A 40 year old woman was admitted to the emergency department (ED) after a syncopal episode. On admission she was in acute respiratory distress and described a two day history of sudden onset breathlessness. She had no previous medical history. Her only regular medication was the oral contraceptive pill. She had had a recent flu-like illness and been less active than usual. On arrival she had a respiratory rate of 30 breaths/minute with accessory muscle use. An ABG on 15L/min oxygen via non-rebreathe mask showed type I respiratory failure (PO2 8.4kPa). She was tachycardic (120bpm) and blood pressure was 98/50. Chest x-ray and bloods were unremarkable although her ECG revealed a sinus tachycardia with right axis deviation, Q waves and inverted T waves in lead III.
The patient had a bedside echocardiogram that revealed a severely dilated right ventricle with poor tricuspid annulus planar systolic excursion (TAPSE). A presumed diagnosis of a pulmonary embolism (PE) was made. Thrombolytic therapy was considered but rejected at this point, in view of the haemodynamic stability. The patient was commenced on enoxaparin at a dose of 1.5mg/kg.
CT pulmonary angiography confirmed the presence of bilateral pulmonary emboli. On return from CT the patient was sat up briefly at which time she became cyanotic and had a brief self-terminating seizure. During this time her blood pressure was not recordable, and significant hypotension secondary to obstructive shock was assumed to be the cause. At this point it was decided to proceed with thrombolysis. The patient was transferred to the Intensive Care Unit, made a rapid recovery without the need for vasopressors or intubation and ventilation, and was discharged from hospital a few days later.
What is the evidence for intravenous thrombolysis for intermediate-risk pulmonary embolism? Read More »
A 70 year old woman suffered an out of hospital cardiac arrest whilst playing golf. She received bystander cardiopulmonary resuscitation and two shocks from an automated external defibrillator which restored spontaneous circulation. She was intubated at the scene and arrived in the resuscitation department cardiovascularly stable, well oxygenated and unconscious in the context of propofol sedation.
There was no prodrome suggestive of a specific aetiology for the cardiac arrest but information from relatives described an ex-smoker with hypercholesterolaemia and diet controlled diabetes mellitus who had previously undergone percutaneous coronary intervention (PCI) for ischemic heart disease. She took regular aspirin, statin and beta-blocker. A post resuscitation 12 lead ECG showed sinus rhythm, left axis deviation and non-specific lateral ischaemia. Troponin was elevated above 200 ng/L.
In view of this she was loaded with dual antiplatelet therapy and underwent emergency coronary angiography which demonstrated occlusion of two small branches (OM1 and PLV) but no large vessel coronary artery occlusion to explain the cardiac arrest. The occluded vessels were not stented. Subsequent echocardiogram and cardiac MRI demonstrated old circumflex territory scar but an otherwise normal heart and ultimately it was agreed that the cause of cardiac arrest was probably ventricular arrhythmia secondary to scar.
She was ventilated for 24 hours with targeted temperature management before being woken and extubated. Although she was initially confused, her neurology improved over approximately 48 hours such that she was discharged with no apparent neurological injury. An implantable cardiac defibrillator was placed prior to discharge to prevent sudden cardiac death from any future arrhythmia.
In survivors of out of hospital cardiac arrest should we proceed to early coronary angiography with a view to PCI?
If so, should we apply this approach to all such patients or only a subset?
If we do proceed to early coronary angiography, should this occur before or after other investigations, specifically computed tomography (CT) of the head and chest to look for intracerebral bleed and pulmonary embolism?
A 35 year old male presented with massive (over 1500mg) propranolol overdose on a background of depression and anxiety. He called for help and was found alert and cardiovascularly stable by paramedics at 50 minutes post ingestion. By 80 minutes his conscious level had fallen to a Glasgow Coma Score of 11 and he had become hypotensive. He started fitting en route to hospital and lost cardiac output as he arrived at hospital. The initial cardiac arrest rhythm was broad complex slow pulseless electrical activity. After a prolonged resuscitation attempt he regained spontaneous cardiac output but never achieved cardiovascular stability and sadly died later that evening.
He was resuscitated according to standard resuscitation algorithms. In addition, several specific therapies were given in line with Toxbase recommendations1: Glucagon was administered as a 10mg slow bolus followed by a 100-150 mcg/kg/hr infusion. Insulin (actrapid) was given as a 60 unit bolus followed by a 1-2 unit/kg/hr infusion along with a glucose bolus of 0.5 g/kg followed by an infusion of 0.5 g/kg/hr. Intralipid was delivered as a bolus (100 ml 20%) followed by an infusion. Atropine 3mg was given and the adrenaline boluses were changed to an infusion at 10 mg/hr.
Cardiac arrest remained refractory until a 100 ml bolus of 8.4% Sodium Bicarbonate was administered prompting almost instantaneous restoration of circulation.
The circulation remained unstable with a broad complex bradycardia resistant to transcutaneous pacing. High dose adrenaline infusion, high dose euglycaemic insulin therapy and glucagon infusion were continued. Transvenous pacing was also ineffective and the patient sadly deteriorated into a refractory cardiac arrest from which he did not recover.
The patient regained his cardiac output when the sodium bicarbonate bolus was given. The temporal association between these two events was profound and led me to question why this therapy sits so far down the toxbase treatment algorithm.1
A 68 year-old gentleman was admitted to the Emergency Department in cardiac arrest. He had complained of sudden onset upper abdominal pain to his wife immediately prior to a collapse, and bystander cardiopulmonary resuscitation (CPR) was commenced whilst emergency services were called. He had a background of ischaemic heart disease, insulin-dependent diabetes, peripheral vascular disease and hypertension.
On arrival, the Paramedic crew found him to be in ventricular fibrillation was the predominant rhythm. Despite appropriate advanced life support with defibrillation and administration of adrenaline and amiodarone over multiple cycles. His airway was supported with an I-Gel supraglottic airway device, and he was transferred to hospital urgently.
Ischaemic heart disease is the leading cause of death in the world, and sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease. Early and effective CPR, early defibrillation and physiological support post-resuscitation form the chain of survival .
Assessment of the patient’s airway on arrival in the Emergency Department revealed evidence of vomit in the pharynx, and endotracheal intubation was performed. Vomitus was aspirated from his endotracheal tube, indicating pulmonary aspiration either at the time of collapse or during the resuscitation attempts. Sidestream capnography was connected to a self-inflating bag administering high-concentration oxygen. The initial capnography indicated a flattened end tidal carbon dioxide (EtCO2) trace with a highest partial pressure of 1.5 kPa. Chest auscultation was performed and air entry was confirmed as being equal bilaterally.
Chest compressions continued uninterrupted and by this stage the overall resuscitation attempt had been ongoing for 45 minutes. The rhythm had changed to pulseless electrical activity, and despite effective CPR, administration of adrenaline and fluids, there was no return of spontaneous circulation (ROSC). Blood gas analysis revealed a severe metabolic acidosis (pH 6.8, lactate 15.2 mmol/L) and by this stage the highest EtCO2 recorded was 0.9 kPa. Following discussion with the team, and on the grounds of futility, the resuscitation attempt was abandoned.
What is the role of capnography in cardiac arrest?
An elderly female was admitted under the care of the orthopaedic team with a 2 week history of decreased mobility due to right knee pain. She had a past medical history of chronic atrial fibrillation, treated with amiodarone, and asthma which was well controlled on salbutamol inhalers. She was not on warfarin. Bony injury was ruled out clinically and radiologically and she was treated with simple analgesia. Whilst on the ward, she deteriorated acutely after complaining of shortness of breath. A cardiac arrest call was put out.
On arrival of the cardiac arrest team, she had a cardiac output. On examination, she was hypotensive (BP 70/50 mmHg) with a heart rate of 55 bpm. She was markedly cyanosed with a respiratory rate of 30 breaths per minute with oxygen saturation of 75% on high flow oxygen through a reservoir bag. Her Glasgow Coma Score was 7 (E1V2M4). There was no evidence of calf swelling or tenderness. Arterial blood gas analysis revealed marked type 1 respiratory failure – pH 7.2, pO2 5.4kPa, pCO2 7.8kPa, HCO3 19mmol/l and lactate 4mmol/l .
She was rapidly intubated, and resuscitated with a total of four litres of crystalloids and colloids. Invasive blood pressure monitoring was established. A clinical diagnosis of acute pulmonary embolus was made. She remained unstable despite resuscitation, requiring frequent boluses of vasopressors and adrenaline thus being too unstable to be transferred for a CT pulmonary angiogram. A bedside echocardiogram showed a markedly dilated right heart with elevated right heart pressures. There was paradoxical movement of the interventricular septum. Left ventricular function was also slightly impaired.
It was decided to thrombolyse the patient. As alteplase was being readied, the patient arrested. The initial rhythm was pulseless electrical activity with a rate of 40 beats per minute. She was resuscitated as per Advanced Life Support (ALS) guidelines and received adrenaline and atropine intravenously. After two cycles of cardio-pulmonary resuscitation (CPR) and the administration of thrombolysis, she regained cardiac output but remained hypotensive and hypoxic. An adrenaline infusion was commenced through a peripheral line. Despite this, she arrested six further times with increasing inotropic support requirement. After two hours from the initial cardiac arrest call, the decision was made to stop resuscitation.
Post-mortem results confirmed the presence of a large pulmonary embolus as well as bilateral deep venous thromboses (DVTs).
What is the evidence for the use of thrombolysis in pulmonary embolism?Read More »
A young adult female with known diagnosis of poorly controlled type 1 diabetes mellitus was admitted with out-of-hospital cardiac arrest. She had only recently been discharged from hospital after an admission with diabetic ketoacidosis. On arrival she had a GCS 3 with minimal respiratory effort. She was in profound DKA. Her temperature was 34.7°C on admission to ICU and she had targeted temperature management aiming for 36°C which was achieved within 2 hours. Her pH had normalised to 7.35 within 8 hours. 48 hours later one pupil became fixed and dilated. CT brain was consistent with global hypoxic ischaemic injury. EEG and SSEP on day 3 revealed severe lack of normal cortical activity. After discussion with family, treatment was withdrawn on day 4.
How do we undertake neuroprognostication after cardiac arrest in the post-TTM era?
A 55 year old presented to ED following a witnessed VF arrest. He received bystander CPR and several shocks from the ambulance crew. He was intubated at the scene, and transferred to ED with return of spontaneous circulation. He had primary PCI to LAD and was transferred to the ICU for therapeutic hypothermia. He was kept at 33 degrees for 24 hours, and rewarmed over 8 hours. He extubated 2 days late with no cognitive impairment, and mild weakness in one arm.
What is the evidence for and against Targeted Temperature Management (TTM) post cardiac arrest?Read More »
A 30 year old man suffered a 30 minute cardiorespiratory arrest secondary to an asthma attack. He was resuscitated, had his severe bronchospasm managed and he was treated with therapeutic hypothermia at 33 degrees. Once rewarmed, his neurology was assessed over several days. He was ventilated on a spontaneous mode, but his pupils remained fixed and dilated and there was no higher motor function seen. A CT brain was consistent with severe hypoxic ischaemic injury. After discussion with the family, treatment was withdrawn.
How reliable is neuroprognostication after cardiac arrest? What modalities are tested? Is there a difference in patients treated with therapeutic hypothermia?
An elderly man was resuscitated from out-of-hospital VF cardiac arrest. He remained deeply comatose post ROSC and was ventilated on the intensive care. His temperature control was not actively managed unless hyperthermia developed. 24 hours post admission he started to have myoclonic jerks and his pupils were fixed and dilated. CT brain showed evidence of severe hypoxic ischaemic injury. Treatment was withdrawn at 72 hours after discussion with family.
What is the rationale for the use of therapeutic hypothermia after cardiac arrest?Read More »