PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
DIAGNOSIS & MANAGEMENT OF PULMONARY HYPERTENSIONKamal Bharathi
Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
DIAGNOSIS & MANAGEMENT OF PULMONARY HYPERTENSIONKamal Bharathi
Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
Apparently a lengthy presentation actually very good for junior physicians as it covers all aspects of assessment, diagnosis and treatment of pleural effusion
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
Apparently a lengthy presentation actually very good for junior physicians as it covers all aspects of assessment, diagnosis and treatment of pleural effusion
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
This presentation covers the methodology of evaluating CTEPH (chronic thromboembolic pulmonary hypertension) case. It starts from the basic concepts of Pulmonary hypertension.
Pulmonary Arterial Hypertension Overview
Michael J. Cuttica MD Assistant Professor of Medicine Northwestern Pulmonary Hypertension Program
Northwestern University
Michael J. Cuttica MD, Assistant Professor of Medicine at the Northwestern Pulmonary Hypertension Program of Northwestern University discusses Pulmonary Arterial Hypertension in scleroderma patients, including how it is diagnosed and treated.
Pulmonary Arterial Hypertension: The Other High Blood Pressure and its association with scleroderma is presented by
Micheal J. Cuttica MD, MS, Assistant Professor of Medicine, Director; Northwestern Pulmonary Hypertension Program, Northwestern University
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PowerPoint presentation on the topic HRCT Chest. This presentation is divided into 5 different parts. 1)Introduction to HRCT chest 2)Technichal aspects of HRCT 3) Relevant anatomy for HRCT interpretation 4)Pattern of lung disease in HRCT 5)HRCT pattern in various ILD’s
PowerPoint presentation on ECMO (Extracorporeal Membrane Oxygenation). Part 2 focuses on Monitoring ECMO patients
Ventilatory strategies, Sedation and pain control, Weaning, Complications and recent advances in ECMO. For better understanding please have a look at ECMO part 1 before going through part 2.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
- 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
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
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
2. Table of Contents
• Definition
• Classification of PH
• Pathology & Pathophysiology
• Approach to diagnosis
• Treatment
• Follow-up.
3. Definition of PAH by WHODefinition of PAH by WHO
• Increase in blood pressure in pulmonary
circulation ( either in the arteries, or both in
arteries and veins)
• Normal pressure is 14-18mmHg at rest.
• 20-25mmHg on exercise.
• Hemodynamically it is defined as an increase in
mean pulmonary arterial pressure to >-25mmHg at
rest.
• Can be measured by right heart catheterization.
4. WHO Classifications of
Pulmonary Hypertension
1. Pulmonary Arterial Hypertension
2. Pulmonary Venous Hypertension
3. PH Secondary to Chronic Hypoxia
4. Chronic Thrombo-Embolic Pulmonary Hypertension
(CTEPH)
5. Miscellaneous (usually extrinsic compression of
pulmonary arteries)
WHO Venice 2003 – Later updated in 2008 (Danapoint)
5. Epidemiology of PH
39%
15%
11% 10% 9.50%
6%
4%
0%
5%
10%
15%
20%
25%
30%
35%
40%
I diopathic Connective
Tissues
Disease
Congenital
Heart Disease
Portal HTN Appetite
Suppressant
HI V Familial
6. Group 1 - PAH
• IPAH
• Familial – BMPR2, ALK 1,Unknown
• Associated with PAH
– Connective Tissue Disease (Scleroderma, SLE, MCTD, RA)
– Congenital Heart Disease
– Portal hypertension (5-7% of patients)
– HIV (0.5% of patients)
– Drugs/toxins (aminorex-, dexfenfluramine-, or fenfluramine-
containing products, cocaine, methamphetamine)
– Other: thyroid disorders, glycogen storage disease, Gaucher’s
disease,
hereditary hemorrhagic telangiectasia, hemoglobinopathies,
myeloproliferative disorders, splenectomy
• Associated with venous/capillary involvement
– Pulmonary veno-occlusive disease (evidence of pulmonary vascular
congestion)
– Pulmonary capillary hemangiomatosis
• Persistent PH of newborn.
7. • Group 2: Pulmonary hypertension due to left heart
disease
– Systolic dysfunction
– Diastolic dysfunction
– Valvular disease
• Group 3: Pulmonary hypertension associated with
lung disease and/or hypoxemia
– Chronic obstructive lung disease
– Interstitial lung disease
– Sleep-disordered breathing
– Alveolar hypoventilation disorders
– Chronic exposure to high altitude
– Developmental abnormalities
8. • Group 4: Pulmonary hypertension due to chronic
thrombotic and/or embolic disease
– Thromboembolic obstruction of proximal pulmonary
arteries
– Thromboembolic obstruction of distal pulmonary
arteries
• Group 5: Miscellaneous
– Sarcoidosis, histiocytosis X, lymphangiomyomatosis,
compression of pulmonary vessels (adenopathy, tumor,
fibrosing mediastinitis
11. Pathophysiology & Pathology – Group 1
• Exact mechanism – unknown.
• Multifactorial.
1)Excessive vasoconstriction -abnormal function or
expression of potassium channels in the smooth muscle
cells .
2) Endothelial dysfunction leads to chronically impaired
production of vasodilator and Vasoconstrictors
(NO,prostacyclin, thromboxane A2 and endothelin-1)
12. 3) Reduced plasma levels of other vasodilator and
antiproliferative substances such as vasoactive
intestinal peptide
4) In the adventitia there is increased production of
extracellular matrix including collagen, elastin,
fibronectin. Inflammatory cells and platelets
(through the serotonin pathway)
5) Prothrombotic abnormalities have been
demonstrated in PAH patients, and thrombi are
present in both the small distal pulmonary arteries
and the proximal elastic pulmonary arteries
14. • Due to lt. heart diseases:
• Pulmonary venous hypertension-most common cause
• Usually due to left-sided heart disease (valvular,
coronary or myocardial), obstruction to blood flow
downstream from the pulmonary veins.
• Reversibility is variable, dependent on lesion.
Pathophysiology & Pathology – Group 2
15. , PH due to lung diseases and/or hypoxia:
Multiple
1) hypoxic vasoconstriction,
2) mechanical stress of hyperinflated lungs,
3) loss of capillaries – emphysema, fibrosis
4) inflammation, and toxic effects of cigarette smoke.
5)endothelium-derived vasoconstrictor–vasodilator imbalance.
Hypoxia induced pulmonary vasoconstriction and anatomical
destruction of the vascular bed due to high pulmonary resistance
and ultimately RV failure.
Pathophysiology & Pathology – Group 3
16.
17. • CTEPH: non-resolution of acute embolic masses which
later undergo fibrosis leading to mechanical
obstruction of pulmonary arteries is the most important
process.
Pathophysiology & Pathology – Group 4
18. • PH with unclear and/or multifactorial mechanisms.
Pathophysiology & Pathology – Group 5
20. Reasons to Suspect PAH
• Unexplained dyspnea despite multiple
diagnostic tests
• Typical symptoms (look for
Raynaud’s)
• Comorbid conditons:
– CREST, liver disease, HIV, sickle cell
– Family history of PAH
– History of stimulant/anorexigen use
21. Symptoms of PAHSymptoms of PAH
• DyspneaDyspnea 60%60%
• FatigueFatigue 19%19%
• Near syncope/syncopeNear syncope/syncope 13%13%
• Chest painChest pain 7%7%
• PalpitationsPalpitations 5%5%
• LE edemaLE edema 3%3%
• Hoarseness of voice 2%
(Ortners syndrome)
24. • Labs
– Autoimmune serologies
– Markers of liver synthetic function
– HIV serologies when dictated by history
25. CXR in PH
Large central
Pulmonary arteries
Right Ventricular
Hypertrophy
Rapid attenuation of
pulmonary vessels
Clear Lung Fields
26. ECG in PH
• Right axis deviation
• An R wave/S wave
ratio greater than one
in lead V1
• Incomplete or
complete right bundle
branch block
• Increased P wave
amplitude in lead II
(P pulmonale) due to
right atrial
enlargement
27. • Echocardiogram
– Order for screening when clinical suspicion exists
– Order for standard interval screening in selected
groups:
• Family of those with IPAH or with known BMPR2 mutation
• Scleroderma spectrum
• Pre-liver transplant
28. Echocardiogram Findings
• TR
• Right atrial and ventricular
hypertrophy
• Flattening of interventricular septum
• Small LV dimension
• Dilated PA
• Pericardial effusion
• Poor prognostic sign
• RA pressure so high it impedes
normal drainage from pericardium
• Do not drain, usually does not
induce tamponade since RV under
high-pressure and non-collapsible
29.
30. Right Heart Catheterization
– RA <6
– RV <30/6
– PA <30/12
– PCWP <12
• Pulmonary Vascular Resistance
• Cardiac Output by the Fick Equation
31. • Mean PAP pressure
– At rest: >25mmHg
– With exercise: >30mmHg
• Wedge Pressure: <15mmHg
• Pulmonary Vascular Resistance: > 240
dynes-cm-sec-5
32. Vasoreactivity Testing During RHC
• Inhaled Nitric Oxide (NO) is a preferential
pulmonary arterial vasodilator
• Positive if:
– Mean PAP decreases at least 10 mmHg and to a value less
than 40 mmHg
– Associated increased or unchanged cardiac output
– Minimally reduced or unchanged systemic blood pressure
• Only patients with Positive Vasoreactivity are given
treatment trials with Calcium Channel Blockers!
33. Always Rule out CTEPH
• Must be excluded in every case of PAH
• Potentially surgically remediable
• V/Q scan is preferred screening test
• CT pulmonary angiography
36. Who do we treat for PAH?
• Treatment is based on functional status
New York Heart Association Functional Classification
Class 1: No symptoms with ordinary physical activity.
Class 2: Symptoms with ordinary activity. Slight limitation
of activity.
Class 3: Symptoms with less than ordinary activity. Marked
limitation of activity.
Class 4: Symptoms with any activity or even at rest.
37. How do we Treat Them?
• General measures:
– Avoid pregnancy
• Contraception imperative
• Maternal mortality 30%
– Immunizations for respiratory illnesses
Influenza & pneumonia vaccinations
– Minimize valsalva maneuvers—increase risk of
syncope
• Cough, constipation, heavy lifting, etc
38. Classes of therapyClasses of therapy
• MedicalMedical
• DiureticsDiuretics
• Anti coagulants (IPAH)Anti coagulants (IPAH)
• DigoxinDigoxin
• OxygenOxygen
• PAH specific therapyPAH specific therapy
• Surgical therapySurgical therapy
• Atrial septostomyAtrial septostomy
• Lung transplantationLung transplantation
39. Diuretics
• Principally to treat edema from right heart failure
• Ventricular interdependence—ensure LV output
preserved.
• May need to combine classes
• -Thiazide and loop diuretics
• Careful to avoid too much pre-load reduction
• Patients often require large doses of diuretics
40. Anticoagulants
• Studies only show benefit in IPAH patients, based
on improved survival.
• Other PAH groups not as clear, use in them
considered expert opinion.
• Generally, keep INR 2.0-2.5.
• Thought to lessen in-situ thrombosis
41. Oxygen
• Formal assessment of nocturnal and
exertional oxygenation needs.
• Minimize added insult of hypoxic
vasoconstriction
• Keep oxygen saturation ≥90%
• May be impossible with large right to left
shunt
• Exclude nocturnal desaturation
• Overnight oximetry
• Rule out concomitant obstructive sleep
apnea and hypoventilation syndromes
44. Calcium Channel Blockers
• Use only when demonstrated vasoreactivity in RHC
(about 10% or less of patients)
• Diltiazem or nifedipine preferred.
• Titrate up to maximum tolerated dose.
• Systemic hypotension may prohibit use
• Only 50% of patients maintain response to CCB.
• Not in FC IV patients or severe right heart failure
45. Endothelin Receptor Antagonists
(ETRA)
• Targets relative excess of endothelin-1 by blocking
receptors on endothelium and vascular smooth muscle
• Bosentan and ambrisentan
• Ambrisentan is ET-A selective.
• Both show improvement in 6MWD and time to clinical
worsening.
• Monthly transaminase monitoring required for both
• Annual cost about $40,000
46. • Potential for serious liver injury (including very rare cases
of unexplained hepatic cirrhosis after prolonged
treatment)
• Oral dosing
• Initiate at 62.5 mg BID for first 4 weeks
• Increase to maintenance dose of 125 mg BID thereafter
• Initiation and maintenance dose of 62.5 mg BID
recommended for patients >12 years of age with body
weight >40kg
• No dose adjustment required in patients with renal
impairment
• No predetermined dose adjustments required for
concomitant warfarin administration.
47. Ambrisentan
• 5 or 10 mg once daily
• Much less risk of transaminase elevation (about
1%), but monthly monitoring still required
• No dose adjustment of warfarin needed.
49. Sildenafil
• Safety
– Side effects: headaches, epistaxis, and
hypotension (transient)
– Sudden hearing loss
– Drug interaction with nitrates
– FDA approved dose is 20 mg tid
51. Epoprostenol
• First PAH specific therapy available in the mid
1990’s
• Lack of acute vasodilator response does not
correlate well with epoprostenol
unresponsiveness.
• Very short half life = 2 minutes
• Delivered via continuous infusion
• Cost about $100,000/year
53. Treprostinil (Remodulin)
• Continuous subcutaneous
infusion or IV infusion
• Longer t1/2 = 4 hours
• Less risk of rapid fatal
deterioriation if infusion stops
• Significant site pain at infusion
site limits use
54. Treprostinil
• Intravenous treprostinil
– Hemodynamic improvements and 6MWD
improvements
– No site pain
– Risk of catheter related bloodstream infection
and embolic phenomenon
– Recent concerns about increased gram-negative
bloodstream infections.
56. Iloprost
• Improvements in 6MW, functional class and
hemodynamics observed
Olschewski H et al. N Engl J Med 2002;347:322-29
• Safety and side effects
– Potential for increased hypotensive effect
with antihypertensives
– Increased risk of bleeding, especially with
co-administration of anticoagulants
– Flushing, increased cough, headache, insomnia
– Nausea, vomiting, flu-like syndrome
– Increased liver enzymes
57.
58.
59. Failure of Medical Therapy: Consider
Atrial Septostomy
• Improved left-sided filling
• Decreased right-sided
pressures
• May serve as bridge to
transplant
60. Failure of Medical Therapy: Indications for
Lung Transplant
• New York Heart Association (NYHA) functional class
III or IV
• Mean right atrial pressure >10 mmHg
• Mean pulmonary arterial pressure >50 mmHg
• Failure to improve functionally despite medical therapy
• Rapidly progressive disease