Heart. Thegross cardiacfindingsdependontheunderlyingdiseaseprocess,forexample,myocardialinfarctionorvalvulardeformitiesmaybepresent.Withtheexceptionoffailureduetomitralvalvestenosisorrestrictivecardiomyopathies(describedlater),theleftventricleusuallyishypertrophiedandcanbedilated,sometimesmassively.Leftventriculardilationcanresultinmitralinsufficiencyandleftatrialenlargement,whichisassociatedwithanincreasedincidenceofatrialfibrillation.Themicroscopic changesinheartfailurearenonspecific,consistingprimarilyofmyocytehypertrophywithinterstitialfibrosisofvariableseverity.Superimposedonthisbackgroundmaybeotherlesionsthatcontributetothedevelopmentofheartfailure(e.g.,recentoroldmyocardialinfarction).
Lungs. Inacuteleft-sidedheartfailure,risingpressureinthepulmonaryveinsisultimatelytransmittedbacktothecapillariesandarteriesofthelungs,resultingincongestionandedemaaswellaspleuraleffusionduetoanincreaseinhydrostaticpressureinthevenulesofthevisceralpleura.Thelungsareheavyandboggy,andmicroscopicallyshowperivascularandinterstitialtransudates,alveolarseptaledema,andaccumulation of edema fluid in the alveolar spaces.Inchronicheartfailure,variablenumbersofredcellsextravasatefromtheleakycapillariesintoalveolarspaces,wheretheyarephagocytosedbymacrophages.Thesubsequentbreakdownofredcellsandhemoglobinleadstotheappearanceofhemosiderin-ladenalveolarmacrophages—so-calledheart failure cells—thatreflectpreviousepisodesofpulmonaryedema.
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Dyspnea (shortness of breath) on exertion is usually the earliest and most significant symptom of left-sided heart failure; cough is also common as a consequence of fluid transudation into air spaces. As failure progresses, patients experience dyspnea when recumbent (orthopnea); this occurs because the supine position increases venous return from the lower extremities and also elevates the diaphragm. Orthopnea typically is relieved by sitting or standing, so patients usually sleep in a semi-seated position. Paroxysmal nocturnal dyspnea is a particularly dramatic form of breathlessness, awakening patients from sleep with extreme dyspnea bordering on feelings of suffocation.
Other manifestations of left ventricular failure include an enlarged heart (cardiomegaly), tachycardia, a third heart sound (S3), and fine ráles at the lung bases, caused by the opening of edematous pulmonary alveoli. With progressive ventricular dilation, the papillary muscles are displaced outward, causing mitral regurgitation and a systolic murmur. Subsequent chronic dilation of the left atrium can cause atrial fibrillation, manifested by an “irregularly irregular” heartbeat. Such uncoordinated, chaotic atrial contractions reduce the atrial contribution to ventricular filling, thus reducing the ventricular stroke volume. Atrial fibrillation also causes stasis of the blood (particularly in the atrial appendage), frequently leading to the formation of thrombi that can shed emboli and cause strokes and manifestations of infarction in other organs.