NUR 837 Exam 3: Thermoregulation Study Guide PDF

NUR 837 Exam 3: THERMOREGULATION Reading: Morgan & Mikhail Ch. 52 Thermodynamics Hypothermia • body temp < 36C o T is a required metric. o if documenting T < 36C → must document intervention • in absence of shivering → hypothermia reduces metabolic O2 requirements • protective during cerebral or car...

NUR 837 Exam 3: THERMOREGULATION Reading: Morgan & Mikhail Ch. 52 Thermodynamics Hypothermia • body temp < 36C o T is a required metric. o if documenting T < 36C → must document intervention • in absence of shivering → hypothermia reduces metabolic O2 requirements • protective during cerebral or cardiac ischemia Perioperative Hypothermia Occurrence • extremes of age mostly affected o elderly → temp drops • abdominal surgery o heat lost to evaporation • long procedures • cold, ambient OR temps • occurs in almost every patient unless measures are taken o ex.: preoperative warming Physiological Effects of Hypothermia • cardiac arrhythmias and ischemia • increased peripheral vascular resistance • left shift of oxyhemoglobin dissociation curve • reversible coagulopathy—platelet dysfunction • increased post-op protein catabolism and stress response o want to avoid! • altered mental status • impaired renal function • delayed drug metabolism • impaired wound healing • increased risk of infection • unintended perioperative hypothermia o associated with increased mortality rate Core Temperature • same as central venous temperature (exception—reperfusion) • if unaddressed, these are the phases of degrees Celsius temperature drop: o phase 1: 1st hour of general anesthesia ▪ 1-2 degrees Celsius drop in temperature ▪ redistribution of heat accounts for initial decrease • warm central blood is redistributed to the cooler periphery secondary to anesthetic vasodilation ▪ prewarming pt for half an hour with convective forced air warming blankets prevents phase 1 hypothermia by eliminating the central-peripheral temperature gradient. o phase 2: more gradual decline in temperature ▪ 3-4 hours ▪ minor heat loss to environment • cold OR air, cold fluids ▪ heat loss in phase 2 is minimized by forced-air warming blankets, warm water blankets, heated humified gases, warm IV fluids, and increasing the temperature in the OR o phase 3: steady state ▪ heat loss = metabolic heat production Normal Temperature Regulation • hypothalamus maintains core body temperature • narrow tolerance for low or high temperatures—inter-threshold range • mechanisms of regulation: o sweating and vasodilation (high temp) o shivering and vasoconstriction (low temp) Anesthesia’s Effect on Normal Temperature Regulation • • • • inhibits central temperature thermoregulation interferes with hypothalamic response general anesthesia: o volatile agents produce dose-dependent decrease in threshold temperature that triggers vasoconstriction ▪ vasodilates AND changes threshold temperature in hypothalamus, which triggers vasoconstriction o isoflurane: 3% decrease in temperature for each percent of inhaled isoflurane o increases inter-threshold range through vasodilation and internal redistribution regional anesthesia: spinal, epidural, neuraxial o increases inter-threshold range through vasodilation and internal redistribution o continued heat loss is allowed. ▪ altered perception by hypothalamus of temperature in anesthetized dermatomes ▪ hypothalamus doesn’t get the message regarding temperature Methods of Heat Transfer • conduction • radiation • convection • evaporation • stop radiation loss by covering pt up • stop conduction loss by having pt touching something with lower conductivity • evaporation—can’t really help Conduction • heat movement through a substance by the transfer of kinetic energy from molecule to molecule • metals have good conduction o metal: pt gets colder faster • air has poor conduction • heat is lost to whatever the patient is touching (Ex.: OR table) Radiation • heat transferred from warmer to cooler objects by emission and absorption of energy radiated in varying wavelengths • objects do not have to be touching • accounts for the largest percentage of normal heat loss from the body • • Radiation accounts for 40% of heat loss from an anesthetized patient. Heat loss from radiation can be minimized by surrounding the object/body with warm objects. It can be accelerated by surrounding the body with cool objects. The difference of temperature between the two objects determines the rate of heat transfer. Cover pts head → prevents radiation loss of heat Convection • heat transfer occurs by moving fluid (liquid or gas) • air adjacent to body is warmed, it expands and moves away, and it carries the heat away • Heat loss of the anesthetized patient is about 32% caused by convection. Examples of this type of heat loss is wind chill and convection air current. Air over hot beach sand warms rises, moves out over water where it cools and moves closer to waters surface and is pushed back to sandy beach. This becomes a cycle. The easiest way to reduce heat loss is covering or insulating the skin surface. Whether using cotton blankets, surgical drapes, or plastic sheeting, a single layer to trap air reduces heat loss about 30 percent. Another important factor is the amount of skin surface covered. It is a popular misconception that a large percentage of heat is lost through the head. In the neonate and infant this is true because their heads account for such a high percentage of the body surface area. But in the adult patient, the amount of surface covered is the important factor. Convection also occurs in the respiratory tract; prevention would include warming inspired gases. Evaporation • the loss of latent heat of vaporation of moisture on the skin’s surface • latent heat of vaporation: the heat required to change liquid into vapor • if evaporation occurs, the remaining liquid loses heat • Evaporation accounts for 28% of heat loss of anesthetized patients. Two factors influence evaporation: difference in vapor pressure between skin surface and surrounding air (amount of heat lost can be increased ten times by sweating), and the amount of surface exposed. Evaporation occurs in surgical wounds and the respiratory tract. • Sources: o anything wet o airway o wounds Intraoperative Considerations of Thermodynamics Factors • cold, ambient temperature in OR • prolonged exposure of open wound • use of large amounts of room-temperature IV fluids • high flows of un-humidified gases o high flows are not humidified o low flows help preserve temperature Intraoperative Management • prewarm patient o 30 minutes with convective forced air warming (Bair Hugger) o prevents phase 1 ▪ phase 1 = vasodilation o eliminates central-peripheral temperature gradient • forced air warming blankets • warm water blankets • heated humification of gases o active vs. passive o passive: HME on end of ETT • warming IV fluids • increase temperature of OR • passive insulators have limited value unless entire body is covered (including head) How is temperature measured in the operating room? • core temp stickers • thermometer • esophageal stethoscope o lies in thorax around the heart o should be pretty close to core temperature • temperature probes o bladder Postoperative Considerations of Thermodynamics Shivering • causes of shivering: o reaction to hypothermia o neurogenic after-effects of general anesthesia • shivering is associated with vasoconstriction • shivering represents the body’s effort to increase heat production and raise body temperature • shivering increases O2 consumption, CO2 production, and CO • occurrence of shivering in anesthesia: o in PACU o postpartum o rationale: the body’s effort to increase heat production and raise the body’s temperature ▪ may be associated with intense vasoconstriction • general anesthesia: o associated in hypothermia and volatile anesthetics ▪ volatile agents take away compensatory mechanism of regulating temperature o more common after longer surgeries; greater concentration of volatile anesthetics • regional anesthesia: o spinal and epidural o lower shivering threshold and vasoconstrictive response to hypothermia • other causes of shivering: o rule out other causes ▪ sepsis ▪ drug allergy ▪ transfusion reaction • effects of shivering: o increases O2 consumption by as much as 5-fold o increases CO2 production o increases CO o decreases arterial O2 saturation o increases risk of MI ▪ increased O2 demand, decreased supply o poorly tolerated by cardiac and pulmonary patients • meperidine 12.5-25 mg → treats shivering Pediatrics and Shivering • older children and adults shiver to create heat • newborns DO NOT shiver o brown adipose tissue burns calories and releases heat o brown adipose tissue is found on babies’ necks, chests, backs, butts o lose brown fat within first few years Treatment of Shivering and Hypothermia • BEST: maintain normothermia • meperidine IV 12.5-25 mg (small doses) • intubated/ventilated patients: o increase sedation and muscle relaxant • postoperatively: o ambient forced air warmer o heated blankets o monitor for: ▪ MI ▪ arrhythmias ▪ increased transfusion requirements ▪ increased/prolongs muscle relaxants Malignant Hyperthermia Overview • rare • genetic • hyper-metabolic disease • triggering agents: o inhaled anesthetics (N2O does not trigger MH) o succinylcholine • presentation time: o when turning agent on o post-op o most likely, will be early o very labile • can present more than an hour after emergence from anesthesia Pathophysiology • uncontrolled increase of intracellular calcium in skeletal muscle • sudden release of calcium from sarcoplasmic reticulum (SR) removes inhibition of troponin, resulting in sustained muscle contraction • marked increase in ATP activity → results in an uncontrolled hypermetabolic state • increased O2 consumption and CO2 production o increased CO2 in blood → acidosis • severe lactic acidosis and hyperthermia • genetic component of MH • drugs known to trigger MH: o ether o halothane o methoxyflurane o enflurane o isoflurane o desflurane o sevoflurane • • • • 4 major components of MH: o rigor—sustained muscle contraction o heat production o CO2 elevated o lactic acidosis o all from SR dumping Ca2+ intracellularly nearly 50% of patients who experience MH have had a previous uneventful exposure to a triggering agent. most MH patients have relatives with MH or abnormal halothanecaffeine contracture test o muscle biopsy exposed to agent chromosome 19, ryanodine receptor (RyR1) o RyR1: calcium channel responsible for release of calcium from SR o important in muscle depolarization Clinical Manifestations • early (2 or more signs increase diagnosis of MH) o muscle rigidity o tachycardia o o • • • • unexplained hypercarbia (rapid increase in ETCO2) increased temperature ▪ core temp can rise 1 degree C every 5 min hypercarbia → tachypnea SNS overactivity → arrhythmias, HTN, mottled cyanosis goal: stop temp from rising to prevent death and end-organ damage what’s the first sign? rise in ETCO2 Signs of MH • markedly increased metabolism • increased SNS activity • muscle damage • hyperthermia Lab Tests for MH • mixed metabolic respiratory acidosis o marked base deficit • hyperkalemia o tx: insulin, dextrose, calcium chloride, bicarbonate • hypermagnesemia • reduced mixed venous O2 saturation • ionized calcium concentration varies; initial increase, but later decreases • increased serum myoglobin o Anectine without MH can also cause increased serum myoglobin. • increased creatinine kinase (CK) o peak CK levels >20,000 → suspect MH o Anectine without MH can also cause elevated CK Diagnosis and Normal Progression of MH • ETCO2—early and sensitive indicator of MH • vital sign changes o SNS stimulation • labs (increased CK, hyperkalemia, hypermagnesemia; decreased SvO2) • AKI and DIC can occur • cerebral edema, seizures • liver failure • MG deaths due to DIC and organ failure due to delayed treatment or no treatment with Dantrolene. • **know what labs will look like for MH** MH & Associated Diseases • musculoskeletal diseases o central-core disease o multi-minicore myopathy o King-Denborough syndrome • controversial associations: o DMD o muscular dystrophies • positive family history • exercise-induced rhabdomyolysis Intraoperative Considerations • treatment overview: o terminate the episode ▪ give something to stop calcium from releasing from the sarcoplasmic reticulum o treat complications (hyperthermia, acidosis) o mortality rate: 5-30% • MHAUS treatment protocol • acute treatment: o discontinue volatile agents and succinylcholine o flush or change soda lime, breathing tubes, breathing bags o hyperventilate with 100% O2 to counteract increased CO2 and increased O2 consumption o volatile agent is still in the entire machine. ▪ • • • turn gas off, give 100% FiO2, get new circuit & machine. Use ambu bag and O2 tank. can use machine, but will need to flush it out. change soda lime, flush with 100% oxygen. can’t do inhalation for MH, so will need to do TIVA, N2O + opioid Dantrolene: o interferes with muscle contraction by binding to RyR1 receptor o inhibits calcium release from SR o dose: 2.5 mg/kg IV every 5 minutes until episode is terminated o preparations: ▪ 20 mg hydrolyzed lypholized powder; reconstitute with 60 ml sterile water. (TAKES LONGER) (Revonto, Dantrium) ▪ 250 mg; reconstitute with 5 ml (MOST EXPENSIVE) (Ryanodex) o half-life: 6 hours o after initial symptoms controlled, 1 mg/kg IV every 6 hours for 24-48 hours o 70 kg pt ▪ 2.5 mg/kg dose, give 175 mg first ▪ supply: 20 mg/60 mls → need 9 vials o MH can reoccur within first 24 hours o used often to treat thyroid storm and neuroleptic malignant syndrome (NMS) o side effect: muscle weakness including respiratory insufficiency and aspiration pneumonia ▪ may need intubation/mechanical ventilation o may cause phlebitis in peripheral veins; give central if possible. Correction of Acid-Base and Electrolyte Imbalances • persisting acidosis—IV sodium bicarbonate (will worsen hypercarbia) • hyperkalemia—glucose, insulin, diuresis o will cause sodium-potassium pump to make in more K+, reducing serum K+ • antiarrhythmics, vasopressors, inotropes as needed • avoid calcium channel blockers if giving Dantrolene o causes hyperkalemia MH → COOL the patient down • surface cooling—ice packs, cold air convection, cooling blankets • lavage (iced saline) • cardiopulmonary bypass if other measures fail • cooling should be initiated IMMEDIATELY MH Postoperative Considerations: Confirm Diagnosis • CK baseline • halothane-caffeine contracture test o requires muscle biopsy • genetic testing • MH registries Differential Diagnosis • MH • CO2 insufflation o CO2 insufflation accidentally placed in arterial or venous system will increase ETCO2. • NMS o NMS: mostly associated with antipsychotics; not usually seen with anesthesia but it closely mimics MH • Thyroid Storm • Pheochromocytoma o hyperdynamic state, but ETCO2 may not be elevated • • • • • • o dumps of E/NE, which may not affect ETCO2 Drug Induced hyperthermia Serotonin Syndrome o not likely seen under anesthesia, but mimics MH o Serotonin syndrome occurs with SSRIs, MAOIs, and foods high in tyrosine. Iatrogenic Hyperthermia Brainstem or hypothalamic injury o if hypothalamus is injured, may interrupt normal compensation for temperature changes. Sepsis Transfusion Reaction Neuroleptic Malignant Syndrome (NMS) • characterized by hyperthermia, muscle rigidity with extrapyramidal signs (dyskinesia), altered consciousness, and autonomic lability in patients receiving antidopaminergic drugs o antidopaminergic drugs: phenothiazines, butyrophenones, thioxanthenes, metoclopramide • imbalance of neurotransmitters in brain o abnormal centra dopamine activity • clinical presentation: o similar to MH o look at patient’s meds o won’t be the acute crisis of MH o mild hyperthermia o tachycardia, labile BP, diaphoresis, increased secretions, urinary incontinence o elevated CK levels • takes hours to weeks to develop; usually within 2 weeks of dose adjustment • NMS is commonly confused with MH, they present similarly. • NMS usually occurs in pts on antipsychotics. • recommended that patients with NMS do not receive succinylcholine or volatile agents.