This podcast episode features a conversation between Dr Oli Flower and his AI co-host, Simon (ChatGPT 4o), focusing on vasospasm and delayed cerebral ischemia (DCI) in aneurysmal subarachnoid haemorrhage (aSAH). The discussion covers:

• The distinction between radiological vasospasm (imaging finding) and DCI (clinical syndrome).
• The evolution of understanding DCI’s multifactorial causes, beyond just vasospasm.
• Evidence and controversies around ICU management, including blood pressure targets, nimodipine use, and the role of other interventions.
• Screening and monitoring strategies: transcranial Doppler, CTA, CTP, and the limitations of each.
• Post-management assessment, therapeutic hypertension, and the emerging role of milrinone.
• The importance of multimodal monitoring and the future potential of AI and global data sharing.
• The episode closes with a lighthearted off-topic discussion about casting for the new Naked Gun movie.

The conversation is rich in clinical nuance, highlights current evidence gaps, and emphasises the need for individualised patient care and ongoing research.

Catherine Bell takes us through how to troubleshoot problems commonly encountered when looking after patients who have an external ventricular drain (EVD) in situ. Issues with using brain tissue oxygen monitors are also discussed. A highly practical session aimed at bedside clinicians.

This presentation was delivered by Catherine Bell at CODA2022. Want more content about EVD? Visit neuroresus.com or subscribe to be notified of new podcast releases via email.

To express your interest in attending the 2024 Neuroresus live course, click here. 

Stuart Browne is a Neuro Rehab specialist from Sydney. He discusses what "severe disability" really means. 

Severe disability is more common than many realise - about 6% of the Australian population.

Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated.

He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being.

Stuart also covers how severely disabled people face various forms of discrimination.

This podcast was recorded at the Brain Symposium which took place in March 2023. For more talks and content like this, visit neuroresus.com or subscribe to be notified of new podcast releases via email.

To express your interest in attending the 2024 Neuroresus live course, click here. 

Acute liver failure for the intensivist by Dr David Anderson

The understanding around the metabolic response to the stress of critical illness has evolved rapidly over the past decade. 

This involves a neuroendocrine and an inflammatory component, which results in perturbations within the sympathetic nervous system, the hypothalamo-pituitary axis and the immune system. 

The clinical consequences are widespread and include changes in metabolic rate, altered use of macronutrients as energy sources, stress hyperglycaemia, muscle wasting and changes in body composition. Many of these manifestations are akin to the metabolic syndrome observed in ambulatory populations. Medium to long-term effects of these metabolic disturbances involve bone health, cognitive and behavioral alterations. 

Knowledge of these effects is relevant due to the potential therapeutic implications, which will be discussed. 

What the boss wants: getting a consultant job by Dr Priya Nair & Dr Ray Raper

The Australian population away from metropolitan areas has the same health care needs and deserves the same level of care (within available resources) as urban residents: we can and should provide it.

This short talk aims to explore work in a non-tertiary centre ICU as a career option and why it’s worth considering.  It will look at what life and work are really like in non-metropolitan areas and how and why working in a regional ICU can be a rewarding career.  It will try and dispel some misconceptions as well as present some of the challenges (and how to overcome them) that arise while working outside capital cities.  This is meant to be a light-hearted look at living and working in the bush or on the beach and an insight into a career path often overlooked by city-based trainees, not a hard-core recruitment drive or a critique of urban life/tertiary centre work.  Come along with an open mind and have a look: you may discover a lifestyle and workplace you didn’t realise could suit you, for the short or longer term.

To pass the Second Part Exam, your performance needs to be at the expected level for a junior consultant. You need to be able to rapidly synthesise clinical information from multiple sources to reach a differential diagnosis and appropriate management decisions. (And achieve this while feeling the equivalent of standing at the top of an Olympic downhill ski-run, simultaneously suffering from a severe bout of gastro.) 

Some general pointers include: 

Get experience running the unit and calling the shots 

Establish a good knowledge base - don’t just practice SAQs 

Write and share your own SAQs and Vivas 

Make every case you see at work a practice Hot Case 

Teach everyone else 

Consider performance coaching  

Finally, if things don’t go to plan the first time, remember it’s an exam not a statement on who you are as a person. Work out what worked and what didn’t and why to change your approach and come back stronger. 

Tips and tricks for getting through the first part: Examiner’s perspective

10% of patients admitted to ICU die and, in some societies over 80% of people die during a hospitalization that included an ICU stay.  Most deaths in ICU are predictable and the overwhelming majority of patients are comatose for the last few days of their life.  Most communication by intensivists is directed at families rather than patients.  This talk will cover some scenarios where this isn’t the case and give guidance on delivering bad news to and discussing organ donation with awake patients.

According to the World Health Organization Training Package for the Health Sector (2008), ‘Children are not little adults’ and specialised care must be targeted to pediatric patients in order to optimize outcomes. In a review of Australia and New Zealand Paediatric Intensive Care (ANZPIC) Registry data from 2006 to 2016, approximately 1600 children <16 years old were admitted each year to one of 21 adult ICUs in Australia and New Zealand who voluntarily submit data. This represents at least 17% of all children (<16 years) admitted to an ICU for care. Respiratory etiology of critical illness was the most common reason for admission (48%), followed by neurological diagnoses (15%) and trauma (11%). According to the ANZPIC data, children from 1 month to 5 years old make up 61% of the admitted patients. Of the total 17 686 children admitted to an adult ICU over the 11 year period, 15 727 (89%) were discharged home directly, 330 (2%) died in the adult ICU, and 1625 (9%) were transferred to tertiary PICU for ongoing care. This data suggests that modern Australia and New Zealand adult ICUs provide a significant proportion of Intensive Care therapies to Australasian children. In this session we will discuss some of the key anatomical, physiological and developmental differences of relevance to critical care of the infant and child. In particular, the translation of common intensive care principles will be highlighted to empower well trained adult intensive care physicians to apply their skills and knowledge to critically ill children.  

You are called to see a 62-year old male now 3 hours post CABG x 4 with hypotension and escalating vasoactive requirements. As you arrive to the bedside, he arrests. How do you manage this situation?  

This talk outlines the management of cardiac arrest in the intensive care unit post open heart surgery, as per the CALS (Cardiac Advanced Life Support) algorithm. Key differences from the standard ALS (Advanced Life Support) algorithm are highlighted, including delaying CPR by up to 1 minute to troubleshoot the initial rhythm, the role of emergency resternotomy, and avoidance of 1mg doses of adrenaline.  

The prevalence of degenerative valvular disease is increasing in the context of an increasingly ageing population, and despite advances in medical and surgical interventions, is associated with a significantly worse outcome when compared with the general population. Data from the EuroHeart Survey (2003) suggests the commonest relates to native valve disease (predominantly aortic stenosis) however, more than one quarter of patients with valve disease have undergone a previous intervention. According to current guidelines, in general treatment for severe, symptomatic aortic stenosis is surgical aortic valve replacement, which is associated with excellent outcomes, however, despite this around 30% of such patients do not undergo surgical intervention.

The last decade has seen a significant change in the potential therapeutic options for patients with aortic valve disease due to the development of transcatheter techniques for valve implantation. Patented in 1991, the first successful human implant of a transcatheter aortic valve was undertaken in 2002, with currently >500,000 implantations having been undertaken in >70 countries worldwide. The evidence supporting transcatheter aortic valve implantation (TAVI) otherwise known as transcatheter aortic valve replacement (TAVR) came originally from the key PARTNER studies, where patients judged to have inoperable aortic stenosis who underwent TAVI having improved survival and a reduction in hospital admission at 1 year. Following the early safety and efficacy studies, and following increasing recommendations for TAVI as an option for patients at high risk in international guidelines, the use of transcatheter techniques is extending to those of lower risk.

Shree Basu is a Paediatric Intensivist in Sydney. She discusses how Paediatric stroke presents, what neuroimaging is required and what interventions are available, including thrombolysis and the role of endovascular thrombectomy.

The blood pressure targets in ICU are discussed; while there isn’t strong evidence to support these targets, it does make sense and is a separate hot topic in adult strokes, especially post ECR!

This podcast was recorded at the Brain Symposium which took place in March 2023. For more talks and content like this, visit neuroresus.com or subscribe to be notified of new podcast releases via email.

The title of the talk is emblematic of the binary way that we have approached structural heart disease where cardiac surgery or an interventional procedure might be required – this thinking is now transitioning to an entirely different paradigm which is that of the “Heart Team”. 

Remarkable advances over the last decade have led to a plethora of interventional options for both coronary and structural heart disease. In the coronary realm, as complex and high risk PCI options continue to evolve, the role for surgery in multi-vessel disease, diabetes and LV dysfunction has become well established. Hybrid revascularization options also evolve and are the subject of ongoing investigation. In structural heart disease, as TAVR application expands to a low risk subset, ongoing investigations will answer questions regarding durability of TAVR as compared to the historical surgical gold standard. Mitral valve repair remains the gold standard for degenerative MR and the Mitraclip has become a well-established option for a high-risk subset. Ongoing studies will answer the role of Mitraclip in functional MR and excitingly multicenter studies are investigating a role for transcatheter mitral valve replacement for mitral valve disease. The role of surgery in tricuspid valve disease, a large and underserved subset remains controversial and transcatheter devices remain investigational at this point. The reality is that decision-making is complex and central to the entire debate is the heart team concept, whereby surgeons and interventionalists sit at the same table as part of the same team to determine the best approach for any given patient. As evidence continues to evolve, lines between cardiac surgery and interventional cardiology continue to blur, with combined expertise from both sides going forward required to best serve our patients in a truly heart team approach.  

CARDIAC REVASCULARIZATION SURGERY IN THE ELDERLY: AN EVIDENCE-BASED HEALTH ECONOMIC APPROACH 

Background: Increasing prevalence of chronic disease in the context of an ageing society has led many to question the value of cardiac revascularization surgery and associated intensive care in elderly (octogenarian) populations. However societal expectations of improved technology and its likely impact on longevity and improved quality of life suggest there is a demand for cardiac surgery in this population. Elderly people are more likely to hold private health insurance, therefore the cost (in terms of waiting time) is likely to be low.  

Objectives: This presentation will consider the value of cardiac revascularization surgery from a health economic perspective, including the various perspectives of patient, family/significant others, providers, healthcare sector and society.  

Method: A theoretical evidence-based health economic model will be presented that is relevant to the evaluation of cardiac surgery in an elderly population. This will be combined with a review of the literature and existing data sources as evidence-based inputs into the development of an economic model to assess cost effectiveness in terms of cost per quality adjusted life year saved. Studies included will be recent published trials (post 2010) where costs and/or quality of life outcomes have been compared between cardiac surgery and conservative management in an elderly (80+ years) population.  

Results/Conclusion: Recent literature and study results will be reviewed against the theoretical health economic model. Where evidence and/or data exist that meet inclusion criteria for the economic analysis these will be summarised in the model. Where gaps in evidence exist these will be highlighted, including appropriate strategies to address data deficiencies.  

A/Prof Jennifer Watts 

Health Economics 

Faculty of Health  

Deakin University 

Introduction: Recent times have witnessed almost half, or sometimes more cardiac surgical procedures are performed in patients above 75 years of age. Traditionally, the EuroSCORE II and STS risk scoring systems have been widely used across the globe. Extensive reviews have shown that EuroSCORE II probably overestimates the perioperative risk at lower score levels while the STS score tends to underestimate the risk. 

Frailty is a broad term that encircles aspects of nutrition, lack of agility, inactivity, lack of strength and wasting; and is seen in 25-50% of elderly patients. It has been defined as a geriatric syndrome reflecting a state of reduced physiological reserve and increased vulnerability to poor resolution of homeostasis after a stressor event. Conversely, pre-frailty, which is potentially reversible, is associated with higher risk of older adults developing cardiovascular disease. 

Frailty assessment includes a variety of physical and cognitive tests, functional assessments and evaluating nutritional status. Literature has highlighted what is referred to as the ‘obesity paradox’, meaning obese patients with heart failure fair better than leaner patients, possibly because they have more metabolic reserve and also because weight loss in itself is a risk factor for frailty. 

Patient Selection: To comprehensively assess a patient, factors that describe the biological status of the patient should be incorporated. There are various methods of assessment and modified Fried criteria or comprehensive assessment of frailty are a couple of systems commonly used. 

Conclusion: Systematic reviews have shown that frail patients have higher chance of mortality, major adverse cardiac and cerebrovascular events and functional decline after cardiac surgery. A holistic assessment not only categorises patients into the apt risk category and hence match goals and treatments; but also, will pick up patients with pre-frailty who will benefit from multidisciplinary intervention and be better prepared for the intervention.  

"The real benefit to the patient [of echocardiography] is not the technical skill, but rather the application of intellectual input... information, communication and teamwork are essential" Jos Roelandt, 1993

Of all the imaging techniques used in intensive care, echocardiography has come to the fore, in particular due to its accessibility, immediate availability and applicability as a point-of-care technique, thereby removing the risks of transportation of the critically ill. Over the preceding 20 years evidence has continued to emerge for its extended use in the acute/emergency setting, to the extent that it is now included in national and international guidelines relating to the universal definition of myocardial infarction, as well as in shock pathways, and as an adjunctive technique in advanced life support. Its potential scope is huge, with applications relating to monitoring, cardiac pathophysiology and coronary perfusion as well as its more evident use to define cardiac anatomy.

The three main uses of ultrasound to interrogate the heart relate to the way in which the technique is used: first, as an extension to the clinical examination using binary questions and 2D imaging only (focused cardiac ultrasound, FoCUS) which forms the basis of 'basic' techniques. Second, incorporating the full range of echocardiographic techniques for diagnostic capability (echocardiography), and third, selective application of the full range of techniques in order to answer specific questions raised in the critical care/emergency arena (targeted echocardiography). This includes speckle strain/strain-rate to determine abnormalities of myocardial function suggestive of myocarditis, calculation of myocardial electromechanical efficiency in order to maximise cardiac output, recognition of parameters that suggest restrictive right ventricular physiology, with the requirement for modification of ventilatory techniques and parameters, detection of myocardial ischaemia, estimation of LVEDP and LAP, and its application in the institution, monitoring and weaning of mechanical circulatory support.

Key questions for the clinician undertaking echocardiography in the critical/acute/emergency setting can be summarised in a checklist format, which includes:

Background questions:

1. What is the clinical context?
2. What does the treating clinician want to know (ie why won't the patient wean from mechanical ventilation? or is this pulmonary oedema, and if so, why?).
3. Can echocardiography answer the required question, and what is the accuracy in this setting?
4. What is the underlying diagnosis (cardiac and non-cardiac)?
5. How is the patient being sedated/ventilated/supported

Specific echocardiographic data:

1. What is limiting the cardiac output/elevating the venous pressure?
2. Is the left atrial pressure elevated?
3. Is the heart rate/AV delay/VV delay appropriate?
4. Is there any other relevant information that the treating clinician needs to know that may inform planned interventions?

To reach its full potential in the critical arena demands therefore not only understanding of the whole range of echocardiographic techniques, but also the confounding factors that will be found in this setting, including filling status, ventilatory parameters, mechanical support and the use of vasoactive agents. Although frequently 'simplified' for application in FoCUS, expert echocardiography in this setting can be extremely challenging, and the potential to cause harm to the patient through misinterpretation should not be underestimated.

The goal of hemodynamic monitoring is to assess the cardiovascular state of the patient, define their reserve and monitor response to treatments and time.  Resuscitation efforts are essentially aimed at restoring and sustaining tissue wellness through maintaining an adequate amount of oxygenated blood flow to the metabolically active tissues. We need to monitor pressure, flow and function. To accomplish these goals one must be able to measure arterial pressure and all its components (i.e. waveforms), cardiac output and stroke volume as well as the adequacy of flow. Presently, there are several devices that can estimate the arterial pressure waveform from a finger plethysmographic device. They are very accurate until profound circulatory collapse makes peripheral pulse not representative of central pressures. These devices can also estimate stroke volume by intuiting the arterial pressure waveform in a fashion similar to that performed by the numerous minimally invasive hemodynamic monitoring devices we now have now. These non-invasive devices can quantify functional hemodynamic monitoring dynamic parameters. Also, pulse oximeter pleth density signals vary with pulse volume into the finger or skin and the pleth variability can also be used as a surrogate of pulse pressure variation. Furthermore, bioreactance can measure both cardiac output and intrathoracic fluid content through surface electrodes. Finally, end-tidal CO2 transiently varies with venous return, increasing if blood flow increases. So both eh bioreactance device and end-tidal CO2 can be used to identify cardiac output changes in response to a passive leg raising maneuver. Thus, one can measure arterial pressure waveforms and cardiac output continuously, assess volume responsiveness and monitor therapy. Finally, the dynamic changes in tissue O2 saturation (StO2) measured by near infrared spectroscopy of the thenar eminence during a vascular occlusion test defines peripheral circulatory insufficiency and local blood flow independent of arterial pressure.  Furthermore, heart rate variability decreases with increasing cardiovascular stress and can be readily measured in real time from the R-R intervals of the surface ECG signal.  Finally, the measure of urine output, skin temperature and sensorium all define effective tissue blood flow as reasonable end-points to resuscitation, if the patient is not overwhelmingly ill. When these measures are coupled to a treatment approach know to improve outcome, there is little reason to believe that such completely non-invasive approaches will be inferior to invasive ones in the management of the critically ill patient. 

Many tools are nowadays available to monitor patients’ hemodynamics in the intensive care unit (ICU) and in the operating room (OR) settings. Some monitoring tools are invasive such as the pulmonary artery catheter (PAC), some others are less invasive such as transpulmonary thermodilution (TPD) systems, some others are called minimally invasive such as uncalibrated arterial pulse wave analysis (PWA) devices, and some others are non invasive such as volume-clamp method, applanation tonometry, esophageal Doppler, bioreactance, CO2 rebreathing, and pulse wave transit time. Recently, the European Society of Intensive Care Medicine has provided recommendations about the use of hemodynamic monitoring in patients with shock. To summarize, except the PAC and the TPD systems, the other hemodynamic monitoring tools are not recommended for the two following reasons: 1) they provide cardiac output but not other important hemodynamic variables, although some of them also provide stroke volume variation (SVV) or pulse pressure variation (PPV), and 2) their validity has been questioned in cases of shock requiring vasopressors. The uncalibrated PWA devices or esophageal Doppler seem to be more suitable in the OR setting when no vasopressor is used. The advantage of the PAC is to provide pulmonary artery pressure and pulmonary artery occlusion pressure. The advantage of TPD systems is to provide global end-diastolic volume (a measure of global cardiac preload), extravascular lung water (a measure of lung edema), pulmonary vascular permeability index (a measure of lung capillary leak), cardiac function index (a measure of systolic cardiac function), PPV and SVV (dynamic indices of fluid responsiveness). The PAC and TPD systems are indicated in cases of shock either when the patient also has a severe ARDS initially or when the shock state does sufficiently respond to the initial therapy administered on the basis of clinical examination, central venous oxygen saturation, carbon dioxide pressure gap, PPV and echocardiography. 

With increasing survival comes morbidity. Pulmonary hypertension in the critical care population represents a secondary disease of myriad pathologies for children and adults. Whilst often cardiac failure or respiratory disease complicated by pulmonary hypertension, the exact aetiology of secondary pulmonary hypertension can be a diagnostic challenge. Yet an understanding of the pathophysiological basis for pulmonary hypertension may allow for patient guided therapy and predictions of reversibility. 

With pulmonary vasodilators of various mechanistic and non-specific sites of action backed by limited disease specific clinical evidence, are we in the jungle treating secondary pulmonary hypertension or can one management regime encompass all critical care patients? 

The right ventricle (RV) is not important, until it is.  Under normal conditions RV function merely keeps central venous pressure low and delivers all the venous return per beat into the pulmonary circulation under low pressure. If pulmonary artery pressures increase due to pulmonary vascular disease (embolism, ARDS, COPD), over-distention (COPD, asthma) or ischemia (embolism, pulmonary hypertension), the RV rapidly dilates decreasing left ventricular (LV) diastolic compliance via ventricular interdependence. Most clinicians presume that the RV is merely a weaker version of the LV, but follows that same rules. But this in not true. Normally, RV filling occurs without any measurable change in RV distending pressure owing to conformational changes in its shape rather than distention of its wall fibers. This effect allows central venous pressure to remain low despite major dynamic change sin venous return associated with breathing. RV ejection is exquisitely dependent of RV ejection pressure. Thus, if disease processes increase pulmonary artery impedance then RV dilation and failure will eventually occur. Furthermore, most of RV coronary blood flow occurs during systole, unlike LV coronary blood flow, which primarily occurs in diastole. Thus, systemic hypotension or relative hypotension where in pulmonary artery pressures equal or exceed aortic pressure must cause RV ischemia. Clinically these findings carry a common end result. For cardiac output to increase RV volumes must increase. If increasing RV volumes also result in increasing filling pressures then RV over distention may be occurring causing RV free wall ischemia. If relative systemic hypotension exists then selective increases in arterial pressure will improve RV systolic function.  Accordingly, fluid resuscitation, if associated with rapid increases in central venous pressure should be stopped until evidence of acute cor pulmonale is excluded. Acute cor pulmonale can be treated by improving LV systolic function, coronary perfusion pressure or reducing pulmonary artery outflow impedance. The normal response of the RV to slowly increasing pulmonary artery pressures is to increase its intrinsic contractility (Anrep effect), but if the pressure load exceeds such adaptation, RV hypertrophy develops in an asymmetric fashion initially in the infundibulum before progressing to the RV free wall and septum. In chronic RV failure, dilation and RV wall thinning occurs as the heart reverts to preload to sustain stroke volume (Starling effect).  Importantly, all these effects and their response to therapies can be assessed at the bedside using echocardiography and pulmonary arterial catheterization.  

The two major causes of acute right ventricular (RV) failure in ICU patients are acute cor pulmonale (ACP) during acute respiratory distress syndrome (ARDS) and ACP during acute massive pulmonary embolism (PE).  

The increase in pulmonary vascular resistance (PVR) in ARDS can be secondary either to « structural » mechanisms related to lung injury per se and to « functional » mechanisms related to the effects of mechanical ventilation with positive end expiratory pressure (PEEP). The latter mechanism is enhanced when PEEP overdistends more than it recruits lung volume and when tidal volume (VT) is high. The recommended protective ventilation with low VT and PEEP adjusted to driving pressure can also reduce the RV afterload. A reduced central blood volume can also play a role in the increase in PVR (extension of the West’s zone 2). In this case, volume administration can reduce the PVR and improve the RV function. Finally, prone positioning also exerts a beneficial effect on RV afterload through a decrease in PVR (lung recruitment, decrease in hypoxic vasoconstriction, increase in central blood volume with decrease in the extent of zone 2).  

In acute PE, RV dysfunction is associated with poor outcome. Thrombolytic treatment, which is indicated in cases of severe PE with shock, prevents hemodynamic decompensation in patients with intermediate risk PE, but also results in increased risk of severe hemorrhage and stroke. In the case of PE with low cardiac output and no RV dilatation, fluid administration can be indicated to improve cardiac output. In cases of systemic arterial hypotension, vasopressors such as norepinephrine can be indicated to restore adequate RV perfusion pressure. Indication of inotropic agents such as dobutamine, which improves the RV-pressure artery coupling should be evaluated individually. Surgical pulmonary embolectomy can be indicated when the thrombolytic therapy is contra-indicated in acute PE with shock.

The use of extracorporeal membrane oxygenation (ECMO), and ventricular assist devices (VADs) for both short-term and long-term management of advanced cardiac (and respiratory) failure is increasing. Both thrombotic and haemorrhagic complications are common in patients receiving mechanical support, and such complications are associated with increased morbidity and mortality. Risks of bleeding and of thrombosis vary over time, and according to technical and patient factors. Careful assessment of the risks and benefits of anticoagulation for each patient is therefore a critical component of successful mechanical support. 

The approach to anticoagulation for patients receiving VADs varies according to stage of recovery and device. In the immediate post-operative period, bleeding is usually a greater risk than thrombosis and a period free from anticoagulation is usually used. Subsequent initiation of anticoagulation is usually with heparin, with the introduction of warfarin and aspirin over a period of days. Current recommendations include warfarin for all continuous flow devices, usually with the addition of aspirin, and in some cases an additional antiplatelet agent. Target INR and platelet inhibition varies with device, and institution. Testing varies according to device also. Potential pitfalls and problems exist, and these will be highlighted in this session, using a case-based approach. 

The management of anticoagulation for patients receiving ECMO varies worldwide, and there are currently limited guidelines. Important factors in decision-making in regards to anticoagulation for ECMO include mode of ECMO, ECMO configuration, ECMO flows, and underlying patient pathology. Strategies for anticoagulation should take each of these factors into consideration. It is also important to recognise that other management techniques to avoid thrombosis are important, such as adequate intracardiac decompression, and promoting cardiac ejection to avoid stasis. Cases will be used to demonstrate important issues and practical management strategies. 

After spinal cord injury (SCI), there aren’t many interventions we have available that actually make a difference. 

Augmenting blood pressure to increase spinal cord perfusion pressure is an attractive concept that may improve neurological outcomes following SCI. We know that hypotension can make SCI worse. Clinical studies looking at blood pressure augmentation are mostly old, retrospective and flawed in various ways. 

Aiming for a MAP of > 85 for 5-7 days is recommended by guidelines but why this pressure and duration are good questions.

Hypertensive therapy is relatively safe and easy to implement but not without risk. 

In this podcast, Tessa Garside discusses the pros and cons, how this is managed practically and what the future may hold in this area.

This is a CODA Podcast that was recorded at CODA2022. Want more content about SCI? Visit neuroresus.com or subscribe to be notified of new podcast releases via email.

Venous thromboembolism (VTE) is one of the most preventable complications in hospitalised patients. Critically ill patients are at risk of VTE due to coexisting of multiple risk factors but, at the same time, often at risk of bleeding. Though not common, fatal pulmonary embolism (PE) continues to occur [1] – due to the alignment of failures (or ‘holes’) in each defensive layer according to the Swiss cheese model [2]. Tackling this is not easy because the pattern of the ‘holes’ in each layer of the cheese is different between patients and, to complicate the matter further, both the size and location of the ‘holes’ also change with time in each individual patient. 

In brief, fatal PE occurs due to one of the three failures – failure to prevent, failure to diagnose and failure to treat (aggressively). It is well established that anticoagulants are very effective in reducing VTE. The golden rule to reduce the size of the ‘holes’ in prevention is to use a multimodal approach, with anticoagulants as a key player. The bottom line is that any anticoagulants, even at a reduced dose, is better than no anticoagulant. Judging bleeding risk to determine when anticoagulant prophylaxis can be safely initiated solely based on INR or aPTT is a last century practice. As for diagnosing PE in the critically ill, computed tomography pulmonary angiography (CTPA) is the practical gold standard. While contrast-induced-nephropathy (CIN) is real and critically ill patients are certainly at risk, the benefits of a CTPA will almost always outweigh the risk of CIN when intensivists suspect their patients may have PE (or when the pre-test probability is >10-15%)[3,4]. Immediate aggressive systemic anticoagulation is pivotal in confirmed PE. It is better to aim at a higher aPTT (80-100s) target than a lower one (e.g. 60-80s) as soon as possible to avoid clot propagation which may lead to requiring even higher risk therapies, such as thrombolysis, extracorporeal membrane oxygenation (ECMO) or surgical embolectomy. For those unfortunate few individuals who continue to deteriorate despite systemic anticoagulation, the options ‘to lyse, suck, use ECMO, or remove’ are endless; but in reality the choice is often limited by what expertise is most available at the time of crisis. 

Finally, the controversial issue of using inferior vena cava filters as a primary VTE prophylaxis in patients with contraindications to anticoagulants will be discussed, including the results of our recently completed randomized controlled trial [5]. 

References: 

[1] Ho KM, Burrell M, Rao S, Baker R. Incidence and risk factors for fatal pulmonary embolism   after major trauma: a nested cohort study. Br J Anaesth 2010;105:596-602. 

[2] Reason J. Human error: models and management. BMJ 2000; 320: 768-70. 

[3] Ho KM. Balancing the risks and benefits of using emergency diagnostic radiocontrast studies to diagnose life-threatening illness in critically ill patients: a decision analysis. Anaesth Intensive Care 2016;44:724-8. 

[4] Ho KM, Harahsheh Y. Predicting contrast-induced nephropathy after CT pulmonary angiography in the critically ill: a retrospective cohort study. J Intensive Care 2018;6:3. 

[5] Ho KM, Rao S, Honeybul S, Zellweger R, Wibrow B, Lipman J, Holley A, Kop A, Geelhoed E, Corcoran T. Detailed assessment of benefits and risks of retrievable inferior vena cava filters on patients with complicated injuries: the da Vinci multicentre randomised controlled trial study protocol. BMJ Open 2017;7:e016747. 

Survival in patients with advanced heart failure (AHF) has improved over the last 2 decades. An increasing number of patients however, are dying with progressive heart failure over the same duration. Optimal utilization of medical therapies and devices like implantable defibrillators and biventricular pacemakers are the likely reasons patients are surviving longer albeit with progressive HF.  

Evolution in mechanical circulatory support (MCS) devices has occurred over the same period, such that they can now be rapidly instituted providing support for pump failure, often percutaneously, with timely restitution of physiologic and metabolic derangements with fewer complications. 

MCS devices can be classified as Short term and Long term. Short term devices such as Intraaortic balloon pumps (IABP), Impella ®, TandemHeart® or Venoarterial extracorporeal membrane oxygenation (VA – ECMO) using a Cardiohelp® device, are usually employed as ‘Bridge to Recovery’(BTR) or Bridge to Decision’(BTD), usually in acute settings. Long term devices such as implantable left ventricular assist devices (LVADs) e.g. Heartmate II® & 3®, Heart ware HVAD® are implanted as ‘Bridge to transplant’ (BTT) or ‘Destination therapy’ (DT) usually in patients ‘sliding’ on inotropes when they are transplant eligible (BTT) or ineligible (DT) respectively.  

Ventricular assist devices have traditionally been developed for left ventricular support in case of severe left heart or biventricular dysfunction. Historically, right ventricular (RV) dysfunction following LVAD implantation or as a component of biventricular dysfunction was managed with either medical therapy, temporary VADs (i.e. ECMO configuration with continuous flow centrifugal pumps like CentriMag®, Rotaflow ®) or occasionally with LVADs placed on the right side. Recently the Impella RP® and ProtekDuo®, percutaneously placed pumps with inflow in the inferior vena cava & right atrium respectively and outflow in pulmonary artery, have become available as less invasive options, for short term RV support. 

The Syncardia® is the only approved total artificial heart system currently in use; however various biventricular, total heart systems (e.g. BiVACOR®) in development show promise.  

Mechanical circulatory devices provide attractive, viable, physiologically plausible ventricular support options that can be used effectively in carefully selected patients. 

When is an arrhythmia important? Can you tell, or should you always refer to a cardiologist? What are the best management strategies for common arrhythmias and are there any potential problems to be aware of? What about the “do not miss” diagnoses? 

Arrhythmias are common in critically unwell patients, and may represent primary cardiac pathology, or the cardiac response to underlying pathology. Estimates for the incidence of arrhythmias in patients in the intensive care unit (ICU) vary widely. Atrial fibrillation is the most common arrhythmia in the ICU, and management varies according to patient instability, underlying comorbidities and conditions, with important features that may favour a rate-control strategy over cardioversion, or a pharmacologic cardioversion over an electrical cardioversion. Atrial tachycardias are less common, but may have important consequences, and be difficult to manage in the intensive care patient. Ventricular arrhythmias are often immediately life threatening, and may require more than an advanced life support (ALS) algorithm to effectively treat and suppress.  

The mainstay of therapy for our patients in ICU is pharmacotherapy, usually with amiodarone or diltiazem, however specific circumstances may dictate the use of other antiarrhythmic drugs. Ablation therapies may offer effective treatment for ICU patients, however have risks specific to ICU patients, associated with transport, procedural risk, delay of ongoing therapies, requirement for personnel, and isolated location. 

This session will outline a practical approach to diagnosis and management of common and important arrhythmias in the ICU, and will include case and ECG discussions.  

Patients admitted to the intensive care unit (ICU) are at increased risk for cardiac arrhythmias. They may be the reason for admission or resulting from the underlying condition. Treating exacerbating and contributing factors is the first step in management, however in certain cases may not be sufficient. Further the diagnosis of the arrhythmia may difficult from the ECG. An invasive cardiac electrophysiology study (EPS) can be helpful in establishing the diagnosis and can be combined with catheter ablation to eliminate the substrate. The field of cardiac electrophysiology is rapidly developing with technological advances providing insights into the mechanism of certain arrhythmias and expanding the therapeutic potential. This presentation will provide an overview of recent developments and insights into the management of common arrhythmias on the ICU. 

The intent of this presentation is to provide an update of coronary assessment and management for the adult intensivist. Discussion points will include:  

1. An assessment of coronary severity, using established methods, in particular fractional flow reserve (FFR),  

2. Which stent- highlight the evolution of the stent to the current generation and what is evolving, 

3. How to keep the stent open with current concepts of antiplatelet therapy and how this impacts the critically ill patient  

4. What to consider if the ECG is abnormal, but the coronaries are not flow limiting obstruction- an occasional dilemma in the critically ill patient and finally  

5.  Discussion around a contemporary study regarding cardiogenic shock and coronary ischemia.  

Debate: Who should care for GUCH?

Presenters: Dr Susanna Price & Dr Peta Alexander. Moderator: Dr Bennett Sheridan

GUCH - A growing problem by Dr Susanna Price.

Congenital Heart Disease (CHD) in infants presents as inadequate systemic or pulmonary blood flow, or heart failure from intra-cardiac shunts. Approaches to surgical intervention comprise primary repair, early palliation with subsequent repair or definitive palliation. 

CHD palliation evolved in the pre-cardiopulmonary bypass era. In 1938 a patent ductus arteriosus was ligated, in 1944 pulmonary blood flow was established via subclavian artery to pulmonary artery anastomosis (Blalock, Taussig and Thomas), and in 1952 pulmonary artery banding was employed to protect pulmonary vasculature. In the 1950s-60s symptomatic infants underwent these palliative procedures with reparative intra-cardiac interventions delayed due to perceived risk. In the late 1960s emerging publications shifted the focus to early primary repair.  

An exponential increase in the complexity of surgical repairs over the past 50 years have built on early innovation, exemplified by management of transposition of the great arteries. Surgical approach transitioned from palliative atrial switch procedures (Senning 1957 and Mustard 1963) with low early mortality but impressive late morbidity to the reparative arterial switch procedure (Jatene 1975) which remains standard of care. 

Despite advances in the field, biventricular repair is not an option for all patients. Children born with a single functional left ventricle benefited from staged palliative procedures to the Fontan circulation. First described in 1971, the Fontan procedure established passive pulmonary blood flow, using the single ventricle for systemic circulation. Further innovation by Norwood (1981) facilitated similar staged palliation of patients with single right ventricles. While for most patients with functionally univentricular CHD, staged palliation is dictated by underlying anatomy, it is increasingly recognized that a proportion of these patients may have anatomy and physiology amenable to biventricular circulation.  

As we embark on the next era of innovation in CHD, patient selection, multicenter collaboration and meaningful outcome measures are challenges to be addressed. 

Inotropic agents are commonly used in critically ill patients to support myocardia contractility either in the setting of cardiac surgery or ischemia or in the setting of sepsis associated myocardial dysfunction. The most commonly used agents are beta-agonist drugs (dobutamine), mixed beta and alpha agents (adrenaline and dopamine), phosphodiesterase inhibitors (inodilators) such as milrinone or enoximone or calcium sensitizers (levosimendan). Such agents are currently used according to clinician and/or unit preference based on tradition, mentorship, belief, inductive physiological reasoning, familiarity, understanding of pharmacokinetic and pharmacodynamics properties, side effects, and cost. No randomized controlled trials exist to support the notion that treatment targeted to similar physiological outcomes (ie cardiac index or MVO2) with one drug versus another would yield a different clinical outcome. More recently, however, two double-blind RCTs have compared adjunctive inotropic therapy with levosimendan in patients with post-operative low-cardiac output syndrome or low pre-operative ejection fraction. Both found that the addition of levosimendan was not superior to the edition of placebo.  

Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.  

Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS). 

Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.  

20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort. 

These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia.

In this podcast Spinal Rehab Specialist Bonne Lee talk about this side of SCI care.

This podcast was recorded at the Brain Symposium which took place in March 2023. For more talks and content like this, visit neuroresus.com or subscribe to be notified of new podcast releases via email.

In non-cardiac ICU patients, the two major causes of acute myocardial dysfunction are sepsis-related cardiac depression (SRCD) and stress-related cardiomyopathy, the most common cause being the former. The main mechanisms responsible for SRCD include release of cardiac-depressant substances such as pro-inflammatory cytokines, hyporesponsiveness of beta-adrenergic receptors, decreased sensitivity of the myofilament to Ca++, and excessive production of perioxynitrite. Echocardiography is the best method to diagnose SRCD. If a cut-off value of 45% left ventricular ejection fraction is used to define SRCD, the occurrence of SRCD is 60% in septic shock patients (40% on the day of admission and in 20% the two following days). Recent advances in ultrasonography such as speckle-tracking (measuring the longitudinal systolic strain) may allow detecting cardiac abnormalities that are not detected by conventional echocardiography. Even when the SRCD is diagnosed, an important issue is to decide to treat it since left ventricular dilatation is an adaptive mechanism associated with a good outcome. The Surviving Sepsis Campaign suggests using dobutamine in patients who show evidence of persistent hypoperfusion despite adequate fluid loading and the use of vasopressor agents. In our opinion, it is more logical to give an inotrope when the shock state persists in the presence of: 1) proven SRCD with echocardiography and, 2) either low (mixed or central) venous blood oxygen saturation or increased veno-arterial carbon dioxide pressure gradient. Dobutamine is still recommended as the first-choice inotropic agent. Levosimendan is considered an alternative as it can restore the sensitivity of the cardiomyocyte myofilament to Ca++. Early administration of norepinephrine can not only increase blood pressure through an alpha1-adrenergic effect but also improve cardiac contractility through a beta1-adrenergic effect and/or an increase in the diastolic arterial pressure (i.e. the perfusion pressure of the left ventricle). 

Ventricular pump function is often compromised during critical illness and for a variety of reasons. The most common cause of a limited cardiac output in acutely ill patients is right ventricular (RV) dysfunction. Exacerbations of chronic obstructive lung disease or the use of high end-expiratory pressure sin acute lung injury to support arterial oxygenation can result in acute elevations of pulmonary arterial pressure impeding RV ejection, causing RV dilation, decreased left ventricular (LV) diastolic compliance. All these effects limit cardiac output and LV stroke volume. Importantly, the treatment is to sustain mean arterial pressure greater than pulmonary artery pressure to prevent RV ischemia and balance RV fluid status to avoid both over-distention (acute cor pulmonale) and under-filling. This delicate fluid balance is greatly facilitated by the immediate and repeated use of bedside echocardiography. Attempts to minimize lung over distention should be a primary focus of therapy.  If one focuses only on the LV, these patients would be said to have a reversible form of diastolic dysfunction, in that LV ejection fraction would be normal but the LV not able to increase its end-diastolic volume without excess filling pressures promoting pulmonary edema. The second most common etiology of impaired heart functional reserve is chronic LV hypertrophy secondary to hypertension, wherein systemic afterload reduction is the primary treatment. Third, decreased systolic pump function is often seen in sepsis owing to reduced myocardial adrenergic responsiveness. However, this is often under-appreciated because of the usually co-existent peripheral vasodilation. In septic patients, measures aimed primarily to increase mean arterial pressure, such as the use of vasopressors often results in a decrease in cardiac output because the septic heart is not able to handle the increased load. Importantly, this form of systolic dysfunction is reversible once the sepsis state resolves, but may require inotropes during its height to sustain flow under pressure.  Finally both chronic heart failure patients can also get sick and acute myocardial infarction will impair both diastolic and systolic function. Their treatments include reversing coronary ischemia, if present, afterload reduction and a balanced fluid response. A clear and logical approach to all critically ill patients is needed to quickly separate these diverse forms of heart failure from each other as they have markedly different therapies and clinical trajectories. 

Over 65,000 people are diagnosed with heart failure every year in Australia. Heart failure is implicated in the deaths of 61,000 individuals per year. Although the need for cardiovascular support is common in patients in the Intensive Care Unit (ICU) with about 60% of ventilated patients requiring some form of inotropic or vasopressor support, a primary diagnosis of acute heart failure on admission to ICU is much less common. There are about 3000 ICU admissions per year primarily due to cardiogenic shock, cardiomyopathy or congestive heart failure in Australia and New Zealand. This represents 2% of all ICU admissions. Only a minority of these patients have a prior history of significant cardiac disease. The mortality of these three conditions are 40%, 17% and 14% respectively. Since the early 2000’s there has been a progressive decline in risk adjusted mortality of all patients admitted to ANZ ICUs. However, the decline in mortality for patients with acute heart failure has lagged behind other diagnoses. This gap is widening.

Shree Basu and Ahmed Osman discuss paediatric traumatic brain injury. They cover initial management, prevention of secondary injury, what is different in paediatrics compared to adults and the latest evidence.

From www.IntensiveCareNetwork.com

Resuscitation is complicated, but the solutions don't have to be. These are the psychological hacks that will help you conquer complexity and excel in dynamic environments.

Shree Basu is joined by Marino Festa to discuss sepsis. They cover epidemiology, challenges in diagnosing sepsis, SEPSIS 3 guidelines and what it means in paediatrics, and some clinical tips on the assessment and management of children with sepsis.

Here's a useful articleon the prognostic accuracy of age-adapted SOFA, SIRS, PELOD-2, and qSOFA for in-hospital mortality among children with suspected infection admitted to the intensive care unit.

From www.IntensiveCareNetwork.com

My own experience by Ms Claire Kerr.

Ms Kerr is a nurse who also spent significant amounts of time in hospital as an adolescent. Claire outlines her own experience in the hospital system and the things that made a difference for her.

In this episode Shree Basu and Ahmed Osman discuss the shocked neonate - both the initial management when they present and the subsequent PICU management. From IntensiveCareNetwork.com

In this episode Shree Basu and Ahmed Osman discuss the tricky issues surrounding management of paeds CICU patients with a single ventricle. From IntensiveCareNetwork.com

The perennial debate of which osmotic agent to use to reduce elevated ICP still rages on.

Who better than Mr Deranged Physiology himself, Aleks Yartsev, to take us through the pros and cons of each and work out a practical strategy.

This podcast was recorded at the Brain Symposium which took place in March 2023. For more talks and content like this, visit neuroresus.com or subscribe to be notified of new podcast releases via email.

Shree Basu and Lily Foster are paediatric intensive care trainees. They discuss post operative management in paediatric cardiac intensive care following surgery for congenital heart disease. 

Matt Anstey is an intensivist from Sir Charles Gardener hospital in Perth, Australia. He gave this talk on outcomes after intensive care at an ICN WA meeting in Perth last year.

Shree Basu and Lily Foster are paediatric intensive care trainees. They give an introductory podcast to paediatric cardiac intensive care, covering recognition of congenital heart disease, early and emergency pre-operative management principles, and classification of the most common lesions.