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    Arsalan Azimi
    Senior Research Fellow
    Rockingham Medical Research Center

    Heart Failure (HF) develops when the heart works effectively but not efficiently (Compensated HF) or when the heart’s function is neither efficient nor effective (Non-compensated HF). In other words, HF develops when the heart fails to maintain the required circulation of body organs or when the heart can do so, but only with the help of compensatory mechanisms.
    Congenital and/or acquired structural alterations of the pulmonary and peripheral circulation, cardiac valves, coronary circulation, endocardium, myocardium, and pericardium impair physiological function of the heart.
    Coronary Artery Disease, high blood pressure, and previous ischemic heart diseases are the most common etiologies of heart failure.
    In general adult population, the prevalence of known HF is generally estimated at 1% to 2%.
    Course of Disease:
    When the heart fails to maintain the required circulation of body organs, compensatory mechanisms such as renin-angiotensin-aldosterone system [RAAS], and sympathetic nervous system [SNS] help the heart to sustain adequate cardiac performance and maintain effective circulation.
    Synergistic effects of RAAS and SNS activation, increase cardiac output, pulmonary and systemic vascular resistance, afterload, preload, and myocardial energy expenditure.
    Although both RAAS and SNS play important compensatory roles in the failing heart, they cause extra work for the heart, and their prolonged activity leads to ventricular hypertrophy, dilation, fibrosis, remodeling, and further cardiac dysfunction.
    In addition, prolonged activity of SNS and subsequent downregulation of β1-adrenoceptors decreases efficiency of both SNS and RAAS mechanisms.
    At this stage, the heart can no longer overcome the increased afterload, and as pulmonary venous and capillary pressures increase, fluid flux out of the capillaries into the alveoli and interstitium and cardiogenic pulmonary edema develops. As a result, deoxygenated blood from the right side of the heart does not participate in gas exchange and pulmonary shunting occurs which leads to hypoxia, pulmonary vasoconstriction, increased right ventricular afterload, and development of Cor-Pulmonale.
    As the patient develops Cor-Pulmonale and right heart pressure increases, venous blood cannot return to the heart, and the patient develops peripheral edema.
    -Respiratory Shunt: Elevated left-sided heart pressure transmits backward into the pulmonary circulation and the patients develop pulmonary edema. Subsequently systemic venous blood does not participate in gas exchange in the pulmonary capillaries and a respiratory shunt ensues.
    -Metabolic Shunt: As elevated right-sided heart pressure is transmitted backward into the Inferior Vena Cava (IVC) and portal vein, it impairs hepatic, gastrointestinal, and renal effective circulation. Subsequently, nutrients cannot be properly absorbed and metabolized and a metabolic shunt develops.
    In this regard, blood cannot deliver sufficient oxygen or nutrients to the cells or transport metabolic waste products away from those cells. In other words, as the disease progresses, respiration and metabolism first lose their efficiency and then their efficacy.
    Heart failure is a sequence of complex chains of events that reinforce themselves through a feedback loop in which complications and causes intensify and aggravate each other, leading to worsening of the situation. Accordingly, both underlying causes and their complications should be treated. Current treatments include diuretics, ACE inhibitors, angiotensin II receptor blockers, beta-blockers, aldosterone antagonists, digitalis, specialized implantable pacemakers, and correction of the underlying disorders.

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