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.
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
This ppt is prepared from content of braunwald, and some latest international journals. In account it make more clear concept about pulmonary hypertension.
it also contain latest ESC 2022 guidelines of pulmonary hypertension.
Pulmonary hypertension and its anesthetic managementprateek gupta
pulmonary hypertension and it pathophysiology. pre operative, intraoperative and post operative complications and anesthetic management.
drugs that can be used in anesthetic management of pulmonary hypertensiom
Pneumonia is an inflammatory condition of the lung affecting primarily the small air sacs known as alveoli. Typically symptoms include some combination of productive or dry cough, chest pain, fever, and trouble breathing. Severity is variable.
Pneumonia is usually caused by infection with viruses or bacteria and less commonly by other microorganisms, certain medications and conditions such as autoimmune diseases. Risk factors include cystic fibrosis, chronic obstructive pulmonary disease (COPD), asthma, diabetes, heart failure, a history of smoking, a poor ability to cough such as following a stroke, and a weak immune system. Diagnosis is often based on the symptoms and physical examination. Chest X-ray, blood tests, and culture of the sputum may help confirm the diagnosis. The disease may be classified by where it was acquired with community, hospital, or health care associated pneumonia.
Vaccines to prevent certain types of pneumonia are available. Other methods of prevention include handwashing and not smoking. Treatment depends on the underlying cause. Pneumonia believed to be due to bacteria is treated with antibiotics. If the pneumonia is severe, the affected person is generally hospitalized. Oxygen therapy may be used if oxygen levels are low.
Pneumonia affects approximately 450 million people globally (7% of the population) and results in about four million deaths per year. Pneumonia was regarded by William Osler in the 19th century as "the captain of the men of death". With the introduction of antibiotics and vaccines in the 20th century, survival improved. Nevertheless, in developing countries, and among the very old, the very young, and the chronically ill, pneumonia remains a leading cause of death. Pneumonia often shortens suffering among those already close to death and has thus been called "the old man's friend"
IPA was first described in 1953. Due to
widespread use of chemotherapy and immunosuppressive agents, its incidence has increased
over the past two decades. Of all autopsies
performed between 1978 and 1992, the rate of
invasive mycoses increased from 0.4% to 3.1%, as
documented. IPA increased
from 17% to 60% of all mycoses found on autopsy
over the course of the study. The mortality rate of
IPA exceeds 50% in neutropenic patients and
reaches 90% in haematopoietic stem-cell transplantation (HSCT) recipients
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult. The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction. A myriad of CNS events, including spinal cord injury, subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), intracranial hemorrhage, status epilepticus, meningitis, and subdural hemorrhage, have been associated with this syndrome.
Obstructive sleep apnea (OSA)—also referred to as obstructive sleep apnea-hypopnea—is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. It is the most common type of sleep-disordered breathing and is characterized by recurrent episodes of upper airway collapse during sleep. These episodes are associated with recurrent oxyhemoglobin desaturations and arousals from sleep.
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).
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to an infection.The definition of sepsis was updated in 2016 following publication of the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). This recommended that organ dysfunction should be defined using the Sequential (or Sepsis-related) Organ Failure Assessment (SOFA) criteria or the "quick" (q)SOFA criteria.
The discovery of malignant cells in pleural fluid
and/or parietal pleura signifies disseminated or
advanced disease and a reduced life expectancy in
patients with cancer.Median survival following
diagnosis ranges from 3 to 12 months and is
dependent on the stage and type of the underlying
malignancy. The shortest survival time is observed
in malignant effusions secondary to lung cancer
and the longest in ovarian cancer, while malignant
effusions due to an unknown primary have an
intermediate survival time.Historically, studies
showed that median survival times in effusions due
to carcinoma of the breast are 5-6 months.
However, more recent studies have suggested
longer survival times of up to 15 months. A
comparison of survival times in breast cancer
effusions in published studies to 1994 calculated
a median survival of 11 months.9
Currently, lung cancer is the most common
metastatic tumour to the pleura in men and breast
cancer in women.Together, both malignancies
account for 50- 65% of all malignant effusions. Lymphomas, tumours of the genitourinary
tract and gastrointestinal tract account for
a further 25% Pleural effusions from an
unknown primary are responsible for 15% of all
malignant pleural effusions.Few studies have
estimated the proportion of pleural effusions due to
mesothelioma: studies from 1975, 1985 and 1987
identified mesothelioma in 1/271, 3/472 and 22/592
patients, respectively, but there are no more recent
data to update this in light of the increasing incidence
of mesothelioma.
Cigarette smoking is one of the major preventable causes
of morbidity and mortality all over the world.
• According to World Health Organization (WHO, 2018)
Tobacco is the second major cause of death. It is currently
responsible for the death of 1 in 10 adults.
Altitude physiology typically focuses on people above 2500 m; ∼8000 ft. Altitudes above that are sometimes subdivided into very high (3500–5500 m; ∼11,500–18,000 ft) and extreme (>5500 m; >18,000 ft). An estimated 40 million people travel each year to altitudes >2500 m (∼8000 ft),1 and as many or more travel to altitude for leisure and sports, and work in mines, military or border operations, and the like. Altitude medicine considers the clinical disorders associated with acclimatization by the travelers, workers and migrants, and with adaptation by people with lifetimes or populations with millennia of residence (an estimated 83 million people).
With a hurried ascent, many (∼80%) will report a transient headache (high-altitude headache or [HAH]), and some will develop one of three forms of acute high-altitude illness: acute mountain sickness (AMS) and HAH, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). AMS and HAH are annoying and interfere with activity and work, however, HACE and HAPE can be fatal with mortality rates approaching 30%. Among some residents, chronic mountain sickness (CMS) and right ventricular hypertrophy develop over months to years of residence at altitude. Birth weights are generally lower and the rate of small-for-gestational-age babies and congenital heart defects are higher than that in lowland populations.
Non–small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. Histologically, NSCLC is divided into adenocarcinoma, squamous cell carcinoma (SCC) (see the image below), and large cell carcinoma. Small cell lung cancer (SCLC), previously known as oat cell carcinoma, is considered distinct from other lung cancers, which are called non–small cell lung cancers (NSCLCs) because of their clinical and biologic characteristics.
Asbestos-related diseases include non-malignant disorders such as asbestosis, diffuse pleural thickening, pleural plaques, pleural effusion, rounded atelectasis and malignancies such as lung cancer and malignant mesothelioma.
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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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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
- 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
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.
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.
1. DIAGNOSIS & MANAGEMENT OF
PULMONARY HYPERTENSION
Dr Kamal Bharathi. S
Department of Pulmonary Medicine
Sri Manakula Vinayagar Medical college and Hospital
2. DIAGNOSTIC STUDIES
• Identify the etiology
• Assess severity and prognosis
• Evaluate the functional and haemodynamic
impairment
• Help guide appropriate therapy
3. Detection of pulmonary hypertension
Detailed history and physical examination Suspicion of pulmonary hypertension and
possible causes/ associations
Electrocardiogram Exclude other causes of cardiopulmonary
symptoms
Chest radiograph
Echocardiogram (at rest. to consider
repeat with exertion)
Evaluate for presence of pulmonary
hypertension, assess chamber sizes and
function, valvular abnormalities, contrast
(bubble) study to evaluate possible shunt
4. Essential testing
Pulmonary function testing Exclude intrinsic lung disease
Lung (V/Q) scan Exclude thromboembolism
Overnight oximetry Screen for sleep-disordered breathing
Blood serologies (e.g., CBC. liver function,
renal function, HIV, ANA, antiphospholipid
antibodies)
Exclude collagen vascular disease, liver
disease, infection, and other possible
causes of pulmonary hypertension
Oxygen desaturation study Assess need for supplemental oxygen
6-Minute walk test Establish baseline
Right cardiac catheterization Confirm diagnosis, assess other cardiac
causes (shunt); consider left heart
catheterization
5. Contingent testing
Transesophageal echocardiogram Assess patent foramen ovale (PFO)
Characterize valvular function
Computed tomogram of chest Assess interstitial lung disease,
adenopathy
Polysomnogram Diagnosis and treatment of sleep-
disordered breathing
Pulmonary angiogram
Blood studies (BNP, clotting studies,
genetic testing)
Assess presence and location of organized
thromboemboli and suitability for
pulmonary thromboendarterectomy
Lung biopsy Exclude subtle interstitial lung disease
vasculitis and other uncommon diseases
(PVOD, PCH) to assist planning
6. Chest Radiograph
Features include:
• elevated cardiac apex due to right ventricular
hypertrophy
• enlarged right atrium
• prominent pulmonary outflow tract
• enlarged pulmonary arteries
• pruning of peripheral pulmonary vessels
9. ECG
• RV hypertrophy with strain pattern (increased
R-wave amplitude with ST-segment
depression and T-wave inversion in the
precordial leads)
• Right atrial enlargement (increased P-wave
amplitude in leads II and V1)
10.
11. Echocardiogram
• Suspicion- first test to assess if PHT is present.
• Modified Bernoulli equation:
RVSP = 4v2 + right atrial pressure;
v = tricuspid jet velocity in meters per second
• assumed equal to the PA systolic pressure
when the pulmonic valve is normal.
• Normal RVSP has been reported as 28 ± 5 mm
Hg.
12. Echocardiogram
• Reveals important anatomical and functional information-
identifying the cause.
• Conditions that Predispose to Pulmonary Hypertension
• Congenital or acquired valvular disease (MR, MS, AS, prosthetic
valve dysfunction)
• Left ventricular systolic dysfunction
• Impaired left ventricular diastolic function (hypertensive heart
disease, HCM, Fabry disease, infiltrative cardiomyopathies)
• Other obstructive lesions (aortic coarctation, supravalvular AS,
subaortic membrane, cor triatriatum)
• Congenital disease with shunt (ASD, VSD, coronary fistula, patent
ductus arteriosus, anomalous pulmonary venous return)
• Pulmonary embolus (thrombus in IVC, right-sided cardiac chamber,
or PA; tricuspid or pulmonic valve vegetation)
• Pulmonary vein thrombosis/stenosis
13. 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
14. Four-chamber view. Right atrial (RA) enlargement, right
ventricular
(RV) enlargement. The left atrium (LA) and left ventricle (LV) are
small and underfilled.
15. Short axis view. RV enlargement is present. Flattening of the
intraventricular septum (IVS) results from pressure and volume
overload of the RV
16.
17.
18. SIX-MINUTE WALK DISTANCE
• The 6-minute walk test (6MWT) is the most commonly
employed measure of exercise capacity in patients with
PH.
• In addition to the distance walked, the degree of
dyspnea (Borg score) and oxygen saturation are also
measured.
• A 6-minute walk distance of < 332 m and a drop in
oxygen saturation by > 10% are suggestive of poor
prognosis.
• It is also measured on routine follow-ups and can be
indicative of clinical deterioration.
• It may also be used to assess the response to therapy.
19. • PFT and ABG:
Identify the contribution of underlying airway
or parenchymal lung disease.
• Ventilation/Perfusion lung scan:
should be performed in patients with PH to
look for potentially treatable CTEPH
20. • High-resolution CT provides detailed views of the lung
parenchyma and facilitates the diagnosis of interstitial lung
disease and emphysema. High resolution CT may be very
helpful where there is a clinical suspicion of PVOD
• Blood tests and immunology Routine biochemistry,
haematology, and thyroid function tests are required in all
patients. Serological testing is important to detect
underlying CTD, HIV, and hepatitis.
• Abdominal ultrasound scan Liver cirrhosis and/or portal
hypertension can be reliably excluded by the use of
abdominal ultrasound.
21. Cardiac Catheterization
• Right heart cardiac catheterization is required to
confirm the diagnosis of pulmonary hypertension.
• to assess the severity of the haemodynamic
impairment.
right atrial pressure
mean PAP
pulmonary artery occlusion pressure (PAOP)
cardiac output (CO)
pulmonary vascular resistance (mPAP-PAOP)/CO
Transpulmonary gradient (mPAP-PAOP)
• to test the vasoreactivity of the pulmonary circulation
22. • Usually, the RAP and PCWP also increase,
implying RV failure and left ventricular (LV)
diastolic dysfunction, respectively.
• The latter is the consequence of ventricular
interdependence and abnormal compliance of
the left ventricle produced by an enlarged
right ventricle.
23. Diagnosis of PAH
• requires a mean pulmonary artery pressure
greater than or equal to 25 mm Hg,
• an adequately measured PAWP or a directly
recorded LVEDP of less than or equal to 15
mm Hg;
• An elevated PVR >3 Wood units is also seen
and required in some published diagnostic
criteria for PAH.
24. Vasodilator testing
• to identify those few patients in whom a trial of
treatment with oral calcium channel antagonists is
appropriate.
• Agents commonly used include inhaled nitric oxide,
intravenous adenosine, or epoprostenol administered
by either route.
• the definition has varied, a decrease in the mPAP of
at least 10 mm Hg to a value less than 40 mm Hg,
together with a CO that is unchanged or increased
(but not decreased) is generally considered a
“positive” acute vasodilator response
25. THERAPY FOR PAH
• Therapy must be driven by an appropriately
established diagnosis
26. Exercise and the Avoidance of
Deconditioning
• Regardless of the cause, patients with
pulmonary hypertension and cor pulmonale
should be encouraged to maintain as active a
lifestyle as possible.
• Regular, steady aerobic exercise should be
encouraged, and is often best initiated under
guidance of a pulmonary or cardiac
rehabilitation program.
27. Oxygen Therapy
• To avoid acute hypoxia- as hypoxic pulmonary
vasoconstriction will add to the burden on the
right ventricle.
• Oxygen relieves hypoxic pulmonary
vasoconstriction, thus decreasing vascular
resistance and improving CO.
• Levels of arterial oxygen saturation < 90% -
supplemental oxygen.
28. Immunizations
• against influenza and pneumococcal
pneumonia are important preventive
measures in all patients with pulmonary
hypertension and cor pulmonale.
29. Fluid Management and Diuretics
• to avoid fluid overload is central to the
management of cor pulmonale.
• dietary habits and to restrict sodium intake.
• Spironolactone is often used to manage mild
fluid retention.
30. Anticoagulation
• In the absence of contraindications,
anticoagulation with warfarin is
recommended.
• The generally recommended target INR for
warfarin therapy in patients with PAH is 1.5 to
2.5.
31. Contraception and Pregnancy
• Pregnancy in women with IPAH is associated
with a high mortality, on the order of 30% to
50%.
• pregnancy should be avoided, and early
termination recommended on account of the
high maternal mortality.
34. Calcium Channel Antagonists
• 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
35. Endothelin Receptor Antagonists
• Targets relative excess of endothelin-1 by
blocking receptors on endothelium and vascular
smooth muscle
• Bosentan, Ambrisentan, Sitaxentan, Macitentan
• Ambrisentan is ET-A selective.
• Both show improvement in 6MWD and time to
clinical worsening.
• Monthly transaminase monitoring required for
both
• Annual cost is high
36. • 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.
37. 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.
38. Macitentan
- able to achieve enhanced tissue penetration,
- long-lasting pharmacologically active metabolites,
- an increased receptor affinity and
- more sustained receptor binding
• These properties allow a once-a-day regimen with lower
doses and optimised safety profile, and with no effect on liver
enzymes in phase II trials
40. Sildenafil
• Safety
– Side effects: headaches, epistaxis, and
hypotension (transient)
– Sudden hearing loss
– Drug interaction with nitrates
– FDA approved dose is 20 mg TID
– Tadalafil 40mg OD
– Vardenafil 5mg OD
42. 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
44. Treprostinil (Remodulin)
• Continuous subcutaneous
infusion or IV infusion
• Longer t1/2 = 4 hours
• Less risk of rapid fatal
deterioriation if infusion stops
• Intravenous treprostinil
– Hemodynamic improvements and
6MWT improvements
– No site pain
– Risk of catheter related
bloodstream infection and embolic
phenomenon
– Recent concerns about increased
gram-negative bloodstream
infections.
45. Iloprost
• Inhaled prostacyclin
• Administered 6-9 times
daily via special
nebulizer
• Reported risk of
morning syncope
• Improvements in 6MW,
functional class and
hemodynamics
observed
46. • 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
47. Guanylate cyclase stimulant
• Stimulators of the nitric oxide receptor.
• Dual mode of action.
• They increase the sensitivity of sGC to
endogenous nitric oxide (NO)
• Directly stimulate the receptor to mimic the
action of NO.
• Riociguat is an oral sGC stimulant that has
reported benefit in patients with inoperable and
persistent chronic thromboembolic pulmonary
hypertension (CTEPH)
48.
49. ATRIAL SEPTOSTOMY
• patients with RV failure and associated PH in whom medical
therapy has failed.
• This approach has been proposed by some experienced centers
to improve peripheral oxygen delivery, despite a fall in
systemic arterial saturation due to a compensatory rise in
cardiac output.
• It is recommended not to perform AS in patients with
(1) severe RV failure on cardiorespiratory support,
(2) mean right atrial pressure (mRAP) >20mmHg,
(3) room-air resting O2 saturation <90%,
(4) left ventricular end diastolic pressure (LVEDP) >18mm
Hg
50.
51. Pott’s shunt
• An alternative method of right
ventricular decompression is via
the creation of an anastomosis
between the descending aorta and
left pulmonary artery or Potts
shunt.
• In the setting of suprasystemic
PAP, a theoretical advantage of
Potts shunt over septostomy is the
sparing of the cerebral and
coronary circulation from
deoxygenated blood.
52. Pulmonary Artery Denervation
• pulmonary artery denervation is a novel
nonmedical therapy for PAH and the
presumed mechanism of action is via the
abolishment of sympathetic nerve supply to
the pulmonary circulation.
53. Lung Transplantation
• Lung transplantation remains a destination therapy for a
significant number of patients despite targeted PAH
therapy.
• Because of limited organ availability and the high mortality
rates of PAH patients awaiting transplantation, eligible
patients for whom first-line treatment strategies have failed
should be referred early for transplantation assessment.
• Double-lung transplantation is the preferred option for PAH,
but heart-lung transplantation remains necessary for some
patients in the context of complex Eisenmenger physiology
and is also adopted by some centers for patients with
refractory right heart failure