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109 Cards in this Set
- Front
- Back
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how does a nerve signal cause release of a neurotransmitter
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1. action potential travels down the motor neuron
2. depolarization of the axon terminal causes voltage gated calcium channels to open and calcium to enter 3. calcium binds to the vesicles containing neurotransmitters and causes them to migrate to the presynaptic membrane 4. the vesicles fuse to the membrane and release acetylcholine into the synaptic cleft |
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how does the release of acetylcholine from the presynaptic membrane affect the postsynaptic membrane and cells
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5. Acetylcholine is a ligand that binds to acetylcholine gated channels. acetylcholine receptors are nicotinic receptors which open the protein channel via conformational change. The channel allows Na, Ca, and K to move. interior of channel is negative so negative ions do not move. two acetylcholine molecules needed to make channel open.
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how does the opening of the ion channels in response to acetylcholine cause muscle contraction
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1. the ions entering the cell, changes the interior of the cell, allowing the signal to propagate throughout the muscle fiber
2. the t-tubules provide the path for depolarization. t-tubules are adjacent to the sarcoplasmic reticulum so when the t-tubules depolarize, they trigger the release of calcium from the sarcoplasmic reticulum 3. calcium then binds to the troponin complex causing a conformational change in the tropomyosin strand which exposes the binding sites on the actin filament. |
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depolarization of the t-tubules activates
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L-type voltage dependent calcium channels (dihydropyridine receptor) in the t-tubule membrane which are in close proximity to the calcium release channels (ryanodine receptor) in the sarcoplasmic reticulum
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the L-type voltage dependent channels are aka
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dihydropyridine receptors
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the receptors in the sarcoplasmic reticulum that are the calcium release channels are
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the ryanodine receptors
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the primary receptor that is the problem for MH
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ryanodine receptor
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definition of MH
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acute hyper metabolic state in muscle tissue following exposure to triggering agents and is potentially fatal
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mortality rate of untreated Malignant Hyperthermia
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>70%
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mortality rate of Malignant Hyperthermia that is treated in a timely manner
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4%
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a defect in what receptors can cause Malignant Hyperthermia
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either the dihydropyridine or the ryanodine receptors
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is Malignant Hyperthermia a functional or structural disorder
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functional
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whether the defect is in the dihydropyridine receptor or the ryanodine receptor, the end result is a
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functional disorder of the ryanodine receptor
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what is the problem with the ryanodine receptor in malignant hyperthermia
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it opens to nonphysiologic stimuli and remains open for a long time allowing a huge amount of calcium to be released from the sarcoplasmic reticulum - leading to prolonged interaction between the actin and myosin filaments
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the intense metabolic state and prolonged muscle contraction in malignant hyperthermia leads to
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muscle rigidity, increased lactic acid, increased CO2, muscle breakdown and many secondary events to these
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why don't the muscle contractions stop
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not enough ATP to combat all that calcium
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what contributes to the heat production with malignant hyperthermia
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muscle breakdown, tearing, increased metabolic rate
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triggering agents for malignant hyperthermia
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halothane, sevoflurane, isoflurane, desflurane, succinylcholine
maybe heat and exercise |
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safe to use with malignant hyperthermia
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opioids, NDMRs, ketamine
propofol, anxiolytics, nitrous oxide and gayle said (I think etomidate too) |
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pediatric incidence of malignant hyperthermia
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1:15,000
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adult incidence of malignant hyperthermia
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1:40,000
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high incidence areas in the US
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west Virginia, wisconsin, and the thumb of Michigan
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genetic relationship of malignant hyperthermia
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autosomal dominant
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overall incidence of malignant hyperthermia
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1:10,000
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what percent of malignant hyperthermia cases have had a previous uneventful surgery
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50%
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most specific and sensitive sign of malignant hyperthermia
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unexpected and sudden rise in ETCO2 but could be masked by rigorous hyperventilation
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initial signs of malignant hyperthermia
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tachycardia and tachypnea
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symptoms of MH
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tachycardia, tachypnea
increase ETCO2 hypertension ventricular dysrhythmias muscle rigidity (80%) increasing body temperature (1-2 degrees every 5 minutes) CO2 absorbent will be hot to the touch |
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ventricular arrhythmias occur in malignant hyperthermia because
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the activation of the sympathetic nervous system, hypercarbia, or increased serum potassium
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why does the potassium rise in malignant hyperthermia
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tearing of muscle cells releases the intracellular contents
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if you have NDMRs on board, why will you still see muscle rigidity with malignant hyperthermia
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because malignant hyperthermia does not affect the nicotinic receptors that are affected by NDMRs
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the CO2 absorbent reaction is
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exothermic
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the ABG of a patient with malignant hyperthermia will show
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acidosis and carbon dioxide retention
hyperkalemia, hypercalcemia, lactic acid |
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even if treated death from malignant hyperthermia can result from
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renal failure and DIC
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why is renal failure a problem with malignant hyperthermia
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myoglobinuria - muscle breakdown releases myoglobin that gets stuck in the kidneys
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other clinical signs of malignant hyperthermia
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hyperkalemia, hypercalcemia, lactic acid, myoglobinuria, elevated CK (>20,000 at 12 hours)
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24 - 36 hours after malignant hyperthermia has been treated
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it may redevelop
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what can accelerate the manifestation of malignant hyperthermia
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when succs is used in conjunction with a volatile anesthetic the symptoms can appear in 5-10 minutes
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rigidity of the jaw muscles after the administartion of succs is called
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masseter muscle rigidity
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masseter muscle rigidity is more common in
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children
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peak age of occurence for masseter muscle rigidity
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8 - 12 years
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less common trigger for masseter muscle rigidity
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is thiopental and propofol
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what is the association between masseter muscle rigidity and malignant hyperthermia
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25% of the people having had masseter muscle rigidity test positive for MH, if limb rigidity is also involved, the association is even greater
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other causes of masseter muscle rigidity
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myotonic syndrome
temporormandibular joint dysfunction underdosing succs intubating before succs works increased succs tension in presence of fever or elevated plasma epinephrine |
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will additional dose of succs or NDMRs help with masseter muscle rigidity
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no
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if your patient develops MMR, what should you do?
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if possible, discontinue surgery
if continuing surgery, move to TIVA have dantrolene available and monitor temperature and ETCO2 closely pt should be watched 12 - 24 hours for myoglobinuria and signs of MH possible dosing of dantrolene 1-2 mg/kg tell family risk of MH and episode of MMR check CK levels q 6 hours for 24 hours |
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CK levels over what in a patient that has experienced MMR means
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patient is very likely to have MH
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what are the three levels of rigidity associated with MMR
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mild, moderate, jaws of steel
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if patient develops jaws of steel -
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if can ventilate, wait it out
if can't ventilate, surgical airway |
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why don't we give succs to young boys?
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originally thought to be associated with MH and undiagnosed muscular dystrophy - but now know it is not directly linked to MH, but it is still a dangerous event
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death rate for young boys who react to succs by extreme hyperkalemia
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60% death
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what is core central disease
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a congenital myopathy characterized by muscle weakness
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core central disease is a mutation of
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the ryanodine receptor
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diseases that are associated with malignant hyperthermia
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core central disease, hypokalemic periodic paralysis, other myotonias, king-denborough syndrome, osteogenesis imperfecta, strabismus or ptosis, localized muscle weakness
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the myotonias are disorders affecting what 2 channels
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chloride and sodium ion channels
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remember Steinhert's disease?
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thinking it is to do with muscle weakness, laryngeal and respiratory insufficiencies, cognitive impairment, adult
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a patient with King-Denborough will show
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marked slanted eyes
low set ears pectus deformity scoliosis small stature |
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MH may possibly be linked to
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heat intolerance
caffeine intolerance SIDS |
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pneumonic for remembering treatment for malignant hyperthermia
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Some Hot Dude Better Give Iced Fluids Fast, Ladies
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treatment for malignant hyperthermia
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Stop volatiles, purge circuit, change absorbers (new circuit)
Hyperventilate with 100% O2 at >10L Dantrolene 2.5 ml/kg q 15 minutes up to 10 ml/kg or symptoms resolve, catheter Bicarbonate for severe metabolic acidosis (2-4 meq/kg to start) Glucose/Insulin/bicarb/hyperventilate to treat hyperkalemia, CaCl 10 mg/kg or 1 gm IV for arrhythmias IV fluids (without K), ice packs, cooling blankets, cold gastric lavage furosemide to flush kidneys Lidocaine for arrhythmias - no Ca channel blockers Laboratory data |
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treatment for Malignant Hyperthermia - step 1 - (Some)
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stop volatiles
purge circuit new circuit new absorbent |
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treatment for Malignant Hyperthermia - step 2 - (Hot)
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hyperventilate with 100% O2 at >10L/minute
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treatment for Malignant Hyperthermia - step 3 - (Dude)
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Dantrolene - 2.5 mg/kg q 15 minutes to a max of 10 mg/kg or symptoms resolve
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treatment for Malignant Hyperthermia - step 4 - (Better)
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Bicarb for severe metabolic acidosis - 2-4 meq/kg to start
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treatment for Malignant Hyperthermia - step 5 - (Give)
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Glucose, Insulin, Bicarb, hyperventilate to treat hyperkalemia
CaCl 10 mg/kg or 1 gm IV if arrhythmias present |
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treatment for Malignant Hyperthermia - step 6 - (Iced)
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IV fluids
Ice packs cooling blankets cold lavages |
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at what point do you stop cooling the patient
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when core body temperature reaches 38 degrees
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treatment for Malignant Hyperthermia - step 7 - (fluids)
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furosemide - to flush kidneys and protect from myoglobinuria
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treatment for Malignant Hyperthermia - step 8 - (Fast)
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Lidocaine to treat tachycardia, VT, vfib
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what drugs don't you use to treat arrhythmias in a patient with malignant hyperthermia?
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calcium channel blockers because they will react with dantrolene to cause/worsen hyperkalemia
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ideal treatment for arrhythmias associated with Malignant Hyperthermia
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ideally resolve the electrolyte disturbances and usually the arrhythmias resolve too
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treatment for Malignant Hyperthermia - step 9 - (Ladies)
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laboratory data - mixed venous, ABGs, electrolytes, BUN/Creatinine, CK, urine test for myoglobinuria, coags
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additional labs to consider ordering for malignant hyperthermia
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coags - because of risk of DIC
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how do you reconstitute dantrolene
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with 50 - 60 ml of sterile water
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how much dantrolene comes in one vial
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20 mg
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what is the dose for dantrolene
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2.5 mg/kg
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max dose of dantrolene
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10 mg/kg
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half life of dantrolene
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12 hours but levels begin reducing at 6 hours
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repeat doses of dantrolene at
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4 - 6 hours
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dantrolene was used for what before its use in MH
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muscle spasticity
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how does dantrolene work
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directly inside the muscle cell by binding to a site on the ryanodine receptor and reduces release of calcium from the sarcoplasmic reticulum
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does dantrolene affect the myocardium
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little effect with prescribed doses
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dantrolene dissolves faster if
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the sterile water is warmer
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dantolene also contains
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300 mg of mannitol per vial
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even though dantrolene contains mannitol, remember to
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give lasix for hyperkalemia and myoglobinuria
give lots of fluids |
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institutions that use general anesthetics are required
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to have 36 vials of dantrolene available (about $909 a year)
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is muscle rigidity always present in MH
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no
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is temperature increase an early or late sign
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late sign
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is ETCO2 increase an early or late sign
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early sign
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at what point can MH occur
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anytime during the anesthetic, even on emergence and in PACU
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managing a MH crisis - delegate what to the orderly
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ice and refrigerate IV fluids
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managing a MH crisis - delegate what to the surgical team
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finish surgery ASAP
place a foley catheter |
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managing a MH crisis - delegate what to the anesthesia tech
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Get the MH cart
begin mixing dantrolene and sterile water (Gayle says use a big sterile basin) |
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managing a MH crisis - delegate what to the circulating nurse
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phone for anesthetic assistance
send for more dantrolene prepare cath kit notify ICU assist with mixing dantrolene |
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managing a MH crisis - delegate what to you
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some hot dude better give iced fluids fast ladies
place an art line if you got time |
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MH research testing done on
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pigs with a ryanodine receptor mutation
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the gold standard for MH testing
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halothane/caffeine contracture test using a muscle biopsy
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drawback of the halothane/caffeine contracture test for MH
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only 5 centers in the US can do it
>$5,000 but insurance will cover it many false positives |
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alternate testing for MH
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genetics looking for RYR-1 receptor mutation hits only 30% of MH positives so far
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take the muscle biopsy from
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the vastus lateralis muscle
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genetic testing for RYR-1 mutations takes a while because
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the gene is huge and takes 3 months full time to get it sequenced
over 80 mutations of the gene but do not know if they all cause MH |
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family members that test negative for the RYR-1 genetic mutation
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are not necessarily MH-
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when is the genetic test useful
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if a member of a family is known to have it, then they can sequence the gene, figure out what mutation it is, and look at other family members for the same mutation
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conditions that mimic MH
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thyroid storm
pheochromocytoma sepsis drug induced hyperthermia iatrogenic hyperthermia hypothalmic or brainstem injury |
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two types of drug induced hyperthermia
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neuroleptic malignant syndrome
serotonin syndrome |
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pheochromocytoma is
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an adrenal gland tumor that pumps out catecholamines
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thyroid storm looks like MH because
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releases massive amounts of T3, T4 causing increased metabolic rate leading to increased ETCO2 and increasing temperature
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north american MH hotline
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1-800-MH-HYPER
www.mhaus.org |
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if you have a patient at high risk of MH, what should you do
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avoid triggers (lock succs in the drawer)
antianxiolytics change soda lime and breathing circuit remove vaporizers (or tape over obviously so no one turns them on) flush with 10 L O2 for 10 - 20 minutes and change fresh gas hose monitor very closely cooling blanket on bed to begin with have the cart handy to ward off evil have 3L of cold fluids in the fridge |
