Residual neuromuscular blockade

Residual neuromuscular blockade

Residual neuromuscular blockade can be defined by inadequate neuromuscular recovery as measured  by objective neuromuscular monitoring. It is also referred to as residual paralysis, residual  curarisation, and residual neuromuscular block. More specifically, recent opinion suggests a definition  of inadequate train of four recovery of less than 0.9 (TOF <0 .9="" p="">

On a practical level, the concept of adequate neuromuscular recovery is intended as the return to a  basline muscular function, particularly the ability to breathe normally, maintain a patent airway, and  retain protective airway reflexes.

 INCIDENCE

current estimates are that around 40% of post-operative patients (who have been paralised)

arrive in PACU with TOF <0 .9="" 12="" and="" p="" tof="" with="">

ADVERSE EFFECTS OF RESIDUAL NEUROMUSCULAR BLOCKADE

The following tables detail the implications of residual neuromuscular blockade (these are more

illustrative than exhaustive)

Table 1: Physiological changes

Impaired muscle tone and Coordination	Upper airway pharyngeal and oesophageal muscles	Increased risk of aspiration Increased risk of airway obstruction
	Laryngeal muscles	Increased risk of aspiration Impaired phonation Impaired cough
	Respiratory muscles	Impaired ventilation and oxygenation
	Impaired function of other muscles throughout                the body

Table 2: Clinical implications

Symptoms and signs of  muscle weakness	Difficulty breathing         Generalised weakness  Difficulty speaking           Visual disturbances         Patient distress
Immediate critical respiratory events  in PACU	Post-operative  hypoxaemia                Upper   airway   obstruction
Later respiratory events	Prolonged ventilator weaning                Post-operative  pulmonary complications    (eg. atelectasis, pneumonia)

INVESTIGATIONS

 Clinical criteria for evaluating adequacy of muscle function include: assessment of a patient’s ability to maintain adequate head lift, jaw clench, grip strength, and tidal volume. These are unreliable predictors of neuromuscular recovery. For example, it is possible to maintain a 5 second head lift with  TOF <0 .52.="" addition="" are="" for="" function.="" in="" many="" not="" of="" p="" respiratory="" specific="" tests="" these="">

Train-of-four neuromuscular monitoring is commonly conducted with a subjective measurement, either  as a simple train of four count (TOFC) or train of four ratio (TOF). The latter refers to when there is  already a TOFC of 4, and subsequent assessment is made for fade in T4 compared to T1.

Double Burst Stimulation (DBS) is another method of neuromuscular monitoring, but is also

commonly measured in a subjective manner..

Objective measurement of neuromuscular monitoring is the only way of accurately assessing residual  neuromuscular blockade. In general, it is conducted via quantitative measurement of the strength of  contraction of a peripheral muscle (eg. adductor pollicis muscle in thumb) in response to peripheral  nerve stimulation (eg. ulnar nerve at wrist) produced by 2 stimulating electrodes. Each measurement  technique measures the force of contraction, either directly or by a factor that is proportional to force.

 Table 5: Common sites of peripheral nerve stimulation

Nerve:  Ulnar     nerve                   

Muscle:                Adductor             pollicis  

Action:  Thumb  adduction                           

Black:    1-2cm    proximal              to            wrist      crease  

Red:       2-3cm    proximal              to            black     

Nerve:  Facial    nerve                   

Muscle:                Orbicularis           oculi       and        Corrugator          supercilii                             

Action:  Twitching             of            eyelid    and        eyebrow                             

Black:    Just        anterior                to            tragus  

Red:       Lateral  to            outer     canthus                of            eye

Nerve:  Posterior tibial nerve    (sural    nerve)                 

Muscle:                Flexor   hallicus brevis                   

Action:  Plantar  flexion  of great                toe                        

Black:    Over posterior aspect of medial                malleolus, over posterior tibial   artery   

Red:       2-3cm    proximal to black             

REVERSAL  AGENT

It is good practice to always consider giving a reversal agent, unless there is objective neuromuscular  monitoring demonstrating a TOF >0.9 (giving neostigmine to fully recovered patients may decrease  upper airway muscle activity and tidal volume) . Adequate spontaneous recovery of train of four count should be established BEFORE giving reversal. When using anaesthetic techniques that do not potentiate neuromuscular blockers, eg. TIVA, a  minimum TOFC of 2 should be established. When using anaesthetic techniques that do potentiate        neuromuscular blockers, eg. inhalational volatiles, a TOFC of 4 should be established. This is to

ensure adequate antagonism by the reversal agent of the additional depth of neuromuscular blockade.

Table 5: Train of four count and physiological correlation              

Trainof  four count  %     neuromuscular blockade at muscle        

    4                                                      0–75%      

    3                                                      75%           

    2                                                      80%            

    1                                                      90%            

    0                                                      100%         

Reversal with subjective neuromuscular monitoring     

- TOFC 1 or zero = delay reversal

- TOFC 2 or 3 = give reversal

- TOFC 4 with fade = give reversal

- TOFC 4 with no perceived fade = give reversal, consider low dose (20 µg/kg) neostigmine

- TOFC 4 and >0.9 = withhold reversal

               

Reversal with objective neuromuscular monitoring       

- TOFC 0 or 1 = delay reversal

- TOFC 2 or 3 = give reversal

- TOFC 4 with < 0.4 = give reversal

- TOFC 4 with 0.4-0.9 = give reversal, consider low dose neostigmine

- TOFC 4 and >0.9 = withhold reversal

               

Reversal guidelines with clinical neuromuscular monitoring

- Only consider reversal when spontaneous muscle activity is present

- Remember that clinical tests of adequate reversal are unreliable indicators of neuromuscular

Blockade

TREATMENT OF RESIDUAL NEUROMUSCULAR BLOCKADE

1. ABC. Basic resuscitation is the foundation on which the following steps are to be considered:

support the patient’s airway, breathing, and circulation.

2. Rule out other potential causes. Is this really residual neuromuscular blockade? Check nerve

stimulator, use a different nerve-muscle combination.

3. Consider giving reversal. In some institutions, it is still not routine for reversal to be used,

largely due to concerns of cholinergic symptoms of nausea and bradycardia with  cholinesterase inhibition.

4. Wait. Have you given enough time for the reversal to have effect? Is the patient stable enough  to tolerate watchful waiting.

5. Consider giving additional reversal. Note however, that if there is already complete

inhibition of acetylcholinesterase, giving further neostigmine will not serve any useful

purpose.

6. Treat potentiating factors. Many factors prolong neuromuscular blockade, such as

inhalational agents, opioids, acidosis, hypothermia, hypercarbia, hypoxia.

7. Consider alternative methods of reversal (Sugammadex if available)

Anesthetic management of patients with aortic stenosis

Anesthetic management of patients with aortic stenosis 

Preoperative consideration 

Etiology: 

Valvular aortic stenosis is nearly always congenital, rheumatic or degenerative. 

Congenitally bicuspid valves are prone to calcification with eventual stenosis. 

Rheumatic stenosis is rarely isolated; it is more commonly associated with AR or mitral valve diseases. 

Clinical picture: 

Classically patients with advanced AS HAVE THE TRIAD OF  

• DYSPNEA ON EXERTION 
• ANGINA 
• SYNCOPE(EXERTIONAL) 

Angina caused by increased o2 demand due to lt ventricular hypertrophy and decreased o2 supply due to compression of intramyocardial  vessels by high LV pressure. 

Pathophysiology and hemodynamic consequences 

• Obstruction of LV outflow caused by AS is almost always gradual allowing the lv to initially compensate and maintain stroke volume. 
• Concentric ventricular hypertrophy enable LV to maintain SV by generating a significant transvalvular pressure gradient   and reduce  ventricular wall stress. 
• With long standing AS, myocardial contractility deteriorates and further compromise LV function. 
• A prominent feature of AS is a decrease in LV compliance as a result of hypertrophy. 
• Diastolic dysfunction  result from an increase in ventricular mass, fibrosis, or ischemia. 
• The decreased diastolic pressure gradient between LA and LV impairs ventricular filling which become quite dependent on normal atrial contraction. 
• Loss of atrial contraction can precipitate CHF or hypotension in patients with AS.  

TEE severity scale: 

Normal aortic valve area 2.5 – 3.5 cm2  

Normal pressure gradient less than 10 mmhg 

Aortic stenosis 

Indicator	Mild	Moderate	severe
Valve area cm2	2-1.2	1.1-.8
Pressure gradient mmhg	20-30	30-50	>50

Doppler Echo and cardiac cauterization data 

Using Gorlin equation 

[Equation] 

K= 44 

Aortic valve area[Equation] 

The pressure gradient can be determined by using continuous wave Doppler Echo: 

Δp= 4V2 

Δp= peak pressure gradient 

V= peak blood flow 

Aortic valve area(V2) =[Equation] 

A1 cross sectional area of LVOT 

V1 maximum blood flow velocity in LVOT 

V2 maximum blood flow velocity through aortic valve 

 

 The hallmark of Pressure-volume loop of AS are high left ventricular systolic pressure and upward and counterwise rotation AB segment indicative of decreased LV compliance. 

Treatment of AS: 

• Percutaneous balloon valvuplasty is generally indicated for younger patients or elderly who are poor candidate for valve replacement. 
• Valve replacement. 
• Medical treatment for CHF: digoxin, Na restriction, and small dose of diuretics. 

Preoperative evaluation: 

These patients need to be evaluated for CHF and angina: 

ECG: look for any arrhythmia or evidence of LV hypertrophy or MI. 

Exercise tests: exercise tolerance test or cardiopulmonary exercise test for patients with disabilities. 

Echo: to assess ventricular and valvular function 

Coronary angiography 

Dobutamine stress echo 

Anesthetic management: 

Hemodynamic objectives or goals: 

The important considerations are  

• To maintain SVR and DBP. This is essential to maintain coronary perfusion. 
• To maintain the preload at the upper end of the normal by giving fluids and avoiding excessive VD. 
• To avoid tachycardia or bradycardia,  and maintain sinus rhythm if present preoperatively and treat AF aggressively. 
• Aim of HR between 60-70\min. 
• To maintain myocardial contractility 

Premedication: 

Patients with AS may benefit from premedication by preventing unnecessary increase of HR. 

Concerns must be taken to ensure adequate venous return and preservation of sinus rhythm. 

Monitoring: 

In addition to the standard monitors, intraarterial pressure monitoring is desirable in severe AS. 

Pulmonary artery pressure monitoring is useful and a prominent ‘a’ wave is often seen on PCWP waveform. 

Close monitoring of ECG for signs of myocardial ischemia. 

TEE can be useful for monitoring ischemia, preload, valvular function, and the effect of therapeutic interventions. 

Anesthetic technique: 

The selection of general anesthetic agents is most critical in patients with symptomatic (moderate tosevere) aortic stenosis. In these patients, a primarily opioid-based anesthetic technique generally results inminimal cardiac depression.

suitable nonopioid induction agents include etomidate and the combination of ketamine and abenzodiazepine.

If a volatile agent is used, the concentration should be carefully controlled to avoid excessive myocardialdepression, vasodilation, or loss of normal atrial systole.

Tachycardia and hypertension, which can precipitate ischemia, should be treated by increasing anestheticdepth. If a -adrenergic blocking agent is used, esmolol may be preferable because of its short half-life.Most patients with aortic stenosis are extremely sensitive to vasodilators. Moreover, because of an alreadyprecarious myocardial oxygen demand–supply balance, they tolerate even mild degrees of hypotensionpoorly.

Hypotension should generally be treated with small doses (25–50 g) of phenylephrine. Intraoperativesupraventricular tachycardias with hemodynamic compromise should be treated with immediatesynchronized cardioversion. Frequent ventricular ectopy (which often reflects ischemia) is usually poorlytolerated hemodynamically and should be treated with intravenous lidocaine. Amiodarone is generallyeffective for both supraventricular and ventricular arrhythmias.