This document provides information on congestive cardiac failure (CCF), including its definition, pathophysiology, clinical features, investigations, and management. CCF occurs when the heart muscle is weakened and cannot maintain adequate cardiac output. The pathophysiology involves changes in preload, afterload, and contractility that decrease cardiac output. Compensatory mechanisms initially help but later worsen symptoms. Clinically, CCF presents with dyspnea, edema, elevated JVP, hepatomegaly, and other signs. Investigations include BNP, ECG, echocardiogram. Management focuses on treating the underlying cause, reducing preload/afterload, and improving contractility. Diuretics, ACE inhibitors, beta
Heart failure is a clinical syndrome characterized by dyspnea, fatigue, and clinical signs of congestion leading to frequent hospitalizations, poor quality of life, and shortened life expectancy. It is a final common pathway to various cardiac conditions. It is a growing problem worldwide with serious consequences in Sub-Saharan Africa where it occurs at a younger age with limited resources to manage the condition. The incidence and prevalence vary worldwide. In this mini-review, we looked at the definition, classification, and pathophysiology of the condition.
Heart failure is a clinical syndrome characterized by dyspnea, fatigue, and clinical signs of congestion leading to frequent hospitalizations, poor quality of life, and shortened life expectancy. It is a final common pathway to various cardiac conditions. It is a growing problem worldwide with serious consequences in Sub-Saharan Africa where it occurs at a younger age with limited resources to manage the condition. The incidence and prevalence vary worldwide. In this mini-review, we looked at the definition, classification, and pathophysiology of the condition.
Coronary artery Disease [CAD] is the most common , serious, chronic life threatening diseases in the USA.
More than 11 million Persons have CAD in USA.
Myocardial Ischemia [Reduced blood & oxygen supply to Heart Muscle ], Caused by
Lack of oxygen due to Inadequate perfusion which result from an Imbalance
Between oxygen supply & Demand.
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently. You have four heart chambers.
Heart failure is a clinical syndrome that develops when –
The heart can not maintain adequate output
or
Can do so only at the expense of elevated ventricular filling pressure
Coronary artery Disease [CAD] is the most common , serious, chronic life threatening diseases in the USA.
More than 11 million Persons have CAD in USA.
Myocardial Ischemia [Reduced blood & oxygen supply to Heart Muscle ], Caused by
Lack of oxygen due to Inadequate perfusion which result from an Imbalance
Between oxygen supply & Demand.
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently. You have four heart chambers.
Heart failure is a clinical syndrome that develops when –
The heart can not maintain adequate output
or
Can do so only at the expense of elevated ventricular filling pressure
Heart failure is a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return.
Definition
Causes
Pathophysiology
Types Of Heart Failure
Symptoms
Signs
Complications
Investigations
Treatment
Etiopathogenesis and pharmacotherapy of CONGESTIVE CARDIAC FAILURE
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
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.
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!
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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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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
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.
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
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.
3. Congestive Cardiac Failure
Definition:
CCF or Heart Failure in a clinical syndrome that
develops when the heart muscle is weakened
and cannot maintain the adequate cardiac
output or can do so only at an expence of
elevated ventricular filling pressure.
4.
5.
6.
7. Pathophysiology
Cardiac output is determined by :
• Preload (the volume and pressure of blood in
the ventricles at the end of diastole)
• Afterload (the volume and pressure of blood
in the ventricle during systole)
• Myocardial contractility
Basis of starling law.
8. Frank-Starling mechanism
Represents the relationship between stroke volume and end
diastolic volume.
• The law states that the stroke volume of the heart increases in
response to an increase in the volume of blood in the
ventricles, be for e contraction (the end diastolic volume),
when all other factors remain constant.
• As a larger volume of blood flows in to the ventricle, the blood
stretches the cardiac muscle fibers, leading to an increase in
the force of contraction.
9. severe (D) heart failure. Ventricular performance is related to the degree of myocardial
stretching. An increase in preload (end-diastolic volume, end-diastolic pressure, filling pressure or
atrial pressure) will therefore enhance function; however, overstretching causes marked
deterioration. In heart failure, the curve moves to the right and becomes flatter. An increase in
myocardial contractility or a reduction in afterload will shift the curve upwards and to the left
(green arrow).
10. • Heart failure is characterised by: a decrease in cardiac output. Cardiac
output in turn is a function of preload, after load and myocardial
contractility. In heart failure, preload is increased, afterload is increased
and myocardial contractility is decreased.
• In initial stages of heart failure with the reduction in CO, certain
compensatory mechanisms come into operation. These compensatory
mechanisms are initially beneficial, but later become counterproductive
and account for most of the manifestations of heart failure.
• These compensatory mechanisms are renin-angiotensin system and
autonomic nervous system.
• Increased myocardial contractility: As the ventricles dilates (resulting in
increased preload), the ventricular contractility increases resulting in
relatively increased volume of blood ejected (Frank-Starling law).
• The increase left ventricular filling pressures are transmitted to the
pulmonary veins which results in alveolar transduction of fluid and
pulmonary congestion. Finally, oxygen demand is enhanced due to
increased contractility.
11. • Myocardial hypertophy occurs due to volume and pressure overload in the
ventricles and helps in enhanced contractility and hence increased CO.
• However, it produces the increased oxygen demand and reduced
compliance of the ventricle that results in increased preload which is again
transmitted to the pulmonary vasculature.
• Sympathetic stimulation results in peripheral vascularisation which in turn
leads to Na+-water retention due to direct and indirect effects of RAS.
• Sympathetic stimulation also produces increased heart rate and enhances
contractility. Increased afterload maybe deleterious as it tends to reduce
cardiac output and increases oxygen demand of the heart.
• Myocardial remodelling: Changes in structure and function of myocardium
and includes hypertrophy and apoptosis of myocytes and alterations in the
quantity and composition of extracellular matrix. Remodelling involves not
only the ischaemic area, but also the viable myocardium resulting in
gradual loss of contractility over a period of time.
12.
13. Types of heart failure
• Left, right and biventricular heart failure
• The left side of the heart comprises the functional unit of the LA and LV,
together with the mitral and aortic valves; the right heart comprises the
RA, RV, and tricuspid and pulmonary valves.
• Left-sided heart failure. There is a reduction in left ventricular output and
an increase in left atrial and pulmonary venous pressure. An acute
increase in left atrial pressure causes pulmonary congestion or pulmonary
oedema; a more gradual increase in left atrial pressure, as occurs with
mitral stenosis, leads to reflex pulmonary vasoconstriction, which protects
the patient from pulmonary oedema. This increases pulmonary vascular
resistance and causes pulmonary hypertension, which can, in turn, impair
right ventricular function.
14. • Right-sided heart failure. There is a reduction in right
ventricular output and an increase in right atrial and
systemic venous pressure. Causes of isolated right
heart failure include chronic lung disease (cor
pulmonale), pulmonary embolism and pulmonary
valvular stenosis.
• Biventricular heart failure. Failure of the left and right
heart may develop because the disease process, such
as dilated cardiomyopathy or ischaemic heart disease,
affects both ventricles or because disease of the left
heart leads to chronic elevation of the left atrial
pressure, pulmonary hypertension and right heart
failure.
17. Clinical Features
Left Sided Heart Failure:
1) Pulmonary Edema
a) Dyspnea (SOB)
b)Orthopnea
c)Paroxysmal Nocturnal Dyspnea
2)Decreased forward Perfusion
Activated Renin Angiotensin Aldosterone System, which
cause fluid retention
and worsenen CHF.
18. Clinical Features
Right Sided Heart Failure:
Most common cause of cause of Right Heart Failure is
Left side
Heart Failure.
a) Dyspnea(SOB)
b)Jugular Venous Distention
c)Pitting Edema
d)Ascitis
e)Nutmeg Liver “Hepatomegaly”
21. • General appearance
Cool Peripheral extrimities
Cynosis of lips and nail beds
Dyspnea:-
Early stage of HF-while exertion
Orthopnea- later manifestation of HF
Chronic or severe stages-even at rest
22. • Pulmonary examination
Pulmonary crackles (Rales or crepitations) can be
heard.
Rales are frequently absent in patients with chronic
HF
But patients without concomitant lung diseases,
rales are specific
For HF
• Cardiac examination
S3(gallop rhythm) is audible and palpable at apex
Murmurs of mitral and tricuspid regurgitation are
frequently
present in patients with advanced HF
23. • Abdomen and extrimities
Hepatomegaly is seen (frequently tender
and pulsating)
Ascities and jaundice are late signs of HF
Peripheral edema is cardinal
manifestation of HF
(Usually symmetric) but is also
nonspecific
24. • Jugular Veins
JVP-Usually elevated
• Cardiac Cachexia
With severe chronic HF there is marked
weight loss and cachexia
25. Investigations
• BNP>100pg/mL
• Electrocardiogram may be normal or it could show numerous
abnormalities including acute ST-T–wave changes from
myocardial ischemia, atrial fibrillation, bradycardia, left
ventricular hypertrophy
• Serum creatinine may be increased because of hypoperfusion.
Pre existing renal dysfunction can contribute to volume
overload.
• Complete blood count useful to determine if heart failure is a
result of reduced oxygen-carrying capacity
26. • Chest radiography is useful for detection of cardiac
enlargement, pulmonary edema, and pleural
effusions
• Echocardiogram assesses left ventricle size, valve
function, pericardial effusion, and ejection fraction
• Hyponatremia, serum sodium <130mEq/L, is
associated with reduced survival and may indicate
worsening volume overload and/or disease
progression
