Heart failure is defined as the inability of the heart to produce adequate cardiac output. The cardiac output of the heart depends on the heart rate and stroke volume of the heart. Stroke volume is the amount of blood ejected by the ventricle during contraction (Mosby 1998). There are 3 main determinants of stroke volume: preload, afterload, and contractility. Preload is the pressure in the left or right ventricle at the end of diastole. It is also known as left or right ventricular end diastolic volume (LVEDV or RVEDV). Afterload is the pressure that the left or right ventricle must overcome to eject blood form the heart. This can be greatly affected by the pressure in the vasculature (peripheral or pulmonary vascular resistance). Contractility is the ability of the heart to contract to expel blood during each contraction (McCance & Huether 2006).
Hypertension can have a great affect on the afterload of the left ventricle. Hypertension increases the peripheral vascular resistance in the body. This in turn causes the heart to overcome a greater afterload to obtain an adequate cardiac output. Overtime, untreated hypertension can lead to structural changes in the heart, which can eventually lead to heart failure (McCance & Huether 2006). In response to the increased workload and oxygen demand the cardiac muscle in the left ventricle will hypertrophy, or enlarge. This is the heart’s attempt to produce an adequate cardiac output for the rest of the body. The mass of the heart is increased due to the replication of more myofibrils and thickening of myocytes in the heart tissue (Taccetta-Chapnick 2002). As the muscle tissue enlarges it is able to keep up with the increased workload and oxygen demands. Over time, the muscle will become too big and inhibit the ability of the heart to adequately pump oxygen. This resulting ischemia and hypertrophy leads to a remodeling of the heart tissue. In ventricular remodeling, the muscle tissue is destroyed when the myofibrils are broken down and fibrous tissue and collagen are deposited between the cells or replace the cells entirely. This causes a change in the actual myofibril, which can leave them larger than normal. This change in the actual structure of the heart muscle further impairs the contractile ability of the heart and cardiac output is further reduced (McCance & Huether 2006).
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