Heart failure is a common condition that results in impaired pumping of the heart. It can be caused by structural or functional issues in the heart. There are over 5 million patients with heart failure in the US, with 500,000 new cases diagnosed each year. The two main types are systolic heart failure, characterized by reduced pumping ability, and diastolic heart failure, characterized by stiffening of the heart muscle. Treatment involves medications such as ACE inhibitors, beta blockers, diuretics, and device-based therapies like biventricular pacing for certain patients. Ongoing research is exploring new drugs and approaches for the treatment of heart failure.
Pharmacotherapy of congestive heart failure symptomatic benefitsRAVISHANKARMANCHUKON
This presentation enables learners to understand the medicines used in the symptomatic treatment of Congestive Heart Failure. This knowledge makes the prescriber emulate the rational drug prescription for this particular diseased condition.
Pharmacotherapy of congestive heart failure symptomatic benefitsRAVISHANKARMANCHUKON
This presentation enables learners to understand the medicines used in the symptomatic treatment of Congestive Heart Failure. This knowledge makes the prescriber emulate the rational drug prescription for this particular diseased condition.
sudden spike in blood pressure to 180/120 or higher
abt how we deal with it
what we need to do immediate action
maintain ASAP blood pressure in order to save the patients
sudden spike in blood pressure to 180/120 or higher
abt how we deal with it
what we need to do immediate action
maintain ASAP blood pressure in order to save the patients
- 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.
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
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
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
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.
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.
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
Ocular injury ppt Upendra pal optometrist upums saifai etawah
Hf. final
1. Heart Failure: the changing
paradigm
The most common reason for hospitalization in adults >65 years old.
2. Heart Failure-Heart Failure- Clinical syndrome … can result fromClinical syndrome … can result from
any structural or functional cardiac disorder thatany structural or functional cardiac disorder that
impairs ability of ventricle to fill with or eject bloodimpairs ability of ventricle to fill with or eject blood
Impact!Impact!
5 million patients- have heart failure
500,000 new cases every year
300,000 deaths/year300,000 deaths/year
3. Types of Heart Failure
• Systolic heart failure (HFrEF)
– Decreased pumping function of the heart, which results
in fluid back up in the lungs and heart failure
– EF =<35%
• Diastolic heart failure (HFpEF)
– Involves a thickened and stiff heart muscle
– As a result, the heart does not fill with blood properly
– This results in fluid backup in the lungs and heart
failure
– EF =>50%
5. Classification of HF: Comparison
Between ACC/AHA HF Stage and
NYHA Functional Class
ACC/AHA HF Stage1
NYHA Functional Class2
A At high risk for heart failure but without
structural heart disease or symptoms
of heart failure (eg, patients with
hypertension or coronary artery disease)
B Structural heart disease but without
symptoms of heart failure
C Structural heart disease with prior or
current symptoms of heart failure
D Refractory heart failure requiring
specialized interventions
I Asymptomatic
II Symptomatic with moderate exertion
IV Symptomatic at rest
III Symptomatic with minimal exertion
None
6. Adapted from Cohn JN. N Engl J Med. 1996;335:490–498.
Pathologic
remodeling
Low ejection
fraction Death
Symptoms:
Dyspnea
Fatigue
Edema
Chronic
heart
failure
•Neurohormonal
stimulation
•Myocardial
toxicity
Sudden
Death
Pump
failure
Coronary artery
disease
Hypertension
Cardiomyopathy
Valvular disease
Myocardial
injury
Pathologic Progression of CV
Disease
Diabetes
7. Compensatory Mechanisms:Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone SystemRenin-Angiotensin-Aldosterone System
Renin + Angiotensinogen
Angiotensin I
Angiotensin II
Peripheral
Vasoconstriction
↑ Afterload
↓ Cardiac Output
Heart FailureHeart Failure
↑ Cardiac Workload
↑ Preload
↑ Plasma Volume
Salt & Water Retention
Edema
Aldosterone Secretion
ACE
Kaliuresis
BetaBeta
StimulationStimulation
• COCO
• NaNa++
Fibrosis
10. Stage A At high risk for developing heart failure.
Includes people with:
Hypertension
Diabetes mellitus
CAD (including heart attack)
History of cardiotoxic drug therapy
History of alcohol abuse
History of rheumatic fever
Family history of CMP
Exercise regularly
Quit smoking
Treat hypertension
Treat lipid disorders
Discourage alcohol or illicit drug
use
If previous heart attack/ current
diabetes mellitus or HTN, use
ACE-I
Stage B Those diagnosed with “systolic” heart
failure- have never had symptoms of
heart failure (usually by finding an ejection
fraction of less than 40% on
echocardiogram
Care measures in Stage A +
Should be on ACE-I
Add beta -blockers
Surgical consultation for coronary
artery revascularization and valve
repair/replacement (as appropriate
Stage C Patients with known heart failure with
current or prior symptoms.
Symptoms include: SOB, fatigue
Reduced exercise intolerance
All care measures from Stage A apply,
ACE-I and beta-blockers should be used
+ Diuretics, Digoxin,
Dietary sodium restriction
Weight monitoring, Fluid restriction
Withdrawal drugs that worsen
condition
Maybe Spironolactone therapy
Stage D Presence of advanced symptoms, after
assuring optimized medical care
All therapies -Stages A, B and C +
evaluation for:Cardiac transplantation,
VADs, surgical options, research
therapies, Continuous intravenous
inotropic infusions/ End-of-life care
Therapies
12. Heart Failure Treatments:
Medication Types
•ACE inhibitor (angiotensin-
converting enzyme)
•ARB (angiotensin receptor
blockers)
•Beta-blocker
•Digoxin
•Diuretic
•Aldosterone blockade
Type What it does
•Expands blood vessels which lowers blood
pressure, neurohormonal blockade
•Similar to ACE inhibitor—lowers
blood pressure
•Reduces the action of stress hormones
and slows the heart rate
•Slows the heart rate and improves the heart’s
pumping function (EF)
•Filters sodium and excess fluid from the blood
to reduce the heart’s workload
•Blocks neurohormal activation and controls
volume
14. Lifestyle Changes
•Eat a low-sodium, low-fat diet
•Lose weight
•Stay physically active
•Reduce or eliminate alcohol
and caffeine
•Quit Smoking
What Why
•Sodium is bad for high blood pressure, causes
fluid retention
•Extra weight can put a strain on the
heart
•Exercise can help reduce stress and
blood pressure
•Alcohol and caffeine can weaken an already
damaged heart
•Smoking can damage blood vessels and make
the heart beat faster
15. • Ivabradine can be beneficial to reduce HF
hospitalization for patients with symptomatic (NYHA
class II-III) stable chronic HFrEF (LVEF ≤35%) who
are receiving GDEM, including a beta blocker at
maximum tolerated dose, and who are in sinus rhythm
with a heart rate of 70 bpm or greater at rest.
• IIa, ACC/ AHA focused update 2016
16. PERIPHERAL ULTRAFILTRATION
• Removes sodium and water in hospitalized HF patients
who are refractory to pharmacologic therapy.
• (UNLOAD) trial enrolled 200 patients with AHFS and
reduced or preserved ejection fraction,
Dyspnea and renal function were not improved..
• ESC 2016 Class IIb , (Level of Evidence: C)
18. Although tolvaptan and conivaptan have been
approved for the treatment of clinically
significant hypervolemic and euvolemic
hyponatremia, their value in the
management of AHFS, with or without
hyponatremia, remains to be determined.
Class IIb (Level of evidence B)
19. Cinaciguat
• Soluble guanylate cyclase(sGC) activator
• Preliminary studies shows beneficial hemodynamic
profile
• At higher doses associated with significant
hypotension, but did not affect 30 days post
discharge mortality
• COMPOSE Trial
20. Advantages over Nitrates
• Heme independent means no tolerance
• More predicatable vasodilatory response
21. Chimeric Natriuretic Peptides(CD-NP)
• C type natriuretic peptide (CNP)
• lacks the natriuretic property of ANP and BNP
• Less hypotension – primaraly a venodilator
• Dendroaspis (DNP)
• Significant natriuretic
• Cause hypotension – both artery and venodilator
22. Aliskiren
• Direct renin inhibitor
• Approved for treatment of hypertension
• Oral treatment
• ACE inhibitors and ARBs are of proven
benefit in treatment of CHF
23. ASTRONAUT
• Addition of alikiren to standard therapy
delays time to events including CV deaths
of HF rehopitalization within 6 mths in pts
hospitalized for AHFS and EF < 40 %
25. Rolofylline
• Highly selective Adenosine A 1 receptor
antagonist
• Increases RBF
• Enhances diuresis
• But does not activate the tubulo glomerular
feedback
26. • Pilot study was PROTECT trial which
showed positive trends in AHF
• But PROTECT II showed only mild
benefits on symptoms and no effects on
renal protection and other pre specified
outcomes and was associated with more
CNS adverse effects
• Hence current status : doubtful
27. Ularitide
• Synthetic analouge of urodilatin
• Urodilatin is natriuretic and diuretic
hormone ( ANP family)
• Ularitide has additional vasodilatory
properties due to effect on vascular c GMP
28. • SIRIUS I and II(Safety and Efficacy of an
Intravenous Placebo /controlled
Randomized infusion of Ularitide in
Prospective double blind Study in patients
with Symptomatic Decompansated Chronic
Heart Failure)
• Improved clinical status, hemodynamics
and neurohormonal profile
• S/E : significant hypotension
29. Endothelin antagonists
• Endothelin 1 ,2 , 3
• Receptors : ET A and ET B
• Most potent endogenous vasoconstriction
via ET A receptos
• Levels of Endothelin increase in HF and
correlates with patient outcomes
• Currently aproved for treatement of PAH
with moderated dysability (Functional Class
III)
30. Tezosentan
• Non selective ET A/B antagonist
• VERITAS trial
• > 1400 pts with AHF were given tezosentan
infusion 24 – 72 hrs v/s placebo
• Did not improve symptoms or decrease mortality
at day 7 post randomization
31. Istaroxime
• Prototype of a new class of drug
• M/A : inhibits membrane bound Na+/K+
ATPase and stimulates SERCA 2a
• Hence increase inotropic and lusitropic
effects
• Improves both systolic and diastolic
function, reduce LV dimension in diastole
and increase SBP
32. HORIZON HF trial
• Studied 120 pts with AHF and reduced EF
• Addition of istaroxime to standard therapy
lowered PCWP and heart rate and increased
SBP
• Higher dose infusion (1.5 mcg/k/min)
increased cardiac index and reduced LVEDV
• No changes in neurohormones , renal function
and trop I levels during 6 hr infusion
33. Relaxin
• Pre – RELAX – AHF study
• Dose response effect of relaxin v/s placebo on symptom
relief, other clinical outcomes and safety in pts with AHF
and normal to incresed BP
• Associated with improvement in dyspnea and other clinical
outcomes
• Currently being studied in RELAX-AHF
trial- phase II/III
39. Cardiac Resynchronization Therapy
Key Points
Recommendations
• CRT is recommended for symptomatic patients with HF in
sinus rhythm with a QRS duration ≥150 msec and LBBB QRS
morphology and with LVEF ≤35% despite OMT in order to
improve symptoms and reduce morbidity and mortality.
• Timing of Referral Important
– Patients often not on optimal Medical Rx
– Patients referred too late- Not a Bail Out
41. Heart Failure and Sudden Cardiac
Death
– SCD is one of the leading causes of death in the U.S. –
approximately 450,000 deaths a year
– Patients with heart failure are 6-9 times as likely to develop
sudden cardiac death as the general population
42. How does a defibrillator for
sudden cardiac death work?
44. • ICD is recommended in patients:
a) with asymptomatic LV systolic dysfunction
(LVEF ≤30%) of ischaemic origin, who are at
least 40 days after acute myocardial infarction,
b) with asymptomatic non-ischaemic dilated
cardiomyopathy (LVEF ≤30%), who receive
OMT therapy, in order to prevent sudden death
and prolong life.
47. In Summary….
• Heart failure is common and has high mortality
• Drug therapy improves survival
– Betablockers, ACE-I, aldosterone antagonists
• Newer device therapies are showing promise for
symptom relief and improved survival
– Biventricular pacing, ICD’s
• Transplants remain rare, but technology for
mechanical assist devices continues to improve,
stay tuned …! ! !
The major risk factors that are associated with HF are CAD, a history of previous MI, hypertension, valvular heart disease, alcoholism, diabetes, and congenital heart defects.
Additional HF risk factors are obesity, age, reduced or falling vital capacity, smoking, and high of low hematocrit level.
The New York Heart Association (NYHA) classification system is based largely on the assessment of symptoms.1
The new American College of Cardiology and American Heart Association (ACC/AHA) classification guidelines were designed to compliment the NYHA classification system. These new guidelines focus more on underlying disease and the need to treat early in the disease process, even before overt symptoms of heart failure are present.2
Lifestyle changes involved in managing heart failure:
Discuss diet and exercise in some detail:
Staying active does not mean training as if you were going to run a marathon: but can simply mean regular walks. You can start slowly and build up under the direction of your doctor.
Can reduce sodium in your diet by focusing on eating fresh meats, fruits, and vegetables; reading labels: asking questions when you eat out; and getting a low-sodium cookbook.
Lifestyle changes are things you can do to influence how your feel.
It may seem difficult to accomplish these things, but they are an essential part of treating heart failure.
There are many resources to help you get started in incorporating these changes into your life. List any.
Also, ask your friends and family for support.
Many patients with advanced systolic heart failure exhibit significant inter- or intraventricular conduction delays that disturb the synchronous beating of the left and right ventricles so that they pump less efficiently. This delayed ventricular activation and contraction is referred to as ventricular dysynchrony and is easily recognized by a wide QRS complex on an ECG.
This IVCD (inter- or intraventricular conduction delay) typically has left bundle branch morphology.
Dr. (Name) says:
Sudden Cardiac Arrest is as scary as it sounds. It means that your heart suddenly starts beating very fast and quivers instead of beating in a regular and organized way. No blood gets pumped, and you will die unless you get treatment within minutes. We’ll talk more about treatments in a moment.
Unlike a heart attack, SCA is caused by an electrical problem in your heart.
SCA can strike without warning, and there are no symptoms.
Click on animation. Dr. (Name) says:
Some people with Class III and IV heart failure can benefit from a heart failure pacemaker that can help your heart beat more efficiently by coordinating or synchronizing the way the heart beats, so your heart pumps more efficiently.
It works by automatically checking your heart function 24 hours a day.
This type of heart device is also called cardiac resynchronization therapy or CRT. You may also hear the term biventricular pacing. All refer to the same kind of treatment.
Treatment with a heart device may make you feel better.
Although many people experience dramatic improvements in their quality of life and in their heart failure symptoms, results may vary. Not everyone responds to the treatment in the same way.
It is also important to note that heart failure pacemakers do not cure heart failure--a heart failure pacemaker is part of an overall treatment plan.
Describe heart failure pacemaker device:
A heart failure pacemaker is about the size of a small pocket watch that contains a battery and computer circuitry to correct your heart rhythm and help your heart beat more efficiently. Small insulated wires called leads connect the device to the heart.
We’re going to pass around a plastic replica of a Medtronic combination heart failure pacemaker and defibrillator pacemaker . Facilitators circulate and pass around replicas and collect them.
Before I move on, I’d like to say a few words about Medtronic, the company helping us put on the seminar today.
Medtronic was the first company to introduce a pacemaker in the United States. Physicians worldwide have prescribed heart failure pacemakers for more than 120,000 patients.
Other people with heart failure are in danger of having heartbeats that are irregular and/or too fast.
These irregular heart beats can cause you to feel short of breath and light headed. Such episodes may also be life threatening if not treated quickly.
Some heart devices also contain a defibrillator in addition to the special kind of pacemaker. This combination device also sends out small electrical signals to restore your normal heart rhythm. If the small signals do not work, the device sends out a shock to reset your heart rhythm. This kind of device is also used to treat SCA.