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Chronic Heart Failure
Done by :
Raniya.Khaled
@Rania199730
References:
ACCP Updates in Therapeutics® 2020 : Acute Care In Cardiology
AHA Heart Failure Guideline Updates 2019
Rxprep course book 2018 edition : Chronic Heart Failure
Heart Failure
• Heart "failure" occurs when the heart is not able to supply
sufficient oxygen-rich blood to the body, because of impaired
ability of the ventricle to either fill or eject blood.
• HF is commonly classified as either:
• Ischemic(due to a decrease in blood supply, such as from an
MI) or
• Non-ischemic, such as f rom long-standing uncontrol led
hypertension.
Raniya.Khaled
@Rania1997301
Heart Failure
Signs And
Symptoms Of
Systolic
Heart Failure
Labs
Increase BNP (B-type natriuretic peptide):
normal < 100 pg/mL
Increase NT-proBNP (N-terminal pro B-
type natriuretic pep- tide):
normal < 300 pg/mL
BNP and proBNP are used to distinguish
between cardiac and non-cardiac causes of
dyspnea
General Signs and Symptoms
Dyspnea
[shortness of breath (SOB);
at rest or upon exertion]
Cough
Fatigue, weakness
Reduction in exercise capacity
Left-Sided Signs and Symptoms
Orthopnea: SOB when lying flat
Paroxysmal nocturnal dyspnea (PND):
nocturnal cough and SOB
Hypoperfusion (renal impairment, cool
extremities)
Right-Sided Signs and Symptoms
Peripheral edema
Ascites: abdominal fluid accumulation
Jugular venous distention (JVD): neck vein
distention
Hepatojugular reflux (HJR): neck vein
distention that occurs when pressure is placed on
the abdomen
Hepatomegaly: enlarged liver due to fluid
congestion
Raniya.Khaled
@Rania1997301
Heart Failure
• An ultrasound of the heart (echocardiography or ECHO)
Provides useful information when HF is suspected, including an estimate of left
ventricular ejection fraction (LVEF).
LVEF is a measurement of how much blood is pumped out of the left ventricle (the
main pumping chamber of the heart) with each contraction.
Diagnosis
Ejection Fraction Ranges
> 50%
- Heart Failure with
Preserved EF (HFpEF)
Diastolic Dysfunction
-Impaired ventricular
relaxation and filling during
diastole
40-49%
-Heart Failure with
Mid-Range EF
(HFmrEF)
-Likely mixed systolic
and diastolic dysfunction
< 40%
-Heart Failure with
Reduced EF (HFrEF)
Systolic Dysfunction
-Impaired ability to eject
blood during systole
Raniya.Khaled
@Rania1997301
Heart Failure
Classification Systems
1-Types of Heart Failure
Systolic heart failure (HFrEF) : Diastolic heart failure (HFpEF) :
Failure of contraction to pump blood out of the chambers. Failure of relaxation to fill the chambers with blood
2-NYHA Functional Classification
I (Mild)
No limitation of physical activity
- Ordinary physical activity doesn't cause
tiredness, heart palpitations, or shortness of
breath
II (Mild)
Slight limitation of physical activity, comfortable
at rest, but ordinary physical activity results in
tiredness, heart palpitations, or shortness of
breath
III (Moderate)
Marked or noticeable limitations of physical
activity, comfortable at rest, but less than ordinary
physical activity causes tiredness, heart
palpitations, or shortness of breath
IV (Severe)
Severe limitation of physical activity, unable to
carry out any physical activity without discomfort.
Symptoms also present at rest. If any physical
activity is undertaken, discomfort increases.
3-AHA/ACC Staging System of Heart
A
People at high risk for
developing heart failure but
without structural heart disease
or symptoms of heart failure.
B
People with structural heart
disease but without signs and
symptoms of heart failure NYHA
Class I
C
People with structural heart
disease with prior or current
symptoms of heart failure NYHA
Class II and III
D
People who have advanced heart
failure and severe symptoms
difficult to manage with standard
treatment
NYHA Class IV
Raniya.Khaled
@Rania1997301
Treatment
Raniya.Khaled
@Rania1997301
Heart Failure
Drug Treatment
The cornerstones of HF treatment are RAAS inhibition
[withACE inhibitor, ARB or angiotensin receptor and neprilysin inhibitor (ARNI)],beta blockers and loop diuretics
CO
SNS RAAS Vasopressin
(ADH)
Natriuretic
Peptides
HR
Contractility
(+ inotropic effect)
Vasoconstriction
( Afterload)
Fluid Retention
( Preload)
Vasodilation
Diuresis
BB
ACEI-ARBS
ARA
Loop
Diuretics Digoxin Sacubitril
The body’s
compensatory
mechanisms
Effect
Drug
therapy
targets
Raniya.Khaled
@Rania1997301
Heart Failure
ACE inhibitors or
angiotensin receptor
blockers (ARBs)
Block neurohormonal activation of the RAAS, resulting in vasodilation and improved EF
Angiotensin receptor and
neprilysin inhibitor (ARNI)
Sacubitril/valsartan (Entresto) Inhibit the risk of cardiovascular death and hospitalization
for HF
In NYHA Class ll-IV patients who have a decreased EF In patients with chronic
symptomatic HF (NYHA Class ll-lll) who tolerate an ACE inhibitor or ARB, an ARNI is
preferred to an ACE inhibitor/ARB to further reduce morbidity and mortality
Beta blockers Block the activation of the SNS by blocking EPI and NE; also provide benefit in
controlling heart rate and reducing arrhythmia risk
Loop diuretics
Reduce blood volume, which inhibit edema and congestion.
Drug Treatment..1
Raniya.Khaled
@Rania1997301
Heart Failure
Aldosterone receptor
antagonists (ARAs)
Provide added diuresis; improve symptoms and EF
Inhibits morbidity and mortality in NYHA Class ll-IV
Digoxin Provides a small increase in cardiac output.
Hydralazine and nitrates
Prevent morbidity and mortality in black patients with NYHA Class lll-IV (when added to an
ACE inhibitor or ARB) and
in other patients who cannot tolerate an ACE inhibitor or ARB
Ivabradine (Corlanor) Inhibit risk of hospitalization in patients with stable NYHA Class ll-lll HF in normal sinus
rhythm with a resting heart rate > 70 BPM
Drug Treatment..2
Raniya.Khaled
@Rania1997301
Heart Failure
Sodium Nitroprusside (Nipride) IV Nitroglycerin
MOA Nitric oxide–induced stimulation of GC to convert GTP to cGMP Combines with sulfhydryl groups
in vascular endothelium to create S-nitrosothiol compounds that mimic nitric oxide’s
stimulation of GC and production of cGMP
Clinical effect Balanced arterial and venous vasodilator Preferential venous vasodilator
> arterial vasodilator, arterial vasodilation at high doses
Indication Warm and wet ADHF, alternative to inotropes in cold and wet ADHF, hypertensive
crises
Warm and wet ADHF, ACS, or hypertensive crises
Dosing 0.1–0.2 mcg/kg/min IV, increase by 0.2–3 mcg/kg/min every 10–20 min 5 mcg/min IV, increase by 5 mcg/min every 5–10 min up to 200 mcg/min
Typical dose 0.5–1 mcg/kg/min IV 25–100 mcg/min IV, titrated to response
Half-life < 10 min 1–3 min
Elimination Cyanide hepatically metabolized, thiocyanate renally excreted Inactive metabolites in urine
AEs Hypotension or cyanide or thiocyanate toxicity Hypotension, reflex tachycardia, headache, tachyphylaxis
Drug Treatment.. Vasodilator Therapy
Raniya.Khaled
@Rania1997301
Heart Failure
Dobutamine (Dobutrex) Milrinone (Primacor)
MOA β1-Agonist: Stimulates AC to convert ATP to cAMP to ↑ CO; slight peripheral
vasodilation
PDE inhibitor: Inhibits cAMP breakdown in heart to ↑ CO and in vascular smooth muscle to
↓ SVR
Clinical effect Positive inotropic, chronotropic, lusitropic effects Positive inotropic and lusitropic effects, no direct chronotropic effects
Indication ADHF: Cold and wet (Forester subset IV) or cold and dry exacerbations (Forester III) (if
PCWP > 15 mm Hg)
ADHF: Cold and wet (Forester subset IV) or cold and dry exacerbations (Forester III) (if
PCWP > 15 mm Hg)
Dosing Start 2.5–5 mcg/kg/min IV; may titrate to max of 20 mcg/kg/min 50 mcg/kg IVB (rarely administered),
then 0.1–0.2 mcg/kg/min IV; may titrate to max of 0.75 mcg/kg/min
Typical dose 5 mcg/kg/min IV No bolus, 0.1–0.375 mcg/kg/min IV
Half-life 2 min 1 hr, prolonged to 2–3 hr if HF or CrCl < 50 mL/min/1.73 m2
Elimination Hepatically metabolized (inactive), renally eliminated 90% renal
AEs Proarrhythmia, tachycardia, hypokalemia, myocardial ischemia, tachyphylaxis (> 72 hr);
possible increased mortality with long-term use
Proarrhythmia, hypotension (avoid bolus), tachycardia, < 1% thrombocytopenia, possible
increased mortality with long-term use
Other comments Consider in severe hypotension Consider if receiving a β-blocker or in those with high pulmonary artery pressures
Drug Treatment.. Inotropic Therapy
Raniya.Khaled
@Rania1997301

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Chronic heart failure

  • 1. Chronic Heart Failure Done by : Raniya.Khaled @Rania199730 References: ACCP Updates in Therapeutics® 2020 : Acute Care In Cardiology AHA Heart Failure Guideline Updates 2019 Rxprep course book 2018 edition : Chronic Heart Failure
  • 2. Heart Failure • Heart "failure" occurs when the heart is not able to supply sufficient oxygen-rich blood to the body, because of impaired ability of the ventricle to either fill or eject blood. • HF is commonly classified as either: • Ischemic(due to a decrease in blood supply, such as from an MI) or • Non-ischemic, such as f rom long-standing uncontrol led hypertension. Raniya.Khaled @Rania1997301
  • 3. Heart Failure Signs And Symptoms Of Systolic Heart Failure Labs Increase BNP (B-type natriuretic peptide): normal < 100 pg/mL Increase NT-proBNP (N-terminal pro B- type natriuretic pep- tide): normal < 300 pg/mL BNP and proBNP are used to distinguish between cardiac and non-cardiac causes of dyspnea General Signs and Symptoms Dyspnea [shortness of breath (SOB); at rest or upon exertion] Cough Fatigue, weakness Reduction in exercise capacity Left-Sided Signs and Symptoms Orthopnea: SOB when lying flat Paroxysmal nocturnal dyspnea (PND): nocturnal cough and SOB Hypoperfusion (renal impairment, cool extremities) Right-Sided Signs and Symptoms Peripheral edema Ascites: abdominal fluid accumulation Jugular venous distention (JVD): neck vein distention Hepatojugular reflux (HJR): neck vein distention that occurs when pressure is placed on the abdomen Hepatomegaly: enlarged liver due to fluid congestion Raniya.Khaled @Rania1997301
  • 4. Heart Failure • An ultrasound of the heart (echocardiography or ECHO) Provides useful information when HF is suspected, including an estimate of left ventricular ejection fraction (LVEF). LVEF is a measurement of how much blood is pumped out of the left ventricle (the main pumping chamber of the heart) with each contraction. Diagnosis Ejection Fraction Ranges > 50% - Heart Failure with Preserved EF (HFpEF) Diastolic Dysfunction -Impaired ventricular relaxation and filling during diastole 40-49% -Heart Failure with Mid-Range EF (HFmrEF) -Likely mixed systolic and diastolic dysfunction < 40% -Heart Failure with Reduced EF (HFrEF) Systolic Dysfunction -Impaired ability to eject blood during systole Raniya.Khaled @Rania1997301
  • 5. Heart Failure Classification Systems 1-Types of Heart Failure Systolic heart failure (HFrEF) : Diastolic heart failure (HFpEF) : Failure of contraction to pump blood out of the chambers. Failure of relaxation to fill the chambers with blood 2-NYHA Functional Classification I (Mild) No limitation of physical activity - Ordinary physical activity doesn't cause tiredness, heart palpitations, or shortness of breath II (Mild) Slight limitation of physical activity, comfortable at rest, but ordinary physical activity results in tiredness, heart palpitations, or shortness of breath III (Moderate) Marked or noticeable limitations of physical activity, comfortable at rest, but less than ordinary physical activity causes tiredness, heart palpitations, or shortness of breath IV (Severe) Severe limitation of physical activity, unable to carry out any physical activity without discomfort. Symptoms also present at rest. If any physical activity is undertaken, discomfort increases. 3-AHA/ACC Staging System of Heart A People at high risk for developing heart failure but without structural heart disease or symptoms of heart failure. B People with structural heart disease but without signs and symptoms of heart failure NYHA Class I C People with structural heart disease with prior or current symptoms of heart failure NYHA Class II and III D People who have advanced heart failure and severe symptoms difficult to manage with standard treatment NYHA Class IV Raniya.Khaled @Rania1997301
  • 7. Heart Failure Drug Treatment The cornerstones of HF treatment are RAAS inhibition [withACE inhibitor, ARB or angiotensin receptor and neprilysin inhibitor (ARNI)],beta blockers and loop diuretics CO SNS RAAS Vasopressin (ADH) Natriuretic Peptides HR Contractility (+ inotropic effect) Vasoconstriction ( Afterload) Fluid Retention ( Preload) Vasodilation Diuresis BB ACEI-ARBS ARA Loop Diuretics Digoxin Sacubitril The body’s compensatory mechanisms Effect Drug therapy targets Raniya.Khaled @Rania1997301
  • 8. Heart Failure ACE inhibitors or angiotensin receptor blockers (ARBs) Block neurohormonal activation of the RAAS, resulting in vasodilation and improved EF Angiotensin receptor and neprilysin inhibitor (ARNI) Sacubitril/valsartan (Entresto) Inhibit the risk of cardiovascular death and hospitalization for HF In NYHA Class ll-IV patients who have a decreased EF In patients with chronic symptomatic HF (NYHA Class ll-lll) who tolerate an ACE inhibitor or ARB, an ARNI is preferred to an ACE inhibitor/ARB to further reduce morbidity and mortality Beta blockers Block the activation of the SNS by blocking EPI and NE; also provide benefit in controlling heart rate and reducing arrhythmia risk Loop diuretics Reduce blood volume, which inhibit edema and congestion. Drug Treatment..1 Raniya.Khaled @Rania1997301
  • 9. Heart Failure Aldosterone receptor antagonists (ARAs) Provide added diuresis; improve symptoms and EF Inhibits morbidity and mortality in NYHA Class ll-IV Digoxin Provides a small increase in cardiac output. Hydralazine and nitrates Prevent morbidity and mortality in black patients with NYHA Class lll-IV (when added to an ACE inhibitor or ARB) and in other patients who cannot tolerate an ACE inhibitor or ARB Ivabradine (Corlanor) Inhibit risk of hospitalization in patients with stable NYHA Class ll-lll HF in normal sinus rhythm with a resting heart rate > 70 BPM Drug Treatment..2 Raniya.Khaled @Rania1997301
  • 10. Heart Failure Sodium Nitroprusside (Nipride) IV Nitroglycerin MOA Nitric oxide–induced stimulation of GC to convert GTP to cGMP Combines with sulfhydryl groups in vascular endothelium to create S-nitrosothiol compounds that mimic nitric oxide’s stimulation of GC and production of cGMP Clinical effect Balanced arterial and venous vasodilator Preferential venous vasodilator > arterial vasodilator, arterial vasodilation at high doses Indication Warm and wet ADHF, alternative to inotropes in cold and wet ADHF, hypertensive crises Warm and wet ADHF, ACS, or hypertensive crises Dosing 0.1–0.2 mcg/kg/min IV, increase by 0.2–3 mcg/kg/min every 10–20 min 5 mcg/min IV, increase by 5 mcg/min every 5–10 min up to 200 mcg/min Typical dose 0.5–1 mcg/kg/min IV 25–100 mcg/min IV, titrated to response Half-life < 10 min 1–3 min Elimination Cyanide hepatically metabolized, thiocyanate renally excreted Inactive metabolites in urine AEs Hypotension or cyanide or thiocyanate toxicity Hypotension, reflex tachycardia, headache, tachyphylaxis Drug Treatment.. Vasodilator Therapy Raniya.Khaled @Rania1997301
  • 11. Heart Failure Dobutamine (Dobutrex) Milrinone (Primacor) MOA β1-Agonist: Stimulates AC to convert ATP to cAMP to ↑ CO; slight peripheral vasodilation PDE inhibitor: Inhibits cAMP breakdown in heart to ↑ CO and in vascular smooth muscle to ↓ SVR Clinical effect Positive inotropic, chronotropic, lusitropic effects Positive inotropic and lusitropic effects, no direct chronotropic effects Indication ADHF: Cold and wet (Forester subset IV) or cold and dry exacerbations (Forester III) (if PCWP > 15 mm Hg) ADHF: Cold and wet (Forester subset IV) or cold and dry exacerbations (Forester III) (if PCWP > 15 mm Hg) Dosing Start 2.5–5 mcg/kg/min IV; may titrate to max of 20 mcg/kg/min 50 mcg/kg IVB (rarely administered), then 0.1–0.2 mcg/kg/min IV; may titrate to max of 0.75 mcg/kg/min Typical dose 5 mcg/kg/min IV No bolus, 0.1–0.375 mcg/kg/min IV Half-life 2 min 1 hr, prolonged to 2–3 hr if HF or CrCl < 50 mL/min/1.73 m2 Elimination Hepatically metabolized (inactive), renally eliminated 90% renal AEs Proarrhythmia, tachycardia, hypokalemia, myocardial ischemia, tachyphylaxis (> 72 hr); possible increased mortality with long-term use Proarrhythmia, hypotension (avoid bolus), tachycardia, < 1% thrombocytopenia, possible increased mortality with long-term use Other comments Consider in severe hypotension Consider if receiving a β-blocker or in those with high pulmonary artery pressures Drug Treatment.. Inotropic Therapy Raniya.Khaled @Rania1997301