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Case Presentation Ventricular Standstill Ventricular Asystole with residual P wave activity 29th August, 2012 History • 85 year old female presented to Redland hospital Emergency Department with a 4 week history of recurrent pre syncopal episodes • Lightheaded • Dizzy • Nausea • Lasted no more than a few seconds History • Denies chest pain, palpitations, shortness of breath, neurology or seizure activity • Has never fully lost consciousness • But with two of the episodes she did fall • Has been otherwise well, eating, drinking and no infective symptoms Background • • • • • • Chronic obstructive pulmonary disease Hypertension Dyslipidemia Gastro-oesophageal reflux disease Denies history of ischaemic heart disease Last in hospital 1952 Medications • • • • • • Indacaterol Tiotropium Ciclesonide Irbesartan Atorvastatin Aspirin Social • • • • Lives by herself in retirement village Mobilises with a 4WW Ex-smoker – quit 40 years ago Occasional glass of wine Examination • Alert and oriented • Blood pressure 132/68 • Pulse 110 on review but telemetry showed it varied from 40 to 128 while in the emergency department • Heart sounds dual no murmurs • Jugular venous pressure not elevated • Remainder of physical examination unremarkable Investigations • • • • • Electrolytes and renal function normal Full blood count normal Troponin I - 0.01 CT brain done as an outpatient normal CXR normal Baseline ECG Telemetry Telemetry • • • Several runs of complete heart block with ventricular standstill overnight Most were symptomatic: lightheadedness, presyncope No loss of consciousness Impression • • • Ventricular Standstill Ventricular asystole with persistent p wave activity Unknown cause - likely old age Diagnosis • • • This as opposed to complete heart block When QRS complex returned there was a clear association between the P wave and QRS and hence reflecting an intact AV node Thus the cause was due to the ventricle being unable to capture the impulse from the atria Telemetry Management • • • • • Admitted HDU overnight on telemetry Isoprenalin infusion 2mcg/minute started in the AM Morning transfer to PAH where a DDD pacemaker was inserted the same day Ambulance transfer had external pacing available if needed Discharged five days from PAH later with no issues Ventricular Standstill • Pathophysiology • Diagnosis • Guidelines for Pacing Conduction Pathway (70x per minute) (40-60x per minute) (ventricle = 40x per minute) Action Potentia Myocyte QRS ST T wave Pacemaker Action Potential Causes • • • Literature very scant Hypoxemia, hyperkalemia, acute coronary syndromes Closely associated with complete heart block • • • • • • • • Fibrosis and sclerosis of the cardiac skeleton associated with ageing Ischaemic heart disease (40% of cases) - It is estimated that approximately 20 percent of patients with an acute MI develop AV block: 8 percent with first degree; 5 percent with second degree; and 6 percent with third degree Cardiomyopathy and myocarditis: SLE, viruses, Chagas Congenital heart disease Drugs: digoxin, calcium channel blockers(Verapamil, Diltiazem), beta blockers, amiodarone, adenosine Surgery/procedures - TAVI, VSD repair Increased vagal tone e.g. carotid sinus massage Numerous case reports: vagal nerve stimulation in the treatment of epilepsy, defibrillator implantation and upper gastrointestinal variceal electrocoagulation Escape Rhythm • If third degree AV block occurs within the AV node, about two-thirds of the escape rhythms have a narrow QRS complex, ie, a junctional or AV nodal rhythm • Block at the level of the bundle of His is also typically associated with a narrow QRS complex • Patients with trifascicular block have a sub-junctional escape rhythm with a wide QRS complex Escape Rate • • As a general rule, the more distal the block, the slower will be the escape pacemaker. Low pacemakers have a rate of 40 beats per minute or less and often are unreliable, resulting in a very slow rate or asystole. Syncope is most common in this group Signs and Symptoms • • • • • • Dizziness/lightheadedness Presyncope Syncope (Stokes-Adams attacks) Ventricular tachycardia Ventricular fibrillation Exacerbation of the symptoms of heart failure and angina pectoris Management • Correct reversible causes: myocardial ischemia, increased vagal tone, and drugs. Multiple case reports have demonstrated this. • Resolution of complete heart block after prednisolone in a patient with systemic lupus erythematosus. Lupus [0961-2033] Lim, L-T Year:2005 Volume:14 Issue:7 Page:561 -563 • Complete heart block induced by intravenous metoclopramide. Anales de medicina interna [0212-7199] Huerta Blanco, R Year:2000 Volume:17 Issue:4 Page:222 -223 (Spanish) Pharmacotherapy • • • • • Emergent setting, atropine may also be effective by reversing the decrease in AV nodal conduction induced by vagal tone. Australian therapeutic guidelines recommend: Atropine 0.5 - 1.5mg IV can be given every 15 minutes If atropine not effective and trancutaneous pacing not available Adrenalin infusion 2 - 10 mcg IV/minute or Isoprenaline 20mcg bolus followed by infusion at 1 - 4 mcg/hour Pacing • • Transcutaneous pacing should be provided if there is no resolution with pharmacotherapy Most patients will need permanent pacing in the absence of an acutely reversible cause 2008 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) Levels of Evidence Pacemaker Indications • Class I Indication • Permanent pacemaker implantation is indicated for third • degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients in sinus rhythm, with documented periods of asystole greater than or equal to 3.0 seconds or any escape rate less than 40 bpm, or with an escape rhythm that is below the AV node. (Level of Evidence: C) I.e. pause > 3 seconds or pulse <40 or wide QRS escape with no pre existing aberrancy Pacemaker Indications • Class I Indication • Permanent pacemaker implantation is indicated for third • degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients with AF and bradycardia with 1 or more pauses of at least 5 seconds or longer. (Level of Evidence: C) I.e. in AF the pause needs to be 5 seconds in absence of symptoms (as opposed to 3 seconds in sinus rhythm) Pacemaker Indications • Class I Indication • Permanent pacemaker implantation is indicated for third degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block. (Level of Evidence: C) • I.e. if they have symptomatic heart block Pacemaker Indications • Class I Indication • Permanent pacemaker implantation is indicated for third degree and advanced second-degree AV block at any anatomic level associated with arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycardia. (Level of Evidence: C) • I.e. if they have another medical condition such as AF that needs drug treatment and this cannot be modified then they can have a pacemaker Pacemaker Indications • • • Class IIa Permanent pacemaker implantation is indicated for third degree and advanced second-degree AV block at any anatomic level associated with neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle muscular dystrophy) Level of Evidence B Pacemaker Indications • • Class IIa Permanent pacemaker implantation is indicated for asymptomatic persistent thirddegree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster if cardiomegaly or LV dysfunction is present or if the site of block is below the AV node. (Level of Evidence: B) Pacemaker Indications • • Class IIa Permanent pacemaker implantation is indicated for secondor third-degree AV block during exercise in the absence of myocardial ischemia. (Level of Evidence: C) Pacemaker Indications • • Class IIa Permanent pacemaker implantation is reasonable for persistent third-degree AV block with an escape rate greater than 40 bpm in asymptomatic adult patients without cardiomegaly. (Level of Evidence: C) Pacemaker Indications • • Class IIa Permanent pacemaker implantation is reasonable for asymptomatic second-degree AV block at intra- or infraHis levels found at electrophysiological study. (Level of Evidence: B) Pacemaker Indications • Class IIb • Permanent pacemaker implantation may be considered for neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) Pacemaker Indications • Class III • Permanent pacemaker implantation is not indicated for asymptomatic first-degree AV block. (Level of Evidence: B) Pacemaker Indications • • Class III Permanent pacemaker implantation is not indicated for asymptomatic type I seconddegree AV block at the supra-His (AV node) level or that which is not known to be intraor infra-Hisian. (Level of Evidence: C) Pacemaker Indications • • Class III Permanent pacemaker implantation is not indicated for AV block that is expected to resolve and is unlikely to recur 100 (e.g., drug toxicity, Lyme disease, or transient increases in vagal tone or during hypoxia in sleep apnea syndrome in the absence of symptoms). (Level of Evidence: B) Choice of Pacemaker • VVI pacing was most commonly used in the past, and is still used in the emergent setting for temporary pacing • Easier to implant and less expensive • Synchrony between atrial and ventricular contraction is lost, which is hemodynamically unfavorable. • In order to maintain physiologic pacing, dual chamber pacing is recommended. • The advantages of physiologic pacing may be less significant in very elderly patients with AV block Pacing Modalities Case Report • Describe a case in which the haemodynamic data from manual external, transthoracic and transvenous pacing in ventricular asystole was compared. Case Report • A 55-year-old Caucasian female with insulin treated type 2 • • • • diabetes mellitus presented to the emergency department with a 3-day history of diarrhoea, vomiting, abdominal pain and malaise Taken for an abdominal CT scan Suffered a sudden asystolic cardiac arrest Return of spontaneous circulation occurred after 3 min advanced cardiac life support and the patient was admitted to the intensive care unit following intubation and the institution of intermittent positive pressure ventilation. She required an infusion of adrenaline (epinephrine) at 0.14 μg/kg per min which was subsequently changed to noradrenaline (norepinephrine) at 0.4 μg/kg per min. Method • The patient developed ventricular asystole with persisting • • • • electrocardiographic p wave activity. 2 boluses atropine - no effect Manual external pacing (cardiac percussion) was commenced over the lower end of the sternum at a rate of 52 beats/min and electrical capture was evident electrocardiographically. This generated a palpable pulse and a blood pressure (BP) of 108/62 mmHg with a mean arterial pressure (MAP) of 78 mmHg. Transthoracic pacing resulted in capture at 90 mA and produced a BP of 140/71 (MAP 105) mmHg at a rate of 80 beats/min. Transvenous pacing resulted in an BP of 148/76 (MAP 112) mmHg at a heart rate of 90 beats/min. Results Conclusion • Our data demonstrate that manual external pacing is as effective as transvenous and transthoracic pacing, as long as electrical capture occurs. Training in resuscitation should stress the usefulness of this technique as a temporary measure while more definitive pacing methods are prepared. Critique One patient Emergency environment Did not compare percussion to standard CPR The End