Basic-muscle relaxants

Question 1

Tell me about the NM junction: what is it composed of? What type of receptors? Are actions moving against or down their concentration gradient? Is ATP required?

Answer 1

The neuromuscular junction is composed of a neuron which releases Ach and a muscle (motor) endplate which has numerous nicotinic (not muscarinic) Ach receptors. Binding of two Ach molecules to the paired alpha (not beta) subunits results in sodium and calcium to flow down their concentration gradients into the cell and potassium to flow down its concentration gradient out of the cell. Because the cations are moving down their concentration gradients, utilization of ATP is not necessary. The net movement of cations leads to an end-plate potential and depolarizes the perijunctional membrane, resulting in the opening of voltage-gated sodium channels. This in turn propagates an action potential of the muscle membrane, which then activates the sodium channel receptors on the T-tubule system, calcium is released by the sarcoplasmic reticulum and contraction occurs.

Question 2

Phase I block following end plate depolarization requires:

A. A high proportion of acetylcholine (Ach) receptors to be activated at once
B. An increase in the number of Ach receptors at the muscle endplate
C. Pretreatment with nondepolarizing muscle relaxants
D. Activation of voltage gated potassium channels
E. Activation of voltage gated calcium channels

Increasing the number of ACh receptors-is that needed for phase 1 block?

Answer 2

A high proportion of acetylcholine (Ach) receptors to be activated at once

Following a very high proportion (super-physiologic) of Ach receptors being activated , the perijunctional membrane is continually depolarized with resultant activation of voltage gated sodium channels (not K or Ca). During this time further Ach release will not result in a contraction as the endplate is in continuous depolarization and has not recovered (repolarized) for another Ach stimulus. This is accomplished by providing very high levels of Ach (or succinylcholine) to bind a high proportion of Ach receptors at once. Increasing the actual number of Ach receptors is not needed for phase I block. Pretreatment with nondepolarizing muscle relaxants can be used to prevent fasiculations, or at a higher dose, prevent depolarization in the first place (prevent phase I block).

Question 3

What is myasthenia gravis? Do you need more or less depolarizong muscle relaxant?

Answer 3

Myasthenia gravis is a condition in which there are a decreased number of normal (not mutant) Ach receptors on the muscle endplate. Because of this, exposure to normal doses of depolarizing muscle relaxants may not activate enough Ach receptors to result in perijunctional depolarization and thus Phase I block

Question 4

On train of four (TOF) peripheral nerve stimulation, the fourth twitch is absent. What does that mean? Go through a loss of each twitch down to one.

Answer 4

Approximately 25% of the Ach-R are unblocked

I was asked to make more tricky questions, so here you go! TOF with absence of the fourth twitch represents a 75% blockade of Ach-R, so therefore “Approximately 25% of the Ach-R are unblocked”must also be true. Fade on TOF can be due to two situations: First, use of nondepolarizing muscle relaxants, and Second: phase II block following succinylcholine. Phase II block is where prolonged depolarization of the perijunctional muscle endplate results in conformational changes to the Ach-R, such that it resembles the block of a nondepolarizer. Absence of the third twitch represents blockade of 80% of Ach-R and second twitch 90%. Tetanus is a related concept to TOF and is best used to gauge recovery from muscle relaxation, not so much redosing. In the situation of 4th twitch absence, one would expect fade on tetanus, regardless of the Hz used.

Question 5

Which three groups are more resistant to the effects of nondepolarizing muscle relaxants? Do they recover sooner or later? Where does adductor policies fit in with all of this?

Answer 5

diaphragm, larynx, and rectus abdominus are more resistant to the effects of nondepolarizing muscle relaxants and recover sooner as compared to peripheral muscles on the extremities*.
It just so happens that monitoring eyebrow twitch parallels the characteristics of these important muscle groups for breathing and airway patency

Because adductor pollicis is more sensitive to muscle relaxation, its recovery is theoretically a better indicator that all of the muscles of the patient have recovered from blockade

Question 6

Which of the following conditions would succinylcholine duration be LEAST LIKELY prolonged:

A. Concomitant use of ecothiophate eye drops
B. Concomitant use of atropine eye drops
C. Concomitant use of cyclophosphamide
D. Pregnancy
E. Cirrhosis

Answer 6

B: Concomitant use of atropine eye drops

First, cholinesterase inhibitors can also inhibit (to variable degrees) pseudocholinesterase, so neostigmine, physostigmine, etc, can cause a prolongation. Of the cholinesterase inhibitors, however, the most “famous” is ecothiophate. An assortment of other drugs can inhibit psedocholinesterase as well, and memorizing them is pretty low yield, but common ones are: esmolol, pancuronium, cyclophosphamide, and phenelzine. Another cause of prolongation of succinylcholine is reduction in the amount of pseudocholinesterase per liter of blood, either by decreased production or dilution (pregnancy and cirrhosis).

Question 7

Pseudochokineaterase variants-how Kong in a heterogenous block vs homogenous?

Answer 7

The heterozygote (one normal, one variant gene) results in about a 30 minute block. Two abnormal genes result in a 4-8 hour block

Question 8

Dibucaine-what is it, and what do the numbers mean in relation to heterogeneity?

Answer 8

Dibucaine, an inhibitor of normal pseudocholinesterase, will inhibit its activity by 80%. In heterozygotes the inhibition is 40-60% and in homozygotes it is 20% (therefore 20% dibucaine number, answer A). This patient is therefore a heterozygote, given a 30 minute blockade.

Question 9

Does pretreatment with Other NM blockers help with the dibucaine numver? Esmolol and sux?

Answer 9

Pretreatment with other muscle relaxants has no bearing on the dibucaine number (answer D), as the dibucaine number is purely a function of the drugs effects on the enzyme (in vitro). Esmolol is metabolized by an esterase located in the red blood cell, which is distinctly different than the pseudocholinesterase responsible for succinylcholine metabolism (answer E), therefore the metabolism of esmolol will be normal (normal esmolol half life is 10-20 minutes).

Esmolol can mess with sux, but esmolol is not broken down by pseudocholinesterase-it’s broken down by RBC esterase

Question 10

Which of the following patients is most likely at the highest risk of hyperkalaemic cardiac arrest following succinylcholine:

A. Patient with ejection fraction below 35%
B. Patient with left sided weakness following a stroke 5 years ago
C. Patient with spinal cord transection at T3 twelve hours earlier
D. Patient with 3rd degree burns over torso and legs 7 days ago
E. Patient with massive blunt abdominal trauma and sepsis 2 days ago

Answer 10

D: Patient with 3rd degree burns over torso and legs 7 days ago

Up-regulation of nicotinic acetylcholine receptors (Ach-Rs) outside the neuromuscular junction occurs following upper motor neuron injuries, and is referred to extra-junctional Ach-Rs (this also occurs following major trauma, prolonged sepsis, and myopathies, to name a few). Normally, following an intubating dose of succinylcholine, serum potassium will rise by 0.5 mEq/L (due to wide spread coordinated depolarization). The presence of exrajunctional Ach-Rs means that the number of receptors and muscle cells affected increases, and life-threating hyperkalaemic cardiac arrest can occur. The odds are increased with the amount of tissue affected and the chronicity of the injury (greatest period of risk is probably 7-10 days following denervation). A typical rule-of-thumb is to absolutely avoid succinylcholine 24 hours after the injury until at least a year. Of the above choices, the patient with burns has the highest risk due to the substantial size of the burns and the timing of drug administration. “Patient with massive blunt abdominal trauma and sepsis 2 days ago” also describes a situation at risk, but 48 hours following injury remains a grey area (less risk than 7 days, some even consider no risk). “Patient with spinal cord transection at T3 twelve hours earlier” chronicity is too acute (12 hours), and the patient with a stroke had the injury 5 years ago (another grey area as far as risk goes). Patients with low ejection fractions are at increased risk of cardiac arrest, but not due to hyperkalaemia.

Question 11

Which of the following is the most likely to result from muscle fasciculations following succinylcholine administration?

A. Increased intracranial pressure (ICP)
B. Pulmonary aspiration of gastric contents
C. Masseter muscle spasm (MMS)
D. Diffuse myalgia
E. Increased intraoccular pressure

Answer 11

Increased intracranial pressure (ICP)

Question 12

Which muscle relaxants tend to release histamine?

Answer 12

Benzylisoquinolone muscle relaxants (ending with –curium) tend to release histamine and steroidal muscle relaxants (ending with –curonium) tend to be vagolytic

Question 13

Of the muscle blockers that release histamine-which ones are the worst? Does six release histamine? What about cisatricurium? Tell me about the side effects of the steroidal compounds?

Answer 13

Of benzylisoquinolone muscle relaxants, atracurium and mivacurium (answer D) are most likely to result in mast cell degranulation with resultant histamine release leading to flushing, vasodilatation, and of course, bronchospasm. Slow injection rates and pretreatment with H1 & H2 blockers are recommended. Succinylcholine also causes histamine release with variable frequency, although in the great majority of cases no adverse effects other than a transient rash are present. Cisatracurium does not appear to result in histamine release even at very high doses. Steroidal coumponds tend to be vagolytic, with the prototype being pancuronium, which predictably results in dose dependent tachycardia and hypertension primarily through vagolytic mechanisms, but also sympathetic stimulation as well. Rocuronium and vecuronium have mild (if any) vagolytic properties at high doses.

Question 14

What is priming dose?

Answer 14

Priming dose is a concept where about 1/10th the intubation dose of a nondepolarizer is given about 3-5 minutes prior to intubation so that when the actual intubation dose is given, onset will be greatly accelerated.

Question 15

If you give neostigmine and then give sux-then what?

Answer 15

Neostigmine inhibits pseudocholinesterase, therefore, succinylcholines duration of action will be prolonged.

Question 16

Which of the following is LEAST likely to potentiate nondepolarizing muscle blockade:

A. Hypothermia
B. Hypermagnesaemia
C. Concurrent morphine
D. Acidosis
E. Desflurane

Are neonates more sensitive to relaxants than adults?

Answer 16

Volatile anesthetics (less so nitrous oxide), magnesium supplementation (as in obstetrics), hypocalcaemia, hypokalaemia, acidosis, and hypothermia are classics. Also worth knowing is neonates are more sensitive than adults to muscle relaxants.

Question 17

General rules about being more sensitive to muscle relaxant:

Answer 17

Extremes of age, MS, most peripheral neuropathies, most neuromuscular junction disorders, most myopathies, muscular dystrophies, some channelopathies…as a general rule anything that makes one weak all the time will most ilk have sensitivity whereas periodic (episodic) weakness is less profound (some sensitivity in MS probably no sensitivity in hyper- or hypo-kalaemic periodic paralysis).

Question 18

Just because a condition has up-regulation of nicotinic receptors does not mean there will for sure be resistance—-T or F? Give an example.

Answer 18

True-multiple sclerosis is an example of this!

Question 19

Myasthenic syndrome is another name for:

With that syndrome, how do patients do with depolarizing vs ND NMB?

Answer 19

Lambert Eaton syndrome

With ELS there is an up-regulation of acetylcholine receptors at the neuromuscular junction due to decreased acetylcholine release. Because there are more receptors, depolarization is easier (requires a smaller dose) with succinylcholine. As for nondepolarizers, although there are more receptors that need to be bound, nondepolarizers work through competitive inhibition and with less acetylcholine present, a lower dose of nondepolarizing muscle relaxant is needed.

Question 20

Does edrophonium have an effect on pseudocholinesterase?

Answer 20

No!

Question 21

MG-sensitivity to NDMB? Sux? How does this compare to ELS?

Answer 21

In MG there are fewer acetylcholine receptors (due to antibodies), again making a reduced dose of nondepolarizing muscle relaxant necessary (fewer receptors to occupy for a given effect); therefore making both ELS and MG sensitive to nondepolarizers for completely different reasons! Because of the fewer acetylcholine receptors at the muscle endplate, depolarization is more difficult (requires a higher proportion of receptors to be activated) making these patients resistant to succinylcholine**. The patients use physostigmine (or other anticholinesterases) which can result in prolonged succinylcholine duration as well as phase II block from supranormal baseline levels of acetylcholine. It should be noted that physostigmine inhibits pseudocholinesterase to a less extent than neostigmine (and the inhibition of pseudocholinesterase can prolong the half-life of succinylcholine)

ELS: less release of ACh, so less competition for NDMB, and
With ELS there is an up-regulation of acetylcholine receptors at the neuromuscular junction due to decreased acetylcholine release. Because there are more receptors, depolarization is easier (requires a smaller dose) with succinylcholine. As for nondepolarizers, although there are more receptors that need to be bound, nondepolarizers work through competitive inhibition and with less acetylcholine present, a lower dose of nondepolarizing muscle relaxant is needed.

Question 22

A patient with cerebral palsy:

A. Sensitivity to nondepolarizing muscle relaxants and hyperkalaemia with succinylcholine
B. Resistance to nondepolarizing muscle relaxants and hyperkalaemia with succinylcholine
C. Normal response to nondepolarizing muscle relaxants and hypersensitivity to succinylcholine
D. Sensitivity to nondepolarizing muscle relaxants and resistance to succinylcholine
E. Resistance to nondepolarizing muscle relaxants and normal response with succinylcholine
Is there a proliferation of receptors?

Answer 22

Cerebral palsy (CP) is a harder condition to make generalizations with, see Neurology Question 17. CP does not have an increased risk of hyperkalaemia with succinylcholine, even in the setting of contractures, as there is no proliferation of extrajunctional nicotinic acetylcholine receptors.

E: Resistance to nondepolarizing muscle relaxants and normal response with succinylcholine

Question 23

A patient with SLE and muscle relaxants-which ones are they sensitive to?

Answer 23

A: Sensitivity to nondepolarizers, sensitivity to succinylcholine

Autoimmune disorders, in general, are reported to have hypersensitivity to all muscle relaxants. This is likely only true for those disorders associated with rheumatologically derived weakness, with muscle relaxants simply just exacerbating this. The ABA has had a long-standing love affair with SLE and that’s why it was included here.

Question 24

There are 3 bird relevant things to know about cisatricurium-
1-how is it metabolized, and what slows that?
2-what does it metabolize to? Who metabolizes OT and excretes it? At high levels-what are it’s negatives? Can it help with muscular blockade?
3-is Cisatricurium associated with histamine release?

Answer 24

First, it is metabolized by organ-independent Hoffman elimination in the plasma, and that process is slowed in hypothermia. Second, one of the breakdown products of cisatracurium is a compound called laudanosine, which is metabolized by the liver and excreted by the kidneys. At extremely high levels, it can result in CNS excitation (increased MAC requirements) and seizures, but has no intrinsic ability for neuromuscular blockade. Atracurium (cis-atracurium is a stereoisomer of atracurium) also produces laudanoside, and since it is less potent, a greater dose (number of molecules needed) of atracurium is needed than cisatracurium. This results in increased levels of laudanosine with atracurium as compared to cisatracurium. Cisatracurium is not associated with histamine release (atracurium is, see MUS 10).

Question 25

Does atracurium produce laudanosine? If so, more or less that cisatricurium?

Answer 25

Atracurium (cis-atracurium is a stereoisomer of atracurium) also produces laudanoside, and since it is less potent, a greater dose (number of molecules needed) of atracurium is needed than cisatracurium. This results in increased levels of laudanosine with atracurium as compared to cisatracurium.

Question 26

patient with a dibucaine number of 20% has a prolonged neuromuscular blockade for four hours. Which of the following muscle relaxants were most likely used:

A. Pancuronium or succinylcholine
B. Vecuronium or succinylcholine
C. Mivacurium or succinylcholine
D. Rocuronium or succinylcholine
E. Only succinylcholine could have been used
Expand/Contract Explanation

Answer 26

The correct answer is: C: Mivacurium or succinylcholine

Both Mivacurium and succinylcholine are metabolized by pseudocholinesterase, and in the setting of homozygous atypical pseudocholinesterase, both can result in a blockade for hours. Of the nondepolarizing muscle relaxants in clinical use, pancuronium has the longest duration of action, but would not be expected to produce a 4 hour long blockade (even in renal failure).

Question 27

Which NDMB is broken down by pseudocholineaterases?

Answer 27

Mivacurium

Question 28

A patient in the ICU is difficult to ventilate with mechanical ventilation and a vecuronium gtt is initiated. Which of the following muscle relaxants would be a better choice for this purpose:

A. Succinylcholine gtt
B. Cisatracurium gtt
C. Rocuronium gtt
D. Atracurium gtt
E. Pancuronium gtt

Answer 28

B: Cisatracurium gtt

Prolonged vecuronium gtt has led to cases of prolonged polyneuropathy with weakness lasting months, and is therefore contraindicated for this purpose. This was especially true in the setting of steroid use (which was more common in the past). Cisatricurium has been shown to be a much safer alternative with far less risk of polyneuropathy. It is important to note that even long cases in the OR with steroids do not lead to polyneuropathies using vecuronium or other steroidal based compounds (pancuronium & rocuronium).

Question 29

In comparing vecuronium to rocuronium, which of the following is true:

A. Rocuronium is metabolized by the liver to a greater extent than vecuronium
B. Rocuronium is devoid of metabolites
C. Both rocuronium and vecuronium have about a quarter of their clearance through the kidney
D. Vecuronium, but not rocuronium, can precipitate with thiopental
E. Rocuronium is more potent than vecuronium

How are each of these metabolized?

Answer 29

is: B: Rocuronium is devoid of metabolites

Pancuronium, vecuronium, and rocuronium are very similar molecues with minor difference between each one (especially vecuronium and rocuronium). The metabolism and excretion of each of these drugs can be thought of a spectrum from pancuronium having the most metabolism (by the liver, of course) and the greatest amount of renal excertion (40%) and the least amount of bile excretion (10%). Rocuronium, on the other side of the spectrum undergoes (essentially) no metabolism and is cleared by the liver via the bile (~10% excreted unchanged in the urine). Vecuronium is in the middle with minimal metabolism (and therefore metabolites), 25% renal excretion and 75% bile excretion. Therefore, in the setting of a dysfunctional liver with poor bile excretion, rocuronium is not metabolized and not excreted, prolonging its blockade. Both rocuronium and vecuronium can precipitate with thiopental leading to pulmonary emboli . A greater dose of rocuronium is needed for an equipotent effect as compared to vecuronium, and is therefore less potent than vecuronium.

Question 30

Parameters for extubation: 
TV 
Vital capacity
NIF 
PACO2 
RR 
Head lift
Tetanus

Answer 30

There are seemingly endless criteria for extubation, and each one is meaningless without clinical context. But in the spirit of the ABA written boards, we provided nothing but dogmatic numbers. The following are minimal levels that generally appear as guidelines: tidal volume should be over 5 cc/ kg, vital capacity over 10 cc/ kg, NIF more negative than -20 cc H20, PaCO2 < 50, RR < 30, sustained tetanus at least 5 seconds, head lift of at least 5 seconds. RSBI is a calculation of RR/ tidal volume and should be less than 105. Fast discharge from the PACU is associated with good pulmonary status, lack of confusion, and pain control (among other factors).

Question 31

Max dose of naloxone:

Answer 31

A “full dose” of naloxone is typically considered >0.4 mg, although 0.2 will reverse the effects of opioids, including pain control, which could be difficult to control in the PACU.

Question 32

Neostigmine is an

Answer 32

acetylcholineaterase inhibitor

Question 33

Following a dose of glycopyrrolate, which of the following would be LEAST likely:

A. Bronchodilatation
B. Tachycardia
C. Decreased gastrointestinal motility
D. Decreased salivation
E. Mydriasis

Why is the answer what it is? Effects of atropine and scopolamine? How to reverse the effects of atropine and scopolamine?

Answer 33

E: Mydriasis

Anticholinergic drugs (prototype atropine) have the opposite effect as anticholinesterases, and are used to offset their effects. All of the answer choices are predictable effects of anticholinergics, including bronchodilitation, tachycardia, decreased GI motility, urinary retention, decreased salivation, confusion and mydriasis. Atropine is a tertiary amine, which means it easily crosses the blood brain barrier; therefore,you will see central effects such as mydriasis, disorientation, and delirium (depending on dose, of course). Glycopyrrolate has a quaternary structure which means it mostly does not cross the blood brain barrier, therefore CNS and pupillary effects are not seen.

Remember in practice there are two terry amines we use: atropine and scopolamine. They both cross the blood brain barrier. At high doses they can cause CNS effects:

Atropine: restlessness, hallucinations, delirium

Scopolamine: sedation, amnesia, euphoria

Glycopyrrolate does not have CNS effects at the doses we use. So its safe to use with narrow-angle glaucoma, for example.

Finally, remember to reverse the CNS effects of tertiary amines, you can use physostigmine. Therefore it would be a good choice if you used so much atropine (due to a glycopyrrolate shortage…which has happened!) that you developed central anticholinergic syndrome

Question 34

How does suggamadex work?

Answer 34

Sugammadex binds steroidal muscle relaxants and removes them from being able to compete for nicotinic acetycholine receptors.

Question 35

Why does neostigmine not work when there are no twitches?

Answer 35

Anticholinesterases such as neostigmine and edrophonium will not reverse the muscle blockade when no tetanus is present, as the increased doses of acetylcholine cannot overcome the competitive blockade.

Question 36

A 45 year old man undergoes laproscopic cholecystectomy under general anesthesia with rocuronium that is reversed with neostigmine at the end of the case and has had a stable course for the past 45 minutes in the PACU. Over the next 15 minutes, the patient begins desaturating to 92%. Physical exam demonstrates weak handgrip, small tidal volumes, clear lungs, and normal mental status. His other vital signs are normal. Which of the following would be the best treatment at this time:

A. Redose neostigmine
B. Noninvasive positive pressure ventilation (NPPV)
C. Draw an arterial blood gas (ABG)
D. Tracheal intubation
E. Heliox

Answer 36

A: Redose neostigmine

Recurization of rocuronium is an elusive concept, that I very much doubt will be on the boards as it is poorly defined. There is no accepted standard treatment for recurization (not due to subsequent administration). Some authors think that in some individuals that the rocuronium excreted in the bile can be reabsorbed and therefore auto-transfused for a subsequent dose (remember, rocuronium is not metabolized, so it is still potentially active). Only at very high doses of rocuronium could one imagine the duration of action outlasting that of neostigmine. The first step for a patient who is mildly desaturating but still stable, is to redose neostigmine (with an anticholinergic, of course). In more emergent situations, tracheal intubation may be safest. NPPV is a poor choice in this situation because the patients course is unknown (could have complete respiratory arrest). Confirming desaturation, hypoxia, or hypercarbia with an ABG will only delay treatment and not change management. Heliox employs helium gas mixed with oxygen to decrease its density in cases where turbulent flow is restricting good airflow. That is not the case here

Question 37

Which of the following is most true regarding neostigmine in regards to reversing muscle relaxation:

A. Neostigmine does not cross the placenta
B. Neostigmine effects peak 30 minutes after administration
C. It typically takes about 20 seconds for the effects of neostigmine to be apparent
D. Neostigmine’s duration of action is greater than 1 hour
E. Intrathecal administration of neostigmine can reverse neuromuscular blockad

Answer 37

D: Neostigmine’s duration of action is greater than 1 hour

Neostigmine’s onset is about 5 minutes, its effects peak at 10 minutes, and its duration is at least an hour. Neostigmine can cross the placenta, whereas glycopyrolate cannot. Therefore, in pregnant patients atropine can be used (even though its onset is quicker and duration of action shorter; whereas glycopyrolate has a more similar profile to neostigmine). Neostigmine can be used as an adjuvant for spinal anesthesia, prolonging sensory blockade, but is associated with many side-effects. Furthermore, intrathecal administration (usually less than 100 mcg) will not reverse muscle relaxation.

Question 38

75 year old man was administered scopolamine for sedation preoperatively and is confused and disoriented in the PACU after a 1 hour surgery. Which of the following would be the BEST next step:

A. Sedation and restraints
B. Reassurance
C. Neostigmine
D. Physostigmine
E. Atropine

Answer 38

D: Physostigmine

Scopolamine has significant CNS effects, causing sedation, amnesia, and sometimes delirium. Its anticholinergic effects on other organ systems are generally far less pronounced than with atropine, with the exception of its potency as an antisalagogue. Physostigmine has a tertiary amine structure, making it able to cross the blood brain barrier (unlike neostigmine and edrophonium), to “reverse” the effects of scopolamine. Sedation and restraints is a last resort and almost should NEVER be used on the boards. Reassurance will likely be ineffective with a confused, disoriented post-operative patient. Atropine is another anticholinergic that also crosses the blood brain barrier, and would worsen the disorientation. This is a case of possible central anticholinergic syndrome (which could appear on the boards either by history and symptoms (as is the case here) or by its name). The treatment will always be physostigmine.

Question 39

Your favorite! Hypokalemic and hyperkalemia metabolic acidosis:
What do they have in common?
How are they different?
How to treat?

Answer 39

Precipitating factors for both hypokalaemic and hyperkalaemic periodic paralysis include hypothermia and rest after exercise. With both diseases, trunk and extremity muscles are mostly affected and diaphragm and cranial muscles are mostly preserved. Response to muscle relaxants would be expected to be normal and a standard reversal with neostigmine should work as expected. Twitch monitoring as far as I can tell should be reliable and normal as well. These diseases are way over-represented on the boards.
For the hypokalaemic form, decreased levels of potassium lead to periodic paralysis* and administration of insulin, respiratory or metabolic alkalosis, etc (anything that decreases potassium) will precipitate or worsen an attack. For the hyperkalaemic form, increased levels of potassium leads to paralysis*, which includes succinylcholine, fasting, respiratory or metabolic acidosis, and, of course, potassium administration (food or drug). In this patient, we see a history of fasting, and a respiratory acidosis, both of which are more specific for the hyperkalaemic form. Hypothermia is consistent with both forms of familial periodic paralysis.
Calcium, in itself would do little to reverse the hyperkalaemia, but it does help decrease the activity of sodium channels that is at the root of this pathophysiology (remember in the setting of hyperkalaemia, membranes are more excitable and calcium reduces this hyperexcitablitiy).
With hypokalaemic familial periodic paralysis treatment includes K+ replacement, acetazolamide, and reversing causes of hypokalaemia (hypothermia, alkalosis, etc). The causative mutations in this disease are voltage-gated calcium channels (not sodium channels).