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What Is The Cause Of Respiratory Acidosis?

Respiratory Acidosis

Respiratory Acidosis

Sort Medical Management improve respiratory ventilation via: -mechanical ventilation -bronchodilators, antibiotics, anticoagulants -pulmonary hygiene; coughing, turning, deep breathing INCENTATIVE SPIROMETER postural drainage -adequate hydration -supplemental oxygen (beware if chronic hypercapnia) *COPD pt's are accustomed to increased CO2 levels; a lack of O2 called hypoxic drive stimulates these pt's to breathe -monitor I&O, VS (always include O2 sat), ABGs In a patient with respiratory acidosis you will see... decreased pH & increased CO2 hypoventilation rapid, shallow respirations increased BP dyspnea headache hyperkalemia disorientation increased cardiac output muscle weakness hyppoxia Continue reading >>

The Four Primary Disturbances Of Acid-base Balance

The Four Primary Disturbances Of Acid-base Balance

Primary Respiratory Acidosis initiating event: V�A (hypoventilation) chronic obstructive pulmonary disease (COPD) weak respiratory muscles (neuromuscular diseases) barbiturate poisoning (central nervous system depression) resultant effects: CO2 retention PaCO2, [H+] and pH compensations: 2� metabolic alkalosis HCO3- retention via PaCO2 effect on renal proximal tubules Primary Respiratory Alkalosis initiating event: V�A (hyperventilation) salicylate intoxication (over-aggressive aspirin therapy) hyperexcitability psychogenic paroxysmal hyperventilation ("brown paper bag" therapy) artificial ventilation resultant effects: CO2 elimination PaCO2, [H+] and pH compensations: 2� metabolic acidosis HCO3- retention via reverse PaCO2 effect on renal proximal tubules Primary Metabolic Acidosis initiating events: renal and extrarenal diabetes mellitus and ketoacidosis (larger than normal anion gap) severe shock or heart failure and lactic acidosis (larger than normal anion gap) diarrhea and loss of bicarbonate ions (normal anion gap) renal tubular acidosis and retention of hydrogen ions (normal anion gap) resultant effects: [H+] and/or [HCO3-], pH compensations: 2� respiratory alkalosis (with renal participation if possible) CO2 elimination via acid drive on ventilation Kussmaul respiration (characteristic deep labored breathing) Primary Metabolic Alkalosis initiating events: renal and extrarenal chronic potassium ion depletion (aggressive diuretic therapy, hyperaldosteronism) protracted vomiting (pyloric obstruction, gastric ulcers) and loss of gastric acids dehydration and depletion of extracellular fluid volume (contraction alkalosis) resultant effects: [H+] and/or [HCO3-], pH urine pH will be paradoxically low (acidic) if there is chronic depletion of potassium ions c Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] 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 mm Hg). Causes[edit] Acute[edit] 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. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>

Causes Of Respiratory Acidosis And Alkalosis - Deranged Physiology

Causes Of Respiratory Acidosis And Alkalosis - Deranged Physiology

Causes of Respiratory Acidosis and Alkalosis Respiratory acidosis and alkalosis are featured in virtually every paper, and being able to identify a respiratory acid-base disturbance is a vital skill for the CICM fellowship candidate. The SAQs will frequently require the application of the usual rules of compensation to reveal a hidden acid-base disorder, eg. "this patient has a low CO2 but it is not low enough". Questions which involve respiratory acid-base disturbances are too numerous to list. Some representative examples include the following: Question 12.3 from the second paper of 2014 Question 3.4 from the first paper of 2013 Question 3.5 from the first paper of 2013 Question 8.3 from the first paper of 2012 Question 9.1 from the first paper of 2011 Question 7.2 from the first paper of 2009 Several CICM fellowship questions revolve around the core question, "what possible causes for this respiratory acid-base disturbance can you think of ?" The causes can be split into aetiological categories, as below: Causes of Respiratory Acidosis and Alkalosis Rebreathing of CO2-containing expired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) CO2 increases by 3mmg for every minute of apnoea central respiratory depression eg. by drugs or post-ictally neuromuscular disorders resulting in weakness lung or chest wall defects resulting in restriction The pH change in response to a chronic respiratory acid-base disturbance 0: An acute change in PaCO2 will not change the Standard Base Excess. 4: In chronic disorders, the expected change in SBE will be 0.4 times the change in PaCO2 ... i.e. expected SBE = 0.4 (40 - PaCO2) 1: In compensation for metabolic acidosis, the compensatory change in PaCO2 will be proportional to the SBE. ..i.e. expected CO2 = 40 + (1.0 Continue reading >>

Acid-base Disturbance In Copd

Acid-base Disturbance In Copd

Summarized from Bruno M, Valenti M. Acid-base disorders in patients with chronic obstructive pulmonary disease: A pathophysiological review. J Bomedicine and Biotechnology (2012) Article ID 915150 8 pages ( available at :) Arterial blood gases are frequently useful in the clinical management of patients with chronic obstructive pulmonary disease (COPD) to assess both oxygenation and acid-base status. A recent review article focuses on disturbance of acid-base in these patients, which occurs in advanced disease when pulmonary gas exchange is so compromised that the rate of carbon dioxide production in the tissues exceeds the rate of carbon dioxide elimination by the lungs. The article begins with an explanation of how the resulting carbon dioxide accumulation in blood leads to respiratory acidosis, the acid-base disturbance that commonly occurs in advanced COPD. An important distinction is made between acute and chronic respiratory acidosis; compensation is less effective in the former. Then follows a detailed description of the several renal mechanisms involved in the compensatory response to chronic respiratory acidosis. Although this mitigates the acidosis to a considerable extent, it often does not result in normalisation of pH. The deleterious effects of acidosis are enumerated and the authors also briefly review the epidemiological study that links severity of acidosis to poorer outcome among COPD patients. The significance of renal compensatory mechanisms is highlighted again in the discussion of the co-existence of renal failure in patients with COPD who to a greater or lesser extent lack these mechanisms and thereby have worse acidosis and poorer outcome. Many COPD patients with respiratory acidosis are suffering other conditions or prescribed drugs that affect Continue reading >>

Evaluation Of Respiratory Acidosis

Evaluation Of Respiratory Acidosis

Respiratory acidosis occurs when acute or chronic derangements of the respiratory system lead to inefficient clearance of carbon dioxide. These derangements may involve: A disorder of central control of ventilation. When alveolar gas exchange units are unable to sufficiently excrete carbon dioxide, this leads to an increase in the arterial carbon dioxide levels above the normal range of 35 to 45 mmHg (4.7-6.0 kPa). With the increase in carbon dioxide, hydrogen ions accumulate, causing the arterial pH to fall below the normal range (i.e., <7.35). [1] O'Driscoll BR, Howard LS, Earis J, et al. BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax. 2017;72(suppl 1):ii1-ii90. Respiratory acidosis may be acute or chronic. Acute respiratory acidosis is usually secondary to acute respiratory failure. In acute respiratory failure, there is insufficient buffering capacity to handle the dramatic increase in arterial and venous carbon dioxide. Over time, more and more carbon dioxide is processed by carbonic anhydrase to bicarbonate (the Hamburger shift). This leads to chloride excretion by the kidney with ammonium, and the pH gradually rises. [2] Alfaro V, Torras R, Ibez J, et al. A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease. Can J Physiol Pharmacol. 1996;74:1229-1235. The consequences of failing to recognize acute respiratory failure include marked hypoxemia, hyperkalemia, cardiovascular instability, and cardiac arrest. Drug use (narcotics, alcohol, sedatives, anesthetics) Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory Acidosis is a pathophysiological category of acidosis and refers to those acidoses caused by primary disturbances in ventilation. Although ventilatory defects can cause significant decreases in the blood pH, renal compensatory mechanisms can largely correct the pH over several days. The fundamental cause of all respiratory acidoses is insufficient alveolar ventilation, resulting in an increase in the partial pressure of arterial carbon dioxide (PaCO2). Increased PaCO2 results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the reduced ECF pH results from an increase in the ratio between PaCO2 relative to the ECF concentration of bicarbonate ([HCO3-]). More colloquially, deficiencies in alveolar ventilation result in an inability of the lungs to "Breathe Off" gaseous CO2 which is immediately converted to carbonic acid H2CO3 in the extracellular fluid. H2CO3 immediately releases a free hydrogen ion (H+) which serves to reduce the ECF pH, thus causing acidosis. Respiratory Acidoses can be compensated by the actions of the kidneys which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of several days. As described in Renal Response to Acid-Base Imbalance, the kidneys respond to acidosis by secreting free hydrogen ions in the urine, synthesizing novel bicarbonate which is added to the ECF, and reducing any urinary excretion of bicarbonate. By secreting acid in the urine, the kidneys may slightly reduce the PaCO2 over several days. However, the most important renal contribution is the synthesis of novel bicarbonate and reduction in urinary bicarbonate excretion which serve to slowly increase the ECF bicarbonate concent Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory Acidosisis an acid-base imbalance characterized by increased partial pressure of arterial carbon dioxide and decreased blood pH. The prognosis depends on the severity of the underlying disturbance as well as the patients general clinical condition. Compensatory mechanisms include (1) an increased respiratory rate; (2) hemoglobin (Hb) buffering, forming bicarbonate ions and deoxygenated Hb; and (3) increased renal ammonia acid excretions with reabsorption of bicarbonate. Acute respiratory acidosis:Associated with acute pulmonary edema, aspiration of foreign body, overdose of sedatives/barbiturate poisoning, smoke inhalation, acute laryngospasm, hemothorax / pneumothorax , atelectasis, adult respiratory distress syndrome (ARDS), anesthesia/ surgery , mechanical ventilators, excessive CO2intake (e.g., use of rebreathing mask, cerebral vascular accident [CVA] therapy), Pickwickian syndrome. Chronic respiratory acidosis:Associated with emphysema , asthma , bronchiectasis; neuromuscular disorders (such as Guillain-Barr syndrome and myasthenia gravis); botulism; spinal cord injuries. Condition, prognosis, and treatment needs understood. Plan in place to meet needs after discharge. This condition does not occur in isolation, but rather is a complication of a broader health problem/disease or condition for which the severely compromised patient requires admission to a medical-surgical or subacute unit. Main Article: Respiratory Acidosis Nursing Care Plan Remain alert for critical changes in patients respiratory, CNS and cardiovascular functions. Report such changes as well as any variations in ABG values or electrolyte status immediately. Maintain patent airway and provide humidification if acidosis requires mechanical ventilation . Perform tracheal suctioning frequ Continue reading >>

Metabolic Acidosis And Alkalosis

Metabolic Acidosis And Alkalosis

Page Index Metabolic Acidosis. Metabolic Alkalosis Emergency Therapy Treating Metabolic Acidosis Calculating the Dose Use Half the Calculated Dose Reasons to Limit the Bicarbonate Dose: Injected into Plasma Volume Fizzes with Acid Causes Respiratory Acidosis Raises Intracellular PCO2 Subsequent Residual Changes Metabolic Acidosis. The following is a brief summary. For additional information visit: E-Medicine (Christie Thomas) or Wikepedia Etiology: There are many causes of primary metabolic acidosis and they are commonly classified by the anion gap: Metabolic Acidosis with a Normal Anion Gap: Longstanding diarrhea (bicarbonate loss) Uretero-sigmoidostomy Pancreatic fistula Renal Tubular Acidosis Intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants Renal failure Metabolic Acidosis with an Elevated Anion Gap: lactic acidosis ketoacidosis chronic renal failure (accumulation of sulfates, phosphates, uric acid) intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene, sulfates, metformin. rhabdomyolysis For further details visit: E-Medicine (Christie Thomas). Treating Severe Metabolic Acidosis. The ideal treatment for metabolic acidosis is correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO2. If it is decided to administer bicarbonate, the SBE and the size of the treatable space are used to calculate the dose required: Metabolic Alkalosis Etiology: Primary Metabolic alkalosis may occur from various causes including: Loss of acid via the urine, stools, or vomiting Transfer of Continue reading >>

Respiratory Acidosis: Causes And Regulation

Respiratory Acidosis: Causes And Regulation

This lesson will discuss an important relationship between the kidneys and the lungs and how both of them play a role in respiratory acidosis. We'll also discuss some of the major causes of respiratory acidosis. Mutualistic Relationships A mutualistic relationship refers typically to a couple of different species of animals helping one another out. Take, for example, the birds that clean an alligator's teeth. The alligator gets a free dental exam, no insurance necessary, and the birds get a nice meal. It's really weird in a way that a bird and a reptile would rely on one another. They are just so different in terms of their size, function, and appearance, but their relationship is nonetheless very important. Well, the kidneys have a relationship with the lungs that is equally weird but important. I mean, the lungs are much bigger, look totally different, and don't seem to be related to the kidneys at all! But these two organ systems are in a very important mutualistic relationship, only one fourth of which can be discussed in this lesson. A Couple of Important Terms Before we get to everything, I want to clarify some terms. 'Acidemia' refers to an abnormally low pH of the blood. pH is inversely proportional to the concentration of H+ (hydrogen ions, aka protons). Hydrogen ions confer acidity upon a substance. So if we raise the concentration of hydrogen, we actually lower the pH. Acidemia is a result of acidosis. 'Acidosis' refers to a pathological state or process that leads to acidemia. We'll be using these terms later, so keep them in mind. To help remember that acid has a low pH, just think about the fact that gastric acid sits 'down' in your stomach. Therefore, something acidic moves 'down' the pH scale. Respiratory Acidosis Okay, with that out of the way for a bit Continue reading >>

Surgical Procedures/acid Base Disorder

Surgical Procedures/acid Base Disorder

(Usually in clinical practice, H+ concentration is expressed as pH.) PaCO2 (Arterial CO2 concentration normal = 3545 mm Hg). HCO3 (Serum electrolytes normal = 2231 mmol/liter). Acidosis is a process that causes the accumulation of acid. Alkalosis is a process that causes the accumulation of alkali. The most common causes in the surgical practice include: Diuretic therapy (e.g., contraction alkalosis). Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting). Exogenous administration of HCO3 or HCO3 precursors (e.g., citrate in blood). Chloride-unresponsive metabolic alkalosis is comparatively less common and includes: Renal tubular Cl wasting (Bartters syndrome) Measurement of urinary chloride concentration. Suggestive causes of the metabolic alkalosis if Urine Cl concentration is <15 mmol/liter: Sughgestive causes of the metabolic alkalosis if Urine Cl concentration is > 20 mmol/liter: Treatment principles in metabolic alkalosis:[ edit ] Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl, K+, and volume deficits. Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia. H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning. Acetazolamide (5 mg/kg/day IV or PO) can be used. Eases fluid mobilization while decreasing renal HCO3 reabsorption. Tolerance to this diuretic may develop after 23 days. Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3 >40 mmol/liter; rate not exceeding 5 ml/minute). Approximately one-half of the calculated volume of NH4Cl is usually administered and the acid-base status and Cl concentration is usually rechecked to determine the need of further treatment. Hepatic failure is contraindication for NH4Cl. HCl m Continue reading >>

Respiratory Failure (types I And Ii)

Respiratory Failure (types I And Ii)

Respiratory failure (types I and II) References What is Respiratory failure (types I and II) Respiratory failure is a disease of the lungs. The respiratory system basically consists of a gas exchanging organ (the lungs) and a ventilatory pump (respiratory muscles and the thorax). Either or both of these can fail and cause respiratory failure. Respiratory failure occurs when gas echange at the lungs is sufficiently impaired to cause a drop in blood levels of oxgyen (hypoxaemia); this may occur with or without an increase in carbon dioxide levels. The definition of respiratory failure is PaO27kPa (55mmHg). Respiratory failure is divided into type I and type II. Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels. Type II respiratory failure involves low oxygen, with high carbon dioxide. Statistics on Respiratory failure (types I and II) Respiratory failure is common, as it occurs in any severe lung disease it can also occur as a part of multi-organ failure. Risk Factors for Respiratory failure (types I and II) Causes of Type I respiratory failure: disease that damage lung tissue, including pulmonary oedema , pneumonia , acute respiratory distress syndrome , and chronic pulmonary fibrosing alveoloitis. Causes of Type II respiratory failure: the most common cause is chronic obstructive pulmonary disease (COPD). Others include chest-wall deformities, respiratory muscle weakness (e.g. Guillain-Barre syndrome ) and central depression of the respiratory centre (e.g. heroin overdose). Progression of Respiratory failure (types I and II) Type I respiratory failure occurs because of damage to lung tissue. This lung damage prevents adequate oxygenation of the blood (hypoxaemia); however, the remaining normal lung is still sufficient to excrete th Continue reading >>

Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Received 29 September 2011; Accepted 26 October 2011 Copyright 2012 Cosimo Marcello Bruno and Maria Valenti. 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. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. Chronic obstructive pulmonary disease (COPD) is a major public health problem. Its prevalence varies according to country, age, and sex. On the basis of epidemiologic data, the projection for 2020 indicates that COPD will be the third leading cause of death worldwide and the fifth leading cause of disability [ 1 ]. About 15% of COPD patients need admission to general hospital or intensive respiratory care unit for acute exacerbation, leading to greater use of medical resources and increased costs [ 2 5 ]. Even though the overall prognosis of COPD patients is lately improved, the mortality rate remains high, and, among others, acid-base disorders occurring in these subjects can affect the outcome. The aim of this pa Continue reading >>

Respiratory Effects Of Morphine In Humans

Respiratory Effects Of Morphine In Humans

Respiratory Effects of Morphine in Humans Naomi Parks has been a freelancing professional since 2004. She is a biochemist and professional medical writer with areas of interest in pulmonology, pharmaceuticals, communicable diseases, green living and animals. She received her Bachelor of Arts in biological anthropology from San Francisco University and her Master of Science in biochemistry from Pace University. Morphine is an opiate derived from poppy seeds. Morphine is an opiate drug that is derived from poppy seeds. According to the book "Basics of Anesthesia," it is a base opiate with which pharmacological chemists compare all other opiates to determine dosage and intensity proportions. Medically, doctors prescribe morphine as an anesthetic, but some people abuse the drug because it causes euphoria, sedation and analgesia. The onset of morphine's affects manifests more quickly in men than women, according to "Basics of Anesthesia." According to "Brunner and Suddarth's Textbook of Medical-Surgical Nursing," epidural opioids like morphine cause respiratory depression, which can occur within anywhere between an hour and 24 hours of administration, but usually peaks within 6 to 12 hours. Respiratory depression essentially indicates that the respiratory system has slowed, resulting in reduced oxygenation and contributing to feelings of sedation. Nurses monitor patients receiving morphine injections for the first time for at least 24 hours to ensure that respiratory depression does not result in progressive respiratory issues, physiological damage due to respiratory depression or loss of consciousness. The respiratory depression caused by morphine can lead to respiratory acidosis, particularly in patients recovering from relaxant anesthesia, according to "Handbook of Drug Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Causes of respiratory acidosis include: Diseases of the lung tissue (such as pulmonary fibrosis, which causes scarring and thickening of the lungs) Diseases of the chest (such as scoliosis) Diseases affecting the nerves and muscles that signal the lungs to inflate or deflate Drugs that suppress breathing (including powerful pain medicines, such as narcotics, and "downers," such as benzodiazepines), often when combined with alcohol Severe obesity, which restricts how much the lungs can expand Obstructive sleep apnea Chronic respiratory acidosis occurs over a long time. This leads to a stable situation, because the kidneys increase body chemicals, such as bicarbonate, that help restore the body's acid-base balance. Acute respiratory acidosis is a condition in which carbon dioxide builds up very quickly, before the kidneys can return the body to a state of balance. Some people with chronic respiratory acidosis get acute respiratory acidosis because an illness makes their condition worse. Continue reading >>

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