This document discusses acute decompensated heart failure (ADHF), including:
1. ADHF is characterized by rapidly developing symptoms of new or worsening chronic heart failure requiring hospitalization. It carries a high risk of rehospitalization and mortality.
2. Causes of ADHF include non-adherence to medications, acute myocardial ischemia, arrhythmias, infections, and other cardiovascular disorders.
3. Management involves aggressive diuresis, treatment of underlying causes, optimization of disease-modifying medications, and consideration of inotropes or mechanical circulatory support for severe cases.
4. Biomarkers like BNP are useful for diagnosis, assessing severity, and guiding therapy, while
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
Renal artery stenosis is the leading cause of secondary hypertension and may lead to :
Resistant (refractory) hypertension,
Progressive decline in renal function, and
Cardiac destabilization syndromes (Flash pulmonary edema, recurrent heart failure, or acute coronary syndromes)
Hyperthyroidism, Reference: Hyperthyroid, Harrison's Principles of Internal Medicine, Soheil Elahi, Islamic Azad University of Medicine- International Branch (IAUM-int)
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
Renal artery stenosis is the leading cause of secondary hypertension and may lead to :
Resistant (refractory) hypertension,
Progressive decline in renal function, and
Cardiac destabilization syndromes (Flash pulmonary edema, recurrent heart failure, or acute coronary syndromes)
Hyperthyroidism, Reference: Hyperthyroid, Harrison's Principles of Internal Medicine, Soheil Elahi, Islamic Azad University of Medicine- International Branch (IAUM-int)
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
Drugs Used in Heart Failure
Drugs without positive inotropic effects used in Heart Failure:
Diuretics
ACE/ARB & Related agents
Vasodilators
β-Adrenergic Blockers
Others
Drugs with positive inotropic effects used in Heart Failure:
Digitalis
Other positive inotropic drugs:
Bipyridines
Beta-Adrenergic agonists
Investigational positive inotropic drugs: Istaroxime, Levosimanden, Omecamtiv mecarbil
There are two distinct goals of drug therapy in CHF.
Relief of congestion/ low cardiac output symptoms and restoration of cardiac performance.
Ionotropic agents, Vasodilators, Diuretics, BETA Blockers.
Arrest/reversal of disease progression and prolongation of survival.
ACE inhibitors, ARBs, Beta Blockers, Aldosterone Antagonists.
Trauma Outpatient Center is a comprehensive facility dedicated to addressing mental health challenges and providing medication-assisted treatment. We offer a diverse range of services aimed at assisting individuals in overcoming addiction, mental health disorders, and related obstacles. Our team consists of seasoned professionals who are both experienced and compassionate, committed to delivering the highest standard of care to our clients. By utilizing evidence-based treatment methods, we strive to help our clients achieve their goals and lead healthier, more fulfilling lives.
Our mission is to provide a safe and supportive environment where our clients can receive the highest quality of care. We are dedicated to assisting our clients in reaching their objectives and improving their overall well-being. We prioritize our clients' needs and individualize treatment plans to ensure they receive tailored care. Our approach is rooted in evidence-based practices proven effective in treating addiction and mental health disorders.
Gemma Wean- Nutritional solution for Artemiasmuskaan0008
GEMMA Wean is a high end larval co-feeding and weaning diet aimed at Artemia optimisation and is fortified with a high level of proteins and phospholipids. GEMMA Wean provides the early weaned juveniles with dedicated fish nutrition and is an ideal follow on from GEMMA Micro or Artemia.
GEMMA Wean has an optimised nutritional balance and physical quality so that it flows more freely and spreads readily on the water surface. The balance of phospholipid classes to- gether with the production technology based on a low temperature extrusion process improve the physical aspect of the pellets while still retaining the high phospholipid content.
GEMMA Wean is available in 0.1mm, 0.2mm and 0.3mm. There is also a 0.5mm micro-pellet, GEMMA Wean Diamond, which covers the early nursery stage from post-weaning to pre-growing.
INFECTION OF THE BRAIN -ENCEPHALITIS ( PPT)blessyjannu21
Neurological system includes brain and spinal cord. It plays an important role in functioning of our body. Encephalitis is the inflammation of the brain. Causes include viral infections, infections from insect bites or an autoimmune reaction that affects the brain. It can be life-threatening or cause long-term complications. Treatment varies, but most people require hospitalization so they can receive intensive treatment, including life support.
Rate Controlled Drug Delivery Systems, Activation Modulated Drug Delivery Systems, Mechanically activated, pH activated, Enzyme activated, Osmotic activated Drug Delivery Systems, Feedback regulated Drug Delivery Systems systems are discussed here.
Letter to MREC - application to conduct studyAzreen Aj
Application to conduct study on research title 'Awareness and knowledge of oral cancer and precancer among dental outpatient in Klinik Pergigian Merlimau, Melaka'
PET CT beginners Guide covers some of the underrepresented topics in PET CTMiadAlsulami
This lecture briefly covers some of the underrepresented topics in Molecular imaging with cases , such as:
- Primary pleural tumors and pleural metastases.
- Distinguishing between MPM and Talc Pleurodesis.
- Urological tumors.
- The role of FDG PET in NET.
DECODING THE RISKS - ALCOHOL, TOBACCO & DRUGS.pdfDr Rachana Gujar
Introduction: Substance use education is crucial due to its prevalence and societal impact.
Alcohol Use: Immediate and long-term risks include impaired judgment, health issues, and social consequences.
Tobacco Use: Immediate effects include increased heart rate, while long-term risks encompass cancer and heart disease.
Drug Use: Risks vary depending on the drug type, including health and psychological implications.
Prevention Strategies: Education, healthy coping mechanisms, community support, and policies are vital in preventing substance use.
Harm Reduction Strategies: Safe use practices, medication-assisted treatment, and naloxone availability aim to reduce harm.
Seeking Help for Addiction: Recognizing signs, available treatments, support systems, and resources are essential for recovery.
Personal Stories: Real stories of recovery emphasize hope and resilience.
Interactive Q&A: Engage the audience and encourage discussion.
Conclusion: Recap key points and emphasize the importance of awareness, prevention, and seeking help.
Resources: Provide contact information and links for further support.
Feeding plate for a newborn with Cleft Palate.pptxSatvikaPrasad
A feeding plate is a prosthetic device used for newborns with a cleft palate to assist in feeding and improve nutrition intake. From a prosthodontic perspective, this plate acts as a barrier between the oral and nasal cavities, facilitating effective sucking and swallowing by providing a more normal anatomical structure. It helps to prevent milk from entering the nasal passage, thereby reducing the risk of aspiration and enhancing the infant's ability to feed efficiently. The feeding plate also aids in the development of the oral muscles and can contribute to better growth and weight gain. Its custom fabrication and proper fitting by a prosthodontist are crucial for ensuring comfort and functionality, as well as for minimizing potential complications. Early intervention with a feeding plate can significantly improve the quality of life for both the infant and the parents.
Michigan HealthTech Market Map 2024. Includes 7 categories: Policy Makers, Academic Innovation Centers, Digital Health Providers, Healthcare Providers, Payers / Insurance, Device Companies, Life Science Companies, Innovation Accelerators. Developed by the Michigan-Israel Business Accelerator
The dimensions of healthcare quality refer to various attributes or aspects that define the standard of healthcare services. These dimensions are used to evaluate, measure, and improve the quality of care provided to patients. A comprehensive understanding of these dimensions ensures that healthcare systems can address various aspects of patient care effectively and holistically. Dimensions of Healthcare Quality and Performance of care include the following; Appropriateness, Availability, Competence, Continuity, Effectiveness, Efficiency, Efficacy, Prevention, Respect and Care, Safety as well as Timeliness.
Stem Cell Solutions: Dr. David Greene's Path to Non-Surgical Cardiac CareDr. David Greene Arizona
Explore the groundbreaking work of Dr. David Greene, a pioneer in regenerative medicine, who is revolutionizing the field of cardiology through stem cell therapy in Arizona. This ppt delves into how Dr. Greene's innovative approach is providing non-surgical, effective treatments for heart disease, using the body's own cells to repair heart damage and improve patient outcomes. Learn about the science behind stem cell therapy, its benefits over traditional cardiac surgeries, and the promising future it holds for modern medicine. Join us as we uncover how Dr. Greene's commitment to stem cell research and therapy is setting new standards in healthcare and offering new hope to cardiac patients.
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardso...rightmanforbloodline
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardson, Verified Chapters 1 - 18, Complete Newest Version
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardson, Verified Chapters 1 - 18, Complete Newest Version
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardson, Verified Chapters 1 - 18, Complete Newest Version
LGBTQ+ Adults: Unique Opportunities and Inclusive Approaches to CareVITASAuthor
This webinar helps clinicians understand the unique healthcare needs of the LGBTQ+ community, primarily in relation to end-of-life care. Topics include social and cultural background and challenges, healthcare disparities, advanced care planning, and strategies for reaching the community and improving quality of care.
2. Acute Decompensated Heart
Failure
• Syndrome complex characterized by rapidly
developing symptoms of new onset de novo heart
failure or worsening of chronic heart failure
culminating in acute decompensation and
requiring monitored therapy including
hospitalization
• Sentinel prognostic event with 50% risk of
rehospitalization at 6 months and 30% mortality at
1 year
4. Acute Heart Failure
• >80% have decompensation of existing HF
• Often several days of gradual weight gain and
worsening dyspnoea precede ADHF
• Fluid overloading is the acute presentation
• Close to 50% have HF and preserved EF
• Cardiogenic shock is a rare presentation
• ACS and renal dysfunction to be assessed
early
5. Acute Decompensated Heart Failure
Optimize Outcome: Opportunities
• Recognition of AHF and instituting prompt life saving
intervention: time saved is life saved
• Aggressive intervention to support circulation when a
treatable/ reversible cause is identified: especially in
De novo AHF
• Optimize disease modifying medications/ interventions
once stabilized
• Prognostic markers/ risk score for intense out of
hospital monitoring
• At hospital discharge: Guideline directed medical
therapy as re-hospitalization for AHF is 50% at 6
months
8. Acute heart Failure
( TVM HF Registry 624 pts)
• Mean Age 60 years
• Acute de novo HF 40%
• Males 69%
• IHD 69.5%
• DCM 14.5%
• RHD 8%
• Diastolic HF 3%
• HT55%, DM 52%, Smoking 44%, AF 14%, CKD
15%
• In hospital mortality 9%
9. ADHF pts characteristics
(OPTIMISE registry)
• Preserved LV function
• EF 55%
• Age 75yrs
• Males 38%
• IHD 38%
• BNP 601pg/ml
• Reduced LV function
• EF 24%
• Age 70 yrs
• Male 62%
• IHD 55%
• BNP 1170 pg/ml
10. General Concepts in management of
ADHF
• 1. Severity of ADHF presentation does not
always predict long term outcome
• 2. LVEF at presentation and improvement/
worsening influence outcome
• 3. Hemodynamic improvement should come
from amelioration of myocardial dysfunction
rather than by increasing contractility with
inotropes
11. General Concepts in management of
ADHF
• 4. Ischemic Viable myocardium requires
revascularization
• 5. Attempt to limit myocardial and renal
damage: intervention to improve clinical signs
and symptoms like diuretics, vasodilators,
inotropes may worsen myocardial and renal
damage
12. Clinical Scenario at presentation
• High SBP > 160 mmHg 25%
• Normal to High normal BP 50%
• Hypotension (SBP<90) 10%
• Cardiogenic shock 1%
• Flash pulmonary edema 3%
15. ADHF: Noninvasive Investigations
• Chest X ray, ECG
• 2D Echo Doppler: EF, LV dimension, wall
thickness, wall motion, valve function, PAH,
RV function
• Myo. Viability/ reversible ischemia study if
CAD suspected and suitable for
revascularization
• CMRI for myocardial infiltration/ fibrosis/ scar
16. ADHF: Invasive Investigations
• PA catheterization: hypoperfusion with uncertain
volume status/respiratory disease
• CAD suspected and eligible for revascularization
• Endo myocardial Biopsy when specific diagnosis
suspected & can alter therapy
Transplant rejection, giant cell myocarditis,
infiltrative process, active myocarditis with
progressive ventricular dysfunction
17. Acute De-compensated HF: Management
Hypoxemia and respiratory failure due to pulmonary
Edema
• Usual treatment for acute pulmonary edema
• O2 by mask : O2 sat>= 90%/
– Noninvasive ventilation CPAP, NIPPV (avoid if
hypotension/altered sensorium)
– Intubated ventilation
• Vasodilators if SBP >110mmHg
– NTG
– Nitroprusside
– Nesiritide
18. Acute De-compensated HF
Diuretic Therapy
• Bolus parenteral Loop diuretics: equal to pt’s
oral maintenance dose: Infusion / intermittent
bolus/ high dose diuretics
• Add another diuretic like thiazide group/
metolazone
• Add small dose dobutamine at 2-5 mic/kg/m
• Resistant fluid overload: Ultra filtration
• Aquaretics if euvolumic hyponatremia
19. Ultra filtration in ADHF
CARESS trial(188 pts)
• In patients with volume overload ADHF as it
reduces volume and electrolytes equally
• UNLOAD(200 pts): superior to diuretics
• CARESS study:High risk ADHF pts.: Similar
outcome for weight reduction, but higher rise
in ser creatinine, need for dialysis, and other
adverse events.
• AVOID HF: Ongoing trial
20. Inotropes in Heart failure
Inotropes/ Vasopressors/ both
• Inotrope: Dobutamine: minimal vasodilatory
effect (beta 2 stimulation)
• Inotrope with vaso dilatation: Milrinone,
Levosimendan
• Vasopressor with Inotropic action: Dopamine,
Nor epinephrine
21. Pts with hypotension/ Hypo-
perfusion
SBP <85 mmHg/ reduced urine output/ lactate
• Exclude hypovolumia
• Modify dose of ACEI/ beta blockers
• Dobutamine infusion
• Short term circulatory support
• I/V levosimendan if exposed to beta blockers
• Vasopressor like dopamine/ norepinephrine if in
cardiogenic shock despite an inotrope, to maintain
SBP and end organ perfusion
22. ADHF: Inotropic Support
Indications
• Until definitive therapy( MCS/transplant) or
resolution of precipitating cause in Pts with
cardiogenic shock , to maintain systemic
perfusion and preserve end organ function
• Short term inotropic support in pts with
severe systolic LV dysfunction, low BP, low
CO : to preserve end organ function
• Long term palliation with inotropic support
23. Mechanical Circulatory Support
• MCS for resistant HF: definitive management
( transplant) or recovery anticipated.
• Percutaneous/ extra corporeal assist devices:
bridge to recovery/ bridge to decision when in
acute profound hypotension
24. Pts with AF and fast VR
• Anticoagulation with heparin
• Rhythm control:
– Emergent DC cardioversion if hemodynamically
unstable
-- Elective DC cardioversion if recent AF(<48hrs) or
TEE echo excludes LA thrombus
• Rate control: Digoxin, ? amiodarone
25.
26. Potential New Therapies
• Cinaciguat: Soluble Guanilate cyclase activators
• Chimeric natriuretic peptides: Avoids arterodilating
hypotensive effects of BNP, with venodilating and
natriuretic action intact
• Istaroxime: membrane Na+ K+ ATPase inhibitor with
SERCA2a activation.
• Stresscopin: Human peptide Urocortin2: Activates
myocardial reperfusion injury protection pathways:
increase EF and CO, decrease SVR,
27. Vaso active drugs in ADHF
Relaxin
• Endogenous peptide associated with
pregnancy and acts through relaxin receptor:
reduce inflammation, decrease fibrosis,
increase vasodilation, promote renal blood
flow, increase vascular endothelial growth
factor, and angiogenesis.
28. Vaso active drugs in ADHF
Relaxin: Serelaxin
• RELAX HF:1161 pt. of ADHF with preserved SBP >115
mmHg.
• Serelaxin 30 ug/kg/day x48 hrs vs Placebo
• Significant improvement in dyspnoea scale
• No impact on short term mortality/ HF readmission
at 60 days, though 180 day mortality was
significantly lower.
• Hypotensive episodes higher but renal dysfunction
less than placebe group
29. Investigational drugs in ADHF
Omecamptive Mecabril
• First selective cardiac Myosin activator: acts
through greater binding of myosin to actin:
– Increases myo. contractility without increase in O2
consumption: increased EF, stroke volume,
decreased LVES and LVED volume
– Chest pain, tachycardia and myo. Ischemia more
common
ATOMIC- AHF study is Phase 3 trial: ongoing
30. Vaso active drugs in ADHF
Ularitide
• Synthetic form of Urodilantin: human natriuretic
peptide produced in kidney: induces natriuresis and
diuresis. Also potent vasodilator( increases
intracellular cyclic GMP) and increased renal blood
flow) : Two double blind studies have shown
favorable outcome in ADHF by symptom
improvement and hemodynamics
• Phase 3 trial(TRUE-AHF >2110 pts) ongoing
31. Investigational drugs in ADHF
Adenosine A1 receptor antagonist:
Rolophylline
• Preserve GFR, improve diuresis, increase
sodium excretion by kidney
• Phase 2 trial: better relief of dyspnoea and
lesser renal dysfunction
• Phase 3 trial: PROTEC:2033 pts.: negative trial
with none of the primary end points
significant and safety was questioned due to
neurological side effects: seizure and stroke
32. Newer Molecules in treatment of
AHF
• Overall impact in treatment is small
• Mechanical Circulatory support will continue
to be used more frequently to bridge to
recovery/ transplant/ destination therapy
• Newer strategies will be required, for any
major impact in management of AHF
34. Biomarkers in AHF
• To diagnose HF in ER
• To predict outcome of HF therapy
• To plan follow up strategy at discharge and
prognostication
35. Acute Heart Failure
Biomarkers: BNP
• BNP/ NT pro BNP : to support clinical judgement for
diagnosis of ADHF
• BNP/ NT pro BNP and/or cardiac troponins in
establishig diagnosis severity and prognosis of ADHF
• BNP/ NT pro BNP to guide therapy in ADHF
• Other biomarkers of myocardial injury/ fibrosis: ST2
36. Biomarkers in HF
BNP/ NT pro BNP
• PROTECT (150 pts): Compensated CHF
• HOME HF outpatient monitoring
evaluation(350 pt.)ADHF pts: BNP based home
management vs BNP blinded (use wt/
symptoms/signs) vs Controls (usual care)
• GUID-IT: ADHF pts monitored with NT pro
BNP guided therapy
37. Novel Cardiac Biomarkers in ADHF
• Soluble ST2 receptor: interleukin family: upregulated
by myocardial strech: predicts 1 year mortality
• NGAL: neutrophil gelatinase ass. Lipocalin: marker of
kidney injury: higher levels predict 30 day mortality
• Copeptin: C terminal protein of pre pro vasopressin:
highest quartile predicted very high 90 day mortality
38. Novel Cardiac Biomarkers in ADHF:
contd.
• Midregion pro adrenomedullin
• Galactin 3: indicator of myocardial collagen
deposition and fibrosis: marker of early HF
Will a multi marker approach help in
prognostication of ADHF
42. Heart Failure Risk Scores
• SHOCKED predictor: (900pts):
Age>75, NYHA>II, AF, COPD, CKD, LVEF<20%, DM
• PACE: (900 pts) PVD, Age >70, Creatinine >2,
EF < 20%,
• ADHERE registry( for acute mortality): SBP, Ser
creatinine and BUN
• Frankenstein: BNP , 6 WT′
43. In multivariable models, nearly all tested covariates performed similarly across LVEF
strata for the outcome of death from any cause, as well as for HF-related and all-
cause hospitalizations.
Conclusions—We found that in a large, diverse contemporary HF population, risk
assessment was strikingly similar across all LVEF categories. These data suggest that,
although many HF therapies are uniquely applied to patients with reduced
LVEF, individual prognostic factor performance does not seem to be significantly
related to level of left ventricular systolic function. (Circ Heart Fail. 2013;6:635-646.)
44. Post Discharge Multi disciplinary
Management Program
• Cardiac Rehabilitation: periodic follow up,
education, optimize drug treatment, general
medical care, exercise program, ensure access to
hospital care
• Palliative Care: frequent hospitalization, not
listed fro transplant or mechanical circulatory
support, poor quality of life, dependence for daily
needs, close to end of life
• Heart failure team: practitioner, nurse,
pharmacist, dietician, psychologist,
physiotherapist
45. Conclusion
• Acute Heart Failure, is a medical emergency
and rapid, coordinated multi disciplinary
approach can significantly reduce mortality.
• Stabilized patients of AHF, to have GDMT/
devices/ revascularization as indicated
• At discharge: patient education, counseling,
compliance with GDMT and frequent clinic
visits can prevent re-hospitalization for AHF
48. General Concepts in management of
ADHF
• 1. AHF with preserved EF is being recognized
more often and carry similar long term prognosis
• 2. Severity of ADHF presentation does not always
predict long term outcome
• 3. LVEF at presentation and improvement/
worsening influence outcome
• 4. Hemodynamic improvement should come
from amelioration of myocardial dysfunction
rather than by increasing contractility with
inotropes
49. General Concepts in management of
ADHF
• 5. Ischemic Viable myocardium requires
revascularization
• 6. Attempt to limit myocardial and renal
damage: intervention to improve clinical signs
and symptoms like diuretics, vasodilators,
inotropes may worsen myocardial and renal
damage
50. Risk Score to Predict Acute
Decompensated HF: PRIDE Score
• Elevated NT Pro BNP>450 pg/ml(<50yrs) 4
• Interstitial pulm edema
2
• Orthopnea 2
• Lack of fever(r/o infection) 2
• Current diuretic use/Age>75/ rales on lung exam/
lack of cough 1
• Early identification and institution of treatment/
correction of causative factors improve outcome
51. European Heart failure Study
• Worsening of chronic HF: 65%
• Acute pulmonary edema: 16%
• Hypertensive HF: 11%
• Cardiogenic shock: 4%
• Acute right heart failure: 4%
ACS presenting as HF :10% of all ACS
52. ADHF: Prognostic markers
• Mathematical model using NT pro BNP value as a
continuous variable with age and pretest probability
of HF had 96% sensitivity and 84% specificity for
predicting a ADHF
• Mid regional pro ANP >120pmol/l: also affected by
age, ender, BMI, AF,renal function
53. Positive Inotropes in HF
Indications
• Advaced HF,
• Reduced EF, LV dilatation,
• Euvolumic hypotensive ( adequate filling
pressure)
• Intolerant to vaso dilators
• Signs of diminished peripheral perfusion or
renal other end organ dysfunction
54. Old drugs: New dosage strategy
Dopamine and furosemide
• Low dose dopamine 5 mic/kg/min and low
dose furosemide appears safer for renal
fuction deterioration (DAD HF study)
• Phase 3 trials ongoing : DAD HF 2, ROSE AHF
55. Diuretic Strategy in ADHF
Low vs high dose furosemide:
DOSE trial(308pts)
• Low( usual Furosemide dose)vs High(2.5 times) X
continuous vs intermittent parenteral dosing
• No significant difference in safety/ efficacy
• Acutely, high dose group had higher creatinine
elevation, but at 7 days, this was not significant
• Secondary end points: greater dyspnoea relief, fluid
loss and weight loss with higher dose
Editor's Notes
Characteristics, treatments, and outcomes of patients with preserved systolic function hospitalized for heart failure: A report from the OPTIMIZE-HF Registry. J Am Coll Cardiol 50:768, 2007.
Data from the ADHERE registry have been used to develop a classification and regression tree (CART) analysis to identify the best predictors of in-hospital mortality and to develop a risk stratification model. Of the 39 variables evaluated, the CART method identified elevated blood urea nitrogen (BUN), lower systolic blood pressure (SBP), and higher serum creatinine at the time of admission to be the best discriminators between hospital survivors and nonsurvivors. A similar model from the OPTIMIZE registry identified serum creatinine, SBP, age, heart rate, and serum sodium as the most powerful predictors of in-hospital mortality in AHFS.[52] A combination of two variables (creatinine concentration and SBP) that were powerful predictors in both ADHERE and OPTIMIZE-HF was able to risk stratify patients into risk groups (Fig. 27-5).
FIGURE 27-5 In-hospital mortality by serum creatinine (SCr) concentration and systolic blood pressure (SBP) in the ADHERE registry.(From Abraham WT, Fonarow GC, Albert NM, et al: Predictors of in-hospital mortality in patients hospitalized for heart failure: Insights from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients With Heart Failure [OPTIMIZE-HF]. J Am Coll Cardiol 52:347, 2008.)
Mortality and rehospitalization rates postdischarge in patients admitted with HF may be as high as 15% and 30% within 60 to 90 days, respectively. Recent claims data using the U.S. Medicare sample suggest an even more striking rate of rehospitalization in elderly patients, with a 30-day rehospitalization rate of 27%.[49] Approximately 30% of patients hospitalized with HF and reduced ejection fraction die suddenly within several months after discharge, and 40% die of progressive HF in spite of receiving evidence-based therapy (Fig. 27-4).[50] Of note, approximately half of the rehospitalizations are not HF related.[50] Rates of early postdischarge events in patients with HFpEF appear to be similar to those in patients with reduced ejection fraction. However, the modes of death and reasons for rehospitalization have not been studied in the former group. It is possible that a significant number of morbid events in the HFpEF population are related to coexisting cardiac or noncardiac comorbidities, such as CAD, hypertension, atrial fibrillation, renal insufficiency, or stroke.[17]
FIGURE 27-4 Postrandomization causes of death of 4,133 patients admitted with worsening HF and reduced ejection fraction in the EVEREST trial. The overall mortality at 9.9 months was 26%.(From O’Connor CM, Miller AB, Blair JE, et al: Causes of death and rehospitalization in patients hospitalized with worsening heart failure and reduced left ventricular ejection fraction: Results from Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan [EVEREST] program. Am Heart J 159:841, 2010.)