Heart failure is a common clinical syndrome that can result from any structural or functional impairment of the ventricle that reduces its ability to fill or eject blood. It is the leading cause of hospitalization in adults over 65 years old. The document defines heart failure, discusses its key concepts like cardiac output and ejection fraction, classifications like NYHA and ACC/AHA stages, risk factors, pathophysiology including compensatory mechanisms and remodeling, symptoms, complications, diagnostic tests and emergency management.
Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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.
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.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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.
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
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
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!
1. Heart Failure
Heart Failure
Dr. Fuad Farooq
Dr. Fuad Farooq
Consultant Cardiologist
Consultant Cardiologist
The most common reason for hospitalization in adults >65 years old.
2. • Heart Failure-
Heart Failure- Clinical syndrome … can result from
Clinical syndrome … can result from
any structural or functional cardiac disorder that impairs
any structural or functional cardiac disorder that impairs
ability of ventricle to fill with or eject blood
ability of ventricle to fill with or eject blood
• Impact!
Impact!
– 5 million Americans- have heart failure
– 500,000 new cases every year
– 25-50 billion dollars a year to care for people with HF
– 6,500,000 hospital days / year and 300,000 deaths/year
6,500,000 hospital days / year and 300,000 deaths/year
3. Heart Failure
Heart Failure
Definition
Definition
• It is the pathophysiological process in which the heart as a
pump is unable to meet the metabolic requirements of the
tissue for oxygen and substrates despite the venous return
to heart is either normal or increased
4. Heart Failure
Heart Failure
Key Concepts
Key Concepts
• Cardiac output (CO) = Stroke Volume (SV) x Heart Rate (HR)
– Becomes insufficient to meet metabolic needs of body
• SV – determined by preload, afterload and myocardial
contractility
• Ejection Fraction (EF) (need to understand)
• Classifications HF
Classifications HF
– Systolic failure – decrease contractility
– Diastolic failure – decrease filling
– Mixed
5.
6.
7. Preload
Preload
• Volume of blood in ventricles
at end diastole
• Depends on venous return
• Depends on compliance
Afterload
Afterload
• Force needed to eject blood into
circulation
• Depends upon arterial BP,
pulmonary artery pressure
• Valvular disease increases
afterload
Factors Effecting Heart Pump
Factors Effecting Heart Pump
Effectiveness
Effectiveness
8. Ejection Fraction (EF)
Ejection Fraction (EF)
• One of the measurements used by physicians to assess how well
a patient’s heart is functioning
• “Ejection” refers to the amount of blood that is pumped out of
the heart’s main pumping chamber during each heartbeat
• “Fraction” refers to the fact that, even in a healthy heart, some
blood always remains within this chamber after each heartbeat
• An ejection fraction is a percentage of the blood within the
chamber that is pumped out with every heartbeat
• Normal EF = 55 to 75 percent
10. Keys To Understanding HF
Keys To Understanding HF
• All organs (liver, lungs, legs, etc.) return blood to heart
• When heart begins to fail/ weaken unable to pump blood
forwardfluid backs up Increase pressure within all organs
• Organ response
Organ response
– LUNGS:
LUNGS: congested increase effort to breathe fluid starts to escape
into alveoli (pulmonary edema) fluid interferes with O2 exchange
(hypoxia) aggravates shortness of breath
– Shortness of breath during exertion may be early symptoms
progresses later require extra pillows at night to breathe (orthopnea)
and experience "P.N.D." or paroxysmal nocturnal dyspnea
11. • LEGS, ANKLES, FEET:
LEGS, ANKLES, FEET: blood from feet and legs back-up of fluid
and pressure in these areas, as heart unable to pump blood as promptly
as received increase fluid within feet and legs (pedal/dependent
edema) and increase in weight
Keys To Understanding HF
Keys To Understanding HF
13. Heart Failure
Heart Failure
Etiology
Etiology
• Systolic Failure
Systolic Failure - most common
– Hallmark finding: Decrease in left ventricular ejection
fraction <40% (EF)
• Due to
– Impaired contractile function (e.g., MI)
– Increased afterload (e.g., hypertension)
– Cardiomyopathy
– Mechanical abnormalities (e.g., valve disease)
14. Heart Failure
Heart Failure
Etiology
Etiology
Diastolic failure
Diastolic failure
– Impaired ability of ventricles to relax and fill during
diastole decrease stroke volume and CO
– Diagnosis based on presence of pulmonary congestion,
pulmonary hypertension, ventricular hypertrophy
– Normal ejection fraction (EF)- Know why!
Not have much blood to eject
Not have much blood to eject
15. Heart Failure
Heart Failure
Etiology
Etiology
• Mixed systolic and diastolic failure
Mixed systolic and diastolic failure
– Seen in disease states such as dilated cardiomyopathy (DCM)
– Poor EFs (<35%)
– High pulmonary pressures
• Biventricular failure
Biventricular failure
– Both ventricles may be dilated and have poor filling and
emptying capacity
18. B.
B. Homeostatic Compensatory Mechanisms
Homeostatic Compensatory Mechanisms
Activation of Sympathetic Nervous System (First line)
1. In vascular system resulting in vasoconstriction
(What effect on afterload?)
2. Kidneys
i. Decrease renal perfusion Renin angiotensin release
ii. Aldosterone release Na and H2O retention
3. Liver
i. Stores venous volume causing ascites, hepatomegaly
Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
19. • Increase Na release of Anti diuretic hormone
(ADH)
• Release of atrial natriuretic factor (ANP) and BNP
Na and H20 excretion
– Thus Prevents
Prevents severe cardiac decompensation
Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
Counter Regulatory Response
Counter Regulatory Response
20. Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
– Neurohormonal responses:
Neurohormonal responses: Endothelin - stimulated by
ADH, catecholamines, and angiotensin II
• Arterial vasoconstriction
• Increase in cardiac contractility
• Hypertrophy
Counter Regulatory Response
Counter Regulatory Response
21. Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
– Neurohormonal responses
Neurohormonal responses: Proinflammatory cytokines (e.g.,
tumor necrosis factor)
• Released by cardiac myocytes in response to cardiac injury
• Depress cardiac function cardiac hypertrophy, contractile
dysfunction, and myocyte cell death
Counter Regulatory Response
Counter Regulatory Response
23. Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
– Natriuretic peptides: atrial natriuretic peptide (ANP) and
b-type natriuretic peptide (BNP)
• Released in response to increase in atrial volume and
ventricular pressure
• Promote venous and arterial vasodilation, reduce
preload and afterload
• Prolonged HF depletion of these factors
Counter Regulatory Response
Counter Regulatory Response
24. • Consequences of compensatory mechanisms
Consequences of compensatory mechanisms
• Ventricular dilation:
Ventricular dilation: Enlargement of heart chambers elevated
left ventricular pressure initially effective adaptive mechanism
then mechanism inadequate cardiac output decrease
• Frank-Starling law:
Frank-Starling law: Initially increase venous return results in
increase in force of contraction later increase ventricular filling
and myocardial stretch eventually results in ineffective contraction
• Hypertrophy:
Hypertrophy: Increase in muscle mass and cardiac wall thickness
in response to chronic dilation heart muscle poor contractility,
increase in oxygen needs, poor coronary artery circulation, prone
to ventricular dysrhythmias (sudden cardiac death)
Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
25. Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
• Ventricular remodeling/ cardiac remodeling
Ventricular remodeling/ cardiac remodeling
– Refers to the changes in size, shape, structure and physiology of
the heart after injury to the myocardium
28. End Result
End Result
FLUID OVERLOAD Acute Decompensated Heart Failure
/Pulmonary Edema
Medical Emergency!!
Medical Emergency!!
29. Heart Failure
Heart Failure
Classification Systems
Classification Systems
• New York Heart Association (NYHA) Functional
Classification of HF
– Classes I to IV
• ACC/AHA Stages of HF (newer)
– Stages A to D
35. 1.
1. Systolic versus Diastolic
Systolic versus Diastolic
– Systolic - loss of contractility get decease CO
– Diastolic - decreased filling or preload
1.
1. Left sided versus Right sided
Left sided versus Right sided
– Left ventricle - lungs
– Right ventricle - peripheral
1.
1. High output vs Low output
High output vs Low output
– Hypermetabolic state
1.
1. Acute versus Chronic
Acute versus Chronic
– Acute MI
– Chronic Cardiomyopathy
Heart Failure
Heart Failure
Causes
Causes
37. • Signs and symptoms
– Dyspnea
– Orthopnea & PND ??
– Cheyne Stokes
– Fatigue
– Anxiety
– Rales
• Orthopnea: dyspnea on lying flat - due to increased distribution of
blood to the pulmonary circulation while recumbent
Heart Failure
Heart Failure
Symptoms
Symptoms
38. Paroxysmal Nocturnal Dyspnoea
Paroxysmal Nocturnal Dyspnoea
• Attacks of severe shortness of breath and coughing that
generally occur at night
• It usually awakens the person from sleep, and may be quite
frightening
• Cause:
Cause:
– Caused in part by the depression of the respiratory center during sleep,
which may reduce arterial oxygen tension, particularly in patients with
reduced pulmonary compliance
– Also, in the horizontal position there is redistribution of blood volume
from the lower extremities and splanchnic beds to the lungs
• Little effect in normal individuals, but in patients with failing left ventricle,
there is a significant reduction in vital capacity and pulmonary compliance
with resultant shortness of breath
39. Heart Failure
Heart Failure
Clinical Manifestations
Clinical Manifestations
• Acute decompensated heart failure (ADHF)
Pulmonary edema
Pulmonary edema, often life-threatening
• Early
– Increase in the respiratory rate
– Decrease in PaO2(hypoxia)
• Later
– Tachypnea
– Respiratory acidosis
41. Person Literally Drowning In
Person Literally Drowning In
Secretions
Secretions
Immediate Action Needed
42. Right Heart Failure
Right Heart Failure
• Signs and Symptoms
Signs and Symptoms
– Fatigue, weakness, lethargy
– weight gain
– Increase abdominal girth
– Anorexia
– Right upper quadrant pain
– elevated neck veins
– Hepatomegaly
– May not see signs of LVF
44. What is present in this extremity, common to right sided HF?
45. Can You Have RVF Without LVF?
Can You Have RVF Without LVF?
• What is this called?
COR PULMONALE
COR PULMONALE
46. Heart Failure
Heart Failure
Complications
Complications
• Pleural effusion
• Atrial fibrillation (most common dysrhythmia)
– Loss of atrial contraction (kick) – necessary for 20-
25% of cardiac output
• Reduce CO by 20% to 25%
– Promotes thrombus/embolus formation
• Increase risk for stroke
47. Heart Failure
Heart Failure
Complications
Complications
• High risk of fatal dysrhythmias
fatal dysrhythmias (e.g., sudden cardiac death,
ventricular tachycardia) with HF and an EF <35%
• HF lead to severe hepatomegaly, especially with RV
failure
– Fibrosis and cirrhosis (cardiac cirrhosis) - develop over time
• Renal insufficiency or failure (cardiorenal syndrome
cardiorenal syndrome)
48. Heart Failure
Heart Failure
Initial Evaluation
Initial Evaluation
Primary goal -
Primary goal - Determine underlying cause
• Thorough history and physical examination – to identify cardiac
and noncardiac disorders or behaviors that might cause or
accelerate the development or progression of HF
• Volume status and vital signs should be assessed
49. Heart Failure
Heart Failure
Diagnostic Tests
Diagnostic Tests
Initial Lab workup includes
Initial Lab workup includes
1. ECG
2. Chest X ray
3. Complete blood count
(CBC)
4. Urinalysis
5. Serum electrolytes
(including calcium and
magnesium)
6. Blood urea nitrogen
(BUN) and serum
creatinine (Cr)
7. Glucose
8. Fasting lipid profile (FLP)
9. liver function tests (LFT)
10. Thyroid-stimulating
hormone (TSH)
11. Cardiac Troponins
12. Beta naturetic peptide
(BNP)
13. Arterial Blood gas (ABG)
51. • 2-dimensional echocardiogram (2-D echo) with
Doppler should be performed during initial
evaluation of patients presenting with HF to assess
ventricular function, size, wall thickness, wall
motion, and valve function
Heart Failure
Heart Failure
Diagnostic Tests
Diagnostic Tests
53. Heart Failure
Heart Failure
Diagnostic Studies
Diagnostic Studies
• Invasive hemodynamic monitoring
Invasive hemodynamic monitoring
– Can be useful for carefully selected patients with acute HF who
have persistent symptoms despite empiric adjustment of standard
therapies and
a. Whose fluid status, perfusion, or systemic or pulmonary vascular
resistance is uncertain
b. Whose systolic pressure remains low, or is associated with
symptoms, despite initial therapy
c. Whose renal function is worsening with therapy
d. Who require parenteral vasoactive agents
• Coronary angiography
Coronary angiography if ischemia is likely cause of heart
failure
54. Heart Failure
Heart Failure
Emergency Management
Emergency Management
U Upright Position
N Nitrates
L Lasix
O Oxygen
A ACE, ARBs, Aldactone, Amiodarone
D Digoxin, Dobutamine, Dopamine
M Morphine Sulfate
E Extremities Down
55. Heart Failure
Heart Failure
Stage
Stage A
At Risk Of Developing Heart Failure but no structural heart
At Risk Of Developing Heart Failure but no structural heart
disease yet:
disease yet:
– Adequate BP control
– Adequate Diabetes control
– Weight reduction
– Quit smoking
– Avoid cardiotoxins
– Lipid management
– Atrial fibrillation management
56. Heart Failure
Heart Failure
Stage B
Stage B
Structural Heart Disease Without Overt Symptoms
Structural Heart Disease Without Overt Symptoms
• Care measures as in Stage A along with:
– Should be on ACE-I
– Add beta blockers
– Spironolactone – if LVEF <40%
• Surgical consultation for coronary artery revascularization
and valve repair/replacement (as appropriate)
57. Structural Heart Disease With Overt Symptoms
Structural Heart Disease With Overt Symptoms
Nonpharmacological Interventions
Nonpharmacological Interventions
• Therapeutic life style changes:
Therapeutic life style changes: Diet
Diet low salt, low fat, rich in fruit
and veggie, increase fiber, water intake limited to 1.5 liters
• Smoking cessation
Smoking cessation
• Activity & exercise
Activity & exercise
– Duration of activity:
Duration of activity: Exercise training and rehab atleast 30 min
aerobic exercise/brisk walking with 5 days and ideally 7 days a
week
– Benefits:
Benefits: improve HRQOL, increase in functional status, improve
exercise capacity and reduce hospitalization and mortality,
improve endothelial function and improve O2 extraction from
peripheral tissue
Heart Failure
Heart Failure
Stage C
Stage C
HRQOL – Health related quality of life
58. Nonpharmacological Interventions
Nonpharmacological Interventions
• Salt
Salt :1.5gm for stage A&B and <3gm for stage C&D
• BMI:
BMI: 30-34.9kg/m2 (grade 1 obesity) lowest mortality –
weight U-shaped mortality curve (cardiac cachexia
cardiac cachexia)
– daily weight monitoring – same time with same clothing
– Weight gain
Weight gain of 3 lb (1.5 kg) over 2 days or a 3- to 5-lb (2.5 kg)
gain over a week – report to health care provider
Heart Failure
Heart Failure
Stage B
Stage B
59. • Pharmacological Interventions
Pharmacological Interventions
– All measures of stage A and B
Diuretics
Diuretics
– Furosimide
Furosimide (20-40mg once or twice)
– Hydroclorothiazide
Hydroclorothiazide (25mg once or twice)
– Metolazone
Metolazone (2.5-5mg OD )
– Spironolactone
Spironolactone (12.5-25 once or twice)
• Aim of diuretic therapy on outpatient is to decrease weight 0.5-1kg
daily with adequate diuresis and adjust the dose accordingly until
evidence of fluid retention resolved
– Then daily wt and adjust the dose accordingly
Heart Failure
Heart Failure
Stage C
Stage C
60. Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
ACE Inhibitors
ACE Inhibitors
• Capotopril:
Capotopril: 6.25mg thrice till
50mg thrice a day
• Enalapril :
Enalapril : 2.5mg twice to 10-
20mg twice a day
• Lisinopril:
Lisinopril: 2.5-5mg once to 20-
40mg once a day
• Ramipril:
Ramipril: 1.25-2.5mg once till
10mg once a day
• C/I
C/I – Cr >3mg/dl, angioedema,
pregnant, hypotension
(SBP<80mmHg), B/L RAS, inc.
K(>5mg/dl)
• Initiation:
Initiation: start low dose – if
tolerated then gradual increase in
few days to weeks to target dose
or max tolerable dose.
– Renal function monitoring
before starting, 1-2weeks
after and periodically
thereafter and after changing
dose
• ACE induced cough – 20%
61. • When ACEI intolerant or
alternative to ACEI
• AT 1 receptor blocker
• Can be substituted to ACEI with
angioedema history but with
caution (pt can develop
angioedema with ARB as well)
• Losartan:
Losartan: 25-50mg once till 50-
150mg once a day
• Valsartan:
Valsartan: 20-40mg twice till
160mg twice
• Same initiation and monitoring as
ACEI
• Titration by doubling the dose
Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
Angiotensin Receptor Blockers
Angiotensin Receptor Blockers
62. • To all pt with LV dysfunction
• Start early
early when Symptoms
improved
• Caution:
Caution: Can worsen heart failure
• START LOW AND GO SLOW
START LOW AND GO SLOW
• Start in low dose even during
hospitalization (careful in pt require
inotropic support) gradually increase
dose in weeks duration and try to
reach target dose
• Bisoprolol:
Bisoprolol: 1.25-2.5mg once till
10mg once
• Carvedilol:
Carvedilol: 3.125 twice till 50mg
twice
• Metoprolol Succinate:
Metoprolol Succinate: 12.5 once till
200mg once
• Continue even Sx not improved
• Abrupt withdrawal avoided
• S/E:
S/E: fluid retention and worsening
HF, slow heart rate, fatigue, blocks,
hypotension (minimize by different
dosing timings of BB and ACEI)
Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
Beta Blockers
Beta Blockers
63. • Indications:
Indications: NYHA II-IV, EF
≤35%, no C/I (GFR >30, Cr:
2.5mg/dl male and 2.0mg/dl
female, K<5mg/dl
• Dosing: Spironolactone
Dosing: Spironolactone 12.5-
25mg once till 50mg daily
• Monitoring:
Monitoring:
– stop all K supplements, check K+
and
Cr 2-3 days after starting then one
week and every month for 3 months
and every 3 month & when clinically
indicated .
– Cycle restarted after changing dose of
ARA or ACEI
• High K containing food: Prunes,
banana, salmon fish, dark green
leafy vegetables, mushrooms,
yogurt, white beans and dried
apricot
• S/E:
S/E: Increase K+
(10-15%),
gynecomastia
Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
Aldosterone Receptor Antagonists
Aldosterone Receptor Antagonists
64. • No mortality benefit
• Only decrease frequency of hospitalizations, Symptoms and
HRQOL
• Don’t stop digoxin if patient is not on ACEI or BB, but try to initiate
them
• No loading required – usual dose 0.125-0.25mg daily (low dose
0.125mg alternate day if >70yrs, CKD, Low lean body mass
• 0.5-0.9 ng/dl plasma conc. (narrow therapeutic range)
• S/E: Nausea, vomiting and diarrhea, visual disturbances (yellow-green
halos and problems with color perception), supraventricular and ventricular
arrhythmias
Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
Digoxin
Digoxin
65. • Indication:
Indication: African-American origin, NYHA III-IV, HFrEF
on ACEI and BB
• Bildil (37.5mg hydralazine and 20mg ISDN) start one tab
TID to increase till 2tab TID
• If given separately then both at least TID
Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
Hydralazine Nitrate Combination
Hydralazine Nitrate Combination
66. • Drugs not to be used:
Drugs not to be used:
– Statins (no benefit – unless there is ischemic etiology)
– CCB (except Amlodipine)
– NSAIDS
– Thiozolidinidinones
– Most anti arrhythmics drugs (except Amiodarone, dofelitide)
– Nutritional Supplements
– Hormonal therapy
Heart Failure
Heart Failure
Stage C
Stage C
Pharmacological Interventions
Pharmacological Interventions
67. Pharmacologic Treatment for Stage C
Pharmacologic Treatment for Stage C
Heart Failure Stage C
NYHA Class I – IV
Treatment:
For NYHA class II - IV patients .
Provided estimated creatinine
>30 mL/ min and K + <5.0 mEq/dL
For persistently symptomatic
African Americans ,
NYHA class III -IV
Class I, LOE A
ACEI or ARB AND
Beta Blocker
Class I, LOE C
Loop Diuretics
Class I, LOE A
Hydral -Nitrates
Class I, LOE A
Aldosterone
Antagonist
Add
Add Add
For all volume overload ,
NYHA class II - IV patients
68. • Implantable Cardioverter Defibrillator (ICD)
Implantable Cardioverter Defibrillator (ICD)
– Nonischemic or ischemic heart disease (at least 40 days post-MI)
with LVEF of ≤35% with NYHA class II or III symptoms or
NYHA 1 with EF ≤30% on chronic medical therapy, who have
reasonable expectation of meaningful survival for more than 1
year
• Cardiac Resynchronization Therapy (CRT)
Cardiac Resynchronization Therapy (CRT)
– Indicated for patients who have LVEF of 35% or less, sinus
rhythm, left bundle-branch block (LBBB) with a QRS duration of
150 ms or greater, and NYHA class II, III, or ambulatory IV
symptoms on GDMT
Heart Failure
Heart Failure
Stage C
Stage C
Device Therapy
Device Therapy
69. 1. Repeated (≥2) hospitalizations or ED visits for HF in the past year
2. Progressive deterioration in renal function (e.g., rise in BUN and creatinine)
3. Weight loss without other cause (e.g., cardiac cachexia)
4. Intolerance to ACE inhibitors due to hypotension and/or worsening renal function
5. Intolerance to beta blockers due to worsening HF or hypotension
6. Frequent systolic blood pressure <90 mm Hg
7. Persistent dyspnea with dressing or bathing requiring rest
8. Inability to walk 1 block on the level ground due to dyspnea or fatigue
9. Recent need to escalate diuretics to maintain volume status, often reaching daily
furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone
therapy
10. Progressive decline in serum sodium, usually to <133 mEq/L
11. Frequent ICD shocks
Heart Failure
Heart Failure
Stage D
Stage D
Clinical Events and Findings Useful for Identifying Patients With Advanced HF
Clinical Events and Findings Useful for Identifying Patients With Advanced HF
70. • All the measures of Stage A, B & C
• Until definitive therapy [e.g., coronary revascularization,
Mechanical circulatory support, heart transplantation or
resolution of the acute precipitating problem], patients
with cardiogenic shock should receive temporary
intravenous inotropic support to maintain systemic
perfusion and preserve end-organ performance.
Heart Failure
Heart Failure
Stage D
Stage D
71. Heart Failure
Heart Failure
Stage D
Stage D
Mechanical Circulatory Support
Mechanical Circulatory Support
• Intraaortic balloon pump
Intraaortic balloon pump (IABP) therapy
– Used for cardiogenic shock
– Allows heart to rest
• Ventricular assist devices
Ventricular assist devices (VADs)
– Takes over pumping for the ventricles
– Used as a bridge to transplant
• Destination therapy-permanent
Destination therapy-permanent, implantable VAD
• Cardiomyoplasty
Cardiomyoplasty-
- wrap latissimus dorsi around heart
• Ventricular reduction
Ventricular reduction -
-ventricular wall resected
• Transplant/Artificial Heart
Transplant/Artificial Heart
72. Stage A
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
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
Heart Failure
Heart Failure
Therapies
Therapies
73. Stage C
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
Heart Failure
Heart Failure
Therapies
Therapies
74. Stage D
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
Heart Failure
Heart Failure
Therapies
Therapies
76. SBP
SBP
Admission and early post-discharge SBP inversely correlates
with post-discharge mortality
Coronary artery disease
Coronary artery disease
(CAD)
(CAD)
Extent and severity of CAD appears to be a predictor of poor
prognosis
Troponin release
Troponin release
Results in a 3-fold increase in in-hospital mortality and
rehospitalization rate, a 2-fold increase in post-discharge
mortality
Ventricular dyssynchrony
Ventricular dyssynchrony
Increase in QRS duration occurs in approximately 40% of
patients with reduced systolic function and is a strong predictor of
early and late post-discharge mortality and rehospitalization
Renal impairment
Renal impairment
Worsening renal function during hospitalization or soon after
discharge is associated with an increase in in-hospital and post-
discharge mortality
Heart Failure
Heart Failure
Prognostic Factors
Prognostic Factors
77. Hyponatremia
Hyponatremia
Defined as serum sodium < 135 mmol/l, occurs in approximately
25% of patients, and is associated with a 2- to 3-fold increase in
post-discharge mortality
Clinical congestion at time
Clinical congestion at time
of discharge
of discharge
An important predictor of post-discharge mortality and morbidity
EF
EF
Similar early post-discharge event rates and mortality between
reduced and preserved EF
BNP/NT-proBNP
BNP/NT-proBNP
Elevated natriuretic peptides associated with increased resource
utilization and mortality
Functional capacity at
Functional capacity at
time of discharge
time of discharge
Pre-discharge functional capacity, defined by the 6-min walk test,
is emerging as an important predictor of post-discharge outcomes
Heart Failure
Prognostic Factors
78. Take Home Message
Take Home Message
• Heart failure is common problem in elderly and having prognosis
worse then Carcinoma Lung
• It is clinical diagnosis supplemented by lab test and echo
• Echo can suggest the etiology of heart failure
• Diuretics are for acute relief and also for chronic management of
fluid overload
• Look for the precipitating event for acute decompensation
• ACE inhibitors/ARB, Beta blockers, Spironolactone improve
prognosis in patient with reduced ejection fraction
79. • Maintain patient on 2- to 3-g sodium diet. Follow daily weight and
determine target/ideal weight, which is not the dry weight - In order
to prevent worsening azotemia and adjust the dose of diuretic
accordingly
• Use Digoxin in most symptomatic heart failure
• Encourage exercise training
• Consider a cardiology consultation in patients who fail to improve
• Heart transplantation is for end stage heart failure
Take Home Message
Take Home Message