This document discusses venous thrombosis and pulmonary embolism. It covers risk factors, pathophysiology, diagnostic evaluation, and treatment options. The main points are:
1. Venous thrombosis and pulmonary embolism are concerns in postoperative and ICU patients. Thrombi often form silently in leg veins and can break off and travel to the lungs.
2. Diagnostic evaluations include D-dimer, ventilation-perfusion scans, echocardiograms, angiograms. Imaging shows defects from clots blocking blood flow.
3. Treatment involves anticoagulation initially with heparin or low molecular weight heparin. Warfarin is used long-term. Thrombolytics or inferior v
Deep vein thrombosis (DVT) and Pulmonary embolism (PE)Aminul Haque
Deep vein thrombosis (DVT) and pulmonary embolism (PE), collectively referred to as venous thromboembolism (VTE), constitute a major global burden of disease.
This was powerpoint was requested by an attending physician to be shared with the Psychiatric providers regarding DVT prophylaxis in patients who may have been on the unit. They include recommendations as outlined by the ACCP 2012 Guidelines for prevention of venous thromboembolism
Deep vein thrombosis (DVT) and Pulmonary embolism (PE)Aminul Haque
Deep vein thrombosis (DVT) and pulmonary embolism (PE), collectively referred to as venous thromboembolism (VTE), constitute a major global burden of disease.
This was powerpoint was requested by an attending physician to be shared with the Psychiatric providers regarding DVT prophylaxis in patients who may have been on the unit. They include recommendations as outlined by the ACCP 2012 Guidelines for prevention of venous thromboembolism
Deep Venous Thrombosis and Pulmonary Embolism : Diagnostic Approach and Curre...Bassel Ericsoussi, MD
Acute pulmonary embolism: Overview, Diagnosis, Treatment
DVT/PE in pregnancy
Prevalence of PE in COPD exacerbations
Diagnostic vascular ultrasonography
Venous thromboembolism (VTE) is a disorder that includes deep vein thrombosis and pulmonary embolism. A deep vein thrombosis (DVT) occurs when a blood clot forms in a deep vein, usually in the lower leg, thigh, or pelvis.
A lecture highlighting the role of Echocardiography as a major hemodynamic monitoring tool in the Intensive Care settings and the assessment of loading conditions.
Deep Venous Thrombosis and Pulmonary Embolism : Diagnostic Approach and Curre...Bassel Ericsoussi, MD
Acute pulmonary embolism: Overview, Diagnosis, Treatment
DVT/PE in pregnancy
Prevalence of PE in COPD exacerbations
Diagnostic vascular ultrasonography
Venous thromboembolism (VTE) is a disorder that includes deep vein thrombosis and pulmonary embolism. A deep vein thrombosis (DVT) occurs when a blood clot forms in a deep vein, usually in the lower leg, thigh, or pelvis.
A lecture highlighting the role of Echocardiography as a major hemodynamic monitoring tool in the Intensive Care settings and the assessment of loading conditions.
Physician should have a high suspicion to diagnose patient with pulmonary Embolism, this slides will give you precise Diagnosis, Investigation and guideline directed Treatment.
Introduction to afib, Epidemiology of afib, etiology of afib, Clinical presentation of people with afib, Investigation and management
AF related outcomes and complications and differential Diagnosis
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These 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
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
3. • The threat of venous thrombosis and acute pulmonary embolism is a daily
concern in the post operative period and ICU.
• Thrombi usually form in proximal leg veins and are often clinically silent,
becoming evident only when a portion of the thrombus breaks loose and
travels to the lungs to become a pulmonary embolus.
• Because it is possible to prevent thrombus formation in the legs , deaths from
pulmonary emboli are considered preventable.
6. Pulmonary embolism
• When a thrombus completely or partially obstructs a pulmonary artery or its
branches,
• the alveolar dead space is increased.
• The area, although continuing to be ventilated,
• receives little or no blood flow.
• Thus, gas exchange is impaired or absent in this area.
• In addition, various substances are released from the clot and surrounding area,
causing regional blood vessels and bronchioles to constrict.
• This causes an increase in pulmonary vascular resistance. This reaction compounds
(the ventilation–perfusion imbalance.)
7. • The hemodynamic consequences are increased from the regional
vasoconstriction and reduced size of the pulmonary vascular bed.
• increase in right ventricular work to maintain pulmonary blood flow.
• When the work requirements of the right ventricle exceed its capacity, right
ventricular failure occurs,
• leading to a decrease in cardiac output followed by a decrease in systemic
blood pressure
• the development of shock.
8. Conditions High-risk regimens
Acute medical illness LDUH/LMWH
Major abdominal surgeries LDUH/LMWH+GCS/IPC
Thoracic surgery LDUH/LMWH+GCS/IPC
Cardiac surgeries with complications LDUH/LMWH+IPC
craniotomy IPC
Hip/knee surgery LMWH
Major trauma LDUH/LMWH/IPC
Head/spinal cord trauma LDUH/LMWH+IPC
Above conditions+active bleeding/risk
of bleeding
IPC
Thromboprophylaxis
9. Unfractionated heparin
• Mucopolysaccharide
• Heparin+anti thrombin forms heparin AT complex which inhibits factor
2(10times) and factor 10
• It also binds to plasma protiens,endothelial cells and macrophages
• Platelet binding-heparin induced thrombocytopenia(HIT)
10. HIT
• 2 types
1)non immune type
2)immune type
Pathogenesis:
• Heparin+platelets forms antigenic complex which produces anti bodies
induces thrombosis.
• Anti bodies also binds to endothelial cells forms fibrin -thrombosis
11. Risk factors:
• Flushes for intravascular catheters, heparin coated pulmonary catheters
• HIT is 10times greater with unfractionated heparin than LMWH
• Post orthopaedic and cardiac surgeries
Clinical features:
• Appears after 5 days and in 24hrs in patient with HIT anti bodies
12. Thrombosis:
• Venous>arterial
Diagnosis:
• ELISA for anti bodies for platelet factor 4 heparin complex
Acute management:
• Withhold heparin
• Stop heparin flushes
• Direct thrombin inhibitors: Argatroban, Lepirudin
13. • Argatroban : 2mcg/kg/min and titrate dose to aPTT= 1.5-3*control
• : 0.5mcg/kg/min in liver failure
• : maximum dose 10mcg/kg/min
• Lepirudin : 0.4mg/kg or 0.2mg/kg(renal failure) bolus/ followed by
• 0.15mg/kg/hr titrate dose to aPTT= 1.5-3*control
15. LOW MOLECULAR WEIGHT HEPARIN
• Anti 10 a activity 2- 4times more than anti thrombin activity.
• Reduced binding to plasma proteins.-more potent anticoagulant.
• Reduced binding to endothelial cells and macrophages – longer duration of
action
• Reduced binding to platelets – low risk of HIT –major advantage.
• Major draw back is clearance by kidney.
16. Anticoagulant regimen for Thromboprophylaxis
Unfractionated heparin :
• Usual dose:5000U SC every 12th /8th hrly
• Obesity:5000U SC 8th hrly(BMI<50),7000U SC 8th hrly(BMI>50)
LMWH:
Enoxaparin: usual dose : 40mg SC once daily/30mg SC twice daily.
• obesity : 0.5mg/kg SC once daily(BMI >40)
• renal failure : 30mg SC once daily
• Dalteparin: usual dose:2500 SC OD
18. Diagnostic evaluation:
• DVT is silent only but symptomatic pulmonary embolus appears.
• The clinical presentation of acute pulmonary embolism is non-specific, and
there are no clinical or laboratory findings that will confirm or exclude
the diagnosis of pulmonary embolism.
19.
20.
21. PERC FOR LOW RISK OUTPATIENT POPULATIONS
• This approach has been best studied in the emergency department
1. Age < 50 years
2. HR < 100 bpm
3. SPO2 ≥ 95 %
4. No haemoptysis
5. No oestrogen use
6. No prior DVT or PE
7. No unilateral leg swelling
8. No surgery or trauma requiring hospitalization within the past 4 weeks
22. LABORATORY
1. Leucocytosis
2. Increased ESR
3. Elevated serum LDH
4. ABGs: hypoxemia, hypercapnia, and respiratory alkalosis. Massive PE with
hypotension can cause hypercapnia and a combined respiratory and metabolic
acidosis (due to lactic acidosis)
23. • Elevated Troponin
1. 30-50 % of pts who have a moderate to large PE
2. Due to acute right heart overload
3. Resolve within 40 hrs (more prolonged elevation after acute MI).
24. • ELECTROCARDIOGRAPHY
1. 70 % of pts with acute PE had ECG abnormalities
2. Most commonly
Sinus tachycardia
nonspecific ST-segment and T-wave changes
• S1 Q3 T3 pattern of acute cor pulmonale (acute right heart strain) is classic
infrequent during acute PE
Common among patients with massive acute PE and cor pulmonale
25.
26. ELECTROCARDIOGRAPHY
• The following ECG abnormalities are associated with a poor prognosis
1. Atrial arrhythmias
2. Right bundle branch block
3. Inferior Q-waves
4. Precordial T-wave inversion and ST-segment changes
27.
28. • CXR shows RLL collapse.
Ventilation perfusion scan
showing perfusion defect in right
side + corresponding ventilation
defect
29. • classical’ appearance of a
pulmonary infarction – a
wedge-shaped lesion
peripherally set against the
pleura
31. ULTRASOUND
• Only 29 % of pts with PE had venous thrombosis detected by compression
ultrasound
32. D-DIMER
• ELISA (results in >8 hrs)
• Quantitative rapid ELISA (results in 30 min)
• Semi-quantitative rapid ELISA (results in 10 min)
• Qualitative rapid ELISA (results in 10 min)
• Quantitative latex agglutination assay (results in 10 to 15 min)
• Semi-quantitative latex agglutination assay (results in 5 min)
• Erythrocyte agglutination assay (SimpliRED) (results in 2 min)
33. • ANGIOGRAPHY - gold standard in the diagnosis of acute PE
• A negative pulmonary angiogram excludes clinically relevant PE
34.
35.
36.
37. ALVEOLAR DEAD SPACE
• Alveolar dead space fraction (ADF) increases
• 98% pts with PE have an abnormal ADF (defined as >20 %) or a positive D-
dimer
• Common false positive results
• Difficulty obtaining accurate ADF measurements
38. ECHOCARDIOGRAPHY
• Useful if a rapid diagnosis is required to justify the use of thrombolytic
therapy
• PE related mortality increases with RV dysfunction,RV thrombus
• 35% of pts with RV thrombus have PE
• only 4 % of pts with PE have an RV thrombus
39. Echocardiographic findings in PE
• RV dilation and dysfunction
• RV thrombus
• RA dilation
• TR
• Pulm HTN
• Paradoxical septal movement
• Increases in RV pressure will displace the septum towards the LV during systole and/or
diastole
• Dilated and invariable IVC
• McConnell Sign
• Regional wall motion abnormalities that spare the right ventricular apex
• 77% sensitivity, 94% specificity
42. Low-Molecular-Weight Heparin
• Enoxaparin, 1 mg/kg by SC every 12h
• LMWH is cleared by the kidneys, and dose adjustments are necessary in renal
impairment
• In patients with renal failure and thromboembolism who require heparin,
UFH is recommended over LMWH .
43. • LMWH no need to monitor anticoagulant activity, and the ability
to treat outpatients (which could help to reduce hospital
admissions for deep vein thrombosis).
• For these reasons, LMWH is slowly replacing UFH for the initial
management of thromboembolism
44. Monitoring Anticoagulation
• The aPTT can be used , because it is a reflection of coagulation factor IIa activity, and
one of the prominent effects of UFH is inhibition of factor IIa (antithrombin effect).
• The aPTT cannot be used to monitor anticoagulation with LMWH.
• Monitoring of anticoagulation is usually not necessary with LMWH.
• If needed, the anticoagulant response to LMWH can be assessed by measuring factor
Xa activity .
45. Warfarin Anticoagulation
• patients with a reversible cause of venous thromboembolism (e.g., major
surgery),oral anticoagulation with warfarin can be started on the first
day of heparin therapy.
• When the PT reaches an (INR) of 2 to 3, the heparin can be discontinued.
• Oral anticoagulation with Coumadin is continued for at least 3 months
Patients with cancer-related or recurrent VTE require longer periods of
anticoagulation
46. Thrombolytic Therapy
• Pulmonary embolism accompanied by hemodynamic instable
• Hemodynamically stable patients with right ventricular dysfunction
• Cardiac arrest
• The major problem with this is bleeding
47. The two drug regimens shown below are designed to achieve rapid clot
lysis.
• Alteplase: 0.6 mg/kg over 15 minutes.
• Reteplase: 10 Units by bolus injection, and repeat in 30 minutes.
48. • The usual Alteplase dose is 100 mg infused over 2 hours
• Reteplase is not currently approved for treatment of
thromboembolism , but the bolus administration of this drug is
well-suited for rapid clot dissolution .
49. Inferior Vena Cava Filters
• Mesh like filter devices can be placed in the inferior vena cava to
trap thrombi that break
• loose from leg veins and prevent them from traveling to the lungs
50. Indications
A. Patient has proximal deep vein thrombosis in the legs and has one of the
following conditions:
• 1. A contraindication to anticoagulation
• 2. Pulmonary embolization during full anticoagulation
• 3. A free-floating thrombus (i.e., the leading edge of the thrombus is not
adherent to the vessel wall).
• 4. Poor cardiopulmonary reserve and unlikely to tolerate a pulmonary
embolus.
51. B. Patient does NOT have proximal deep vein thrombosis in the legs but has one of
the following conditions:
• 1. Requires long-term prophylaxis of pulmonary embolism (e.g., patients with a
history of recurrent pulmonary embolism)
• 2. Has a high risk of thromboembolism and a high risk of hemorrhage from
anticoagulant drugs (e.g., trauma victims)
52. The Greenfield Filter
• The major advantage of this filter is its elongated, conical
shape, which allows the basket to fill with thrombi to 75% of
its capacity without compromising the cross-sectional area of
the vena cava.
• This limits the risk for vena cava obstruction and
troublesome leg oedema, which plagued earlier models of
IVC filters.
53.
54. References:
• Paul Marino's, The ICU Book, 4th Edition.
• Venous thromboembolism: risks and prevention:Contin Educ Anaesth Crit
Care Pain (2011) 11 (1): 18-23.