Heart Failure Flashcards
Define HF
An abnormality of cardiac structure/function leading to failure of the heart to deliver enough O2 to meet metabolic and physiological demands despite normal filling pressures
Define forward failure
reduced CO
When does forward failure occur?
When the LV contracts and cannot exert sufficient CO
Define backward failure
elevated A/V filling pressures
When does backward failure occur?
When either ventricles contract and are unable to reject all blood from chambers -> returning blood cannot refill due to no space
Describe HF-REF (systolic HF)
- reduced LVEF <40%
- inability of the heart to contract effectively
Describe HF-PEF (diastolic HF)
- normal LVEF > 40%
- inability of the heart to relax effectively
Describe the difference between acute and chronic HF
- rapid onset (hrs/days)
- sudden decline in cardiac function
- potentially life threatening
- chronic is slow onset (months/years)
State 4 causative factors of HF-REF
- intrinsic myocardial damage
- pressure overload
- volume load
- inadequate filling
Describe the pathophysiology of HF-PEF
Occurs a result of multiple comorbidites such as obesity, HPT, AF, Type 2 diabetes
State & describe 3 pathophysiological mechanisms of HF-REF
- cardiorenal model - fluid retention secondary to forward failure & reduced renal BF
- cardio-circulatory model - forward failure due to peripheral vasoconstriction & increases PVR
- neurohormonal model - maladpative neurohormonal activation -> cardiac remodelling
Describe how the neurohormonal model works
- Cardiac injury reduces CO output -> reduced BP & organ perfusion
- reflex activation of several neurohormonal pathways which are initially beneficial but then become harmful
- progressive deterioration of cardiac function
Describe the effects of the neurohormonal model on the sympathetic nervous system
- Increase in catecholamines, myocardial contractility, HR, systemic & pulmonary vasoconstriction
- Increased secretion of renin from juxtaglomerular apparatus of kidney activates RAAS
What effect do catecholamines (adrenaline & noradrenaline) have?
aggravates ischaemia, potentiate arrhythmias, directly toxic to myocytes, promote cardiac remodelling
Describe the renin-angiotensin-aldosterone system
- increased angiotensin II increases systemic vasoconstriction and peripheral SNS activation
- increased aldosterone increases Na & H2O retention, endothelial dysfunction, organ fibrosis
- angiotensin II & aldosterone are directly toxic to cardiac myoctyes & promote cardiac remodelling