Heart failure Flashcards
Lambl excrescences
Fibrous thickening of valves in the aging heart
Brown atrophy
Lipofuscin deposits in aging heart
Causes of high output heart failure
Thyrotoxicosis induced
Anemia induced
tachycardia induced
Causes of increased afterload contributing to HF
Severe HTN
Severe aortic stenosis
Pathologic causes of increased preload contributing to HF
Aortic regurgitation
Mitral regurgitation
MI
Dilated cardiomyopathy
Physiologic cause of increased preload
Exercise
Effect of increased contractility on isovolumic P/V curve
Shifts left
Six principal mechanisms of CVS dysfunction
Pump failure
Flow obstruction
Regurgitant flow
Shunted flow
Disorders of cardiac conduction
Rupture of the heart or major vessel
Causes of systolic dysfunction causing reduced ejection fraction
Impaired ventricular contractility
Increased afterload
Change in PV loop in systolic dysfunction
Shifts right and SV decreases
PV loop in compensation by Frank Starling mechanism
Increased preload, SV, and contraction
Extends to the right
PV loop compensation by catecholamine release
Increased HR, contractility, SV, and filling
PV loop shifts left
PV loop compensation by increasing ventricular volume or elasticity
Increased EDV and SV, slightly right
Causes of diastolic relaxation or ventricular filling leading to diastolic dysfunction with preserved EF
LV hypertrophy
Restrictive cardiomyopathy
Myocardial fibrosis
Transient MI
Pericardial constriction or tamponade
Amyloid deposition
PV loop changes in heart failure with preserved ejection fraction
EDV decreased and increased LVEDP
Shifts up and left
Most common cause of RHF
LHF
Compensatory response of the myocardium to increased mechanical work
Cardiac hypertrophy
Collective molecular, cellular, and structural changes that occur as a response to injury or changes in loading conditions in the heart
Ventricular remodeling
Arrangement of new sarcomeres in pressure overload of the heart
In parallel –> thicken
Arrangement of new sarcomeres in volume overload of the heart
In series –> elongate
Changes that regulate excitation-contraction that occur in the failing cardiac myocyte that contribute to depressed LV systolic function in HF
Decreased function of SR Ca adenosine triphosphates (SERCA2A)
Decreased Ca uptake into the SR and hyperphosphorylation of the ryanodine receptor
Ca leakage from the SR
Changes that occur in the cross-bridges that occur in the failing cardiac myocyte that contribute to depressed LV systolic function in HF
Decreased expression of alpha-myosin heavy chain
Increased expression of beta-myosin heavy chain
Myocytolysis
Disruption of the cytoskeletal links between the sarcomeres and the ECM
Activation of neurohumoral systems that occur in the failing cardiac myocyte that contribute to depressed LV systolic function in HF
Adrenergic nervous system
Renin-angiotensin-aldosterone system
Increased production of ADH
Produced when ventricular myocardium is subjected to hemodynamic stress and able to be detected in the blood
BNP
Effect of the release of natriuretic peptides
Excretion of Na and water
Vasodilation
Inhibition of renin secretion
Antagonism of the effects of ATII on aldosterone and vasopressin levels
Function of enothelin-1, released in HF
Potent vasoconstrictor
Regions of liver affected by cell death in RHF
Centrilobular regions
Possible causes of high output HF
Hyperthyroidism
Severe anemia
Thiamine deficiency
Septic shock
Trauma
Surgical shunt - AV fistula
Paget disease
Type of hypertrophy seen in endurance athletes
Eccentric
Type of hypertrophy seen in strength athletes
Concentric
