What is heart disease?
structural/functional abnormality
What is heart failure
inadequate output or needs high filling pressures.
Compliance definition?
ΔV/ΔP (distensibility); stiffness = 1/compliance.
What is passive compliance?
the inherent elasticity and distensibility of blood vessels or heart chambers, allowing
them to expand and store blood without active muscle contraction
what is active compliance?
the dynamic ability of arteries to expand and contract, which can be altered or regulated
by smooth muscles in their walls.
What determines pressure in a segment?
≈ Volume ÷ Compliance (or Volume × Stiffness).
Equation for flow?
≈ ΔPressure ÷ Resistance.
Where is resistance clinically meaningful?
Precapillary arterioles (small radii).
Biggest determinant of resistance?
Radius^−4.
Normal valves → resistance?
Essentially negligible.
Preload mainly reflects...
Ventricular end-diastolic volume (filling).
Afterload approximated by...
(Systolic pressure × Radius) ÷ Wall thickness.
↑ Afterload → ESV?
Increases.
↑ Contractility → ESV?
,Decreases.
Cardiac output equation?
SV × HR
SV equation?
EDV – ESV
Effect of ↑ HR on diastolic filling?
Decreases (less time).
A-fib effect on pulses?
Irregular rate with variable/weak pulses due to variable filling.
Where is most blood volume?
Systemic veins.
Why do veins hold the most blood?
High compliance + large capacity.
Venoconstriction effect on RA flow?
↑ Venous pressure → ↑ VR to RA.
Angiotensin II effect on venous system?
↓ Compliance (↑ stiffness) → ↑ venous pressures.
Why do high venous pressures cause edema?
↑ Capillary hydrostatic pressure → ↑ filtration.
Left-sided failure edema location?
Lungs (pulmonary edema).
Right-sided failure edema location?
Systemic (legs/abdomen—ascites).
Lymphatics prevent edema until...
Filtration > lymph drainage capacity.
Concentric hypertrophy stimulus?
Pressure overload (↑ afterload).
Eccentric hypertrophy stimulus?
Volume overload (↑ preload).
Concentric outcome?
Wall thickening, relatively normal chamber size; normalizes wall stress.
, Eccentric outcome?
Chamber dilation with proportional wall mass increase.
MMVD (dogs) primary lesion → sequence?
Mitral regurg → volume overload → eccentric LV hypertrophy.
DCM core defect?
Primary contractile weakness → dilation + low forward output.
HCM core defect?
Primary myocardial thickening → diastolic dysfunction.
How DCM breaks compensation?
Fails to generate pressure; dilation worsens MR/volume overload → neurohormonal
drive.
Major systems in chronic HF?
RAAS, SNS, vasopressin.
Short term effects of neuroendocrine activation?
maintains BP
Long term effects of neuroendocrine activation?
fibrosis, Na/H2O retention, vasoconstriction.
Hypovolemia (dehydration) hemodynamics?
↓ Preload → ↓ SV/CO → hypotension.
Rapid fluid bolus effect on pressures?
Increases venous/arterial pressures (if compliance unchanged).
Renal hypoperfusion: two causes?
↓ Arterial pressure gradient or ↑ renal arteriolar resistance.
High venous pressures risk?
Edema upstream of the failing side.
Diuretics main hemodynamic effect?
↓ Volume → ↓ venous pressures → relieve edema
ACE inhibitors key effects?
↓ Ang II → vasodilation, ↓ venous stiffness, ↓ remodeling
Arteriolar vasodilators lower BP by...
↓ Precapillary resistance → ↓ arterial volume/pressure.