Tachycardia

This is the term used by the medical profession to describe
a fast heart rate of greater than 100 per minute. Tachycardias
include:
1. Sinus tachycardia
2. Paroxysmal atrial tachycardia (PAT)
3. Atrioventricular nodal reentrant tachycardia (AVNRT)
4. Atrial fibrillation
5. Atrial flutter
6. Wolff-Parkinson-White syndrome (WPW)
7. Ventricular tachycardia

These tachycardias are usually differentiated for diagnostic
purposes into narrow QRS and wide QRS and then
into regular or irregular tachycardias.

A. Sinus Tachycardia
When the fast beat arises from the normal sinus node
pacemaker, it is called a sinus tachycardia. This is a normal
physiologic occurrence during exercise, infections causing
fever, anxiety states, loss of blood, dehydration, and
thyroid overactivity. This is one of the most common
abnormal tachycardias occurring in young healthy adults.

B. Paroxysmal Atrial Tachycardia
Those who have episodes of very fast heart beat, usually
150–190 beats per minute, may have a condition known
as PAT. If episodes are frequent, drug treatment may be
necessary. The term paroxysmal atrial tachycardia was
introduced more than 50 years ago and was formerly used
to include AVNRT, but these two conditions have subtle
differences. Most cases called PAT are truly AVNRT.
There is no conclusive evidence that excessive adrenaline
triggers PAT.

In a few individuals, excessive adrenaline may play a
role during stress or a heart attack. Excessive adrenaline
is liberated in the heart muscle during a heart attack and
increases the occurrence of premature beats and other
abnormal heart rhythms. Pacemaker cells outside the sinus
node commence an electrical discharge and take over the
heart rhythm for up to a few hours. The ECG reveals a
P-wave that precedes the QRS and its contour is different
from the sinus P-wave; the rhythm may be regular or
irregular. Some cases are caused by digoxin toxicity.

C. Atrioventricular Nodal Reentrant
Tachycardia
The most common type of paroxysmal narrow regular
tachycardia is one originating in the AV node; it is called
atrioventricular nodal reentrant tachycardia. There is
no conclusive evidence that excessive adrenaline triggers
this type of tachycardia. In a few individuals, excessive
adrenaline may play a role during stress or during a heart
attack. Excessive adrenaline is liberated in the heart
muscle during a heart attack and increases the occurrence
of premature beats and other abnormal heart rhythms.
Beta-blockers can be useful when excessive adrenaline from
stress or a heart attack precipitates tachycardias.

Additionally, in a normal heart AVNRT does not cause
heart failure or angina, nor does it lead to a heart attack.
At the time of her visit to the emergency room, the patient
was being treated with quinidine and had nausea and
diarrhea. The quinidine was discontinued and she was
advised to suppress the attacks through the use of certain
maneuvers that increase the activity of the vagus nerve;
the vagus nerve slows the heart and keeps it in check.
Simple maneuvers to suppress AVNRT are (1) gagging
by putting a finger at the back of the tongue to cause
retching, (2) holding both nostrils tightly and breathing
out against the resistance for about 30 seconds, and
(3) holding the breath and immersing the face in cold
water for about 10 seconds. The patient was warned not
to apply pressure on the eyeball because detachment of
the retina may occur.

On a few occasions the attack was stopped in the
emergency room by massaging her right carotid artery
(carotid sinus massage) for 3–6 seconds. This stimulates
the vagus nerve and suddenly stops the abnormal fast heart
rhythm in more than 50% of individuals. This technique
should not be tried until the patient is hooked up to
a cardiac monitor or ECG. If these facilities are not
available, someone needs to listen to the heartbeat while
the doctor presses the carotid sinus. This technique is
not used in individuals over age 60 or in those whose
carotid arteries are known to be obstructed by atheroma
due to the rare possibility of stroke.

The above patient’s attacks became more frequent
after age 50. She was tried on digoxin, which was a 75%
success for about two years. She later required a betablocker,
which often helps in this situation. Very rarely
a combination of digoxin and beta-blocker is necessary to
suppress attacks, and this was tried with success for about
two years. Finally, at age 51 she was tried on a beta-blocker
alone and this was effective. At age 76, except for two
or three one-hour episodes per year, her heart remained
normal.

The majority of patients with AVNRT get immediate
relief in the emergency room when given adenosine IV
or IV verapamil. Verapamil cannot be used, however, inindividuals who have heart failure or who have a weak
heart muscle, because it can precipitate heart failure in
such cases. Adenosine, is as effective as verapamil, but safer.
Intravenous adenosine corrects the condition within a
few seconds. Adenosine 6 mg is given, but the drug has a
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