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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
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
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.
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.
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BOX 45.1
Understanding atrial fibrillation
