S2: Heart Failure Flashcards
What is Heart Failure?
It is a clinical syndrome (collection of sign and symptoms) caused by inability of the heart to supply sufficient blood flow to meet the body’s need
List mechanical causes of pump failure
- Impaired ventricular function
- Pressure overload of ventricle
- Inflow obstruction of ventricle
- Valvular disease
- Volume overload of ventricle
What diseases cause impaired ventricular function?
- Myocardial infarction
- Cardiomyopathy
What diseases cause impaired pressure overload of ventricle?
- Systemic hypertension
- Pulmonary hypertension
What diseases cause inflow obstruction of ventricle?
- Restrictive cardiomyopathy (heart is small and cannot stretch to allow blood in)
- Diastolic heart failure
- Mitral stenosis
What diseases cause Valvular disease?
- Aortic stenosis/regurgitation
- Mitral stenosis/regurgitation
- Tricuspid stenosis/regurgitation
What diseases cause Volume overload of ventricle?
- Ventricular and Atrial septal defect (VSD and ASD) –> too much blood on one side of the heart
- Patent ductus arteriosus (PDA)
What are the 3 ways Heart Failure can be classified?
- Reduced ejection fraction, preserved ejection fraction or midrange ejection fraction
- Acute or Chronic
- Left ventricular failure vs Right ventricular failure
Describe class I and class IV of the NYHA Functional Class for heart failure
Class I : No limitations even with physical activity
Class IV: Inability to carry out any physical activity without discomfort. Symptoms also during rest - this is severe heart failure.
Why is heart failure increasing?
- HF is very strongly related to age and we live in an aging population in the UK.
- The other major factor for increasing prevalence of HF is better treatment for HF so it is no longer a fatal condition but a long term condition so patients with HF will live longer.
What are the compensatory mechanisms of a weakened heart?
- Ventricular dilation - natural (to maintain SV at reduced ejection fraction because there is a larger volume to start with)
- Increased myocardial contractility (sympathetic drive increases in surviving parts of the heart)
- Myocardial hypertrophy
- cardiac failure –> sustained increase in chamber radius (dilation)
- Laplace’s law ( radius decreases increases CO) - Renin-Angiotensin-Aldosterone System (RAAS) - increasing BV and therefore pressure for a short term solution
- Sympathetic Stimulation
Describe Deleterious effects of prolonged compensatory mechanism
- Continuous sympathetic activation:β-adrenergic downregulation and desensitization ‘immune’ (less inotropic response)
- Increased heart rate:Increased metabolic demands which will increase myocardial cell death
- Increased preload:Beyond limits of Starling’s law (ventricular dilation), pressure is transmitted to pulmonary vasculature leading to pulmonary oedema
- Increased total peripheral resistance:Higher afterload leading to decreased stroke volume and cardiac output
- Continuous neurohumoral activation:Chronically elevated angiotensin-II and aldosterone trigger production of cytokines, which stimulate macrophages and stimulate fibroblasts resulting in myocardial remodelling which leads to loss of contractility.
Describe the frank-starlings curve
- In health, increased filling of the ventricle (heart will dilate) results in increased force of contraction. SV increases as LVEDV increases
- In heart failure this mechanism fails, as the ventricle is over-stretched reducing ability to cross-link actin and myosin filaments (weaken).
Describe ventricle dilation as a compensatory mechanism for HF
- CO = SV x HR
- The ventricle dilates to maintain SV
- When this compensatory mechanism is exhausted, the pressure in the stretched ventricle steadily increases resulting in restriction to filling (back pressure into LA - pulmonary oedema) and increased venous pressures
- Preload can be reduced by vasodilators (GTN) and diuretics
What are the two main drugs prescribe for heart failure?
Beta blockers which block sympathetic NS and reduce HR and contractility
Ace inhibitors which block the activation of RAAS which decreases afterload, preload and Na+ and H2O retention.