The document discusses several respiratory emergencies including asthma, COPD, pneumonia, pneumothorax, and pulmonary embolism. Asthma is a chronic inflammatory disease characterized by recurrent episodes of impaired breathing. COPD is defined as a preventable disease involving persistent airflow limitation usually due to smoking. Pneumonia involves lower respiratory infection signs with abnormal chest x-rays. Pneumothorax is the presence of air in the pleural space ranging from benign to life-threatening. Pulmonary embolism occurs when a blood clot lodges in the pulmonary arteries.
Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, and refractory (non-reversible) asthma. This disease is characterized by increasing breathlessness
Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, and refractory (non-reversible) asthma. This disease is characterized by increasing breathlessness
Dr Kishore Kumar Ubrangala, MD
Professor, Dept. of Medicine,
Yenepoya Medical College,
Yenepoya (Deemed to be) University, Mangalore, India.
sankish@gmail.com
Chronic obstructive pulmonary disease, commonly referred to as COPD, is a group of progressive lung diseases. The most common are emphysema and chronic bronchitis. Many people with COPD have both of these conditions.
Emphysema slowly destroys air sacs in your lungs, which interferes with outward air flow. Bronchitis causes inflammation and narrowing of the bronchial tubes, which allows mucus to build up.
The top cause of COPD is tobacco smoking. Long-term exposure to chemical irritants can also lead to COPD. It’s a disease that usually takes a long time to develop.
Diagnosis usually involves imaging tests, blood tests, and lung function tests.
There’s no cure for COPD, but treatment can help ease symptoms, lower the chance of complications, and generally improve quality of life. Medications, supplemental oxygen therapy, and surgery are some forms of treatment.
Untreated, COPD can lead to a faster progression of disease, heart problems, and worsening respiratory infections.
It’s estimated that about 30 million people in the United States have COPD. As many as half are unaware that they have it.
Presented by Mr B.Kalyankumar Msc(N) Dept Of MSN
Bronchitis is an acute inflammation of the air passages within the lungs. It occurs when the trachea (windpipe) and the large and small bronchi (airways) within the lungs become inflamed because of infection or irritation from certain causes. Homeopathy is the best treatment with no side effects. For further information contact Ph. : +91-265-2250212,
(M) +91 97236 69210
Skype Id : cosmic1021
Email:
drmahavrat@homeopathyhealing.net
Bronchitis is an inflammation of the bronchial tubes, the airways that carry air to your lungs. It causes a cough that often brings up mucus. It can also cause shortness of breath, wheezing, a low fever, and chest tightness. There are two main types of bronchitis: acute and chronic.
Dr Kishore Kumar Ubrangala, MD
Professor, Dept. of Medicine,
Yenepoya Medical College,
Yenepoya (Deemed to be) University, Mangalore, India.
sankish@gmail.com
Chronic obstructive pulmonary disease, commonly referred to as COPD, is a group of progressive lung diseases. The most common are emphysema and chronic bronchitis. Many people with COPD have both of these conditions.
Emphysema slowly destroys air sacs in your lungs, which interferes with outward air flow. Bronchitis causes inflammation and narrowing of the bronchial tubes, which allows mucus to build up.
The top cause of COPD is tobacco smoking. Long-term exposure to chemical irritants can also lead to COPD. It’s a disease that usually takes a long time to develop.
Diagnosis usually involves imaging tests, blood tests, and lung function tests.
There’s no cure for COPD, but treatment can help ease symptoms, lower the chance of complications, and generally improve quality of life. Medications, supplemental oxygen therapy, and surgery are some forms of treatment.
Untreated, COPD can lead to a faster progression of disease, heart problems, and worsening respiratory infections.
It’s estimated that about 30 million people in the United States have COPD. As many as half are unaware that they have it.
Presented by Mr B.Kalyankumar Msc(N) Dept Of MSN
Bronchitis is an acute inflammation of the air passages within the lungs. It occurs when the trachea (windpipe) and the large and small bronchi (airways) within the lungs become inflamed because of infection or irritation from certain causes. Homeopathy is the best treatment with no side effects. For further information contact Ph. : +91-265-2250212,
(M) +91 97236 69210
Skype Id : cosmic1021
Email:
drmahavrat@homeopathyhealing.net
Bronchitis is an inflammation of the bronchial tubes, the airways that carry air to your lungs. It causes a cough that often brings up mucus. It can also cause shortness of breath, wheezing, a low fever, and chest tightness. There are two main types of bronchitis: acute and chronic.
Chronic obstructive pulmonary disease..It is one of the most affecting lung disease.. In detailed explanation of disease is there and including its ayurvedic aspect of management is also there...
#Ayurveda#Emphysema#Chronic brochitis
the scenario given at the start of ppt z nt interstitial lung diseases... its a similar diseases to it.... diagnose it urself to differniate it and hv better command over diffferntial diagnosis.
Etiopathogenesis and pharmacotherapy of Asthma
the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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
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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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
- 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
2. Asthma
• Asthma is a chronic respiratory disease characterized by periods of
variable and recurring symptoms, airflow obstruction, and bronchial
hyperresponsiveness that manifests clinically as attacks of impaired
breathing
• Asthma is an inflammatory disease; repetitive episodes of acute
superimposed on chronic airway inflammation are responsible for
alterations in airway function and result in irreversible structural
airway changes
• Asthma is thus a complex interaction of the immune system, the
environment, and genetic predispositions, which combine to alter
airway structure and function
3.
4.
5.
6.
7.
8. European Respiratory Society/American Thoracic Society Definitions
of Severe and Uncontrolled Asthma
• Severe asthma for patients 6 years old and older is defined as:
Asthma which requires treatment with guidelines suggested
medications for Global Initiative for Asthma steps 4 to 5 asthma (high-
dose ICS and LABA or leukotriene modifier/ theophylline) for the
previous year or systemic corticosteroids for ≥50% of the previous
year to preventing it from becoming “uncontrolled” or which remains
“uncontrolled” despite this therapy
9.
10. Uncontrolled asthma is defined as one of the following:
• Poor symptom control (ACQ consistently >1.5, ACT <20 (or “not well controlled” by
NAEPP/Global Initiative for Asthma guidelines)
• Frequent severe exacerbations: Two or more bursts of systemic corticosteroids (>3
days each) in previous year
• Serious exacerbations: At least one hospitalization, ICU stay, or mechanical
ventilation in the previous year
• Airflow limitation: After appropriate bronchodilator, withhold FEV1<80% predicted
(in the face of reduced FEV1 as less than the lower limit of normal)/FVC defined
• Controlled asthma that worsens on tapering of these high doses of ICS or systemic
corticosteroids (or additional biologics)
20. COPD
• Global Initiative for Chronic Obstructive Lung Disease (GOLD)
collaborators have updated their defnition of COPD as “a preventable and
treatable disease characterized by persistent airflow limitation that is
usually progressive and associated with an enhanced chronic inflamatory
response in the airways and the lungs to noxious particles or gas.”
• The definition specifically avoids mention of chronic bronchitis and
emphysema, two entities that have been traditionally included in the
definition of COPD
• the GOLD collaborators focus on airflow limitation as the principle feature
of the disease. Airflow limitation is a direct result of a combination of
parenchymal destruction and small airways disease. Both processes are a
consequence of chronic inflammatory changes and present clinically in
varying degrees amongst patients with COPD
21.
22. • Progressive inflammation in COPD leads to airway limitation and obstruction.
However, not all patients who smoke or have exposure to noxious stimuli
develop COPD, raising the possibility that other contributory factors such as
genetics and environmental factors
• In COPD, evidence of airway inflammation is found from the trachea down to
the smallest peripheral airways. In the larger, more proximal airways, an
increase in both the number and size of mucous-secreting goblet cells can
result in the formation of mucous plugs, which further contributes to airflow
obstruction.
• Damage to the endothelium impairs the mucociliary response that clears
bacteria and mucous. Airway resistance and flow limitation are mainly due to
damage to the distal, smaller airways where the diameter is 2 mm or less.
• In cigarette smokers, the parenchymal damage will typically present in a
centriacinar pattern, especially in the early stages of the disease. Emphysema
is no longer routinely used in the definition of COPD, because it is a pathologic
and anatomically defined condition.
23. • Chronic bronchitis on the other hand is a clinical condition defined by the
presence of chronic productive cough for 3 months in each of 2 successive
years, where other causes of chronic cough have been excluded. Most patients
with COPD will have mixed features of both conditions.
• There is compelling evidence that protease/anti-protease imbalance plays a role
in the modification of the inflammatory cascade and resultant parenchymal
destruction seen in COPD. Protease-mediated destruction of connective tissues,
including elastin results in lung parenchymal damage and resultant emphysema.
• Anti-proteases protect against connective tissue destruction and are an integral
component in the pathogenesis of patients with congenital α1-antitrypsin
deficiency.
• Congenital α1-antitrypsin deficiency accounts for a small percentage of COPD
patients and is recognized by the lack of the anti-protease enzyme that inhibits
the protease enzyme, neutrophil elastase. The deficiency of this anti-protease
results in uninhibited protease action, parenchymal destruction, and severe
panacinar emphysema.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33. Proposed Indications for Mechanical Ventilation
• Respiratory arrest Worsening level of consciousness despite maximal
therapy
• Cardiovascular instability (shock, heart failure)
• NIPPV failure or exclusion criteria
• Severe dyspnea with use of accessory muscles and paradoxical abdominal
motion
• Severe tachypnea
• Life-threatening hypoxia
• Severe acidosis and hypercapnia
• Other complications (metabolic abnormalities, sepsis, pneumonia,
pulmonary embolism [PE], barotraumas, massive pleural effusion)
34. Pneumonia
• Pneumonia involves symptoms and signs of lower respiratory tract
infection (breathlessness, productive cough, and fever) usually
associated with CXR abnormalities. Pneumocystis pneumonia may
occur with minimal or no CXR changes. Consider pneumonia in
patients with septicaemia or acute confusional states.
• Pneumonia commonly results from microaspiration of upper
respiratory pathogens into the sterile lower respiratory tract. If the
challenge of invading organisms overwhelms host defenses, microbial
proliferation leads to inflammation, an immune response, and clinical
pneumonia.
35.
36. • In patients admitted in the ICU the most common aetiologies were S. pneumoniae
(62%), atypical pathogens (14%) and polymicrobial aetiologies (11%). The most
frequent polymicrobial pattern was S. pneumoniae and viral infection, particularly
influenza virus .
• The microbial pattern of the severe CAP has changed over the years, with the decrease
of atypical pathogens, especially Legionella and the increase of viral pneumonia
• A large number of micro-organisms other than S. pneumoniae must be considered,
especially Pseudomonas aeruginosa, and CA—MRSA. The risk factors for Pseudomonas
pneumonia include
o ◆ Recent hospitalization.
◆ Frequent (>4 courses per year) or recent administration of antibiotics (last 3 months).
◆ Severe disease (FEV1 < 30%) and oral steroid use (>10 mg of prednisolone daily in the last 2
weeks).
• Accordingly, the risk factors for community-acquired methicillin-resistant
Staphylococcus aureus (CA-MRSA), an emerging problem, are participating in contact
sport, living in crowded or unsanitary conditions, intravenous drug abuse
• CA-MRSA is the most common pathogen isolated in community-acquired skin and soft
tissue infections. It causes severe, rapidly progressing pneumonia with sepsis, often in
children or healthy young adults with influenza
37. American Thoracic Society/Infectious Disease Society of America
Definitions of Hospital Acquired, Ventilator-Associated, and Health
Care–Associated Pneumonia
• Hospital-acquired pneumonia (HAP)—occurs ≥48 hr after admission and
does not appear to be incubating at the time of admission
• Ventilator-associated pneumonia (VAP)—occurs >48–72 hr after
endotracheal intubation
• Health care–associated pneumonia (HCAP)—occurs in a non hospitalized
patient with extensive health care contact defined by one or more of the
following exposures
• IV therapy, wound care, or IV chemotherapy within the prior 30 days Residence in a
nursing home or other long-term care facility
• Hospitalization in an acute care hospital for 2 or more days within the past 90 days
• Received hemodialysis within the prior 30 day.
38. Organ colonization time-evolution during ICU stay.
*At 48 hours 80% of ETT are colonized, but heavy colonization occurs at
60–96 hours.
39.
40.
41.
42.
43.
44. Criteria for ICU admission.
One of the major or three
or more of the minor
criteria would indicate ICU
admission
45.
46.
47.
48.
49. Pneumothorax
• Pneumothorax is defined as the presence of air in the intrapleural space
and can range from a benign to a life-threatening process.
• A spontaneous pneumothorax occurs in the absence of any external
precipitating factor, traumatic or iatrogenic.
• Primary spontaneous pneumothorax occurs in individuals without clinically
apparent lung disease.
• Secondary spontaneous pneumothorax arises in the context of an
underlying pulmonary disease process.
• Tension pneumothorax is a life-threatening complication resulting from
pressure in the pleural cavity causing hemodynamic compromise.
57. The classic radiographic appearance is that of a thin, visceral pleural line lying parallel to the chest wall,
separated by a radiolucent band devoid of lung markings. The average width of this band can be used to
estimate the size of the pneumothorax, such as with the Rhea method
58. British Thoracic Society
guidelines define size
based on measurement
of the intrapleural
distance at the level of
the hilum: small, less than
1 cm; moderate, 1 to 2
cm; and large, more than
2 cm.
The American College
of Chest Physicians
measures from the apex
to the cupola(chest wall
apex)—small is less than
3 cm, and large is more
than 3 cm.
62. • The triad of venous injury, slow blood flow, and hypercoagulability are the
cardinal inciting mechanisms for VTE, and most clinical decision rules for VTE
incorporate these factors.
63.
64.
65. Diagnosis
• Diagnosis of DVT and PE starts with an estimation of the pretest
probability (PTP).
• the LEFt score:
• 1 point in case of left (L) leg suspicion,
• 1 point for edema (E), and
• 1 point if the suspicion occurred during the first trimester (Ft) of pregnancy,
• with a score of 0 or 1 tantamount to a low PTP
• The PTP dictates the pathway for diagnostic testing
66.
67. A three-point
ultrasound includes
the common femoral,
femoral, and
popliteal veins. A
whole-leg ultrasound
includes a three-
point ultrasound and
the peroneal and
tibial calf veins.
68.
69.
70. • Upper extremity DVT can cause PE, and all patients with DVT above the elbow
require definitive treatment.: About half of all upper extremity DVTs are
associated with an indwelling catheter, and peripherally inserted central
catheters (PICCs) carry the highest risk.
• Acute PE from an axillary vein Isolated upper occurs in about 9% of patients
with arm DVT, although the PE tends to be less severe from upper extremity
DVT
• only venous ultrasound has been adequately validated as a method to
diagnose and exclude upper extremity DVT
71. PULMONARY EMBOLISM
• A PE results when a clot that formed hours, days, or sometimes weeks
earlier in the deep veins dislodges, travels through the venous system, and
traverses the right ventricle into the pulmonary vasculature.
• The mortality of diagnosed and treated pulmonary embolism is 7%. Many
more people die from undiagnosed PE. Venous thromboembolism
develops in patients already suffering from sepsis, cancer, or COPD or in
patients recovering from stroke, MI, surgery, and joint replacement.
• Pulmonary embolic disease can result in a variety of symptoms often
misdiagnosed as asthma, anxiety, pneumonia and ACS
72.
73.
74. • The right ventricle normally pumps through a pulmonary vascular tree with a
low resistance to fluid flow, and young persons without cardiopulmonary
disease (eg, congestive heart failure, chronic obstructive lung disease,
advanced sarcoidosis, pulmonary fibrosis, scleroderma, primary pulmonary
hypertension) can tolerate at least 30% obstruction from a clot, with minimal
symptoms or signs.
• Pulmonary infarction, in contrast, can produce severe pleuritic pain Although
a segmental pulmonary artery constitutes only about 1/16 of the entire
pulmonary vascular circuit, a clot lodged deeply in a segmental artery can
obstruct blood flow to a sufficient degree to cause tissue necrosis.
75.
76.
77.
78. Pulmonary Embolism Rule-Out Criteria (PERC
Rule)
Low pretest probability for PE by the treating emergency clinician’s
unstructured estimate, plus all the following must be true:
• Age < 50 yr
• Pulse rate < 100 beats/min
• Oxygen saturation < 94%
• No hemoptysis
• No unilateral leg swelling
• No recent major surgery or trauma
• No prior pulmonary embolism or deep venous thrombosis
• No hormone use
79.
80. • Chest radiography seldom provides specific information, but is useful to
suggest alternative diagnoses, such as pneumonia, congestive heart failure, or
pneumothorax.
• If symptoms have been present for 3 days or more, a pulmonary infarction may
be visible on chest x-ray as an apex central, pleural-based, wedge-shaped area
of infiltrate, producing the so-called Hampton’s hump finding. Unilateral lung
oligemia (Westermark’s sign) is a rare radiographic manifestation of a large PE.
• When PE causes electrocardiographic changes, this is usually a result of acute
or subacute pulmonary hypertension. The most common effects of pulmonary
hypertension on the ECG are rapid heart rate, symmetric T-wave inversion in
the anterior leads (V1–V4), the McGinn White S1Q3T3 pattern, and incomplete
or complete right bundle branch block
• In the ED, inability to identify a cause of chest symptoms or specific signs may
be an important cue to evaluate the patient for PE
81.
82. PLEURAL INFLAMMATION AND
EFFUSION
• Pleural effusion implies the presence of an abnormal collection of fluid in
the pleural space.
• A pleural effusion associated with bacterial pneumonia or lung abscess is
termed a parapneumonic effusion. The term pleural empyema (or
pyothorax) implies the presence of actual pus in the pleural space. Fluid
that is anatomically confined and not freely flowing within the pleural
space is termed a loculated effusion.
• Loculated effusions occur when there are adhesions between the visceral
and parietal pleurae