LipPharmCh16HeartFailure.txt

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mcaster24
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76912
Filename:
LipPharmCh16HeartFailure.txt
Updated:
2011-04-03 04:50:41
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Heart failure drugs
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Heart failure drugs
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  1. Heart Failure Overview
    Heart failure (HF) is a complex, progressive disorder in which the heart is unable to pump sufcient blood to meet the needs of the body. Its car-dinal symptoms are dyspnea, fatigue, and fuid retention. HF is due to an impaired ability of the heart to adequately fll with and/or eject blood. It is often accompanied by abnormal increases in blood volume and inter-stitial fuid, hence the term “congestive” HF because symptoms include dyspnea from pulmonary congestion in left HF, and peripheral edema in right HF. Underlying causes of HF include arteriosclerotic heart disease, myocardial infarction, hypertensive heart disease, valvular heart dis-ease, dilated cardiomyopathy, and congenital heart disease. Left systolic dysfunction secondary to coronary artery disease is the most common cause of HF, accounting for nearly 70 percent of all cases. The number of newly diagnosed patients with HF is increasing, because more individuals now survive acute myocardial infarction.
  2. Role of Physiologic Compensatory Mechanisms in Progression of HF
    Chronic activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis is associated with remodeling of cardiac tissue, characterized by loss of myocytes, hypertrophy, and fbrosis. The geometry of the heart becomes less elliptical and more spheri-cal, interfering with its ability to efciently function as a pump. This prompts additional neurohumoral activation, creating a vicious cycle that, if left untreated, leads to death
  3. Goals of pharmacologic intervention in HF
    illeviate symptoms, slow disease progression, and improve survival.

    • six classes of drugs have been shown to be efective:
    • 1) inhibitors of the renin-angiotensin system, 2) β-adrenoreceptor blockers,
    • 3) diuretics,
    • 4) inotropic agents,
    • 5) direct vasodilators, and
    • 6) aldosterone antagonists

    • Depending on the severity of cardiac failure and individual patient factors, one or more of these classes of drugs are administered. Benefcial efects of pharmacologic intervention include
    • 1. reduction of the load on the myo-cardium,
    • 2. decreased extracellular fuid volume,
    • 3. improved cardiac contractility,
    • 4. slowing of the rate of cardiac remodeling.

    Knowledge of the physiology of cardiac muscle contraction is essential to understand-ing the compensatory responses evoked by the failing heart as well as the actions of drugs used to treat HF
  4. PHYSIOLOGY OF MUSCLE CONTRACTION: Overview
    The myocardium, like smooth and skeletal muscle, responds to stimulation by depolarization of the membrane, which is followed by shortening of the contractile proteins and ends with relaxation and return to the resting state. However, unlike skeletal muscle, which shows graded contractions depend-ing on the number of muscle cells that are stimulated, the cardiac muscle cells are interconnected in groups that respond to stimuli as a unit, contract-ing together whenever a single cell is stimulated.
  5. PHYSIOLOGY OF MUSCLE CONTRACTION: Action Potential
    Cardiac muscle cells are electrically excitable. However, unlike the cells of other muscles and nerves, the cells of cardiac muscle show a spon-taneous, intrinsic rhythm generated by specialized “pacemaker” cells located in the sinoatrial and atrioventricular nodes. The cardiac cells also have an unusually long action potential, which can be divided into fve phases (0–4). Figure 16.2 illustrates the major ions contributing to depolarization and polarization of cardiac cells. These ions pass through channels in the sarcolemmal membrane and, thus, create a current. The channels open and close at diferent times during the action potential. Some respond primarily to changes in ion concentration, whereas oth-ers are sensitive to adenosine triphosphate, or to membrane voltage.
  6. PHYSIOLOGY OF MUSCLE CONTRACTION: Cardiac contraction 1: OverviewSources of Free Intracellular Calcium
    • Overview:
    • Cardiac muscle cells are electrically excitable. However, unlike the cells of other muscles and nerves, the cells of cardiac muscle show a spon-taneous, intrinsic rhythm generated by specialized “pacemaker” cells located in the sinoatrial and atrioventricular nodes. The cardiac cells also have an unusually long action potential, which can be divided into fve phases (0–4). Figure 16.2 illustrates the major ions contributing to depolarization and polarization of cardiac cells. These ions pass through channels in the sarcolemmal membrane and, thus, create a current. The channels open and close at diferent times during the action potential. Some respond primarily to changes in ion concentration, whereas oth-ers are sensitive to adenosine triphosphate, or to membrane voltage.

    • Sources of Free Intracellular Calcium:
    • 1. Calcium comes from several sources. The frst is from outside the cell, where opening of voltage-sensitive calcium channels causes an immediate rise in free cytosolic calcium. Calcium may aslo enter by exchange with sodium. Calcium is also released from the sarcoplasmic reticulum and mitochondria, which further increases the cytosolic level of calcium (Figure 16.3).

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