Hergen Buscher is an Intensivist from St Vincent's hospital in Sydney. He has extensive experience with ECMO, in both veno-venous and veno-arterial contexts. Listen to this talk he gave on the most recent developments in ECMO and where things are heading.
This talk was given live in September 2014 for an Intensive Care Network (ICN) NSW meeting.
Go to www.intensivecarenetwork.com for more.
ECMO, DEFINITION, ETIOLOGY, INDICATION, CONTRAINDICATION, TYPES OF ECMO, VENOVENOUS ECMO, VENO ARTERIAL ECMO, NURSING CARE OF PATIENT ON ECMO, WEANING FROM ECMO,
ECMO, DEFINITION, ETIOLOGY, INDICATION, CONTRAINDICATION, TYPES OF ECMO, VENOVENOUS ECMO, VENO ARTERIAL ECMO, NURSING CARE OF PATIENT ON ECMO, WEANING FROM ECMO,
This workshop will outline the basic principles of extracorporeal life support made easy by key-experts in the field. During the course delegates will gain a good understanding of ECMO in the following areas: Theoretical concepts, basic physiology and pathophysiology, cardiac and respiratory support and monitoring, alarm settings and monitoring, role of cardiac ultrasound during ECMO, newest technologies, circuits and devices, practical hands-on sessions and simulations.
A brief yet comprehensive coverage of ICU role in ECMO cases. Presentation has been prepared in order to help ICU fellows and registrars to understand the importance of their role and to know necessary actions they have to take in case of need.
This workshop will outline the basic principles of extracorporeal life support made easy by key-experts in the field. During the course delegates will gain a good understanding of ECMO in the following areas: Theoretical concepts, basic physiology and pathophysiology, cardiac and respiratory support and monitoring, alarm settings and monitoring, role of cardiac ultrasound during ECMO, newest technologies, circuits and devices, practical hands-on sessions and simulations.
This workshop will outline the basic principles of extracorporeal life support made easy by key-experts in the field. During the course delegates will gain a good understanding of ECMO in the following areas: Theoretical concepts, basic physiology and pathophysiology, cardiac and respiratory support and monitoring, alarm settings and monitoring, role of cardiac ultrasound during ECMO, newest technologies, circuits and devices, practical hands-on sessions and simulations.
This workshop will outline the basic principles of extracorporeal life support made easy by key-experts in the field. During the course delegates will gain a good understanding of ECMO in the following areas: Theoretical concepts, basic physiology and pathophysiology, cardiac and respiratory support and monitoring, alarm settings and monitoring, role of cardiac ultrasound during ECMO, newest technologies, circuits and devices, practical hands-on sessions and simulations.
A brief yet comprehensive coverage of ICU role in ECMO cases. Presentation has been prepared in order to help ICU fellows and registrars to understand the importance of their role and to know necessary actions they have to take in case of need.
This workshop will outline the basic principles of extracorporeal life support made easy by key-experts in the field. During the course delegates will gain a good understanding of ECMO in the following areas: Theoretical concepts, basic physiology and pathophysiology, cardiac and respiratory support and monitoring, alarm settings and monitoring, role of cardiac ultrasound during ECMO, newest technologies, circuits and devices, practical hands-on sessions and simulations.
This workshop will outline the basic principles of extracorporeal life support made easy by key-experts in the field. During the course delegates will gain a good understanding of ECMO in the following areas: Theoretical concepts, basic physiology and pathophysiology, cardiac and respiratory support and monitoring, alarm settings and monitoring, role of cardiac ultrasound during ECMO, newest technologies, circuits and devices, practical hands-on sessions and simulations.
PowerPoint presentation on ECMO (Extracorporeal Membrane Oxygenation). Part 2 focuses on Monitoring ECMO patients
Ventilatory strategies, Sedation and pain control, Weaning, Complications and recent advances in ECMO. For better understanding please have a look at ECMO part 1 before going through part 2.
There might be no safe ventilation. Much too often, all there is for us to measure at the bedside are nothing but global indicators of stress/strain, more or less refined. Heterogeneity at the alveolar level-inhomogeneities or stress raisers - render global parameters less useful than previously predicted. In fact, Mead had already stated it through his work on stress distribution at the alveolar level.
ECMO (VA ECMO) might be regarded as one other way of decatecholaminization (M.Singer). Stop stressing the already stressed heart. Unfortunately, fem-fem VA ECMO still needs inotropic support to lessen the LV distension. Levosimendan and IABP combined could help decrease the catecholamine usage in this context.
Roger Pye is a world leading ECMO specialist. This talk on starting ECMO during CPR resuscitation is serious and backed up by some extraordinary cases. Roger presents his experience and the literature on this topic.
The presentation can be heard on wwwintensivecarenetwork.com.
Shay McGuinness talks about what ECMO is, the history of its use in New Zealand and how their ECMO retrieval system works there. This was recorded live at the inaugural ICN NZ meeting, with support from ANZICS NZ.
A study to assess the effectiveness of structured teaching program on knowledge regarding care of patients after cardiac surgery among staff nurses at Shree Narayana, Hospital, Raipur, chhattisgarh.
CORTICAL SPREADING DEPOLARISATION IN NEUROLOGICAL DISEASE – AN INTRODUCTION
By Toby Jeffcote
Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury.
It was first described by Leão in 1944, a disturbance in neuronal electrophysiology has since been demonstrated in a number of animal studies, and recently a few human studies that examine the occurrence of this depolarizing phenomenon in the setting of a variety of pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, and traumatic brain injuries. The onset of CSD has been demonstrated experimentally following a disruption in the neuronal environment leading to glutamate-induced toxicity. This initial event leads to pathological changes in the activity of ion channels that maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps that aim to restore homeostasis fail, leading to osmolar shifts of fluid, swelling of the neuron, and ultimately a measurable depression in cortical activity that spreads in the order of millimeters per minute. Equally important is the resulting change in vascular response. In healthy tissue, increased electrical activity is coupled with release of vasodilatory factors such as nitric oxide and arachidonic acid metabolites that increase local blood flow to meet increased energy expenditure. In damaged tissue, not only is the restorative vascular response lacking but a vasoconstrictive response is promoted and the ischemia that follows adds to the severity of the initial injury. Tissue threatened by this ischemic response is then at elevated risk for CSD propagation and falls into a vicious cycle of electrical and hemodynamic disturbance. Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.
Celia Bradford takes us through the latest on the management of subdural haemorrhage (SDH). She covers acute SDH, chronic SDH and middle meningeal artery embolisation, a novel treatment for chronic SDH management in certain circumstances.
Andy Neill - More neuroanatomy pearls for neurocritical careSMACC Conference
Andy Neill shares some more neuroanatomy wisdom that's highly practical for anyone working with neuro emergencies. This time he covers brain herniation syndromes, hydrocephalus, extradural vs subdural haematomas, cervical spinal imaging, vertebral artery dissection and "things you read on CT reports but don't know what they mean"!
Andrew Udy talks about Brain Tissue Oxygen Monitoring:
It’s Not What You’ve Got It’s What You Do With It
The BONANZA Trial
Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail!
More on BONANZA here
More on BOOST3 here
R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.
By Catherine Bell and Andrew Udy
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.
There is no such thing as mild, moderate and severe TBI - by Andrew UdySMACC Conference
Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.
TBI Debate - Mild, moderate and severe categories workSMACC Conference
Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations
Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.
Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics.
However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.
Managing Complications of Chronic SCI by Bonne LeeSMACC Conference
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
Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care.
Keywords
SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI
Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus.
So why do we do cEEGs for patients with suspected SE?
To confirm the diagnosis
To see if patient just post ictal or still seizing
To establish that the clinical and electric seizures have stopped
To see if burst suppression is achieved
To exclude other differential diagnoses
She makes a good argument for why cEEG is such an important tool in managing SE.
In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.
Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. 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.
Shree Basu is a Paediatirc Intensivist in Sydney. These slides from the Brain Symposium 2023 accompany the talk she gave. She discusses how Paediatric stroke presents, what neuroimaging is required and what interventions are available, including thrombolysis and the role of endovascular thrombectomy.
Hypertensing Spinal Cord Injury - gold standard or wacky?SMACC Conference
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.
Tessa discusses the pros and cons, how this is managed practically and what the future may hold in this area.
Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.
Social Worker Victoria Whitfield and Bereavement councilor Louise Sayers discuss the power of words when health professionals are communicating topics around of death and serious injury with relatives and patients in critical care. They use role plays to bring theories to life.
Sepsis and Antimicrobial Stewardship - Two Sides of the Same CoinSMACC Conference
Appropriate use of antimicrobials is primarily a patient safety issue, and is the key aim of an effective antimicrobial stewardship program. We discuss the challenges in the management of a patient with sepsis, and how decision-making is usually done in the absence of effective diagnostics. Time dependent protocols and the knowledge that undertreatment of a patient with sepsis will lead to poor outcomes will lead to prescribing that may be driven by fear. Antimicrobial resistance is associated with over-use of antimicrobials but is usually not the immediate concern. Antimicrobial stewardship programs should work closely with sepsis teams to ensure that sepsis pathways are implemented across the whole hospital, and that key principles of judicious use are embedded within the clinical pathway.
Being able to prognosticate in the aftermath of a traumatic brain injury (TBI) is important as it assists with counselling patients and families. Moreover, it helps rationally allocate healthcare resources.
However, due to the heterogenous nature of TBI and variable pre brain injury patient factors and post brain injury course, this has proven to be a difficult task.
Large cohort studies have enabled improved accuracy in the prediction of 6 month mortality and unfavourable outcome.
Furthermore, many of the factors that contribute to long-term outcome have also emerged. However, it is not yet possible to use them in prediction algorithms or mathematical models.
There is emerging evidence that pre injury psychosocial and demographic factors may be of more relevance than injury severity. Moreover, that 'outcome' becomes increasingly subjective and complex as the post injury duration increases.
We end with three brief vignettes which highlight the fraught nature of long term outcome prediction.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
1. What’s new in extracorporeal life
support
Hergen Buscher
2.
3. Definition
• External artificial circuit carries venous blood from the patient to an
oxygenator.
• Blood becomes enriched with oxygen and has carbon dioxide removed.
• The blood is than returned to the patient via a central vein or an artery.
4.
5. Allow time to recovery
It most cases recovery is seen between 7 to 14 days
6. 16 year old boy with goodpasture syndrome
On admission 28 days later
7. 51 year old patient with
polypharmacy overdose
No pulsatility Same patient 6 days later
20. Indications VV
Inability to maintain SaO2 > 88 or pH > 7.20 with safe mechanical ventilation
• Plateau pressure < 35cmH2O and
• Tidal volume <6ml/Kg predicted body weight
• Need for inter-hospital transport in severe respiratory failure
Despite
• Trial of high PEEP (18-22)
• Prone positioning
• Nitric Oxide or alternative pulmonary vasodilators
21. Conditions VV
Good:
• ARDS with primary lung injury (infection, aspiration or direct trauma)
• Primary graft dysfunction following lung transplantation (within 7 days)
• Pulmonary vasculitis (Goodpasture’s, ANCA-associated, other Autoimmune)
Variable:
• ARDS from secondary lung injury (from non-pulmonary sepsis, burns or pancreatitis)
• Lung transplant recipients 7-30 days post transplant
• Age >70
22. Conditions VA
Good
• Acute fulminate myocarditis
• Cardiomyopathy (first presentation)
• Chronic cardiomyopathy (suitable for VAD)
• Primary Graft Failure post heart transplant
• AMI (with early revascularisation)
• Drug overdose
• Pulmonary Embolism
Variable
• Multiple organ failure
• Late revascularisation
• Septic shock
• Post cardiotomy
23. Contraindications
• Age: > 70 years
• Active malignancy
• Severe brain injury
• Previous Bone marrow transplant, previous transplant (>30 days), AIDS
• End stage chronic organ failure (hepatic, renal)
• End stage cardiomyopathy (except for bridge to VAD/transplant)
• Chronic lung disease (except for bridge to transplant)
• Multi organ failure
• Severe mitral or aortic valvular insufficiency or aortic dissection (VA only)
25. • ECMO (n=90 patients)
• Conventional management (n=90)
• 68 (75%) patients actually received
ECMO
• 63% of patients consideration for
treatment by ECMO survived
• 47% of patients on conventional
management survived
• Relative risk 0.69; 95% CI 0.05–0.97,
p=0.03
• Quality-adjusted life-year: £19 252
26. Research
EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO) FOR SEVERE
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
A multicenter, randomized, controlled open trial
EOLIA : ECMO to rescue Lung Injury in severe ARDS
Promoter:
Département de la Recherche Clinique et du Développement (DRCD)
Assistance Publique–Hôpitaux de Paris
42. ASAP –ECMO: Antibiotic, Sedative and Analgesic Pharmacokinetics during Extracorporeal
Membrane Oxygenation: A multi-centre study to optimise drug therapy during ECMO
Authors:
Kiran Shekar1
Jason A Roberts2
Susan Welch3
Hergen Buscher3
Sam Rudham3
Sussan Ghassabian4
Steven C Wallis2
Bianca Levkovich5
Vin Pellegrino5
Shay Mcguinness6
Rachael Parke6
Paul Forrest6
Adrian G Barnett8
James Walsham9
Daniel V Mullany1
Maree T Smith4
John F Fraser1
Affiliations:
1Critical Care Research Group, Adult Intensive Care Services, The Prince Charles Hospital and The
University of Queensland, Brisbane, Queensland, Australia
2Burns Trauma and Critical Care Research Centre, Royal Brisbane and Women’s Hospital and The
University of Queensland, Brisbane, Queensland, Australia
3 Intensive Care Services, St Vincent’s Hospital, Sydney, New South Wales, Australia
4Centre for Integrated Preclinical Drug Development, University of Queensland, Brisbane, Queensland,
Australia
5 Intensive Care Services, The Alfred Hospital, Melbourne, Victoria, Australia
6 Intensive Care Services, Auckland City Hospital, Auckland, New Zealand
6 Intensive Care services, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia
8Institute of Health and Biomedical Innovation, School of Public Health & Social Work, Queensland
University of Technology, Queensland, Australia
9Intensive Care Services, Princess Alexandra Hospital, Brisbane, Queensland, Australia
Day/Month/Year Footnote to go here Page 42
49. Complications - Bleeding
Zapol et al: Extracorporeal membrane oxygenation in severe acute
respiratory failure. A randomized prospective study. JAMA (1979)
Morris et al: Randomized clinical trial of pressure-controlled inverse ratio
ventilation and extracorporeal CO2 removal for adult respiratory distress
syndrome. Am J Respir Crit Care Med (1994)
50. How to anticoagulate and how to treat
bleeding
• As higher the flow as lower the heparin
• APTT targets of 1.5 to 2 times normal
• Low dose heparin??
• Heparin free ECMO is possible (in adults)
• Longest reported run without heparin: 25 days
• But higher risk during VA-ECMO
• Point of care testing to manage bleeding
52. ECMO and Blood Management
• 52 ECMO runs in St Vincent’s Hospital
• 363 ECMO days
• Daily median (interquartile range) transfusions
(unpublished data)
60. Hemolung Catheter 15.5 Fr
60
26 cm Femoral Catheter
350 – 450 ml/min flow
Infusion Lumen (Red)
Drainage Lumen (Blue)
17 cm Jugular Catheter
450 - 550 ml/min flow
Drainage Port
Infusion Port
Infusion Lumen (Red)
Drainage Lumen (Blue)
Drainage Port
Infusion Port
61. • Blood Flow
350-450 ml/min
• CO2 Removal
30% - 50% of total CO2 production
62. Indications
• To avoid intubation
• To facilitate extubation
• To reduce invasiveness of ventilation (ultraprotective ventilation)
Contraindications:
• Whenever oxygenation failure is that severe that more support is
used for that reason alone
62
63. Carbon Dioxide and
Mechanical Ventilation
Christopher Reeve Stephen Hawking
1995 to 2004 ~1985 to present
64. A real case
64
• 59 year old male with exacerbation of COPD
• Admission to ICU after respiratory arrest in the ward
70. NIV IMV pre ECCOR ECCOR
0 10 20 30 40 50 60 70 80
Page 70
Patient 5
Patient 4
Patient 3
Patient 2
Patient 1
hours
Abrams et al. Ann Am Thorac Soc 2013
ECCOR to facilitate extubation
71. Extubation was possible after
a few hours
Page 71
NIV IMV pre ECCOR ECCOR Time to extubation post ECCOR
21.5
2
1.5
5
4
0 10 20 30 40 50 60 70 80 90
Patient 5
Patient 4
Patient 3
Patient 2
Patient 1
hours
Abrams et al. Ann Am Thorac Soc 2013
72. 3 to 11 days on ECCOR
post extubation
NIV IMV pre ECCOR ECCOR Time to extubation post ECCOR ECCOR and extubated
0 50 100 150 200 250 300 350 400
Page 72
Patient 5
Patient 4
Patient 3
Patient 2
Patient 1
hours
Abrams et al. Ann Am Thorac Soc 2013
73. Mobilizing patients on ECCOR
NIV IMV pre ECCOR ECCOR Time to extubation post ECCOR ECCOR and extubated
Page 73
150 ft
450 ft
70 ft
600 ft
240 ft
0 50 100 150 200 250 300 350 400
Patient 5
Patient 4
Patient 3
Patient 2
Patient 1
hours
Abrams et al. Ann Am Thorac Soc 2013
75. Where to use it: ARDS
• Mortality rate up to 45% despite lung protective ventilation
• Lung hyperinflation in 30%
• TV<4 ml/kg (ultraprotective ventilation)
• Hypercapnia
• Immunosuppression
• impairs pulmonary epithelial repair
• worsens right heart function
• barrier to achieve LPV
80. What we used to do
severe
moderate
ECMO
IABP
Inotropes
Recovery
Tandem Heart, Impella, Levitronix…..
OR
Death
Durable VADs
Heart Transplantation
acute chronic
Heart Failure
81. What we are doing now
severe
moderate
ECMO-Tandem Heart-Impella …..
IABP
Inotropes
Durable VADs
Heart Transplantation
acute chronic
Heart Failure
82. What we are doing now
severe
moderate
ECMO-Tandem Heart-Impella …..
IABP
Inotropes
Durable VADs
Heart Transplantation
acute chronic
Heart Failure
84. Incidence and Mortality of Cardiogenic
Shock Post Myocardic Infarct
Mann, Nolan: Current Opinion in Critical Care 2006
85. Incidence of Cardiogenic Shock (CS)
Compared to ECMO runs
30000
25000
20000
15000
10000
5000
0
ECMO runs CS post MI CS on admission post MI
Total ECMO runs (ELSO)
Cardiogenic Shock from MI (NRMI)
(US data 1995-2004)
87. Should there be a RCT on cardiac extracorporeal life support
on patients with an expected mortality of 50-80%?
88. Prophylactic ECMO for interventional
aortic valve replacement
Before
• 8/131 (6%) needed rescue ECMO
• 2/8 (25%) died
After
• 9/83 (11%) had prophylactic ECMO
• 0% Mortality
• 1 needed Rescue ECMO and died
Husser, Regensburg Medical Center
89. ECMO Implantation to Optimize Renal
Function as a Bridge to Decision
ECMO Implantation
72 hours
Creatinine improved
to normal values
3 days after
ECMO implantation
90. ECMO could be more than a rescue
treatment in cardiogenic shock
91. What if the patient does not recover?
severe
moderate
IABP
Inotropes
Durable VADs
Heart Transplantation
acute chronic
Heart Failure
ECMO-Tandem Heart-Impella …..
93. … But is Heart Transplantation
an Option?
In the US
• 5.000.000 people have heart failure
• 500.000 are newly diagnosed each year
• 200.000 are refractory to standard treatment
• 2.200 will have a heart transplant
94. “TREATING CONGESTIVE HEART
FAILURE WITH CARDIAC
TRANSPLANTATION IS
ANALOGOUS TO TREATING
POVERTY WITH LOTTERY
TICKETS”
R. Robbins
Director of the Stanford Institute of Cardiovascular Medicine
103. Get ECMO in less than 45 min from collapse
Non-survivors are not expensive
104. One of our cases
• 58 year old male presented to ED on a Sunday morning
• Found on the street, GCS 12, hypothermia (32.1 C)
• 08:01 VF cardiac arrest in ED
• 08:10 call for E-CPR
• 08:15 team arrives, 5 shocks, now asystolic
• 08:20 start of cannulation
• 08:38 total of 37 min of CPR, 5 shocks, 10mg adrenalin total
• 08:39 start of ECMO, CPR ceased
• 08:44 patients localized to the ETT, still asystolic, sedation given
• 08:51 temperature up to 34.5 C, VF
• 08:52 one shock, ROSC
• 24 hrs of temperature control at 36.0 C
• Pt. decannulated, extubated on day 1
• Ward the next day
105. Summary
• ECMO has been used as rescue therapy for many indications and has
shown to be safe and to improve outcome
• Extracorporeal life support devices become less invasive and more
integrated in general patient care
• Durable VADs evolve rapidly and become safer for long term treatment and
destination therapy
• Further studies are needed to investigate the rule of ECMO (and other
mechanical support devices) for high risk patients
• Patient selection and ethical considerations remain essential
Editor's Notes
How much is the nonpulsatile ECMO flow and how much is the heart contributing? There are other clues besides just echo. Here is an extreme example of what is potentially possible with ECMO.
Still alive? See the CO2 trace, also the difference in oxygenation (color difference of the 2 cannula with O2 extraction that continues if still alive)
The Avalon catheter is frequently used in MSICU. With this cannula correct positioning is vital-we will see why with the next slide.
The blood gets taken in from the IVC and SVC ports and returned through a single port that needs to be positioned in the central part of the RA.
The reported incidence of acute respiratory distress syndrome ranges from 7 to 59 per 100,000 people with an associated with a mortality rate of 40 to 45%. This rate remains unacceptably high despite the introduction of lung protective.
When surveyed, health care providers reported that hypercapnia or its related effects were significant barriers to achieving LPV.
Studies have shown that while 6 ml.kg-1 is superior to 12 ml.kg-1 and <4 ml.kg-1 might be superior to 6 ml.kg-1 [9-11].
Hypercapnia harms injured lung through immunosuppression and impaired pulmonary epithelial repair. Furthermore, hypercapnia worsens right heart failure and is undesirable in patients with elevated intracranial pressure.