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
What happens as a result of increased ADH release?
Increased water retention & vasoconstriction
describe the 2 symptom complexes of clinical features of HF
Reduced CO - hypoperfusion symptoms
- fatigue & decreased exercise tolerance
Impeded venous return - congestive symtpoms
- pulmonary & systemic congestion
- ankle oedema, cough, elevated JVP
Describe the classification & staging of HF
classification Class I (asymptomatic) -> Class IV (severe)
staging stage A (high risk) -> Stage D (end/refractory)
State the different drugs used to manage chronic HF and which model they apply to
Cardiorenal - diruetics, inotropes
Cardiocirculatory - inotropes, vasodilators
Neurohormonal - ACEIs, BBs, ARBs, ARNIs, aldosterone antagonists
Describe the integrated approach for management of chronic HF
general measures:
- Reduces cardiac workload
- Restrict dietary salt & fluid intake
- Smoking cessation & alcohol moderation
Drug therapy
Other - heart transplant
List the treatment goals for CHF
- improve CO (decrease forward failure)
- reduce A/V filling pressures
- stop/reverse cardiac remodelling
State 3 treatment strategies of HF
- myocardial stimulation
- reduce cardiac workload
- arrest/reverse cardiac remodelling
Describe the treatment of myocardial stimulation
increases myocardial contractility with inotropic agents
Describe treatment of reducing cardiac workload
reduces afterload/preload with diuretics/vasodilators
Describe how cardiac remodelling is reversed
inhibits chronic neurohormonal activation with ACEIs, BBs, ARBs, ARNIs, aldosterone antagonists
