McKenna's Pharmacology for Nursing, 2e

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P A R T 8  Drugs acting on the cardiovascular system

To pump effectively, these muscles need to contract together. If this orderly initiation and conduction of impulses is altered, the result can be a poorly coordi- nated contraction of the ventricles that is unable to deliver an adequate supply of oxygenated blood to the brain and other organs, including the heart muscle. If these haemodynamic alterations are severe, serious com- plications can occur. For example, lack of sufficient blood flow to the brain can cause syncope or precipitate stroke; lack of sufficient blood flow to the myocardium Atrial fibrillation (AF) is a relatively common arrhythmia of the atria. It has been associated with coronary artery disease (CAD), myocardial inflammation, valvular disease, cardiomegaly and rheumatic heart disease. The cells of the atria are connected side to side and top to bottom, and are relatively simple cells. In contrast, the cells of the ventricles are connected only from top to bottom, with one cell connected only to one or two other cells. It is much easier, therefore, for an ectopic focus in the atria to spread that impulse throughout the entire atria, setting up a cycle of chaotic depolarisation and repolarisation. It is more difficult to stimulate fibrillation in the ventricles, because one ectopic site cannot rapidly spread impulses to many other cells, only to the cells connected in its two- or three-cell set. Fibrillation results in lack of any coordinated pumping action, because the muscles are not stimulated to contract and pump out blood. In the ventricles, this is a life- threatening situation. If the ventricles do not pump blood, no blood is delivered to the brain, the tissues of the body, or the heart muscle itself. However, loss of pumping action in the atria per se does not usually cause much of a problem. The atrial contraction is like an extra kick of blood into the ventricles; it provides a nice backup to the system, but the blood will still flow normally without that kick. DANGER OF BLOOD CLOTS One of the problems with AF occurs when it exists for longer than 1 week. The auricles (those appendages hanging on the atria to collect blood; see Chapter 42) fill with blood that is not effectively pumped into the ventricles. Over time, this somewhat stagnant blood tends to clot. Because the auricles are sacks of striated muscle fibres, blood clots form around these fibres. In this situation, if the atria were to contract in a coordinated manner, there is a substantial risk that those clots or emboli would be pumped into the ventricles and then into the lungs (from the right auricle), which could lead to pulmonary emboli, or to the brain or periphery (from the left auricle), which could cause a stroke or occlusion of peripheral vessels. ■■ BOX 45.1  Understanding atrial fibrillation

can exacerbate atherosclerosis and cause angina or myo- cardial infarction (MI).

Types of arrhythmias Various factors can change the cardiac rate and rhythm, resulting in an arrhythmia. Arrhythmias can be caused by changes in rate ( tachycardia , which is a faster-than-normal heart rate, or bradycardia , which is a slower-than-normal heart rate); by stimulation from

TREATMENT CHOICES Treatment of AF can be complicated if the length of time the person has been in AF is not known. If a person goes into AF acutely, drug therapy is available for rapid conversion. In some situations, digoxin has been effective in converting AF. Electrocardioversion, a DC current shock to the chest, may break the cycle of fibrillation and convert a person to sinus rhythm, after which the rhythm will need to be stabilised with drug therapy. If the onset of AF is not known and it is suspected that the atria may have been fibrillating for longer than 1 week, the person is better off staying in AF without drug therapy or electrocardioversion. Prophylactic oral anticoagulants are given to decrease the risk of clot formation and emboli being pumped into the system. Conversion in this case could result in potentially life-threatening embolisation of the lungs, brain or other tissues. SVT: ANOTHER DANGER The other danger of AF is rapid ventricular response to the atrial stimuli, a condition called supraventricular tachycardia (SVT). With the atria firing impulses, possibly 200 to 300 a minute, the number of stimuli conducted into the ventricles is erratic and irregular. If the ventricle is responding too rapidly—more than 120 times a minute— the filling time of the ventricles is greatly reduced, causing cardiac output to fall dramatically. In these situations, and when AF is anticipated (such as with atrial flutter or paroxysmal atrial tachycardia), drugs may be given to slow conduction and protect the ventricles from rapid rates. Flecainide and propranolol are often used to convert rapid SVT. Esmolol and adenosine are used intravenously to convert SVT with rapid ventricular response, which could progress to AF. IMPLICATIONS FOR HEALTH PROFESSIONALS Careful assessment is essential before beginning treatment for AF. If the person’s history cannot be established from information and medical records are not available, it is usually recommended that AF be left untreated and anticoagulant therapy started. This can pose a challenge for the nurse or midwife in trying to teach people about why their rapid and irregular heart rate will not be treated and explaining all of the factors involved in the long-term use of oral anticoagulants.