exposed to contamination, but saves himself by increasing his respiratory rate to induce alkalosis. See also References Further reading External links Acid–base disturbances

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 (mmol/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. 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.

Physiology, Acid Base Balance -- Related Testing

Arterial blood gas (ABG) sampling, is a test often performed in an inpatient setting to assess the acid-base status of a patient. A needle is used to draw blood from an artery, often the radial, and the blood is analyzed to determine parameters such as the pH, pC02, pO2, HCO3, oxygen saturation, and more. This allows the physician to understand the status of the patient better. ABGs are especially important in the critically ill. They are the main tool utilized in adjusting to the needs of a patient on a ventilator. The following are the most important normal values on an ABG: pH = 7.35 to 7.45 pCO2 = 35 to 45 mmHg pO2 = 75 to 100 mmHg HCO3- = 22 to 26 mEq/L O2 Sat = greater than 95% The ability to quickly and efficiently read an ABG, especially in reference to inpatient medicine, is paramount to quality patient care.

Comparison of arterial and venous blood gases analysis in patients with exacerbation of chronic obstructive pulmonary disease.

To investigate whether venous blood gases (VBG) test can be replace by an arterial blood gases (ABG) in exacerbation of chronic obstructive pulmonary disease (COPD). From October 2005 to March 2006, at the Emergency Room of Kashan Beheshti Hospital, the data of 107 patients with exacerbation of COPD were assessed. Arterial blood gases and VBG samples were obtained simultaneously, and indexes of pH, carbon dioxide partial pressure (PCO2), bicarbonate (HCO3), oxygen partial pressure (PO2) and Oxygen (O2) saturation level were analyzed. The mean +/- SD of indexes in ABG and VBG samples were as follows: pH = 7.37 +/- 0.47 versus 7.34 +/- 0.047; PCO2 = 53.88 +/- 7.63 mm Hg versus 59.55 +/- 8.96 mm Hg, HCO3= 30.66 +/- 4.49 mEq/L versus 31.94 +/- 4.39 mEq/L; PO2 = 55.37 +/- 11.19 mm Hg versus 43.08 +/- 10.54 mm Hg. The average difference between indexes in ABG and VBG samples were as follows: pH = 0.0241 +/- 0.004, p<0.001, r = 0.864; PCO2 = 5.673 +/- 1.126 mm Hg, p<0.001, r = 0.761; HCO3 = 1.279 +/- 0.604 mEq/L, p<0.001, r = 0.749; and PO2 = 12.294 +/- 2.115 mm Hg, p<0.001, r = 0.702. Venous blood gases, especially pH and PCO2 levels have relatively good correlation with ABG values. In view of the fact that, this correlation is not close, VBG cannot be substitute for ABG in exacerbation of COPD.


We are presented with a case of RSV-positive bronchiolitis. According to current recommendations, it would be indicated to initiate supplemental oxygen therapy.

A 2-month-old infant with an upper respiratory tract cold of 3 days of evolution, who begins with moderate respiratory distress and pulmonary auscultation with expiratory wheezing. Oxygen saturation is 89 %. Respiratory syncytial virus is isolated in the nasopharyngeal exudate. Which of the following treatments do you consider more indicated for this condition?

[Comparative study of nebulized sambutol against placebo in the acute phase of bronchiolitis in 33 infants aged 1 to 6 months].

The therapeutic role of bronchodilators in bronchiolitis remains controversial. The aim of this study is to evaluate the safety and the clinical response to nebulized salbutamol in infants with mild acute bronchiolitis. Thirty-three infants, aged 1 month to 5 months and 22 days (mean: 92.4 days) were included in the study. Patients received either nebulized salbutamol (0.15 mg/kg per dose: 16 infants) or a placebo (normal saline aerosol: 17 infants), delivered by an oxygen propellent, three times at intervals of 1 hour, as part of a double-blind randomized trial. Effect of treatment was evaluated by measuring respiratory and heart rate, clinical scores based on the degree of retraction and wheezing, and oxygen saturation. Clinical assessment was repeated 30 minutes after each nebulization. A nasopharyngeal swab was obtained for detection of respiratory syncytial virus (VRS) antigens by immunofluorescence assay in all patients. Patients in the salbutamol group exhibited significantly greater improvement in respiratory rate (P = 0.01), accessory muscle score (P < 0.001) and wheezing score (P < 0.001). There was no significant difference in oxygen saturation between both groups. Infants treated with salbutamol exhibited a non-significant increase in heart rate after the three sprays; no other adverse effects were noted. VRS was identified in 78% of the children tested. Salbutamol is safe and effective in relieving the respiratory distress of young infants with acute bronchiolitis. Our study confirms previous observations that infants younger than six months of age respond as well as older children when given three doses of nebulized salbutamol. Responders could not be differentiated from non responders by personal or family histories of atopy and VRS isolation. A longitudinal study could establish a correlation between response to bronchodilator therapy and later development of asthma.

Respiratory Syncytial Virus Bronchiolitis in Children.

Bronchiolitis is a common lower respiratory tract infection in infants and young children, and respiratory syncytial virus (RSV) is the most common cause of this infection. RSV is transmitted through contact with respiratory droplets either directly from an infected person or self-inoculation by contaminated secretions on surfaces. Patients with RSV bronchiolitis usually present with two to four days of upper respiratory tract symptoms such as fever, rhinorrhea, and congestion, followed by lower respiratory tract symptoms such as increasing cough, wheezing, and increased respiratory effort. In 2014, the American Academy of Pediatrics updated its clinical practice guideline for diagnosis and management of RSV bronchiolitis to minimize unnecessary diagnostic testing and interventions. Bronchiolitis remains a clinical diagnosis, and diagnostic testing is not routinely recommended. Treatment of RSV infection is mainly supportive, and modalities such as bronchodilators, epinephrine, corticosteroids, hypertonic saline, and antibiotics are generally not useful. Evidence supports using supplemental oxygen to maintain adequate oxygen saturation; however, continuous pulse oximetry is no longer required. The other mainstay of therapy is intravenous or nasogastric administration of fluids for infants who cannot maintain their hydration status with oral fluid intake. Educating parents on reducing the risk of infection is one of the most important things a physician can do to help prevent RSV infection, especially early in life. Children at risk of severe lower respiratory tract infection should receive immunoprophylaxis with palivizumab, a humanized monoclonal antibody, in up to five monthly doses. Prophylaxis guidelines are restricted to infants born before 29 weeks' gestation, infants with chronic lung disease of prematurity, and infants and children with hemodynamically significant heart disease.

Childhood Respiratory Conditions: Lower Respiratory Tract Infection.

Bronchiolitis, a lower respiratory tract infection, commonly affects infants and children younger than 2 years. Respiratory syncytial virus is the most common cause. Nasal congestion, rhinorrhea, and mild fever occur in the first 1 to 3 days. Symptoms worsen for several days to include wheezing and other lower respiratory tract signs, and then resolve over days to weeks. However, some children develop hypoxemia and/or respiratory distress and require hospitalization. The diagnosis is clinical, based on the history and physical examination findings. Routine chest x-rays and blood tests are not recommended. Management is supportive, including nasal suctioning, oxygen (in cases of hypoxemia), and hydration. Use of bronchodilators (ie, albuterol, epinephrine) and systemic corticosteroids is not recommended in infants and children ages 1 to 23 months. Pneumonia, another common infection in infants and children, typically is caused by viruses or bacteria. The diagnosis is clinical, and chest x-rays and blood cultures are not required for patients well enough to be treated as outpatients. Antibiotics are not routinely required for preschool-aged children (ie, younger than 5 years) with pneumonia because most have viral infections. For immunized school-aged children with mild to moderate pneumonia suspected to be of bacterial origin, amoxicillin is recommended. In school-aged children, if atypical pathogens (eg, Mycoplasma) are suspected, a macrolide antibiotic should be prescribed.

[An epidemic of respiratory syncytial virus bronchiolitis among infants in northern Israel].

In the wake of a community outbreak of bronchiolitis in northern Israel from December 1993 to March 1994, we conducted a retrospective study of 108 infants aged 2 weeks to 14 months with proven respiratory syncytial virus (RSV) infection (diagnosed by a rapid RSV antigen test in nasopharyngeal secretions). 47% of the infants were less than 8 weeks old. Mean hospital stay was 6.6 days (range 1-60). The characteristic clinical findings were: cough in all patients, dyspnea in 96%, rhinitis in 95% and fever in 55%. In those younger than 8 weeks, or in those with underlying diseases, hospitalization was longer, the disease was more serious and complications more frequent (p < 0.002). 4 children (3%) died, 3 of whom had severe congenital heart defects. All children were treated with oxygen and beta-agonist inhalations. The 33% who also received corticosteroids were older and most had a history of pulmonary diseases, such as asthma or bronchopulmonary dysplasia. There was no difference between those who did or did not receive corticosteroids with regard to severity of disease or rate of complications. Ribavirin was used to treat 19 (17.5%), most of whom had underlying lung disease. The others were otherwise healthy infants younger than 8 weeks. 13 were cared for in the intensive care unit, 11 of whom required mechanical ventilation. A rapid test for detection of RSV infection enabled prompt isolation of infected patients so that the risk of nosocomial infection was reduced and Ribavirin therapy could be started early, if required.

The efficacy of nebulized metaproterenol in wheezing infants and young children.

The benefit of beta-adrenergic agonists in the treatment of acutely wheezing infants and young children has not been well documented in the outpatient setting. To determine the efficacy of nebulized metaproterenol sulfate, 74 children aged 36 months or younger with acute wheezing participated in a double-masked, randomized, placebo-controlled clinical trial. Children received nebulized metaproterenol, either as an initial treatment or after a control treatment with normal saline solution. At baseline and 20 minutes after each treatment, an assessment was made that included measurements of heart rate, respiratory rate, oxygen saturation, and clinical variables related to respiratory compromise with the use of a standardized respiratory distress index (RDI). Children who received saline solution as initial therapy had no significant differences from baseline in any of the assessment measures. After metaproterenol therapy, children demonstrated an increase in heart rate ([mean +/- SD] 147 +/- 14 beats per minute vs 153 +/- 16 beats per minute), a decrease in respirations (50/min +/- 5/min vs 45/min +/- 7/min), improvement (lower scores) on the RDI (24 +/- 4 vs 15 +/- 2), and an increase in oxygen saturation (94.1% +/- 2.7% vs 95.3% +/- 3.0%). Patients aged 12 months or younger (n = 37) benefited from metaproterenol treatment (improvement in respiratory rate and RDI) but not to the same degree as children aged 24 months or older (n = 23) (improvement in respiratory rate, RDI, and oxygen saturation). Compared with assessments made before metaproterenol treatment, patients with respiratory syncytial virus infection (n = 21) had improvement in respirations (52/min +/- 7/min vs 45/min +/- 6/min) and RDI scores (22 +/- 4 vs 14 +/- 3). Based on a priori criteria (reduction in a premedication respiratory rate of 20% and an RDI score of 50%), responders to metaproterenol therapy included 45% of the entire sample and, respectively, 40% of those aged 12 months or younger, 52% of those aged 24 months or older, and 48% of patients who tested positive for respiratory syncytial virus. Although there appears to be an age-dependent degree of response, metaproterenol is effective in relieving the respiratory distress of young acutely wheezing children, including those with documented respiratory syncytial virus bronchiolitis.

Bronchiolitis.

Bronchiolitis, a lower respiratory tract illness most often caused by respiratory syncytial virus, generally affects children under two years of age, commonly during the winter months. Necrosis of epithelial cells in the small airways leads to inflammation and airway obstruction, causing decreased oxygen saturation, with cough and wheezing. Hospital admission should be considered for children with pulse oximetry levels less than 95 percent at rest. Treatment consists of humidified oxygen, intravenous hydration and administration of nebulized albuterol. Infants with mild disease who are identified early in the course of illness should be reevaluated in 24 hours. Infants with congenital heart disease, bronchopulmonary dysplasia or a history of prematurity, who are at high risk for severe disease, should be treated with ribavirin.

Predictors of bronchodilator responsiveness in infants with wheezing associated respiratory tract infection.

The responsiveness to bronchodilator is variable in infants with wheezing associated respiratory illness (WARI). Factors for prediction of the response will lead to more rational use of the bronchodilator in these infants. We examined the possible predictive factors in 44 children under 2 years of age who had their first episode of WARI. All of them were treated with 0.15 mg/kg of nebulized salbutamol. Thirty patients (68%) with decreasing clinical score > or = 3 after treatment were considered as the responders while the remainder (14 infants) were non responders. By using Chi-square test, Fisher exact test and Mann-Whitney U test to compare the data of the 2 groups, the significant factors for the responders were older than 6 months and history of previous LRI (p < 0.01). The significant factors for the non-responders included concurrent diarrhea, patchy pulmonary infiltration and positive RSV in the nasopharyngeal secretion (p < 0.01). These results suggested effective bronchodilator therapy in infants older than 6 months or having a history of previous LRI. Those who had acute RSV infection or patchy infiltration in chest X-ray and associated diarrhea were less likely to respond.

Lower airway disease caused by respiratory syncytial virus.

Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in infants and young children. Most infections due to RSV are mild and do not require hospitalization. RSV causes both upper respiratory tract infections as well as lower respiratory tract infections. Infants with underlying disease states like bronchopulmonary dyslasia, congenital heart disease and prematurity appear more prone to develop severe infection and have a higher incidence of hospitalization. The exact pathogenesis of RSV is not well understood. The mortality associated with primary RSV infection in healthy children is estimated to be between .005% to .02%. In hospitalized children the mortality rate is estimated to be from 1% to 3%. Several treatment modalities in the form of bronchodilators, corticosteroids, ribavirin, intravenous immune gammaglobulin and antibiotics are available. Studies have failed to show the true beneficial effect of any of the above treatment modalities. Supportive care is only needed. The best treatment is the supportive care in the form of oxygen and fluids and close monitoring of the vital signs including oxygen saturation.

Efficacy of corticosteroids in acute bronchiolitis: short-term and long-term follow-up.

Corticosteroids continue to be used by many physicians to treat infants with bronchiolitis. The aim of this study was to examine the short-term and long-term efficacy of oral corticosteroid therapy when added to beta2-agonists in infants with mild to moderate bronchiolitis (defined as the first episode of wheezing associated with low grade fever, rhinitis, tachypnea, and increased respiratory effort in a previously healthy infant during the winter months). Infants with mild to moderate bronchiolitis, were randomly assigned to receive either oral prednisone (2 mg/kg/day) or placebo for 3 days. All patients received nebulized albuterol q.i.d. during this period. Upon admission and after 3 days of therapy, a clinical score was assigned based on respiratory rate, use of accessory muscle, and the presence of wheeze. Oxygen saturation (SaO2) was also measured. On day 7, we inquired as to the well-being of each child. Two years later, the development of chronic respiratory symptoms was assessed. Thirty-eight infants were enrolled in the study; 20 received prednisone and 18 received placebo. Both groups were similar in terms of age, duration of illness prior to enrollment, pretrial medication use, clinical severity of bronchiolitis, history of atopy, and family history of atopy. After 3 and 7 days of treatment, both groups showed similar clinical improvement and there were no statistically significant differences between the two groups in the clinical score or in the SaO2. No major side effects were observed. Two years later, 32% of the infants continued to suffer from chronic respiratory symptoms, with a similar prevalence in both groups. We conclude that a 3-day course of oral corticosteroids is of no benefit to infants with mild to moderate bronchiolitis who are also treated with an inhaled beta2-agonist.

Respiratory syncytial virus infections: characteristics and treatment.

In this review, we describe the history, epidemiology and clinical manifestations of infections attributed to respiratory syncytial virus (RSV) in children. At present, no cure exists for RSV infection but commonly employed palliative treatments include oxygen and inhaled beta(2)-adrenoceptor agonists, such as salbutamol, to relieve the wheezing and increased bronchiolar smooth muscle constriction. Adrenaline (epinephrine) has been found to be superior to the selective beta(2)-adrenoceptor agonists. Oral or inhaled corticosteroids should counteract the inflammatory response to RSV infection but their effectiveness is controversial. Inhaled ribavirin is the only licensed antiviral product approved for the treatment of RSV lower respiratory-tract infection in hospitalized children, although its use is now restricted to high-risk infants. Other treatments considered are nasopharyngeal suctioning, surfactant therapy, recombinant human deoxyribonuclease I, heliox (helium:oxygen) and inhaled nitric oxide. Prevention of infection by RSV antibodies is another strategy and, currently, palivizumab is the only safe, effective and convenient preventative treatment for RSV disease in high-risk populations of infants and young children. Its cost-effectiveness, however, has been questioned. Both live attenuated and subunit vaccines against RSV infection have been developed but so far there is no safe and effective vaccine available. Finding effective treatments and prophylactic measures remains a major challenge for the future.

Evaluation of the efficacy of prednisolone in early wheezing induced by rhinovirus or respiratory syncytial virus.

The role of systemic corticosteroids in the treatment of early childhood wheezing in children is not clear. We sought to determine whether prednisolone is effective in rhinovirus-induced early wheezing. We conducted a controlled trial comparing oral prednisolone (2 mg/kg per day in three divided doses for 3 days) with placebo in 78 hospitalized children (mean age, 1.1 year; standard deviation, 0.7) experiencing their first or second episode of wheezing induced by rhinovirus or respiratory syncytial virus. Mixed viral infections were excluded. Our primary end point was the time until the patient was ready for discharge; secondary end points included oxygen saturation during hospitalization, duration of symptoms, occurrence of relapses during the next 2 months and blood eosinophil counts at discharge and 2 weeks later. In multivariate regression analysis, prednisolone did not influence the time until ready for discharge, but it decreased relapses during the subsequent 2-month period in rhinovirus-affected children (prednisolone versus placebo, 22% versus 56%; odds ratio, 19.06; 95% confidence interval, 2.52-144.03; P = 0.004) and in children with blood eosinophils > or = 0.2 x 10/L (respectively, 24% versus 71%; odds ratio, 10.57; 95% confidence interval, 1.99-56.22; P = 0.006). Rhinovirus-affected children had more blood eosinophils on admission (mean, 0.44 versus 0.086 x 10/L), had a higher prevalence of atopy (44% versus 8%) and were older (mean, 1.4 versus 0.9 years, P < 0.001 for all) than respiratory syncytial virus-infected children. Prednisolone reduced relapses during a 2-month period after first episodes of wheezing associated with rhinovirus infection or blood eosinophils > or = 0.2 x 10/L.

Respiratory syncytial virus

Treatment for severe illness is primarily supportive, including oxygen therapy and more advanced breathing support with CPAP or nasal high flow oxygen, as required. In cases of severe respiratory failure, intubation and mechanical ventilation may be required. Ribavirin is the only antiviral medication currently licensed for the treatment of RSV in children, although its use remains controversial. Signs and symptoms RSV infection can present with a wide variety of signs and symptoms that range from mild upper respiratory tract infections (URTI) to severe and potentially life-threatening lower respiratory tract infections (LRTI) requiring hospitalization and mechanical ventilation. While RSV can cause respiratory tract infections in people of all ages and is among the most common childhood infections, its presentation often varies between age groups and immune status. Reinfection is common throughout life, but infants and the elderly remain at highest risk for symptomatic infection.

Respiratory syncytial virus

Bronchiolitis is a common lower respiratory tract infection characterized by inflammation and obstruction of the small airways in the lungs. While several viruses can cause bronchiolitis, RSV is responsible for about 70% of cases. It usually presents with 2 to 4 days of runny nose and congestion followed by worsening cough, noisy breathing, tachypnea (fast breathing), and wheezing. As infants work harder to breathe, they can also show signs of respiratory distress, such as subcostal retractions (when the belly pulls under the ribcage), intercostal retractions (when the muscles between the ribs pull inward), grunting, and nasal flaring. If the child has not been able to feed adequately, signs of dehydration may also be present. Fever may be present, but high-grade fever is uncommon. Crackles and wheezing can often be heard on auscultation, and oxygen saturation levels may be decreased.

Respiratory syncytial virus

Adults Reinfection with RSV remains common throughout life. Reinfection in adulthood often produces only mild to moderate symptoms indistinguishable from the common cold or sinus infection. Infection may also be asymptomatic. If present, symptoms are generally isolated to the upper respiratory tract: runny nose, sore throat, fever, and malaise. In the vast majority of cases, nasal congestion precedes the development of cough. In contrast to other upper respiratory infections, RSV is also more likely to cause new onset wheeze in adults. Only about 25% of infected adults will progress to significant lower respiratory tract infection, such as bronchitis or tracheobronchitis.

Respiratory syncytial virus

Treatment Supportive care Treatment for RSV infection is focused primarily on supportive care. This may include monitoring a patient's breathing or using suction to remove secretions from the upper airway. Supplemental oxygen may also be delivered though a nasal cannula or face mask in order to improve airflow. In severe cases of respiratory failure, intubation and mechanical ventilation may be required to support breathing. If signs of dehydration are present, fluids may also be given orally or through an IV.

Management strategies for respiratory syncytial virus infections in infants.

Management of respiratory syncytial virus lower respiratory tract infection in infants is predominantly supportive and symptomatic. Outpatient management requires close attention to feeding, oral hydration, and monitoring of fever, behavior, and respiratory effort. In the small proportion of patients who need hospitalization, clinicians are concerned primarily with oxygenation and the possibility of oxygen desaturation. Appropriate interventions depend on the level of oxygenation as indicated by pulse oximetry or arterial blood gases. Hydration and symptomatic treatment with alpha- or ss(2 )-adrenergic agonist bronchodilators may lessen the work of breathing. The role of these agents remains controversial, however, and anticholinergic bronchodilators are considered ineffective. Current antiviral therapy is limited to aerosolized ribavirin. Immunotherapy with respiratory syncytial virus immune globulin or a monoclonal antibody has not been rewarding in terms of clinical outcome, although the antiviral effect of these agents has been impressive. There is concern about long-term pulmonary sequelae after respiratory syncytial virus lower respiratory tract infection early in life. Several recent studies, including new data reported here, suggest that ribavirin may have a beneficial effect on some of these sequelae, whereas other studies have failed to demonstrate any benefit. Future studies may help resolve this question.

[Respiratory syncytial infections in the elderly. Seven cases and review of the literature].

We report 7 cases of respiratory syncytial virus (RSV) infections among elderly patients hospitalized for acute lower tract infection during the winter months. The median age was 95 years (range: 79-106 years). 6 patients were living in nursing homes. All patients had chronic cardiopulmonary conditions. Clinical symptoms included upper respiratory tract symptoms for 3 of them and lower respiratory tract symptoms for all of them. Three patients developed a severe infection with acute respiratory failure. The chest X ray showed an interstitial infiltrate in 3 cases, a consolidation in one case. All patients received oxygen, respiratory physical therapy, nebulized B-agonists and antibiotics. Corticosteroids were used for 4 patients. Progress was favorable for all patients and none died. Diagnosis was obtained in a few hours by direct antigen detection by enzyme immunoassays (EIA) in sputum. Respiratory syncytial virus infection is a common cause of respiratory tract infection in the elderly, during the winter months. Clinical manifestations are similar to influenza infections. Detection of RSV antigens from sputum specimens may be a useful and rapid diagnostic method and merits further evaluation in the elderly. Early diagnosis of respiratory syncytial virus infection should be encouraged to allow the implementation of effective infection control procedures and avoid inadequate therapies.

Management of bronchiolitis: current practices in Ireland.

To establish current practice for hospital-based treatment of uncomplicated respiratory syncytial virus (RSV) infection in the Republic of Ireland. A questionnaire was sent to all consultant general paediatricians in the Republic of Ireland. The questionnaire described a clinical scenario and this was followed by a list of management questions. The scenario was of a 3-month-old infant with uncomplicated but moderately severe RSV infection requiring hospitalization. Seventy-three questionnaires were sent. 63/73 (86%) of the questionnaires were returned. With respect to management of this case almost all (61/63) the paediatricians felt that oxygen therapy was necessary (oxygen saturation described in the case was 90%). With respect to bronchodilator therapy, ipratropium bromide (38/63--60%) was chosen much more frequently than salbutamol (15/63--24%). Chest physiotherapy would have been prescribed by 8/63--13% of paediatricians. Oral steroids were infrequently chosen (1/63--2%) but nebulised steroids were selected in 7/63 (11%) cases. The routine use of RSV monoclonal antibody, palivizumab, for RSV prophylaxis was reported by 49% (31/63) of paediatricians. Prematurity with bronchopulmonary dysplasia was considered an indication for its administration by all of these but only 23% considered prematurity alone to be an indication. The management of infants with RSV bronchiolitis varies greatly among consultant paediatricians in Ireland. Evidence based guidelines may be of value in establishing a more uniform national treatment approach.

Respiratory syncytial virus

Additional supportive treatments have been investigated specifically in infants hospitalized with RSV bronchiolitis. These include the following: Nebulized hypertonic saline has been shown to reduce length of hospitalization and reduce clinical severity in infants with viral bronchiolitis. It is thought that this treatment may help by reducing airway edema and mucus plugging to decrease airway obstruction. Heliox, a mixture of oxygen with helium, may improve respiratory distress within the first hour after starting treatment. It works by reducing airway resistance and decreasing the work of breathing. However, it has not been shown to impact overall illness outcomes. Chest physiotherapy has not been found to reduce disease severity and is not routinely recommended. Inhaled recombinant human deoxyribonuclease (rhDNase), an enzyme that digests the DNA that contributes to mucus plugging and airway obstruction, has not been shown to improve clinical outcomes in this group.

First_Aid_Step2

Treatment is primarily supportive; treat mild disease with outpatient management using ﬂuids and nebulizers if needed. Hospitalize in the setting of marked respiratory distress, O2 saturation of < 92%, toxic appearance, dehydration/poor oral feeding, a history of prematurity (< 34 weeks), age < 3 months, underlying cardiopulmonary disease, or unreliable parents. Treat inpatients with contact isolation, hydration, and O2. A trial of aerosolized albuterol may be attempted; continue albuterol therapy only if effective. RSV is the most common cause of bronchiolitis. Ribavirin is an antiviral drug that has a controversial role in bronchiolitis treatment. It is sometimes used in high-risk infants with underlying heart, lung, or immune disease. RSV prophylaxis with injectable polyor monoclonal antibodies (RespiGam or Synagis) is recommended in winter for high-risk patients ≤ 2 years of age (e.g., those with a history of prematurity, chronic lung disease, or congenital heart disease).

Asthma

Humidified Oxygen to alleviate hypoxia if saturations fall below 92%. Corticosteroid by mouth are recommended with five days of prednisone being the same 2 days of dexamethasone. One review recommended a seven-day course of steroids. Magnesium sulfate intravenous treatment increases bronchodilation when used in addition to other treatment in moderate severe acute asthma attacks. In adults intravenous treatment results in a reduction of hospital admissions. Low levels of evidence suggest that inhaled (nebulised) magnesium sulfate may have a small benefit for treating acute asthma in adults. Overall, high quality evidence do not indicate a large benefit for combining magnesium sulfate with standard inhaled treatments for adults with asthma. Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases. Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.

Inhaled corticosteroids during and after respiratory syncytial virus-bronchiolitis may decrease subsequent asthma.

Respiratory syncytial virus (RSV) bronchiolitis in infancy can lead to bronchial hyper-reactivity or recurrent obstructive bronchitis. The aim of the present study was to determine whether the type of treatment has an influence on respiratory status after RSV bronchiolitis. The study involved 117 infants (mean age 2.6 months), who needed hospital treatment because of RSV bronchiolitis. The patients were divided randomly into three groups. All received the same symptomatic treatment. Group I children received symptomatic treatment only, group II children were treated for 7 days with inhaled budesonide, 500 microg three times per day, administered via a nebulizer. Group III children received nebulized budesonide, 500 microg twice per day for two months. Follow-up consisted of out-patient check-ups 2 and 6 months after the infection, and telephone contact two years after the infection. Statistically significant differences were seen between the groups. In group I 37% of the children had asthma, in group II 18%, and in group III 12%. According to the present study it seems that inhaled corticosteroid treatment during and after the acute phase of infant RSV bronchiolitis may have a beneficial effect on subsequent bronchial wheezing tendency.

Seasonal respiratory viral infections. Impact on infants with chronic lung disease following discharge from the neonatal intensive care unit.

To determine the frequency and severity of acute respiratory infections in infants with bronchopulmonary dysplasia following discharge from the neonatal intensive care unit. A prospective cohort study of 30 oxygen-dependent children who were younger than 2 years (mean age, 9.8 months; range, 3 to 24 months) were studied from September 1990 through April 1991. During the study, 101 (90.2%) of 112 visits for illness were prompted by new or worsening respiratory symptoms. Diagnoses included upper respiratory tract infection (30.4%), otitis media (26.0%), pneumonia (11.1%), acute exacerbation of bronchopulmonary dysplasia (10.4%), reactive airway disease (9.6%), and bronchiolitis (5.9%). Among these children, an increase in the fraction of inspired oxygen was necessary during 43% of visits. Ten children were hospitalized on 25 occasions for a mean of 37.6 hospital days per child (range, 1 to 107 days), and mean length of stay for each hospitalization was 15 days (median, 6 days). Five children were admitted to the pediatric intensive care unit. Respiratory viruses isolated included respiratory syncytial virus (n = 7), parainfluenza 3 virus (n = 3), and adenovirus (n = 2). No isolates of influenza A or B were detected. Anthropometrics at study entry and study end were converted to z scores as descriptors of weight for age, height for age, and weight for height. Growth improved during the 8 months of the study; however, overall, the children were leaner at study end than at study entry. In children with bronchopulmonary dysplasia, respiratory viral infections led to significant morbidity, which included long and frequent hospitalizations during the peak of the respiratory viral season. Although weight and linear growth increased throughout the study, patients were leaner at study conclusion than at study entry.

The impact of respiratory syncytial virus infection: a prospective study in hospitalized infants younger than 2 years.

We analyzed the influence of respiratory syncytial virus (RSV) on the clinical course and management of infants hospitalized due to viral upper and lower respiratory tract infections (U/LRTI). Infants younger than 2 years were prospectively tested for RSV infection by antigen detection in nasopharyngeal aspirates between November 1999 and October 2000. Of 281 infants hospitalized during the study period, 58 (21%) tested RSV positive. Seasonal distribution of RSV infections showed a peak in March (45% of all U/LRTI). Infants with RSV infection (12% were preterm, 5% had congenital heart disease) were younger (p < 0.001), had more severe U/LRTI (p < 0.001), longer hospitalizations (p < 0.001), more days with oxygen requirement (p < 0.001) and respiratory support (p = 0016) and more frequent requirements for bronchodilators (p = 0.002) and corticosteroids (p = 0.02). RSV contributed to prolonged hospitalizations and more severe clinical courses of disease both in very young term and preterm infants.

[Is the use of ribavirin aerosols in respiratory syncytial virus infections justified? Clinical and economic evaluation].

The controversy about the use of ribavirin aerosol for children at risk (cardiopathy, pneumopathy, premature and immunodeficient patients), in case of respiratory syncytial virus (RSV) infection, led us to stop its prescription in 1993 and study prospectively the patients admitted during the following winters. Criterias of inclusion for this study were those of the Committee on Infectious Diseases of the American Academy of Pediatrics concerning the use of ribavirin aerosol. Two cohorts of patients were studied: the first group included treated patients (ribavirin group: n = 22, ribavirin and support treatment: salbutamol aerosols, respiratory physiotherapy and oxygen-therapy; winters 1989-1990 to 1992-1993); the second group included patients with support treatment only (control group: n = 22; winters 1993-1994 and 1994-1995). The clinical gravity score at admission (4.55 vs 5.23, P = 0.46) and the risk factor scores (3.05 vs 3.27, P = 0.69) of the two groups were identical. Results showed that the children of the ribavirin group stayed much longer in hospital (14.2 vs 8.2 days, P = 0.002) and in the intensive care unit (7.2 vs 0.2 days, P < 0.001) than those of the control group. More support treatment was necessary for the ribavirin group as regard respiratory physiotherapy (3.8 vs 2.7 sessions a day, P = 0.026), the duration of oxygen-therapy (7.3 vs 3.7 days, P = 0.030) and the number of children requiring respiratory assistance (4 vs 0 children, P = 0.116). Administration of ribavirin aerosols (480 US$ a dose) and the way in which such treatment was carried out meant high daily costs for the ribavirin group (1,076 vs 604 US$, P < 0.001). As hospitalization was longer for children treated with ribavirin, the global cost was therefore much higher (15,552 vs 5,156 US$, P < 0.001). The antiviral effect of ribavirin is undeniable. However ribavirin is known to be the cause of severe bronchospasms (two cases in our study) and can also cause moderate and long term bronchospasms, aggravating therefore the clinical evolution of the disease. Our experience shows that administration of ribavirin aerosols in case of RSV infection of inferior respiratory airways seems not to be justified.

[Prednisolone treatment of respiratory syncytial virus infection. A randomized, controlled trial of 147 children].

Our objective was to evaluate the effect of systemic prednisolone as an adjunct to conventional treatment with beta 2-agonist, fluid replacement and respiratory support in hospitalized infants younger than 24 months with respiratory syncytial virus (RSV) infection. The study was randomized, double-blind and placebo-controlled. During the winter of 1995-96, 147 infants less than two years of age hospitalized with RSV infection were allocated to treatment with either systemic prednisolone mixture 2 mg/kg daily or placebo for 5 days. Our main outcome measures were: 1. Acute effect variables: duration of stay in hospital, use of medicine and supportive measures while in hospital. 2. At follow-up one month after discharge: duration of illness, start in day care center, morbidity and use of medicine. 3. At follow-up one year after discharge: morbidity, use of medicine and skin prick tests with allergens. Prednisolone treatment had no effect on any of the outcome measures. We find our results in agreement with the largest studies reported earlier; therefore, corticosteroid, whether by systemic route or by inhalation, should not be prescribed to infants with RSV infection.

[A case of bronchiolitis obliterans secondary to human metapneumovirus bronchiolitis].

Human metapneumovirus (hMPV), formerly classified in Paramyxoviridae family is now moved into Pneumoviridae, which was described as a novel family. It causes upper and lower respiratory tract infections (LRTIs) usually in children younger than five years old. The recent epidemiological studies indicated that hMPV is the second most frequently detected virus in LRTIs of young children, following the respiratory syncytial virus (RSV). Bronchiolitis obliterans (BO) is a chronic obstructive lung disease characterized by fibrosis of the distal respiratory airways. It is usually a result of an inflammatory process triggered by a LRTI related to adenovirus, RSV, Mycoplasma pneumoniae, measles virus, Legionella pneumophila, influenza virus or Bordetella pertussis as a causative agent. In this report, a case of hMPV bronchiolitis complicated with BO has been reported to point out the complications and severity of the clinical progress belongs to this virus. A three-month-old female patient has admitted to our pediatric intensive care unit with the diagnosis of acute bronchiolitis and respiratory failure. She was born at term, weighing 2950 gram and had been hospitalized in newborn intensive care unit for 11 days with the diagnosis of transient tachypnea of the newborn and neonatal sepsis. On auscultation, there were bilateral crepitant rales, wheezing and prolonged expirium. Her oxygen saturation was 97-98% while respiratory support was given with a non-rebreathing reservoir mask. Complete blood count, procalcitonin and C-reactive protein levels were in normal ranges. The chest radiography yielded right middle lobe atalectasia, left paracardiac infiltration and bilateral air trapping. A nasopharyngeal swab sample was analyzed by a commercial multiplex real-time reverse transcriptase-polymerase chain reaction (Thermo Fisher Scientific®, USA) developed for the detection of 15 respiratory viruses. Her sample yielded positive result for only hMPV. On the 4th day of hospitalization, the patient was intubated because of respiratory failure and carbon dioxide retention. She was extubated on the 19th day but could not tolerate. In the thorax computed tomography (CT), bilateral hyperinflation, patchy infiltration, mosaic perfusion and atelectasis especially bilateral posterior areas were detected. Bronchoscopy was normal except mild bronchomalacia in right middle lobe bronchus. The patient was diagnosed as BO secondary to hMPV bronchiolitis, according to the clinical, virological, bronchoscopic and thorax CT results. On the 76th day of admission, she was discharged with respiratory support with home ventilation via a tracheostomy cannula and medical treatments of oral metilprednisolone, nebulized salbutamol and budesonide. In conclusion, hMPV should not be undervalued especially in infants with severe LRTI that can be complicated with BO.

[Childhood croup].

Hoarseness, whooping cough and stridor are elements of a syndrome of upper airway obstruction. In childhood, acute laryngotracheobronchitis is by far the commonest cause of this syndrome. Yet, the differential diagnosis includes a number of rare and severe entities. In many cases, the traditional distinction between viral and spasmodic types is not possible. The value of humidifying therapy has not been established. In severe cases, nebulized adrenaline is of benefit but should be reserved for hospital. The effect lasts only two hours and at times a rebound effect is observed. It is now realized that some patients treated with adrenaline can safely be discharged after a two to three hours observation. There is a large body of evidence that all children arriving at the emergency department with croup should receive steroids without delay. This policy results in a much better outcome, with important reduction in hospitalizations, intensive care unit admissions and incubations. Oral dexamethasone is the drug of choice: it is as effective, easier to administer and cheaper than nebulised budesonide. In most studies, dexamethasone has been used at a dose of 0.6 mg/kg but there is some evidence that 0.15 mg/kg may be just as effective.

[Respiratory morbidity after hospital discharge in premature infants born at < or = 32 weeks gestation with bronchopulmonary dysplasia].

Bronchopulmonary dysplasia (BPD) is the most frequent cause of respiratory morbidity in the first 2 years of life among preterm infants who survive the first 28 days. To evaluate respiratory morbidity in the first 2 years of life in a group of preterm infants born at (32 weeks' gestation with BPD (oxygen requirement at 36 weeks' postconceptional age) by comparing it with that in preterm infants born at (32 weeks without BPD and with a control group of full term infants without neonatal morbidity. To determine whether respiratory morbidity in children with BPD decreases after the age of 2 years. Group I: preterm children with BPD (n = 29). Group II: preterm children without BPD (n = 29). Group III: children with appropriate gestational age and weight (n = 32). A cross-sectional, descriptive study of the three groups was performed over a 2-year period. In 17 children in group 1, the study was prolonged to the age of 4 years. We analyzed wheezing on at least two occasions, use of inhaled bronchodilators, use of inhaled glucocorticosteroids for more than 6 months, and hospitalization for respiratory illness. The chi-square test and Fischer's exact test were performed. At least one episode of wheezing occurred in 25 children (86.2%) in group I compared with 12 children (41.4%) in group II and 6 (18.8%) in group III. Nineteen children (65.5%) in group I and none in the remaining two groups received treatment with inhaled glucocorticosteroids for more than 6 months (p < 0.001). Inhaled bronchodilators were used by 25 children (86.2%) in group I compared with 12 (41.4%) in group II and 6 (18.8%) in the control group (p < 0.001). Twelve children (41.3%) in group I were hospitalized for respiratory illness compared with 8 (27.6%) in group II. There were no admissions among the control group. None of the children with BPD who received prophylaxis with palivizumab contracted respiratory syncytial virus infection. Seventeen children with BPD were evaluated until the age of 4 years. Episodes of wheezing decreased from 88.2% in the first year to 41 % between the third and fourth years (p < 0.001). Treatment with inhaled glucocorticosteroids for more than 6 months was given to 88.2% in the first year, 41.2 % between the first and second year and to 0 % after the second year (p < 0.001). Hospital admissions for respiratory illness decreased from 52.9% in the first year to 17.6% in the second year. None of the children were hospitalized after the age of 2 years (p < 0.001). During the first 2 years of life, children with BPD showed a greater number of admissions and episodes of wheezing and a greater need for medical treatment. Respiratory morbidity improved with age, 40% showed recurrent wheezing episodes at the age of 4 years.

First_Aid_Step2

Presents with low-grade fever, rhinorrhea, cough, and apnea (in young infants). Exam reveals tachypnea, wheezing, intercostal retractions, crackles, prolonged expiration, expiratory wheezing, and hyperresonance to percussion. Predominantly a clinical diagnosis; routine cases do not need blood work or a CXR. CXR may be obtained to rule out pneumonia and may show hyperinﬂ ation of the lungs with ﬂattened diaphragms, interstitial infiltrates, and atelectasis. Nasopharyngeal aspirate to test for RSV is highly sensitive and specific but has little effect on management (infants should be treated for bronchiolitis regardless of whether RSV is or not). Treatment is primarily supportive; treat mild disease with outpatient management using ﬂuids and nebulizers if needed.

New approaches to respiratory infections in children. Bronchiolitis and croup.

Croup is a disease that is commonly seen in children younger than the age of 6 years. The cause is viral, with parainfluenza viruses and RSV being the two most common pathogens. Treatment consists primarily of supportive care, and parents usually have tried humidification and cool air exposure before the child presents to the ED. Children with moderate to severe croup are usually seen in the ED. The use of steroids in an oral preparation results in a clinical improvement of outpatients with mild to moderate croup and reduces the need for hospitalization. The dosage range for oral dexamethasone is 0.15 mg/kg to 0.6 mg/kg. Nebulized budesonide may also be used. Racemic or L-epinephrine, both of which are equally effective, can be used for symptomatic treatment in severe croup. After administration of racemic or L-epinephrine, hospitalization is not automatic and patients can be discharged safely from the ED after a 3-hour of observation period. There should be no respiratory distress, and the patient should have access to follow-up and emergency care if needed.

Infant respiratory distress syndrome

Oxygen is given with a small amount of continuous positive airway pressure (CPAP), and intravenous fluids are administered to stabilize the blood sugar, blood salts and blood pressure. CPAP application to preterm neonates with respiratory distress is associated with a reduction in respiratory failure, mechanical ventilation and mortality. However, CPAP is associated with an increased rate of pneumothorax compared to spontaneous breathing with or without supplemental oxygen. If the baby's condition worsens, an endotracheal tube (breathing tube) is inserted into the trachea and intermittent breaths are given by a mechanical device. An exogenous preparation of pulmonary surfactant, either synthetic or extracted from animal lungs, is given through the breathing tube into the lungs. Surfactant medications can decrease the risk of death for very low-birth-weight infants who are hospitalized by 30%. Such small premature infants may remain ventilated for months. A study shows that an aerosol