References

Abedin Z. Differential diagnosis of wide QRS tachycardia: A review. J Arrhythm. 2021; 37:(5)1162-1172 https://doi.org/10.1002/joa3.12599

AlKalbani A, AlRawahi N. Management of monomorphic ventricular tachycardia electrical storm in structural heart disease. J Saudi Heart Assoc. 2019; 31:(3)135-144 https://doi.org/10.1016/j.jsha.2019.05.001

Alzand BS, Crijns HJ. Diagnostic criteria of broad QRS complex tachycardia: decades of evolution. Europace. 2011; 13:(4)465-72 https://doi.org/10.1093/europace/euq430

Ashraf MM, Rea R. Effect of dehydration on blood tests. Pract Diabetes. 2017; 34:(5)169-171 https://doi.org/10.1002/pdi.2111

Battle C, Hutchings H, Evans PA. Blunt chest wall trauma: A review. Trauma. 2013; 15:(2)156-175 https://doi.org/10.1177/1460408613488480

British Heart Foundation. Implantable cardioverter defibrillators (ICDs). https://tinyurl.com/mr4crmws (accessed 12 May 2023)

British Heart Foundation. Heart failure. 2022. https://www.bhf.org.uk/informationsupport/conditions/heart-failure (accessed 12 May 2023)

British Heart Rhythm Society. Standards for continuous cardiac monitoring in hospital (telemetry). 2020. https://tinyurl.com/422h5wf9 (accessed 15 May 2023)

Ventricular tachycardia – monomorphic VT. 2023a. https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library (accessed 15 May 2023)

Polymorphic VT and torsades de pointes (TdP). 2023b. https://litfl.com/polymorphic-vt-and-torsades-de-pointes-tdp/ (accessed 15 May 2023)

Hypomagnesemia. 2021. https://litfl.com/hypomagnesaemia-ecg-library (accessed 15 May 2023)

DiNicolantonio JJ, Liu J, O'Keefe JH. Magnesium for the prevention and treatment of cardiovascular disease. Open Heart. 2018; 5:(2) https://doi.org/10.1136/openhrt-2018-000775

Fischbach F, Dunning MB. A manual of laboratory and diagnostic tests, 9th edn. Philadelphia: Wolters Kluwer Health; 2013

Pulseless ventricular tachycardia. 2022. https://www.ncbi.nlm.nih.gov/books/NBK554467/ (accessed 15 May 2023)

Ventricular tachycardia. 2023. https://www.ncbi.nlm.nih.gov/books/NBK532954/ (accessed 15 May 2023)

Ismail TF, Strugnell W, Coletti C Cardiac MR: From theory to practice. Front Cardiovasc Med. 2022; 9 https://doi.org/10.3389/fcvm.2022.826283

Joint Formulary Committee. Arrhythmias (treatment summaries). 2023. https://bnf.nice.org.uk/treatment-summaries/arrhythmias/ (accessed 12 May 2023)

Mahida S, Sacher F, Dubois R Cardiac imaging in patients with ventricular tachycardia. Circulation. 2017; 136:(25)2491-2507 https://doi.org/10.1161/CIRCULATIONAHA.117.029349

Marca-Frances G, Frigola-Reig J, Menéndez-Signorini JA, Compte-Pujol M, Massana-Morera E. Defining patient communication needs during hospitalisation to improve patient experience and health literacy. BMC Health Serv Res. 2020; 20:(1) https://doi.org/10.1186/s12913-020-4991-3

Martindale Pharma. Amiodarone 30 mg/ml solution for injection/infusion in pre-filled syringe. Summary of product characteristics. Electronic Medicines Compendium. 2021. https://www.medicines.org.uk/emc/product/3453 (accessed 12 May 2023)

NHS website. Cardiac catheterisation and coronary angiography. 2022. https://www.nhs.uk/conditions/coronary-angiography/ (accessed 15 May 2023)

National Institute for Health and Care Excellence. Implantable cardioverter defibrillators and cardiac resynchronisation therapy for arrhythmias and heart failure. NICE technology appraisal TA314. 2014. https://www.nice.org.uk/guidance/ta314/chapter/2-clinical-need-and-practice (accessed 15 May 2023)

Hypokalaemia. 2020. https://litfl.com/hypokalaemia/ (accessed 15 May 2023)

Nursing and Midwifery Council. The Code: Professional standards of practice and behaviour for nurses, midwives and nursing associates. 2018. https://tinyurl.com/y588npaj (accessed 15 May 2023)

O'Neill SM, Clyne B, Bell M Why do healthcare professionals fail to escalate as per the early warning system (EWS) protocol? A qualitative evidence synthesis of the barriers and facilitators of escalation. BMC Emerg Med. 2021; 21:(1) https://doi.org/10.1186/s12873-021-00403-9

Pannone L, D'Angelo G, Gulletta S Amiodarone in ventricular arrhythmias: still a valuable resource?. Rev Cardiovasc Med. 2021; 22:(4)1383-1392 https://doi.org/10.31083/j.rcm2204143

Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol. 2010; 35:(9)453-504 https://doi.org/10.1016/j.cpcardiol.2010.08.001

Advanced life support (manual), 8th edn. London: Resuscitation Council UK; 2021a

Resuscitation Council UK. Adult tachycardia algorithm. Adult advanced life support guidelines. 2021b. https://tinyurl.com/4vy67cxn (accessed 12 May 2023)

Royal College of Emergency Medicine. UK NHS Ambulance Services pre-alert guideline for the deteriorating adult patient. 2020. https://tinyurl.com/2pzfbmd8 (accessed 15 May 2023)

Ruthven AKB. Essential examination, 3rd edn. Banbury: Scion Publishing; 2019

Sara JD, Toya T, Taher R, Lerman A, Gersh B, Anavekar NS. Asymptomatic left ventricle systolic dysfunction. Eur Cardiol. 2020; 15 https://doi.org/10.15420/ecr.2019.14

Assessment of tachycardia. 2023. https://bestpractice.bmj.com/topics/en-gb/830 (accessed 17 May 2023)

Adult advanced life support guidelines. 2021. https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines (accessed 16 May 2023)

Spartalis M, Spartalis E, Tzatzaki E Novel approaches for the treatment of ventricular tachycardia. World J Cardiol. 2018; 10:(7)52-59 https://doi.org/10.4330/wjc.v10.i7.52

Tung R, Boyle NG, Shivkumar K. Catheter ablation of ventricular tachycardia. Circulation. 2010; 122:(3)389-391 https://doi.org/10.1161/circulationaha.110.963371

University Hospitals of Derby and Burton NHS Foundation Trust. Arrhythmias – full clinical guideline. 2018. https://tinyurl.com/3dtx5xv8 (accessed 15 May 2023)

University Hospitals of Derby and Burton NHS Foundation Trust. Hypomagnesemia in adults – full clinical guideline. 2021. https://tinyurl.com/2p8uw5a6 (accessed 01/07/2022)

University Hospitals of Derby and Burton NHS Foundation Trust. Sepsis of unknown origin in non-pregnant adults – microbiology full clinical guideline. 2022. https://tinyurl.com/mbtdhas8 (accessed 17 May 2023)

University Hospitals of Derby and Burton NHS Foundation Trust. Community acquired pneumonia – microbiology full clinical guideline. 2023. https://tinyurl.com/bdcuf339 (accessed 17 May 2023)

Van Herendael H, Dorian P. Amiodarone for the treatment and prevention of ventricular fibrillation and ventricular tachycardia. Vasc Health Risk Manag. 2010; 6:465-472 https://doi.org/10.2147/vhrm.s6611

Wellens HJ. Electrophysiology: ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001; 86:(5)579-585 https://doi.org/10.1136/heart.86.5.579

Pulsed ventricular tachycardia: a case study

25 May 2023
Volume 32 · Issue 10

Abstract

Ventricular tachycardia (VT) is an arrhythmia that originates from the ventricles of the heart and presents as a wide and prolonged QRS complex on the electrocardiograph of greater than 120 milliseconds, with a heart rate of over 100 beats per minute. VT can occur as a pulsed or pulseless rhythm. Pulseless VT occurs when the ventricles cannot effectively pump blood out of the heart, therefore resulting in no cardiac output. Pulsed VT can manifest with the patient presenting asymptomatically, or with symptoms of reduced cardiac output resulting from poor ventricular filling. There is the potential for the patient to quickly become haemodynamically unstable if not treated. This article discusses a case of pulsed VT, diagnosed and treated out of hours in an acute hospital.

This article will focus on a case seen in clinical practice, from the perspective of the first author, who was at the time a trainee advanced clinical practitioner (ACP) working in the hospital out of hours team within an acute hospital. To maintain the patient's privacy and dignity as per the Nursing and Midwifery Council (2018)Code, the pseudonym ‘Max’ will be given to the patient.

Case presentation

Max, a 65-year-old gentleman with no prior past medical history, had been admitted to the emergency department as a ‘resus pre-alert’ at the beginning of this admission 1 week previously. Ambulance crews are required to pre-alert the receiving hospital of any patient who may require immediate clinical interventions, or to activate any relevant protocol or treatment pathway (Royal College of Emergency Medicine, 2020). Max had described a history of progressively feeling dizzy and experiencing shortness of breath with fevers following a fall from his bicycle 5 days earlier. Max called the 111 service, who promptly sent a paramedic crew to his home. They found Max to be in pulsed ventricular tachycardia (VT) of a rate of 180 beats per minute, with a blood pressure reading of 125/70, and a oxygen saturation level of 80% on 15 litres oxygen via a non-rebreathe mask. This saturation level could be attributed to poor cardiac output, however, given the history of trauma, this raised the suspicion of a possible respiratory complication. Of note, the patient also had a pyrexia of 38.7 °C. It was therefore very important to rule out the possibility of rib fractures, lung contusions and chest infections in addition to the initial presentation of pulsed VT.

In this instance, due to Max's low oxygen saturations on maximal oxygen therapy, and the increased risk of Max becoming more haemodynamically unstable, the pre-alert was warranted to ensure the receiving team had the space and appropriate monitoring equipment ready – for example, a defibrillator and cardiac monitor.

Pulsed and pulseless VT

A heart rate of greater than 100 beats per minute is defined as a tachycardia, which may originate from the atria or the ventricles (Shadman and Rho, 2023). VT presents as a wide complex tachyarrhythmia, with a prolonged QRS complex on the electrocardiograph (ECG) of greater than 120 milliseconds (Foth et al, 2023). Abedin (2021), however, suggested that a QRS of greater that 140 milliseconds will almost certainly be VT.

The QRS denotes the depolarisation of the ventricles and demonstrates the electrical impulse journey from the atrioventricular node, down the bundle branches into the Purkinje's fibres, and finally entering the myocardial cells (Fischbach and Dunning, 2015). The approximate origin of the VT can be identified by the width of the QRS complex, with arrhythmias originating in the lateral walls of the ventricles causing very wide complexes, whereas narrower QRS complexes are created when the origin of the VT is close to the interventricular septum (Wellens, 2001).

VT can occur as ‘non-sustained’, lasting fewer than 30 seconds at a time, or ‘sustained’ if the complexes last longer than 30 seconds, or if cardioversion was required sooner due to haemodynamic instability (AlKabani and AlRawahi, 2019; Soar et al, 2021). In addition, VT can also present as ‘monomorphic’, a uniform waveform that demonstrates the arrhythmia is originating from a primary focus, or polymorphic, which is observed on the ECG as a changing QRS morphology from beat to beat (Foth et al, 2023; Buttner and Burns, 2023a;). Torsades de pointes is a form of polymorphic VT in which the QRS characteristically twists around the baseline of the ECG (Foglesong and Mathew, 2022; Buttner and Burns, 2023b).

VT can occur as a pulsed or pulseless rhythm (Soar et al, 2021). Pulseless VT occurs when the ventricles cannot effectively pump blood out of the heart, therefore resulting in no cardiac output (Foglesong and Mathew, 2022). Pulsed VT, as demonstrated in this case study, can present with the patient presenting asymptomatically, however, there is the potential for the patient to quickly become haemodynamically unstable if not treated (Resuscitation Council UK, 2021a).

It is acknowledged that other arrhythmias may be mis-diagnosed as broad-complex tachycardias, such as supraventricular tachycardias with aberrant conduction, for example, in the presence of a left or right bundle branch block (Foth et al, 2023). Other causes may include cases of poisoning or overdose of sodium-channel blocking drugs (Buttner and Burns, 2023a).

Epidemiology

It is estimated that 80% of all cases of wide complex tachycardias are VT (Pellegrini and Scheinman, 2010). Patients over the age of 35 years presenting with a wide complex tachyarrhythmia are more likely to be in VT, with a positive predictive value of 92% (Alzand and Crijns, 2011). Furthermore, patients with a clinical history of myocardial infarction, recent angina episodes and heart failure each have a positive predictive value of 95% for VT (Pellegrini and Scheinman, 2010).

The National Institute for Health and Care Excellence (NICE) (2014) estimated that in 2010, out of the 70 000 sudden cardiac deaths in England and Wales, 75-80% were due to ventricular arrhythmias. Accurate diagnosis of the VT is vital, as misdiagnosis and subsequent inappropriate treatment may cause further deterioration and may provoke cardiac arrest (Alzand and Crijns, 2011).

First-line treatment

In the emergency department, Max received a 300 mg dose of amiodarone. Initially introduced as an anti-anginal, amiodarone has since become widely used due to its anti-arrhythmic effects (Van Herendael and Dorian, 2010). By blocking the potassium channels within cardiac tissue, amiodarone works by prolonging the refractory period of the action potential, resulting in fewer ectopic beats, and the prevention of re-entry arrhythmias (Martindale Pharma, 2021). A single 300 mg dose of amiodarone may fail to convert the pulsed VT to sinus rhythm. In this case study, the treatment failed to cardiovert the pulsed VT to sinus rhythm, therefore Max was commenced on an intravenous infusion of amiodarone of 900 mg over 24 hours following local guideline recommendation and advice from the on-call cardiology consultant.

For all patients who present with a cardiac arrhythmia, it is vital that electrolytes such as magnesium, potassium and calcium are monitored and corrected as necessary (Foth et al, 2023).

Magnesium is an integral part of the cardiovascular conduction system, affecting vascular tone and electrical activity (DiNicolantonio et al, 2018). Hypomagnesaemia of levels of less than 0.8 millimoles per litre can result in prolongation of the QT interval, which in turn increases the risk of ventricular arrhythmias (Buttner and Larkin, 2021). Max's serum magnesium level on arrival was 0.5 millimoles per litre. Magnesium was given via intravenous infusion while in the emergency department, as per local guidelines, which recommend maintaining magnesium levels greater than 0.9 millimoles per litre, aiming towards the upper limit, rather than the normal range of magnesium of 0.7–1.05 millimoles per litre (University Hospitals of Derby and Burton NHS Foundation Trust (UHDB), 2018; 2021).

Hypokalaemia and hypomagnesaemia often occur concomitantly as low magnesium levels increase renal potassium losses (Nickson, 2020). Max's serum potassium level on arrival was 3.2 millimoles per litre, indicating mild hypokalaemia. It is essential that hypomagnesaemia is treated in the first instance, as magnesium is required to support the uptake and maintenance of potassium, specifically in the myocardium (DiNicolantonio et al, 2018).

Following initial replacement of magnesium and potassium, the repeat serum magnesium level was 0.96 millimoles per litre, and although this is within the normal range, given the protective factors that magnesium provides, as previously discussed, the target range in patients with significant cardiac complications is 1.0-1.5 millimoles per litre (Buttner and Larkin, 2021). For Max, he continued on magnesium replacement to ensure his levels were maintained towards the higher end of normal. Repeat potassium levels following replacement were 3.6 mmols per litre

Max had also been commenced on intravenous antibiotics, namely co-amoxiclav and clarithromycin, as it was suspected that he had an underlying chest infection. These antibiotics are often prescribed in conjunction where community-acquired pneumonia is suspected. Local guidelines recommend this dual antibiotic pairing in high severity cases (UHDB, 2023). This is likely due to Max presenting with a fever, new oxygen requirement and a history of breathlessness.

Blood tests revealed a rise in inflammatory markers, and, as per local guidelines, blood cultures were obtained before commencing antibiotic therapy, which once resulted showed no growth. A chest X-ray was taken on admission, which showed no obvious rib fractures, and no areas of consolidation, although it must be acknowledged that up to 50% of rib fractures are missed on chest radiographs (Battle et al, 2013). Shortly after admission, these antibiotics were switched to piperacillin with tazobactam, a broad-spectrum antibiotic, due to no clear focal indication of a pneumonia, and the treatment was directed towards an infection of unknown origin, as per local guidelines (UHDB, 2022).

Despite this treatment, during the 24-hour infusion, Max remained in stable pulsed VT, therefore the decision was made by the cardiology consultant to attempt cardioversion using direct current (DC) electricity. DC cardioversion is a procedure performed under sedation whereby a synchronised shock is administered via defibrillator pads with the aim of restoring a normal cardiac rhythm (Docherty and Morris, 2020). Following sedation by the anaesthetic team, a single shock was delivered at 150 joules, which restored the patient's sinus rhythm.

Once fully recovered from sedation and it was confirmed that sinus rhythm was sustained, Max was admitted to the coronary care unit and monitored via telemetry. The British Heart Rhythm Society (BHRS) (2020) describes telemetry as a method of cardiac monitoring using a wireless transmitter, to allow greater freedom of movement for the patient. The BHRS (2020) standards for telemetry highlight potential safety issues with telemetry, such as alarm fatigue, whereby constantly sounding alarms from monitors are overlooked, and the inaccurate setting of individual parameters for patients. As such, telemetry beds are situated in areas where staff are trained in their use and which have limited beds for such monitoring, such as the coronary care unit and cardiology wards.

It was felt by the admitting team that there was a low possibility of thrombus formation following this initial episode of sustained VT, therefore anticoagulation was not prescribed at this time, but Max was prescribed prophylactic low molecular weight heparin during admission.

Max continued on intravenous amiodarone following DC cardioversion, which was later switched to an oral beta blocker, bisoprolol, as a method of prevention.

Pulsed VT

A week later, the co-ordinator for the hospital out-of-hours team received a phone call from the cardiology ward, where Max had been transferred from the coronary care unit, informing the team that he had reverted into pulsed VT and required urgent medical assistance. Max had remained an inpatient while being administered intravenous antibiotics and undergoing further cardiac investigations.

The on-call medical registrar was informed verbally and arrived on the ward alongside a foundation year two (FT2) junior doctor and the trainee ACP. Pre-empting the confirmation of pulsed VT, the trainee ACP, a provider of advanced life support, was able to identify that the algorithm for adult tachycardia would be used to guide this patient's management (Resuscitation Council UK, 2021b).

ABCDE approach

As per the Resuscitation Council UK (2021b) guidelines, a rapid assessment was undertaken using the airway, breathing, circulation, disability and exposure approach. On initial assessment, the patient was alert, orientated and asymptomatic, with no complaints of palpitations, chest pain or breathlessness. Telemetry monitoring showed VT at a rate ranging between 155 and 198 bpm, with a blood pressure of 113/70. A 12-lead ECG was performed at the bedside, which further confirmed monomorphic VT. The trainee ACP changed the ECG electrodes for defibrillator pads, which allowed for continuous monitoring, but also would reduce time needed to defibrillate should Max's condition deteriorate.

The patient appeared stable, with no sign of adverse features of syncope or shock (Soar et al, 2021). The trainee ACP took this opportunity to ask Max about his admission so far. Gaining an understanding of the patient's journey from their perspective is useful to determine how much the patient comprehends of their diagnosis, investigations, and plan of care (Marca-Frances et al, 2020). The trainee ACP obtained a history from the patient, understanding that prior to this admission, Max was fit and healthy, with no medical problems, no regular or over-the-counter medications, and no family history of any cardiac illnesses.

The examination, other than profound tachycardia, was unremarkable. Auscultation of the chest was difficult due to the transmitted cardiac sounds; on percussion, the chest was globally resonant, with no areas of dullness or hyper-resonance. There was no raised jugular venous pressure, examined by observing the left side of the neck once turned at a 45° angle, observing for any double pulsations above 4 centimetres above the sternal angle (Ruthven, 2019). Although there were no abnormal findings in this case, ‘cannon’ A waves, visible pulsations or waves which are seen in the jugular veins can be seen in patients with VT, as a result of atrioventricular dissociation (Pellegrini and Scheinman, 2010). Other clinical findings may include varying intensity of the S1 heart sound on chest auscultation (Foth et al, 2023), but this was not identified in this case, due to the extreme tachycardia. There was no pitting peripheral or sacral oedema, which can be seen in patients with raised venous pressure, such as fluid overload, or right-sided heart failure (Ruthven, 2019). Max's blood pressure, respirations, oxygen saturations on air and temperature were all within normal limits.

This initial assessment concluded that, although Max was having a prolonged episode of pulsed VT, he was not showing concerning signs of shock, syncope, heart failure or myocardial ischaemia. Nevertheless, the faster the heart rate, the less likely the patient's body will be able to compensate (Resuscitation Council UK, 2021a).

Importance of team-work

The clinicians worked as a team to obtain further intravenous access. Max already had a 20-gauge cannula in situ in the back of his hand; however, it was identified that a second site of intravenous access with a wider-bore cannula would be of benefit. This proved beneficial as amiodarone was to be given, which ideally should not be given peripherally due to its high potency and increased probability of developing thrombophlebitis, however, alternative access is not always possible in emergency situations (Van Herendael and Dorian, 2010). Given that this episode had occurred overnight, there was not the available provision to place a central line, therefore it was deemed most appropriate to use peripheral cannulas.

The FT2 doctor, under instruction from the registrar, administered an intravenous bolus of amiodarone 300 mg over 10 minutes. Intravenous bolus doses of amiodarone are not recommended due to the potential for rapid administration causing undesirable effects on the patient (Martindale Pharma, 2021). Foth et al (2023) state that amiodarone is effective in cardioverting 30% of VT, and is particularly effective in reducing the re-occurrence rate of monomorphic VT. The bolus amiodarone had no immediate effect on the patient, therefore a further amiodarone intravenous infusion of 900 mg over 23 hours was prescribed. Amiodarone has been found to increase the success of cardioversion and is also recommended for longer-term maintenance therapy if given alongside a beta blocker (Pannone et al, 2021; Joint Formulary Committee, 2023).

There was a delay in commencing this treatment, as it requires a pharmacist to prepare and dispense the infusion. Meanwhile, the trainee ACP and the registrar reviewed the recent investigations that had been undertaken since the patient had been admitted, while the FT2 doctor monitored the patient at the bedside.

Investigations

The following day after admission and cardioversion, Max underwent an angiogram to examine the cardiac blood supply and to assess for any cardiac disease (NHS website, 2022). This revealed the left anterior descending and left circumflex arteries were both ‘sluggish’ with mild disease, and the right coronary artery was dominant, again with sluggish flow and mild disease, however, overall no flow-limiting coronary artery disease was identified.

While Max remained in sinus rhythm, an echocardiogram was performed, which revealed left ventricular systolic dysfunction, which is characterised as reduced left ventricular function with the absence of clinical heart failure (Sara et al, 2020). This diagnosis was supported with a measured left ventricular ejection fraction (LVEF) of 30-35%. This indicates that only 30-35% of the blood within the left ventricle is pumped with each cardiac contraction, whereas a recording of greater than 50% is considered normal (British Heart Foundation, 2022). No other finding of note was identified on the echocardiogram report.

Transthoracic echocardiograms and angiography are the recommended initial investigations for identifying a potential cause for the VT (Mahida et al, 2017). Angiography is helpful in identifying or excluding ischaemic causes for the arrhythmia (Foth et al, 2023). Echocardiograms, however, have limited success in providing quality imaging, with 10-15% of echocardiograms providing sub-optimal image results, thus resulting in a margin of error in relation to the interpretation of these images (Mahida et al, 2017).

Considering these findings did not indicate a clear cause for the patient's abnormal heart rhythm, the cardiology team had requested a cardiac magnetic resonance (CMR) scan (sometimes referred to as a cardiac MRI), which had been performed earlier that afternoon, but the formal report was yet to be released. The CMR was vital to look for any accessory pathways or structural abnormalities, and can review perfusion territories, quantifying the viability of cardiac muscle (Mahida et al, 2017; Ismail et al, 2022). It is estimated that 90% of patients who experience VT have structural heart disease, whereas the remaining 10% of patients have idiopathic VT, with no structural abnormalities (AlKabani and AlRawahi, 2019). CMR is deemed the gold standard imaging method for structural abnormalities in cases of VT (Mahida et al, 2017), allowing for visualisation of the heart structures including vessels and valves, and CMR scans are often reviewed alongside the ECG to help prevent any misdiagnosis due to motion artefacts (Fischbach and Dunning, 2015).

Blood tests showed normal inflammatory markers, which had been raised on admission, and Max had completed a course of intravenous antibiotics for a suspected lower respiratory tract infection resulting from his initial fall from his bicycle. The registrar identified that although the patient's urea and electrolyte levels were within normal ranges, his haemoglobin and haematocrit were raised compared with his baseline level, which had been within normal limits on admission, indicating that Max might be dehydrated. Dehydration can cause the laboratory values of haemoglobin and haematocrit to increase (Ashraf and Rea, 2017). The serum haemoglobin levels indicate the amount of stored haemoglobin in the red blood cells, and haematocrit measures the percentage of red blood cells compared with the volume of the blood sample (Fischbach and Dunning, 2013). Thus, the more dehydrated a patient, the more viscous the blood, indicated in the haematocrit level, and the higher the concentration of haemoglobin.

The medical registrar requested that fluids were prescribed for Max, however, given his reduced ejection fraction identified on the echocardiogram, it was agreed that a bolus of 250 ml of 0.9% sodium chloride would be administered, and to re-review Max following this to ensure no overt signs of fluid overload.

Early discussion with senior colleagues helps to prevent future delays in patient care in the case of deterioration (O'Neill et al, 2021). Given that this episode occurred early in the night shift, the registrar contacted the on-call cardiology consultant at home, first to highlight this patient to them, and second, to form a plan, should the amiodarone infusion not revert the patient. The cardiology consultant advised the team to transfer the patent to the coronary care unit for the amiodarone infusion and to alert the on-call anaesthetist due to the high probability that they could be required to sedate the patient in preparation for repeat DC cardioversion. The hospital out-of-hours team were informed to observe the patient for up to 2 hours after starting the amiodarone infusion, and if Max remained in pulsed VT, the plan was to proceed with another DC cardioversion.

While waiting for the infusion to arrive from the pharmacy, the team prepared the patient for transfer to the coronary care unit, during which time, 80 minutes after first going into pulsed VT, the patient reverted to sinus rhythm. The patient was re-assessed, and discussions held with the cardiology ward nurses who were happy to commence the infusion of amiodarone on the ward and transfer the patient to the coronary care unit.

Amiodarone was still administered as an infusion even though the patient had self-reverted, due to its protective factor and prevention of further episodes of VT, with this being the second episode of pulsed VT in a week (Van Herendael and Dorian, 2010; Spartalis et al, 2018).

The team, satisfied that the patient remained stable with a clear treatment plan, documented the events, and ensured that the nursing team were fully informed of the plan, should Max's condition deteriorate again.

Forward planning

The onward plan for Max, should he remain in sinus rhythm, was to await the CMR results, which would determine his future management. Should the findings be normal, Max would be scheduled for an implantable cardioverter-defibrillator (ICD).

An ICD is a matchbox-sized electrical device made up of a pulse generator and up to three electrode leads, which, once fitted, continuously monitors the cardiac rhythm, delivering electrical cardioversion or pacing if required (British Heart Foundation, 2017).

Max may be a candidate for ablation should the CMR identify any areas of scar tissue or possible accessory pathways. Ablation involves radiofrequency heat to burn away possible abnormal electrical pathways within the heart (Tung et al, 2010). Pellegrini and Scheinman (2010) report that greater than 90% of ablations undertaken for treatment of sustained VT are successful, with only 5% of cases re-occurring.

Conclusion

This was the trainee ACP's first encounter with pulsed VT, having only previously seen VT in a cardiac arrest setting. In this asymptomatic case, maintaining a calm environment and early involvement of senior clinicians' expertise to facilitate a clear and sensible plan helped to ensure the best possible outcome for the patient.

On reflection, the delay in acquiring the amiodarone infusion following the second episode of pulsed VT could be an area where improvements could be made for future practice. For the trainee ACP, it has been beneficial to improve their knowledge of the causes of VT and the modalities used to identify a cause in this case and it is hoped that information shared in this article can be used to support other health professionals' practice.

KEY POINTS

  • Ventricular tachycardia may present as a pulsed or pulseless rhythm, both requiring different considerations for immediate treatment
  • Pulsed ventricular tachycardia presents as a sustained rhythm with the patient appearing stable, however, there is always the possibility of decompensation and quickly becoming haemodynamically unstable
  • Thorough ABCDE assessments are vital in facilitating appropriate treatment and ensuring the best possible outcome for the patient
  • Hypomagnesaemia and hypokalaemia often occur simultaneously, and magnesium should be replaced first

CPD reflective questions

  • What would you have done if faced with this situation? Would you have done anything differently?
  • Have you ever nursed a peri-arrest patient? How did you identify and escalate it?
  • How might you support a patient in pulsed ventricular tachycardia who may be distressed or frightened?