Heart Failure Flashcards
notes
Define heart failure
clinical syndrome caused by the inability of the heart to supply sufficient blood flow to meet the body’s needs
Classification of heart failure?
Reduced EF (Ejection Fraction) or Preserved EF (HFrEF, HFmrEF, HFpEF) Acute or Chronic heart failure
Describe the NYHA Functional Class
4 : breathless at rest
1 : heart muscle damaged/abnormal but no symptoms
Describe heart failure epidemiology
- Prevalence 1-2% (6-10% in >65yo)
- In 2030 50% increase due to increasing prevalence rather than increasing incidence
- Commonest cause for emergency admission >65y
- 2% total NHS health care costs
- 70% of cost = hospital admissions
- Quality of life affected most
Prevalence in over 85?
1/7
Compensatory mechanisms of failing heart?
Ventricular dilatation Increased myocardial contractility Myocardial hypertrophy Sympathetic stimulation Renin-Angiotensin-Aldosterone-System (RAAS)
What’s the Frank-Starling Law?
-increased filling of the ventricle
-increased force of contraction
SV α LVEDV (left ventricular ejection end diastolic volume)
How does heart failure affect the Frank-Starling Law?
ventricle is over-stretched reducing ability to cross-link actin + myosin filaments.
Long term effects of compensatory mechanisms?
Continuous sympathetic activation Increased HR Increased preload Increased TPR Continuous neurohumoral activation
Describe the effect of continuous sympathetic activation
β-adrenergic downregulation + desensitization (less inotropic response)
Describe the effect of increased HR
Increased metabolic demands+myocardial cell death
Describe the effect of increased preload
Beyond limits of Starling’s law, pressure is transmitted to pulmonary vasculature –> pulmonary oedema
Describe the effect of increased TPR
Higher afterload –> decreased SV + CO
Describe the effect of continuous neurohumoral activation
- chronically elevated Ang II + aldosterone
- production of cytokines
- stimulate macrophages + fibroblasts
- myocardial remodelling
- loss of contractility
Equation of CO?
CO = SV x HR
Effect of ventricular dilation?
- maintains SV but exhausted
- pressure in stretched ventricle steadily increases
- restriction to filling + increased venous pressures
Why was β-blocker last option for HF?
negatively iontropic so reduce contractility of muscle but decreases afterload
Effect of increased sympathetic drive?
- decreased CO detected by baroreceptors
- central + peripheral chemoreflex activation induce A, NA, VP release
- adrenergic activation increases HR + contractility via vasoconstriction
- increased afterload
- increased cardiac work
- myocyte damage
Effect of β-blocker?
decrease BP, afterload, HR, contractility
Effect of renin-angiotensin cctivation?
-decreased CO
-renin-angiotensin activation:
vaoconstriction increases afterload
Na + H2O retention increases preload
-increases cardiac work
-myocyte damage via myocyte fibrosis, + eccentric ventricular hypertrophy