Neuro Resus

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The menagerie of monitoring tools Aug 20, 2018

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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.

Pulmonary hypertension and ICU therapies Aug 20, 2018

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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?

Acute right heart failure: Adaptation, interdependence and external influences Aug 20, 2018

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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.

Management of acute right heart failure Aug 19, 2018

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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.

Anticoagulation during mechanical support Aug 19, 2018

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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.

How to prevent fatal pulmonary embolism Aug 19, 2018

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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.

RVADs/LVADs and all things mechanical Aug 19, 2018

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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.

Arrhythmias in the ICU: An Intensivist's approach. Aug 19, 2018

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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.

Cardiac Electrophysiology: What's new? Aug 09, 2018

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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.

Coronary flow for the critically ill Aug 09, 2018

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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.

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