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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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 »

Mechanical Ventilation of Chronic Obstructive Airways Disease

A 68-year-old went into respiratory arrest on the chest ward. He had been admitted 2 weeks previously for an exacerbation of chronic obstructive airways disease (COAD). He has had two previous episodes of reduced conscious level due to hypercapnoea, which resolved with non-invasive ventilation and oxygen titration.

He was immediately intubated on the ward and transferred to the intensive care unit for ventilation. Hypoxia was corrected to a PaO2 >8.0kPa with a moderate FiO2. However he remained very difficult to ventilate and maintained a persistently high PaCO2. The highest level was 21kPa. He was treated with B2 agonist nebulisers, anti-muscarinic nebulisers, systemic steroids, aminophylline infusions, magnesium infusions and a ketamine infusion. He also needed vasopressor support and for a period of time continuous renal replacement therapy. After a week when his ventilator pressures reduced he had an uneventful percutaneous tracheostomy. Sedation was then reduced and he was awake and spontaneously breathing but with a high level of support. He was recurrently troubled by episodes of bronchospasm and air trapping. The lowest settings for inspiratory pressure were 14 cmH2O. He deteriorated a number of times before care was withdrawn and he died 20 days later.

Can we predict which COAD patients will benefit from mechanical ventilation?

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Post Operative Cognitive Deficit after Cardiac Surgery

A middle-aged  man underwent an elective re-do aortic arch replacement for a 6.1cm ascending aortic aneurysm distal to a pre-existing composite graft. Past medical history included a Bentall procedure (metallic aortic valve replacement, aortic root and ascending aorta replacement with coronary re-implantation into the composite graft) 20 years ago. Preoperative echocardiogram showed a well seated AVR and good biventricular function. Drug history included Warfarin (target INR 2-3) and Atenolol.

Anaesthetic induction and re-sternotomy were uneventful. Cerebral oximetry (rSO2) monitoring was utilized in this case. Cardiopulmonary bypass (CPB) was achieved uneventfully and deep hypothermic circulatory arrest (DHCA) was instituted. The patient was cooled to 18°C using CPB and icepacks. Prior to CPB and DHCA being commenced, intravenous thiopentone and methylprednisolone were administered for neuroprotection. Total DHCA time was 40 minutes and selective anterograde perfusion via the right axillary artery (chosen as it is relatively free of atheroma) was employed when rSO2 dropped to <40% and they remained >40% for the remainder of DHCA. Total CPB time was 105 minutes.

Following successful insertion of a new graft, the patient was carefully rewarmed to normothermia and weaned off CPB uneventfully, only requiring minimal vasopressor support. The patient was transferred to the cardiothoracic critical care unit.

After optimization of cardiorespiratory physiology, correcting coagulopathy and maintaining normothermia, with strict avoidance of hyperthermia, the patient was extubated the following day. For the first 48-72 hours postoperatively, delirium was the most active medical issues and this was managed according to conventional treatment. There was no focal upper or lower limb neurology. The patient did not require any other organ system support.

Following resolution of his delirium the patient was discharged to the ward to continue his rehabilitation. Prior to discharge, at approximately postoperative days 7-10, he was complaining of loss of short-term memory, reduced attention span and difficulty with finding words. A neurology review attributed this to cognitive dysfunction but no formal tests were carried out. A neurology clinic follow-up and an outpatient MRI scan were arranged.

What are the neurological complications after cardiac surgery?Read More »

Scoring Systems for Acute Hepatic Dysfunction

Scoring Systems for Acute Hepatic Dysfunction

A 40 year old was admitted to hospital with his first presentation of alcoholic liver disease with symptoms of jaundice (bilirubin 248), poor mobility, hallucinations and passing of black stool. On admission to hospital, he was lethargic with features of Grade II encephalopathy, was coagulopathic (INR 3.1), had deranged electrolytes (sodium 114, potassium 2.9), but a normal creatinine (54) and a raised white cell count (15.9). He was haemodynamically stable and had a haemoglobin of 119g/L with no signs of active bleeding. His abdomen was distended (ascites), he was visibly jaundiced and had spider naevi on his chest. An abdominal ultrasound was performed that showed liver cirrhosis, borderline splenomegaly, small volume ascites and normal kidneys. A full liver screen revealed no infective cause and his AST:ALT ratio suggested alcoholic liver disease. His prognostic indicator scores were all suggestive of severe alcoholic liver hepatitis (Maddrey score: 131; Childs: C; Lille Score: 1; GAHS: 10; MELD: 29). His serum ammonia level was 170. He was commenced on terlipressin, prednisolone and pentoxyphylline and thiamine. Despite this, his encephalopathy progressed to grade 4 and he required intubation and ventilation for airway protection and a presumed aspiration pneumonia. His liver function and coagulopathy continued to worsen, and he developed an acute kidney injury necessitating commencement of renal replacement therapy. He required noradrenaline to support his blood pressure. Ascitic tap ruled out spontaneous bacterial peritonitis. He was discussed with regional liver centres, but was not felt to be a transplant candidate. His liver and renal function continued to deteriorate and eventually treatment was withdrawn nearly 3 weeks into his admission.

Describe the scoring systems for assessing the severity of acute hepatic dysfunction.

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Rapid Response Systems

Rapid Response Systems

An elderly man was admitted with an acute abdomen and free air visible under the diaphragm on CXR. He was fluid resuscitated before undergoing emergency laparotomy, where a perforated duodenal ulcer was oversewn. He was admitted to ICU postoperatively, extubated the next morning and deemed fit for discharge to the surgical ward later that day. Due to a lack of surgical beds, he was eventually discharged from ICU at 22:30. Eight hours post discharge, he was urgently re-referred to ICU after being found moribund on the ward. Before he could be seen and assessed he suffered an unrecoverable asystolic arrest. Review of his observation charts showed that there had been a clear deterioration in recorded observations, including hypotension for the two preceeding hours. However, the Early Warning Score had been calculated incorrectly, and no escalation had occurred.

What evidence is there that rapid response systems are effective in preventing patient deterioration and improving outcomes?

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Lactate Physiology and Predicting Disease Severity

Lactate Physiology and Predicting Disease Severity

A middle aged man presented with urosepsis after several days antibiotic therapy in the community. He was in septic shock, with tachypnoea, tachycardia and hypotension. He had raised inflammatory markers and acute kidney injury. His initial lactate level was 14mmol/L with a significant metabolic acidosis (base deficit 21). He was commenced on iv antibiotics, noradrenaline and renal replacement therapy. Lactate levels cleared to less than 2mmol/L over the next 24hrs. He weaned off noradrenaline in 72 hours and CVVHDF over the next 5 days.

How is lactate produced and what is its significance in predicting the severity of critical illness?

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Neuroprognostication Post Cardiac Arrest (Post TTM Era)

Neuroprognostication Post Cardiac Arrest (Post TTM Era)

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?

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Intensive Care Acquired Weakness

Intensive Care Acquired Weakness

A cardiovascularly fit 65 year old man was admitted with septic shock secondary to community acquired pneumonia, which progressed to multi-organ failure. During his recovery it was noted that he had generalised weakness with no focal neurology. He underwent respiratory weaning, and rehabilitation therapy over the next 4 weeks but had persistent weakness at his ICU discharge.

How can ICU-acquired weakness be diagnosed and managed?Read More »

Therapeutic Hypothermia after Cardiac Arrest (Post-TTM)

Therapeutic Hypothermia after Cardiac Arrest (Post-TTM)

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 »