1) Chronic HF is a progressive syndrome that impairs the heart's ability to pump blood effectively. It can be caused by structural or functional changes to the heart and has two main types: HFrEF with reduced ejection fraction and HFpEF with preserved ejection fraction. 2) Risk factors include age, with risk doubling each decade, and prior conditions like hypertension, diabetes and myocardial infarction. Five-year mortality is around 50% and sudden cardiac death causes 40% of HF deaths. 3) Treatment involves managing symptoms, slowing disease progression, and preventing hospitalizations through lifestyle changes, medications, and devices. Diuretics, ACE inhibitors, beta-blockers, and aldosterone antagon

2. • Chronic HF: is a progressive clinical syndrome that can
result from any changes in cardiac structure or function
that impairs the ability of the ventricle to fill with or eject
blood. (affects ability of heart to contract (systolic) or
relax (diastolic)
• HFrEF: there is decrease in cardiac output (reduced
systolic function).
• HFpEF: Preserved LV systolic function (normal LVEF)
with presumed diastolic dysfunction.
• HF is the final common pathway for many cardiac d/o
including those affecting pericardium, heart valves, and
myocardium.

3. • Risk doubles with every decade in life
• Major cause for hospitalization among elderly
• 5-year mortality rates around 50% for all pt with HF.
• Around 40% of deaths from HF come as sudden cardiac
death
• About 50% of HF pts have HFpEF.

4. • HFrEF is often caused by previous MI while pts with
HFpEF are usually elderly, female, obese, have HTN,
Afib, or diabetes. (survival is similar in both)
• Causes of HF: ACS, Volume/ pressure overload and HTN
Systolic dysfunction (decreased contractility)
•Reduction in muscle mass (eg, myocardial infarction)
•Dilated cardiomyopathies
•Ventricular hypertrophy
• Pressure overload (eg, systemic or pulmonary hypertension, aortic or
pulmonic valve stenosis)
• Volume overload (eg, valvular regurgitation, shunts, high-output states)
Diastolic dysfunction (restriction in ventricular filling)
•Increased ventricular stiffness
• Ventricular hypertrophy (eg, hypertrophic cardiomyopathy)
• Infiltrative myocardial diseases (eg, amyloidosis, sarcoidosis, endomyocardial
fibrosis)
• Myocardial ischemia and infarction
•Mitral or tricuspid valve stenosis
•Pericardial disease (eg, pericarditis, pericardial tamponade)

5. • CO: volume of blood ejected per unit time (L/min)
CO= HR X SV
MAP= CO X systemic vascular resistance (SVR)
• HR is controlled by the ANS (autonomic nervous system)
• SV: Stroke volume or the volume of blood ejected during
systole, depends on preload, afterload, and contractility.

8. • 1) Tachycardia and increased contractility through SNS
activation
• 2) the Frank-starling mechanism (increase in Preload
causes increase in SV)
• 3) vasoconstriction
• 4) ventricular
hypertrophy and
remodeling

10. • Angiotensin II: It is a potent vasoconstrictor. Angiotensin
II facilitates release of NE. It promotes sodium retention
through direct effects on the renal tubules and by
stimulating aldosterone release.
• NE: causes tachycardia, vasoconstriction, and increased
contractility and plasma renin activity in HFrEF. Plasma
NE concentrations are elevated in correlation with the
degree of HF. Excess catecholamines increase the risk of
arrhythmias and can cause myocardial cell loss by
stimulating both necrosis and apoptosis.
• Aldosterone: aldosterone-mediated sodium retention
and its key role in volume overload and edema.

11. • Natriuretic peptides: has three members, atrial natriuretic
peptide (ANP), B-type natriuretic peptide (BNP), and C-type
natriuretic peptide (CNP). Of these, BNP is the most useful in
the diagnosis and management of HF. BNP and its related
biologically inactive peptide, NT-proBNP, are synthesized and
released from the ventricle in response to pressure or volume
overload. BNP or NT-proBNP plasma concentrations are
elevated in patients with HF functioning to increase natriuresis
and diuresis and attenuate activation of the RAAS and SNS.
BNP and NT-proBNP are biomarker for prognostic, diagnostic,
and therapeutic use.
• Arginine vasopressin: AVP is a pituitary peptide hormone
that regulates renal water excretion and plasma osmolality.
Plasma concentrations of AVP are elevated in patients with
HF. This causes (a) increased renal free water reabsorption in
the face of plasma hypoosmolality resulting in volume
overload and hyponatremia; (b) increased arterial
vasoconstriction that contributes to reduced CO; and (c)
stimulation of remodeling by cardiac hypertrophy and

12. • Cardiac events: Myocardial ischemia and infarction, Atrial
fibrillation, and HTN.
• Noncardiac events: Pulmonary infections (pneumococcal
and influenza), pulmonary embolism, diabetes,
worsening renal fcn, hypothyroidism, and
hyperthyroidism.
• Non-adherence with prescribed HF medications or
dietary recommendations.
• Some drugs may cause or exacerbate HF: 1) negative
inotropic effects 2) cardiotoxic 3) Na/Water retention 4)
other mechanism.

13. • Symptoms: Dyspnea, particularly on
exertion, Orthopnea, Paroxysmal nocturnal
dyspnea, Exercise intolerance, Tachypnea,
Cough, Fatigue, Nocturia, Hemoptysis,
Abdominal pain, Anorexia, Nausea,
Bloating, Poor appetite, early satiety,
Ascites, Mental status, changesWeight gain
or loss.
• Signs: Pulmonary rales, Pulmonary edema,
S3 gallop, mitral regurgitant murmur, Cool
extremities, Pleural effusion, Cheyne-Stokes
respiration, Tachycardia, Narrow pulse
pressure, Cardiomegaly, Peripheral edema,
Jugular venous distention, Hepatojugular
reflux, Hepatomegaly, Venous stasis
changes, Lateral displacement of apical

14. • Labs:
BNP > 100 pg/mL
NT-proBNP > 300 pg/mL
Electrocardiogram
Serum creatinine
Chest X-ray
Echocardiogram
Hyponatremia: serum sodium < 130 mEq/L

15. • New York Heart Association Functional Classification:
• I: Patients with cardiac disease but without limitations of
physical activity. Ordinary physical activity does not cause
undue fatigue, dyspnea, or palpitation.
• II: Patients with cardiac disease that results in slight limitations
of physical activity. Ordinary physical activity results in fatigue,
palpitation, dyspnea, or angina.
• III: Patients with cardiac disease that results in marked
limitation of physical activity. Although patients are comfortable
at rest, less than ordinary activity will lead to symptoms.
• IV: Patients with cardiac disease that results in an inability to
carry on physical activity without discomfort. Symptoms of
congestive heart failure are present even at rest. With any
physical activity, increased discomfort is experienced.

17. • Improve pts quality of life, relieve/ reduce symptoms,
prevent or minimize hospitalization, slow progression of
the disease and prolong survival.
• Non- Pharmacological therapy:
• smoking and alcohol cessastion.
• Exercise tailored to pt, restrict when decompensated.
• Na restriction: <2g/day
• General fluid restriction: <2L/d if Hyponatremia or
persistent fluid overload
• Daily wt measurements and logging: intervene if wt
increases >1 kg in 1 day or > 2kg over 5 days.
• Implantable devices.

18. • Symptom-targeted treatment
• Disease-targeted treatment
• Mechanism-targeted treatment

19. Recommendations
Diuretics
•A loop or a thiazide diuretic should be considered for patients with volume overload. However,
with more severe volume overload or inadequate response to a thiazide, a loop diuretic should be
implemented. Caution is warranted not to lower preload excessively, which may reduce stroke
volume and cardiac output.
ACE inhibitors
•ACE inhibitors should be considered in all patients who have symptomatic atherosclerotic
cardiovascular disease or diabetes and one additional risk factor.
Angiotensin receptor blockers
•In patients who are intolerant of ACE inhibitors, an angiotensin receptor blocker can be
considered an alternative.
Aldosterone antagonists
•reduce the risk of hospitalization in patients that do not have contraindications or are at risk for
hyperkalemia.
β-Blockers considered in pts w/:
•Myocardial infarction
•Hypertension
•Atrial fibrillation requiring ventricular rate control
Calcium channel blockers
•In patients with atrial fibrillation warranting ventricular rate control who either are intolerant to or
have not responded to a β-blocker, diltiazem or verapamil should be considered.
•for symptom-limiting angina and HTN

22. • As advanced, refractory, or end-stage HF.
• A poor quality of life, and are at high risk for morbidity
and mortality. Recurrent hospitalizations
• Referred to HF management programs including:
 Mechanical circulatory support, continuous IV positive
inotropic therapy, and cardiac transplantation
 Restriction of sodium and fluid( High doses of diuretics
or mechanical methods of fluid removal such as
ultrafiltration may be required).

23. • For patients with fluid o/l -> decrease edema by reduction
of preload
• Chronic use to maintain euvolemia.
• Relief symptoms but does not prolong survival. Improve
QOL and exercise tolerance.
• Use with caution, 2/2 risk of overdiuresis which lead to a
reduction in CO (HoTN), renal perfusion, and symptoms
of volume depletion.
• Start with low dose, adjust dose according to daily wt
measurements. Intervene if wt increases >1 kg in 1 day
or > 2kg over 5 days.

24. • Thiazide diuretics: hydrochlorothiazide used in pt with
mild fluid o/l and high BP.
• Loop diuretics restore and maintain euvolemia in HF.
• Loop diuretics: Furosemide, torsemide and bumetanide.
Only pharmacokinetic differences.
• “ceiling effect” overcome it with increasing frequency or
dose or adding thiazide (metolazone).
• S.E: Hypovolemia, hypotension, hyponatremia,
hypokalemia, hypomagnesemia, hyperuricemia, renal
dysfunction, thirst.

25. • decrease development of severe HF, and reduce
reinfarction and HF hospitalization rates, improve
symptoms, slow disease progression, and decrease
mortality in patients with HFrEF.
• S.E. of ACEi: 1) Hypotension 2) renal insuffeciency 3)
hyperkalemia 4) cough 5) angioedema
• ACEi C/I in pregnancy, angioedema and renal artery
stenosis.
• Renal function and serum potassium should be evaluated
at baseline and within 1 to 2 weeks after therapy is
started.

26. • candesartan, losartan, or valsartan are recommended by
the guidelines.
• ARBs reduced mortality and hospitalizations and
improved symptoms.
• Used in pts. who can’t tolerate ACE inhibitors.
• Blood pressure, renal function, and serum potassium
should be evaluated within 1 to 2 weeks after initiation of
therapy and after increases in dose.
• S.E: hyperkalemia, decrease in renal function and
hypotension.
• Candesartan and valsartan have no drug drug
interactions.

27. • Metoprolol succinate, carvedilol, and bisoprolol reduce
mortality.
• Carvedilol preferred in pts with uncontrolled BP.
• metoprolol or bisoprolol may be preferred in patients with
low BP or dizziness and in patients with significant airway
disease.
• S.E: bradycardia or heart block, hypotension, fatigue,
impaired glycemic control in diabetic patients,
bronchospasm in patients with asthma, and worsening
HF. May mask hypoglycemia s/s. except sweating
• monitor vital signs and carefully assess for signs and
symptoms of worsening HF during β-blocker initiation and
uptitration.
• The strategy of starting a β-blocker prior to an ACE
inhibitor is safe and effective

28. • Start low and go slow with up titration. Dose should not
be doubled more than every 2 weeks.
• β-blockers slow disease progression, decrease
hospitalizations, and improve survival, improve quality of
life in HFrEF.
• β-blocker are C/I uncontrolled bronchospastic disease,
symptomatic bradycardia, advanced heart block without a
pacemaker, and acute decompensated HF.

29. • Spironolactone and eplerenone block the
mineralocorticoid receptor, the target site for aldosterone.
• It improves symptoms, reduce the risk of HF
hospitalization, and increase survival in select patients
• 2 groups benefit from this drug: those with mild to
moderately severe HFrEF (NYHA class II-IV) who are
receiving standard therapy and those with left ventricular
dysfunction and either acute HF or diabetes early after
MI.
• It has high incidence of hyperkalemia and may cause
gynecomastia and menstrual irregularities.
• Monitor renal fcn. & K levels

30. • Nitrates result in venodilation and decreased preload.
• Hydralazine is a direct-acting arterial vasodilator causing
a decrease in SVR and resultant increases in SV and
CO. reduces oxidative stress.
• useful in patients unable to tolerate either an ACE
inhibitor or ARB because of renal insufficiency,
hyperkalemia, or possibly hypotension.
• Problems: 1) need for frequent dosing 2) high cost 3)
adverse effects e.g. dizziness, HA, and GI distress.

31. • have positive inotropic effect on heart.
• improves cardiac function, quality of life, exercise
tolerance, and HF symptoms in patients with HFrEF.
• the target SDC should be 0.5 to 0.9 ng/mL (0.6-1.2
nmol/L). Cam ne achieved with daily dose of 0.125mg.
• Help control ventricular response in pts with HFrEF.
• blood samples for measurement of SDCs should be
collected at least 6 hours and preferably 12 hours or
more after the last dose.

32. • provide symptom-targeted treatment in patients with
HFpEF by decreasing HR and increasing exercise
tolerance.
• nondihydropyridines (verapamil and diltiazem) are the
most effective because they lower heart rate in addition
to lowering BP. Used to treat the co-morbidities of
hypertension and atrial fibrillation in patients with HFpEF.
• Initial daily doses are verapamil 120 to 240 mg, diltiazem
90 to 120 mg, and amlodipine 2.5 mg.
• S.E.: bradycardia, heart block, peripheral edema and HA.
• NDHP CCB Contraindicated in heart block.

33. • HYPERTENSION:
Both HFrEF and HFpEF
 ACE inhibitors or ARBs, β-blockers, and diuretics,ARB,
aldosterone antagonist, ISDN/hydralazine, or a second-
generation calcium channel blocker such as amlodipine.
• ANGINA:
• Nitrates and β-blockers , amlodipine and felodipine
appear to be safe
• ATRIAL FIBRILLATION:Digoxin , β-Blockers OR
Combination therapy with digoxin and a β-blocker.
Calcium channel blockers with negative inotropic effects
such as verapamil or diltiazem.
• DIABETES: the treatment of diabetes in this population
remains uncertain.

34. • Evaluation :
o (a) functional capacity
o (b) volume status
o (c) laboratory monitoring