Hypothermia

hypothermiaHypothermia is when you get really cold. Generally, hypothermia is defined as a core temperature less than 35C (95F). The Swiss staging system is fairly commonly used for correlating core temperature and clinical signs:

  • Stage I (35 – 32C; 90 – 95F): conscious, shivering
  • Stage II (28 – 32C; 82 – 90F): altered mental status, not shivering
  • Stage III (24 – 28C; 75 – 82F): unconscious, not shivering, vital signs present
  • Stage IV (< 24C; < 75F): apparent death (but resuscitation possible!)
  • Stage V (< 13.7C; < 58F): death due to irreversible hypothermia

Healthy people have fairly effective mechanisms for maintaining a normal temperature (37C; 99F) (e.g., shivering, peripheral vasoconstriction) but these can be overwhelmed by extreme cold (Primary Hypothermia). Some comorbid patients can develop hypothermia even in a warm environment (Secondary Hypothermia). For instance, severely-burned patients can have increased heat loss, while acute spinal cord injury can impair peripheral thermoregulation.

For the development of hypothermia, it is sometimes helpful to remember that heat can be lost by 4 physical mechanisms:

  • Radiation: heat exchange by infrared electromagnetic radiation
  • Evaporation: molecules converting from liquid to gas phase (e.g., sweat)
  • Convection: heat exchange by air/fluid currents
  • Conduction: heat exchange by direct contact with a colder surface
  • Brown DJA, Brugger H, Boyd J, Paal P. 2012. Accidental hypothermia. NEJM; 367:1930.
  • Zafran K, Mechem CC. 2017. Accidental hypothermia in adults. In: UpToDate.

Waveform Capnography

capnography Waveform capnography is a commonly used monitor in the operating room, and is increasingly seen in non-operating room environments too! The capnographic waveform can be described as having several phases:

  • Phase 0 (inspiratory baseline) represents the inspiratory phase of the respiratory cycle.
  • Phase 1 is the initial part of expiration, when dead space gases are being exhaled. Since the exhaled gas in this phase did not take part in gas exchange, the PCO2 is 0.
  • Phase 2 (expiratory upstroke) involves exhaled gases from alveoli reaching the detector. There is a sharp rise in PCO2 during this phase.
  • Phase 3 is a (more or less) flat plateau showing continued exhalation of alveolar gas. The last, maximal part of this phase is the end-tidal point (ETCO2), which is usually 35-40 mmHg. ETCO2 tends to be 2-5 mmHg lower than PaCO2, though this difference can be increased/decreased under a variety of conditions, such as ventilation-perfusion mismatch.

The shape of the capnograph waveform can tell you a lot!

For example:

  1. A slanting upslope can represent airway obstruction (e.g., chronic obstructed pulmonary disease, bronchospasm, blocked endotracheal tube).
  2. In patients paralyzed with a neuromuscular blocker, as the paralytic wears off they may try to breathe asynchronously against the ventilator, producing a notch called a curare cleft.’
  3. Quantitative capnography during resuscitation can be very useful. During CPR, there should be a visible waveform during high quality chest compressions; its absence may indicate accidental esophageal intubation
  4. A sudden loss is bad, as it means that the tube is fully obstructed or disconnected or that there has been a sudden loss of circulation
  5. You can also just simply tell is someone is hypo- or hyperventilating

  • Dorsch JA, Dorsch SE. 2007. Gas monitoring. In: Understanding anesthesia equipment (Dorsch and Dorsch, Eds.) Lippincott Williams & Wilkins, Philadelphia PA.
  • Kodali BS. 2013. Capnography outside the operating rooms. Anesthesiology; 118:192.

Paracentesis: Anatomic Landmarks

paracentesisToday’s post follows up on one of the first ones on this site, about abdominal paracentesis!

Paracentesis is the process of drawing out fluid from the peritoneum. It is useful for diagnosing ascites when its cause is unclear, and the procedure be used to therapeutically remove large volumes of ascites fluid.

While it is overall a quite safe procedure, the risks of paracentesis include: bleeding, bowel or bladder perforation, persistent ascites fluid leak, infection.

Paracentesis is usually done in a lateral decubitus position (or supine, for large volumes). The level of the ascites fluid is percussed and a needle is inserted in either in the midline (2-3 cm below umbilicus) or lateral lower quadrant (lateral to rectus abdominus muscle, 2-4 cm superomedial to anterior superior iliac spine). This positioning prevents puncture of the inferior epigastric arteries; visible superficial veins and surgical scars should be avoided too. To reduce risk of ascites fluid leak, the needle is inserted either with a z-tracking technique, or at a 45-degree angle.

  • Lee SY, Pormento JG. 2009. Abdominal paracentesis and thoracentesis. Surgical Laparoscopy, Endoscopy & Percutaneous Techniques; 19:e32.
  • McGibbon A, Chen GI, Peltekian KM, Veldhuyzen van Zanten S. 2007. An evidence-based manual for abdominal paracentesis. Digestive Disease Science; 52:3307.
  • Thomson TW, Shaffer RW, White B, Setnik GS. 2006. Paracentesis. NEJM; 355:e21.

Jugular Venous Pulse (JVP)

jvpThe jugular venous pulse/pressure (JVP) is a favourite topic on the wards!

The jugular veins fill with blood and pulsate in relation to filling in the right atrium. Since the JVP correlates well with central venous pressure, it’s used as an indirect marker of intravascular fluid status.

Traditionally, the right internal jugular (IJ) vein is used in JVP measurement; it’s preferred since it is directly in line with the superior vena cava and right atrium. The external jugular (EJ) vein is not commonly used to assess the JVP because it has more valves and an indirect course to the right atrium, but EJ is easier to see than IJ, and JVP measurements from both sites correlate fairly well. The left-sided jugular veins are also uncommonly used, since they can be inadvertently compressed by other structures and thus be less accurate!

Learners on the ward are often asked how to identify the JVP and distinguish it from carotid artery pulsations. The mnemonic POLICE describes the distinguishing features of the JVP:

  • Palpation: The carotid pulse is easy felt but the JVP is not.
  • Occlusion: Gentle pressure applied above the clavicle will dampen the JVP but will not affect the carotid pulse.
  • Location: The IJ lies lateral to the common carotid, starting between the sternal and clavicular heads of the sternocleidomastoid (SCM), goes under the SCM, and when it emerges again can be followed up to the angle of the jaw. The EJ is easier to spot because it crosses SCM superficially.
  • Inspiration: JVP height usually goes down with inspiration (increased venous return) and is at its highest during expiration.
    • (Kussmaul’s Sign describes a paradoxical rise in JVP during inspiration that happens in right-sided heart failure or tamponade)
  • Contour: The JVP has a biphasic waveform, while carotid pulse only beats once.
  • Erection/Position: Sitting up erect will drop the meniscus of the JVP, while lying supine will increase filling of the JVP.

To measure the JVP, the patient lies supine in bed at a 30 – 45 degree angle, with their head turned slightly leftward and jaw relaxed. A hard light source (e.g., penlight) pointed tangential to the patient’s neck will accentuate the visibility of the veins. Once the highest point of JVP pulsation is seen, measure high how it is at its maximum, in terms of centimeters above the sternal angle (aka Angle of Louis, at the 2nd costal cartilage). The JVP normally is 4 cm above the sternal angle or lower; increased in fluid overload and decreased in hypovolemia.

  • Beigel R et al. 2013. Noninvasive evaluation of right atrial pressure. Journal of the American Society of Echocardiography: 26;1033.
  • Chua Chiaco JMS, Parikh NI, Fergusson DJ. 2013. The jugular venous pressure revisited. Cleveland Clinic Journal of Medicine. 80;638.
  • Cook DJ, Simel DL. 1996. Does this patient have abnormal central venous pressure? Journal of the American Medical Association: 275;630.
  • Vinayak AG, Pohlman AS. 2006. Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients. Archives of Internal Medicine: 166;2132.
  • Wang CS et al. 2005. Does this dyspneic patient in the emergency department have congestive heart failure? Journal of the American Medical Association: 294;1944.

Streptococcal Pharyngitis

strep-pharyngitis

Sore throats (pharyngitis) are a common complaint in primary and emergency care settings. Most of the time, pharyngitis is caused by viral infection (most commonly rhinovirus).

Streptococcus pyogenes, aka Lancefield group A streptococci, (GAS) is the most common bacterial cause of pharyngitis. The possible complications of GAS infection include:

  • Rheumatic fever
  • Post-streptococcal glomerulonephritis
  • Peritonsillar/retropharyngeal abscess
  • Otitis media
  • Mastoiditis
  • Pediatric autoimmune neuropsychiatric disorder associated with Group A streptococci (PANDAS) *controversial!

Signs and symptoms

GAS pharyngitis may also include fever, chills, malaise, headache, nausea, vomiting, abdominal pain, or maculopapular rash (scarlet fever). Cough, coryza/rhinitis, and conjunctivitis are uncommon symptoms for GAS pharyngitis. However, clinically diagnosing GAS pharyngitis based on history and physical is incredibly unreliable, so patients with a convincing presentation would benefit from laboratory confirmation (i.e., throat culture, rapid antigen detection test of throat swab). The Centor and McIsaac criteria are useful for helping rule out GAS pharyngitis, but shouldn’t be used exclusively to diagnose it.

The Centor criteria are scored based on the presence of:

  1. Fever (subjective or >38 C)
  2. Lack of cough
  3. Tender lymphadenopathy (anterior cervical)
  4. Tonsillar exudate

The MacIsaac criteria add an extra point for patients < 14 years old (since this age group is more prone to GAS pharyngitis) and subtract a point if >45 years old. A low score on these criteria help to exclude GAS pharyngitis, but higher scores indicate a need for lab tests.

The first-line treatment for GAS pharyngitis is penicillin. Other antimicrobial agents vary between different guidelines. Guidelines vary about whether empiric treatment should be considered before lab results have confirmed a diagnosis.

References

  • Aalbers J et al. 2011. Predicting streptococcal pharyngitis in adults in primary care: A systematic review of the diagnostic accuracy of symptoms and signs and validation of the Centor score. BMC Medicine: 9;67.
  • Kociolek LK, Shulman ST. 2012. Pharyngitis. In: Annals of Internal Medicine: In the Clinic (Cotton D, Taichman D, Williams S, Eds.). ITC3-1.
  • Weber R. 2014. Pharyngitis. Primary Care Clinics in Office Practice: 41;91.
  • Wessels MR. 2011. Streptococcal pharyngitis. New England Journal of Medicine; 364:648.
  • Worrall G. 2011. Acute sore throat. Canadian Family Physician: 57;791.

Side Effects of Atypical Antipsychotics

antipsychotics

BUY THIS AS A STUDY CARD

Atypical (a.k.a., “second-generation”) antipsychotics are commonly used in the treatment of psychotic disorders, and mood disorders as well. Compared to typical (first-generation) antipsychotics, the atypical antipsychotics have lower affinity for dopamine D2 receptors, and they also act at serotonin (5-HT) receptors (they are antagonists for these receptors). Other neurotransmitter receptors are affected as well, and each atypical antipsychotic preferentially antagonizes different receptors.

When atypical antipsychotics were first introduced, it was hoped that they would be more effective than typical antipsychotics and have fewer extrapyramidal side effects (see below). While these expectations may have been somewhat overblown and atypicals are not markedly superior in decreasing psychosis symptoms, most atypicals certainly have a lower risk of developing extrapyramidal side effects. However, they do come with their own array of side effects.

Extrapyramidal side effects (EPSE): These are movement-related side effects caused by dopamine antagonism. These include acute dystonia (torticollis, an uncomfortable muscular spasm of the neck; as well as spasms of the eyes, tongue, jaw), akathisia (motor restlessness and a need to remain in motion), tardive dyskinesia (repetitive, involuntary movements usually involving facial muscles), parkinsonian symptoms (resting tremor, rigidity, slowed movements), and neuroleptic malignant syndrome (potentially fatal!).
Elevated prolactin (PRL): This can lead to gynecomastia (breast growth) and galactorrhea (milk-production), which can be very distressing for male patients! Can also cause infertility and sexual dysfunction. It also happens with typical antipsychotics.
Weight gain: This can be very a troublesome symptom, and may lead to diabetes in some patients.
Sedation: This may prevent patients from engaging in their usual activities and work.
Orthostatic hypotension: Drop in blood pressure after standing from sitting position.

Some antipsychotics have especially severe side effects. Clozapine, for example, is extremely effective in treating psychosis but can lead to fatal agranulocytosis (drop in white blood cells), as well as tremendous weight gain and sedation. Ziprasidone use can lead to QTc prolongation and increase the risk for serious cardiac arrhythmia.

The above chart shows the relative side effect profiles of eight atypical antipsychotics (aripiprazole, clozapine, lurasidone, olanzepine, paliperidone, quetiapine, risperidone, ziprasidon) versus two typical antipsychotics (chlorpromazine, haloperidone).

  • Haddad PM, Sharma SG. 2007. Adverse effects of atypical antipsychotics: Differential risk and clinical  implications. CNS drugs; 21:911.
  • Leucht S, Cipriani A, Spineli L, Mavridis D, Orey D, Richter F, Samara M, Barbui C, Engel RR, Geddes JR, Kissling W, Stapf MP, Lassig B, Salanti G, Davis JM. 2013. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: A multiple treatments meta-analysis. Lancet; 382:951.
  • Meltzer HY. 2013. Update on typical and atypical antipsychotic drugs. Annual Review of Medicine: 64:393.
  • Sadock BJ, Sadock VA (Eds.). 2007. Serotonin-dopamine antagonists: Atypical antipsychotics. In: Kaplan & Sadock’s Synopsis of Psychiatry. Lippincott Williams & Wilkins, Philadelphia PA.

Mechanical Ventilation Basics

ventilator

Volume control (VC) and pressure control (PC) are two common modes of positive pressure mechanical ventilation. In VC, the clinician sets the tidal volume that is given for every breath; pressure is allowed to vary over the course of the breath. In PC, the ventilator is programmed to deliver the same pressure throughout inspiration, so tidal volume is allowed to vary based on the pressure and timing settings, as well as the patient’s own lung compliance.

The timing of ventilation can be set according to a trigger. Continuous mandatory ventilation (CMV) involves setting the respiratory rate and having the ventilator deliver breaths at exactly that rate. This is generally used in paralyzed patients (e.g., general anesthesia), where the patient is not expected to trigger any breaths. In Synchronized Intermittent Mandatory Ventilation (SIMV), mandatory breaths are still given but they are synchronized to the patients’ own respiratory efforts (if present). Also, the patient is allowed to take additional breaths on their own. SIMV is often used to wean patients from the ventilator, by decreasing the rate of mandatory breaths and having patients take more of their breaths spontaneously.

Pressure support (PS) is another mode that is used for weaning. No mandatory breaths are programmed. The patient actively takes their own breaths, and the ventilator simply gives an additional boast of inspiratory pressure to help them out.

Positive End Expiratory Pressure (PEEP) is a setting that is used to prevent alveolar collapse, increase functional residual capacity, and generally improve gas exchange. PEEP involves programming a small amount of additional airway pressure (often ~5-10 cmH2O) to be present at the end of expiration.

  • Nugent K, Nourbaksh E (Eds.). 2011. A bedside guide to mechanical ventilation. Createspace.
  • Owens W. 2012. The ventilator book. First Draught.
  • Kacmarek RM, Hess DR. 2008. Mechanical ventilation for the surgical patient. In: Anesthesiology (Longnecker DE, Brown DL, Newman MF, Zapol WM, Eds.). McGraw Hill, New York.

 

Complex Regional Pain Syndrome

crps

Hypo/Hyperalgesia:Decreased/increased sensitivity to a usually-painful stimulus (e.g., pinprick).
Hypo/Hyperesthesia: Decreased/increased sensation to a usually-innocuous stimulus (e.g., light touch).
Allodynia: Sensation of pain from a usually-innocuous stimulus (e.g., light touch).

Complex Regional Pain Syndrome (CRPS) refers to a chronic neuropathic pain condition with a broad and varied range of  clinical presentations. CRPS patients experience severe pain out of proportion to their original injury, and this may start at the time of injury or weeks later. The pain is described as deep-seated and burning/aching/shooting. Sesnory changes are common, including hypo/hyperesthesia, hypo/hyperalgesia, and allodynia. For instance, many patients describe not being able to tolerate the sensation of bedsheets on their painful limb.

In the affected area, there is often marked edema, temperature asymmetry (usually cooler), and sweating changes (usually increased). Loss of hair and nail growth is common, and disuse of the limb can result in weakness, muscle atrophy, and contractures.

The diagnosis is made clinically, using the Budapest Criteria. Some pain physicians use a nuclear medicine test, three-phase bone scintigraphy, for CRPS diagnosis but this test is becoming less popular, since it has a low positive predictive value.

Budapest Criteria

  1. Pain, ongoing and disproportionate to any inciting event
  2. Symptoms: at least one symptom in three of the four categories:
    • Sensory: reports of hyperesthesia and/or allodynia
    • Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetr
    • Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. Physical Signs: at least one sign at time of evaluation in two or more categories:
    • Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or 
joint movement)
    • Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry
    • Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  4. No other diagnosis better explains the signs and symptoms

CRPS is classified as Type I when there is no apparent history of nerve damage, and Type II when associated with definite peripheral nerve injury. CRPS most commonly occurs following fractures and immobilization, but can happen even with little to no trauma.The pathophysiology is thought to involve autonomic dysfunction and inflammation, but much is still unknown.

CRPS affects females about 2-4 times more often than males, and onset is usually in middle age (though there are rare pediatric cases reported). It is a progressive disease that can result in spread of pain, sensory disturbances, and physical changes to other limbs.

Treatment for CRPS may involve physiotherapy, complementary medicine (e.g., acupuncture, qi gong) psychological therapies, and a variety of pharmacologic (e.g., NSAIDs, anticonvulsants, antidepressants, opioids, ketamine, bisphosphonates) and interventional procedures (nerve blocks, sympathectomy, neurostimulators). As with all things CRPS, there isn’t great evidence for any particular intervention.

  • Harden RN, Bruehl S, Perez RSGM, Birklein F, Marinus J, Maihofner C, Lubenow T, Buvanendran A, Mackey S, Graciosa J, Mogilevski M, Ramsden C, Chont M, Vatine J-J. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for Complex Regional Pain Syndrome. Pain; 150:268.
  • Hord E-D. Complex regional pain syndrome. In: Massachusetts General Hospital Handbook of Pain Management (Eds: Ballantyne JC, Fields HL). Lippincott Williams & Wilkins.
  • Moon JY, Park SY, Kim YC, Lee SC, Nahm FS, Kim H, Oh SW. 2012. Analysis of  patterns of three-phase bone scintigraphy for patients with complex regional pain syndrome diagnosed using the proposed research criteria (the ‘Budapest Criteria’). British Journal of Anesthesia; 108:655.
  • O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome – an overview of systematic reviews. Cochrane Database of Systematic Reviews; 4:CD009416.
  • Schwartzman RJ, Erwin KL, Alexander GM. 2009. The natural history of complex regional pain syndrome. Clinical Journal of Pain; 25:273.
  • Smith H, Popp AJ. The patient with chronic pain syndromes. In: A Guide to the Primary Care of Neurological Disorders (Eds: Popp AJ, Deshaies EM). Thieme.
  • Tran DQH, Duong S, Bertini P, Finlayson RJ. Treatment of complex regional pain syndrome: a review of the evidence. Canadian Journal of Anesthesiology; 57:149.

Internuclear Opthalmoplegia

ino.v2Internuclear opthalmoplegia (INO) is an impairment in lateral conjugate gaze (both eyes looking toward one side), caused by a lesion in the medial longitudinal fasciculus (MLF), and associated with multiple sclerosis.

Lateral conjugate gaze requires coordination of adduction (medial rectus muscle, CN III) in one eye and abduction (lateral rectus muscle, CN VI) in the other eye. These movements are coordinated by the paramedian pontine reticular formation (PPRF), also known as the pontine gaze centre. The pathway is as follows:

  1. To look to the left, the right frontal eye field (FEF) sends a signal to the left PPRF.
  2. The left PPRF innervates the left abducens (CN VI) nucleus, which controls the left lateral rectus muscle and causes the left eye to abduct (gaze to the left).
  3. Additionally, the left CN VI nucleus innervates the right oculomotor (CN III) nucleus, which controls the right medial rectus muscle and causes the right eye to adduct (gaze to the left). The MLF is the tract connecting the CN VI nucleus to the contralateral CN III nucleus.

In INO, there is damage to the MLF, giving a deficit in adduction of the corresponding eye during conjugate lateral gaze, but convergence (eye crossing) is classically preserved because that is controlled by a different pathway. In very mild cases of INO, the only deficit is a slowed velocity of the affected eye. For naming, a right INO (as in the sketch) involves damage to the right MLF, which means that the right eye can’t adduct to look to the left, but can abduct to look to the right.

INO may also be associated with gaze abnormalities such as nystagmus, skew deviation, and even abduction or convergence deficits.

The causes of INO include: multiple sclerosis, pontine glioma, and stroke.

  • Flaherty AW, Rost NS. 2007. Eyes and vision. In: Massachusetts General Hospital Handbook of Neurology. Lippincott Williams & Wilkins.
  • Frohman EM, Frohman TC, Zee DS, McColl R, Galetta S. 2005. The neuro-opthalmology of multiple sclerosis. The Lancet Neurology; 4:111.
  • Ropper AH, Brown RH. 2005. Disorders of ocular movement and pupillary function. In: Adams and Victor’s Principles of Neurology. McGraw-Hill.
  • Wilkinson I, Lennox G. 2005. Cranial nerve disorders. In: Essential Neurology. Blackwell.

 

Monitoring Neuromuscular Blockade

nmb

As mentioned in a previous post, neuromuscular blocking drugs are used in anesthesia to ensure paralysis during surgery. The degree of neuromuscular block is assessed using nerve stimulation, where two electrodes impose a pulse of current on a peripheral nerve (e.g., ulnar n., facial n., posterior tibial n.) and induce muscle twitches which can then be monitored through the surgery. There are a few different ways to do nerve stimulation :

Tetany: A sustained stimulation (5 s)
Train-of-four (TOF): Four pulses in rapid succession
Double-burst stimulation (DBS): A series of 3 pulses followed after a pause by 2 or 3 pulses.
Post-tetanic potentiation: When a pulse is sent after a tetanic stimulation, it will bring on a stronger twitch than at first.

With non-depolarizing muscle blockers, there is a fade phenomenon where twitch amplitude decreases from the first stimulation. For instance, in a TOF each twitch is weaker than the last; the last twitch is the first to disappear with non-depolarizing blockade, while the first twitch is the last to disappear. This non-depolarizing fade is also seen in DBS and tetany, though there is still post-tetanic potentiation.

With a depolarizing muscle blockade, no fade will be seen. Instead, all twitches in response to stimulation will be uniformly decreased, and there is no post-tetanic potentiation. This pattern is known as a Phase I block. But, if there is a ton of succinylcholine or the blockade is of a long duration, the pattern of response will look like a non-depolarizing block. This would be a Phase II block.

Recovery of neuromuscular function
Throughout a surgery, the TOF ratio is often mentioned as a means of assessing neuromuscular blockade on an ongoing basis. This means dividing the amplitude of the fourth (and most influenced  by neuromuscular blockers) twitch in a TOF by the amplitude of the first (which is the least affected). In normal people, the 4:1 amplitude is the same, for a TOF ratio of 1. In a Phase I depolarizing block, the TOF ratio is also 1. The TOF ratio will be less than 1 in a non-depolarizing block (remember the fade?). It is commonly mentioned that a TOF ratio of 0.7 represents an full recovery of neuromuscular function, but these days it is thought that a TOF ratio of at least 0.9 is needed before extubation.

It is very hard to tell what the TOF ratio is by sight or feel alone! DBS ratio is more sensitive than TOF ratio for assessing neuromuscular block, and it’s easier to gauge by tactile evaluation than the TOF ratio. So, quantitative monitoring by electomyography (EMG), mechanomyography (MMG), or accelerometry is ideal!

  • Fuchs-Buder T. 2010. Neuromuscular monitoring in clinical practice and research. Springer.
  • McGrath CD, Hunter JM. 2006. Monitoring of neuromuscular block. Continuing Education in Anesthesia, Critical Care & Pain; 6:7.
  • Neuromuscular blocking agents. 2006. In: Clinical Anesthesiology (Eds: Morgan GE, Mikhail MS, Murray MJ). Lange.
  • Viby-Mogensen J. 2005. Neuromuscular monitoring. In: Miller’s Anesthesia (Eds: Miller RD, Erikkson LI, Fleisher LA, Wiener-Kronish JP, Young WL). Elsevier.
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