HEART
FAILURE
M Nor MD
INTRO
•A clinical syndrome
• Caused by structural or functional dysfunction
• Affecting systole or diastole or both
• Leading to impaired ability of one or both ventricles to pump
• Associated with objective evidence of pulmonary or systemic
congestion
• Corroborated by elevated natriuretic peptide
Universal Definition and Classification of Heart Failure - Journal of Cardiac Failure
CAUSES
•Ischemia & infraction
•Hypertension
•Valvular disorders
•Myocardial damage
• Cardiomyopathy
• Myocarditis
•Arrhythmias
•Some chemotherapy
drugs
•Systemic Disorders that
increase demand for CO
• Anemia
• Hyperthyroidism
•Amyloidosis
•Chronic fibrosis
(eg, systemic sclerosis)
•Hemochromatosis
•Reduced substrate
availability (free fatty acids
or glucose)
CALSSIFICATION
CALSSIFICATION
https://www.jacc.org/doi/10.1016/j.jacc.2021.04.070
- HFrEF (Reduced EF) :
• EF ≤40%.
• Impaired systolic function
- HFmrEF (Mid-Range EF):
• EF 41–49%.
• Intermediate category
• With mixed systolic/diastolic dysfunction
- HFpEF (Preserved EF):
• EF ≥50%.
• Impaired diastolic function
• Stiff ventricles affecting filling
- HFimpEF (Improved EF):
• EF previously ≤40%
• but increased to >40% after treatment
1. By E j e cti on Fr acti on (E F):
2. By Ti me Course:
- Acute HF:
• Sudden onset HF
- Chronic HF:
• Long-standing
• Stable symptoms
• Usually managed with therapies
- Acute Decompensated HF:
• Worsening of chronic HF
• Requiring urgent care
- Cardiogenic Shock:
• Severe acute HF
• With life-threatening hypotension
• EF <25%, systolic BP <90 mmHg
Types of Heart Failure | American Heart Association
CLASSIFICATION
3. By Anat omical Invol vement :
- Left-Sided HF:
• Causes pulmonary congestion
• Dyspnea
• Pulmonary edema
- Right-Sided HF:
• Leads to systemic venous congestion
• Peripheral edema
• Jugular distension
- Biventricular HF:
• Both sides affected, common in advanced disease.
Types of Heart Failure | American Heart Association
CLASSIFICATION
NYHA Functional Classification:
Class Symptoms Severity Relation to daily activity
I No fatigue, dyspnea, or palpitations. None
Can complete any activity requiring ≤ 7 MET:
• Carry 11 kg up 8 steps
• Carry objects weighing 36 kg
II
With normal Physical activity
Fatigue, dyspnea, palpitations, or angina Mild
Can complete any activity requiring ≤ 5 MET:
• Sexual intercourse without stopping
• Gardening
• Walk 7 km/hour on level ground
• Climb one flight of stairs at a normal pace
without symptoms
III
Comfortable at rest
Less than ordinary physical activity
Causes fatigue, dyspnea, palpitations, or angina
Moderate
Can complete any activity requiring ≤ 2 MET:
• Shower or dress without stopping
• Strip and make a bed
• Clean windows
• Walk 4 km/hour
IV
Symptoms occur at rest
Any physical activity increases discomfort. Severe
Cannot do or cannot complete any activity
requiring ≥ 2 MET; cannot do any of the above
activities
Table: New York Heart Association (NYHA) Classification of Heart Failure-MSD Manual Professional Edition
4. By St aging S ystem
CLASSIFICATION
Classes and Stages of Heart Failure | American Heart Association
ACC/AHA Stages:
Stage Severity Description
A At risk • Hypertension, diabetes without structural heart disease
B Pre HF
• Structural disease reduced EF, hypertrophy) without
symptoms
C HF • Reduced EF, hypertrophy) Symptomatic
D Advanced HF • Refractory HF requiring advanced therapies.
CLASSIFICATION
4. By St aging S ystem
CV Physiology | Combined Ventricular Systolic and Diastolic Dysfunction
- Systolic Dysfunction:
• Impaired contraction (HFrEF).
- Diastolic Dysfunction:
• Impaired relaxation/stiffness (HFpEF).
- Mixed Dysfunction:
• Features of both (common in HFmrEF)
Systolic Heart Failure | Johns Hopkins Medicine
Diastolic Heart Failure: HFPEF, Left-Sided Heart Failure, Symptoms
5. By P athophysi ol ogy
CLASSIFICATION
• Ischemic HF
• Hypertension
• Valvular disease
• Cardiomyopathy (dilated, hypertrophic, restrictive)
• Arrhythmias, congenital defects, or toxins (e.g., chemotherapy)
• High-Output HF:
• Elevated metabolic demands (e.g., anemia, hyperthyroidism, AV shunts)
• Special Considerations
- Pediatric HF: Often due to congenital or genetic causes
- Comorbidities: Diabetes, CKD, and COPD…
6. By Et iol ogy
CLASSIFICATION
PATHOPHYSIOLOGY
• Ability of the heart to increase its performance
above resting levels in response to stress
• Increasing heart rate
• Increasing systolic and diastolic volumes
• Increasing stroke volume
• Increasing extraction of oxygen
• It is about:
• 200% to 250% in old age
• 300% to 400% in a normal young healthy
• 500% to 600% in athletes
1621324608PHYSIOLOGY_SEM-2_k-sembulingam-essentials-of-medical-physiology.pdf
Car di ac r eser ve:
PATHOPHYSIOLOGY
•Determined by:
•Preload
•Afterload
•Heart rate and rhythm
•Oxygen supply
•Amount of viable myocardium
•Substrate availability (fatty acids, glucose)
CV Physiology | Combined Ventricular Systolic and Diastolic Dysfunction
Ventricular performance :
PATHOPHYSIOLOGY
•Frank-Starling principle
•Systolic contractile performance
•Represented by stroke volume
•Is proportional to preload
•Within the normal physiologic
range
Effect of changes in myocardial contractility on the Frank-Starling... | Download Scientific Diagram
Mo r phol og i cal Chang e:
PATHOPHYSIOLOGY
Vent Pressure mm Hg
Vent Volume
EDV
ESV
EDP
Systolic
pressure
Diastolic pressure
Stroke Volume
Iso
volumetric
Relaxation
Diastolic filling
Iso
volumetric
Contraction
Systolic ejection
Aortic valve closes
Mitral valve closes
Aortic valve open
Mitral valve open
P r e s s u r e - Vo l u m e R e l a t i o n s h i p :
PATHOPHYSIOLOGY
• Systolic heart failure:
• Decreased contractility
• Predominant in :
• Myocardial infarction
• Myocarditis
• Dilated cardiomyopathy
• Reduced ejection fraction (HFrEF)
• Increased diastolic volume
and pressure
• Decreased ejection fraction
(≤ 40%)
• Affect primarily the LV
1 . C o r e M e c h a n i s m s :
PATHOPHYSIOLOGY
• Diastolic heart failure:
• Increased Afterload
• Results from :
• Hypertension
• Valvular disease
• Constrictive pericarditis
• Global contractility is preserved
• Increased ventricular stiffness
• Impaired ventricular relaxation
• LV filling is impaired
• Cause inappropriately low
LV end-diastolic volume
• Ejection fraction remain normal (≥ 50%)
1 . C o r e M e c h a n i s m s :
PATHOPHYSIOLOGY
• Left Side Heart Failure:
• Pulmonary venous pressure increases
• Fluid extravasates (from the capillaries into the interstitial space and alveoli )
• Reduced pulmonary compliance
• Increasing the work of breathing
• Deoxygenated pulmonary arterial blood passes through poorly
ventilated alveoli
• Decreasing oxygenation ( PaO2)
• Dyspnea
• Respiratory alkalosis early ( CO2)
• But elevating PaCO2 is a sign of impending respiratory failure
1 . C o r e M e c h a n i s m s :
PATHOPHYSIOLOGY
•Right sided heart failure:
• systemic venous pressure increases
• Fluid extravasation and edema (feet and ankles of ambulatory patients and abdominal
viscera )
• Liver is affected
• Hepatic congestion and dysfunction
• Fluid accumulation in the peritoneal cavity (ascites)
• Breaks down less aldosterone, further contributing to fluid accumulation.
• Chronic venous congestion in the viscera:
• Anorexia
• Malabsorption of nutrients and drugs
• Protein-losing enteropathy
• Rarely ischemic bowel infarction
1 . C o r e M e c h a n i s m s :
PATHOPHYSIOLOGY
• Compensatory mechanisms:
• Initially maintain perfusion
• Finally worsen HF
• Sympathetic Overdrive:
• Short-term compensation
• Chronic activation causes:
• Myocardial toxicity
• Arrhythmias
• β-receptor downregulation.
• Renin-Angiotensin-Aldosterone System
(RAAS):
• Reduced renal perfusion
• Triggers renin release → angiotensin II (vasoconstriction, aldosterone release)
• Sodium/water retention (↑ preload), vasoconstriction (↑ afterload), and myocardial fibrosis
• Natriuretic Peptides (BNP, ANP):
• Released in response to ventricular stretch
• Promote vasodilation and diuresis
• Overwhelmed in advanced HF
• Leading to persistent fluid retention
2 . N e u r o h o r m o n a l A c t i v a t i o n :
PATHOPHYSIOLOGY
• Thickened ventricular walls :
• Myocyte Hypertrophy
• In pressure overload, e.g., hypertension).
• Dilation:
• Thin, enlarged chambers
• Volume overload
• May be valvular regurgitation
• Both …. Turn Pathologic :
• Stretching of cardiac muscle increases contractility (up to a certain point)
• Fails in advanced HF due to excessive stretch
• ↓ CO, ↑ congestion
• Fibrosis:
• Scar tissue replaces functional myocardium
• Reducing compliance and contractility
• Molecular Changes:
• Altered calcium handling
• Mitochondrial dysfunction
• And apoptosis
3. Ventr i cul ar Rem od el i ng :
PATHOPHYSIOLOGY
• Forward Failure:
• Reduced CO → hypoperfusion of organs (fatigue, renal dysfunction,
confusion)
• Backward Failure:
• Elevated ventricular filling pressures → pulmonary congestion
(dyspnea, orthopnea) or systemic venous congestion (jugular
distension, hepatomegaly, edema).
• Cardiorenal Syndrome:
• Worsening kidney function due to reduced renal perfusion and venous
congestion
• Cardiac cirrhosis
4-S ystemi c Conse qu ences :
PATHOPHYSIOLOGY
Cardiorenal Syndrome: Symptoms & Treatment
Cardiac Cirrhosis - StatPearls - NCBI Bookshelf
• Ischemic HF:
• Coronary artery disease → myocardial necrosis → scar tissue →
impaired contractility
• Hypertensive HF:
• Chronic pressure overload → left ventricular hypertrophy → diastolic
dysfunction.
• Valvular HF:
• Stenosis/regurgitation → volume/pressure overload → remodeling
• Non-ischemic Cardiomyopathy
• Viral myocarditis, alcohol toxicity
• Direct myocardial damage
5-E ti o l ogy- Sp eci fi c P ath w ays :
PATHOPHYSIOLOGY
•Cytokines:
• TNF-α, IL-6
• Promote inflammation, apoptosis, and cachexia
•Oxidative Stress:
•Free radicals
•Damage myocardium and endothelial cells
•Insulin Resistance:
• Common in HFpEF
• Exacerbates diastolic dysfunction
6. I nfl amm ator y an d Meta bol i c :
PATHOPHYSIOLOGY
MANAGEMENT
MANAGEMENT
STRUCTURED APPROACH
1. Initial Assessment & Stabilization
• ABCs (Airway, Breathing, Circulation)
• Intubation if respiratory failure:
• PaO₂ <60 mmHg
• Hypercapnia
• Altered mental status
• Monitor vital signs (BP, HR, SpO , respiratory rate).
₂
• Physical Exam:
• Jugular venous distension
• Pulmonary crackles
• Peripheral edema
• S3 gallop
• Diagnostics:
• .
• Imaging: Chest X-ray (pulmonary edema, cardiomegaly), echocardiogram (EF, valvular function).
• ECG: Detect ischemia/arrhythmias (e.g., AF, STEMI).
• Clinical picture
• Chest radiograph
• Echocardiogram
• Electrocardiogram
• Labs:
• ANP
• Troponin
• Electrolytes
• Renal/liver function
• Exercise test
• Catheterization or coronary angiography
2 . Di agn osi s
MANAGEMENT
• Hemodynamics:
• Arterial line (continuous BP)
• CVP
• Swan-Ganz catheter ?
• Daily Assessments:
• Weight
• Fluid balance
• Lactate
• Renal function.
• Echocardiography:
• Repeat to assess response to therapy.
3. Mon i t or i ng
MANAGEMENT
• Oxygen Therapy:
• Nasal cannula or non-rebreather mask for hypoxemia
• Non-Invasive Ventilation (NIV):
• CPAP/BiPAP for acute pulmonary edema to reduce work of breathing.
• Mechanical Ventilation:
• If NIV fails
• Or patient fatigues
• Use low tidal volumes (6–8 mL/kg) to minimize barotrauma.
4. R espi r ato r y S upp or t
MANAGEMENT
• Monitor:
• Urine output
• Electrolytes (K , Mg² ),
⁺ ⁺
• Renal function
• Fluid Restriction:
• Typically, 1.5–2 L/day
• Adjust based on volume status
• Diuretics:
• IV loop furosemide
• 40–80 mg IV bolus
• Then infusion.
• Ultrafiltration:
• Considered if:
• Diuretic resistance
• CKD
• ESRD.
5 . F l u i d M a n a g e m e n t
MANAGEMENT
•Vasodilators:
• If SBP >110 mmHg
• Nitroglycerin:
• Start at 10–20 mcg/min
• Titrate
• Nitroprusside:
• Reserved for severe hypertension
• 0.3–5 mcg/kg/min
• Monitor for cyanide toxicity.
6. H emodyn ami c Sup por t
MANAGEMENT
• Inotropes:
• For low cardiac output
• For SBP <90 mmHg:
• Dobutamine:
• 2–20 mcg/kg/
• Avoid in cardiogenic shock with arrhythmias
• Milrinone - Amrinone :
• Phosphodiesterase inhibitors
• Dose:
• Milrinone: 0.125–0.75 mcg/kg/min
• Amrinone : Load: 0.75 mg/kg IV bolus over 2-3 minutes,
THEN 5-10 mcg/kg/min IV
• Caution in renal failure.
• Levosimendan: (Calcium sensitizer)
• Preferred in β-blocker use
6. H emodyn ami c Sup por t
MANAGEMENT
•Vasopressors:
•If persistent hypotension:
•Norepinephrine:
• First-line
• 0.05–0.5 mcg/kg/min
6. H emodyn ami c Sup por t
MANAGEMENT
•Arrhythmias:
• Rate control (β-blockers, amiodarone) for AF
• Cardioversion if unstable.
•Ischemia:
• Revascularization (PCI/CABG) for ACS.
•Infection:
• Empiric antibiotics if sepsis suspected.
•Electrolytes:
• Correct hypokalemia/hypomagnesemia to prevent arrhythmias
7. C omor b i di ty Managem ent
MANAGEMENT
•Hypertensive Crisis:
• Aggressive vasodilation
• Nitroprusside
• + diuresis
•Diastolic HF:
• Focus on BP control
• Diuresis
• And rate control
•Cardiogenic Shock:
• Inotropes
• + mechanical support (e.g., Impella).
8. S p eci a l Scenar i os
MANAGEMENT
•Intra-Aortic Balloon Pump
(IABP):
• For cardiogenic shock complicating
acute MI
• Controversial efficacy
9. Mechani cal Ci r cul ator y S up port
MANAGEMENT
•Percutaneous Ventricular Assist
Device (Impella) :
• Refractory shock
• Requires specialized centers
9. Mechani cal Ci r cul ator y S up port
MANAGEMENT
•VA-ECMO:
9 . M e c h a n i c a l C i r c u l a t o r y S u p p o r t
MANAGEMENT
• Increases the level of natriuretic peptides
• Get rid of more sodium (salt)
• Vasodilation
• Guideline-directed Medical Therapy (GDMT):
• Initiation
• Once stable
• Angiotensin receptor- neprilysin inhibitor
(ARNI) /
Angiotensin Receptor Blocker (ARB)/
Angiotensin-Converting Enzyme Inhibitor
(ACE-I) :
• Cornerstone of therapy
• Start at low doses
• Sacubitril/valsartan 24/26 mg bid).
10. Transi ti on to O r al T her apy:
MANAGEMENT
• Beta-Blockers:
• Long-term outcomes improved
• Carvedilol/bisoprolol
• Avoid in acute decompensation
• Spironolactone/eplerenone:
• If K <5.0 and Cr <2.5 mg/dL.
⁺
• SGLT2i “sodium-glucose co-transporter 2”:
• Empagliflozin/dapagliflozin
• Even without diabetes
• Digoxin :
• If as a component of chronic therapy
• Digoxin is not an agent for stabilization of patients with an acute
exacerbation
• Loading doses (as may be used for rate control in patients with atrial fibrillation) are not
indicated in patients with HF
1 0 . Tr a n s i t i o n t o O r a l T h e r a p y :
MANAGEMENT
• Renal Failure:
• Avoid nephrotoxins
• Balance diuresis
• Arrhythmias:
• Correct electrolytes
• Minimize inotrope duration
• Thromboembolism:
• Prophylactic heparin if needed
11. Co mpl i cat i ons & P r even ti on :
MANAGEMENT
• Education:
• Sodium/fluid restriction
• Medication adherence
• Daily weights.
• Multidisciplinary team involvement:
• ICU
• Cardiology
• Pharmacy
• Nutrition
• Follow-Up:
• Early cardiology visit
12. Di schar g e Pl anni ng
MANAGEMENT
THANK YOU

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Heart failure in the ICU unit for non cardiologists

  • 2. INTRO •A clinical syndrome • Caused by structural or functional dysfunction • Affecting systole or diastole or both • Leading to impaired ability of one or both ventricles to pump • Associated with objective evidence of pulmonary or systemic congestion • Corroborated by elevated natriuretic peptide Universal Definition and Classification of Heart Failure - Journal of Cardiac Failure
  • 3. CAUSES •Ischemia & infraction •Hypertension •Valvular disorders •Myocardial damage • Cardiomyopathy • Myocarditis •Arrhythmias •Some chemotherapy drugs •Systemic Disorders that increase demand for CO • Anemia • Hyperthyroidism •Amyloidosis •Chronic fibrosis (eg, systemic sclerosis) •Hemochromatosis •Reduced substrate availability (free fatty acids or glucose)
  • 5. CALSSIFICATION https://www.jacc.org/doi/10.1016/j.jacc.2021.04.070 - HFrEF (Reduced EF) : • EF ≤40%. • Impaired systolic function - HFmrEF (Mid-Range EF): • EF 41–49%. • Intermediate category • With mixed systolic/diastolic dysfunction - HFpEF (Preserved EF): • EF ≥50%. • Impaired diastolic function • Stiff ventricles affecting filling - HFimpEF (Improved EF): • EF previously ≤40% • but increased to >40% after treatment 1. By E j e cti on Fr acti on (E F):
  • 6. 2. By Ti me Course: - Acute HF: • Sudden onset HF - Chronic HF: • Long-standing • Stable symptoms • Usually managed with therapies - Acute Decompensated HF: • Worsening of chronic HF • Requiring urgent care - Cardiogenic Shock: • Severe acute HF • With life-threatening hypotension • EF <25%, systolic BP <90 mmHg Types of Heart Failure | American Heart Association CLASSIFICATION
  • 7. 3. By Anat omical Invol vement : - Left-Sided HF: • Causes pulmonary congestion • Dyspnea • Pulmonary edema - Right-Sided HF: • Leads to systemic venous congestion • Peripheral edema • Jugular distension - Biventricular HF: • Both sides affected, common in advanced disease. Types of Heart Failure | American Heart Association CLASSIFICATION
  • 8. NYHA Functional Classification: Class Symptoms Severity Relation to daily activity I No fatigue, dyspnea, or palpitations. None Can complete any activity requiring ≤ 7 MET: • Carry 11 kg up 8 steps • Carry objects weighing 36 kg II With normal Physical activity Fatigue, dyspnea, palpitations, or angina Mild Can complete any activity requiring ≤ 5 MET: • Sexual intercourse without stopping • Gardening • Walk 7 km/hour on level ground • Climb one flight of stairs at a normal pace without symptoms III Comfortable at rest Less than ordinary physical activity Causes fatigue, dyspnea, palpitations, or angina Moderate Can complete any activity requiring ≤ 2 MET: • Shower or dress without stopping • Strip and make a bed • Clean windows • Walk 4 km/hour IV Symptoms occur at rest Any physical activity increases discomfort. Severe Cannot do or cannot complete any activity requiring ≥ 2 MET; cannot do any of the above activities Table: New York Heart Association (NYHA) Classification of Heart Failure-MSD Manual Professional Edition 4. By St aging S ystem CLASSIFICATION
  • 9. Classes and Stages of Heart Failure | American Heart Association ACC/AHA Stages: Stage Severity Description A At risk • Hypertension, diabetes without structural heart disease B Pre HF • Structural disease reduced EF, hypertrophy) without symptoms C HF • Reduced EF, hypertrophy) Symptomatic D Advanced HF • Refractory HF requiring advanced therapies. CLASSIFICATION 4. By St aging S ystem
  • 10. CV Physiology | Combined Ventricular Systolic and Diastolic Dysfunction - Systolic Dysfunction: • Impaired contraction (HFrEF). - Diastolic Dysfunction: • Impaired relaxation/stiffness (HFpEF). - Mixed Dysfunction: • Features of both (common in HFmrEF) Systolic Heart Failure | Johns Hopkins Medicine Diastolic Heart Failure: HFPEF, Left-Sided Heart Failure, Symptoms 5. By P athophysi ol ogy CLASSIFICATION
  • 11. • Ischemic HF • Hypertension • Valvular disease • Cardiomyopathy (dilated, hypertrophic, restrictive) • Arrhythmias, congenital defects, or toxins (e.g., chemotherapy) • High-Output HF: • Elevated metabolic demands (e.g., anemia, hyperthyroidism, AV shunts) • Special Considerations - Pediatric HF: Often due to congenital or genetic causes - Comorbidities: Diabetes, CKD, and COPD… 6. By Et iol ogy CLASSIFICATION
  • 13. • Ability of the heart to increase its performance above resting levels in response to stress • Increasing heart rate • Increasing systolic and diastolic volumes • Increasing stroke volume • Increasing extraction of oxygen • It is about: • 200% to 250% in old age • 300% to 400% in a normal young healthy • 500% to 600% in athletes 1621324608PHYSIOLOGY_SEM-2_k-sembulingam-essentials-of-medical-physiology.pdf Car di ac r eser ve: PATHOPHYSIOLOGY
  • 14. •Determined by: •Preload •Afterload •Heart rate and rhythm •Oxygen supply •Amount of viable myocardium •Substrate availability (fatty acids, glucose) CV Physiology | Combined Ventricular Systolic and Diastolic Dysfunction Ventricular performance : PATHOPHYSIOLOGY
  • 15. •Frank-Starling principle •Systolic contractile performance •Represented by stroke volume •Is proportional to preload •Within the normal physiologic range Effect of changes in myocardial contractility on the Frank-Starling... | Download Scientific Diagram Mo r phol og i cal Chang e: PATHOPHYSIOLOGY
  • 16. Vent Pressure mm Hg Vent Volume EDV ESV EDP Systolic pressure Diastolic pressure Stroke Volume Iso volumetric Relaxation Diastolic filling Iso volumetric Contraction Systolic ejection Aortic valve closes Mitral valve closes Aortic valve open Mitral valve open P r e s s u r e - Vo l u m e R e l a t i o n s h i p : PATHOPHYSIOLOGY
  • 17. • Systolic heart failure: • Decreased contractility • Predominant in : • Myocardial infarction • Myocarditis • Dilated cardiomyopathy • Reduced ejection fraction (HFrEF) • Increased diastolic volume and pressure • Decreased ejection fraction (≤ 40%) • Affect primarily the LV 1 . C o r e M e c h a n i s m s : PATHOPHYSIOLOGY
  • 18. • Diastolic heart failure: • Increased Afterload • Results from : • Hypertension • Valvular disease • Constrictive pericarditis • Global contractility is preserved • Increased ventricular stiffness • Impaired ventricular relaxation • LV filling is impaired • Cause inappropriately low LV end-diastolic volume • Ejection fraction remain normal (≥ 50%) 1 . C o r e M e c h a n i s m s : PATHOPHYSIOLOGY
  • 19. • Left Side Heart Failure: • Pulmonary venous pressure increases • Fluid extravasates (from the capillaries into the interstitial space and alveoli ) • Reduced pulmonary compliance • Increasing the work of breathing • Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli • Decreasing oxygenation ( PaO2) • Dyspnea • Respiratory alkalosis early ( CO2) • But elevating PaCO2 is a sign of impending respiratory failure 1 . C o r e M e c h a n i s m s : PATHOPHYSIOLOGY
  • 20. •Right sided heart failure: • systemic venous pressure increases • Fluid extravasation and edema (feet and ankles of ambulatory patients and abdominal viscera ) • Liver is affected • Hepatic congestion and dysfunction • Fluid accumulation in the peritoneal cavity (ascites) • Breaks down less aldosterone, further contributing to fluid accumulation. • Chronic venous congestion in the viscera: • Anorexia • Malabsorption of nutrients and drugs • Protein-losing enteropathy • Rarely ischemic bowel infarction 1 . C o r e M e c h a n i s m s : PATHOPHYSIOLOGY
  • 21. • Compensatory mechanisms: • Initially maintain perfusion • Finally worsen HF • Sympathetic Overdrive: • Short-term compensation • Chronic activation causes: • Myocardial toxicity • Arrhythmias • β-receptor downregulation. • Renin-Angiotensin-Aldosterone System (RAAS): • Reduced renal perfusion • Triggers renin release → angiotensin II (vasoconstriction, aldosterone release) • Sodium/water retention (↑ preload), vasoconstriction (↑ afterload), and myocardial fibrosis • Natriuretic Peptides (BNP, ANP): • Released in response to ventricular stretch • Promote vasodilation and diuresis • Overwhelmed in advanced HF • Leading to persistent fluid retention 2 . N e u r o h o r m o n a l A c t i v a t i o n : PATHOPHYSIOLOGY
  • 22. • Thickened ventricular walls : • Myocyte Hypertrophy • In pressure overload, e.g., hypertension). • Dilation: • Thin, enlarged chambers • Volume overload • May be valvular regurgitation • Both …. Turn Pathologic : • Stretching of cardiac muscle increases contractility (up to a certain point) • Fails in advanced HF due to excessive stretch • ↓ CO, ↑ congestion • Fibrosis: • Scar tissue replaces functional myocardium • Reducing compliance and contractility • Molecular Changes: • Altered calcium handling • Mitochondrial dysfunction • And apoptosis 3. Ventr i cul ar Rem od el i ng : PATHOPHYSIOLOGY
  • 23. • Forward Failure: • Reduced CO → hypoperfusion of organs (fatigue, renal dysfunction, confusion) • Backward Failure: • Elevated ventricular filling pressures → pulmonary congestion (dyspnea, orthopnea) or systemic venous congestion (jugular distension, hepatomegaly, edema). • Cardiorenal Syndrome: • Worsening kidney function due to reduced renal perfusion and venous congestion • Cardiac cirrhosis 4-S ystemi c Conse qu ences : PATHOPHYSIOLOGY Cardiorenal Syndrome: Symptoms & Treatment Cardiac Cirrhosis - StatPearls - NCBI Bookshelf
  • 24. • Ischemic HF: • Coronary artery disease → myocardial necrosis → scar tissue → impaired contractility • Hypertensive HF: • Chronic pressure overload → left ventricular hypertrophy → diastolic dysfunction. • Valvular HF: • Stenosis/regurgitation → volume/pressure overload → remodeling • Non-ischemic Cardiomyopathy • Viral myocarditis, alcohol toxicity • Direct myocardial damage 5-E ti o l ogy- Sp eci fi c P ath w ays : PATHOPHYSIOLOGY
  • 25. •Cytokines: • TNF-α, IL-6 • Promote inflammation, apoptosis, and cachexia •Oxidative Stress: •Free radicals •Damage myocardium and endothelial cells •Insulin Resistance: • Common in HFpEF • Exacerbates diastolic dysfunction 6. I nfl amm ator y an d Meta bol i c : PATHOPHYSIOLOGY
  • 27. MANAGEMENT STRUCTURED APPROACH 1. Initial Assessment & Stabilization • ABCs (Airway, Breathing, Circulation) • Intubation if respiratory failure: • PaO₂ <60 mmHg • Hypercapnia • Altered mental status • Monitor vital signs (BP, HR, SpO , respiratory rate). ₂ • Physical Exam: • Jugular venous distension • Pulmonary crackles • Peripheral edema • S3 gallop • Diagnostics: • . • Imaging: Chest X-ray (pulmonary edema, cardiomegaly), echocardiogram (EF, valvular function). • ECG: Detect ischemia/arrhythmias (e.g., AF, STEMI).
  • 28. • Clinical picture • Chest radiograph • Echocardiogram • Electrocardiogram • Labs: • ANP • Troponin • Electrolytes • Renal/liver function • Exercise test • Catheterization or coronary angiography 2 . Di agn osi s MANAGEMENT
  • 29. • Hemodynamics: • Arterial line (continuous BP) • CVP • Swan-Ganz catheter ? • Daily Assessments: • Weight • Fluid balance • Lactate • Renal function. • Echocardiography: • Repeat to assess response to therapy. 3. Mon i t or i ng MANAGEMENT
  • 30. • Oxygen Therapy: • Nasal cannula or non-rebreather mask for hypoxemia • Non-Invasive Ventilation (NIV): • CPAP/BiPAP for acute pulmonary edema to reduce work of breathing. • Mechanical Ventilation: • If NIV fails • Or patient fatigues • Use low tidal volumes (6–8 mL/kg) to minimize barotrauma. 4. R espi r ato r y S upp or t MANAGEMENT
  • 31. • Monitor: • Urine output • Electrolytes (K , Mg² ), ⁺ ⁺ • Renal function • Fluid Restriction: • Typically, 1.5–2 L/day • Adjust based on volume status • Diuretics: • IV loop furosemide • 40–80 mg IV bolus • Then infusion. • Ultrafiltration: • Considered if: • Diuretic resistance • CKD • ESRD. 5 . F l u i d M a n a g e m e n t MANAGEMENT
  • 32. •Vasodilators: • If SBP >110 mmHg • Nitroglycerin: • Start at 10–20 mcg/min • Titrate • Nitroprusside: • Reserved for severe hypertension • 0.3–5 mcg/kg/min • Monitor for cyanide toxicity. 6. H emodyn ami c Sup por t MANAGEMENT
  • 33. • Inotropes: • For low cardiac output • For SBP <90 mmHg: • Dobutamine: • 2–20 mcg/kg/ • Avoid in cardiogenic shock with arrhythmias • Milrinone - Amrinone : • Phosphodiesterase inhibitors • Dose: • Milrinone: 0.125–0.75 mcg/kg/min • Amrinone : Load: 0.75 mg/kg IV bolus over 2-3 minutes, THEN 5-10 mcg/kg/min IV • Caution in renal failure. • Levosimendan: (Calcium sensitizer) • Preferred in β-blocker use 6. H emodyn ami c Sup por t MANAGEMENT
  • 34. •Vasopressors: •If persistent hypotension: •Norepinephrine: • First-line • 0.05–0.5 mcg/kg/min 6. H emodyn ami c Sup por t MANAGEMENT
  • 35. •Arrhythmias: • Rate control (β-blockers, amiodarone) for AF • Cardioversion if unstable. •Ischemia: • Revascularization (PCI/CABG) for ACS. •Infection: • Empiric antibiotics if sepsis suspected. •Electrolytes: • Correct hypokalemia/hypomagnesemia to prevent arrhythmias 7. C omor b i di ty Managem ent MANAGEMENT
  • 36. •Hypertensive Crisis: • Aggressive vasodilation • Nitroprusside • + diuresis •Diastolic HF: • Focus on BP control • Diuresis • And rate control •Cardiogenic Shock: • Inotropes • + mechanical support (e.g., Impella). 8. S p eci a l Scenar i os MANAGEMENT
  • 37. •Intra-Aortic Balloon Pump (IABP): • For cardiogenic shock complicating acute MI • Controversial efficacy 9. Mechani cal Ci r cul ator y S up port MANAGEMENT
  • 38. •Percutaneous Ventricular Assist Device (Impella) : • Refractory shock • Requires specialized centers 9. Mechani cal Ci r cul ator y S up port MANAGEMENT
  • 39. •VA-ECMO: 9 . M e c h a n i c a l C i r c u l a t o r y S u p p o r t MANAGEMENT
  • 40. • Increases the level of natriuretic peptides • Get rid of more sodium (salt) • Vasodilation • Guideline-directed Medical Therapy (GDMT): • Initiation • Once stable • Angiotensin receptor- neprilysin inhibitor (ARNI) / Angiotensin Receptor Blocker (ARB)/ Angiotensin-Converting Enzyme Inhibitor (ACE-I) : • Cornerstone of therapy • Start at low doses • Sacubitril/valsartan 24/26 mg bid). 10. Transi ti on to O r al T her apy: MANAGEMENT
  • 41. • Beta-Blockers: • Long-term outcomes improved • Carvedilol/bisoprolol • Avoid in acute decompensation • Spironolactone/eplerenone: • If K <5.0 and Cr <2.5 mg/dL. ⁺ • SGLT2i “sodium-glucose co-transporter 2”: • Empagliflozin/dapagliflozin • Even without diabetes • Digoxin : • If as a component of chronic therapy • Digoxin is not an agent for stabilization of patients with an acute exacerbation • Loading doses (as may be used for rate control in patients with atrial fibrillation) are not indicated in patients with HF 1 0 . Tr a n s i t i o n t o O r a l T h e r a p y : MANAGEMENT
  • 42. • Renal Failure: • Avoid nephrotoxins • Balance diuresis • Arrhythmias: • Correct electrolytes • Minimize inotrope duration • Thromboembolism: • Prophylactic heparin if needed 11. Co mpl i cat i ons & P r even ti on : MANAGEMENT
  • 43. • Education: • Sodium/fluid restriction • Medication adherence • Daily weights. • Multidisciplinary team involvement: • ICU • Cardiology • Pharmacy • Nutrition • Follow-Up: • Early cardiology visit 12. Di schar g e Pl anni ng MANAGEMENT

Editor's Notes

  • #2: a condition that develops when your heart doesn't pump enough blood for your body's needs.
  • #4: HFpEF (Preserved EF): There has been debate about the correct name for this condition including originally Diastolic Heart Failure (DHF), Heart Failure with a Normal Ejection Fraction (HFNEF), and more recently Heart Failure with a Preserved Ejection Fraction,
  • #5: HFpEF (Preserved EF): There has been debate about the correct name for this condition including originally Diastolic Heart Failure (DHF), Heart Failure with a Normal Ejection Fraction (HFNEF), and more recently Heart Failure with a Preserved Ejection Fraction,
  • #12: HFpEF (Preserved EF): There has been debate about the correct name for this condition including originally Diastolic Heart Failure (DHF), Heart Failure with a Normal Ejection Fraction (HFNEF), and more recently Heart Failure with a Preserved Ejection Fraction,
  • #15: link between the initial length of myocardial fibers and the force generated by contraction
  • #16: Patients with systolic heart failure require a large end-diastolic volume to produce an adequate stroke volume and cardiac output. This is represented as the rightward shift of the LV end-diastolic pressure-volume relation 
  • #17: EF = (SV/EDV) x 100. Heart failure with reduced ejection fraction (HFrEF)
  • #18: Heart failure with preserved ejection fraction (HFpEF
  • #19: Heart failure with reduced ejection fraction (HFrEF)
  • #20: Heart failure with reduced ejection fraction (HFrEF)
  • #22: Calcium Dysregulation in HF Systolic Dysfunction: Reduced SERCA2a Activity: Decreased reuptake of calcium into the SR, leading to lower calcium stores and impaired contraction. Phospholamban Dysregulation: Reduced phosphorylation (e.g., due to β-adrenergic downregulation) exacerbates SERCA2a inhibition. Diastolic Dysfunction: Delayed Calcium Removal: Slower SR reuptake and increased NCX activity prolong relaxation, causing stiffness. Calcium Overload: Leaky RyR2 Channels: Promote diastolic calcium leaks, triggering arrhythmias and activating pro-apoptotic pathways. Mitochondrial Dysfunction: Calcium overload in mitochondria induces oxidative stress and cell death.
  • #26: HFpEF (Preserved EF): There has been debate about the correct name for this condition including originally Diastolic Heart Failure (DHF), Heart Failure with a Normal Ejection Fraction (HFNEF), and more recently Heart Failure with a Preserved Ejection Fraction,
  • #28:  over 100 pg/mL may be a sign of heart failure
  • #38: Impella is a brand name, and the manufacturer makes various heart pumps that help with different purposes cost of treating people with mechanical devices rose from $47,000 to $51,00
  • #40: Neprilysin is an endopeptidase that cleaves a variety of peptides such as natriuretic peptides, bradykinin, adrenomedullin, substance P, angiotensin I and II, and endotheli Neprilysin inhibitors:  Cause an increase in levels of natriuretic peptides Get rid of more sodium (salt). Open your blood vessels wide
  • #41: Spironolactone Reasonable to continue if: Renal function is stable Without hyperkalemia
  • #44: HFpEF (Preserved EF): There has been debate about the correct name for this condition including originally Diastolic Heart Failure (DHF), Heart Failure with a Normal Ejection Fraction (HFNEF), and more recently Heart Failure with a Preserved Ejection Fraction,