heart failure

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Heart Failure:

Heart Failure

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According to the latest WHO data published in April 2011 Coronary Heart Disease Deaths in Egypt reached 78,897 or 21.73% of total deaths (Ranking Egypt #33 in the world).

Epidemiology :

Epidemiology A recent medical study concern heart disease conducted in 14 countries from the countries of the Middle East and Africa simultaneously It was reported that : 70 % with high levels of bad cholesterol 68% with Abdominal obesity 25 % of people with diabetes 14 % of the smokers

Heart Failure:

Heart Failure Introduction: is a progressive clinical syndrome that can result from any abnormality in cardiac structure or function that impairs the ability of the ventricle to fill or eject blood

Heart Failure will lead to:

Heart Failure will lead to Backward failure Forward Failure Congestion of pulmonary or systemic circulation Reduced output to body tissues (decrease perfusion) So Heart Failure can be referred as Congestive Heart F ailure

Normal cardiac function:

Normal cardiac function CO = HR × SV where; CO the volume of blood ejected per time (L/min). HR heart rate SV stroke volume ( volume ejected during systole ) HR is controlled by autonomic nervous system (discussed later). SV is controlled by : Preload Afterload Contractility Ejection fraction (EF) is the volumetric fraction of blood pumped out of the left and right ventricle with each heartbeat or cardiac cycle; normally (60-65%)

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Preload Forces acting on the venous side of circulation to affect myocardial wall tension As defined by Frank Starling mechanism, the ability of heart to alter the force of contraction depend on changes in preload. As heart muscle stretches(increase in its length) increases the force of contraction Heart muscle length is determined primarily by volume of blood in ventricle ( left ventricle end-diastolic volume ), therefore LVEDV is the primary determent of preload. Afterload Simply; it’s the sum of all forces preventing active forward ejection of blood by ventricle, depending on: Ejection impedance or systemic vascular resistance (SVR) Wall tension Wall geometry Contractility its intrinsic property of cardiac muscle describing fiber shortening and tension development (isotonic & isometric contraction)

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Preload Heart contraction Afterload Heart cycle

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It was believed that reduced myocardial contractility (systolic dysfunction) was the sole disturbance in cardiac function responsible for heart failure Later, it is noticed that some HF pt have normal systolic function & is believed to be primarily due to diastolic dysfunction

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Heart failure may caused by Systolic dysfunction (contraction) Diastolic dysfunction (relaxation) Both Systolic and Diastolic dysfunction

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Systolic dysfunction Impaired ventricular contraction (inotropic disturbances) The left heart cannot pump with enough force to push a sufficient amount of blood into the systemic circulation. This leads to fluid backing up into the lungs and pulmonary congestion Ejection fraction is reduced (less than 40%) It is a characteristic of dilated cardiomyopathy (most common)& may be seen in patients with hypertrophic cardiomyopathy (HCM) .

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Systolic Dysfunction (70%) Is due to Ischemic cardiomyopathy (2/3) Non –ischemic cardiomyopathy (1/3) Coronary artery disease 2ry to diseases as; ( HTN, Thyroid disease, valvular Heart disease, cardiotoxins (alcohol & chemotherapeutics), idiopathic )

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Diastolic dysfunction Impaired ventricular relaxation & filling (lusitrophic disturbances) or stiffiness This leads to muscle hypertrophy which then leads to inadequate filling which may lead to accumulation of fluids mainly in the feet, ankles, and legs Ejection fraction is preserved (greater than 50%) So its called (HF with preserved LVEF ) It is a characteristic of both Hypertrophy and restrictive cardiomyopathies & may be seen in patients with dilated cardiomyopathy

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Diastolic Dysfunction (30%) Age (decrease in heart elastic Properties) Diseases (HTN, diabetes, AF,…..) Cardiomyopathies (restrictive(infiltrative), hypertrophic)

Dilated Cardiomyopathy:

Dilated Cardiomyopathy The most common form of cardiomyopathy It is characterized by enlargement of one or both ventricles The heart muscle becomes thin and weakened and is unable to pump the blood efficiently These structural changes decrease the amount of blood ejected Due to several factors genetic & toxic

Hypertrophic Cardiomyopathy:

Hypertrophic Cardiomyopathy It is a common autosomal dominant genetic disorder that affects 1 in 500 persons The heart muscle increases in size and mass (stiff)especially along the intraventricular Septum These structural changes decrease the amount of blood ejected

Restrictive Cardiomyopathy:

Restrictive Cardiomyopathy It is the least common type of Cardiomyopathy It is characterized by the deposition of abnormal substances that cause the ventricular walls to become rigid , thereby impeding ventricular filling Due to myocardial or endomyocardial disease of diverse causes which "stiffen" the heart by infiltration or fibrosis

Classification of heart failure:

Classification of heart failure According to :

NYHA functional classification According to symptoms & physical activity:

NYHA functional classification According to symptoms & physical activity

ACC/AHA According to structural & damage to heart muscle :

ACC/AHA According to structural & damage to heart muscle Structural heart disease develops HF symptoms develops Treatment-resistant symptoms

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1ry etiological factor Compensatory mechanism (cardiac reserve) Myocardial damage Impaired contractility Chronic compensated heart failure Persistent Etiological factor Excessive compensation Decompensation (maladaptation) Acute decompensated heart failure

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Shortness of breath (dyspnea) Important symptoms

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Persistent cough

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Rise jugular venous pressure

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Pitting edema

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Abdominal discomfort

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cold extremities

Signs & symptoms of HF:

Signs & symptoms of HF Chronic compensated HF Shortness of breath (dyspnea) then progressed into orthopnea Fatigue & exercise intolerance Persistent cough Edema in legs, ankles, Feet, abdomen (ascites) Hepatic congestion Loss of appetite, but wt gain due to Fluid retention Tachycardia

Signs & symptoms of HF:

Signs & symptoms of HF Acute decompensated HF (more sever) Increased SNS activity (cold extremities & diaphoresis) Arrhythmia Hyperthyroidism or Hypothyroidism Crackles at the lung bases reflect transudation of fluid into the alveoli. Expiratory wheezing & rhonchi Hepatic enlargement, Peripheral pitting edema Incase of RT HF Rise jugular venous pressure

Heart Failure theories (paradigms):

Heart Failure theories (paradigms) Cardiorenal model At first, It was thought that the only problem is the excess sodium & water retention Diuretic therapy was the main therapeutic approach Cardiocirculatory model It is focused on impaired CO due to reduced pumping capacity of the heart and systemic vasoconsriction The treatment was focused on positive inotropes & later vasodilators The therapeutic approaches of these paradigms provide some symptomatic benefits but they don’t limit progression of HF

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Neurohormonal model They found that the problem moves beyond the heart as it involves systemic disease which is mediated by neurohormones that drive myocyte injury, oxidative stress, inflammation & extracellular matrix remodeling Neurohormonal activation include: Norepinephrine Angiotensin II Vasopressin Endothelin Aldosterone Natriuretic peptides TNF- α Cytokines

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In healthy heart End diastolic volume (110-120ml) SV ~70ml Residual end systolic Volume ~40 -50ml In early HF End diastolic volume ( ~ 200ml) SV ~70ml Residual end systolic Volume (~100ml) EF 60% EF 33% Sympathetic stimulation

Pathophysiology of Heart Failure:

Pathophysiology of Heart Failure

Cardiac Cachexia:

Cardiac Cachexia It is unintentional severe weight loss caused by heart disease (life-threatening). Swelling of the intestine may not allow for adequate absorption of nutrients from the food you eat. Heart failure may force you to work harder to breathe and cause your body temperature to increase. Both of these conditions burn calories.

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Cytokines Activates nuclear transcription factor- KB (NF-KB) Inc. ubiquitin (proteolytic activity) Dec. Myo-D gene expression Hyper catabolism Dec. myofibril synthesis

Natriuretic peptides:

Natriuretic peptides Peptide hormones released in response to volume overload inducing natriuresis It have been referred to as cardiac neurohormones There are 3 types of NP : Atrial NP Brain NP Type-c NP

Natriuretic peptides:

Natriuretic peptides Atrial NP Released from atrial In response to dilation & stretch of myocardium Brain NP Released from ventricle In response to volume overload & high end diastolic pressure Type-c NP Released from lung, Kidney & vascular endothelium In response to shear stress

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Concentrations of BNP in the myocardial tissue were found to be higher than those of ANP. Therefore, BNP considered as a clinically useful marker of increased ventricular filling pressure.

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Cardiac myocytes Pre-pro BNP Pro BNP NT-proBNP (inactive) half-life is long ~1-2 hr. Due to absence of NP receptors CT-BNP (active) half-life is short ~ 20 min Due to presence of NP receptors and plasma endopeptidases As a laboratory specimen, NT-proBNP is more stable during storage than BNP. NT-proBNP samples are stable at room temperature for 72 hours, versus less than 4 hours for BNP samples.

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BNP levels in( pg /ml): ≤ 100-400 ≤ Absence of HF High incidence of HF May be (pulmonary Embolism, pul. HTN, Chronic hypoxia, HF, RF) Drugs used NP analogs NP metabolism inhibitors Nesiritide (analog) Recombinant produced human BNP approved by FDA For IV management of acute HF exacerbation

Principles & goal of therapy:

Principles & goal of therapy

Non pharmacological therapy:

Non pharmacological therapy

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Stage A Stage D Stage C Stage B High risk No symptoms Structural H.D No symptoms Structural H.D Presence of symptoms Refractory symp. Require special intervention Control risk factor Stop smoking Stop alcohol Reg. exercise Use (ACEI or ARBS) Incase of vascular d. Or DM LVH, LVEF <40 Stop smoking Stop alcohol Reg. exercise Use (ACEI or ARBS) & BETA BLOCKERS titrated to target dose Stop smoking Stop alcohol Reg. exercise Salt restriction Use (ACEI or ARBS) & BETA BLOCKERS titrated to target dose Use Diuretics for fluid retention If symp. Continue may use (aldosterone ant., hydralazine, nitrates, digoxin) Refractory HF Heart transplant Permanent mech. Support

Major sites of drug action in HF :

Major sites of drug action in HF

Angiotensin-converting enzyme (ACE) Inhibitors:

Angiotensin-converting enzyme (ACE) Inhibitors

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ACEIs only that have effect on cardiac cachexia As it decrease Il-1 Il-6 TNF- α While TNF antibodies and TNF receptor blocker Have no effect on cardiac cachexia

Beta blockers:

Beta blockers

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If there is significant hypotension, bradycardia or dizziness when β -blocker is titrated slowly Lower the dose by 50 % If pt. has heart block or is in cardiogenic shock Discontinue the drug If there is hypotension alone is the problem Reduce ACEI dose first

Aldosterone receptor antagonist:

Aldosterone receptor antagonist spironolactone Eplerenone

Digoxin :


Hydralazine-isosorbide dinitrate (vasodilators):

Hydralazine-isosorbide dinitrate (vasodilators)

Angiotensin receptor blocker (ARB):

Angiotensin receptor blocker (ARB) Alternative to ACEI incase of cough & angioedema Best ARBS used in HF : Candesartan 32 mg/day Valsartan 160 mg 2 times/day Losartan 150 mg/day

Diuretics :


Renin inhibitor (Aliskiren):

Renin inhibitor (Aliskiren) Mechanism of action Renin inhibitors bind to the active site of renin and inhibit the binding of renin to angiotensinogen (rate-determining step). According to ACC (2013), it is failed to improve outcomes for patients with stable heart failure at 6 months or at 12 months

FDA approved 2008:

FDA approved 2008 left ventricular assist device used to replace the function of a failing heart

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