Alterations in the Specific Gravity of the Blood Plasma with Onset of Diuresis in Heart Failure

Total Page:16

File Type:pdf, Size:1020Kb

Alterations in the Specific Gravity of the Blood Plasma with Onset of Diuresis in Heart Failure MECHANISM OF DIURESIS: ALTERATIONS IN THE SPECIFIC GRAVITY OF THE BLOOD PLASMA WITH ONSET OF DIURESIS IN HEART FAILURE Harold J. Stewart J Clin Invest. 1941;20(1):1-6. https://doi.org/10.1172/JCI101189. Research Article Find the latest version: https://jci.me/101189/pdf MECHANISM OF DIURESIS: ALTERATIONS IN THE SPECIFIC GRAVITY OF THE BLOOD PLASMA WITH ONSET OF DIURESIS IN HEART FAILURE By HAROLD J. STEWART (From the Department of Medicine of.the New York Hospital and Cornell University Medical College and the Hospital of the Rockefeller Institute for Medical Research, New York) (Received for publication July 3, 1940) There are divergent views concerning the Moreover, its duration may be brief before res- mechanism by which diuresis is initiated. Many toration is attempted, or it may be long enough of the observations on this subject relate to mer- and of such magnitude that it can be detected. curial drugs. Crawford and McIntosh (1) con- On the other hand, if diuresis is initiated at cluded that novasurol induced primary dilution, the tissue side of the system so that fluid enters followed by concentration of the blood in edema- the blood stream first, dilution of the blood would tous patients. Bryan, Evans, Fulton, and Stead occur. Equilibrium would be disturbed until the (2) thought that salyrgan resulted in concentra- kidneys began to excrete the surplus fluid. If di- tion of the blood, since sustained rise in its spe- lution of the blood was of sufficient duration and cific gravity occurred coincident with diuresis in magnitude, it might be detected. dogs made edematous by plasmapheresis. Schmitz It appeared that frequent observations of the (3) did not find evidence that salyrgan mobilized specific gravity of the blood would reflect changes fluid into the blood stream before the onset of in dilution and concentration of the blood and give diuresis. Blumgart, Gilligan, Levy, Brown, and data which would contribute to one or the other Volk (4) concluded from observations on normal of these points of view. Moore and Van Slyke subjects that diuresis following xanthine and mer- (7) demonstrated a linear relationship between curial drugs was not initiated by the kidneys in the observed specific gravity of the plasma of the response to measurable changes in specific gravity blood and the observed protein content of the or sodium or chloride contents of the blood. plasma of normal individuals and nephritic pa- Brown and Rowntree (5) found an increase in tients. They found also that when the specific blood volume with the onset of diuresis in cardiac gravity of the plasma was below 1.0223 in certain patients. On the other hand, using more accurate types of nephritis, edema was present, and that methods, Evans and Gibson (6) observed in dogs when the specific gravity was above this level, the a diminution of plasma volume during diuresis so-called edema zone, edema did not occur. induced by salyrgan. In cardiac patients, Moore and Stewart (8) For purposes of analysis the circulatory-renal also found that the specific gravity of the plasma system consists of the kidneys on the one hand and had a linear relationship to the protein content of the tissues which retain fluid on the other, the cir- the plasma and demonstrated that the plasma pro- culating blood connecting them. Tissue fluid to teins and specific gravity of cardiac patients were be excreted as urine must be carried by the blood above the edema level of nephritic patients. to the kidneys. The stimulus to inaugurate diu- Moore and Stewart's (8) observations relating to resis may be applied at different points in this the behavior of the specific gravity of the plasma system. If the mechanism is initiated in the kid- of normal individuals provided the background neys and increased secretion of urine is the first for turning Moore and Van Slyke's method to this step, concentration of the blood should occur on purpose. They found that the specific gravity of the withdrawal of fluid from it. How far this the blood plasma of normal individuals and of imbalance in the blood constituents can proceed cardiac patients in water equilibrium remained and how long it can be present before restoration constant to within 0.0004 from day to day. Di- occurs by the entrance of fluid from the edema- lution of blood by the injection of normal salt solu- tous tissues might vary with different diuretics. tion and following hemorrhage in dogs gave paral- 1 2 HAROLD J. STEWART Jan. Feb. 10270 6 . 1.0260 10240 A FIG. 1. RELATIONSHIP BETWEEN ONSET OF DIGITALIs, THEOCALCIN, AND SPONTANEOUS DiuREsis To SPECIFIC GRAvrTY OF THE BLOOD PLASMA In this figure is shown the relation of onset of diuresis to the level of specific gravity of the blood plasma. In B. McL., 58 years (Figure 1A), in whom heart failure was a consequence of hypertension, diuresis re- sulted from giving digitan 12 grams in 24 hours. In L. C., 64 years (Figure 1B), in whom heart failure resulted from hypertension, the administration of theocalcin 4.5 grams on April 14, and daily thereafter, re- sulted in marked diuresis. In J. McM., 44 years (Figure 1C), in whom heart failure resulted from arteriosclerotic heart disease, diuresis occurred spontaneously. SPECIFIC GRAVITY OF PLASMA IN DIURESIS 3 £ 53 1.0270 e 1.0260 c0- O u,, [0250 ta o E. -5 1.0270-_ n Zn 10240 1.0260 1.0230 ° 8 1.0250 1.0220 H Q s 1.0240C B C FIG. 1 (conttintued) lel decreases in specific gravity of the plasma and gestive heart failure was estimated by the method of plasma proteins. The oral administration of 1000 Moore and Van Slyke (7). Duplicate samples were cc. of water did not alter specific gravity of the checked to within 0.00002. The daily fluid and salt in- plasma; during the urine concentration test, how- takes of the patients were 1200 cc. and 5 grams, respec- tively. Patients remained in bed. There was a control ever, the specific gravity and the plasma proteins period before giving diuretics. Since samples of blood increased, indicating concentration of the blood. were taken frequently before and after the administration In short, when concentration of the blood occurs, of diuretics, it was not expedient to keep the subjects in the specific gravity rises and when dilution occurs, the basal or postabsorptive state. The patients ate break- it decreases. fast at 7:30 a.m., after which they received no fluid 1 It appeared from these observations that during until samples of blood were taken without stasis at 10:30 a.m. The was a time in which nothing was done to deplete the diuretic then given. A rubber stopper was plasma proteins, the specific gravity of the plasma used to eliminate evaporation. Clotting was prevented by use of heparin. could be used to indicate dilution or concentration of the blood. METHODS AND PLAN OF OBSERVATIONS 1 It is recalled, however, that Moore and Stewart (8) The specific gravity of the plasma of the blood of found that drinking 1000 cc. water did not alter the cardiac patients exhibiting signs and symptoms of con- specific gravity of the blood. 4 HAROLD J. STEWART OM PATIEMr S *:DURIS fAILURE SP. GR. OF bLOOD PLASMA CAROIAC OaRECOVIRED C RELATIOM OF OCCURREnCE Of DIURES3S TO SP. OR. OF bLOOD PLASMA 5 1o*%v*@|DIU%v] *" |RI1l o RELAT1on or IfITIATIOMfOFOIURESIS TO SP. CR. Of BLOOD PLASMA A l'l~.Ia?I?D¶?uII''IIi'eI~I,~I4 LA 1468 IUR4ST~'0'- .,,t, iL A & 16"1"8' o 2 "'8"o2 I 4,Wo"l4 % I'''~~~9IAl& o,4I8w - o & 6 ao u0 o ' O X, O. Ot a #4 - - w - #4 0 4 #4 o4 0 0. 0t ~ FIG. 2. RELATION OF INITIATION AND OCCURRENCE OF DiuREsis TO, SPECIFIC GRAVITY OF THE BLOOD PLASMA In Figure 2A are plotted specific gravity estimations of the plasma to show the level at which diuresis was initiated. Closed circles indicate that diuresis was initiated at the level shown. In Figure 2B are plotted data to show the relation of occurrence and persistence of diuresis to specific gravity of the blood plasma. Closed circles in- dicate occurrence of diuresis and open ones that diuresis was not taking place. In Figure 2C are plotted specific gravity estimations of patients during (closed circles) and recovered (open circles) from heart failure. OBSERVATIONS diuresis. Similar patterns were recorded in one other patient with auricular fibrillation and 3 patients with Specific gravity of the blood plasma was observed in instances of diuresis occurring spontaneously without the normal sinus mechanism. The case of J. McM. (Figure 1C) illustrates the re- use patients), in diuresis resulting from of drugs (8 auricular fibrillation and 5 patients digitalis (9 patients), and, finally, in diuresis following sults in 3 patients with with normal sinus rhythm in whom diuresis occurred the use of theocalcin (Merck) (5 patients). Patients spontaneously with rest in bed and limitation of fluid having auricular fibrillation, as well as those with normal intake. There was a fall in specific gravity when diuresis sinus rhythm, were subjects. when the first Patient B. McL. (Figure 1A) illustrates the effect of occurred; or, if diuresis had been initiated sample was taken, the specific gravity was low, rose with digitalis. Rest in bed and restriction of fluids did not the continuance of diuresis, and had risen to a normal result in diuresis. When digitan 1.2 grams (Merck) 2 level when excess fluid had been eliminated. were given in 24 hours, diuresis with loss in weight For all the level of specific gravity of the occurred promptly.
Recommended publications
  • Therapeutic Hypothermia: Where Do We Stand?
    5/29/2015 Therapeutic Hypothermia: Where Do We Stand? Melina Aguinaga-Meza, MD Assistant Professor of Medicine Gill Heart Institute University of Kentucky Disclosure Information Melina Aguinaga-Meza, MD “Therapeutic Hypothermia: Where Do We Stand?” • FINANCIAL DISCLOSURE: – No relevant financial relationship exists • UNLABELED/UNAPPROVED USES DISCLOSURE: – No relevant relationship exists 1 5/29/2015 The Clinical Problem • Out-of-hospital cardiac arrest (OHCA) is a leading cause of death among adults in the US • Approx. 300,000 OHCA events occur each year in the US • Resuscitation is attempted in 100,000 of these arrests • Less than 40 000 survive to hospital admission MMWR / July 29, 2011 / Vol. 60 / No. 8 2 5/29/2015 Consequences From Cardiac Arrest Myocardial Brain injury dysfunction Post-Cardiac Arrest Syndrome Systemic ischemia Disorder that + reperfusion caused the cardiac responses arrest • The effects of this syndrome are severe and pervasive MMWR / July 29, 2011 / Vol. 60 / No. 8 Survival and Neurological Outcomes after OHCA • Only one third of patients admitted to the hospital survive to hospital discharge • Approx. one out of ten people who experience OHCA survive to hospital discharge • Only 2 out of 3 of them have a good/moderate neurologic recovery MMWR / July 29, 2011 / Vol. 60 / No. 8: CARES 3 5/29/2015 “Chain of Survival” • Actions needed to improve chances of survival from out-of-hospital cardiac arrest Circulation 2010; 122:S676-84 • Try to identify and treat the precipitating causes of the arrest and prevent recurrent
    [Show full text]
  • Critical Care in the Monoplace Hyperbaric Chamber
    Critical Care in the Monoplace Hyperbaric Critical Care - Monoplace Chamber • 30 minutes, so only key points • Highly suggest critical care medicine is involved • Pitfalls Lindell K. Weaver, MD Intermountain Medical Center Murray, Utah, and • Ventilator and IV issues LDS Hospital Salt Lake City, Utah Key points Critical Care in the Monoplace Chamber • Weaver LK. Operational Use and Patient Care in the Monoplace Chamber. In: • Staff must be certified and experienced Resp Care Clinics of N Am-Hyperbaric Medicine, Part I. Moon R, McIntyre N, eds. Philadelphia, W.B. Saunders Company, March, 1999: 51-92 in CCM • Weaver LK. The treatment of critically ill patients with hyperbaric oxygen therapy. In: Brent J, Wallace KL, Burkhart KK, Phillips SD, and Donovan JW, • Proximity to CCM services (ed). Critical care toxicology: diagnosis and management of the critically poisoned patient. Philadelphia: Elsevier Mosby; 2005:181-187. • Must have study patient in chamber • Weaver, LK. Critical care of patients needing hyperbaric oxygen. In: Thom SR and Neuman T, (ed). The physiology and medicine of hyperbaric oxygen therapy. quickly Philadelphia: Saunders/Elsevier, 2008:117-129. • Weaver LK. Management of critically ill patients in the monoplace hyperbaric chamber. In: Whelan HT, Kindwall E., Hyperbaric Medicine Practice, 4th ed.. • CCM equipment North Palm Beach, Florida: Best, Inc. 2017; 65-95. • Without certain modifications, treating • Gossett WA, Rockswold GL, Rockswold SB, Adkinson CD, Bergman TA, Quickel RR. The safe treatment, monitoring and management
    [Show full text]
  • A Rare Complication of Carbon Monoxide Poisoning
    International Clinical Pathology Journal Case Report Open Access Compartment syndrome of the lower limb: a rare complication of carbon monoxide poisoning Abstract Volume 6 Issue 5 - 2018 Carbon monoxide poisoning (CO) nicknamed “Silent killer” remains the leading cause Ghassen Drissi, Mohamed Khaled, Houssem of poisoning deaths in most countries. In Tunisia, an estimated number of 2000 to 4000 cases of poisoning was noted per a year with an estimated percentage of death up Kraiem, Khaled Zitouna, Mohamed lassed to 90% at the site of intoxication. This intoxication is very exceptionally complicated kanoun by a compartment syndrome that can aggravate the functional and vital prognosis Department of Orthopaedics and Traumatology, La Rabta Hospital of Tunis, Tunisia when it is dominated by other symptoms, particularly neurological ones. We report the case of a patient who presented a compartment syndrome during CO intoxication Correspondence: Ghassen Drissi, Department of that evolved favorably. Orthopaedics and Traumatology, La Rabta Hospital of Tunis, Tunisia, Email Received: October 08, 2018 | Published: November 15, 2018 Introduction an inhalation syndrome causing acute respiratory failure associated with a compartmental syndrome of the left lower limb syndrome Carbon monoxide is a colorless, odourless, non-irritating gas. It is causing acute kidney failure (tubular necrosis) with rhabdomyolysis particularly toxic to mammals but undetectable by them giving it an requiring intubation associated to mechanical ventilation with insidious “Silent killer” character. In humans, it is the cause of much emergency hemodialysis sessions. With regard to the compartmental domestic intoxication, often fatal. Its causes are most often accidental, syndrome, two fasciotomies in emergency were made in our service.
    [Show full text]
  • THE EFFECT of CONTINUOUS NEGATIVE PRESSURE BREATH- ING on WATER and ELECTROLYTE EXCRETION by the HUMAN KIDNEY by HERBERT 0
    THE EFFECT OF CONTINUOUS NEGATIVE PRESSURE BREATH- ING ON WATER AND ELECTROLYTE EXCRETION BY THE HUMAN KIDNEY By HERBERT 0. SIEKER,1 OTTO H. GAUER,2 AND JAMES P. HENRY (From the Aero-Medical Laboratory, Wright-Patterson Air Force Base, Ohio) (Submitted for publication September 4, 1953; accepted December 30, 1953) The effects of decreased intrathoracic pressure ment. Negative pressure breathing during both inspiration on arterial blood pressure (1), venous pressure and expiration was applied through a standard U. S. Air (2, 3), cardiac output (4), and pres- Force pressure breathing oxygen mask attached by a pulmonary short tubing to a 40 liter cylinder. This cylinder was sure and volume (5) have been investigated in the ventilated by a suction pump with fresh air at the rate of past. The present study was prompted by the as- 100 to 160 liters per minute and rebreathing was pre- sociation of marked diuresis with continuous nega- vented by means of a two-way valve in the face mask. tive pressure breathing in anesthetized animals (6) The desired negative pressure, which in these experiments and the observation that in unanesthetized man was a mean pressure of 15 to 18 centimeters of water, was obtained by varying the air inlet to the container. continuous positive pressure breathing leads to an Control studies duplicated the procedure exactly except oliguria (7). The purpose of this investigation that the negative pressure breathing was omitted. Re- was to demonstrate that human subjects like an- peat studies were done in all but two subjects. esthetized animals have an increased urine flow in The urine volume for each 15-minute interval was noted response to continuous negative pressure breathing.
    [Show full text]
  • Renal Function in Hyperbaric Environment
    APPLIED HUMAN SCIENCE Journal of Physiological Anthropology Renal Function in Hyperbaric Environment Yang Saeng Park1), John R. Claybaugh2), Keizo Shiraki3) and Motohiko Mohri4) 1) Kosin Medical College, Korea 2) Tripler Army Medical Center, USA 3) University of Occupational and Environmental Health 4) Japan Marine Science and Technology Center Abstract. During mixed gas saturation diving (to 3– diuresis. This topic has been reviewed previously by Hong 49.5 ATA) daily urine flow increases by about 500 ml/ (1975), Hong et al. (1983; 1995), Hong and Claybaugh day, with no changes in fluid intake and glomerular (1989), Shiraki (1987), and Sagawa et al. (1996). filtration rate. The diuresis is accompanied by a significant decrease in urine osmolality and increase in excretion Characteristics of Hyperbaric Diuresis of such solutes as urea, K+, Na+, Ca2+ and inorganic phosphate (Pi). The fall in urine osmolality is mainly Fig. 1 depicts time courses of urine flow in subjects due to a reduction of free water reabsorption which is exposed to 31 ATA He-O2 atmosphere determined in associated with a suppression of insensible water loss three saturation dives, Seadragon IV (Nakayama et al., and the attendant inhibition of antidiuretic hormone 1981), Seadragon VI (Shiraki et al., 1987), and New (ADH) system. The increase in urea excretion may be Seatopia (Sagawa et al., 1990), conducted in Japan associated with a reduction of urea reabsorption at the Marine Science and Technology Center (JAMSTEC). The collecting duct as a consequence of ADH suppression. daily urine flow increased rapidly upon compression to a The rise in K+ excretion is due to a facilitated K+ secretion value 700–1000 ml/day above the predive level, then it at the distal tubule as a result of increased aldosterone, dropped off slightly to a steady level of approximately 500 urine flow and excretion of impermeable anions such ml/day above the predive level.
    [Show full text]
  • Hyperthermia & Heat Stroke: Heat-Related Conditions
    Hyperthermia & Heat Stroke: Heat-Related Conditions Joseph Rampulla, MS, APRN,BC eat-related conditions occur when excess heat taxes or overwhelms the body’s thermoregulatory mechanisms. Heat illness is preventable and occurs more Hcommonly than most clinicians realize. Heat illness most seriously affects the poor, urban-dwellers, young children, those with chronic physical and mental illnesses, substance abusers, the elderly, and people who engage in excessive physical The exposure to activity under harsh conditions. While considerable overlap occurs, the important the heat and the concrete during the syndromes are: heat stroke, heat exhaustion, and heat cramps. Heat stroke is a life- hot summer months places many rough threatening emergency and occurs when the loss of thermoregulatory control results sleepers at great risk in hyperpyrexia (very high fever) and severe damage to many internal organs. for heat stroke and hyperthermia. Photo by Epidemiology Sharon Morrison RN Heat illness is generally underreported, and the deaths than all other natural disasters combined in true incidence is unknown. Death rates from other the USA. The elderly, the very poor, and socially causes (e.g. cardiovascular, respiratory) increase isolated individuals are disproportionately affected during heat waves but are generally not reflected in by heat waves. For example, death records during the morbidity and mortality statistics related to heat heat waves invariably include many elders who died illness. Nonetheless, heat waves account for more alone in hot apartments. Age 65 years, chronic The Health Care of Homeless Persons - Part II - Hyperthermia and Heat Stroke 199 illness, and residence in a poor neighborhood are greater than 65.
    [Show full text]
  • Hyperbaric Diuresis at a Thermoneutral 31 ATA He-O2 Environment
    〔日 生 気 誌 、20(1)38-15,1983〕 Original Hyperbaric Diuresis at a Thermoneutral 31 ATA He-O2 Environment K. SHIRAKI*, S. SAGAWA*, N. KONDA* and H. NAKAYAMA** * Department of Physiology , University of Occupational and Environmental Health, Japan School of Medicine ** Department of Hyperbaric Medicine , University of Occupational and Environmental Health, Japan School of Medicine (Yahatanishi-ku, kitakyushu-shi, 807 JAPAN) Abstract The basic pattern of body water exchange was studied in four Japanese male divers during exposure to a thermoneutral 31 ATA (He-O2) environment for 3 days (Seadragon V). The hyperbaric chamber temperature was raised from 25•}0.5•Ž at 1 ATA (air) pre-dive to 31.5 f 0.3•Ž at 31 ATA. Both rectal and mean skin temperatures were measured every hour (including during sleep) and were maintained at the same level at both pressures. The exposure to 31 ATA induced an increase in the daily urine flow, and a corresponding reduction in the insensible (and evaporative) water loss without changing the total daily water output. However, the daily fluid intake decreased by 600 ml at 31 ATA, and hence the divers developed a state of negative fluid balance, as reflected by a reduction in body weight and an increase in hematocrit. All changes in the pattern of body water exchange observed at 31 ATA were gradually reversed during subsequent decompression. As observed in a previous dive to 31 ATA (Seadragon IV) in which there was a subtle cold stress (as indicated by the 1•Ž reduction in mean skin temperature at 31 ATA), the increase in daily urine flow at pressure was almost entirely due to the increase in overnight urine flow.
    [Show full text]
  • Diuretics and Chronic Lung Disease of Prematurity
    Editorial &&&&&&&&&&&&&& Diuretics and Chronic Lung Disease of Prematurity Luc P. Brion, MD supplementation, mortality, oxygen dependency at 28 days or 36 Sin Chuen Yong weeks, length of stay, and number of hospitalizations during the first Iris A. Perez year of life. The complete list of eligible randomized trials and details Robert Primhak of selection criteria and methods of analyses are all available at {http:/ /www.nichd.nih.gov/cochraneneonatal}. Despite the widespread use of diuretics in CLD, there have Babies leaving today’s neonatal nurseries with chronic lung been surprisingly few randomised clinical trials of their clinical disease of prematurity (CLD) are very different to those initial safety or efficacy. The 20 eligible studies used very variable survivors followed by Northway et al.1 The definition of the disease outcome measures, and most concentrated on short-term has changed; most now consider an oxygen requirement beyond physiological measures such as pulmonary mechanics. Only three 36 weeks post conceptional age to be a more important defining of the studies extended beyond 8 days duration: two compared criterion than the 28 days of oxygen dependency used initially for thiazide and spironolactone to placebo,7,8 and a third evaluated bronchopulmonary dysplasia.2 Early stages of the disease are the addition of spironolactone to thiazide treatment.9 The studies associated with alveolar and interstitial edema,1,3 which could spanned a 16-year period, during which the pattern of disease reduce lung compliance as well as increase airway resistance by and survival in preterm infants have changed, and the narrowing terminal airways.3 Diuretic administration could assumptions made to calculate summary statistics from the often improve pulmonary mechanics by three mechanisms: (1) limited data available may have underestimated real differences immediate diuresis-independent reabsorption of lung fluid, (2) between treatments.
    [Show full text]
  • Malignant Hyperthermia.Pdf
    Malignant Hyperthermia Matthew Alcusky PharmD, MS Student University of Rhode Island July, 2013 Financial Disclosure I have no financial obligations to disclose. Outline • Introduce malignant hyperthermia including its causes and implications • Describe the underlying pathophysiology • Detail the clinical presentation of MH • Summarize the necessary pharmacological and non-pharmacological treatment of MH • Highlight necessary considerations with the use of dantrolene • Discuss recrudescence Malignant Hyperthermia • A life threatening reaction that is most often triggered by the use of inhalational anesthetics • Estimated incidence of 1 in 5,000 to 1 in 100,000 anesthesia inductions • Early recognition and treatment is essential in reducing morbidity and mortality • Screening patients for past anesthesia history and family history, as well as conducting testing on at risk individuals is necessary to reduce MH occurrence Rosenberg H, Davis M, James D, Pollock N, Stowell K. Malignant hyperthermia. Orphanet J Rare Dis. 2007 Apr 24;2:21. Review. Drugs Triggering Malignant Hyperthermia • Desflurane • Succinylcholine- • Enflurane only non-inhalational • Halothane anesthetic that triggers MH • Isoflurane • Nitrous Oxide- only • Methoxyflurane inhalational anesthetic • Sevoflurane that does not cause MH Hopkins PM. Malignant hyperthermia: pharmacology of triggering. Br J Anaesth. 2011 Jul;107(1):48-56. doi: 10.1093/bja/aer132. Epub 2011 May 30. Review. Pathophysiology • MH partially attributed to a dominant mutation in the ryanodine receptror 1 (RYR1) – Ryanodine receptors are activated by elevated Ca2+ levels, known as store overload induced calcium release (SOICR) – Mutant receptors are activated by lower Ca2+ levels – Volatile anesthetics further lower the SOICR threshold MacLennan DH, Chen SR. Store overload-induced Ca2mutations + release as a triggering mechanism for CPVT and MH episodes caused by in RYR and CASQ genes.
    [Show full text]
  • Guidelines for Management of a Malignant Hyperthermia (MH) Crisis
    Guidelines for the management of a Malignant Hyperthermia Crisis Successful treatment of a Malignant Hyperthermia (MH) crisis depends on early diagnosis and aggressive treatment. The onset of a reaction can be within minutes of induction or may be more insidious. Previous uneventful anaesthesia does not exclude MH. The steps below are intended as an aide memoire. Presentation may vary and treatment should be modified accordingly. Know where the dantrolene is stored in your theatre. Treatment can be optimised by teamwork. Call for help Diagnosis - consider MH if: 1 1. Unexplained, unexpected increase in end-tidal CO2 together with 2. Unexplained, unexpected tachycardia together with 3. Unexplained, unexpected increased in oxygen consumption Masseter muscle spasm, and especially more generalised muscle rigidity after suxamethonium, indicate a high risk of MH susceptibility but are usually self-limiting. Take measures to halt the MH process: 2 1. Remove trigger drugs, turn off vaporisers, use high fresh gas flows (oxygen), use a new, clean non-rebreathing circuit, hyperventilate. Maintain anaesthesia with intravenous agents such as propofol until surgery completed. 2. Dantrolene; give 2-3 mg.kg-1 i.v. initially and then 1 mg.kg-1 PRN. 3. Use active body cooling but avoid vasoconstriction. Convert active warming devices to active cooling, give cold 3 intravenous infusions, cold peritoneal lavage, extracorporeal heat exchange. Monitor: 4 ECG, SpO2, end-tidal CO2, invasive arterial BP, CVP, core and peripheral temperature, urine output and pH, arterial blood gases, potassium, haematocrit, platelets, clotting indices, creatine kinase (peaks at 12-24h). Treat the effects of MH: 5 1. Hypoxaemia and acidosis: 100% O2, hyperventilate, sodium bicarbonate.
    [Show full text]
  • Hypothermia After Cardiac Arrest December 2013
    Hypothermia after Cardiac Arrest December 2013 Managing Common Issues: Bradycardia: Bradycardia alone (even to as low as 35 bpm) may occur during induced hypothermia and, except in rare cases, is NOT a reason to discontinue the protocol. If bradycardia is severe, associated with persistent hypotension, and is not responsive to fluid and vasopressor therapy, a decision in conjunction with Neurocritical Care may be made to discontinue the protocol and rewarm the patient to 36⁰C. In this case, the endovascular device should be left in and temperature should remain at 36⁰C for the duration of the “maintenance” phase. Rewarming can then proceed to 37ᵒC per protocol. Lactate: Due to multiple factors (decreased cardiac output, shivering, lab measures, vasopressor administration), lactate levels will often be mildly elevated (usually < 5 mmol/L) during hypothermia. Once patient has reached target temperature, lactate should remain stable. Thus, the lactate trend during the protocol should be noted. An increasing lactate during the maintenance phase may indicate underresuscitation, which should be treated aggressively. Methods of Temperature Measurement: The benefit of therapeutic hypothermia relies on the induction and maintenance of an appropriate core body temperature without overcooling or accidental rewarming, both of which may be harmful to the patient. For this reason, temperature must be monitored closely and the method used to do so must be accurate and continuous. Of the methods available, both esophageal and bladder measurements have been shown to most accurately reflect core body temperature in most circumstances. Due to the importance of continuous temperature measurement and the possibility of inaccuracies, it is safest to measure BOTH esophageal and Foley temperatures continuously throughout the protocol.
    [Show full text]
  • Drowning – January 2018
    CrackCast Show Notes – Drowning – January 2018 www.canadiem.org/crackcast Chapter 145 – Drowning Episode Overview: 1) List risk factors for drowning 2) List 5 variables that portend poor outcome 3) Describe the diving reflex 4) Describe the management of a drowning patient with respiratory distress 5) Discuss the indications for rewarming the drowning patient. To what temperature do we warm to? 6) What are late complications of drowning? Wisecracks 1. What is immersion syndrome? Key Points: ▪ Drowning is a leading cause of death and loss of years of life with over 90% of cases occurring in lower- and middle-income countries. ▪ All significant drownings induce pulmonary injury and hypoxia by the amount of water aspirated and the duration of submersion. ▪ Pulmonary and neurologic support is essential to optimize the victim’s chance of a favorable outcome from this hypoxic event. ▪ Electroencephalography may be indicated in obtunded drowning victims to assess for subclinical seizures. ▪ No prognostic scale or clinical presentation accurately predicts long-term neurologic outcome; normal neurologic recovery is documented in patients with prolonged submersions, persistent coma, cardiovascular instability, and fixed and dilated pupils. ▪ Hyperventilation, steroids, dehydration, barbiturate coma, and neuromuscular blockade do not improve outcome after resuscitation. ▪ Comatose patients who have been resuscitated after reasonable submersion time regardless of rhythm should not be rewarmed above 34°C. Rosen’s in Perspective Traditionally, the terminology
    [Show full text]