Some patients with severe refractory heart failure are kept alive thanks to implantable pumps such as the left ventricular assist device (LVAD). Many emergency physicians are likely to be unfamiliar with these but could encounter patients who have them. One particular peculiarity is that latter generation devices maintain non-pulsatile flow and provide or assist cardiac output independent of cardiac rhythm. In extreme situations patients can have life-sustaining cardiac outputs without palpable pulses or even audible heart sounds.
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A great example of how weird this can get is provided by a case of a 66 year male with an LVAD (HeartMate II (Thoratec Corporation)) who presented due to spontaneous discharge of his internal cardioverter-defibrillator (ICD). He was alert but had no pulses, and no detectable blood pressure using both a manual sphygmomanometer and an automated non-invasive blood pressure device. His 12 lead showed ventricular fibrillation. An invasive blood pressure showed a mean arterial pressure (mAP) of 80 mmHg. Several hours later his VF was successfully terminated and his mAP remained 80 mmHg
Some interesting points made by the authors include:
CPR was unnecessary in this guy but in cases of severe RV dysfunction it might need to be done to provide flow into the LV.
A danger of CPR in patients with an LVAD is the risk of damage to the device or ventricular rupture
LVAD use is significantly increasing so we can expect to encounter more episodes of previously impossible presentations to our emergency departments.
ABSTRACT
Optimal medical treatment, cardiac resynchronization, and the use of an implantable cardioverter defibrillator are established therapies of severe congestive heart failure. In refractory cases, left ventricular assist devices are more and more used not only as bridging to cardiac transplantation but also as destination therapy. Ventricular arrhythmias may represent a life-threatening condition and often result in clinical deterioration in patients with congestive heart failure. We report a case of asymptomatic sustained ventricular fibrillation with preserved hemodynamics caused by a nonpulsatile left ventricular assist device. Consecutive adequate but unsuccessful discharges of the implantable cardioverter defibrillator were the only sign of the usually fatal arrhythmia, prompting the patient to consult emergency services. Electrolyte supplementation and initiation of therapy with amiodarone followed by external defibrillation resulted in successful restoration of a stable cardiac rhythm after 3.5 hours.
We all like to treat selected post cardiac arrest patients with hypothermia now, but isn’t hypothermia associated with a drop in potassium, which of course can precipitate pesky ventricular dysrhythmias in patients who would really rather not arrest again. Maybe the hypothermia itself is protective against the dysrhythmias?
A study from the Mayo Clinic updates our knowledge of this area:
METHODS: We retrospectively analyzed potassium variability with Therapeutic Hypothermia (TH) and performed correlative analysis of QT intervals and the incidence of ventricular arrhythmia.
RESULTS: We enrolled 94 sequential patients with OHCA, and serum potassium was followed intensively. The average initial potassium value was 3.9±0.7 mmol/l and decreased to a nadir of 3.2±0.7 mmol/l at 10 h after initiation of cooling (p<0.001). Eleven patients developed sustained polymorphic ventricular tachycardia (PVT) with eight of these occurring during the cooling phase. The corrected QT interval prolonged in relation to the development of hypothermia (p<0.001). Hypokalemia was significantly associated with the development of PVT (p=0.002), with this arrhythmia being most likely to develop in patients with serum potassium values of less than 2.5 mmol/l (p=0.002). Rebound hyperkalemia did not reach concerning levels (maximum 4.26±0.8 mmol/l at 40 h) and was not associated with the occurrence of ventricular arrhythmia. Furthermore, repletion of serum potassium did not correlate with the development of ventricular arrhythmia.
CONCLUSIONS: Therapeutic hypothermia is associated with a significant decline in serum potassium during cooling. Hypothermic core temperatures do not appear to protect against ventricular arrhythmia in the context of severe hypokalemia and cautious supplementation to maintain potassium at 3.0 mmol/l appears to be both safe and effective. Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis Resuscitation. 2010 Dec;81(12):1632-6
How can you not love those guys at hqmeded.com?
Here’s a great case of theirs demonstrating the echocardiographic appearance of ventricular fibrillation – something we talk about on the BEAM course.
Drowning is one of the leading causes of accidental death in children. Some apparent drownings may be related to sudden cardiac death, in particular to unidentified channelopathies, which are known to precipitate fatal arrhythmias during swimming-related events.
The majority of cases of sudden cardiac death in children and adolescents are secondary to either hypertrophic or right ventricular cardiomyopathy with coronary artery abnormalities also prevalent, and reports have demonstrated these cardiac abnormalities on autopsy following sudden swimming-related deaths.
However, the majority of autopsies in swimming-related sudden deaths are normal suggesting causation at molecular level, in particular ion channel defects such as type 1 long-QT syndrome (LQT1) and catecholaminergic polymorphic ventricular tachycardia (CPVT). The gene deletion in LQT1 (KCNQ1) leads to a reduction in the repolarising potassium current (IKs) and prolongation of repolarisation. This lengthens the QT interval (which may be lengthened further by facial immersion in cold water). A premature ventricular contraction (PVC) again which may be initiated by swimming occurring during the vulnerable part of repolarisation leads to establishment of polymorphic ventricular tachycardia (torsades de pointes). The ryanodine receptor gene mutation (RyR2) in catecholaminergic polymorphic ventricular tachycardia leads to defective closure of the receptor on the surface of the sarcoplasmic reticulum during diastole. This leads to increased calcium (Ca2+) leakage from the sarcoplasmic reticulum and increased potential for delayed afterdepolarisations and subsequent ventricular tachycardia.
Some recommendations are made in an article in Archives of Disease in Childhood: Proposed implementations to improve detection and appropriate management of apparent drownings secondary to cardiac channelopathies
Improving awareness in the coronial service of the possibility of a cardiac cause for poorly explained drownings.
Education of lifeguards and provision of automated defibrillators in swimming pools.
Molecular autopsy for non-survivors to look for potential channelopathies.
Screening for survivors and family members of non-survivors to identify those with a channelopathy.
Proper counselling for those identified to have a channelopathy on family screening.
One of the dilemmas in selecting appropriate therapy for atrial fibrillation in the emergency situation is determining whether the AF is of acute onset or not. AF causes release of natriuretic peptide from the heart, so measuring these peptides may give a clue to the recency of onset if the kinetics are known. This of course can only apply to those patients without heart failure, who have another cause for elevated natriuretic peptide levels.
A study of N-terminal pro-BNP levels in patients with acute onset AF, and without clinical or radiological evidence of heart failure, showed the pattern of rise and fall. The key finding in this study is the rapid rise of plasma NT-proBNP levels to peak followed by a rapid decline, probably due to depletion of the granules in atrial myocytes in which pro-BNP is stored.
The authors describe the following implication of the study: According to our observations, a rising trend is markedly indicative of the fact that AF onset did not happen more than 24–48 h before presentation. As a consequence, obtaining two to three plasma NT-proBNP levels within 24 h of presentation in patients with AF without heart failure who cannot satisfactorily pinpoint the time of onset may assist in determining whether the onset of the arrhythmia was recent. Such information is pertinent to decisions concerning anticoagulation and cardioversion. Short-term fluctuations of plasma NT-proBNP levels in patients with new-onset atrial fibrillation: a way to assess time of onset? Heart. 2010 Jul;96(13):1033-6
Investigators at the Royal North Shore Hospital in Sydney (it’s good there) did a literature review to determine the best ‘gold standard’ way of performing a Valsalva manoeuvre for SVT, and assessed success rates before and after its introduction into the ED.
The technique required the patient to lie supine on the bed in a Trendelenberg position, and forcefully expire into a section of suction tubing and pressure gauge for at least 15 seconds and at a pressure of at least 40 mm Hg. The theory behind increased success in a supine position lies in augmenting the patients’ vagal tone and attenuating the sympathetic tone in addition to increased venous return during phase IV of Valsalva. The ‘standardised’ technique improved the rate of successful termination of SVT from 5.3% to 31.7%
The Ottawa Aggressive Protocol is used to treat recent onset (< 48 hours) atrial fibrillation or flutter with procainamide and/or cardioversion to allow discharge from the emergency department.
A cohort of 660 patient visits is described in a paper in the Canadian Journal of Emergency Medicine, 95.2% involving atrial fibrillation and 4.9% involving atrial flutter. The mean age of patients enrolled was 64.5 years. In total, 96.8% were discharged home and, of those, 93.3% were in sinus rhythm. All patients were initially administered intravenous procainamide, with a 58.3% conversion rate. A total of 243 patients underwent subsequent electrical cardioversion with a 91.7% success rate. Adverse events occurred in 7.6% of cases: hypotension 6.7%, bradycardia 0.3% and 7-day relapse 8.6%. There were no cases of torsades de pointes, stroke or death. The median lengths of stay in the ED were as follows: 4.9 hours overall, 3.9 hours for those undergoing conversion with procainamide and 6.5 hours for those requiring electrical conversion.
This proactive approach by emergency physicians seems excellent for patients who in some centres probably still get admitted for this presentation. I’m not sure why they continue to use a drug with a conversion percentage in the 50’s, which the authors have demonstrated before. Many of us routinely use flecainide for recent onset AF in patients likely to have structurally normal hearts, as it has been shown to be superior to procainamide in AF. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter
Canadian Journal of Emergency Medicine 12.3 (May 2010): p181(11)
Previous studies have suggested the following are necessary for a successful Valsalva manoeuvre with maximum vagal effect:
Supine posturing
Duration of 15 seconds
Pressure of 40 mmHg (with an open glottis)
One popular method of generating a Valsalva Manoeuvre is to get the patient to blow into a syringe in an attempt to move the plunger. Different syringe sizes were tested. A 10ml (Terumo) syringe was best The 10 mL syringe is useful in generating the recommended standard of 40 mmHg intrathoracic pressure for the Valsalva manoeuvre Emerg Med Australas. 2009 Dec;21(6):449-54
Based on a study of 453 consecutive patients undergoing their first transthoracic electrical cardioversion for atrial tachyarrhythmias, recommendations were developed to aim at delivering the lowest possible total cumulative energy with ≤2 consecutive shocks using the specific truncated exponential biphasic waveform incorporated in Medtronic Physio-Control devices: they recommend an initial energy setting of 50 J in patients with atrial flutter or atrial tachycardia, of 100 J in patients with atrial fibrillation (AF) of 2 or less days in duration, and of 150 J with AF of more than 2 days in duration. If the initial shock fails to restore sinus rhythm, a rescue shock of 250 J for AFL/AT or of 360 J for AF should be applied to secure the highest possible probability of successful cardioversion for each patient. Optimization of initial energy for cardioversion of atrial tachyarrhythmias with biphasic shocks Am J Emerg Med. 2010 Feb;28(2):159-65
