Emergency Coronary Angiography After Out-of-Hospital Cardiac Arrest



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.

Clinical questions:

  1. In survivors of out of hospital cardiac arrest should we proceed to early coronary angiography with a view to PCI?
  2. If so, should we apply this approach to all such patients or only a subset?
  3. 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?

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Facilitation Of Donation After Circulatory Death


A previously fit and well 45 year old man presented to the emergency department with a two-hour history of a sudden onset severe headache associated with weakness, vomiting and photophobia. He had a normal breathing pattern and oxygen saturations of 96% in air. He was hypertensive with a non-invasive blood pressure of 220/115mmHg and a pulse rate of 85 beats/minute in sinus rhythm. Neurological examination revealed a Glasgow Coma Scale (GCS) of 14/15 with a dense hemiparesis, with hemisensory neglect and dysarthria.

He deteriorated and dropped his GCS to 5/15. He was intubated and an urgent computed tomographic (CT) brain scan was performed that revealed a large right-sided intraparenchymal haemorrhage with 4mm of midline shift. Blood tests including full blood count, urea and electrolytes and clotting screen were normal.

He was discussed with the neurosurgeons who felt transfer to institute intracranial pressure monitoring or surgical intervention was not indicated. His blood pressure was managed with a labetalol infusion aiming for a target systolic blood pressure of ≤ 160mmHg. Seizure activity was managed with a 15mg/kg loading dose of phenytoin followed by a maintenance dose of 300mg once daily nasogastrically. Sodium levels were monitored closely and hypotonic fluids avoided.

By day 5 he was making spontaneous respiratory effort, and his pupils were equal and sluggishly reactive. His GCS remained 3/15. A repeat CT was performed on day 9 due to no improvement in his clinical condition and revealed extension of the intraparenchymal haemorrhage with 8mm midline shift, effacement of the ventricles and loss of sulcal definition. A discussion regarding end of life care was held with his family who raised the possibility of organ donation. In agreement with his family, end of life care was instituted and he became an organ donor after circulatory death was confirmed.

How can we facilitate Donation After Circulatory Death?Read More »

Graft versus Host Disease

A 34-year-old woman received a small bowel, pancreas and abdominal wall transplant.

Despite the operation being technically very difficult and prolonged, she initially recovered well after the procedure and her transplanted bowel started to work. However, after a few days she started developing respiratory complications eventually requiring re-intubation despite antibiotics. She went on to develop multi-organ dysfunction requiring vasopressor support and renal replacement therapy. Antifungals and co-trimoxazole were added, with no additional benefit noted.

A skin rash started to develop, which raised the suspicion of Graft versus Host Disease (GvHD). A diagnostic test was performed (chimerism of peripheral blood leucocytes), and it confirmed the diagnosis of GvHD.

Doses of immunosuppressants such as tacrolimus, mycophenolate mofetil were increased and steroids were started too.

An experimental therapy of mesenchymal stem cells infusion was also employed, but she continued to deteriorate further and she eventually died after a prolonged admission on ICU.

Graft versus Host Disease – what it is, how to diagnose it, how to treat itRead More »

Extracorporeal CO2 removal

A 42 year old man presented with a week-long history of increasing shortness of breath, cough  (productive of purulent sputum) and fevers on a background of significant chronic lung disease. He had a ten year history of interstitial lung disease and was on the waiting list for a lung transplant. He used oxygen at a rate of 2 litres per minute at home, 24 hours a day. His usual exercise tolerance of 200 metres had been significantly reduced for the past week. His regular medications included seretide and salbutamol inhalers, lansoprazole, azathioprine, prednisolone alendronate.

On arrival in hospital, he was alert and orientated. He had a patent airway, but was tachypnoeic (rate of 50/minute) using his respiratory accessory muscles and a tracheal tug was evident. An arterial blood gas revealed type two respiratory failure (pH 7.26; pO2 8.14, pCO2 7.52 on 15 liters/min of face mask oxygen). He was hypotensive (80/40mmHg) and tachycardic (130/minute, sinus rhythm). A pyrexia of 39.2°C was recorded. Blood results showed normal renal function, a slightly elevated white cell count of 14.

The patient was admitted to the high dependency for close monitoring in view of his history and presentation. He was commenced on treatment for a presumed infection (viral or bacterial) with oseltamivir, co-amoxiclav and clarithromycin and given three “pulsed” doses (750mg) of methylprednisolone. He remained stable for the next twelve hours.

Early the next morning, he became very hypoxic (oxygen saturations less than 50%), bradycardic (<35 beats per minute) and had a brief hypoxic respiratory arrest. He received 1 cycle of cardiopulmonary resuscitation and was intubated. There was subsequently a return of spontaneous circulation.

The next 24 hours involved a period of difficulty with ventilation. His peak airway pressures were very high, despite being paralysed and a low volume/high respiratory rate strategy being employed. He was discussed with a tertiary respiratory centre and it was decided that he should be transferred for insertion of a pumpless arteriovenous interventional lung assist (for extracorporeal carbon dioxide removal) as a bridge prior to lung transplantation. He had formal ultrasound measurement of his femoral arteries. His left common femoral artery was widely patent (AP and transverse diameter of 8-9mm throughout), but the right was only 4-5mm throughout.

In the meantime, his peak airway pressures were consistently between 35 and 40cmH2O, despite tidal volumes of 230ml, 3.8ml/kg). With a rate of 32-35 breaths per minute, his pH was  initially maintained above 7.2, with a pCO2 of 9-11kPa. Over the course of the next few hours, this became increasingly difficult to achieve. His oxygen requirements did not escalate (an FiO2 of 0.6 provided a pO2 of 8-9kPa). When his pCO2 increased to 15.4kPa and his pH dropped to 7.17, further adjustments were made and the PEEP decreased to 5cmH2O from 10cmH2O. His noradrenaline requirements were increasing and with the aid of the cardiac output monitoring, he was cautiously given fluid with a good response.

He was transferred to the centre in which a lung transplant could be performed within hours of the referral. A Novalung device was inserted and he underwent a bilateral lobar lung transplant several days later. He was in hospital for 6 weeks and made a very good long-term recovery. At six months, he was extremely well and was undertaking his activities of daily living completely normally with stable lung function. He even managed to complete an eight mile bike ride.

What is the rationale for extracorporeal lung assist?
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Declining Admission to Intensive Care

An 86 year-old man was referred to ICU because of oliguria, acidaemia and decreased conscious level. He had originally been referred by the general practitioner to the acute general medicine team with unexplained weight loss, malaise and reduced mobility, 19 days previously. He had a longstanding history of bronchiectasis and COPD. He had been able to mobilise independently around his house and garden until suffering a pneumonia several months before this admission, and since required a four-times-daily care package.

During the current admission the patient had been treated for a further pneumonia on the basis of new chest x-ray changes, breathlessness and raised inflammatory markers. He had also undergone a CT chest/abdomen/pelvis for the unexplained weight loss. This was consistent with chronic COPD and bronchiectasis but no other positive findings. A week prior to ICU referral he was found to have acute kidney injury (creatinine 280 µmol/mL, baseline 90 µmol/mL) which had failed to improve. In the 24 hours prior to referral had become progressively drowsy and oliguric.

The patient appeared frail, cachectic and oedematous. He groaned in response to voice and could not follow commands. He had Kussmaul breathing at a rate of about 18 breaths per minute with SaO2 of 91% on 35% oxygen via facemask. Arterial blood gas showed pH 7.09, pCO2 7.1 kPa, pO2 9.1 kPa, base excess -9.3 mEq/L, lactate 1.3 mmol/L, glucose 8.7 mmol/L, creatinine 294 µmol/mL. His chest x-ray showed persistent bilateral patchy consolidation. He had a blood pressure of 98/55 mmHg with a pulse of 110 beats/min and cool peripheries. ECG showed sinus tachycardia. He was afebrile. Abdomen was soft and a urinary catheter had drained only 25 mL in the last 4 hours. Other than reduced responsiveness, neurological survey was non-diagnostic.

Evaluation of this patient revealed an elderly man who was severely unwell with acute kidney injury, probable sepsis, and a poor response to treatment to date. This was on the background of chronic suppurative lung disease, and diminished health for several weeks. No specific treatment limitations were in place. His next-of-kin was unaware of any prior expressed wishes and was under the impression that the patient would prefer active treatment. The referring team were of the opinion that intensive care should be considered.

Although no unifying diagnosis for this gentleman’s kidney injury had been identified, a single, rapidly-reversible condition was not apparent. The principal indication for intensive care was for renal replacement therapy for an unknown duration. In view of the status of his neurological, respiratory and cardiovascular systems, it was deemed that airway protection, invasive respiratory support and vasopressor treatment would almost certainly be required. His overall health status made the prospect of survival from a prolonged period of multi-organ support on intensive care highly unlikely. After discussion with the intensive care consultant and the referring consultant it was decided to withhold admission to the intensive care unit. Appropriate family discussions were held. The patient was actively managed on the ward for a further 12 hours, after which fluid management, antimicrobials and further investigation were ceased. He died the following day.

What uncertainties do we face when declining admission to intensive care?Read More »

Transplantation After Brainstem Death

A 38-year-old previously fit man suffered a grade five subarachnoid haemorrhage. Attempts at coiling failed and he suffered a catastrophic rebleed on-table whereupon his pupils became fixed and dilated. After a suitable sedation washout period he underwent testing which confirmed brainstem death at which point he was referred to the specialist nurse for organ donation. Following counselling of the family and appropriate assessment, donation of his kidneys, liver and heart was agreed.

Upon confirmation of brainstem death, mechanical ventilation was continued to ensure PaO2 greater than 10 kPa and limit peak inflation pressure to less than 30 cmH20. Vasoactive support was switched from noradrenaline to vasopressin 0.02 iu/kg/min. Methylprednisolone and intravenous triiodothyronine were administered whilst awaiting harvest. Blood antibody testing for HIV1+2, Hepatitis B and C, HTLV-1 and CMV IgG were all negative. A transthoracic echocardiogram confirmed good biventricular function; following discussion with the transplant retrieval team a pulmonary artery catheter was floated. Clinical measurements of cardiac output and mixed venous oxygen saturation were satisfactory. Adequate hydration was maintained with crystalloid by infusion and glucose control optimised in the range 8-10 mmol/L with insulin. The dedicated retrieval team performed the organ retrieval eighteen hours after confirmation of brainstem death.

How can we optimise organ function for organ donation?Read More »

Advance Directives

An elderly man presented to hospital with an acute abdomen. He was fit and well, with a background of well-controlled hypertension and chronic back pain. He had previously had admissions with a recurrent gastric volvulus, each time it had resolved spontaneously.

A CT scan was performed and revealed a gastric volvulus which was decompressed endoscopically. He was transferred to the high dependency ward post-procedure for observation as it was deemed high risk for recurrence and therefore likely that he would need surgery to correct it. Overnight he required increasing amounts of fluid and analgesia and suddenly deteriorated with a tachycardia, rising lactate and peritonitic abdomen. He was taken for an emergency laparotomy and had a gastrectomy. A feeding jejunostomy was inserted during the procedure.

The post-operative course involved a period of septic shock and multi-organ failure. He remained intubated, on a noradrenaline infusion and was receiving CVVH for renal failure. On the third post-operative day, despite a 24 hour sedation hold, he was showing no sign of any neurological recovery and was not eye-opening or obeying commands. It was at this point that his wife presented the team with an advance directive.

The advance directive was presented at a point in the care whereby the patient was already receiving high levels of support for his cardiovascular system (noradrenaline 0.3mcg/kg/min), respiratory system, renal system (CVVH) and gastrointestinal system (jejunostomy feed). It was discussed and a plan was made to, for the current time, continue management, but it was explained that the outlook was bleak.

His renal function worsened over the next few days (urea 27, creatinine 400) and despite a long sedation hold, he was still unable to obey commands. However,care was continued as both the cardiovascular and respiratory support was decreasing, with the noradrenaline having been weaned by day 6. He was extubated by day, but remained mildly confused and agitated. The following day, he became more tachycardic, tachypneoic and hypotensive. He deteriorated significantly to the extent where he became peri-arrest and was re-intubated. A CT confirmed an intra-abdominal/mediastinal catastrophe.

He once again developed severe septic shock with multi-organ dysfunction. His antiobiotics were restarted (meropenum) and an anti-fungal (fluconazole) introduced. NJ feed was commenced. He improved to the point of extubation on day 11, but again deteriorated. At this point, a decision involving his wife was made to palliate him. He died later that day

What are the implications of advance directives on the ICU?Read More »

High Dose Insulin Infusion for Calcium Channel Blocker Overdose

A 24-year-old was admitted following an intentional overdose of 10mg amlodipine tablets following an argument with his family. Approximately 10 tablets were ingested. On self-presentation two hours after the event, he was clinically stable with no haemodynamic compromise. There was no airway or respiratory compromise and a 12 lead electrocardiogram demonstrated sinus rhythm at 98 beats per minute. Both an arterial blood gas and electrolyte analysis were normal. Ionised calcium was 1.14 mol/L.

Over the following two hours he developed hypotension down to a nadir of 58/32 mmHg without change in heart rate or rhythm or the development of metabolic abnormalities. This was initially treated with intravenous fluids without significant response. A bolus of calcium chloride was administered without success; at this time he was referred to the intensive care team for assessment. Careful clinical examination revealed no other abnormality except hypotension. Neurological function remained intact and there appeared to be a vasodilated state with warm peripheries and relative tachycardia at 110 beats per minute in sinus rhythm.

The patient was transferred to the intensive care unit where an infusion of noradrenaline was commenced, rapidly escalating to a rate of 0.92 mcg/kg/min with little improvement in mean arterial pressure beyond 30-40 mmHg and relative oliguria. After consultation with the National Poisons Service, a high dose infusion of actrapid was commenced at rate of 0.5 units/kg/hour, with subsequent improvement of his haemodynamic parameters and a reduction in his noradrenaline requirement. Over the following 4 hours, both this infusion and the noradrenaline infusion were subsequently weaned off. The patient was discharged to the ward after eight hours and after assessment by the psychiatric team, from hospital the following day.

What are the clinical features of calcium channel blocker overdose and what is the role of high dose insulin infusion?Read More »

Attempted Suicide and Treatment Withdrawal

A elderly man  was found unconscious at home having taken an overdose of prescription medication. This event may have been precipitated by a recent bereavement and worsening of his preexisting depression for which he had recently been reviewed by psychiatric services and commenced on an SNRI. He left a note at the scene of the suicide attempt, clearly stating that he intended to take his own life and did not wish to be resuscitated in the event of being found alive. He was discovered in his home by a relative who had been growing increasingly concerned as to his welfare, having not spoken to him for several days. On arrival in ED his Glasgow coma score (GCS) was 3/15. He was known to be taking venlafaxine for depression and amitriptyline for chronic back pain, and empty packets of each drug were found at his home.

He was intubated and transferred to the intensive care unit. Supportive care was provided including vasopressors (noradrenaline) for hypotension, electrolyte correction and ventilatory support. Plain chest radiograph showed a probable aspiration pneumonitis affecting the right upper and middle lobe. He was hypoxic with a high Fi 02 requirement and needed high levels of PEEP to maintain adequate oxygenation. His conscious level fluctuated over several days and he became increasingly agitated and exhibited signs of distress. At this stage it was not clear if he was orientated in time, place or person. He underwent percutaneous tracheostomy to facilitate weaning and reduce sedation requirements.

We were then able to wean him from sedation by day 11 of his admission. The patient’s ventilatory requirements were still high requiring mean airway pressures of 30 cmH2O, PEEP of 10 cmH2O, and an inspired oxygen concentration of 60%. At this stage he indicated to the ITU team that he did not wish treatment to be continued. We found him to be fully orientated in terms of time and place and he was aware of the preceding events and his intentional overdose. It was clearly explained to him that if treatment were discontinued he would die. He indicated to us that he had no intention of changing his mind.

We referred him to the liaison psychiatrist for the hospital who independently assessed and found him to be competent and able to fully understand the implications of such a decision, i.e. his likely death from respiratory failure. The psychiatrist also found him to be depressed but noted that this did not interfere with his competence and ability to give or withhold his consent. With his consent, his family were informed of this development. They had been agonizing for some time over whether they had made the right decision to call emergency services when they first found him. They attempted to dissuade him but his resolve was unshakeable. Invasive ventilation was withdrawn on the morning of his 15th day of ITU as per his wishes. Diamorphine was administered to reduce symptoms of respiratory distress. He died of hypoxia later that day. Cause of death was recorded as aspiration pneumonia.

Describe the ethical and legal framework utilised in the management of this patient.Read More »

Major Haemorrhage and Recombinant Factor VIIa Concentrate

Major Haemorrhage and Recombinant Factor VIIa Concentrate

A 40-year-old female intravenous drug user presented with a diffusely swollen right lower leg. She had injected heroin into her right thigh one week previously. The swelling started 3 days later. Initial observations revealed T 39.6, HR 135, NIBP 100/87, RR 32, Sats 96% on air. On examination, she was pale and sweaty. She had a swollen right lower leg with mottling of her foot and poor pedal pulses. Following initial fluid resuscitation, chest X-ray, cultures and broad-spectrum antibiotics (Flucloxacillin, Metronidazole and Gentamicin), she underwent CT angiogram of her lower limbs which showed oedematous and expanded muscle compartments of the thigh and calf but patent arterial flow to the feet. There was also right common femoral vein thrombosis with some vessel patency. Initial labs revealed neutrophilia (9.2), thrombocytopaenia (16) and deranged coagulation (PT 16, APPT 33, Fib 2.6). CK was 57000. She underwent right leg fasciotomies and was brought to ICU ventilated and on Noradrenaline to maintain MAP >65. She commenced Immunoglobulin IV 1gram/kg per day for 2 days for suspected Streptococcus Group A sepsis. That night she had massive transfusion requirements due to ongoing haemoserous ooze from her fasciotomy sites, losing up to 1 litre of haemoserous fluid per hour. Overnight she received 10 units RCC, 8 x FFP, 6 x Platelets and 2 x Cryoprecipitate, as well as Vitamin K (guided by Hb on ABG, formal lab results and thromboelastography). She was discussed with the Haematology Consultant and it was decided that, if rapid blood loss continued despite full correction of her clotting factors, fibrinogen and platelets then Factor VII could be given. However, over the next 2 hours, losses were much reduced following product replacement, and since she already had clot in her femoral vein, Factor VII Concentrate was not given.

What is the role of Recombinant Factor VIIa in major haemorrhage?

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