الفهرس 
Anatomical and Pathophysiological AspectOnly 14 pages are availabe for public view
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Abstract
Chronic heart failure (HF), a clinical syndrome in which abnormalities of ventricular function and neurohormonal regulation lead to pulmonary venous congestion, exercise intolerance, and decreased life expectancy, remains the one major cardiovascular (CV) disorder that has increased both in incidence and prevalence in recent years.
Heart failure can be broadly subdivided into two distinct forms, and distinguishing between the two forms is often difficult. Diastolic heart failure is due to inadequate ventricular relaxation preventing adequate end-diastolic filling (HF with preserved systolic function). This type of heart failure affects the left ventricle (LV). The second is the more common, systolic heart failure is due to inadequate force generation to eject blood normally. This type of heart failure can affect either ventricle but failure of the left heart is more common.
A four-stage classification of HF is recently recommended, according to the progressive nature of HF and the importance of neurohormonal antagonism in trying to delay its progression.
HF may be the end result of hypertension, coronary artery disease, valvular heart disease, cardiomyopathy, as well as a variety of other conditions. A combination of changes in size, shape and function of the LV, commonly termed LV Remodeling which results in neurohumoral stimulation, is a key event in the development of HF, leading to progressive impairment of function, and ultimately resulting in reduced contractile function and ejection fraction.
The pharmacological therapy of chronic HF has evolved dramatically during the last 20 years, where digoxin has moved to the end of the list, Angiotensin Converting Enzyme (ACE) inhibitors are first line drugs, and β-adrenergic blockers that were classically contraindicated, are now known to reduce mortality and symptomatology.
The rationale is towards antagonism of the neurohumoral changes that initiate, perpetuate and aggravate ventricular dysfunction.
Non pharmacological and surgical options include Cardiac Resynchronization Therapy, Ventricular Assist Devices, revascularization of hibernating myocardium, Ventricular Restoration Surgery (Left Ventricular Reshaping), correction of mitral regurge and heart transplantation.
A comprehensive preoperative evaluation of coronary, valvular and myocardial pathology and the presence of pulmonary hypertension, is needed for ensuring hemodynamic stability during induction and maintenance of anesthesia.
The anesthetic plan should take into account other extracardiac comorbidities (hepatic, renal, cerebral). Careful intraoperative management of these patients should include proper choice of anaesthetic technique (general or regional) and proper monitoring for prevention and early detection of cardiac complication.
Anesthesia goal are to maintain stable haemodynamic, control pain, maintenance of body temperature, control heart rate and avoid anemia.
Postoperative period appears to present the highest risk for cardiac morbidity. So good postoperative management is needed to avoid tachycardia, stress and increased oxygen consumption, which may not be tolerated by patients with markedly impaired LV function.