This document provides an overview of circulatory care and treatments for cardiogenic shock. It discusses:
1. Outcomes of cardiogenic shock, which has high early mortality despite early intervention and is difficult to support medically.
2. Trials of IABP support that have shown no clear benefit on mortality. Ongoing large trials are investigating IABP further.
3. Inconclusive evidence on the benefits of inotropes for cardiogenic shock.
4. Evidence that ECMO can successfully support patients with cardiogenic shock, with survival rates over 50-75% reported for various conditions. Early application of ECMO seems to provide major benefits to patients.
5.
Value Analysis Committee Presentation - PleuraFlow® ACT® SystemPaul Molloy
Presentation explaining how the PleuraFlow® ACT® System from ClearFlow,Inc.can Reduce Complications and Costs for your Cardiothoracic surgery patients.
Dr Vanita Arora - Arrhythmia Diagnosis in IndiaDr Vanita Arora
Dr Vanita Arora is a Senior Consultant Cardiac Electrophysiologist & Interventional Cardiologist, Cardiac Electrophysiology Lab and Arrhythmia Services, 3D Mapping Radio frequency Ablation of the Complex Arrtymias and Arrhythmia Cardiac Diagnosis in India.
Value Analysis Committee Presentation - PleuraFlow® ACT® SystemPaul Molloy
Presentation explaining how the PleuraFlow® ACT® System from ClearFlow,Inc.can Reduce Complications and Costs for your Cardiothoracic surgery patients.
Dr Vanita Arora - Arrhythmia Diagnosis in IndiaDr Vanita Arora
Dr Vanita Arora is a Senior Consultant Cardiac Electrophysiologist & Interventional Cardiologist, Cardiac Electrophysiology Lab and Arrhythmia Services, 3D Mapping Radio frequency Ablation of the Complex Arrtymias and Arrhythmia Cardiac Diagnosis in India.
Atrial fibrillation (afib) is one of the main causes of strokes in the US. New treatment options are available - both medical therapy (such as new blood thinners) and procedures (watchman left atrial appendage closure).
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.
Interpreting toe and ankle pressure curves and results when using PeriFlux 6000Perimed
The aim of this document is to provide an
understanding for the interpretation of the curves
generated during toe and ankle pressure measurements using PeriFlux 6000.
he Citrate Story
David Gattas gives an update on today's go-to anti-coagulant for renal replacement therapy: Citrate
David is a key figure in the ANZICS CTG, with a growing list of publications and was involved in the RENAL and POST-RENAL studies.
Long-Term Survival and Dialysis Dependency Following Acute Kidney Injury in Intensive Care: Extended Follow-up of a Randomized Controlled Trial is available free.
This talk was recorded live at an ICN NSW / ANZICS meeting in September 2014.
Workshop of Low Cardiac Output Management, 2018Isman Firdaus
Low cardiac output or shock or circulatory failure was the terminal state of any disease including cardiovascular problem. It is consist distributive, volume, obstructive and cardiogenic circulatory failure leading multi organ failure and mortality. Hemodynamic monitoring is important evaluation to guide the medication and treatment.
Exercise tolerance testing (also known as exercise testing or exercise stress testing) is used routinely in evaluating patients who present with chest pain, in patients who have chest pain on exertion, and in patients with known ischaemic heart disease.
Isicam, high bleeding risk pci,2016,ismanIsman Firdaus
Presented by Dr. Isman Firdaus in ISICAM 2016
PCI in high bleeding risk patient was tricky management
Drug Coated Stent vs Bare Meta stent regarding LEADERS FREE trial.
BCC4: Michael Parr on ICU - Surviving Trauma GuidelinesSMACC Conference
Michael Parr, director of Liverpool ICU in Australia, speaks about "Surviving Trauma Guidelines". He does so through the use of an interesting case of a patient admitted to ICU following a MVA. This educational podcast was recorded at BCC4.
Atrial fibrillation (afib) is one of the main causes of strokes in the US. New treatment options are available - both medical therapy (such as new blood thinners) and procedures (watchman left atrial appendage closure).
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.
Interpreting toe and ankle pressure curves and results when using PeriFlux 6000Perimed
The aim of this document is to provide an
understanding for the interpretation of the curves
generated during toe and ankle pressure measurements using PeriFlux 6000.
he Citrate Story
David Gattas gives an update on today's go-to anti-coagulant for renal replacement therapy: Citrate
David is a key figure in the ANZICS CTG, with a growing list of publications and was involved in the RENAL and POST-RENAL studies.
Long-Term Survival and Dialysis Dependency Following Acute Kidney Injury in Intensive Care: Extended Follow-up of a Randomized Controlled Trial is available free.
This talk was recorded live at an ICN NSW / ANZICS meeting in September 2014.
Workshop of Low Cardiac Output Management, 2018Isman Firdaus
Low cardiac output or shock or circulatory failure was the terminal state of any disease including cardiovascular problem. It is consist distributive, volume, obstructive and cardiogenic circulatory failure leading multi organ failure and mortality. Hemodynamic monitoring is important evaluation to guide the medication and treatment.
Exercise tolerance testing (also known as exercise testing or exercise stress testing) is used routinely in evaluating patients who present with chest pain, in patients who have chest pain on exertion, and in patients with known ischaemic heart disease.
Isicam, high bleeding risk pci,2016,ismanIsman Firdaus
Presented by Dr. Isman Firdaus in ISICAM 2016
PCI in high bleeding risk patient was tricky management
Drug Coated Stent vs Bare Meta stent regarding LEADERS FREE trial.
BCC4: Michael Parr on ICU - Surviving Trauma GuidelinesSMACC Conference
Michael Parr, director of Liverpool ICU in Australia, speaks about "Surviving Trauma Guidelines". He does so through the use of an interesting case of a patient admitted to ICU following a MVA. This educational podcast was recorded at BCC4.
Important Trials of the Day & Basics of Biostatistics | IACTS SCORE 2020IACTSWeb
This presentation emphasizes on the importance of biostatistics in the interpretation, analysis and design of studies and trials in the daily life of an academic surgeon. It also sheds light on some important clinical trials of the present milieu that are playing a vital role in the course that cardiothoracic surgery is taking.
Courtesy of Dr. Prasanna Simha Mohan Rao, MS, MCh, DNB, PGDHHM. He presently serves as Professor and Unit Chief of Cardiothoracic and Vascular Surgery at Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru.
This presentation accompanies a video that is part of the lecture series of IACTS SCORE 2020 held at the SSSIHMS Whitefield, Bengaluru between 7th and 8th March, 2020.
Remote Ischaemic Conditioning: A Paper Review & Uses in Paramedic Practicebgander23
A 2 part presentation. Part 1 reviews a paper on the long-term clinical outcomes of STEMI patients undergoing remote ischaemic perconditioning prior to primary percutaneous coronary intervention. The 2nd part looks at how this technique can be used in Paramedic practice.
Don’t Miss a Beat: Arrhythmia Detection for Preclinical ECG ResearchInsideScientific
In this webinar sponsored by Data Sciences International, scientists discuss arrhythmia detection in pre-clinical research applications including common challenges and how scientists can improve their data analysis process through the application of Data Insights software.
Dr. Belal A. Mohamed from George-August University discusses how arrhythmia scoring correlates with the stage of myocardial remodeling in a mouse model of transaortic constriction-induced heart failure.
Hank Holzgrefe, a safety pharmacology consultant at Charles River Laboratories, presents his research on dose dependent polymorphic arrhythmia detection in dogs, specifically, on large datasets with time and dose-dependent proarrhythmic effects using Ouabain.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
4. 1992: First ICU
Rotation
• 1800-0800 (14 beds) RMO only cover
• Closed loop control of circulation
• Open loop control of feeding
• Open loop control of tonicity
10. PAC - Clinical Trials
•
Intensive Care 19882006
•
•
•
•
ARDS
General ICU
High Risk Surgery
12 Prospective RCT
11. PAC - Clinical Trials
•
•
•
Evaluated different targets
•
CO / Oxygen Delivery (explicit) or Physician
determined
•
+/- MAP, Urine output, skin changes
Used different guidance (rules)
•
CVP and PAOP (explicit) or Physician determined
Applied different therapy
•
•
Fluids (crystalloids/colloids or RBC)
Drugs (inotropes or pressors)
12. PAC - Clinical Trials
•
•
•
•
•
Intensive Care 1988-2006
ARDS
General ICU
High Risk Surgery
12 Prospective RCT
13. PAC - Clinical Trials
• Various approaches to haemodynamic care in
numerous patient populations using either....
• explicit targeting of cardiac output /
oxygen delivery
• guiding care based on perceived needs
does not improve outcome in a number of high
risk patient groups
18. Fluids - Obsevational
Liberal fluids
associated
with
increased
ICU and
ventilator
time and no
reduction in
renal failure
•
Outcome
Death at 60 days (%)
Ventilator-free days
from day 1 to day 28
ICU-free days
Days 1 to 7
Days 1 to 28
Organ-failure-free days
Days 1 to 7
Cardiovascular failure
CNS failure
Renal failure
Hepatic failure
Coagulation abnormalities
Days 1 to 28
Cardiovascular failure
CNS failure
Renal failure
Hepatic failure
Coagulation abnormalities
Dialysis to day 60
Patients (%)
Days
Conservative Strategy
Liberal Strategy
P Value
25.5
28.4
0.30
14.6 ± 0.5
12.1 ± 0.5
<0.001
0.9 ± 0.1
13.4 ± 0.4
0.6 ± 0.1
11.2 ± 0.4
<0.001
<0.001
3.9 ± 0.1
3.4 ± 0.2
5.5 ± 0.1
5.7 ± 0.1
5.6 ± 0.1
4.2 ± 0.1
2.9 ± 0.2
5.6 ± 0.1
5.5 ± 0.1
5.4 ± 0.1
0.04
0.02
0.45
0.12
0.23
19.0 ± 0.5
18.8 ± 0.5
21.5 ± 0.5
22.0 ± 0.4
22.0 ± 0.4
19.1 ± 0.4
17.2 ± 0.5
21.2 ± 0.5
21.2 ± 0.5
21.5 ± 0.4
0.85
0.03
0.59
0.18
0.37
10
14
0.06
11.0 ± 1.7
10.9 ± 1.4
0.96
ARDS Clinical Trial Network, NEJM 2006
19. Fluids - Observational
After correcting for
age and APACHE II,
positive fluid balance
correlated with
increased mortality
Boyd J.H.et al Crit Care Med 2011
21. Currently
Low Blood Pressure
Low Blood Pressure
Fluids
Fluids
Low Cardiac Output
Low Cardiac Output
Inotropes
Inotropes
Organ Failure
Organ Failure
Vasopressors
Vasopressors
22. Currently
Low Blood Pressure
Low Blood Pressure
Fluids
Fluids
Low Cardiac Output
Low Cardiac Output
Inotropes
Inotropes
Organ Failure
Organ Failure
Vasopressors
Vasopressors
23. The Future ??
• Each decade we reject a new haemodynamic
variable, on which, to base interventions
• 1980: PAWP
• 1990:VO2-DO2 relationship
• 2000: LVEDV GEDVI
• 2010: Forget about monitoring - just
ECHO everything (over and over)
25. Where does that leave
us ?
• Prescriptive Approaches
• RELIEF (Restrictive versus Liberal Fluid
Therapy in Major Abdominal Surgery)
• Clinical Trials.gov Id: NCT 01424150
• Random allocation of drugs
• Targeting Fluid Balance
26. A Physiological Approach
• Instead of targeting MAP or CO/O2D indices
• using DEPENDENT circulatory variables
(e.g. CVP, EDV, PPV) to guide therapy
• Target BOTH simultaneously using
• INDEPENDENT circulatory variables
-
Volume state
Cardiac function
Systemic vascular resistance
35. Independent variables of
the circulation
• MSFP = Volume state
= 0.96(CVP) + 0.04(MAP) + c(CO)
• HP (Heart Performance) = Inotropy state
=(MSFP - RAP) / MSFP
• SVR = Arteriolar tone state
These are the numerical descriptors (indicators) of the circulation
36. Choosing the Target
• Cardiac output
• Mean arterial pressure
• (Cardiac Power = CO x MAP)
• Captures both kinetic and potential energy of
the circulation
• Allows assessment of volume responsiveness
39. Navigator Guidance
Heart efficiency axis
Mean systemic
filling pressure axis
Data from
Monitors
Target zone
Targets set
by clinician
Other data
Systemic
resistance axis
Main menu
area
Data link
Status area
Patient’s
current position
Arrow shows next therapeutic direction
40. •
Intended Control:
Following the arrow
Vertical Axis Control
If Cardiac Power Low: increase MSFP or
Inotropy (depending on HP)
•
•
•
If Cardiac Power High: decrease MSFP or
Inotropy* (depending on HP)
Horizantal Axis Control
•
If Cardiac Power is not well “geared” (SVR too
high or too low): dilators and constrictors
43. What we learned
• Even if you know the independent
determinants of circulatory variables (like
CO)......
• Even if you use them to direct therapy to a
meaningful target (like cardiac power).....
• You don’t necessarily know when you
should change the target and when you
should change the treatments
44. Structured approach to circulatory
care using Navigator
1. Medical
assessment
2. Nursing
assessment
3. Continual
maintenance
Determine Targets
Targets attained and
maintained (ASD < 1.5)
within intervention limits
No change
+
Define (allowable)
interventions
Targets not maintained within
intervention limits (ASD >1.5)
New Target
or
New Intervention
46. Improving Circulatory
Care .....
• Further investigations into physiologically
based treatments
• Cannot accept that understanding the
circulation can’t lead to improved care
50. Cardiogenic Shock
Outcomes
•High early mortality (despite early
intervention)
•Difficult to support medically
•Reasonable quality of life post
•Not invariably associated with irrecoverable myocardial damage
51. IABP
Krischan D. Sjauw
Krischan D. Sjauw
European Heart Journal (2009)
European Heart Journal (2009)
30, 459–468
30, 459–468
56. ECMO
• Extra Corporeal Membrane
Oxygenation is a form of
extracorporeal life support where
an external artificial circuit carries
venous blood from the patient to
a gas exchange device
(oxygenator) where blood
becomes enriched with oxygen
and has carbon dioxide removed.
This blood then re-enters the
patient circulation
• Veno-arterial ECMO
– Percutaneous cardiopulmonary
support (bypass)
67. Alfred CS-AMI
•25 patients (20032012)
•Average Age: 52.4
•Average Days on
Support: 9.14
•56% Survival to
hospital discharge
• 5 NW
• 8 SB
• 12 SW
68. Current Mechanical Treatment
Options for Severe Acute Heart
Failure
•Veno-arterial ECMO
•Centrifugal VAD
• Tandem Heart LVAD
• RVAD, LVAD, BiVAD
•Impella Recover
•B2B (Bridge to Bridge)
•Long term VAD
71. Conclusion
• Cardiogenic shock remains a challenging
syndrome to treat but the early application
of safe ECMO seems possible to provide
major patient benefits
• Simple
• Transferable
Editor's Notes
Consider the interface in two halves:
On the right side are the patient values (red and blue) and adjacent are the entered physician determined target values. For the purposes of the trial, the ranges for cardiac output and mean arterial pressure were automatically set around a single value:
+/- 12% for MAP and +/- 15% for CI
Patient values for age, size and Hb were entered at set up and Hb and SaO2 were updated as the data became available. Current DO2I targets were also represented
On the left hand side, is the target zone and the patient’s current position relative to the target zone. The axes are: Vertical: Volume state and Heart performance and on the horizontal axis the familiar SVR.
The yellow arrow gives the next therapeutic move.
Notice this patient is guided to receive volume (or inotrope depending on the defined HP starting point for commencing inotropes) followed by vasodilation