Susan P Pilbeam presented on patient-ventilator asynchrony and how monitoring the diaphragm's electrical activity (Edi) can help identify and reduce asynchrony. Asynchrony is common, occurring in 25-53% of patients, and can lead to longer ventilation times and muscle atrophy. Edi monitoring provides insights not available from ventilator waveforms alone and can guide modes like NAVA that use Edi to synchronize breathing. Case studies showed rapid resolution of respiratory issues when switching to NAVA-guided ventilation.
Patient ventilator interactions during mechanical ventilationDr.Mahmoud Abbas
Patient Ventilator Interaction during Mechanical Ventilation lecture presented by Dr.Lluis Blanch at Pulmonary Critical Care Egypt Meeting and Exhibition, January 2014. www.pccmegypt.com
An excellent tool to treat refractory hypoxia. Target audience are ICU junior physicians and Respiratory Therapists. It will take away the fear of "What is APRV?" from your hearts and you will feel ready to give it a try.
Patient ventilator interactions during mechanical ventilationDr.Mahmoud Abbas
Patient Ventilator Interaction during Mechanical Ventilation lecture presented by Dr.Lluis Blanch at Pulmonary Critical Care Egypt Meeting and Exhibition, January 2014. www.pccmegypt.com
An excellent tool to treat refractory hypoxia. Target audience are ICU junior physicians and Respiratory Therapists. It will take away the fear of "What is APRV?" from your hearts and you will feel ready to give it a try.
Presentation of Dr. Dean Hess at 10th Pulmonary Medicine Update Course, Cairo, Egypt. Pulmonary Medicine Update Course is organized by Scribe : www.scribeofegypt.com
Presentation of Dr. Lluis Blanch at 10th Pulmonary Medicine Update Course, Cairo, Egypt. Pulmonary Medicine Update Course is organized by Scribe : www.scribeofegypt.com
Mehmed 2015 - effect of vagal stimulation in acute asthmaSAIF MEHMED
vagus nerve stimulation in the carotid sheath was my interest in the past 3 years and the results was amazing that i can share my experience may be in a workshop, the results was interesting patient suffering from bronchial asthma in acute attack this papaer was the first and followed by another one with 52 participant 10 normal ,10 with asthma not in acute attack 32 in acute attack 11 of them treated with placebo and 21 treated with vagus nerve stimulation it takes time was difficult but it deseve
Predictors of weaning from mechanical ventilator outcomeMuhammad Asim Rana
This is a very useful presentation for respiratory therapists and ICU and Emergency physicians. Intended to teach how to assess you patient's readiness for weaning from mechanical ventilator and successful separation from machine.
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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
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
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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
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
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
The POPPY STUDY (Preconception to post-partum cardiovascular function in prim...
Identifying Asynchrony and Solving the Problem - Pilbeam
1. Susan P Pilbeam, MS, RRT, FAARC
Clinical Applications Specialist
Maquet, Inc
Within the past 12 months, the presenter has had an affiliation with the
Maquet, Inc who is sponsoring this presentation.
Objectives
Review the definition and the causes of patient-
ventilator asynchrony.
Show the frequency that asynchrony occurs.
Demonstrate how the electromyograph (EMG) of the
diaphragm can be used to identify asynchrony and
improve synchrony
Discuss how an alternative method of ventilation can
use the EMG of the diaphragm to reduce asynchrony.
Demonstrate the use of Edi and NAVA.
2. What is Patient-Ventilator
Asynchrony?
“…a mismatch between the patient and
the ventilator inspiratory and expiratory
times.” (Thille, Inten Care Med; 32, 1515, 2006)
What is the Most Commonly
Reported Form of Asynchrony?
“Wasted Effort” – The patient wants a breath and
doesn’t get one.
The most severe form of asynchrony:
A combination of oversensitivity trigger setting, high
sedation levels and high assist levels.
Leaks also contribute to asynchrony.
Sinderby C, Beck J: Neurally adjusted assist for infants in critical
Condition. Pediatric Health 2009, 3(4):297-301 (edit)
3. Ventilator Waveform Identification
Georgopoulos (2006)
“Flow, volume, and airway pressure waveforms are
valuable real-time tools in identifying various aspects
of patient-ventilator interaction.”
However, “If you aren’t looking for something, you
surely will not to find it.”
Can You Identify Asynchrony?
4. Experts Versus Non-Experts
Columbo, et al, CCM 2011, 39:11
Experts Versus Non-Experts
Columbo, et al, CCM 2011, 39:11
5. Experts Versus Non-Experts
Columbo, et al, CCM 2011, 39:11
Experts Versus Non-Experts
Columbo, et al, CCM 2011, 39:11
7. SAME PATIENT SHOWING DIAPHRAGM ACTIVITY
1 2 3
1 2 3
Courtesy: Dan Rowley
PRESSURE SUPPORT –
IS THE PATIENT TRIGGERING THE VENTILATOR?
8. YOU HAVE SEEN A PATIENT LIKE
THIS
John Marini, 1992, Resp Care
Patient-Ventilator Asynchrony
How much of asynchrony is “us”?
How much is the machine?
9. How Do Ventilator Parameters We Set
Affect Patient-Ventilator Synchrony?
Setting sensitivity appropriate to the patient
Inappropriate trigger increases ventilation time. (deWit,
et al: CCM 2009, 37:2740)
Providing adequate inspiratory flow
Insuring appropriate volume or pressure delivery
Ending the breath when the patient is done
10. How Often is Asynchrony Really Present?
One in four patients (25%) exhibited asynchrony during
assist/control or PSV ventilation. (Thille et al: Inten Care Med
2006:32:1515; De Wit, et al (CCM 37(10): 2009)
Exhibited as inability to trigger or double triggering, or
inappropriate Ti time.
During SIMV 53% of the total mandatory breath time was
asynchronous compared to the measured neural drive.
Every mandatory breath was asynchronous
(Beck et al: Ped Research, 65(6), 2009, 663)
But…(With Heavy Sedation)…!
Lack of use of the diaphragm and mechanical
ventilation can also lead to wasting (severe atrophy)
and damage to the respiratory muscles. (ventilator
induced diaphragm dysfunction, VIDD)
“Specifically related to the use of mechanical
ventilation is the loss of diaphragmatic force generating
capacity.” Levine, et al NEJM 2008, 358:13
Increased length of intubation and ventilation (Petrof,
et al Curr Opin Crit Care 16:19-25, 2010)
11. DISUSE ATROPHY IN NEONATES
Long term ventilatory assistance may
predispose diaphragmatic myofibers to
disuse atrophy or failure of normal
growth. (1988)
47 Days of mechanical ventilation
0 Days of mechanical ventilation
Source: Knisely A.S., et al. Abnormalities of diaphragmatic muscle in
Neonates with ventilated lungs. The Journal of Pediatrics. 1988; 113:1074-7
ATROPHY AND DAMAGED OF THE
DIAPHRAGM MUSCLE
“The diaphragm is not a biologically inert organ that
can be light-heartedly substituted by the ventilator:
the vital pump is both malleable and vulnerable.”
Vassilakopoulos T et al. AJRCCM,2004;169: 336-341.
12. Ventilator Induced Diaphragm
Dysfunction (VIDD)
“…18 – 69 hours of complete diaphragmatic inactivity
and MV results in marked (50%) atrophy of human
diaphragm fibers.” Levine et al. NEJM 2008; 358(13):1327-1335.
Additional study of volunteers and a second group of
organ donors.
Ventilation between 2 and 4 hours and up to 10 days.
Leads to diaphragm disuse degeneration. (Hussain
SNA, et al, 2010, AJRCCM 182:1377)
PROBLEMS WITH MECHANICAL
VENTILATION
Not only…
Asynchrony
Atrophy and ventilator induced
diaphragm dysfunction (VIDD)
VILI (Baro/volume/biotrauma)
VAP
13. PURPOSE OF VENTILATION?
A major goal is to reduce a patient’s work of
breathing, not increase it.
Achievement of this goal is dependent on
satisfactory patient-ventilator interaction.
“The machine needs to cycle in unison with the
rhythmic contractions of a patient’s diaphragm.”
Parthasarathy S, Jurbran A, Tobin MJ. Amer J of Crit Care Med 2000; 162:546-552
ACHIEVING SYNCHRONY
Synchronous ventilation can potentially be
achieved by:
Manipulation of rate
Inspiratory time
Employment of patient triggered ventilation
Largely achieved by the practitioner
Greenough A, Dimitriou G, Prendergast M, Milner AD. Synchronized mechanical ventilation for respiratory support in newborn
infants. Cochrane Database of Systematic Reviews 2008, Issue 1. Art.No.:CD000456. DOI:
14. Respiratory Therapist
Have Hard Jobs
This seminar has presented important issues that are
a part of our job.
Patients with asthma are another example of the
serious problem we deal with.
Another Asynchrony Phenomena
Double Triggered Breath
Double triggering is defined as two cycles of breath
delivery separated by a very short expiratory time.
15. Not using ventilator graphics, but…
Identifying asynchrony using
esophageal pressures and
the diaphragm’s electrical activity
(Edi)
Thille & Brochard, Inten Care Med 2007; 33:744
16. Possible Causes Double Trigger
Patients with ALI/ARDS and high ventilatory demand
and low PaO2/FIO2 ratio, high Ppeak and high levels of
PEEP.
In patients on PSV, set pressure too high for patient and
over-sedation can lead to double trigger.
17. BENEFITS OF SYNCHRONY
During synchronized mechanical ventilation
Positive airway pressure and spontaneous inspiration
coincide.
If synchronous ventilation is provided:
Adequate gas exchange
Lower peak airway pressures
Potentially reducing baro/volutrauma and, in infants,
bronchopulmonary displasia (BPD)
Greenough A, Dimitriou G, Prendergast M, Milner AD. Synchronized mechanical ventilation for respiratory support in newborn
infants. Cochrane Database of Systematic Reviews 2008, Issue 1. Art.No.:CD000456. DOI:
WHAT TO DO WHEN THE PATIENT
IS NOT SYNCHRONIZED?
What is our current clinical practice when the patient
is out of sync with the ventilator?
Can you say…
Propofol
18. Problems With Sedation
Already identified VIDD
Increased length of intubation
Increased length of stay
Sedation Trials
Spontaneous awakening trials (SAT, interruption
of sedation) paired with spontaneous breathing
trials(SBT).
Resulted in better outcomes than with standard
approaches.
Improve ventilator free days 14+7 vs. 11+6 = 3+1 Day
Decrease time in coma
Decrease time in the ICU and Hospital
Sedation trials (awakening trials) should become
the standard approach.
Lancet 2008; 371: 126–34, Ely’s group
19. ECG Waveforms
An ECG is the standard of care for a variety of
patient problems.
What if we could monitor the ECG of the
diaphragm?
ECG OF THE DIAPHRAGM
Monitoring diaphragmatic electrical activity permits monitoring between neural
drive and the ventilator breath delivery.
Monitoring diaphragmatic electrical activity comes closest to representing the
ideal in ventilator monitoring.
Source: MacIntyre N. Evolving Approaches to assessing and monitoring patient ventilator interaction.
Current Opinion in Critical Care. 2010 Published ahead of print.
20. How Edi is Monitored?
Nasogastric Tube with Monitoring
Electrodes
Similar to the leads on
an EKG
Electrodes are internal
(esophagus)
Edi is 1/10th and 1/100th
the strength of the
heart’s electrical activity.
22. Monitoring Available in Any Mode
USING EDI TO MONITOR THE DIAPHRAGM
AND IMPROVE SYNCHRONY
What is a normal Edi
signal?
What causes a low Edi
signal?
What causes a high Edi
signal?
23. Low Edi signal
Sedation
Neural disorder
Muscle relaxants
Paralytics
Brain injury or
Brain dead
Hyperventilation
24. High Edi Signal
Increased respiratory drive
High CO2 values or low O2 values
Increased resistance
Increased respiratory
workload
Sigh Breath
Assist/Control Volume
26. PC Card
Edi Catheter
What is the Ideal Ventilator?
Laghi, Franco, NAVA: Brain over Machine? Intensive Care Medicine; 2008
“Ideal ventilator should be able to record the activity of
the respiratory neural system, and use that
measurement to select a satisfactory tidal volume. “
29. Patient Case – 54 y.o. Woman
Post-op for draining of an intracraneal bleed.
Three days on ventilatory support with difficulty
weaning.
Patient became very agitated whenever sedation level
was reduced (40 mg of propofol)
Unknown cause of agitation
ABG on current settings: 7.43/ PC02 38/ P02 281.
30. Ventilator Settings
Edi Catheter Inserted
No activity from the diaphragm
Still receiving sedation
Propofol was weaned
NAVA was implemented as soon as Edi was
restored.
The patient was calm and not agitated!
Vital signs stable
32. Patient Extubate – 1.5 Hours
Ventilator on Standby
NAVA catheter staying in place
Used to monitor patient after extubation
The physician said that this patient would have been
intubated at least a day or two longer.
Used Catheter to monitor patient after
extubation.
33. Patient Admitting Information
A women in her late 50s year was brought into the
Emergency Department by ambulance shortly after
midnight.
She had signs of respiratory failure.
Blood gases were drawn on a non-rebreathing mask:
Ph 7.11 PaCO2 = 56, PaO2 = 51 SpO2 60%
Chest radiograph report: Ground glass pattern with
left upper lobe opacity, possible the beginning of
ARDS and extensive bilateral infiltrates.
34. Day 1 – 00:05 (After Midnight)
Mechanical Ventilation
The patient was intubated and placed on mechanical
ventilation.
Aspiration of secretions from the ET tube showed the
contents of a recently eaten meal.
PRVC, Vt = 600 , rate =18 , PEEP = 7, 100% oxygen.
(VE = 10.8 L/min)
Blood gases: pH = 7.11, PaCO2 = 56, PaO2 = 51 SpO2 =
89%
Physician stated this patient was in early ARDS: low
compliance, poor PaO2/FiO2 ratio.
35. Day 1 Continued:
Protective Ventilation
Vt decreased to 500 ml (6 mL/kg IBW) and rate
increased to 20 b/min (VE = 10 L/min)
Blood gases: pH = 7.20, PaCO2 = 50, PaO2 = 62, SpO2
= 90%.
Physician stated this patient was in early ARDS: low
compliance, poor PaO2/FiO2 ratio.
Difficulty Oxygenating the Patient
Same day adjustments to ventilator.
PRVC: Vt = 350, rate = 22,
PEEP = 14, oxygen at 100%
pH = 7.31, PaCO2 = 37, PaO2 = 92 SpO2 = 98%
Ventilation was improved, but oxygenation was not.
36. Day 2 – Not Much Change
With no significant improvement by the morning of
the next day, the RTs discussed the use of NAVA with
the patient’s physician.
NAVA was instituted the afternoon of the second day.
During the night the RT reported the patient
tolerated NAVA well without the need for excessive
sedation.
The RT stated that the patient was coughing so much
that they had to change the expiratory filter 4 times
during their shift. “You should have seen the stuff
(secretions) coming out of her lungs.”
Day 3- Morning Chest Radiograph
37. RADIOLOGIST’S REPORT
Results of chest radiograph in the morning following
institution of NAVA the night before.
“Significant clearing of infiltrates. What did you do to
this patient?”
QUICK TURN AROUND FOR PATIENT
Morning ABGs while on NAVA at 50% FiO2
pH = 7.43, PaCO2 = 40, PaO2 = 92 SpO2 = 96%
After about 14 hours on NAVA they were able to
extubate the patient.
The patient was on the ventilator a total of only three
days and was transferred out of the unit the next
morning.
38. Case Review
Physician noted that typically a patient with
aspiration pneumonia and ALI would have been on
ventilation for 5-7 days.
Resolution occurred very quickly following the use of
NAVA
This is a novel case which suggests benefit of the
mode NAVA.
A study done on weaning patients with ARDS
PS vs NAVA (Terzi N, et al,CCM 2010 vol 38)
NAVA significantly reduced asynchrony and may help
avoid over-assist.
Questions in Neonates
(Howard Stein, MD)
Is central apnea really ‘central’ in
origin?
Is SIMV (pressure control) in
premature infants really
‘synchronized’?
Is the neural trigger synchronous?
39. True central apnea in a 1 month old 23 week infant.
Is SIMV (pressure control) in Premature
Infants Really ‘Synchronized’?
41. SIMV (pressure control) with EDI superimposed shows the lack of
synchrony on the flow triggered breaths
Is Neural Ventilation synchronous
NAVA in a 1 month old ex 23 week infant.
42. Patient Case
28 week old
Self-extubated following ventilation with NAVA
Not reintubated but put on high flow therapy
Edi catheter still in place and used to monitor
Bubble Cpap 7cmH20
45. Summary
Ventilator Asynchrony is a serious and prevalent
problem for ventilated pateints.
Edi allows monitoring of the diaphragm’s activity to
evaluate ventilator asynchyrony.
With the NAVA mode, the patient’s neural center
activity (Edi) controls the ventilator.
Improves patient-ventilator synchrony and reduce
work of breathing
Potential Benefits – less sedation, lung protective,
fewer ventilator days, monitor diaphragm fatigue
Providing Ventilation is Lifesaving