McKenna's Pharmacology for Nursing, 2e

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C H A P T E R 4 4 Cardiotonic agents

and increased demand for oxygen and energy as the heart muscle must constantly contract harder. (Valvular heart disease is seen less often today owing to the success of cardiac surgery and effective treatment for rheumatic fever.) The end result of all of these conditions is that the heart muscle cannot pump blood effectively through­ out the vascular system. If the left ventricle pumps inefficiently, blood backs up into the lungs, causing pulmonary vessel congestion and fluid leakage into the alveoli and lung tissue. In severe cases, pulmonary oedema (manifested by rales, wheezes, blood-tinged sputum, low oxygenation and development of a third heart sound [S 3 ]) can occur. If the right side of the heart is the primary problem, blood backs up in the venous system leading to the right side of the heart. Liver congestion and oedema of the legs and feet reflect right- sided failure. Because the cardiovascular system works as a closed system, one-sided failure, if left untreated, eventually leads to failure of both sides, and the signs and symptoms of total HF occur. Clinincal management of a person with heart failure Compensatory mechanisms Because effective pumping of blood to the cells is essential for life, the body has several compensatory mechanisms that function if the heart muscle begins to fail (Figure 44.2). Decreased cardiac output stimulates the baroreceptors in the aortic arch and the carotid arteries, causing increased sympathetic activity (see Chapter 29). This stimulates an increase in heart rate, blood pressure and rate and depth of respirations, as well as a positive inotropic effect (increased force of con­ traction) on the heart and an increase in blood volume (through the release of aldosterone). The decrease in cardiac output also stimulates the release of renin from the kidneys and activates the renin–angiotensin– aldosterone system, which further increases blood pressure and blood volume. If these mechanisms work effectively, compensa­ tion is occurring and the person may show no signs or symptoms of HF. Over time, however, all of these effects increase the workload of the heart, contribut­ ing to further development of HF. Eventually, the heart muscle overstretches from the increased workload, and the chambers of the heart dilate secondary to the increased blood volume that they have had to handle. This hypertrophy (enlargement) of the heart muscle, called cardiomegaly , leads to inefficient pumping and eventually to increased HF. Cellular changes The myocardial cells are changed with prolonged HF. Unlike healthy heart cells, the cells of the failing heart

↓ Myocardial function or failure

↓ Cardiac output

↓ Blood flow to kidneys

Baroreceptor stimulation

Activation of renin–angiotensin system

Sympathetic activation

↑ BP ↑ P ↑ Respirations + Inotropic effect ↑ Cardiac output

↑ BP ↑ Cardiac output

↑ Aldosterone synthesis and release

↑ Na + retention ↑ K + excretion ↑ H 2 O retention

ADH release

↑ Blood volume

↑ Cardiac workload

FIGURE 44.2  Compensatory mechanisms in heart failure (HF), which lead to increased cardiac workload and further HF. ADH, antidiuretic hormone; BP, blood pressure; P, pulse.

seem to lack the ability to produce the energy needed for effective contractions. Movement of calcium ions into and out of the cell is no longer effective, leading to further deterioration because the muscle contracts inefficiently and is unable to deliver blood to the cardiac muscle. Clinical manifestations The person with HF presents a predictable clinical picture that reflects not only the problems with heart pumping, but also the compensatory mechanisms that are working to balance the problem. Radiography, electrocardiography (ECG) and direct percussion and palpation help to detect changes in the heart muscle and function. The heart rate will be rapid secondary to sym­ pathetic stimulation, and the person may develop atrial flutter or fibrillation as atrial cells are stretched and damaged. Anxiety often occurs as the body stimulates the sympathetic stress reaction. Heart murmurs may develop when the muscle is no longer able to support the papillary muscles that support the valve leaflets or the annuli that anchor the heart valves. Peripheral congestion and oedema occur as the organs and vessels become engorged waiting for blood to be pumped through the heart as a result of pump failure. With right-sided failure, there is enlarged liver (hepatomegaly); enlarged spleen (splenomegaly); decreased blood flow to the gastrointestinal (GI) tract