Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
42 Cards in this Set
- Front
- Back
What is the cause of NMS?
|
chronic administration of psychoactive drugs
1. butyrophenones 2. phenothiazines 3. MAOI 4. lithium |
|
What are symptoms of NMS?
|
1. rhabdo,
2. ARF, 3. impaired motor fxn (generalized rigidity), 4. mental status deterioration leading to coma, 6. delirium, 7. hyperpyrexia, 8. autonomic instability - labile BP, inc HR, inc RR 9. respiratory failure, 10. mortality of 15% |
|
What is the difference between NMS and MH?
|
-MH is defect in skeletal muscle metabolism, has a genetic basis,
-NMBDs are able to produce flaccid paralysis in NMS but not MH |
|
Is MH susceptibility present in patients with NMS?
|
probably not, can use SCh
|
|
What is the therapy for NMS?
|
no completely effective therapy,
-bromocriptine (dopamine agonist) can be used, -dantrolene has also been effective |
|
What is the basic underlying problem in MH?
|
SR loses it's ability to bind or reuptake calcium
-there is an intracellular buildup of Ca which leads to heat production, O2 consumption, and activation of contractile elements |
|
How does dantrolene work in MH?
|
decreases the release of Ca from the SR
|
|
How does MH work on the SR?
|
leads to disruption of the ATPase in the SR, resulting in consumption of available energy resources and acidemia which is the hallmark of the condition
|
|
What drugs are unsafe in MH susceptable pts?
|
decamethonium, SCh, volatiles (not nitrous)
|
|
Why should you not give verapamil to a patient being treated for MH?
|
has been shown to depress cardiac function when given with dantrolene
|
|
How should you give dantrolene for treatment of MH?
|
-bolus 2.5mg/kg IV
-repeat every 5min until symptoms abate or a max of 10-20mg/kg is reached -then 24 hours of 10mg/kg/day should be given |
|
What is troponin and what is tropomyosin?
|
-troponin - inhibitory protein that binds to actin (thin filaments) in the resting state (calcium binds to troponin and inhibits the inhibition);
-tropomyosin - inhibitory protein that binds to myosin (thick filaments) in the resting state |
|
how do nondepolarizers affect the muscle rigidity of MH?
|
they don't
|
|
When in relation to the trigger does MH occur?
|
either acute or delayed
-if delayed may not occur until the patient is in recovery |
|
When giving SCh what should raise your suspicion to the possibility of MH? Why? What else?
|
trismus signals the onset of MH about 50% of the time,
-also failure to achieve muscle relaxation |
|
CPK levels of what postop signal MH?
|
>20,000
|
|
If a patient develops masseter spasm during or after a MH triggering anesthetic what should you do? What should you check?
|
Should mandate conversion to a non-triggering anesthetic
-Other signs of MH should be present before anesthesia and surgery are stopped. -serum creatinine kinase levels should be followed for 24 hrs after an episode of masseter spasm bc an elevation may indicate an underlying myopathy |
|
What are the earliest signs of MH?
|
hypercarbia > tachycardia
|
|
What are signs of MH?
|
1. tachycardia,
2. tachypnea, 3. rigidity, 4. hypercarbia 5. hypoxemia 6. acidosis 7. cyanosis 8. hyperthermia, 9. arrhythmias, 10. hyperkalemia |
|
What are complications from MH?
|
1. death from cardiac arrest,
2. death from cerebral or pulmonary edema, 3. renal failure, 4. DIC |
|
What is the differential diagnosis of MH?
|
1. sepsis,
2. pheochromocytoma, 3. thyroid storm, 4. NMS |
|
How is dantrolene prepared?
|
must be dissolved in sterile water (20mg vial with 60cc sterile water)
|
|
What is the half life of dantrolene and what are the routes through which it can be given?
|
T1/2 = 12 hrs,
-highly lipid solube and comes in PO and IV forms |
|
What is the treatment for MH?
|
1. stop anesthesia and surgery,
2. hyperventilate with 100% O2, 3. dantrolene - 2.5 mg/kg Q 5min to 10 mg/kg 4. treat hyperthermia - institute cooling 5. treat hyperkalemia (insulin 10 units/glucose 50cc D50) 6. treat acidosis - bicarbonate 2-4 meq/kg 7. treat arrhythmias - Lidocaine 1-4 mg/kg slow IV push 8. place foley, arterial, and central lines |
|
What is the gold standard for evaluating patients possibly susceptible to MH?
|
halothane contracture test,
-varying doses of halothane and caffeine and measuring muscle tension -caffeine causes a muscle sample to contract when halothane is added muscle contraction is greater -perform on a fresh sample of muscle |
|
What conditions were once thought to be more prevalent in MH pts, but were found to be no more than the general population?
|
1. strabismus,
2. hernia, 3. kyphoscoliosis, 4. muscle cramps 5. muscle weakness |
|
What is the best indicator of MH risk?
|
hx of MH episode in patient or relative
|
|
How does pretreatment with dantrolene affect the occurence of MH?
|
masks the early signs but doesn't prevent the actual event
|
|
When should you do a muscle biopsy?
|
history of masseter spasm or questionable MH (if for sure MH no reason to do the biopsy)
|
|
When do you do a MH test in a child with a distant relative with MH?
|
test the child's parent then only if the childs parent is positive do you test the child
|
|
What size should a child be to test for MH?
|
20kg minimum is recommended to avoid injury to the muscle group
|
|
When is an optimal CPK test done?
|
patient fasting and resting (no exercise for 1-2 days)
|
|
Why should you not do the halothane contracture test in patients with NMS?
|
patients with NMS can have an abnormal response to halothane
|
|
Other than drugs, what are other possible triggers of MH?
|
1. stress
2. high environmental temp 3. muscle trauma 4. exercise |
|
What may be useful for arrhythmias in MH?
|
BBs or Lidocaine, but verapamil should be avoided
|
|
What is the best tx for rhabdo that occurs with MH?
|
Aggressive hydration with forced diuresis and urine alkanization
|
|
What is the sarcotubular system?
|
It is made of the T system and the sarcoplasmic reticulum and surrounds each muscle fiber
-the T system rapidly transmits an action potential to fibrils |
|
Explain the physiology of MH.
|
- During contraction there is "sliding" between actin and mysosin as they break and reform cross linkages
- the action potential is transmitted to the fibrils via the T system and this triggers the release of Ca from the SR - Ca initiates excitation contraction coupling - muscle contraction - Ca inhibits the inhibition - it binds to troponin; in resting muscle, troponin is tightly bound to actin. Ca inhibits this binding and as the union is weakened, tropomyosin is then able to move laterally and actin comes into contact with myosin, ATP is split, and muscle contraction occurs -Shortly after releasing Ca, the SR begins to reaccumulate and store released Ca in its cisterns by active transport (ATP is involved again) - when intracellular Ca falls sufficiently, contraction of muscle ceases - If the SR can't reuptake Ca, muscle contraction continues and is sustained - referred to as contracture |
|
If symptoms of MH appear, what must you immediately do?
|
Obtain an ABG and switch to a nontriggering anesthetic
|
|
What is Dantrolene? How does it work?
|
It is a hydantoin developed as a muscle relaxant
-it inhibits transmembrane Ca flux and excitation contraction coupling -ie it decreases the release of Ca from the sarcoplasmic reticulum |
|
Management of MH susceptible or high risk pts.
|
1. heightened awareness and readiness
2. non-triggering anesthetic techniques |
|
What neurotransmitter system does NMS involve?
|
The dopaminergic system and has been associated with the withdrawal of L-Dopa
|