MH Flashcards

1
Q

What is of the most importance if you suspect MH in your patient?

A

Rapid recognition, diagnosis, and treatment.

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2
Q

what causes MH?

A

sux and volatile anesthetics

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3
Q

how long after the case can MH show up?

A

more than an hour after emergence.

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4
Q

rates of occurance in pediatrics and adults.

A

pediatrics is 1:15,000

adults is 1:40,000

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5
Q

who does MH show up in mostly?

A

young males

almost none reported in infants
and few reported in elderly

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6
Q

what is the basic unit of skeletal muscle?

A

sarcomere

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7
Q

what is the name of the proteins inside the sarcomere?

A

actin and myosin

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8
Q

what has to be exposed so that a muscle contraction can potentially occur?

A

active sites on the actin have to be exposed so that fibrils of myosin can connect.

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9
Q

what electrolyte do you have to have for muscle contraction to occur?

A

Ca++

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10
Q

what happens after the active sites are open?

A

Myosin heads latch to the site and pull actin strands together causing contraction.

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11
Q

What is increased in MH?

A

abnormal increase in Calcium release

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12
Q

what type of leak of calcium is occurring in MH?

A

increased and continuous leak of calcium.

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13
Q

where is the leak coming from in MH?

A

ryanodine receptors of the SR

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14
Q

what type of contraction does MH create? intermittent or sustained?

A

sustained contraction

continuous

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15
Q

in MH is there an increase or decrease in metabolism?

A

increase in metabolism

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16
Q

increase in temp is what kind of sign of MH?

A

LATE SIGN

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17
Q

What causes the increase in temp in MH?

A

prolonged muscle rigidity causes increase in temp.

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18
Q

name some s/s of MH?

A
increased CO2 that never reaches back down to base line
tachycardia
muscle rigidity (specifically masseter)
rhabdo (dark urine color) 
eventually increased temp.  
mottled cynosis
hypertension
arrhythmias
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19
Q

what is rhabdo?

where will you see it occuring?

A

muscle break down

you will see it as a change in urine color- dark, tea color

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20
Q

EARLIEST SIGN of MH?

A

MASSETER MUSCLE RIGIDITY induced by sux and or other muscle rigidity.

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21
Q

what else could be the issue if you have some masseter muscle rigidity - difficulty opening the mouth to intubate?

A

make sure you gave them a full dose of paralytic bc if you under dose them their mouth may stay shut
also make sure you have given the paralytic time to work- they may just need more time.

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22
Q

how much can the core temp of a person in MH rise per five min?

A

increase by 1 C every five min. (cool them down)

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23
Q

in MH the patient will initially have hypertension but it can rapidly be followed by what?

A

low blood pressure because of cardiac depression.

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24
Q

is generalized muscle rigidity consistently present in MH?

A

No, can have muscle rigidity but it does not have to be generalized.

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25
what does dark colored urine reflect?
myoglobinemia and myoglbinuria (blood and urine)
26
what is the most sensitive indicator of MH?
unanticipated doubling or tripling of ETCO2, in the absence of vent changes.
27
so whats the earliest sign and what is the most sensitive sign (the sensitive sign happens pretty early on as well).
earliest = MMR or muscle regidity in general. most sensitive sign = increasing ETCO2
28
what is a diagnosing problem with MH?
variable presentation | quite a few of the signs can be different in diff individuals, may show up may not, may take longer.
29
If they patient survives the first few min. of MH what can happen to the Renal, Hepatic, CNS?
acute kidney failure and DIC Cerebral edema with seizures Hepatic failure
30
most MH deaths are due to what?
DIC and organ failure due to delayed or no treatment with DANTROLENE
31
Who is (for sure) susceptible to MH?
``` Familiar MH (close family) musculoskeletal dz should clue you into the fact that they will be more likely to have MH ``` central core dz muliti minicore mypathy king-denborough syndrome
32
king-denborough what does it look like in kids?
short stature, small jaw, kyphoscoliosis, pigeon chest, facial and skeletal deformities, susceptibility to malignant hyperthermia, and acquired joint contractures
33
potentially susceptible to MH ?
DUCHENNE’S OTHER MUSCULAR DYSTROPHIES NONSPECIFIC MYOPATHIES HEAT STROKE OSTEOGENESIS IMPERFECTA (brittle bone)
34
Tell me about Duchenne's?
``` Duchenne's muscular dystrophy = progressive weakness and wasting of muscles onset 3-5 years old genetic- primarily males motor development delay history clumsiness frequent falls difficulty climbing stairs, running, and riding tricyle waddling gait typically can not ambulate by age 12 do not typically live past 18 birthday ```
35
are people with exercise induced rhabdo susceptible to MH?
several MH reports in patients who have exercise induced rhabdo
36
what should be in the back of your head when you have a patient who you are inducing and they have MMR?
consider that they may be potentially susceptible to MH, try to find any other reason for this to be happening.
37
what do the labs of someone with MH look like in regard to acid base?
mixed metabolic and respiratory acidosis with marked base deficit (base deficit means acid) early on it may be isolated resp. acidosis
38
what will a person with MH electrolytes look like?
increased K increased Mg Increased Ca, then decrease later (ionized calcium which is the free active form)
39
what will their labs in regards to muscle breakdown look like for MH?
INCREASED serum myoglobin, creatinine kinase.
40
when do serum CK levels peak and what does that tell you?
12-18 hours after anesthesia, exceed 20,000 IU/L | The diagnosis is strongly suspected
41
what can sux do to serum myoglobin and CK levels?
sux can increase myoglobin and CK levels markedly without MH (if you have muscle contraction with Sux as it naturally does during phase one depolarization then that can break down muscle)
42
treatment of MH?
Stop the triggering agent (sux volatile gas) notify the surgeon hyperventilate with 100% oxygen (ambu bag) finish case or abort DANTROLENE bicarb cooling insuline (d50) core temp monitor monitor urine output and try to prevent ATN (change out the machine if possible, if not gas it out with air or oxygen)
43
if you suspect a person to be MH possible and you do not have a designated MH machine what should you do to your existing machine? (same thing you would do to a patient who came down with MH and you do not have a seperate MH machine)
CHANGE ABSORBER, CIRCUIT, REMOVE VAPORIZERS, FLUSH 100% OXYGEN THROUGH MACHINE (AT LEAST 5 MIN) could run oxygen through machine longer, hospital specific.
44
while waiting on MH vent, or while clearing out your existing vent what will you be doing to the patient in regards to oxygenation?
bag mask 100% while waiting on vent.
45
If someone has MH, why do you give calcium cl or calcium gluconate? is that your first go to?
For cardiac protection, bc it does NOT lower the potassium and the patient may have life threatening high potassium. you give the calcium only if the potassium is life threatening otherwise you treat it with more normal measures such as insulin/glucose, hyperventilate, bicarb.
46
What drug do you avoid if you have given Dantrolene?
NO CALCIUM CHANNEL BLOCKERS!
47
You would cool a patient with MH, but when is cooling the patient an immediate concern?
you cool them immediately if fever is present!
48
With MH and treatment, what all are you treating by way of labs and metabolic things?
correct acid/base and electrolyte imbalances. lower potassium.
49
MH is family related but what type of family members does it matter more with?
first degree family members (mom dad, sister brother, children)
50
What is the IMMEDIATE main therapy for MH?
Dantrolene
51
what is the dose of dantrolene
Dantrolene 2.5 mg/kg to a max of 10mg/kg given every 5 min. until episode has stopped.
52
how does the normal dantrolene come?
20mg powder that needs to be dissolved in 60ml of steril water that takes 86 sec. for each vial
53
the newer type of dantrolene (ryanodex) takes how long to mix and how much comes in a vial?
20 sec to mix | and contains 250mg
54
half life of dantrolene and why does this matter?
half life is 6 hours and it matters because you may have to re dose someone if they have symptoms again after the half life.
55
How does dantrolene work, what is the MOA?
DIRECTLY INTERFERES WITH MUSCLE CONTRACTION BY BINDING THE Ryr1 RECEPTOR CHANNEL AND INHIBITING CALCIUM ION RELEASE FROM THE SARCOPLASMIC RETICULUM Hydantoin derivative (crystalline compound in sugar beet) used in anticonvulsant drugs.
56
after the initial episode of MH is controlled what is the maintenance dose of Dantrolene?
1mg/kg q 6 hours (half life is 6 hours) for 24-48 hrs to prevent relapse bc MH can recur within 24 hours after initial episode.
57
what is the most serious complication of use with dantrolene?
generalized muscle weakness that may result in respiratory insufficiency or aspiration PNA.
58
dantrolene given through a small peripheral vein can cause what?
phlebitis, consider CVL | IF YOU HAVE TIME throw in a CVL or jugular.
59
What are some other uses of dantrolene that is not MH? | and if used chronically what can occur?
decrease temp in thyroid storm NMS chronic use for spastic disorders has been assoiciated with hepatic dysfunction.
60
ryanodex, tell me about it?
new formulation of dantrolene contains 250mg per vial contains 125mg of mannitol requires 5cc of sterile water to dissolve sufficient dantrolene in a single vial for a loading dose in a 100kg patient!
61
common dantrolene is called what other name?
revonto is the more used form of dantrolene, the more expensive higher concentration dantrolene is called ryanodex
62
how much mannitol in Revonto?
3000mg
63
how many doses of revonto / ryanodex can you give?
revonto you can give subsequent treatment dose, but with ryanodex it is limited to the initial dose only.