HF Pathophysiology Flashcards
Define HF
Affected ability of the ventricle to fill with or pump out blood
Heart fails to pump enough blood to meet the body’s metabolic demands
- affect the whole body
Classification
Focus on ventricle
Left ventricular dysfunction
• reduced LV ejection fraction
• preserved LV Ejection fraction
Right ventricular dysfunction
Movement of blood via ❤️
from body enter via SUPER VENA CAVA
RA - tricuspid valve - RV - pulmonary artery (to lungs get O2)
From lungs (oxygenated blood) LA - bicuspid valve - LV - Aorta ( to body)
LV dysfunction
types
effect
Types
•reduced EF - systolic dysfunction (HF-LVSD)
• preserved EF - diastolic dysfunction (HF-LVDD)
Effect
Stroke vol ⬇️ ->less in body
Systole vs diastole
Contraction vs relaxation
Pump out vs filling
Ejection fraction
Proprotion of blood in the V pumped our at each contraction
Amount pumped out after each filling
Reduced EF (systolic dysfunction) -most common
Enlarged, weakened ventricle -> pump out less than 40-50% ⬇️EF
Failing to pump due to - decreased myocardial contractility
(Impaired squeezing during systole)
Due to:
• coronary artery disease (ischemic- oxy sup decrease to part of heart , which turns hard = hard to contract -> HF)
•systemic arterial hypertension
•valvular heart disease
Preserved EF (diastolic dysfunction)
Stiff V (not able to expand much) fill less blood
Failing to pump due to - decreased ability of V to relax : •impaired filling • end diastolic vol⬇️ • increased diastolic LV stiffness
Contractility NOT impaired
Due to:
• coronary artery disease
• long-standing hypertension
Pattern of HFrEF
Condition of VOL overload
Vol overload Increased diastolic pressure (to fill more) Increased diastolic wall stress Chamber enlargement Vol overload
Pattern of HFpEF
Condition of PRESSURE overload
P overload Increased systolic pressure (to pump more) Increased systolic wall stress Wall thickening Less space P overload
Right V dysfunction
Lung related
Right V fails to pump effectively
Has to work harder to pump blood to lungs
Due to
-pulmonary hypertension secondary to lung disease
May also due to
- LVDysfunction
- tricuspid valvular disease
- congenital heart disease
- ischaemic affecting rv
Pulmonary hypertension leads to remodelling of right side ❤️
Constricted blood vessels in lungs (as fibrosis occur surrounding the vessel)
Weakened RV - as constantly work heard to push blood to ‘Pressured’ areas in lung
Compensatory mechanism
- good in short term (while heart work harder
-bad in long term
(Use drug to stop compensation)
- increased sympathetic tone (⬆️heart rate)
- activation of renin angiotension aldosterone system
- sodium and water retention (⬆️stoke vol)
- other neurohormonal adaptations
- cardiac remodelling
Neurohormonal cardiac compensation
SNS , RAAS
SNS and RAAS activates each other
SNS:
- vasoconstriction
- heart rate ⬆️
- contractility ⬆️
- RAAS activity ⬆️
RAAS
- vasoconstriction
- BP, aldosterone ⬆️
- fibrosis ⬆️( irreversible)
- Sympathetic tone ⬆️
Cardiac remodelling
Progression of disease
Cardiac Dilation
- seen in systolic dysfunction (thinning and weakening of wall)
- ventricles fail to pump adequate amount
- blood accumulate in V , myocardial fibres stretched and V become dilated
Cardiac hypertrophy
- muscle mass and wall thickness ⬆️