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Ventilator Settings For Respiratory Acidosis

Vent Settings In Metabolic Acidosis

Vent Settings In Metabolic Acidosis

SDN members see fewer ads and full resolution images. Join our non-profit community! I recently saw a patient in emerg with acute kidney injury and lithium toxicity who was in resp failure with a bilateral pneumonia/possibly ARDS. She had a pretty significant metabolic acidosis and a resp rate in the 40s, with a pretty low pco2 on blood gas to compensate for her acidosis. ICU came down and intubated and put the patient on a Vt of 500, RR of 12. I let the fellow know that she had a pretty significant metabolic acidosis prior to the tube, and suggested she might want to increase the vent settings. She said it didn't matter and gave some vague explanation as to why. Is compensating for the acidosis a legitimate concern or is it just dogma that we don't need to worry about? I recently saw a patient in emerg with acute kidney injury and lithium toxicity who was in resp failure with a bilateral pneumonia/possibly ARDS. She had a pretty significant metabolic acidosis and a resp rate in the 40s, with a pretty low pco2 on blood gas to compensate for her acidosis. ICU came down and intubated and put the patient on a Vt of 500, RR of 12. I let the fellow know that she had a pretty significant metabolic acidosis prior to the tube, and suggested she might want to increase the vent settings. She said it didn't matter and gave some vague explanation as to why. Is compensating for the acidosis a legitimate concern or is it just dogma that we don't need to worry about? You need to make the minute ventilation appropriate for the patients exsisting metabolic acidosis. So if they are hyperventilating before you should probably match their minute ventilation assuming they were not alkalemic. This patient was getting 6L of minute ventilation, which is not going to keep her PCO2 low enough t Continue reading >>

Ventilatory Failure - Critical Care Medicine - Merck Manuals Professional Edition

Ventilatory Failure - Critical Care Medicine - Merck Manuals Professional Edition

Ventilatory failure is a rise in Paco2 (hypercapnia) that occurs when the respiratory load can no longer be supported by the strength or activity of the system. The most common causes are severe acute exacerbations of asthma and COPD, overdoses of drugs that suppress ventilatory drive, and conditions that cause respiratory muscle weakness (eg, Guillain-Barr syndrome, myasthenia gravis, botulism). Findings include dyspnea, tachypnea, and confusion. Death can result. Diagnosis is by ABGs and patient observation; chest x-ray and clinical evaluation may help delineate cause. Treatment varies by condition but often includes mechanical ventilation. (See also Overview of Mechanical Ventilation .) Hypercapnia occurs when alveolar ventilation either falls or fails to rise adequately in response to increased carbon dioxide production. A fall in alveolar ventilation results from a decrease in minute ventilation or an increase in dead space ventilation without appropriate compensation by increasing minute ventilation. Ventilatory failure can occur when there is excessive load on the respiratory system (eg, resistive loads or lung and chest wall elastic loads) versus neuromuscular competence for an effective inspiratory effort. When the minute ventilation load increases (eg, as occurs in sepsis), a compromised respiratory system may not be able to meet this increased demand (for causes, see Figure: The balance between load (resistive, elastic, and minute ventilation) and neuromuscular competence (drive, transmission, and muscle strength) determines the ability to sustain alveolar ventilation. ). Physiologic dead space is the part of the respiratory tree that does not participate in gas exchange. It includes Anatomic dead space (oropharynx, trachea, and airways) Alveolar dead space Continue reading >>

Managing Hypercapnia In Patients With Severe Ards And Low Respiratory System Compliance: The Role Of Esophageal Pressure Monitoringa Case Cohort Study

Managing Hypercapnia In Patients With Severe Ards And Low Respiratory System Compliance: The Role Of Esophageal Pressure Monitoringa Case Cohort Study

Managing Hypercapnia in Patients with Severe ARDS and Low Respiratory System Compliance: The Role of Esophageal Pressure MonitoringA Case Cohort Study 1Intensive Care Unit, E. Wolfson Medical Center, 62 HaLohamim Street, P.O. Box 5, 58100 Holon, Israel 2Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel Received 4 August 2014; Revised 1 October 2014; Accepted 13 October 2014 Copyright 2015 Arie Soroksky et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Purpose. Patients with severe acute respiratory distress syndrome (ARDS) and hypercapnia present a formidable treatment challenge. We examined the use of esophageal balloon for assessment of transpulmonary pressures to guide mechanical ventilation for successful management of severe hypercapnia. Materials and Methods. Patients with severe ARDS and hypercapnia were studied. Esophageal balloon was inserted and mechanical ventilation was guided by assessment of transpulmonary pressures. Positive end expiratory pressure (PEEP) and inspiratory driving pressures were adjusted with the aim of achieving tidal volume of 6 to 8 mL/kg based on ideal body weight (IBW), while not exceeding end inspiratory transpulmonary (EITP) pressure of 25 cm H2O. Results. Six patients with severe ARDS and hypercapnia were studied. Mean PaCO2 on enrollment was mmHg. One hour after adjustment of PEEP and inspiratory driving pressure guided by transpulmonary pressure, PaCO2 decreased to . EITP pressure before intervention was low with a mean of ) after intervention. Adjustment of PEEP and inspiratory driving pressures did not worsen oxygenation and did not affect c Continue reading >>

Permissive Hypercapnia

Permissive Hypercapnia

Permissive hypercapnia is hypercapnia , (i.e. high concentration of carbon dioxide in blood), in respiratory insufficient patients in which oxygenation has become so difficult that the optimal mode of mechanical ventilation (with oxygenation in mind) is not capable of exchanging enough carbon dioxide. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs . In acute respiratory distress syndrome (ARDS), decreasing the tidal volume on the ventilator (usually 8-12 mL/kg) to 4-6 mL/kg may decrease barotrauma by decreasing ventilatory peak airway pressures and leads to improved respiratory recovery. Hypercapnia (increased pCO2) sometimes needs to be tolerated in order to achieve these lower tidal volumes. The permissive hypercapnia leads to respiratory acidosis which might have negative side effects, but given that the patient is in ARDS, improving ventilatory function is more important. Since hypoxemia is a major life-threatening condition and hypercapnia is not, one might choose to accept the latter. Hence the term, "permissive hypercapnia." Altogether, the negative side effects of permissive hypercapnia may outweigh the benefits. For that reason, the implementation of extracorporeal CO2 removal (iLA Membrane Ventilator, Novalung ) at an early stage of ARDS, has become a well established standard[ citation needed ] to allow for protective ventilation and avoid respiratory acidosis. Continue reading >>

Invasive Mechanical Ventilation

Invasive Mechanical Ventilation

V. National Standards, Core Indicators and Quality Measures. The most difficult challenge to face by a hospitalist in regards to invasive mechanical ventilation are when to intubate, what setting the ventilator should be set at and troubleshooting the ventilator. A hospitalist will need to identify when a patient needs intubation and then be able to successfully select the correct ventilator setting to best suit the needs of the patient and subsequently troubleshoot the ventilator when things go wrong. III. Describe a Step-by-Step approach/method to this problem. A good rule of thumb is if you are considering intubation for a patient then you should probably intubate the patient. Non-invasive ventilation (Bilevel Positive Airway Pressure or BiPAP) should only be implemented in patients that have immediately reversible conditions such as pulmonary edema or chronic obstructive pulmonary disease (COPD) exacerbation. Patients with respiratory failure that have conditions requiring more than a few hours to recover are better candidates for mechanical ventilation (e.g., Pneumonia requiring intravenous [IV] antibiotics). One should consider intubation if any of the following criteria are met: Impaired oxygenation: Hypoxemic respiratory failure Impaired ventilation: Hypercapnic respiratory failure Airway protection: increased work of breathing, facial trauma, severe alcohol withdrawal, upper airway obstruction, severe metabolic acidosis with inadequate respiratory compensation There are 3 most common modes of ventilation to choose from: -volume control ventilation: set volume given, patient determines pressure -pressure control ventilation: set pressure given, patient determines volume 2) Synchronized Intermittent Mandatory Ventilation (SIMV) 3) Pressure Regulated Volume Contr Continue reading >>

Preventing Intubation In Acute Respiratory Failure: Use Of Cpap And Bipap

Preventing Intubation In Acute Respiratory Failure: Use Of Cpap And Bipap

Preventing intubation in acute respiratory failure Preventing intubation in acute respiratory failure: Use of CPAP and BiPAP Until recently, options for the treatment of severe acute respiratory failure were limited. If a patient progressed to the point were he was unable to sustain adequate oxygenation and ventilation on his own, then endotracheal intubation and positive pressure ventilation with a mechanical ventilator became necessary. In the past several years, more aggressive medical therapy with agents such as bronchodilators or nitrates (depending upon the underlying etiology), has resulted in less frequent need for intubation. However, the increasing use of noninvasive ventilatory support (NIVS) has further decreased the need for endotracheal intubation in this patient population. Indeed, the use of NIVS in the Emergency Department is probably one of the most significant advances in the care of patients with acute respiratory failure in recent years. The primary goals of this discussion will be to familiarize physicians with the many advantages of NIVS, to encourage its routine use, and to compare and contrast Continuous Positive Airway Pressure (CPAP) with Bi-level Positive Airway Pressure (BiPAP). There are many possible etiologies for acute respiratory failure and the diagnosis is often unclear or uncertain during the critical first few minutes after ED presentation. Since it is often necessary to initiate treatment before a clear diagnosis can be established, taking a pathophysiologic approach towards the patient can be useful. To that end, the "respiratory equation of motion" can provide a useful conceptual framework in determining why the patient is unable to sustain adequate minute ventilation. Pmuscle + Papplied = E(Vt) + R(V) + threshold load + Inertia Continue reading >>

Ventilation, Ventilator Management

Ventilation, Ventilator Management

There is no doubt that mechanical ventilation is a life-saving procedure that has impacted millions of lives of patients with respiratory failure around the world. It is also beneficially used in patients with chronic irreversible causes of respiratory failure like neuromuscular disease or spinal cord injuries, permitting them to live a life that would not have been possible before the creation of the mechanical ventilator. The need for mechanical ventilation is one of the most common causes of admission to the intensive care unit. It is first imperative to understand some basic terms to understand mechanical ventilation. Ventilation: Exchange of air between the lungs and the air (ambient or delivered by a ventilator), in other words, it is the process of moving air in and out of the lungs. Its most important effect is the removal of carbon dioxide (CO2) from the body, not on increasing blood oxygen content. Ventilation is measured as minute ventilation in the clinical setting, and it is calculated as respiratory rate (RR) times tidal volume (Vt). In a mechanically ventilated patient, the CO2 content of the blood can be modified bychanging the tidal volume or the respiratory rate. Oxygenation: Interventions that provide greater oxygen supply to the lungs, thus the circulation. In a mechanically ventilated patient, this can be achieved by increasing the fraction of inspired oxygen (FiO 2%) or the positive end-expiratory pressure (PEEP). PEEP:The positive pressure that will remain in the airways at the end of the respiratory cycle (end of exhalation) that is greater than the atmospheric pressure in mechanically ventilated patients. For a full description of the use of PEEP, please review the article titled Positive End-Expiratory Pressure (PEEP). Tidal volume: Volume of Continue reading >>

Mechanical Ventilation And The Copd Patient

Mechanical Ventilation And The Copd Patient

RT: For Decision Makers in Respiratory Care Mechanical Ventilation and the COPD Patient The challenge of mechanically ventilating a patient with COPD can be met by preventing autoPEEP and dynamic hyperinflation. During the past 10 years, much of the focus in mechanical ventilation has been on preventing ventilator-induced lung injury and on optimizing care for patients with the preventing ventilator-induced lung injury and on optimizing care for patients with the adult respiratory distress syndrome (ARDS).1 Ventilatory support of the patient with chronic obstructive pulmonary disease (COPD) differs greatly from that of the ARDS patient and remains a challenge. While noninvasive positive-pressure ventilation (NPPV) is now considered the first choice for the treatment of selected patients experiencing COPD exacerbations, there are some patients for whom NPPV may not be suitable due to the severity of their conditions.2 Pathophysiology of COPD Severe airflow obstruction that imposes a significant load on the respiratory system is a major manifestation of COPD. Airflow obstruction develops when the airway diameter is narrowed by bronchospasm, mucosal or interstitial edema, and mucus, causing dynamic airway collapse during exhalation. This increases the time required for exhalation, thus elevating lung volume and alveolar pressure; end-expiratory lung volume (EELV) exceeds functional residual capacity. In contrast, EELV in individuals without COPD approximates the relaxed volume of the respiratory system. The term dynamic hyperinflation is used to describe this phenomenon of increased lung volume and is associated with the increased work of breathing (WOB) and the hypercapneic state observed in the COPD patient.3,4 The reduced expiratory airflow also causes air trapping at Continue reading >>

Acid-base Tutorial - Respiratory Correction

Acid-base Tutorial - Respiratory Correction

by "Grog" (Alan W. Grogono), Professor Emeritus, Tulane University Department of Anesthesiology Acid-Base Therapy: Respiratory Correction The objective is to restore the PCO2 to its customary position for that patient which, for someone with chronic lung disease, will be higher than PCO2 = 40 mmHg (5.7 kPa). Emergency therapy: The body's metabolism produces respiratory (carbonic) acid and, in cardiorespiratory failure also produces metabolic (lactic) acid. In emergencies, therefore, it is usual to find that correction is required for metabolic or respiratory acidosis. For this reason, and in the interest of simplification, the following paragraphs primarily discuss acidosis and its correction: Respiratory acidosis. A physician decides to ventilate a patient to reduce the PCO2 level based on exhaustion, prognosis, prospect of improvement from concurrent therapy and, only in part, on the PCO2 level. Once the clinical decision is made, the PCO2 helps calculate the appropriate correction. The PCO2 reflects the balance between the production of carbon dioxide and its elimination. Unless the metabolic rate changes, the amount of carbon dioxide produced is roughly constant and determines the amount of ventilation required and the level of PCO2. Where VT equals tidal volume and f equals frequency of ventilation: PCO2 x f x VT = K This equation means that the same number of carbon dioxide molecules are eliminated by high ventilation at a low PCO2 as by low ventilation at a high PCO2, The Target Ventilation is calculated by dividing k by the target PCO2: New Ventilation = K/Target PCO2 = PCO2 x f x VT / Target PCO2 Illustrations (Click on Picture on Right): 1) Pure Respiratory Acidosis: This patient has a pure (acute) respiratory acidosis with a PCO2 = 70 mmHG (9.8 kPa) and is v Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

DEFINITION Respiratory acidosis = a primary acid-base disorder in which arterial pCO2 rises to an abnormally high level. PATHOPHYSIOLOGY arterial pCO2 is normally maintained at a level of about 40 mmHg by a balance between production of CO2 by the body and its removal by alveolar ventilation. PaCO2 is proportional to VCO2/VA VCO2 = CO2 production by the body VA = alveolar ventilation an increase in arterial pCO2 can occur by one of three possible mechanisms: presence of excess CO2 in the inspired gas decreased alveolar ventilation increased production of CO2 by the body CAUSES Inadequate Alveolar Ventilation central respiratory depression drug depression of respiratory centre (eg by opiates, sedatives, anaesthetics) neuromuscular disorders lung or chest wall defects airway obstruction inadequate mechanical ventilation Over-production of CO2 -> hypercatabolic disorders Malignant hyperthermia Thyroid storm Phaeochromocytoma Early sepsis Liver failure Increased Intake of Carbon Dioxide Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) EFFECTS CO2 is lipid soluble -> depressing effects on intracellular metabolism RESP increased minute ventilation via both central and peripheral chemoreceptors CVS increased sympathetic tone peripheral vasodilation by direct effect on vessels acutely the acidosis will cause a right shift of the oxygen dissociation curve if the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the left CNS cerebral vasodilation increasing cerebral blood flow and intracranial pressure central depression at very high levels of pCO2 potent stimulation of ventilation this can result in dyspnoea, disorientation, acute confusion, headache, Continue reading >>

Using Abgs To Optimize Mechanical Ventilation

Using Abgs To Optimize Mechanical Ventilation

Using ABGs to optimize mechanical ventilation June 2013, Volume 43 Number 6 , p 46 - 52 This article has an associated Continuing Education component. AN ARTERIAL BLOOD GAS (ABG) analysis can tell you about the patient's oxygenation (via PaO2 and SaO2), acid-base balance, pulmonary function (through the PaCO2), and metabolic status. This article focuses on translating ABG information into clinical benefits, with three case studies that focus on using ABGs to manage mechanical ventilation. Endotracheal (ET) intubation and mechanical ventilation may be prescribed for patients who can't maintain adequate oxygenation or ventilation or who need airway protection. The goal of mechanical ventilation is to improve oxygenation and ventilation and to rest fatigued respiratory muscles. Mechanical ventilation is supportive therapy because it doesn't treat the causes of the illness and associated complications. However, ventilator support buys time for other therapeutic interventions to work and lets the body reestablish homeostasis. When using this lifesaving intervention, clinicians should take steps to avoid or minimize ventilator-induced lung injury (VILI), which will be discussed in detail later. Patients should be weaned from ventilatory support if their condition permits. A critically ill patient's clinical status can change rapidly and dramatically, and the need for ventilatory support in terms of oxygenation or minute ventilation can vary at different stages of the illness. ABG analysis is an indispensable diagnostic tool for monitoring the patient's condition and evaluating the response to interventions. By reviewing the patient's ABGs and clinical status, clinicians can adjust ventilator settings to improve oxygenation, ventilation, and acid-base balance, or wean the pat Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is an abnormal clinical process that causes the arterial Pco2 to increase to greater than 40 mm Hg. Increased CO2 concentration in the blood may be secondary to increased CO2 production or decreased ventilation. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Respiratory acidosis can arise from a break in any one of these links. For example, it can be caused from depression of the respiratory center through drugs or metabolic disease, or from limitations in chest wall expansion due to neuromuscular disorders or trauma (Table 90-1). It can also arise from pulmonary disease, card iog en ic pu lmon a ryedema, a spira tion of a foreign body or vomitus, pneumothorax and pleural space disease, or through mechanical hypoventilation. Unless there is a superimposed or secondary metabolic acidosis, the plasma anion gap will usually be normal in respiratory acidosis. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 Respiratory acidosis is characterized by an increased arterial blood PCO2 and H+ ion concentration. The major cause of respiratory acidosis is alveolar hypoventilation. The expected physiologic response is an increased . The increase in concentration of bicarbonate ions (HCO3) in plasma ( ) is tiny in patients with acute respiratory acidosis, but is much larger in patients with chronic respiratory acidosis. Respiratory alkalosis is caused by hyperventilation and is characterized by a low arterial blood PCO2 and H+ ion concentration. The expected physiologic response is a decrease in . As in respiratory acidosis, this response is modest in patients with acute respiratory alkalosis and much larger in patients with chronic respir Continue reading >>

Mechanical Ventilation Pimer- Clinical Respiratory Diseases & Critical Care Medicine, Seattle - Med 610 - University Of Washington School Of Medicine

Mechanical Ventilation Pimer- Clinical Respiratory Diseases & Critical Care Medicine, Seattle - Med 610 - University Of Washington School Of Medicine

Although mechanical ventilation is a key component of intensive care, unfamiliar jargon and technical detail render it confusing and formidably difficult for many clinicians. The rapidity and complexity of change in this area of respiratory medicine in recent years adds to the problem. Most of the current literature and nearly all the controversy in mechanical ventilation apply to only a small fraction of the patients who are intubated and ventilated in acute care hospitals. This small fraction consists of those with severe respiratory failure due to acute diffuse lung injuryacute lung injury (ALI) or the acute respiratory distress syndrome (ARDS)and also those with severe obstructive lung disease (COPD or asthma). For the other 80 or 90 percent of ventilated patients the issues are much less difficult. At best, mechanical ventilation can support gas exchange and lung inflation in a reasonably normal fashion. It is supportive, replacement therapy only; there is no disease that intubating and ventilating a patient will cure. When done as well as we know how, mechanical ventilation can come close to replacing the normal functions of the lungs and chest bellows. Considering the many adverse consequences of intubation and positive-pressure ventilation, the clinician should always be striving to make the period of ventilatory support as short as possible. This primer summarizes the main issues in mechanical ventilation, explains many of the modes, settings, and terms involved, and reviews aspects of monitoring and complications with which the clinician should be familiar. It focuses on invasive mechanical ventilation (that is, on ventilating intubated patients), and on the care of adults rather than children or infants. Parts of it are adapted from the chapter on invasive m Continue reading >>

Free Respiratory Therapy Flashcards About Mechvent 1

Free Respiratory Therapy Flashcards About Mechvent 1

the amount of force needed to overcome airway resistance and inflate the lung w/ a volume. (= Vt/PIP-PEEP) inspiratory hold of air w/ a Pplat giving the C of the lungs. (= Vt/Pplat-PEEP) How will Cstat and Cdyn change under Raw and stiffness? What changes in pts status can affect Cstat and Cdyn? Cstat will decrease w/ resistance or w/ air-trapping; Cdyn will decrease or become less C w/ an obstruction end of inhalation (i.e. machine stops at end of inhalation) List the various factors used to trigger ventilator breaths. Pressure and Flow (pt.), Timed (vent.), Manuel (operator) the pressure maintained in the airways in an entire respiratory cycle. in Paw then an in PaO2 What ventilator parameters (i.e. PEEP, Ti) that affects Paw. Can be increased w/ PIP, PEEP***, I-Time. SIMV prevents breath stacking, IMV will give a pt a breath no matter where they are in a spontaneous breath. What blood gas value is the primary indicator of adequate ventilation? Describe the possible negative impacts of PEEP therapy. barotraumas, venous return, Qt and renal blood flow, WOB, PVR, ICP, deadspace, mean airway pressure. Describe the negative physiological effects of positive pressure vent. barotraumas*, venous return, Qt*, renal blood flow, urine output, and gastrointestinal function (due to blood flow), also an in ICP, PVR, deadspace and mean airway pressure. What will be the result of an Raw or a in compliance on a volume cycled ventilator? What will be the result of an Raw or a in compliance on a pressure, time cycled ventilator? Pressure, time stays the same as volume s. Less VE then pt could become hypercapnic What are the various ways you can adjust I:E on a vol-cycled vent? flow* or I-Time* or Vt or even RR (changes TCT) Highest PIP on a volume ventilator that can occur before poss Continue reading >>

Respiratory Acidosistreatment & Management

Respiratory Acidosistreatment & Management

Respiratory AcidosisTreatment & Management Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more... Treatment of respiratory acidosis is primarily directed at the underlying disorder or pathophysiologic process. Caution should be exercised in the correction of chronic hypercapnia: too-rapid correction of the hypercapnia can result in metabolic alkalemia. Alkalization of the cerebrospinal fluid (CSF) can result in seizures. The criteria for admission to the intensive care unit (ICU) vary from institution to institution but may include patient confusion, lethargy, respiratory muscle fatigue, and a low pH (< 7.25). All patients who require tracheal intubation and mechanical ventilation must be admitted to the ICU. Most acute care facilities require that all patients being treated acutely with noninvasive positive-pressure ventilation (NIPPV) be admitted to the ICU. Consider consultation with pulmonologists and neurologists for assistance with the evaluation and treatment of respiratory acidosis. Results from the history, physical examination, and available laboratory studies should guide the selection of the subspecialty consultants. Pharmacologic therapies are generally used as treatmentfor the underlying disease process. Bronchodilators such as beta agonists (eg, albuterol and salmeterol), anticholinergic agents (eg, ipratropium bromide and tiotropium), and methylxanthines (eg, theophylline) are helpful in treating patients with obstructive airway disease and severe bronchospasm. Theophylline may improve diaphragm muscle contractility and may stimulate the respiratory center. Respiratory stimulants have been used but have limited efficacy in respiratory acidosis caused by disease. Medroxyprogesterone increases central respiratory drive and may Continue reading >>

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