Category Archives: Comorbid illness and anesthesia

AEQ1: Revised Cardiac Risk Index (RCRI) and ACS-NSQIP

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  • Anaesthesia Exam Question:1
  • Revised Cardiac Risk Index (RCRI) is one of the commonly used perioperative risk indices
  • The RCRI determines preoperative risk based on risk of surgery, history of ischemic heart disease, congestive heart failure, cerebrovascular disease, preoperative use of insulin and creatinine greater than 2.0 mg/ dL. 
  • The total score ranges from 0 to 6, with higher scores indicating a higher risk of major adverse cardiac events (MACE). The risk categories and their corresponding scores are as follows:
  • 0 points: Low risk (MACE rate <1%)
  • 1-2 points: Intermediate risk (MACE rate 1-5%)
  • 3-6 points: High risk (MACE rate >5%)
  • RCRI is less accurate in patients undergoing vascular, noncardiac surgery. In addition, as RCRI does not capture risk factors for noncardiac causes of perioperative mortality, it does not predict all-cause mortality well
  • American College of Surgeons’ National Surgical Quality Improvement Program (ACS-NSQIP) is a universal surgical risk calculator model developed using a web-based tool . The ACS-NSQIP calculator incorporates 20 patient risk factors in addition to the surgical procedure. From this input, it calculates the percentage risk of a MACE, death, and 8 other outcomes. This risk calculator may offer the best estimation of surgery-specific risk of a MACE and death. It has excellent performance for predicting mortality and morbidity. It has not been validated in an external population outside the NSQIP. This classification has poor inter-rater reliability
  • Surgery-specific risk calculation using ACS-NSQIP report the rate of cardiac death or non-fatal MI and are noted to be greater than 5% in high-risk procedures, 1% to 5% in intermediate-risk procedures, and less than 1% in low-risk procedures. Emergency surgery is associated with higher risk of MACEs compared with elective procedures. 

Cricoarytenoid arthritis: an ominous entity for the anesthesiologist

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  • Rheumatoid arthritis is the most common cause of this condition
  • Can also may be associated with bacterial infections, mumps, diphtheria, tuberculosis and ankylosing spondylitis,systemic lupus erythematosus, gout, progressive systemic sclerosis
  • The cricoarytenoid joint has a synovial lining and bursa. Its mobility is vital for speech, respiration, and protection from aspiration.
  • Effusion, pannus formation, joint erosion, and ankylosis may compromise the joint’s functions.
  • Its involvement may be unsuspected or mistaken for asthma until intubation or after extubation and may necessitate a surgical airway.
  • Dysphonia, dyspnea, or stridor should raise suspicion of this possibility.
  • Complete airway obstruction is a well described but an uncommon complication
  • Laryngoscopy may reveal a rough and thick mucosa with narrowing of the vocal chink.
  • Airway obstruction occurs most commonly in patients with long-standing rheumatoid arthritis with polyarticular and systemic involvement
  • But laryngeal stridor has been described as the sole manifestation of this disease too!
  • Always anticipate this as a cause for postoperative stridor in such patients.

HEY ANESTHESIOLOGIST!

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1.TAKE CARE OF YOURSELF
2.ASK OPINION TO SOMEONE WHO ALREADY HAD AN EXPERIENCE
3.GOOD COMMUNICATION BETWEEN ANESTHESIA & SURGERY TEAMS
4.PLAN SUFFICIENTLY EARLY AND DISCUSS INSIDE THE TEAM
5.ASSIGN DUTIES CLEARLY TO EACH MEMBER

COVID 19 AND THE ANAESTHESIOLOGIST: WHAT EXACTLY YOU WILL DO WHEN MANAGING A COVID POSITIVE PATIENT IN OR/ICU OR DURING CPR? A SUMMARY OF 8 SOCIETY GUIDELINES

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GENERAL INSTRUCTIONS FOR PERIOPERATIVE SCENARIO (Source: 1 Consensus guidelines for managing the airway in patients with COVID-19 Guidelines from the Difficult Airway Society, the Association of Anaesthetists the Intensive Care Society, the Faculty of Intensive Care Medicine and the Royal College of Anaesthetists, Source: 2 Editorial, anesthesia-analgesia, May 2020,  Source: 3 Anesthesia Patient Safety Foundation and World Federation of Societies of Anesthesiologists, accessed 3/13/2020, Source: 4 Interim guidance for health care providers during covid-19 outbreak from AHA and 5 CDC guidelines)

  • Remember that your personal protection is the priority. Plan ahead as it takes time to apply all the barrier precautions. Before intubation, review and practice donning and doffing the appropriate respiratory protection, gloves, face shield, and clothing.
  • Practice appropriate hand hygiene before and after all procedures.
  • Anaesthesia/ Intubating personnel should don full PPE (Well fitting N95 mask, goggles+ face shield, splash resistant gown, boot covers, double gloves)
  • Patient should wear a mask; continue it during pre-oxygenation
  • When intubated patient being transferred to ICU or transfer from one circuit / ventilator to other, avoid disconnections in patient’s breathing circuit. Put the ventilator on stand by to turn off flows. Clamp ETT with forceps to prevent aerosolization
  • Tracheal intubation of the COVID positive patient is a high risk procedure for the staff, irrespective of the clinical severity of the disease. Do not rush; priority should be to succeed in the first chance. Avoid unreliable, unfamiliar or repeated techniques
  • Know and communicate the plan before entering the room (Use a checklist). Also plan how to communicate once inside the Operating Room (OR) (It will be difficult with the PPE; You may have to use adequate volume while speaking). You can display your plan/algorithm in the OR.
  • Limit staff present at the tracheal intubation: one intubator, one assistant and one to give drugs, equipments and monitor the patient; A runner should be there outside the room. The most experienced anaesthetist available should perform the intubation, to maximise first-pass success. Technician/assistant to keep a distance of 2 m from patient
  • Touch as less as possible once inside the room
  • Ideally we should intubate in a negative pressure room with >12 air changes per hour
  • If this is not available, switch off air conditioner/ positive pressure, 20 minutes before and 20 mins after Aerosol Generating Procedures

PREPARATION OF DRUG/ EQUIPMENT

PROCEDURE:

  • Most of this should happen outside the room
  • Pre-procedure machine check to ensure no leak. Check circuit
  • Create a COVID Intubation Trolley (This can also be used in the ICUs)
  • Arrange N95 mask and 2 HEPA filters to attach between tracheal tube and breathing circuit and between expiratory limb and anaesthesia machine
  • Standard monitors, cannulas, instruments, drugs
  • If patient is on HCQ, it will be better to avoid glycopyrrolate and ondansetron
  • Sterile plastic covers: for protecting monitors, ventilator or anaesthesia machine and for covering the cable covering the laryngoscope handle. Also keep stylet, appropriate size cuffed tube,10 ml syringe for cuff inflation, oral suction catheter etc
  • Face mask
  • Airways
  • A second generation Supra Glottic Airway device for airway rescue
  • Use 5 minutes of preoxygenation with 100% oxygen and RSI techniques to avoid manual ventilation of patient’s lungs and the potential aerosolization of virus from airways.
  • No bag mask manual ventilation. Holding the mask: 2-person, 2-handed, with a VE grip technique (rather than the C- technique) to improve seal. If you are forced to mask ventilate, use a 2-person, low flow, low pressure technique
  • Intubating dose of Rocuronium or Suxamethonium should be given along with propofol or ketamine (can avoid cardiovascular collapse in some situations): Intubate after 90 seconds (prevent coughing)
  • Indirect laryngoscopy with video laryngoscope & intubation under the transparent plastic sheet on the patient
  • Inflate the ETT cuff immediately after tube placement, before starting ventilation
  • HEPA shield antiviral filter connected to ETT & then connect ETT to ventilator breathing circuit
  • Avoid all Aerosol Generating Procedures (AGP) like high flow nasal oxygen, NIV, bronchoscopy and tracheal suction without a closed suction facility. Routine use of supraglottic airway devices unless in unanticipated difficult airway should be avoided
  • Use a closed suction system
  • Confirm correct position of the tracheal tube. Confirmation of the ETT position will be difficult while wearing PPE; so for this purpose we may have to rely on inspection of bilateral chest examination, observation of ETCO2 waveforms etc.
  • Have a vasopressor ready for managing hypotension if it happen post-intubation
  • Push-twist all connections to avoid circuit disconnections
  • Clamp tube and pause ventilator for all airway manoeuvres and for attempting to resolve circuit disconnections
  • Place a nasogastric tube if necessary.
  • If COVID-19 status has not been confirmed, take a deep tracheal aspirate using closed suction
  • Institute mechanical ventilation and stabilize patient, as appropriate.
  • Lung protective ventilation strategies: Small TV:6 ml/Kg [Predicted body wt= Ht in cm-100 (males) & Ht- 110 (females)]. Plateau pressure </= 30 cm H2O. PEEP= 10-15 mm Hg, Adjust FiO2 to achieve reasonable PaO2 (>60 mm Hg). Target SaO2 88-95%. pH >/= 7.25 (Permissive Hypercapnia)
  • Use only metered dose inhalers if bronchodilators indicated at any point ( avoid nebulisation)
  • Use of intravenous anesthesia would be preferred to the use of a volatile gas anesthetic machine in the ICU environment, especially given that many of these patients are not going to be rapidly recovered and extubated following the procedure. (Source:6)
  • Rule out pneumothorax if there is difficulty in ventilation ( Lung USG, CXR)
  • Clean the room 20 minutes after tracheal intubation or any AGP.
  • Use low gas flows and closed circuits
  • Prophylactic anti emetic before extubation
  • Adequate Pain management: Morphine/Fentanyl boluses
  • All efforts to prevent coughing including lidocaine/dexmedetomidine
  • To prevent aerosol generation extubation also should be performed under transparent sheet
  • O2 by nasal cannula / face mask. When wearing nasal prongs, a surgical mask can be worn by the patient over the prongs to reduce droplet spread. Should higher oxygen requirements necessitate use of a mask, non-rebreather masks with an attached exhalation filter can be used.
  • NIV or High flow O2 can cause aerosol generation: so better to avoid
  • Ensure the availability of ambu bag with filter during transfer
  • After leaving the room, do a meticulous doffing of PPE
  • In the ICU: The use of CPAP/BiPAP may increase the risk of delayed deterioration leading to need for emergent intubation and increased risk of mistakes in donning PPE due to time pressures to resuscitate. In general, CPAP/BiPAP should be avoided in patients with Covid 19 and should never be used outside of appropriate airborne/droplet isolation.
  • All airway equipment must be decontaminated and disinfected according to appropriate hospital policies.
  • After removing protective equipment, avoid touching hair or face before washing hands.
  • NB: N95 mask disinfection: Either cycle through 4 masks in series: one for each day, then repeat (OR heat the mask to 70 degree for 30 minutes (UV light, alcohol, bleach and touching the metal of the oven during heating…all these can degrade the mask)

EMERGENCY INTUBATION IN THE CRITICAL CARE UNIT (Source: 6 Wax, R.S., Christian, M.D. Practical recommendations for critical care and anesthesiology teams caring for novel coronavirus (2019-nCoV) patients. Can J Anesth/J Can Anesth(2020))

  • Here also the same principles cited above should apply; additional points are
  • Higher level of precautions are needed here as there is high-level viral shedding due to severity of patient illness and procedures associated with resuscitation or intubation may generate aerosols
  • All personnel in the room must be using appropriate PPE, including either a fit-tested N95 mask or a PAPR. The procedure should be attempted by the most skilled person. Recurrent traffic of people bringing equipment into the room may increase the risk of viral transmission. 
  • Clinicians should strongly consider pneumothorax in any ventilated patient with sudden respiratory deterioration. Portable ultrasound may be used to quickly assist in the diagnosis of a pneumothorax, as arranging for a CXR will lead to delay in intervention.

DIFFICULT AIRWAY

Compared to the normal patient, after the first failure of intubation itself, we should order for Front Of Neck Access (FONA) set. And in the next step, we can either do step B (SGD) or step C ( Facemask). Because of this, we will move fast towards the final step of FONA in the Covid difficult airway algorithm.

DIFFICULT AIRWAY: NORMAL PATIENT VS COVID PATIENT

Prevention and management of respiratory or cardiac arrest: Protected Code Blue (PCB) (Source: 7 Resuscitation Council. Resuscitation Council UK Statement on COVID-19 in relation to CPR and resuscitation in healthcare settings. 2020. Source: 8 Wax, R.S., Christian, M.D. Practical recommendations for critical care and anesthesiology teams caring for novel coronavirus (2019-nCoV) patients. Can J Anesth/J Can Anesth(2020))

  • Do not listen or feel for breathing by placing your ear and cheek close to the patient’s mouth
  • Full Aerosal Generating Procedure (AGP) Personal Protective Equipment (PPE) must be worn by all members of the resuscitation/emergency team before entering the room.
  • Sets of AGP PPE must be readily available where resuscitation equipment is being locally stored.
  • No chest compressions or airway procedures such as those detailed below should be undertaken without full AGP PPE.
  • Once suitably clothed, start compression-only CPR and monitor the patient’s cardiac arrest rhythm as soon as possible.
  • Do not do mouth-to-mouth ventilation or use a pocket mask. If the patient is already receiving supplemental oxygen therapy using a face mask, leave the mask on the patient’s face during chest compressions as this may limit aerosol spread.
  • If not in situ, but one is readily available, put a simple oxygen mask on the patient’s face. Restrict the number of staff in the room (if a single room). Allocate a gatekeeper to do this. 
  • Tracheal intubation or SGA insertion must only be attempted by individuals who are experienced and competent in this procedure. 
  • Dispose of, or clean, all equipment used during CPR following the manufacturer’s recommendations and local guidelines.
  • Any work surfaces used for airway/resuscitation equipment will also need to be cleaned according to local guidelines.
  • Specifically, ensure equipment used in airway interventions (e.g. laryngoscopes, face masks) is not left lying on the patient’s pillow, but is instead placed in a tray.
  • Do not leave the Yankauer sucker placed under the patient’s pillow; instead, put the contaminated end of the Yankauer inside a disposable glove. 

Lower risk resuscitation interventions:

Placement of an oral airway
Placement of an oxygen mask with exhalation filter on patient (if available)
Chest compressions
Defibrillation, cardioversion, transcutaneous pacing
Obtaining intravenous or intraosseous access
Administration of intravenous resuscitation drugs

Higher risk resuscitation interventions more likely to generate aerosol and/or increase risk of viral transmission to staff

Bag-mask ventilation
CPAP/BiPAP
Endotracheal intubation/surgical airway
Bronchoscopy
Gastrointestinal endoscopy

Broad Complex Tachycardias

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A broad complex tachycardia has a QRS complex greater than 0.12 seconds. They are usually ventricular in origin, but can also be supraventricular with aberrant conduction. Other possible causes for broad complex tachycardias include atrial fibrillation with ventricular pre-excitation, i.e. patients with Wolff–Parkinson–White (WPW) syndrome, or torsades de pointes (polymorphic VT).

Broad complex tachycardia is therefore due to SVT with aberrancy or Ventricular Tachycardia (VT), and differentiating between the two can be challenging. However, there are a few pathognomonic ECG features that diagnose VT

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1.Atrio-ventricular (AV) dissociation. There is a higher ventricular rate than atrial rate (more QRS complexes than P-waves). This can only occur if the ventricular rate is autonomous and no longer under control of the SA node.

2.Capture beats: There is an isolated narrow complex amongst a train of broad complexes. This represents a normally conducted P-wave via the AV node and an intact His-Purkinje system indicating there is no underlying bundle branch block. Therefore, the train of broad complexes are ventricular in origin (i.e. VT).

3.Fusion beats: A normally conducted P-wave may fuse with a simultaneous ventricular beat causing a complex halfway between the appearance of a normal QRS and a broad complex.

4.VT is more likely in patients with a prior history of MI.

5.VT complexes are usually very broad (> 160 ms) due to a very abnormal path taken by the depolarisation wave from the VT focus.

6.The time from R-wave onset to the nadir of the S-wave is prolonged (> 100 ms) in VT, again representing an abnormal activation path through the ventricle.

7.Extreme left axis deviation and positive aVR are more common in VT, as the ventricles are depolarised in the opposite direction to normal conduction.

8.Failure to respond to iv adenosine

9.The absence of typical RBBB or LBBB patterns suggests VT. For example, an RSR pattern in V1 with a taller first R-wave suggests VT (in RBBB the first R-wave is caused by septal depolarisation and is therefore smaller than the second R-wave, which is caused by depolarisation of the RV).

SVT with aberrancy is more likely if previous ECGs demonstrate an accessory pathway or a bundle branch block with identical morphology to the broad complex tachycardia. When in doubt, treat as VT

TORSADES DE POINTES

Is a specific variant of ventricular tachycardia (VT). It has a classic undulating pattern with variation in the size of QRS complex. It is caused by a prolonged QT interval and can precipitate VF and sudden death

QT PROLONGATION: CAUSES

Tricyclic antidepressants, flecainide and quinidine; Hypocalcemia; Acute myocarditis

VENTRICULAR TACHYCARDIA(VT) AND VENTRICULAR FIBRILLATION (VF)

VT is a broad complex tachycardia, defined as a run of at least three consecutive ventricular ectopic beats, at a rate of >120 bpm. Can arise from a single or multiple foci or from a reentry circuit. There may be capture or fusion beats, where a normally conducted beat will join an ectopic beat travelling in the opposite direction

CAUSES: Acute MI, degeneration of other arrhythmias, electrolyte abnormalities etc

VF describes an ECG which is random and chaotic with no identifiable QRS complexes that is incompatible with life and need immediate provision of ACLS with prompt delivery of DC shock. Others: Amiodarone, Lidocaine, beta blockers, Implantable cardioverter defibrillators

 

MANAGEMENT

For VT treat with amiodarone 300 mg IV followed by 900 mg over 24 hours. If the arrhythmia is known to be supraventricular, treat as a narrow complex tachycardia.

An irregular broad complex tachycardia is most likely to be atrial fibrillation with bundle branch block, and should be treated as narrow complex atrial fibrillation

In a stable patient who is known to have WPW, the use of amiodarone is probably safe. Adenosine, digoxin, verapamil and diltiazem must be avoided, as these drugs block the AV node and will cause a relative increase in pre-excitation

Torsades de pointes is treated by stopping all drugs known to prolong the QT interval and correcting electrolyte abnormalities. Magnesium sulphate (2 g IV over 10 minutes) should also be given. Such patients may require ventricular pacing. If the patient’s condition deteriorates proceed to synchronised electrical cardioversion or, if the patient is pulseless, commence the ALS algorithm

Ventricular bigeminy
Ventricular bigeminy is associated with endotracheal intubation (a sympathoadrenal response). Given time the bigeminy will disappear, but if it does not intravenous
lidocaine (50–100 mg) may be helpful

Narrow Complex Tachycardias

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Narrow complex tachyarrhythmias have a QRS duration <0.12 seconds. They arise above the bundle of His.

NARROW COMPLEX TACHYCARDIA

As narrow complex tachycardias involve ventricular activation through the normal His-Purkinje system, they must originate within the atria and are therefore often referred to as supraventricular tachycardia (SVT). There are five common types of SVT. They are: Atrial tachycardia, Atrial fibrillation, Atrial flutter, Atrioventricular nodal
re-entry tachycardia, Atrioventricular re-entry tachycardia. When faced with an ECG of narrow complex tachycardia, (i) we should examine the P-wave and (ii) check the QRS regularity

SINUS ARRHYTHMIA/TACHYCARDIA/BRADYCARDIA (from SA Node)

ATRIAL FIBRILLATION 

There is completely disorganised atrial activity, with P-waves replaced by an irregular baseline due to fibrillation waves, and QRS complexes occur in an irregularly irregular fashion (Please the post on AF)

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ATRIAL FLUTTER 

There is a self-perpetuating wave of atrial depolarisation usually circulating within the right atrium, causing regular, saw-toothed flutter waves at 300 bpm and QRS complexes every second, third, or fourth flutter wave. We can see classical sawtooth flutter waves.Drug control of the ventricular rate is not often successful.

Screen Shot 2019-04-22 at 8.06.10 AM

ATRIAL TACHYCARDIA 

There is an abnormal atrial focus driving the ventricular rate. This rhythm can be difficult to distinguish from sinus tachycardia, but P-wave morphology and axis is usually abnormal. If the atrial focus is close to the AV node, a junctional tachycardia may occur and P-waves may be absent.

In case of Atrial tachycardia with AV block after halting glycoside therapy (and ensuring normokalaemia), lidocaine 1 mg kg−1 IV is the drug
of choice. Alternatively DC cardioversion or atrial
pacing may be effective.

ATRIO VENTRICULAR NODAL REENTRY TACHYCARDIA (AVNRT)

This is the commonest type of paroxysmal supraventricular tachycardia (PSVT). It is often seen in people without any heart disease, and is usually benign. There is a rapid reentry circuit within the AV node resulting in simultaneous atrial and ventricular depolarisation. The P-wave is usually buried within the QRS or ST-segment. There will be fast regular narrow complex tachycardia, and P-waves can be seen buried in the terminal portion of the QRS complex which may easily be mistaken for a second, small R-wave. The very close proximity of the QRS and P-waves implies near simultaneous depolarisation of atria and ventricles.

Screen Shot 2019-04-22 at 8.23.38 AM

ATRIO VENTRICULAR REENTRY TACHYCARDIA (AVRT)

This occurs in patients with WPW, and is usually benign unless there is coexisting structural heart disease. There is an accessory pathway bridging the atria and ventricles allowing antegrade conduction down the AV node (causing a narrow QRS) and retrograde conduction back to the atria via the accessory pathway. Since the depolarisation wave takes time to complete this circuit, the P-wave occurs after the QRS complex and is often buried within the T-wave. AVRT can occur with antegrade conduction to the ventricles via the accessory pathway, but this will result in ventricular depolarisation via an abnormal route and consequently a broad QRS. In sinus rhythm, antegrade conduction via the accessory pathway produces a short PR interval (as the normal delay in the AV node is avoided) and the abnormal activation of the ventricles produces a slurred upstroke
in the QRS called a delta wave. The QRS complex is said to be pre-excited and can be associated with repolarisation abnormalities. There are seven sinus beats followed by a ventricular ectopic beat that conducts to the atria retrogradely through the atrioventricular node and then returns to the ventricles via the accessory pathway. This cycle repeats and triggers a broad complex tachycardia. (Please see post on ‘WPW Syndrome’ also).

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An unstable patient presenting with a regular narrow complex tachycardia should be treated with electrical cardioversion. If this is not immediately available, adenosine should be given as a first-line treatment. A stable patient presenting with a regular narrow complex tachycardia should initially be treated by vagal
manoeuvres such as carotid sinus massage or the Valsalva manoeuvre, as these will terminate up to a quarter of episodes of PSVT. Carotid sinus massage should be avoided
in the elderly, especially if a carotid bruit is present, as it may dislodge an atheromatous plaque and cause a stroke

Management

A stable patient presenting with a regular narrow complex tachycardia should initially be treated by vagal manoeuvres such as carotid sinus massage or the Valsalva manoeuvre, as these will terminate most episodes of PSVT. Carotid sinus massage should be avoided in the elderly, especially if a carotid bruit is present, as it may dislodge an atheromatous plaque and cause a stroke. If the tachycardia persists and is not atrial flutter, 6 mg of adenosine should be given as an IV bolus, followed by a 12 mg bolus if no response. A further 12 mg bolus of adenosine may be given if the tachycardia persists. Vagal manoeuvres or adenosine will terminate almost all AVNRTs or AVRTs within seconds, and therefore failure to convert suggests an atrial tachycardia such as atrial flutter. If adenosine is contraindicated, or fails to terminate a narrow complex tachycardia, without first demonstrating it as atrial flutter, give a calcium-channel blocker, e.g. verapamil 2.5–5 mg IV over two minutes. Atrial flutter should be treated by rate control with a beta-blocker.

An irregular narrow complex tachycardia is most likely to be atrial fibrillation (AF) with an uncontrolled ventricular response, but may also be atrial flutter with variable block. If the patient is unstable, synchronised electrical cardioversion should be used to treat the arrhythmia

ATRIAL FIBRILLATION (AF) AND THE ANESTHESIOLOGIST

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Atrial fibrillation(AF) is a supra-ventricular arrhythmia characterized by the complete absence of co-ordinated atrial contractions. There will not be any discernable p-waves.
The ventricular response rate depends on the conduction of the AV node.

WHAT IS THE DIFFERENCE BETWEEN ATRIAL FIBRILLATION AND ATRIAL FLUTTER

Flutter is a more organised and regular form of atrial activity and classically with an atrial rate of 300 bpm. ‘Saw toothed’ flutter waves are present on the ECG. The ventricular response depends on conduction through the AV node. The classic ECG has 2:1 block, hence a ventricular rate of 150 bpm

CAUSES OF AF IN THE PERIOPERATIVE SETTING

Electrolyte abnormalities especially low potassium or magnesium
Withdrawal of beta blockers
Following cardiac surgery.
ASD or mitral valve disease
Ischaemic heart disease
Thyrotoxicosis
Excess caffeine or alcohol (acute or chronic)
Pulmonary embolism
Pneumonia
Pericarditis

In the context of major vascular surgery, systemic inflammation,hypovolemia and a heightened adrenergic state are likely to play a major role.

WHAT IS LONE AF?

‘Lone AF’ is AF in the absence of any demonstrable medical cause, but this is not usually diagnosed in the peri-operative period. So beta blockers will be efficacious in this setting.

WHAT ARE THE PROBLEMS AF CAN POSE?

Loss of the atrial ‘kick’ as it contracts and empties into the LV can reduce the CO by 10%–20% with a normal ventricle (reduced by 40%–50% in those with a ‘stiff’ ventricle as in
diastolic dysfunction, aortic stenosis etc). The disorganised contractions of the atria cause stasis of blood and the risk of thromboembolism. There is a 3%–7% annual risk of
thromboembolic CVA

AF- EVALUATION

*History *Assessment of volume status and electrolytes *ECG: This will also help to exclude acute ischaemia. *The pulse will be irregularly irregular. *No ‘a wave’ in the jugular venous pulsation as this is caused by sinus atrial contraction. *Chaotic atrial activity can be seen on echocardiography.

READ THIS ECG

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MNEMONIC ‘RIAS QRST’ (Rate & Rhythm, Intervals, Axis, QRS & ST segment T wave)

The rate is 78 bpm; the rhythm is irregularly irregular. There are flutter waves seen in the V1 rhythm strip. The axis is normal (There is borderline LVH by voltage criteria). There are no Q waves and the QRS width is normal. There is evidence of infero-lateral ischaemia shown by the inverted and biphasic T waves in this territory (II, III, aVF and V3−V6).

MANAGEMENT OF AF

Assess for cardiovascular compromise and resuscitate simultaneously if needed. Oxygen should be administered, continuous ECG monitoring instituted and IV access secured.

If the patient is unstable, synchronised electrical cardioversion should be used to treat the arrhythmia.

In a stable patient, treatment options include: Rate control by drug therapy. Drugs used to control the heart rate include beta-blockers, digoxin, magnesium, the non-dihydropyridine calcium channel blockers (verapamil or diltiazem) or a combination of these.

Rhythm control by amiodarone to encourage cardioversion: Amiodarone is given as a 300 mg IV bolus, followed by 900 mg IV over 24 hours.

Rhythm control by electrical cardioversion: This is more likely to restore sinus rhythm than chemical cardioversion.

Treatment to prevent complications. Patients who are in AF are at risk of atrial thrombus formation and should be anticoagulated

Patients who have pre excitation syndromes with an accessory conduction pathway between the atria and ventricles (such as in the Wolff–Parkinson–White syndrome) should not be given AV node blocking drugs if they develop an SVT. This will promote the atrial impulses to travel directly to the ventricle at up to 300 bpm via the accessory pathway. The drugs of choice are amiodarone, flecainide or procainamide.

BEFORE PROCEEDING WITH DC CARDIOVERSION FOR AF, WHAT ALL THINGS SHOULD BE CONSIDERED?

  1. Cardioversion should only be attempted without anticoagulation if the duration of the AF is less than 48 hours. If the duration is unknown or longer than this, 3–4 weeks of anticoagulation (INR 2–3) is required to reduce the incidence of clot embolisation. If there is a contra-indication to anticoagulation, or if the cardioversion is deemed necessary more urgently, then an echocardiogram is needed to exclude thrombus in the atrium and atrial appendage
  2. When did the AF start (history of palpitations or recording on monitor): is it acute or chronic?
  3. What is the likelihood of an atrial thrombus which could be embolised by
    cardioversion?
  4. What is the ventricular rate now? – may need pacing after cardioversion if
    the rate is below 60 bpm
  5. Has there been an ischaemic episode?

ANESTHESIA FOR CARDIOVERSION

This should be done in a critical care or operating room area with the usual preparation, equipment and assistance needed for any routine anaesthetic. Someone independent should be present to perform the defibrillation, preferably with a hands-free device. Elective cardioversion has been done under conscious sedation without any adverse effects, but the usual technique is to use a sleep dose of propofol following pre oxygenation. One can use a facemask or maintain the airway with an LMA. If there is any serious doubt about cardiovascular performance or reserve, an arterial line should be given consideration, but this is a short procedure and the cardiac output should improve with the restoration of sinus rhythm. If the patient has a pacemaker in situ or an implantable cardiac defibrillator, we should place the paddles as far away as possible from the device and preferably in the anterior–posterior position.

IF THE PATIENT DOES NOT GET CARDIOVERTED, WHAT SHOULD YOU DO?

Try a period of 4–6 weeks of medical therapy and anticoagulation. If the patient is still in AF, then a further trial of DCC is reasonable. If a second DCC is unsuccessful, then rate control is the next step to improve symptoms and reduce ventricular failure.

 

Wolff–Parkinson–White syndrome and the Anesthesiologist

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WHAT ARE THE CAUSES OF PALPITATION

Exercise, Anxiety, Caffeine, alcohol, drugs: thyroxine, cocaine, beta 2 agonists, MI, arrthymias, hyperthyroidism, hypoglycaemia, phaeochromocytoma

MECHANISMS OF ARRHYTHMIAS

Reentry circuits, Enhanced automaticity, Triggered activity

EVALUATION AND MANAGEMENT

History and examination, ECG: 12-lead, 24-hour, ambulatory, cardiac electrophysiological study, blood investigations to rule out endocrine causes

ABC, oxygen, etc., Check electrolytes (including Mg2+), Carotid sinus massage, Adenosine – caution in asthma and if taking dipyridamole prolongs half-life

WHAT HAPPENS IN WPW SYNDROME?

Presence of faster accessory pathway (bundle of Kent) between atrium  and ventricle (accessory AV pathway) which conducts impulses faster than the normal AV node. Electrical signals traveling down this abnormal pathway may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia. The ECG may show sinus rhythm, normal axis, short PR interval and the presence of delta waves

DELTA WAVES

The accessory atrio-ventricular pathway conducts the atrial impulse to the ventricles much faster than the A–V node. This results in the start of ventricular depolarisation sooner than normal, hence the short P–R interval. That initial ventricular depolarisation
takes place in normal ventricular tissue (i.e. not specialised conducting tissue). The initial rate of depolarisation is therefore slower, hence the slurred, delta wave. When the rest of the impulse finally arrives the A–V node, the bundle of His and Purkinje carries out the ventricular depolarization as normal; hence, the rest of the QRS looks normal

IMPLICATIONS FOR ANESTHESIA

1.There is a tendency to paroxysmal supraventricular tachycardia in the perioperative period and there may be associated congenital cardiac abnormality.

2.Anaesthetic drugs tend to change the physiology of AV conduction.

3.If the patient is asymptomatic, then risk of perioperative arrhythmias is much less.

4.We should avoid light planes of anaesthesia and drugs that can precipitate tachycardia (like atropine, glycopyrrolate, ketamine) resulting in paroxysmal supraventricular tachycardia or atrial fibrillation

5.There are references showing disappearance of delta waves after propofol administration, making it the drug of choice for induction. For maintenance, Isoflurane and sevoflurane are preferred as they dont have effect on AV node conduction. Short acting nondepolarizing muscle relaxant would be an acceptable choice as reversal of neuromuscular blockade using neostigmine and glycopyrrolate is not required.

6. Regional anaesthesia has significant advantage over general anaesthesia as multidrug
administration, laryngoscopic stimulation, intubation, and light planes leading to sympathetic stimulation are avoided.

WHAT ARE THE COMMON ARRHYTHMIAS IN WPW?

Atrial fibrillation (AF): Patients with WPW who develop atrial fibrillation are at risk of very rapid ventricular responses as the accessory pathway does not provide any ‘protective delay’ like the A-V node. This may result in heart failure or may even deteriorate into ventricular fibrillation. In AF, most conducted impulses reach the ventricles via the accessory pathway, so delta waves are seen on the ECG.
Re-entrant tachycardia: A re-entry circuit is set up. After transmitting an atrial impulse, the A–V node usually recovers before the accessory pathway. If an atrial ectopic occurs at the right time, it will transmit through the A–V node while the accessory pathway is still refractory. By the time it has done this, the accessory pathway may have recovered and the impulse will then pass through it back into the atria. As the impulses are all reaching the ventricles via the A–V node and not the accessory pathway, there are no delta waves on the ECG

INTRAOPERATIVE ARRHYTHMIAS: MANAGEMENT

1. A,B,C and Treat possible triggers of rhythm disturbance such as hypoxia, hypercarbia, acidosis, electrolyte disturbance or any cause of sympathetic stimulation.

2.Assess the degree of cardiovascular compromise. If there is significant compromise, synchronised DC cardioversion starting at 25–50 J would be the treatment of choice. If the blood pressure was stable, then the management would depend on the rhythm.

3. Pharmacological therapy:

(a) For re-entrant tachycardia, adenosine would be the first choice. Class 1a drugs such as procainamide (5–10 mg/kg) and disopyramide prolong the refractory period, decrease conduction in the accessory pathway (by blocking fast sodium channel) and may terminate both re-entrant tachycardia and AF. More conventional drugs such as amiodarone, sotalol and other beta-blockers such as esmolol may also be useful.

(b)AF: The treatment principle is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. This is in direct contradiction to the goal of treatment of non-WPW atrial fibrillation, which is to slow the refractory period of the AV node

DRUGS THAT SHOULD BE AVOIDED

Verapamil and digoxin are contra-indicated as they both preferentially block A–V conduction thereby increasing conduction through the accessory pathway. Although verapamil could, in theory, be used to terminate a re-entrant tachycardia, its use is not advisable, because these patients may then revert to AF or flutter. A further hazard with verapamil is that a tachyarrhythmia that looks like re-entrant tachycardia may actually be VT. Adenosine would preferentially block the A–V node and therefore should not be used in AF.

TOTAL BODY WEIGHT [TBW] , LEAN BODY WEIGHT [LBW], IDEAL BODY WEIGHT [IBW] &ADJUSTED BODY WEIGHT ; THEIR IMPLICATIONS IN Anesthesia AND CriticalCare

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Drug administration in obese patients is difficult because recommended doses are based on pharmacokinetic data obtained from individuals with normal weights

With increasing obesity, fat mass accounts for an increasing amount of TBW, and the LBW/TBW ratio decreases

TBW is defined as the actual weight

IBW is what the patient should weigh with a normal ratio of lean to fat mass

IBW can be estimated from the formula: IBW (kg) = Height(cm) − x ( where x = 100 for adult males and 105 for adult females).

LBW is the patient’s weight , excluding fat

Male LBW = 1.1(weight)-128(weight/height)^2 (Weight in Kg and Height in cm)

Female LBW = 1.07 (weight) -148 (weight/height)^2

Regardless of total body weight, lean body weight rarely exceeds 100 kg in men and 70 kg in women

Below IBW, TBW and LBW are similar.

Adjusted body weight (ABW) Takes into account the fact that obese individuals have increased lean body mass and an increased volume of distribution for drugs.

It is calculated by adding 40% of the excess weight to the IBW : ABW (kg) = IBW (kg) + 0.4 [TBW (kg)]

Drugs with weak or moderate lipophilicity can be dosed on the basis of IBW or more accurately on LBW. These values are not same in obese; because 20–40% of an obese patient’s increase in TBW can be attributed to an increase in LBW. Adding 20% to the ‘estimated IBW based dose’ of hydrophilic medication is sufficient to include the extra lean mass. Non-depolarizing neuromuscular blocking drugs can be dosed in this manner.

In morbidly obese patients, the induction dose of propofol can be calculated on IBW.

In case of midazolam, prolonged sedation can occur from the larger initial dose needed to achieve adequate serum concentrations. #TheLayMedicalMan

Remifentanil dosing regimens should be based on IBW or LBW and not on TBW.

When using succinylcholine in obese adults or adolescents, dosage should be calculated on TBW

The antagonism time of neostigmine has been shown to be independent of TBW and BMI. Therefore, TBW can be used to calculate the dose.

Ref:Association of Anaesthetists of Great Britain and Ireland. Peri-operative management of the obese surgical patient 2015. Anaesthesia 2015, 70, pages 859–876.

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