Basic information on the Graphics displayed on the Ventilators. Prepared to educate about the graphics to train the professionals who work with Ventilators.
Basic information on the Graphics displayed on the Ventilators. Prepared to educate about the graphics to train the professionals who work with Ventilators.
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
Final newer modes and facts niv chandanChandan Sheet
THIS IS THE BASIC POINTS REGARDING NIV, THIS IS COMPILED AND ARRANGED FROM DIFFERENT BOOKS, JOURNALS AND PPTs.
The author is grateful to the teachers and authors of pulmonology and critical care.
Ventilatory management of Acute Hypercapnic Respiratory FailureVitrag Shah
Presentation on ventilatory management in Acute Hypercapnic Respiratory Failure
Updated information till 17/8/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36513-ventilatory-management-acute-hypercapnic-respiratory-failure-presentation.html
Download review articles and guidelines for ventilatory management in COPD & Asthma
http://www.medicalgeek.com/articles-and-news/36514-articles-ventilatory-management-copd-asthma.html
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
Final newer modes and facts niv chandanChandan Sheet
THIS IS THE BASIC POINTS REGARDING NIV, THIS IS COMPILED AND ARRANGED FROM DIFFERENT BOOKS, JOURNALS AND PPTs.
The author is grateful to the teachers and authors of pulmonology and critical care.
Ventilatory management of Acute Hypercapnic Respiratory FailureVitrag Shah
Presentation on ventilatory management in Acute Hypercapnic Respiratory Failure
Updated information till 17/8/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36513-ventilatory-management-acute-hypercapnic-respiratory-failure-presentation.html
Download review articles and guidelines for ventilatory management in COPD & Asthma
http://www.medicalgeek.com/articles-and-news/36514-articles-ventilatory-management-copd-asthma.html
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.
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
11. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
B) Technical quality
C) Report Ventilator findings
12. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
Oxygen Saturations
End Tidal CO2 Trace
Haemodynamics
13. B) Technical qualityReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
Know your ventilator
..and the alarms
14. C) Report Ventilator findingsReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
1) Mode?
2) Parameters set and achieved?
4) Interpretation?
3) Information from waveforms/
manoeuvres ?
24. 4) Interpretation?
C) Report Ventilator findings
Safe ventilation?
TV 6-8ml/kg
Pplat<30
Safe oxygenation?
FiO2<60%
Other problems:
Low Compliance
High Resistance
25. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
B) Technical quality
C) Report Ventilator findings
1) Mode?
2) Parameters set and achieved?
4) Interpretation?
3) Information from waveforms/
manoeuvres ?
Safe ventilation?
Safe oxygenation?
Other problems
26. If you change the ventilator settings
REASSESS the patient
37. INTERPRETATION
IS VENTILATION SAFE?
IS OXYGENATION SAFE?
Other ISSUES?
Safe ventilation?
TV 6-8ml/kg
Pplat<30
Safe oxygenation?
FiO2<60%
Other problems:
Low Compliance
High Resistance
I:E ratio of 1:1
38. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
B) Technical quality
C) Report Ventilator findings
1) Mode?
2) Parameters set and achieved?
4) Interpretation?
3) Information from waveforms/
manoeuvres ?
Safe ventilation?
Safe oxygenation?
Other problems
41. PRESSURE TIME CURVE
Volume mode
Values
Pattern
Increased PIP
Same shape. Higher pressures
Values
Pattern
Expiratory limb back
to baseline
42. FLOW TIME CURVE
Volume mode
Values
Pattern
Increased Expiratory flow rate
Flow pattern normal
Area under curve same in both
Curve finishes earlier
Values
Pattern
No Change
43. HISTORY
Rosa, 36 year old lady with respiratory failure 2’
to Community acquired pneumonia
Day 1 ICU
Weight= 80 Kg (Predicted body weight)
History
51. INTERPRETATION
Severe respiratory failure with P/F ratio of 65
Poor lung compliance, with high plateau
pressures
IS VENTILATION SAFE?
IS OXYGENATION SAFE?
Other ISSUES?
Safe ventilation?
TV 6-8ml/kg
Pplat<30
Safe oxygenation?
FiO2<60%
Other problems:
Low Compliance
High Resistance
53. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
B) Technical quality
C) Report Ventilator findings
1) Mode?
2) Parameters set and achieved?
4) Interpretation?
3) Information from waveforms/
manoeuvres ?
Safe ventilation?
Safe oxygenation?
Other problems
56. PRESSURE TIME CURVE
Increased Airway Resistance
Values
Pattern
Increased PIP
Rapid rise in PIP. Then tapers down
Values
Pattern
Expiratory limb back
to baseline
VOLUME
MODE
57. Values
Pattern
FLOW TIME CURVE
Increased Airway Resistance
Values
Pattern
Decreased Expiratory flow rate
Increased expiratory time
Rises to zero baseline just before next breath
VOLUME
MODE
68. INTERPRETATION
IS VENTILATION SAFE?
IS OXYGENATION SAFE?
Other problems?
Safe ventilation?
TV 6-8ml/kg
Pplat<30
Safe oxygenation?
FiO2<60%
Other problems:
Low Compliance
High Resistance
INCREASED AIRWAY RESISTANCE
NO gas trapping
75. INTERPRETATION
IS VENTILATION SAFE?
IS OXYGENATION SAFE?
Other Problems?
Gas trapping
Safe ventilation?
TV 6-8ml/kg
Pplat<30
Safe oxygenation?
FiO2<60%
Other problems:
Low Compliance
High Resistance
Dyssynchrony
Equipment
77. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
B) Technical quality
C) Report Ventilator findings
1) Mode?
2) Parameters set and achieved?
4) Interpretation?
3) Information from waveforms/
manoeuvres ?
Safe ventilation?
Safe oxygenation?
Other problems
81. A) Patient AssessmentReport ECG
findingsDesc
ribe
Inter
pret
Patient
Assessme
nt
B) Technical quality
C) Report Ventilator findings
1) Mode?
2) Parameters set and achieved?
4) Interpretation?
3) Information from waveforms/
manoeuvres ?
Safe ventilation?
Safe oxygenation?
Other problems
83. References
Critical Care Medicine Tutorials
http://www.ccmtutorials.com/rs/mv/
Puritan Bennett™ , 840 Ventilator, User’s Pocket Guide
http://www.covidien.com/imageServer.aspx/doc228227.pdf?contentID=26430&contentt
ype=application/pdf
Curves and loops in mechanical ventilation
http://www.draeger.net/media/10/08/41/10084127/rsp_curves_and_loops_booklet_90
97339_en.pdf
http://lifeinthefastlane.com/education/ccc/pressure-vs-time-graph/
Oh's Intensive Care Manual, 6e
Andrew D Bersten, Neil Soni
Provide a system for reading the ventilator
Reading the ventilator is just not about the waveforms
Interpret findings in context of the clinical situation
Pragmatic talk. My system for incorporating information from vent in patient assessment
Case based discussions
Test your knowledge
NOT: mechanical vent/ waveform/ modes of ventilation
DISCLAIMER
Assess your patient… with specific attention to …
Assess your patient… with specific attention to …
Assess your patient… with specific attention to …
Resistance and flow PATTERN affect the peak pressure
Compliance and affect the plateau pressure
Change shape
Assess your patient… with specific attention to …
Predicted body weight based on gender and height
Interactions between flow/ IE ratios
Flow: exp limb meet baseline just before next breath
? Secondary to I:E= 1:1
Parameters + Waveforms
Safe ventilation= No
Safe oxygenation= No
Other complications:
Severe respiratory failure with P/F ratio of 65
Poor lung compliance, with high plateau pressures
Assess your patient… with specific attention to …
Also important to exlude problems with pelura and chest wall
Same shape
Hgher
Predicted body weight based on gender and height
Predicted body weight based on gender and height
Predicted body weight based on gender and height
Predicted body weight based on gender and height
Predicted body weight based on gender and height
Interactions between flow/ IE ratios
Parameters + Waveforms
Safe ventilation= No
Safe oxygenation= No
Other complications:
Severe respiratory failure with P/F ratio of 65
Poor lung compliance, with high plateau pressures
I am expecting lady with COPD to have bronchospasm--- leading to high resistnce and Pressure. In this setting impotant to exclude other causes of high P- ETT
The gas takes a long time to leave patients lungs
The gas takes a long time to leave patients lungs
Predicted body weight based on gender and height
Predicted body weight based on gender and height
Interactions between flow/ IE ratios
Parameters + Waveforms
Safe ventilation= No
Safe oxygenation= No
Other complications:
Severe respiratory failure with P/F ratio of 65
Poor lung compliance, with high plateau pressures
Dynamic hyperinflation
The phenomenon that occurs when a new breath begins before the lung has reached the static equilibrium volume is called dynamic hyperinflation.[1]
To qunatify degree of autopeep
Parameters + Waveforms
Safe ventilation= No
Safe oxygenation= No
Other complications:
Severe respiratory failure with P/F ratio of 65
Poor lung compliance, with high plateau pressures