Cardiac arrhythmia

View previous topic View next topic Go down

Cardiac arrhythmia

Post  counselor on Mon Oct 15, 2012 11:44 am

CARDIAC ARRHYTHMIA





Under normal conditions the pulses to the contraction of the myocardium are originated in the sinoatrial node and from this they propagate through the atria, the atrio-ventricular node and the His-Purkinje system of the ventricle.

Cardiac arrhythmias consist of an alteration in the normal sequence of cardiac activation. We can distinguish arrhythmias from:
• Abnormal activation in the genesis of the pulse rate.
• Disturbance of driving with impaired cardiac activation sequence.

Cardiac arrhythmias may compromise the hemodynamic efficiency of the heart pump, thus generating situations of danger to the life of the patient.

The ABNORMALITIES IN GENESIS PULSE MAY BE DUE TO:

Alteration of normal automaticity
Abnormal automaticity in the sinoatrial node to altered activity of the ANS.
Increased automaticity in the His-Purkinje system.
And 'the slope of phase 4 of the action potential which determines the genesis of the pulse.
The sinoatrial node presents under normal conditions the maximum speed of depolarization and constitutes the "pacemaker" normal. Under abnormal conditions other foci may generate momentum for the activation rate.
The slope of the phase 4 of the action potential, due to currents of Ca + +, K + and Na +, determines whether or not the attainment of the depolarization threshold for activation.

The slope is modified by hypokalemia, adrenergic stimulation, mechanical stretching.


Onset of abnormal pulses
May be due to abnormal automaticity in Purkinje fibers, atrial and ventricular cells of the conduction tissue.
Occurs when their resting potential becomes less negative (ie about - 60 mV).


Activity triggered
This term refers to a cardiac activation triggered by an action potential.
Can occur:
a) Post-depolarizations early.
b) Post-delayed depolarizations.

After-depolarizations early.
Occur before completion phase of repolarization.


Post-delayed depolarizations.
Occur at the end of the repolarization. Are an expression of an overload of Ca + + in the myocyte. May be caused by catecholamines and digitalis.

The after-depolarizations may give rise to onset of pulses is reached when a threshold value of depolarization.

Can be no single extrasystoles or premature beat, or repeated discharge pulses.


THE ARRHYTHMIAS, ON THE OTHER HAND, MAY BE DUE TO DEFECTS IN CONDUCTING THE PULSE.

Phenomenon of return
The normal heart rhythm depends on the fact that the PA initiated in the SA node, and have multiplied in the branches of the conduction tissue, meet and extinguish one another, not being able to activate the myocytes because they are in refractoriness.
If not could occur cyclical activation rate.

In pathological conditions may occur a situation of unidirectional conduction block.

The slowdown creates the conditions for a subsequent re-excitation of the conduction tissue (usually refractory).

Reentrant excitations can give one extra beat or abnormal depolarization autopropagantisi cycles (circular motion).

Drugs that prolong the refractory period, or modifying the conduction velocity may be useful to abolish the return.


Wolff-Parkinson-White.
It 'an example of a reentrant arrhythmia, which is due to abnormal conduction fibers (bundle of Kent) that by-pass the atrio-ventricular junction.

It is therefore the phenomenon of return on an anatomical basis.



TYPES OF ARRHYTHMIAS

1) premature beats and extrasystoles.
The premature beat originating from an ectopic focus and interrupts the normal sinus rhythm.
If the atria originates after it you have a normal cycle of activity of the SA node.
If it originates in the ventricle has a compensatory pause.
There is talk of extrasystoles when the ectopic beat is inserted between normal sinus beats.

2) ectopic atrial tachycardia.
Depending on the frequency distinguish:

- Paroxysmal atrial tachycardia.
Atrial ectopic pacemaker
100-180 beats per minute.
Usually the transmission of impulses to the ventricles is normal.

- Atrial Flutter
Atrial ectopic pacemaker
250-350 beats per minute.
Relationship between atrial beats and ventricular 2 to 1.
And 'common rheumatic diseases, hyperthyroidism and coronary heart disease.
Cardiac glycosides may bring the relationship between atrial and ventricular beats to 3:1 or 4:1.


- Atrial Fibrillation
Multiple sites of ectopic foci or reentry.
500-600 beats per minute in the atria and the ventricles about 200.
The heart may not be able to eject blood. Risk of blood clots.

3) nodal tachycardia or AV junction
And 'generally associated with valvular disease with myocardial ischemia.
-Recording inverted P wave (AV node conduction from
atrium).
-Palpitations due to rapid ventricular rhythm.
-L 'arrhythmia can last hours or days.

4) Ventricular tachycardia
We distinguish:
Paroxysmal tachycardia ventricular
-Focus ventricular ectopic.
-100-200 Beats per minute.
-Widened QRS and abnormal forms.
-It can be due to surgery, ischemic heart disease or overdose of digitalis.

5) Ventricular fibrillation
-Multiple or ectopic pacemaker phenomenon of return.
Movements-vermicular without ejection of blood.
ECG activity continued irregular in frequency.
-Frequent cause of death if not corrected immediately with electrical cardioversion


6) atrioventricular block
Grade I: Slow AV conduction, atrial and ventricular beats but ratio = 1:1.
Grade II: Ratio 2:1, 3:1.
Grade III: Complete block. The atrium beats at about 75 beats / min, while the ventricles are beating with idioventricular: 30-45 / min (Purkinje fibers).
If the frequency is too low, you may have periods of dizziness and syncope with cerebral ischemia (syndrome of Morgagni-Stokes-Adams).

7) branch block bundle of His
Transmission delay of the ventricle under the control of the branch.




Antiarrhythmic drugs

The therapeutic approach to arrhythmias now includes the use of automatic defibrillators, pacemakers with a long battery life and the ablation of accessory conduction pathways.

Antiarrhythmic drugs available were classified according to Vaughan Williams into 4 classes. This classification continues to be fairly used, but must be integrated to describe in more detail the pharmacodynamic profile of the individual antiarrhythmics.

Class I: Na + channel blockers

They are attached mainly to the open channel, not the channel at rest. Their use is dependent block, recovery from block is of relatively long duration.

Class IA (quinidine, procainamide, disopyramide).
-Slow down the speed of depolarization in phase 0.
-Decreased the amplitude of phase 0.
-Greatly increase the refractory period.
-Move the threshold potential toward less negative values.
-Decreased the slope of phase 4.

Quinidine
Block:
• sodium channels in the open state,
• potassium channels
• The quinidine also has antimuscarinic action and block -adrenergic
It is used to treat atrial flutter and atrial fibrillation and to prevent recurrence of ventricular tachycardia and ventricular fibrillation.
Frequently causes diarrhea with risk of hypokalemia.

Procainamide and disopyramide
They share similar indications and quinidine, but have less effect on SNA.


The Class B (lidocaine, tocainide, mexiletine)

- Depression of phase 0, blocking Na + channels, mail from the recovery of these block is rapid.
- The refractory period is slightly changed. However, in ischemic tissue PRE is increased!
- Decreased the slope of phase 4 in Purkinje fibers.
- Decreased the abnormal automaticity.

Lidocaine
• Blocks sodium channels is in the activated state than in the rest. The recovery from block is very rapid
E 'used intravenously in the treatment of ventricular arrhythmias of various origins, including those associated with myocardial infarction.
A toxic doses causes convulsions
Tocainide and mexiletine
Are analogs of lidocaine, orally administrable.
They are used for ventricular arrhythmias

Moricizina
Works by blocking the Na + channels.
E 'used for ventricular arrhythmias by oral administration.


The Class C (flecainide, propafenone)

- Marked reduction of the speed of depolarization in phase 0.
- Decrease of the phase 0.
- Increase of the refractory period in both the atria into the ventricles.
- Poor effect on the phase 4.
- Automatic abnormally depressed.

Flecainide
• Blocks sodium channels (slow recovery)
• Blocks potassium channels.
It is used to treat supraventricular arrhythmias.
The main side effect is a possible proarrhythmic effects, especially during initiation of therapy

Propafenone
• Blocks sodium channels
• Blocks potassium channels
• It also has -adrenergic blocking
E 'used primarily for supraventricular arrhythmias

Evokes adverse reactions such as ventricular tachycardia
Cardiac insufficiency and bronchospasm.


Class II: -adrenergic antagonists

-Lack of influence on the speed of the phase 0.
-Lack of influence on the amplitude of phase 0.
Sharp increase in the PRE-A-V node.
-Strong reduction of the slope of phase 4 in the conduction tissue.
-Increases power threshold for ventricular fibrillation.
-Reduced oxygen utilization in the myocardium.

Evoke
Marked slowing of atrio-ventricular conduction.
-Marked reduction in automaticity.
-Lower tendency to ventricular fibrillation in the event of myocardial infarction.

They are used for supraventricular arrhythmias: atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia.
It takes advantage of the increase in refractoriness in the AV node.
They are also used for ventricular arrhythmias triggered by exercise, emotional factors (catecholaminergic etiology) or ischemic heart disease (reduced ischemia).
I'm not used to digital arrhythmias.

Class III (amiodarone, sotalol)

-They prolong the duration of the PA and the PRE in Purkinje fibers and ventricular muscle fibers.
Amiodarone and sotalol-PRE also extend the atrium and the AV node.
-Amiodarone reduces slope and amplitude of phase 0.
-Amiodarone and sotalol reduces the slope of phase 4.
-Increase the threshold for ventricular fibrillation.

Sotalol
• Inhibits potassium channels
• It also has action -blocker

Amiodarone
• It inhibits sodium channels
• Interacts with the calcium and potassium channels

Lengthens the action potential and
Prolongs the refractory period in all cardiac tissues

It has no effect proarrhythmic
However, generates changes in thyroid function
Pulmonary fibrosis
Hepatic dysfunction

Class IV (Ca + + channel blockers)
-Reducing the firing rate of the SA node.
PRE-lengthening of the AV node.
Low-slope of phase 4 of the Purkinje fibers.
-Reduction of post-delayed depolarizations.

Verapamil and diltiazem
• Reduce the speed of conduction and heart rate.
• They are useful for reentrant arrhythmias including the NAV
• They are useful for supraventricular arrhythmias


Digoxin
Increases the refractory period of atrio-ventricular, out of which
Causes reduction of the calcium current
Activation of potassium currents.

E 'used for supraventricular arrhythmias


Adenosine
• Enable potassium current
• Reduces calcium current NAV
• Inhibits effects due to increased cAMP

Produces hyperpolarization
Slows the normal automatic

It is used in recurrent supraventricular arrhythmias.


N-3 PUFAs
Supplementation drug or a diet rich in these polyunsaturated fatty acids are known to have action antiaritmogena.
avatar
counselor
Admin

Posts : 172
Join date : 2012-09-01
Age : 32

View user profile http://www.myhelpforum.net

Back to top Go down

View previous topic View next topic Back to top

- Similar topics

 
Permissions in this forum:
You cannot reply to topics in this forum