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Heart Failure

by B. Mahato

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  • What is heart failure (HF)?
    • It is a condition in which the cardiac output (CO) is so low that it can no longer meet the metabolic demand of the body, or it does so at a cost (see compensated HF below).
  • What are the signs and symptoms of HF?
(Source: http://www.nhlbi.nih.gov/health/health-topics/topics/hf/signs.html)
  • What are the different ways of categorizing HF?
    • Compensated vs decompensated
      • In the beginning CHF can be compensated, and then progress to decompensated
    • Chronic vs acute (and decompensated)
    • Right vs left sided
      • RHF signs/symptoms
        • symptoms due to fluid back up
          • dependent edema
          • hepatomegaly
          • ascites
      • LHF signs/symptoms
        • fatigue
        • cyanosis
        • dyspnea (SOB)
        • orthopnea
        • paroxysmal (intermittent) nocturnal dyspnea (PND)
        • pulmonary edema: can result in cough
    • Systolic vs diastolic
      • systolic: reduced ejection fraction (EF). Heart cannot pump/squeeze enough blood. The causes include:
        • decreased contractility due to ischemic heart disease and dilated CMP (MR, AR)
        • increased afterload due to HTN, AS.
      • diastolic: heart failure with preserved EF (HEPEF). Heart cannot relax enough. This can be due to:
        • left ventricular hypertrophy (LVH). This must be concentric hypertrophy.
  • What are the compensation mechanisms?
    • CO = HR x SV
    • So CO can be increased by increasing HR, or increasing SV. SV, in turn, can be increased by increasing preload (P), decreasing afterload (A), or increasing contractility (C). This can be remembered using the mnemonic SV PAC.
    • There are 3 broad mechanisms to bring about the above mentioned changes.
      • Frank-Starling curve shift
        • During early part of HF, if volume load (preload) increases (e.g. from MR), this leads to increased stroke volume according to the Frank-Starling law.  However, this compensatory mechanism not sustainable for long. In late HF, Frank starling curve shifts down and to the right: at a given preload (EDV), there is lower than normal SV. There is “less bang for the buck.” This is decompensation.
      • Neurohormonal changes: 3 broad mechanisms
        • Increased sympathetic tone (alpha-1, beta-1): 3 mechanisms
          • Increased HR
          • Increased contractility
          • Increased vasoconstriction
            • Arteries –> maintain BP –>  maintain perfusion pressure
            • Veins –> increase venous return –> increase preload
        • Renin-angiotensin-system (RAS)
          • Increased vasoconstriction
          • Increased preload (independent of that via vasoconstriction)
        • Anti-diuretic hormone (ADH)
          • Increased preload via water retention
      • Remodeling
        • Pressure loading lesion leads to concentric hypertrophy. Sarcomeres are laid in parallel, increasing the diameter of the cardiac wall.
        • Volume loading lesion leads to eccentric hypertrophy. Sarcomeres are laid in series, resulting in increased chamber size.
  • How are changes to preload, afterload, and contractility depicted on a pressure-volume loop graph?
    • increased preload: EDV increases (movement along EDPVR line)–>increased SV (ESV stays the same)
    • decreased afterload: Aortic valve opens at a lower pressure–> increased SV (ESV decreases)
    • increased contractility: ESPVR shifts up and to the left–> increased SV
                     (Graphs coming soon)
  • What is the downside of the compensation mechanisms?
(Coming soon)
  • What are the commonly used drugs to counteract the neurohormonal changes?
    • Beta-blockers: counteract increased sympathetic tone (increased HR, contractility, and vasoconstriction)
    • ACE inhibitors: counteract compensation via RAS system (vasoconstriction and increased preload)
    • Diuretics: counteract water retention (and hence increased preload) via ADH
  • What are the causes of acute CHF?
    • salt load –> increases preload
    • MI –> decreases contractility
    • acute valve rupture –> fluid backs up in the chamber–> increases preload. (Better explanation needed)
    • uncontrolled HTN –> increases afterload
    • med non-adherance
    • increased metabolic demand
      • infection
      • neoplasm
      • hyperthyroidism
    • increased fluid intake –> increases preload
  • What are the signs of congestion in HF?
    • Congestion/volume overload can result in
      • increased JVP, seen as jugular veinous distention (JVD)
      • fluid in and around the lung
        • fluid in the lung = pulmonary edema
        • fluid around the lung = pulmonary effusion
      • edema in dependent parts, e.g. lower extremities.
  • Why can there be a metabolic acidosis during HF?
    • HF –> insufficient oxygen supply (hypoxia) –> anaerobic oxidation –> increased lactic acid –> metabolic acidosis
  • How can congenital mitral valve prolapse (MVP) lead to HF?
    • The mitral valve balloons up in the left atrium. It can be benign initially, but can result in mitral regurgitation (MR) later. MR can lead to volume overload, and hence to heart failure. (Talk about 3 phases of MR: acute, chronic compensated, chronic decompensated. Maybe have a separate entry for MVP/MR.)
  • What is a left ventricular  heave (LV heave) ?
    • a diffuse lifting apical impulse felt during heart exam
  • What are the signs related to liver in CHF?
    • hepatomegaly
    • pulsatile liver
Acknowledgment:
The above note is based, at least in part, on the discussion during a Harvard Medical School tutorial lead by Dr. Sonja K Rakowski, M.D.  of Brigham and Women’s Hospital, Boston. Other participants included Annie Nguyen, Bisundev Mahato, Christine Linh-Minh Pham, Joshua Jeffrey Aaron Baugh, Kanika Bharti Sharma,  Lisa Y. Siu, Peter Kirkhoff Olds, and Samira Salari. Errors, if any, are my own.
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