1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves lifestyle modifications, medications like diuretics, ACE inhibitors, beta blockers, and devices or transplantation for refractory cases.
Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.
Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS).
Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.
Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.
Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS).
Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.
Heart Failure (Dr Vosik Presentation) Symposia presented in Milot, Haiti at Hôpital Sacré Coeur.
CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
Definition of heart failure - causes and types of heart failure - pathophysiology and risky factors for heart failure - Diagnosis clinical manifestations and investigations and classification of heart failure- treatment of chronic heart failure
Also Acute heart failure causes - clinical picture and treatment
Heart failure is a serious medical condition that occurs when the heart cannot pump enough blood to meet the body's needs. It can be caused by a variety of factors, including heart disease, high blood pressure, diabetes, and obesity. In this essay, we will explore the symptoms, causes, and treatments of heart failure.
One of the most common symptoms of heart failure is shortness of breath. This occurs because the heart is not able to pump enough oxygenated blood to the lungs, leading to a feeling of suffocation. Other symptoms may include fatigue, swelling in the legs and feet, and a persistent cough. These symptoms can be very uncomfortable and can significantly reduce a person's quality of life.
There are many possible causes of heart failure. In some cases, it may be the result of an underlying heart condition, such as coronary artery disease, a heart attack, or a heart valve problem. In other cases, it may be caused by lifestyle factors such as smoking, high blood pressure, or obesity. Other risk factors for heart failure include a family history of heart disease, diabetes, and certain medications.
Treatments for heart failure may vary depending on the severity of the condition and the underlying causes. In some cases, medications such as diuretics or beta-blockers may be prescribed to help reduce symptoms and improve heart function. Lifestyle changes such as quitting smoking, losing weight, and reducing salt intake may also be recommended. In more severe cases, surgery may be required to repair or replace damaged heart valves or to implant a device such as a pacemaker or defibrillator.
While heart failure can be a very serious condition, there are many effective treatments available. It is important to seek medical attention if you experience any symptoms of heart failure, as early diagnosis and treatment can help improve outcomes and quality of life. With proper care and management, many people with heart failure are able to live healthy, active lives.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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.
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. Heart Failure
Results from any structural or
functional abnormality that impairs
the ability of the ventricle to eject
blood (Systolic Heart Failure) or
to fill with blood (Diastolic Heart
Failure).
3. The Vicious Cycle of Congestive Heart
Failure
Decreased Blood Pressure and
Decreased Renal perfusion
Stimulates the Release
of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure
LV Dysfunction causes
Decreased cardiac output
4. Types of Heart Failure
Systolic Heart Failure:
decreased cardiac output
Decreased Left ventricular ejection fraction
Diastolic Heart Failure:
Elevated Left and Right ventricular end-diastolic
pressures
May have normal LVEF
.
6. Clinical Presentation of Heart Failure
Due to excess fluid accumulation:
Dyspnea (most sensitive symptom)
Edema
Hepatic congestion
Ascites
Orthopnea, Paroxysmal Nocturnal Dyspnea
(PND)
Due to reduction in cardiac ouput:
Fatigue
Weakness
7. Physical Examination in Heart Failure
S3 gallop
Low sensitivity, but highly specific
Cool, pale, cyanotic extremities
Have sinus tachycardia, diaphoresis and peripheral
vasoconstriction
Crackles or decreased breath sounds at bases
(effusions) on lung exam
Elevated jugular venous pressure
Lower extremity edema
Ascites
Hepatomegaly
Splenomegaly
Displaced PMI
Apical impulse that is laterally displaced past the
midclavicular line is usually indicative of left ventricular
enlargement>
8. Lab Analysis in Heart Failure
CBC
Since anemia can exacerbate heart failure
Serum electrolytes and creatinine
before starting high dose diuretics
Fasting Blood glucose
To evaluate for possible diabetes mellitus
Thyroid function tests
Since thyrotoxicosis can result in A. Fib,
and hypothyroidism can results in HF.
Iron studies
To screen for hereditary hemochromatosis as cause of heart
failure.
ANA
To evaluate for possible lupus
Viral studies
If viral mycocarditis suspected
9. Laboratory Analysis (cont.)
BNP
With chronic heart failure, atrial mycotes
secrete increase amounts of atrial natriuretic
peptide (ANP) and brain natriuretic pepetide
(BNP) in response to high atrial and
ventricular filling pressures
Usually is > 400 pg/mL in patients with
dyspnea due to heart failure.
10. Chest X-ray in Heart Failure
Cardiomegaly
Cephalization of the pulmonary
vessels
Kerley B-lines
Pleural effusions
14. Cardiac Testing in Heart Failure
Electrocardiogram:
May show specific cause of heart
failure:
Ischemic heart disease
Dilated cardiomyopathy: first degree AV
block, LBBB, Left anterior fascicular block
Amyloidosis: pseudo-infarction pattern
Idiopathic dilated cardiomyopathy: LVH
Echocardiogram:
Left ventricular ejection fraction
Structural/valvular abnormalities
15. Further Cardiac Testing in Heart
Failure
Coronary arteriography
Should be performed in patients presenting with
heart failure who have angina or significant
ischemia
Reasonable in patients who have chest pain that
may or may not be cardiac in origin, in whom
cardiac anatomy is not known, and in patients with
known or suspected coronary artery disease who do
not have angina.
Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic
pressure.
16. Classification of Heart Failure
New York Heart Association (NYHA)
Class I – symptoms of HF only at
levels that would limit normal
individuals.
Class II – symptoms of HF with
ordinary exertion
Class III – symptoms of HF on less
than ordinary exertion
Class IV – symptoms of HF at rest
17. Classification of Heart Failure (cont.)
ACC/AHA Guidelines
Stage A – High risk of HF, without
structural heart disease or symptoms
Stage B – Heart disease with
asymptomatic left ventricular
dysfunction
Stage C – Prior or current symptoms
of HF
Stage D – Advanced heart disease and
severely symptomatic or refractory HF
18. Chronic Treatment of Systolic Heart
Failure
Correction of systemic factors
Thyroid dysfunction
Infections
Uncontrolled diabetes
Hypertension
Lifestyle modification
Lower salt intake
Alcohol cessation
Medication compliance
Maximize medications
Discontinue drugs that may contribute to heart
failure (NSAIDS, antiarrhythmics, calcium channel
blockers)
19. Order of Therapy
1. Loop diuretics
2. ACE inhibitor (or ARB if not
tolerated)
3. Beta blockers
4. Digoxin
5. Hydralazine, Nitrate
6. Potassium sparing diuretcs
20. Diuretics
Loop diuretics
Furosemide, buteminide
For Fluid control, and to help relieve
symptoms
Potassium-sparing diuretics
Spironolactone, eplerenone
Help enhance diuresis
Maintain potassium
Shown to improve survival in CHF
21. ACE Inhibitor
Improve survival in patients with all
severities of heart failure.
Begin therapy low and titrate up as
possible:
Enalapril – 2.5 mg po BID
Captopril – 6.25 mg po TID
Lisinopril – 5 mg po QDaily
If cannot tolerate, may try ARB
22. Beta Blocker therapy
Certain Beta blockers (carvedilol,
metoprolol, bisoprolol) can improve
overall and event free survival in NYHA
class II to III HF, probably in class IV.
Contraindicated:
Heart rate <60 bpm
Symptomatic bradycardia
Signs of peripheral hypoperfusion
COPD, asthma
Heart block
23. Management of Refractory Heart
Failure
Inotropic drugs:
Dobutamine, dopamine, milrinone,
nitroprusside, nitroglycerin
Mechanical circulatory support:
Intraaortic balloon pump
Left ventricular assist device (LVAD)
Cardiac Transplantation
A history of multiple hospitalizations for HF
Escalation in the intensity of medical therapy
A reproducable peak oxygen consumption with
maximal exercise (VO2max) of < 14 mL/kg
per min. (normal is 20 mL/kg per min. or more)
is relative indication, while a VO2max < 10
mL/kg per min is a stronger indication.