HEART FAILURE Flashcards Preview

Term 5 - PathoPhysio > HEART FAILURE > Flashcards

Flashcards in HEART FAILURE Deck (19):

  • Clinical Presentation:

  • Breathlessness (dyspnea) particularly when lying down (orthopnea) or at night [paroxysmal nocturnal dyspnea (PND)] 
  • Blood-tinged sputum (hemoptysis) 
  • Chest pain (occasional) 
  • Fatigue, nocturia, and confusion


Etiology of LVF:

  • Inappropriate workloads placed on the LV:
    • Volume overload (example: MR or AR) 
    • Pressure overload (example: systemic hypertension) 
  • Restricted filling of the LV (example: constrictive pericarditis) 
  • Myocardial loss - as in MI 
  • Decreased myocardial contractility – as in poisoning or infections


Hemodynamic Changes in Systolic dysfunction

  • Pressure-volume relationship shows a low ejection with a high or low ventricular pressure during ejection
  • Reduction in the stroke volume (SV) & a decrease in cardiac output (CO) (CO = SV x HR) 
  • Reduction in ejection fraction (EF)


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Hemodynamic Changes in Systolic dysfunction

  1. Increased preload (Frank-Starling relationship) Heart operates at a larger end-diastolic volume & pressure
  2. Increased release of catecholamines
  3. Cardiac muscle hypertrophy and ventricular volume increases


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  • Diastolic dysfunction (also called HF with preserved systolic function or HF with preserved EF)
  • Causes?

  • Causes: Any disease that produces 
    • Increased stiffness of ventricle (Eg:Hypertrophic cardiomyopathy, Longstanding hypertension and ischemia)
    • Decreased relaxation (Eg:constrictive pericarditis)


Hemodynamic Changes in Diastolic dysfunction

  • In diastolic dysfunction ventricular filling is impaired, resulting in reduced ventricular filling and increased end-diastolic pressure.
  • Diastolic pressure-volume curve is shifted to the left, with an accompanying increase in left ventricular end-diastolic pressure
  • Contractility and ejection fraction (EF) remain normal
  • Reduced LV filling can produce low CO and systemic symptoms (heart failure)
  • Elevated left atrial pressure can produce pulmonary congestion


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Stroke Volume (SV)

  • SV is the volume of blood ejected by each ventricle in a beat
  • It is the difference between end diastolic volume and end systolic volume
  • SV = (EDV – ESV) ml per beat
  • SV increases with an increase in EDV
  • SV increases with a decrease in ESV
  • When both increase in EDV and decrease in ESV occur, SV increases maximally


Ejection Fraction (EF)

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Neurohumoral Changes in Heart Failure:

  • Increased sympathetic activity
  • Activation of Renin-Angiotensin- Aldosterone System (RAAS)
  • Increased release of ADH (vasopressin)
  • Release of cytokines and peptides


  • Neurohumoral Changes 
  • Increased sympathetic activity:

  • Occurs early in the heart failure
  • Elevated plasma norepinephrine levels
  • Increased cardiac contractility and rate
  • Initially it may be helpful to improve SV
  • Continued effect leads to increased preload and afterload which can worsen heart failure


  • Neurohumoral Changes 
    • Activation of renin-angiotensin-aldosterone system (RAAS):

  • Reduced renal blood flow → Activation of RAAS.
  • Consequence of continued hyperactivity of RAAS initiates a vicious cycle:
  • Severe vasoconstriction combined with increased plasma volume → Increased both preload & afterload → Further reduction in cardiac output → Further reduction in glomerular filtration rate → RAAS activation (cycle repeats)


  • Neurohumoral Changes:
  • Other cytokines/peptides in heart failure:

  • The interleukins (ILs) – IL-1 accelerates myocyte hypertrophy
  • Tumor necrosis factor-α (TNF-α) – causes myocyte hypertrophy and cell death (apoptosis)
  • Endothelin – stimulates vasoconstriction in pulm vasculature, myocyte growth, myocardial fribrosis
  • Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) – cause natriuresis and vasodilatation


B-type natriuretic peptide (BNP):

  • Also known as brain natriuretic peptide 
  • Elevated when ventricular filling pressures are high (myocyte stretching) 
  • Sensitive in patients with symptomatic heart failure (due to systolic or diastolic dysfunction) but less specific in older patients, women, and patients with COPD 
  • Helpful in emergency department in the diagnosis of acute decompensated heart failure  
  • Less sensitive and specific to diagnose heart failure in the chronic setting