fdvdfzfgdzgddfz

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ARRHYTHMIAS
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. ARRHYTHMIAS
 Concept.- Heart rhythm disorders, which are divided into two main
groups: tachyarrhythmias, that is, arrhythmias due to increased electrical
activity, and bradyarrhythmias, caused by a decrease in the electrical
activity of the heart.
PHYSIOLOGY OF THE ELECTRICAL ACTIVITY OF THE HEART.
 Transmembrane action potential.- Cardiac cells possess the property of
excitability. At rest, the electric cell is polarized, with a concentration of
potassium 30 times higher than that of the extracellular medium. In
response to an electrical or mechanical stimulus, the permeability of the
membrane is modified and the transmembrane action potential is divided
into several phases as a result of the different ion fluxes through it. Phase
0: the sodium channels of the membrane are opened to allow the massive
and very rapid entry of sodium into the cell, with which the
transmembrane potential goes from -90 mV to +30 mV. When the sodium
channels are inactivated, ventricular repolarization is initiated through the
activation of the potassium channels (phases 1 to 3), which slowly return
the ionic equilibrium to the resting potential (phase 4). During a large part
of repolarization, the cell is inexcitable, even in the case of stimuli of great
magnitude; It is the so-called absolute refractory period.
Sinus and atrioventricular nodule cells have a lower resting potential, have a
slower depolarization rate and a lower amplitude action potential. As a cardiac
cell depolarizes, its neighbors are depolarized inducing the conductivity
phenomenon.
METHODS OF STUDY OF CARDIAC ARRHYTHMIAS.
1. Anamnesis and physical examination.- The characteristic symptoms are:
palpitations, syncopes, heart failure, angina or sudden death. It is
important to know the frequency of the pulse during the crisis, the
regularity, the form and circumstances of onset and termination, the
duration of the crisis and the accompanying symptoms
2. Complementary explorations: the one that allows to make the definitive
diagnosis of the type of cardiac arrhythmia is the ECG obtained during the

3. crisis. It must be borne in mind that it is not always possible to obtain an
ECG record at the time of the crisis, so several complementary
explorations are used that reproduce the patient's symptoms to capture the
moment of the crisis, within these explorations we have: a) the stress test,
b) the Holter ambulatory monitoring, c) the tilt test and d) the
electrophysiological study.
PREEXCITATION SYNDROME (WOLFF-PARKINSON-WHITE)
 Concept.- Under normal conditions, the atrioventricular node and the
fascicle of His is the path through which the electrical impulse travels
from the atria to ventricles and inversely; When the atrioventricular ring is
formed by fibrous tissue, it can not conduct the electrical stimulus
adequately, so that conduction becomes slow. There are cases of
anomalous anatomical connections of epicardial muscle cells that skip the
fibrous annulus with the ability to drive the impulse via antegrade, giving
rise to a preexcitation and also a retrograde conduction capacity that
produces a tachycardia crisis, these two together make up the so-called
Syndrome Wolff-Parkinson-White (WPW).
 Electrocardiographic diagnosis.- Electrocardiographic alterations are:
 Short P-R interval

4.  Pasting of the initial part of the QRS
 According to the morphology of the QRS complex, two Wolff-
Parkinson-White (WPW) types are distinguished: Type A, leads
V1 and V2 show predominant R waves. Type B, VI and V2 present
predominant S waves and positive delta wave in V5 and V6.
 Repolarization disorder.
 Etiology.- consequence of the existence of an anomalous (congenital)
pathway.
 Clinical picture: paroxysmal supraventricular tachyarrhythmia followed
by atrial fibrillation can often be asymptomatic or tachyarrhythmias (12-
80%). The higher the heart rate reached, the more likely it is to produce
ventricular fibrillation, especially if the R-R intervals are less than 200ms.
 Treatment.- When no premises are given, the practice of an
electrophysiological study is recommended to determine the risk of sudden
death according to the refractory period of the accessory life. The
treatment of tachycardia attacks is adenosine, which causes a transient
block in AV conduction. Adenosine is administered as a bolus of 3 to 12
mg intravenously in progressive doses every 2-3 min until the cessation of
tachycardia or reaching the maximum dose. If the patient presents atrial
fibrillation, drugs of class I should be administered such as ajmaline,
procainamide or intravenous flecainide that block conduction through the
accessory pathway.
FIBRILLATION HEADSET

5.  Concept.- Total disorganization of the electrical activity of the atrium and
absence of atrial contraction.
 Electrocardiographic diagnosis.- absence of P waves, presence of f
waves, frequency of 500 to 600 per minute, irregularity of the ventricular
rhythm, ventricular rate between 100-160 beats / min, QRS can show
widening.
 Etiology.- The main cause is aging.
 Classification.- from the clinical point of view: a) First episode of atrial
fibrillation: patient is seen for the first time in fibrillation; b) Paroxysmal
atrial fibrillation: self-limited to a period of 7 days or less; c) Persistent
atrial fibrillation: atrial fibrillation beyond 7 days; d) Permanent atrial
fibrillation: patients in whom it has been decided not to attempt the return
of sinus rhythm due to the low probability of success.
 Clinical picture.- The repercussions of clinics are multiple:
1. heart failure
2. formation of atrial thrombi
3. the sinus pause after fibrillation can condition the appearance of a
syncope
4. worsening of heart failure, fatigue or dyspnea
5. development of tachycardiomyopathy
6. irregular and rapid arterial pulse, the first heart sound varies in
intensity.
 Treatment.-
1. Reversion to sinus rhythm: electrical cardioversion,
pharmacological or treat the triggering factor. If there is an
immediate relapse after cardioversion, start treatment with
amiodarone IV.
2. Control of the heart rate by means of digitalization IV. In cases of
good ventricular function, the first option will be the use of beta-
blockers or calcium antagonists (verapamil or diltiazem). In a
fibrillation of more than 48 hours and less than 1 year,

6. anticoagulant therapy and oral antiarrhythmic treatment should be
initiated and maintained chronically
3. Prevention of complications: initiate an anticoagulant treatment
both in patients with chronic and paroxysmal atrial fibrillation.
BIBLIOGRAPHIC REFERENCE:
Mont Girbau, L. Brugada Terradellas, J., "Cardiac Arrhythmias" Farreras, V.
Rozman, C, Internal Medicine, Barcelona-Spain, Elsevier, 2016, Vol.1, p. 431-
460.