This document discusses mechanical ventilation, including:
1) The basics of invasive positive pressure ventilation (IPPV) and noninvasive positive pressure ventilation (NIPPV) and how they help reduce work of breathing and restore gas exchange.
2) Important considerations for initiating IPPV including indications like respiratory failure and risks like hypotension and lung injury.
3) Key principles of mechanical ventilation including the equation of motion, partitioning work between the ventilator and patient, and common modes of ventilation.
Learning Objectives Covered1. Explain the importance of monitor.docxsmile790243
Learning Objectives Covered:
1. Explain the importance of monitoring plateau pressures and its use in calculating static compliance
2. Explain the use of volume-controlled ventilation and pressure-controlled ventilation
3. List and describe ventilatory support treatment plans for patient’s based on their clinical diagnosis
Background
Compliance is a measurement of the distensibility of the lung or the ability of the lung to distend. It is expressed as a change in volume divided by a change in pressure using the standard units of Liters/cmH20. The normal lung + thorax compliance of an adult is around 0.1 L/cmH20. When the compliance is low, more pressure will be needed to deliver a given volume of gas to a patient. Diseases that cause low lung compliance are classified as restrictive diseases and include Adult Respiratory Distress Syndrome (ARDS), pulmonary edema, pneumonectomy, pleural effusion, pulmonary fibrosis, and pneumonia among others. Emphysema is a typical cause of increased lung compliance.
When measuring lung compliance one must know the delivered tidal volume and must also know the change in alveolar pressure that results from the addition of that known tidal volume. Alveolar pressure is the pressure in the distensible parts of the respiratory tract and is determined by the tidal volume and the lung/chest compliance. Airway pressure is the pressure measured at the patient’s airway during mechanical ventilation. Airway pressure is equal to alveolar pressure when there is no occurrence of airflow. At the end of a mechanical inspiration, flow to the distal parts of the lungs continues even after inspiratory flow from the ventilator stops, as time is required for gas to reach the periphery of the lung. To measure alveolar pressure, one must measure the airway pressure at a time when both pressures are equal, i.e. when there is no flow.
We normally assume that alveolar and airway pressure starts out at atmospheric (our zero reference) before an inspiration starts. To equalize airway and alveolar pressures, we only have to prevent exhalation after inspiration has ceased by utilizing an inspiratory hold maneuver. The actual calculation is to divide the delivered tidal volume by the plateau pressure where the plateau pressure is the steady-state pressure measured during an inspiratory hold maneuver. Since approximate values are adequate for clinical use, clinicians use the plateau pressure minus the end expiratory pressure that is then divided into the exhaled tidal volume as measured by the ventilator. This compliance measurement is referred to as static compliance since it is measured after an inspiratory hold and there is no gas flow during its measurement.
Cstatic = exhaled VT (ml)
Pplat (cmH2O) – PEEP (cmH2O)
Where:
VT – Tidal Volume
Pplat = Plateau Pressure
A spontaneously breathing person has a normal compliance of approximately 100mL/cmH2O. In intubated patients, normal comp ...
Learning Objectives Covered1. Explain the importance of monitor.docxsmile790243
Learning Objectives Covered:
1. Explain the importance of monitoring plateau pressures and its use in calculating static compliance
2. Explain the use of volume-controlled ventilation and pressure-controlled ventilation
3. List and describe ventilatory support treatment plans for patient’s based on their clinical diagnosis
Background
Compliance is a measurement of the distensibility of the lung or the ability of the lung to distend. It is expressed as a change in volume divided by a change in pressure using the standard units of Liters/cmH20. The normal lung + thorax compliance of an adult is around 0.1 L/cmH20. When the compliance is low, more pressure will be needed to deliver a given volume of gas to a patient. Diseases that cause low lung compliance are classified as restrictive diseases and include Adult Respiratory Distress Syndrome (ARDS), pulmonary edema, pneumonectomy, pleural effusion, pulmonary fibrosis, and pneumonia among others. Emphysema is a typical cause of increased lung compliance.
When measuring lung compliance one must know the delivered tidal volume and must also know the change in alveolar pressure that results from the addition of that known tidal volume. Alveolar pressure is the pressure in the distensible parts of the respiratory tract and is determined by the tidal volume and the lung/chest compliance. Airway pressure is the pressure measured at the patient’s airway during mechanical ventilation. Airway pressure is equal to alveolar pressure when there is no occurrence of airflow. At the end of a mechanical inspiration, flow to the distal parts of the lungs continues even after inspiratory flow from the ventilator stops, as time is required for gas to reach the periphery of the lung. To measure alveolar pressure, one must measure the airway pressure at a time when both pressures are equal, i.e. when there is no flow.
We normally assume that alveolar and airway pressure starts out at atmospheric (our zero reference) before an inspiration starts. To equalize airway and alveolar pressures, we only have to prevent exhalation after inspiration has ceased by utilizing an inspiratory hold maneuver. The actual calculation is to divide the delivered tidal volume by the plateau pressure where the plateau pressure is the steady-state pressure measured during an inspiratory hold maneuver. Since approximate values are adequate for clinical use, clinicians use the plateau pressure minus the end expiratory pressure that is then divided into the exhaled tidal volume as measured by the ventilator. This compliance measurement is referred to as static compliance since it is measured after an inspiratory hold and there is no gas flow during its measurement.
Cstatic = exhaled VT (ml)
Pplat (cmH2O) – PEEP (cmH2O)
Where:
VT – Tidal Volume
Pplat = Plateau Pressure
A spontaneously breathing person has a normal compliance of approximately 100mL/cmH2O. In intubated patients, normal comp ...
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
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.
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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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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Hemodialysis: Chapter 3, Dialysis Water Unit - Dr.Gawad
ventilator_Omar_2016.ppt
1. Basics and Advances of
Mechanical Ventilation
Omar A. Elshaarawy
Senior Resident of Hepatology
1
2. Objectives
To understand:
How positive pressure ventilation helps
• Reduce the work of breathing
• Restore adequate gas exchange
The basics of
• Invasive positive pressure ventilation (IPPV)
• Noninvasive positive pressure ventilation (NIPPV)
The principles of bedside monitoring
• Pressure and volume alarms
• Flow and pressure time curves
2
3. Physiopathology of Respiratory Failure30
ResistanceAW ComplianceR
D VA/Q
Work of Breathing
Fatigue
Hypercapnia
Neuromuscular
disorders
VE
VO2
VCO2
pH
Hypoxemia
AW=Airrway; R=respiratroy system; VE = minute ventilation, VO2 = Oxygen consumption, VCO2=carbon dioxide production
3
4. Indications and Rationale for Initiating IPPV
Unprotected and unstable airways (e.g,, coma)
• Intubation and IPPV allows to
- Secure the airways
- Reduce the risk of aspiration
- Maintain adequate alveolar ventilation
Hypercapnic respiratory acidosis
• IPPV and NIPPV
- Reduce the work of breathing and thus prevents respiratory muscle fatigue or speeds
recovery when fatigue is already present
- Maintain adequate alveolar ventilation (prevent or limit respiratory acidosis as needed)
Hypoxic respiratory failure
• IPPV and NIPPV help correct hypoxemia as it allows to
- Deliver a high FiO2 (100% if needed during IPPV)
- Reduce shunt by maintaining flooded or collapsed alveoli open
Others
• Intubation to facilitate procedure (bronchoscopy), bronchial suctioning
4
5. Important Pitfalls and Problems Associated
with PPV
Potential detrimental effects associated with PPV
• Heart and circulation
- Reduced venous return and afterload
- Hypotension and reduced cardiac output
• Lungs
- Barotrauma
- Ventilator-induced lung injury
- Air trapping
• Gas exchange
- May increase dead space (compression of capillaries)
- Shunt (e.g., unilateral lung disease - the increase in vascular resistance in the normal lung
associated with PPV tends to redirect blood flow in the abnormal lung)
5
6. Decreased preload
• Positive alveolar pressure ↑ lung volume compression of the heart by the inflated lungs
the intramural pressure of the heart cavities rises (e.g., ↑ RAP) venous return decreases
preload is reduced stroke volume decreases cardiac output and blood pressure may
drop. This can be minimized with i.v. fluid, which helps restore adequate venous return and
preload.
• Patients who are very sensitive to change in preload conditions (e.g., presence of
hypovolemia, tamponade, PE, severe air trapping) are particularly prone to hypotension
when PPV is initiated.
Reduced afterload
• Lung expansion increases extramural pressure (which helps pump blood out of the thorax)
and thereby reduces LV afterload.
• When the cardiac performance is mainly determined by changes in afterload than in preload
conditions (e.g., hypervolemic patient with systolic heart failure), PPV may be associated with
an improved stroke volume. PPV is very helpful in patients with cardiogenic pulmonary
edema, as it helps to reduce preload (lung congestion) and afterload. As a result stroke
volume tends to increase.
Important Effects of PPV on Hemodynamics
6
7. Generally speaking, the effects of PPV on the cardiac chamber
transmural pressures vary in parallel with:
• Airway pressure (e.g., ↑ airway pressure ↓ venous return)
• Lung compliance (e.g., ↑ compliance ↓ venous return)
• Chest wall stiffness (e.g., in the obese patients, a given change in airway
pressure and lung volume will have more impact on the
hemodynamics, given that the pressure rise around the
heart is going to be higher than in patients with
compliant chest wall, everything else being equal)
Effects of PPV on Hemodynamics
Marini, Wheeler. Crit Care Med. The Essentials. 1997.
7
8. Alveolar Pressure and Gas Exchange
Intensity
of
the
effects
Alveolar Pressure
PaO2
Dead space
Oxygen transport
Adapted from: Marini, et al. Crit Care Med. 1992.
Note that as airway pressure increases above a certain level (e.g., high
PEEP [positive end-expiratory pressure]):
• Oxygen transport start to decline despite the rising PaO2 as cardiac output starts falling.
• Dead space also tends to increase due to compression of alveolar capillaries by high alveolar
pressure, creating ventilated but poorly perfused alveolar units.
8
9. Other Potentially Adverse Effects of Mechanical
Ventilation
Excessive airway pressure and tidal volume can lead to lung injury
(ventilatorinduced lung injury) and contribute to increased mortality.
The Acute Respiratory Distress Syndrome
Network. N Engl J Med. 2000;342:1301-1308.
Lungs of dogs ventilated for a few hours with large
tidal volume demonstrate extensive hemorrhagic
injury.
9
10. Other Potentially Adverse Effects of Mechanical
Ventilation
In the setting of obstructive physiology (e.g., asthma and COPD),
adjustment of the tidal volume and rate minute ventilation to restore a
normal pH and PaCO2 can lead to air trapping, pneumothoraces, and
severe hypotension.
Upper Panel: When airway resistances are high, there is for a few
breath more air going in than coming out of the lungs (dynamic
hyperinflation). Subsequently, a new equilibrium is reached. The
amount of air trapped can be estimated in a passive patient by
discontinuing ventilation and collecting the expired volume (lower
panel).
The volume of trapped gas is largely determined by:
1. The severity of airway obstruction
2. The ventilator settings (see advance course for details). Of all the
settings, the imposed minutes ventilation (set rate x VT) and the
most important one.
3. The time left between tidal breath for exhalation is less important
if a low VT and VE are targeted.
10
11. Positive Pressure Ventilation:
The Equation of Motion
In a passive subject, airway pressure represents the entire pressure (P) applied
across the respiratory system.
The work required to deliver a tidal breath (Wb) = tidal volume (VT) x airway
pressure
The pressure (P) associated with the delivery of a tidal breath is defined by the
simplified equation of motion of the respiratory system (lungs & chest wall):
P = VT/CR+ VT/Ti x RR + PEEP total
Where CR = compliance of the respiratory system, Ti = inspiratory time and VT/Ti = Flow, RR = resistance of the respiratory system and
PEEP total = the alveolar pressure at the end of expiration = external PEEP + auto (or intrinsic) PEEP, if any. Auto PEEP = PEEP total – P
extrinsic (PEEP dialed in the ventilator) adds to the inspiratory pressure one needs to generate a tidal breath.
P elastic P resistive P elastic
11
12. Work of Breathing
Work per breath is depicted as a pressure-volume area
Work per breath (Wbreath) = P x tidal volume (VT)
Wmin = wbreath x respiratory rate
Pressure Pressure Pressure
Volume
Volume
Volume
V
T
WR = resistive work
WEL = elastic work
The total work of breathing can be partitioned between an elastic and resistive work. By analogy, the pressure needed to inflate a balloon
through a straw varies; one needs to overcome the resistance of the straw and the elasticity of the balloon.
12
13. Intrinsic PEEP and Work of Breathing
Volume
V
T
V
T
FRC
Pressure
PEEPi
Dynamic
Hyperinflation
PEEPi = intrinsic or auto PEEP; green triangle = tidal elastic work; red loop = flow resistive work; blue rectangle = work expended in
offsetting intrinsic PEEP (an expiratory driver) during inflation
When present, intrinsic PEEP contributes to the work of breaking and can
be offset by applying external PEEP.
13
14. +
+
+
+
The Pressure and Work of Breathing can be Entirely
Provided by the Ventilator (Passive Patient)
Ventilator
₊ ₊
14
15. Work of Breathing Under Passive Conditions
When the lung is inflated by constant flow, time and volume are linearly related. Therefore,
the monitored airway pressure tracing (Paw) reflects the pressure-volume work area during
inspiration. A pressure-sensing esophageal balloon reflects the average pressure change in
the pleural space and therefore the work of chest wall expansion.
15
16. The Work of Breathing can be Shared Between the
Ventilator and the Patient
PAW
PES
patient machine
time
AC mode
The ventilator generates positive pressure within the airway and the patient’s
inspiratory muscles generate negative pressure in the pleural space.
Paw = Airway pressure, Pes= esophageal pressure 16
17. Relationship Between the Set Pressure Support
Level and the Patient’s Breathing Effort
Carrey et al. Chest. 1990;97:150.
The changes in Pes
(esophageal
pressure) and in the
diaphragmatic activity
(EMG) associated
with the increase in
the level of mask
pressure (Pmask =
pressure support)
indicate transfer of
the work of breathing
from the patient to
the ventilator.
17
18. Partitioning of the Workload Between the Ventilator
and the Patient
How the work of breathing partitions between the patient and the ventilator
depends on:
• Mode of ventilation (e.g., in assist control most of the work is usually done by the ventilator)
• Patient effort and synchrony with the mode of ventilation
• Specific settings of a given mode (e.g., level of pressure in PS and set rate in SIMV)
18
19. Common Modes of Ventilation
Volume targeted ventilation (flow controlled, volume cycled)
• AC
Pressure targeted ventilation
• PCV (pressure controlled, time cycled)
• PS
Combination modes
• SIMV with PS and either volume or pressure-targeted mandatory cycles
19
20. Pressure and Volume Targeted Ventilation
Pressure and volume targeted ventilation obey the same principles set
by the equation of motion. Pressure and volume targeted ventilation
obey the same principles set by the equation of motion.
In pressure-targeted ventilation: an airway pressure target and
inspiratory time are set, while flow and tidal volume become the
dependent variables.
In volume targeted ventilation (flow-controlled, volume cycled), a target
volume and flow (or inspiratory time in certain ventilator) are preset and
pressure and inspiratory time (or flow in the ventilator where inspiratory
time is preset) become the dependent variables.
The tidal volume is the integral of the flow during inspiration = area
under the curve of the flow time curve during inspiration (see next slide).
20
21. Pressure and Volume Targeted Ventilation
Marini, Wheeler. Crit Care Med. The Essentials. 1997.
VT
21
22. Assist-control
Set variables
• Volume, TI or flow rate, frequency, flow profile (constant or decel)
• PEEP and FIO2
Mandatory breaths
• Ventilator delivers preset volume and preset flow rate at a set back-up rate
Spontaneous breaths
• Additional cycles can be triggered by the patient but otherwise are identical to the
mandatory breath.
22
23. SIMV
Key set variables
• Targeted volume (or pressure target), flow rate (or inspiratory time, Ti), mandated frequency
• PEEP, FIO2, pressure support
Mandatory breaths
• Ventilator delivers a fixed number of cycles with a preset volume at preset flow rate.
Alternatively, a preset pressure is applied for a specified Ti
Spontaneous breaths
• Unrestricted number, aided by the selected level of pressure support
23
24. Peak Alveolar and Transpulmonary Pressures
P(t) = VT/CR+ Flow x RR + PEEP tot
meanPaw
External PEEP
Intrinsic PEEP
Plateau pressure
Peak Airway Pressure
+
_
_ _
_ _
+
+
+
+ Palveolar
Ppleural
Ptranspulmonary = Palveolar - Ppleural Pplat = Maximum Palveolar
Alveolar Pressure
Transpulmonary pressure is a key determinant of alveolar distension.
24
25. Monitoring Pressure in Volume Targeted
Ventilation
Plateau pressure tracks the highest tidal alveolar pressure, a key
determinant of alveolar distension.
Plateau pressure (Pplat) is, however, only a surrogate of peak alveolar
distending pressure (transpulmonary pressure = Pplat – pleural
pressure).
• e.g., in a patient with a low chest wall compliance, a given Pplat is typically
associated with a higher pleural pressure but less alveolar distension (smaller
transpulmonary pressure) than in a patient with a compliant chest wall.
The difference between the Ppeak and Pplat tracks the resistive
pressure, as dictated by the equation of motion. During an inspiratory
pause, flow becomes zero, the resistive pressure is eliminated and the
airway pressure drops from its peak to the plateau pressure.
25
26. Airway Resistance and Respiratory System
Compliance
Under conditions of constant flow, the difference between peak
and plateau airway pressures drives end-inspiratory flow. The
quotient of this difference and the flow setting gives a measure
of airway resistance at end inspiration.
When airflow is stopped in a passively ventilated patient by
occlusion of the expiratory circuit valve at end inspiration
(plateau pressure) and end expiration (total PEEP), the pressure
needed to overcome the elastic recoil of the lungs and chest wall
during delivery of the tidal volume is given as the difference in
these values. Dividing the delivered tidal volume by this
difference quantifies the respiratory system compliance.
26
27. Mean Airway Pressure
Although measured in the connecting circuit, mean airway
pressure is a valid measure of the pressure applied across the
lung and chest wall, averaged across both phases of the
ventilatory cycle - but only under passive conditions.
Changes in mean airway pressure are produced by changes in
minute ventilation, PEEP, and I:E ratio.
Mean airway pressures affect pleural pressure and lung
distention.
Therefore, changes in mean airway pressure during passive
inflation may influence:
• Arterial oxygenation
• Cardiac output
27
28. Pressure Controlled Ventilation
Key set variables:
• Pressure, TI, and frequency
• PEEP and FIO2
Mandatory breaths
• Ventilator generates a predetermined pressure for a preset time
Spontaneous breaths
• PCV-AC mode: same as mandatory breaths
• PCV-SIMV mode: unsupported or PS
Important caveat
• It is important to understand that in pressure-controlled ventilation the relation between the set
rate and minute ventilation is complex. Above a certain frequency (e.g., when intrinsic PEEP is
created due to a reduced expiratory time), the driving pressure (set PC pressure – PEEPtotal)
starts to drop--and so does the delivered tidal volume.
• A pneumothorax or other adverse change in the mechanics of the respiratory system will not
trigger a high alarm pressure but a low tidal volume alarm instead.
28
29. Pressure Support
Pressure = set variable.
Mandatory breaths: none.
Spontaneous breaths
• Ventilator provides a preset pressure assist, which terminates when flow drops to a
specified fraction (typically 25%) of its maximum.
• Patient effort determines size of breath and flow rate.
29
30. PCV: Key Parameter to Monitor is VT
Change in mechanics
• airway resistance:
. e.g., bronchospasm
• respiratory system compliance .
.e.g, pulmonary edema, pneumothorax
AutoPEEP
• expiratory resistance
• expiratory time
e.g., rate
Inspiratory time
• e.g., rate if I:E ratio constant
What Causes a Decreased
VT During PCV?
30
31. Auto-PEEP (Intrinsic PEEP, PEEPi)
Marini, Wheeler. Crit Care Med. The Essentials. 1997.
Note that AutoPEEP is not equivalent to air trapping. Active expiratory muscle contraction is an often under appreciated contributor
(left panel) to positive pressure at the end of expiration
31
32. Suspecting and Measuring AutoPEEP
Time
Pressure
PEEPe
PEEPi
Total PEEP
Suspect AutoPEEP if flow at the end
of expiration does not return to the
zero baseline.
AutoPEEP is commonly measured by performing a pause at the end of expiration. In a passive patient, flow interruption is associated with pressure
equilibration through the entire system. In such conditions, proximal airway pressure tracks the mean alveolar pressure caused by dynamic
hyperinflation.
End expiratory pause
32
33. Interim Summary and Key Points
Mechanical ventilation helps to improve respiratory gas
exchange and can provide complete or partial work of breathing
assistance.
Safe and effective implementation of mechanical ventilation
requires understanding the equation of motion for the respiratory
system.
Monitoring dynamic and static airway pressures and flows yields
vital information for interpreting the mechanics of the respiratory
system and for adjusting machine settings for optimal
performance.
33
35. Hypercapnic Acidosis
Determinants of PaCO2
• PACO2 = 0.863 x VCO2/VA
• VA = VE (1-VD/VT)
Causes of hypercapnia
• Inadequate minute ventilation (VE)
• Dead space ventilation (VD/VT)
• CO2 production (VCO2 )
Corrective measures for respiratory acidosis
• When appropriate, increase the minute ventilation (e.g., the rate or the tidal
volume )
VD = dead space
VA = alveolar ventilation
VE = minute ventilation
VT = tidal volume
VCO2 = CO2 production
35
36. Mechanism for Arterial Hypoxemia
Reduced FiO2 (e.g., toxic fumes, altitude)
Hypoventilation
Impaired diffusion
Ventilation/perfusion (VA/Q) mismatching
• High VA/Q
• Low VA/Q
Shunting
• If significant shunting is present, the FIO2 requirement is typically > 60%
36
37. Minute Ventilation and Gas Exchange
The relationship between PaCO2 and minute ventilation is not linear. In patients
with hypoventilation, small changes in minute ventilation may have large effect on
the PaCO2.
37
38. Shunting: Effects of FiO2 on PaO2
Note that as the % of shunt rises, increasing the
FIO2 has less and less impact on PaO2.
Under such conditions, reducing the shunt
fraction is key to the ability to improve gas
exchange, and this typically requires PPV and
PEEP.
38
39. Key Factors Determining the Effects of Shunting
on Arterial O2 Saturation
450
mmHg
0
mmHg
70%
100%
85%
SvO2
Shunt fraction
Note that inpatients with shunt
physiology a reduction in arterial O2
saturation may be due to a change in:
• the intraparenchymal shunt
fraction (e.g., atelectasis)
or
• the SvO2 (e.g., drop in cardiac
output).
A sudden drop in O2 saturation in
patients with ARDS warrants a
thorough assessment of the
respiratory and cardiovascular system.
50% 50%
39
40. Mean Airway and Alveolar Pressures
Adapted from: Ravenscraft et al. Crit Care Med. 1992.
In normal lungs, the inspiratory resistive pressure is similar to the expiratory resistive pressure (light shaded area under the airway
pressure-time curve) so that mean airway pressure (Paw) can be used to track mean alveolar pressure (Palv).
40
41. PEEP, Regional Lung Volume, and Shunting
ZEEP
CPAP
Lung regions with shunt tend to distribute preferentially in the dependent regions. Tidal ventilation helps open collapsed regions, and
PEEP helps to maintain those regions open throughout expiration and to reduce shunt. Note that level of PEEP required to achieve such
varies along the gravitational axis.
41
42. Effect of PEEP-induced Alveolar
Recruitment on PaO2
Malbuisson et al. AJRCCM. 2001:163:1444-1450. 42
43. Approach to MV
Is MV indicated ?
Conservative
treatment and
periodic
reassessment
NO
YES
Contraindication to NIPPV ?
NIPPV
NO
Success ? Invasive MV
NO
NO
YES
43
45. Key Differences Between NIPPV and IPPV
Allows the patients to
maintain normal functions
• Speech
• Eating
Helps avoid the risks and
complications related to:
• Intubation
• Sedation
Less ventilator-associated
pneumonia
Less airway pressure is
tolerated
Does not protect against
aspiration
No access to airway for
suctioning
Advantages of NIPPV Disadvantages of NIPPV
45
46. Clinical Use of NIPPV in Intensive Care
Decompensated COPD (Hypercapnic Respiratory Failure)
Cardiogenic pulmonary edema
Hypoxic respiratory failure
Other possible indications
• Weaning (post-extubation)
• Obesity hypoventilation syndrome
• Patients deemed not to be intubated
• Post-surgery
• Asthma
Adapted from: Am J Respir Crit Care Med. 2001;163:283-291. 46
47. Contraindications to NIPPV
Cardiac or respiratory arrest
Nonrespiratory organ failure
Severe encephalopathy (e.g., GCS < 10)
Severe upper gastrointestinal bleeding
Hemodynamic instability or unstable cardiac arrhythmia
Facial surgery, trauma, or deformity
Upper airway obstruction
Inability to cooperate/protect the airway
Inability to clear respiratory secretions
High risk for aspiration
Adapted from: Am J Respir Crit Care Med. 2001;163:283-291.
47
48. Initiating NIPPV
Initial settings:
• Spontaneous trigger mode with backup rate
• Start with low pressures
- IPAP 8 - 12 cmH2O
- PEEP 3 - 5 cmH2O
• Adjust inspired O2 to keep O2 sat > 90%
• Increase IPAP gradually up to 20 cm H2O (as tolerated) to:
- alleviate dyspnea
- decrease respiratory rate
- increase tidal volume
- establish patient-ventilator synchrony
48
49. Success and Failure Criteria for NPPV
Improvements in pH and PCO2 occurring within 2 hours predict
the eventual success of NPPV.
If stabilization or improvement has not been achieved during
this time period, the patient should be considered an NPPV
failure and intubation must be strongly considered.
Other criteria for a failed NPPV trial include: worsened
encephalopathy or agitation, inability to clear secretions,
inability to tolerate any available mask, hemodynamic
instability, worsened oxygenation.
49
50. Conclusions
A good understanding of respiratory physiology is required for
the judicious mechanical ventilation.
The equation of motion is the single most useful guide to
understanding mechanical ventilation.
Unless contraindicated, NIPPV is becoming the first modality to
try in many settings.
Monitoring key variables such as Pplateau and auto-PEEP is
mandatory to safe and effective practice.
50
51. Post Module Testing: Case 1
29-year-old patient (weight 120 kg, height 170 cm)
ARDS secondary to bilateral pneumonia
Ventilator settings: AC with VT 800 ml and back-up rate 10/min,
PEEP 5 cmH2O, FIO2 80 %
Measured variables: rate 25, VE = 20 l/min, Ppeak 40 cm H2O,
Pplat 35 cm H2O
ABG: pH 7.40, PaO2 55 mmHg, PaCO2 38 mmHg, O2 saturation
85%
51
52. Question 1
What mechanism best explains the patient’s hypoxemia?
1. V/Q mismatch
2. Shunt
3. Abnormal diffusion
4. Inadequate oxygen delivery and high tissue extraction
52
53. Answer 1
If in a ventilated patient, FIO2 > 60% is needed, shunt is certainly
the main cause for the hypoxemia (correct response: 2).
As a rule, increasing the FIO2 will compensate for VA/Q
mismatching but not for shunt. When VA/Q mismatching is
present, hypoxemia typically corrects with an FIO2 < 60%.
Altered diffusion is rarely a clinically relevant issue.
Increasing the ventilation rate will not exert a significant impact on
oxygenation unless it contributes to air trapping and auto-PEEP.
53
54. Question 2
Which of the following ventilatory setting changes is the next best
step to reduce shunt and increase the PaO2/FIO2 ratio (a
bedside index of oxygen exchange)
1. Increase PEEP to 10 cmH20
2. Increase the FIO2 to 100%
3. Add an inspiratory pause of 1 second
4. Increase respiratory rate to 30/min
54
55. Answer 2
Interventions that target mean airway pressure are the most helpful.
They help recruit flooded or collapsed alveoli and maintain the recruited
alveoli open for gas exchange (reduced shunt).
Increasing PEEP is the first intervention to consider; extending the
inspiratory time and I:E ratio is a secondary option to raise mean airway
pressure.
In the presence of shunt, increasing the FIO2 would reduce the ratio.
Although increasing rate may affect meanPaw, its impact is overall
minor. Rate adjustment is mainly used to control minute ventilation and
its consequences on:
• air trapping
• PaCO2 and pH
55
56. Question 3
PEEP is increased to 10 cmH20
PaO2 is now 85 mmHg, Pplat is 45, and Ppeak 50 cmH2O
The high pressure alarm is now triggered.
Your next step is:
1. Reset the alarm pressure to 55 cmH20.
2. Disconnect the patient from the ventilator and start manual ventilation (bagging).
3. Order a stat chest x-ray to assess for a pneumothorax.
4. Reduce the tidal volume slowly until the alarm turns off.
5. None of the above
56
57. Answer 3
The correct answer is 5. Option 1 does not address the issue of the excessive tidal volume and
airway pressure.
The rise in airway pressure that triggered the alarm was predictable following the increase in
PEEP level (see equation of motion). There is thus no need for 2 and 3.
Tidal volume is never titrated to an arbitrary set alarm pressure.
Pplat, which tracks alveolar pressure and the risk of developing ventilator-induced lung injury
(VILI), is an easy and accessible bedside parameter used to assess the risk of alveolar
overdistension. In this patient, it is the high Pplat associated with the choice of an excessive tidal
volume that puts the patient at risk of VILI.
Patients with ARDS have reduced aerated lung volume (“baby lungs”) and need to ventilated with
small tidal volumes: e.g., 6 ml/kg predicted ideal body weight. This patient is clearly ventilated with
an excessive tidal volume for his size (ideal or predicted body weight). The tidal volume must be
reduced. A tidal volume and PEEP combination associated with a Pplat of less than 25 cmH2O is
generally considered safe. Concerns regarding the risk of overdistension and VILI is significant
when Pplat is > 30 cmH2O.
Remember, however, that the actual distending alveolar pressure is the transpulmonary pressure
(Pplat- Ppleural). Higher Pplat can be accepted in a patient with low chest wall compliance, as
less alveolar distension will be present for the same Pplat, everything else being equal.
57
58. Case 2
67-year-old female (weight 50 kg) with severe emphysema is admitted for
COPD decompensation. She failed NIPPV and required sedation, paralysis,
and intubation.
Soon after intubation and initiation of mechanical ventilation, she became
hypotensive (BP dropped from 170/95 to 80/60). She has cold extremities,
distended neck veins, midline trachea, distant heart sounds, and symmetrical
breath sounds with prolonged expiratory phase.
Ventilatory settings are: assist control, tidal volume 500ml, rate 15/min, PEEP 5
cmH2O, FIO2 1.0 (100%)
ABG: pH 7.20, PaO2 250 mmHg, PaCO2 77 mmHg
Measured variables: rate 15/min, VE = 7.5 l/min, Ppeak 45 cmH2O, Pplat 30
cmH2O
58
59. Question 1
The next step in this patient’s management should be:
1. Order a stat echocardiogram to assess for tamponade.
2. Order a stat AngioCT to assess for pulmonary embolism.
3. Measure AutoPEEP, disconnect the patient briefly from the ventilator, then
resume ventilation with a lower tidal volume and rate and administer intravenous
fluid.
4. Start the patient on intravenous dopamine and adjust the ventilator to normalize
the PaCO2.
59
60. Answer 1
The correct answer is 3. Remember that gas trapping is your key concern in the
ventilated patient with obstructive physiology.
A quick look at the expiratory flow tracing and performing an expiratory pause
maneuver demonstrated that the patient has developed severe dynamic hyperinflation
and intrinsic PEEP (15 cmH2O).
Brief disconnection (1 - 2 minutes) from the ventilator while continuously monitoring
oxygen saturation is safe in this condition and allows for the lung to empty, intrinsic
PEEP to decrease--thus restoring venous return, preload, stroke volume, and BP. The
restoration of BP following ventilator disconnection is not specific for air trapping.
Therefore, intrinsic PEEP needs to be measured to confirm the diagnosis.
It is also important to consider the possibility of a tension pneumothorax in this patient.
The symmetrical chest and midline trachea did not suggest this possibility here.
Also notice that Pplat was elevated (due to gas trapping), but in contrast to a patient
with stiff lungs (ARDS), there is a large difference between Ppeak and Pplat because
airway resistance is markedly elevated in patients with COPD.
60
61. Question 2
You change the ventilator’s tidal volume to 300 ml and the rate to
15/min. After 1 liter of physiologic saline is infused, the BP is now
100/70 mmHg and heart rate is 120/min. ABG: pH 7.30, PaO2 250
mmHg, PaCO2 60 mmHg. Measured variables: rate 20/min, VE = 6.0
l/min, Ppeak 37 cmH2O, Pplat 25 cmH2O, Intrinsic PEEP is now
7cmH2O (total PEEP=12 cmH2O).
The best next step is to:
1. Continue with bronchodilators and tolerate the current mild respiratory acidosis.
2. Increase the rate to normalize PaCO2.
3. Increase the tidal volume but only to normalize the pH.
4. Ask for another ABG since you do not believe the drop in PaCO2--minute
ventilation declined.
61
62. Answer 2
The best next step is continue with bronchodilator and tolerate
the current mild respiratory acidosis (RA).
• The patient has no contraindications to mild RA (history of an acute or chronic
central nervous system problem, that may be worsened by the increase in
intracranial pressure associated with RA, heart failure, cardiac ischemia, or
arrhythmia.
• Although less than present initially, dynamic hyperinflation is still an issue (high
Pplat and relatively low BP). Thus, increasing the minute ventilation to normalize
the pH or PaCO2 will make this worse.
• The reduction in PaCO2 is due to less air trapping, with improved venous return
and reduced dead space ventilation. Hyperinflation tends to compress capillaries
and thus promote ventilation of unperfused alveolar units (dead space).
62
63. References and Suggested Readings
Hubmayr RD, Abel MD, Rehder K. Physiologic approach to mechanical
ventilation. Crit Care Med. 1990;18:103-13.
Tobin MJ. Mechanical ventilation. N Engl J Med. 1994;330;1056-61.
Marini JJ. Monitoring during mechanical ventilation. Clin Chest Med.
1988;9:73-100.
Brochard L. Noninvasive ventilation for acute respiratory failure. JAMA.
2002;288:932-935.
Calfee CS, Matthay MA. Recent advances in mechanical ventilation.
Am J Med. 2005;118:584-91.
63