DOCSLIB.ORG

Acid-Base Disturbances Physiological Approach

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Acid-Base Disturbances Physiological Approach Acid-Base disturbances Physiological approach Pieter Roel Tuinman, M.D., PhD, intensivist Department of Intensive Care, VU Medical Center, Amsterdam, The Netherlands p.tuinman@vumc.nl Content • Introduction • Regulation of acid-base balance • Diagnosis of acid-base disturbances • Examples Acid-Base balance • definition: Bronsted-Lowry (1923) • Homeostasis • Physiologic effects of pH on protein function • normal A:B ratio 1:20 – strength is defined in terms of the tendency to donate (or accept) the hydrogen ion to (from) the solvent (i.e. water in biological systems) Relation pH and H+ pH H+ nanomol/L 7,80 16 7,60 26 7,40 40 7,20 63 7,00 100 Henderson-Hasselbalch equation + - 0.03 PCO2 H + HCO3 + • H = 800 x --------------- K d = ————— - CO HCO3 2 disolved - HCO3 Metabolic by kidneys • pH = 6.1 + log --------- CO2 disolved Respiratory by lungs pH pH is and indirect measure of [H+] CAVE! Hydrogen ions (i.e. protons) do not exist free in solution but are linked to adjacent water molecules by + hydrogen bonds (H3O ) [H+] by a factor of 2 causes a pH of 0.3 normal plasma pH pH 7.4 (7.36-7.44) normal Acidosis <7.35 pH 7.45> alkalosis Range compatible with life 6.80-7.80 (H+ 160-16 nM) Acid-base disturbances Why of interest? • Frequently encountered • Are (first) sign of illness • Can be used to diagnose the disease • Require early treatment Examples of diseases resulting in acid-base disturbance • CZS: CVA, bleeding, trauma • Circulation: hypotension, myocardial infarction • Respiratory: COPD, asthma. • Renal: acute / chronic kidney injury • Tr dig: vomiting, chronic diarrhea. • Liver: acute / chronic liverfailure H+-regulation • Chemical buffering • Control of PCO₂ - • Control of plasma HCO3 Regulation of acid-base balance How ? • Dilution (distribution) • Chemical buffering (intra – and extracellular) • Regulation of CO2 concentration (respiratory) + - • Regulation of H and HCO3 concentration (metabolic) Acid excretion Lungs • 20 – 50 mol volatile acid/day – (2 – 4 liter concentrated HCL) Kidneys • 80 mmol/l non-volatile, sulfate, phosphate, urineacid, citrate, ammoniumsalts. x 1000 times more acid trough lungs than kidneys Respiratory system - CO2 + differences in the stimulation of respiration by pCO2, H and pO2 alveolar ventilation disturbances acidemia respiratory centre of the brain alveolar ventilation CO2 alkalemia respiratory centre of the brain alveolar ventilation CO2 Respiratory regulation Influence of pH on breathing Daily CO2 production : 15.000 mmol/day H+ chemoreceptors medulla oblongata • pH ↑ alveolar ventilation /Minute volume • pH alveolar ventilation /Minute volume↑ Renal regulation - • Serum pH ↑ Urine pH↑ = netto HCO3 excretion • Serum pH Urine pH = netto H+ excretion Regulation kidney in summary serum pH↑ - HCO3 resorption H+ secretion = Netto base loss Urine buffers serum pH - HCO3 resorption ↑ H+ secretion↑ = Netto acid loss Urine buffers ↑ Quantative rules (see Berend et al. NEJM) • Compensation of acid-base disturbance is bound by quantative rules • Are this rules disregarded, than there is a mixed-acid-base disturbance • Over - or undercompensation does not exist - HCO3 ( nier ) Rules in general pH =pK + log ---------------- CO2 ( long ) - • Definition acid-base distubance pH, PCO2 en HCO3 • Compensation is usually not complete pH < 7.35 acidosis pH > 7.45 alkalosis • Inadequate compensation Mixed disturbance - • Direction compensation the same HCO3 / CO2 ratio. Assessment of A-B balance Arterial blood Mixed venous blood range range pH 7.40 7.35-7.45 pH 7.33-7.43 pCO 40 mmHg 35 – 45 pCO2 41 – 51 pO2 95 mmHg 80 – 95 pO2 35 – 49 Saturation 95 % 80 – 95 Saturation 70 – 75 BE 2 BE - - HCO3 24 mEq/l 22 - 26 HCO3 24 - 28 Disorders of A-B balance Acidosis: abnormal condition lowering arterial pH Alkalosis: abnormal condition raising arterial pH Homeostatic response predictable Simple A-B disorders: there is a single primary aetiological acid-base disorder Mixed A-B disorders: more primary aetiological disorders are present simultaneously Causes Respiratory abnormal processes which tend to alter pH because of a primary change in pCO2 levels acidosis alkalosis Metabolic abnormal processes which tend to alter pH because of a - primary change in [HCO3 ] acidosis alkalosis Stepwise approach 1. History 2. Look at the pH 3. Look at PCO2 and HCO3- 4. In metabolic acidosis: what is anion gap? 5. With high AG: delta-ratio? 6. Normal AG: calculate urine AG 7. Is compensation adequate? 8. In respiratory process: acute or chronic? Metabolic acidosis (MA) - • primary disorder is a pH due to HCO3 : – fixed [H+] = high anion gap - – loss or reabsorption of HCO3 = normal anion gap • Anion Gap Use and limitations of Anion Gap • [Na+]- [Cl⁻]-[HCO³⁻] • Calculate the excess of unmeasured anions • Range 8-12 mM/L Correction for albumin (alb ↓1 g/L->↑ 2.5 AG) High Anion Gap Acidosis Berend K, et al. NEJM 2014 (oct): 371:15 Normal Anion Gap Acidosis Berend K, et al. NEJM 2014 (oct): 371:15 Primary acid-base disturbances Disturbance Compensation Classification - pH HCO3 PCO2 metabolic acidosis with respiratory compensation - PCO2 ↑ HCO3 ↑ respiratory acidosis with metabolic compensation - pH ↑ HCO3 ↑ PCO2 ↑ metabolic alkalosis with respiratory compensation - PCO2 HCO3 respiratory alkalosis with metabolic compensation Diagnosis mixed acid-base disturbances There is a discrepancy between real and expected compensation • compensation CO2 ↑↑ : extra acidosis • CO2 : extra alkalosis - • compensation HCO3 ↑↑ : extra alkalosis - HCO3 : extra acidosis Berend K, et al. NEJM 2014 (oct): 371:15 Case 1 44 yr man dehydrated with sever diarrhea. pH 7.31/33/bic 16/93 Na 134/K 2.9/Cl 108/Cr 150/Ur 25 What is the acid base disorder? Answer 1.Based on history: normal AG because of diarrhea or elevated AG because of lactic acidosis due to hypovolemia 2.Look at pH 3.Look at the process (HCO3 and PCO2) 4.Calculate the AG: =10 5.Compensation adequate PCO2= 1.5 x bic +8 (+/-2)= 30-34 C/ Normal AG acidosis with adequate compensation, most likely due to diarrhea Case 2 22 yr female with DM1, N/V+, polyuria, abnormal breathing pH 7.27/23/bic 10 Na 132/K 6/Cl 93/gluc 36/Cr 200 What is acid-base disorder? Answer 1.History: elevated AG because of DKA or lactic acidosis secondary to hypovolemia due to vomiting and polyuria; metabolic alkalosis due to vomiting 2.Look at the pH 3.What is the primary process (bic/pCO2)? 4.Calculate AG=28 5.Is compensation adequate? = 1.5 ×11 + 8 ± 2 = 22.5 - 26.5. C/ High AG metabolic acidosis due to diabetic ketoacidosis Case 3 70 yr man, with history of CHF, increased dyspnoe and leg swelling pH 7.24/60/bic 27/ 52 What is acid-base disorder? Answer 1.History acute respiratory acidosis due to acute pulmonary edema 2.Look at pH 3.What is process? (PCO2/bic)? 4.Acute/chronic? 60-40=20/10=2 +24=26 (is almost bic 27) so acute respiratory acidosis C/ Acute respiratory acidosis secondary to pulmonary edema Questions? http://fitsweb.uchc.edu/student/selectives/TimurGraha m/Welcome.html .
Load more

Recommended publications
  • Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
    Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder.
    [Show full text]
  • Problem-Based Review: a Patient with Metabolic Acidosis
    Acute Medicine 2012 11(4): 251-256 251 Trainee Section Problem-Based Review: A patient 251 with metabolic acidosis saf R Allan & C Foster Abstract Metabolic acidosis is a common metabolic derangement present in the acute medical patient. A thorough and structured investigative approach is required as there are many causes and management is reliant on identifying these. In particular calculation of the anion gap with correction for albumin level and use of the delta ratio can be helpful in complex cases especially in patients where a combination of metabolic derangements may be present. Keywords metabolic acidosis, anion gap, delta ratio, renal tubular acidosis, bicarbonate Key points • Calculation of the anion gap is crucial in identifying the cause of metabolic acidosis. • Metabolic acidosis is often multi-factorial and the delta ratio calculation can be useful in identifying situations where a normal gap acidosis coexists with a raised anion gap cause. • Identification of the specific cause(s) of metabolic acidosis is vital as this will usually guide treatment. • Bicarbonate treatment has a role in some cases but adverse effects should be considered. Case Vignette Although the anion gap calculation will narrow A 37 year old male with no past medical history presents our differential (Table 2), many possible explanations to the acute medical unit (AMU) with a history of general for the acidosis remain, especially when the gap is deterioration in health over the last 8 months. He has lost 10 high. The mnemonic MUDPILERS (Methanol, kg of weight and has severe fatigue. More recently he describes a Uraemia, Diabetic Ketoacidosis or other causes Table 1.
    [Show full text]
  • PHAR 503 Exam 2
    PHAR 503 Exam 2 Rho Chi Acid-Base Disorders Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Diuretics increase loss of H+, vomiting, hypokalemia, citrate is metabolized to HCO3- A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis Hyperventilating -> blowing off CO2 (acid) If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 Metabolic: HCO3- abnormalities, respiratory: PaCO2 What is the normal range for PaCO2? What is the normal range for HCO3-? What is the normal range for PaCO2? 35-45 (40!) What is the normal range for HCO3-? 22-26 (24!) ROME Respiratory Opposite: PaCo2 and pH go in opposite directions Metabolic Equal: HCO3- and pH go in the same direction Which of the following would NOT cause a metabolic acidosis? A.
    [Show full text]
  • Diabetic Ketoalkalosis in Children and Adults
    Original Article Diabetic Ketoalkalosis in Children and Adults Emily A. Huggins, MD, Shawn A. Chillag, MD, Ali A. Rizvi, MD, Robert R. Moran, PhD, and Martin W. Durkin, MD, MPH and DR are calculated because the pH and bicarbonate may be near Objectives: Diabetic ketoacidosis (DKA) with metabolic alkalosis normal or even elevated. In addition to having interesting biochemical (diabetic ketoalkalosis [DKALK]) in adults has been described in the features as a complex acid-base disorder, DKALK can pose diagnostic literature, but not in the pediatric population. The discordance in the and/or therapeutic challenges. change in the anion gap (AG) and the bicarbonate is depicted by an Key Words: delta ratio, diabetic ketoacidosis, diabetic ketoalkalosis, elevated delta ratio (DR; rise in AG/drop in bicarbonate), which is metabolic alkalosis normally approximately 1. The primary aim of this study was to de- termine whether DKALK occurs in the pediatric population, as has been seen previously in the adult population. The secondary aim was iabetic ketoacidosis (DKA), a common and serious dis- to determine the factors that may be associated with DKALK. Dorder that almost always results in hospitalization, is de- Methods: A retrospective analysis of adult and pediatric cases with a fined by the presence of hyperglycemia, reduced pH, metabolic 1 primary or secondary discharge diagnosis of DKA between May 2008 and acidosis, elevated anion gap (AG), and serum or urine ketones. August 2010 at a large urban hospital was performed. DKALK was as- In some situations, a metabolic alkalosis coexists with DKA sumedtobepresentiftheDRwas91.2 or in cases of elevated bicarbonate.
    [Show full text]
  • ABG Analysis in Clinical Setting
    CHAPTER ABG Analysis in Clinical Setting 117 Rajesh Mahajan, Suman Sethi INTRODUCTION defined by the ratio of PCO2 to HCO3 and not by absolute Acid-Base balance is an intricate concept which requires an value of either one alone.5,6 intimate and detailed knowledge of the body’s metabolic Overview of Fundamentals of Acid-Base Disorder pathways used to eliminate the H+ ion. Accurately Normal metabolism of proteins and nucleotides generates interpreting acid-base balance requires simultaneous about 100 mmol H+ per day in the form of sulphuric and measurements of arterial pH and plasma electrolytes, phosphoric acids. By comparison, hydration of CO2 to as well as knowledge of compensatory physiologic form H CO generates 12,500 mmol H+ per day. mechanisms. In this article, we’ll review normal acid-base 2 3 physiology, acid-base disturbances, and lab techniques Carbon dioxide transport and mathematical calculations used to identify the cause 1. Transport of carbon dioxide in the blood is of acid-base derangements. considerably more complex. A small portion of carbon dioxide, about 5 percent, remains BASIC PHYSIOLOGY unchanged and is transported dissolved in blood. Acid-base Chemistry 2. The remainder is found in reversible chemical pH combinations in red blood cells or plasma. Some The concept of pH was put forward by the Danish chemist, carbon dioxide binds to blood proteins, principally Soren Peter Sorensen in 1909 to refer to the negative hemoglobin, to form a compound known as logarithm of hydrogen ion (H+) concentration. An increase carbamate. in the pH indicates a proportionate decrease in the 3., About 88 percent of carbon dioxide in the blood is [H+] and a decrease in the pH indicates a proportionate in the form of bicarbonate ion.
    [Show full text]
  • Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: a Pathophysiological Review
    Hindawi Publishing Corporation Journal of Biomedicine and Biotechnology Volume 2012, Article ID 915150, 8 pages doi:10.1155/2012/915150 Review Article Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Cosimo Marcello Bruno and Maria Valenti Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Correspondence should be addressed to Cosimo Marcello Bruno, cmbruno@unict.it Received 29 September 2011; Accepted 26 October 2011 Academic Editor: Saulius Butenas Copyright © 2012 C. M. Bruno and M. 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. 1. Introduction However, an alteration in respiratory exchanges, as occurs in advanced phase of COPD, results in retention of CO2. Chronic obstructive pulmonary disease (COPD) is a major Carbon dioxide is then hydrated with the formation of public health problem. Its prevalence varies according to carbonic acid that subsequently dissociates with release of country, age, and sex. On the basis of epidemiologic data, hydrogen ions (H+) in the body fluids according to the fol- the projection for 2020 indicates that COPD will be the lowing equation: third leading cause of death worldwide and the fifth leading − + cause of disability [1].
    [Show full text]
  • PGE2 EP1 Receptor Inhibits Vasopressin-Dependent Water
    Laboratory Investigation (2018) 98, 360–370 © 2018 USCAP, Inc All rights reserved 0023-6837/18 PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct Rania Nasrallah1, Joseph Zimpelmann1, David Eckert1, Jamie Ghossein1, Sean Geddes1, Jean-Claude Beique1, Jean-Francois Thibodeau1, Chris R J Kennedy1,2, Kevin D Burns1,2 and Richard L Hébert1 PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1 − / − mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1 − / − , Htn, HtnEP1 − / − . Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1 − / − , but sglt2 was increased in EP1 − / − mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1 − / − or HtnEP1 − / − mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.
    [Show full text]
  • University of Huddersfield Repository
    University of Huddersfield Repository Aburas, Omaro A Emhmed Investigation of aldehyde oxidase and xanthine oxidoreductase in rainbow trout (Oncorhynchus mykiss) Original Citation Aburas, Omaro A Emhmed (2014) Investigation of aldehyde oxidase and xanthine oxidoreductase in rainbow trout (Oncorhynchus mykiss). Doctoral thesis, University of Huddersfield. This version is available at http://eprints.hud.ac.uk/23543/ The University Repository is a digital collection of the research output of the University, available on Open Access. Copyright and Moral Rights for the items on this site are retained by the individual author and/or other copyright owners. Users may access full items free of charge; copies of full text items generally can be reproduced, displayed or performed and given to third parties in any format or medium for personal research or study, educational or not-for-profit purposes without prior permission or charge, provided: • The authors, title and full bibliographic details is credited in any copy; • A hyperlink and/or URL is included for the original metadata page; and • The content is not changed in any way. For more information, including our policy and submission procedure, please contact the Repository Team at: E.mailbox@hud.ac.uk. http://eprints.hud.ac.uk/ Investigation of aldehyde oxidase and xanthine oxidoreductase in rainbow trout (Oncorhynchus mykiss) Omaro Aburas B.Sc., M.Sc. Department of Chemical and Biological Science University of Huddersfield United Kingdom Thesis submitted in partial fulfilment of the requirements for the Degree of Doctor of Philosophy July 2014 Abstract Molybdo-flavoenzymes (MFEs), aldehyde oxidase (AOX) and xanthine oxidoreductase (XOR) are involved in the oxidation of N-heterocyclic compounds and aldehydes, many of which are environmental pollutants, drugs and vitamins.
    [Show full text]
  • Acid Base Cover.Cdr
    Workshop on Electrolyteand Acid-BaseDisturbances Organisers AKAgarwal,RKSingal Editor PraveenAggarwal Governing Body of Association of Physicians of India PresidentElect President PastPresident AKAgarwal, NewDelhi(2009) SKBichile,(Mumbai 2009) RKSingal,(NewDelhi 2009) Vice Presidents BRBansode,(Mumbai 2009) PritamGupta,(NewDelhi 2010) AlakaDeshpande,(Mumbai 2011) Hon.General Secretary Sandhya Kamath,(Mumbai 2010) Hon.Treasurer Milind Y Nadkar,(Mumbai 2009) Members ShyamSundar,(Varanasi 2009) RohiniHanda,(NewDelhi 2010) NarinderPalSingh,(NewDelhi 2011) YSatyanarayanRaju,(Hyderabad 2009) AmalKumarBanerjee,(Howrah 2010) MadhukarRai,(Varanasi 2011) JMukhopadhyay,(Howrah 2009) RSajithkumar,(Kottayam 2010) SurendraDaga,(Kolkata 2011) NKSingh,(Dhanbad 2009) AbhayNRai,(Gaya 2010) SArulrhaj,(Tuticorin 2011) Zonal Members NorthZone–RajeshUpadhyay,(NewDelhi 2011) MidSouthZone–GNarsimulu,(Hyderabad 2011) NorthWestZone–GurpreetSWander,(Ludhiana 2011) SouthZone–AMuruganathan,(Tirupur 2011) CentralZone–SanjivMaheshwari,(Ajmer 2011) MidEastZone–KamleshTewary, Muzaffarpur( 2011) WestZone–AshitBhagwati,(Mumbai 2011) EastZone–SamarKumarBanerjee,(Kolkata 2011) Ex Officio Member Dean ICP AK Das, Pondicherry Invited Members Hon.Editor,JAPI APIHouseChairman Editor-in-chief,APITextBook ShashankRJoshi, Mumbai SiddharthNShah, Mumbai YPMunjal, NewDelhi Co-opted Members Jt.Secretary, President’sPlace ArmedForces, MedicalServices Jt.Secretary(HQ) JMPhadtare, Mumbai(2009) Lt.Gen.SRMehta,(NewDelhi 2007-2008) FalguniParikh, Mumbai OrganisingSecretary, APICON2008 OrganisingSecretary,
    [Show full text]
  • Controversies in the Management of Aneurysmal Subarachnoid Hemorrhage*
    Controversies in the management of aneurysmal subarachnoid hemorrhage* Neeraj S. Naval, MD; Robert D. Stevens, MD; Marek A. Mirski, MD, PhD; Anish Bhardwaj, MD, FCCM Background: The care of patients with aneurysmal subarach- Data Source: Search of MEDLINE and Cochrane databases and noid hemorrhage has evolved significantly with the advent of new manual review of article bibliographies. diagnostic and therapeutic modalities. Although it is believed that Data Synthesis and Conclusions: Many aspects of care in these advances have contributed to improved outcomes, consid- patients with aneurysmal subarachnoid hemorrhage remain erable uncertainty persists regarding key areas of management. highly controversial and warrant further resolution with hypoth- Objective: To review selected controversies in the manage- esis-driven clinical or translational research. It is anticipated that ment of aneurysmal subarachnoid hemorrhage, with a special the rigorous evaluation and implementation of such data will emphasis on endovascular vs. surgical techniques for securing provide a basis for improvements in short- and long-term out- aneurysms, the diagnosis and therapy of cerebral vasospasm, comes. (Crit Care Med 2006; 34:511–524) neuroprotection, antithrombotic and anticonvulsant agents, cere- KEY WORDS: aneurysm; subarachnoid; hemorrhage; vasospasm; bral salt wasting, and myocardial dysfunction, and to suggest ischemia venues for further clinical investigation. he rupture of an intracranial sepsis, and thromboembolism. As many and management of cerebral vasospasm, aneurysm may be associated of these complications are life-threaten- neuroprotective strategies, use of anti- with an array of severe distur- ing but reversible, it is widely believed thrombotic agents (thrombolytic agents, bances in intracranial and sys- that patients with aSAH can benefit from heparin, and platelet inhibitors), prophy- Ttemic physiology that represent a unique laxis of seizures, and the approach to ce- management in an intensive care setting.
    [Show full text]
  • 1. Regarding Targeted Temperature Management TTM After Cardiac Arrest A) TTM Should Be Implemented for at Least 72 Hours After
    1. Regarding targeted temperature management TTM after cardiac arrest a) TTM should be implemented for at least 72 hours after arrest b) Target temperature should be between 32 and 36 degrees c) Rapid infusion of 60ml/kg of IV iced normal saline should be used after ROSC d) Once TTM period is finished, there is no guide on what temperatures should be kept at if a patient remains comatosed 2. Which of the following is incorrect in describing renal handling of acid base balance a) Renal tubular acidosis type 1 distal inhibits H+ extrusion and serum bicarb decreases to a steady state level b) 15% of bicarbonate reclamation occurs in the distal tubule c) If serum is acidotic, formation of new bicarbonate in the distal tubule to may take up to 4 -5 days to reach equilibrium d) Ammonia has no effect on acid excretion 3. Regarding acid and base compensation which is correct a) Correlation between venous and arterial pH is poor especially in DKA b) Compensation in chronic respiratory alkalosis may be efficient enough to normalize pH c) A patient cannot have a normal pH if there is a disease process causing metabolic acidosis d) In an ABG with a high pH, acidosis can be excluded 4. When calculating the anion gap a) Measured values of K is always needed to accurately calculate anion gap b) Anion gap > 12 is always abnormal c) Most of the normal anion gap in healthy individuals consists of albumin d) Anion gap cannot be normal if there is an elevated lactate 5.
    [Show full text]
  • Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders
    1521-0081/68/2/476–532$25.00 http://dx.doi.org/10.1124/pr.115.010652 PHARMACOLOGICAL REVIEWS Pharmacol Rev 68:476–532, April 2016 Copyright © 2016 The Author(s) This is an open access article distributed under the CC-BY Attribution 4.0 International license. ASSOCIATE EDITOR: STEPHANIE W. WATTS Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders F.V. Brozovich, C.J. Nicholson, C.V. Degen, Yuan Z. Gao, M. Aggarwal, and K.G. Morgan Department of Health Sciences, Boston University, Boston, Massachusetts (C.J.N., Y.Z.G., M.A., K.G.M.); Department of Medicine, Mayo Clinic, Rochester, Minnesota (F.V.B.); and Paracelsus Medical University Salzburg, Salzburg, Austria (C.V.D.) Abstract ...................................................................................478 I. Introduction . ..............................................................................478 A. Scope and Limitations..................................................................478 B. Overview of Regulation of Blood Pressure/Vascular Tone. ...............................478 1. Guyton View of Regulation Blood Pressure, Kidney Role, Volume Regulation. .......478 2. Recent Direct Confirmation of Changes in Vascular Tone/Resistance Related to Changes in Systemic Vascular Resistance and Blood Pressure and Downloaded from the Importance of Vascular Smooth Muscle Contraction in both Normal Physiology and Pathophysiology—Hypertension......................................479 3. Racial Differences/Personalized
    [Show full text]