PDA

View Full Version : contraindicated for wolff-parkinson-white syndrome



pharmacology
01-22-2005, 10:38 PM
A 72 year-old man is brought to the emergency department and diagnosed with atrial fibrillation. Shortly after receiving a medication to treat his dysrhythmia, the patient develops ventricular fibrillation. It is discovered that the patient was initially misdiagnosed and should have been diagnosed with Wolff-Parkinson-White syndrome and atrial fibrillation. Inappropriate administration of which of the following drugs most likely resulted in the development of ventricular fibrillation?

A. Adenosine
B. Amiodarone
C. Digoxin
D. Disopyramide
E. Quinidine

hmed
01-26-2005, 12:56 PM
Answer C Digoxin

pharmacology
02-10-2005, 11:29 PM
A 72 year-old man is brought to the emergency department and diagnosed with atrial fibrillation. Shortly after receiving a medication to treat his dysrhythmia, the patient develops ventricular fibrillation. It is discovered that the patient was initially misdiagnosed and should have been diagnosed with Wolff-Parkinson-White syndrome and atrial fibrillation. Inappropriate administration of which of the following drugs most likely resulted in the development of ventricular fibrillation?

A. Adenosine
B. Amiodarone
C. Digoxin
D. Disopyramide
E. Quinidine

The correct answer is C. Accessory pathways between the atria and ventricle that avoid the conduction delay of the atrioventricular node may predispose the myocardium to the development of reentrant tachycardias. Examples of these dysrhythmias include atrial fibrillation, atrioventricular reentry tachycardia (AVRT), and atrial flutter. Most commonly, these specific reentry tachycardias make direct connections between the atria and ventricle though the Kent bundles [Wolff-Parkinson-White syndrome (WPWS)]. This produces a short PR interval but an early delta wave at the onset of a wide, slurred QRS complex owing to early ventricular depolarization of the region adjacent to the pathway. In patients with WPWS and atrial fibrillation, digoxin can enhance transmission of impulses through accessory pathways. This may result in an extremely rapid ventricular rate, and even ventricular fibrillation. Digoxin is an antiarrhythmic used primarily for the treatment of atrial fibrillation and flutter. All the other agents can be used to treat supraventricular tachycardias.

Adenosine (choice A) is primarily used for conversion of paroxysmal supraventricular tachycardia (including that associated with accessory bypass tracts of WPWS) to normal sinus rhythm.

Amiodarone (choice B) is a class III/IA antiarrhythmic used in the treatment of refractory ventricular tachycardia and supraventricular tachycardia and in the prevention of ventricular tachycardia and ventricular fibrillation.

Disopyramide (choice D) and quinidine (choice E) are class IA antiarrhythmics used in the treatment of ventricular tachycardia and supraventricular tachycardia and in the prevention of ventricular fibrillation and symptomatic ventricular premature beats.

pharmacology
02-22-2005, 06:09 PM
Wolff-Parkinson-White

http://www.emedu.org/ecg/images/wpw_2a.jpg
Syndrome:
1.Short PR interval: less than 0.12 seconds with a normal p-wave.
2.Abnormally wide QRS (equal to or greater then 0.11 seconds)

3.Presence of a delta wave (slurring of the QRS complex) When impulses travel
down the accessory pathway in an anterograde manner, ventricular preexcitation
results. This produces a short PR interval and a delta wave as seen in Wolff-Parkinson-White
(WPW) syndrome (see Image 9) (Wolff, 1930).


4.Secondary ST segment and T-wave changes. The delta
wave: Slow conduction through the bypass tract and more rapid
conduction through the Purkinje system. When the delta wave is
negative, this simulates a Q-wave. This is known as a pseudo-infarction
pattern, and is seen n up to
70% of patients with WPW.


ST and T-wave changes: abnormal depolarization results in abnormal repolarization
patterns.

Significance: The WPW pattern is seen in approximately 0.20 percent of the
general population. Paroxysmal tachycardias occur in approximately 13 percent
of healthy individuals with WPW, however much higher incidences of tachycardia
are seen in hospitalized or "cardiac" patients.

The primary dysrhythmia in WPW is PSVT. The heart rate is usually 140-250
and the delta wave is not typically seen.

Atrial fibrillation and flutter is less common (20-35%) and commonly results
in a pattern of wide QRS complexes. The ventricular rate may be as fast as 220-360
beats/minute. Due to the requisite short, fast refractory period these patients
are a high risk for ventricular fibrillation.

"False VT," wide aberrant tachycardia may be seen in WPW in the setting of
atrial fibrillation or flutter.


About Wolff-Parkinson-White syndrome
Also known as preexcitation syndrome,
Wolff-Parkinson-White (WPW) syndrome is a condition in which the normal
electrical signals in the heart travel along an extra electrical
pathway. This can cause an abnormal heart rhythm (arrhythmia).

In a normal heart, electrical signals are generated in the upper right chamber of the heart (right atrium) and travel along a standard conduction system. These signals first stimulate

http://www.heartcenteronline.com/myheartdr/images/Article/Conduction_System.jpg

the atria to contract, then pass through the atrioventricular node to the ventricles
and cause them to contract in a rhythmic, predictable fashion. However,
in patients with WPW syndrome, the electrical signals travel through an
extra, abnormal pathway that bypasses the atrioventricular node. This
pathway is known as the Kent bundles.


Because the electrical signals reach the ventricles via this abnormal
route instead of through the heart’s normal conduction system, they may
signal the ventricles to contract abnormally. This is usually because
of a co-existing arrhythmia called atrial fibrillation, in which the
atria beat very rapidly, or a special kind of arrhythmia called an atrioventricular reentrant tachycardia
(AVRT). An AVRT occurs when the electrical signal “loops” through the
parallel conduction systems in the heart, causing the ventricles to
contract multiple times. This is called a reentrant signal. As a result
of either condition, the patient may experience rapid heart rhythms of
over 100 beats per minute (tachycardias), along with palpitations, lightheadedness and/or loss of consciousness Click the term for moreThe vast majority of patients with WPW syndrome have a good prognosis,
but the condition develops differently in different people. It could:

Go into dormancy, only to recur later in life.

Resolve on its own over time as the Kent bundles lose their ability to conduct electrical impulses.

Cause a potentially fatal abnormal heart rhythm (arrhythmia) such asventricular fibrillation, in which the heart quivers rapidly instead of beating. This
life-threatening complication is extremely rare (less than a 1 percent
chance of occurring in any given individual).
As many as 70 percent of WPW patients have no other sign of heart
disease. The other 30 percent have another heart condition in addition
to WPW syndrome, such as:

Mitral valve prolapse. A condition in which the two flaps of the mitral valve
(which regulates blood flow between the left atrium and the left
ventricle) cannot close properly – either because one of the flaps is
larger than the other, or because the “hinges” of the flaps are
damaged. As a result, one or both of the flaps close in the wrong
direction, and blood can leak back toward the upper chamber (regurgitation).

Cardiomyopathy. A type of heart disease in which the heart muscle is abnormally enlarged, thickened and/or stiffened.

Ebstein’s anomaly. A rare heart condition present from birth that involves a deformed and misplaced tricuspid valve
(which regulated blood flow between the right atrium and the right
ventricle). It leads to a lack of oxygen-rich blood flowing through the
body, which can produce cyanosis (a bluish tint to the skin, lips, fingernails or other parts of the body).
On average, only about 4 out of 100,000 people have WPW syndrome. Men
are at a greater risk of acquiring it than are women. Often, the
condition is first diagnosed in children and young adults, and the
abnormal accessory pathways are believed to be present since birth. WPW
is the leading cause of tachycardia among children and adolescents.
There is interest in studying WPW’s genetic aspects, as there is an
inherited form of the syndrome. It is felt that such changes
(mutations) are responsible for the tachycardia in WPW syndrome.
Understanding the genetics of WPW syndrome may help toward making an
early diagnosis and in offering the most effective therapies.







Copyright © 2003-2018 ValueMD, LLC. All rights reserved.