Ventricular Flutter And Ventricular Fibrillation – Causes, Diagnosis And Treatment

Ventricular Flutter

Ventricular flutter is a rapid ventricular tachycardia, with a rate of 180-250 beats / minute, which degenerates, most frequently, into ventricular fibrillation. Ventricular flutter occurs most often in severe organic heart disease, the most common cause is acute myocardial infarction. Some drugs (digoxin, quinidine, tricyclic antidepressants) may be triggers of ventricular flutter. From a clinically point of view, a patient with ventricular flutter presents secondary signs of hemodynamic deterioration, loss of consciousness, the absence of peripheral pulse and collapsed blood pressure.

Ventricular Flutter

ECG shows the following:

• Electrocardiographic waves with large amplitude, with continues ongoing and sinusoidal aspect, the components of the QRS complex can not be individualized (electrical activity is impossible to identify), a characters that allow the differentiation from a ventricular tachycardia,  in which is possible the distinguish between individual components of the the QRS complex .
• Flutter wave frequency is 180-250 beats / minute.

Ventricular Flutter ECG

Ventricular flutter is a major cardiovascular emergency and therefore the treatment should be done as quickly as possible. This consists in CPR measures and the administration of external electric shock of 200-400 joules, as soon as possible.

Ventricular fibrillation:

Ventricular fibrillation represents the disappearance of organized ventricular electrical activity. It is the most serious cardiac arrhythmia, due to serious hemodynamic consequences which are inducing: loss of pump function of the heart, collapse of cardiac output and of blood pressure. Most of the times, ventricular fibrillation is irreversible, fatal if the measures of CPR  and external electric shock are not quickly applied, to obtain a efficiently heart rate, from haemodynamically point of view.

Causes:

• Myocardial infarction;
• Cardiomyopathy;
• Atrial fibrillation in the presence of Wolf-Parkinson-White syndrome;
• Long QT syndrome;
• Brugada syndrome;
• Drug intoxication (digoxin, quinidine, procainamide, tricyclic antidepressants);
• Heart failure, in terminal phase.

Ventricular Fibrillation

In terms of conditions of appearance, ventricular fibrillation may be primary, in the absence of cardiogenic shock  and heart failure, and secondary, which occurs in patients with cardiogenic shock or heart failure.

Triggering factors of ventricular fibrillation are, most often, a ventricular extrasystole with R / T phenomena,or can occur the degeneration of ventricular tachycardia or torsades de pointes into ventricular fibrillation.

Clinically, patients experience loss of awareness, convulsive movements, respiratory arrest, peripheral pulse and blood pressure are absent. In situations in which the intervention dose not occur quickly, will appear death.

ECG shows the following:

• Chaotic undulations of isoelectric line, with variable amplitude, morphology and duration;
• Ventricular rate is between 150-250 beats / minute.

In terms of the ECG, there are two types of ventricular fibrillation:

1. Tonic ventricular fibrillation with large waves, which usually respond to external electric shock.
2. Atonic ventricular fibrillation, with small waves, hard reducible.

Ventricular Fibrillation ECG

Ventricular fibrillation is a major cardiovascular emergency, so the treatment should be instituted as quickly as possible and is aiming measures of CPR and application of external electric shock of 200-400 joules. If the measures of treatment are not quickly applied, the patient may die.

Prevention of ventricular fibrillation recurrences is achieved by intravenous administration of amiodarone (5-20 mg / kg intravenous infusion for 30-120 minutes, followed by intravenous infusion to a total dose of 1200 mg/24 hours, then is given an oral dose of amiodarone of 100-600 mg / 24 hours), procainamide, lidocaine or tosylate of bretilium. Some patients require implantation of a cardioverter defibrillator.

Preexcitation Syndromes (WPW And LGL Syndrome) – Causes, Diagnosis And Treatment

Ventricular pre-excitation activity is defined as a premature activity of a part or of the entire ventricular myocardium, through a supraventricular impulse, occurred through connections or accessories pathways, which are short-circuiting the normal way of impulse conduction. Pre-excitation syndromes are caused by a defect in embryonic development of the atrioventricular ring. Accessory pathways are composed of myocardial fibers with conduction velocity and refractory period lower than the structures of His bundle and of atrioventricular node.

Preexcitation syndrome

These pathways can lead the excitation both anterograde and retrograde, which allows a reentry circuit. Therefore, in people with pre-excitation syndromes, occur frequently paroxysmal supraventricular tachycardia crises, which are usually initiated by a atrial extrasystole or by ventricular extrasystole, which is lead through the way with shorter refractory period and with a faster velocity conduction.

Pathways by which the ventricular myocardium is early depolarized are:

1. Kent atrioventricular bundle, which makes a connection between the right atrium and right ventricle or between the left atrium and left ventricle.
2. James bundle, connecting atrial myocardium with the lower third of the atrioventricular node or His bundle.
3. Mahaim bundle, which makes the connection between the bottom of the atrioventricular node and the interventricular septum.

WPW Syndrome

Wolff-Parkinson-White Syndrome (WPW syndrome):

Wolff-Parkinson-White syndrome is produced by the presence of Kent bundle and has a frequency in general population of 1-4°. Clinically, patients may present paroxysmal tachyarrhythmia in 20-40% of cases.

Diagnosis of Wolff-Parkinson-White syndrome is based on the  ECG interpretation:

• PR interval <0.12 seconds, P waves of normal appearance;
• QRS complex is wide, with a longer duration than 0.12 seconds;
• The presence of delta waves. Slow enrollment or thickening of the initial portion of the QRS complex (delta wave) is the most important criterion for diagnosis of Wolff-Parkinson-White syndrome. Delta wave length range between 0.02-0.07 seconds;
• Secondary changes of ST segment and T wave, which are showing a opposite direction from the QRS complex and delta wave.

WPW Syndrome ECG

Treatment of Wolff-Parkinson-White syndrome:

Asymptomatic patients, showing only ECG changes do not require treatment.

Arrhythmic chronic treatment, designed to prevent crisis of ventricular tachycardia and to control ventricular rate in case of atrial fibrillation is realized by the administration of class IC  antyarrhythmics (flecainide, propafenone), class III antiarrhythmics (amiodarone, sotalol), drugs that are increasing the refracted period in Kent bundle.

Elective treatment of Wolff-Parkinson-White syndrome, in the patients with symptoms, is the ablation of the accessory bundle with radiofrequency current.

Treatment of supraventricular tachycardia access is done by: vagal maneuvers, intravenous administration of adenosine and verapamil. After administration of adenosine can occur an episode of atrial fibrillation with rapid ventricular rate, which necessitate, sometimes, electrical defibrillation.

LGL Syndrome

Lown-Ganong-Levine Syndrome (LGL syndrome)

Lown-Ganong-Levine syndrome is produced by the presence of James bundle and has a frequency, in general population, of 0.5%. Clinically, patients with this syndrome may present ventricular tachycardia.

The diagnosis of Lown-Ganong-Levine syndrome is based on  ECG interpretation:

• PR interval with a duration of less than 0.12 seconds, with normal P waves;
• The QRS complex duration is normal;
• The absence of delta waves;
• Episodes of paroxysmal supraventricular tachycardia.

Ventricular Tachycardia

Ventricular tachycardia is a sequence of four or more depolarizations, with ventricular origin, meaning that this depolarizations are arising from an outbreak that is located below the bifurcation of His fascicle, and have a frequency of 100 beats / minute. Onset and end of ventricular tachycardia crisis are sudden, realizing short-term (paroxysmal) form or long-term form of ventricular tachycardia.

Causes:

• Ischemic heart disease: myocardial infarction in the acute phase (monomorphic or polymorphic ventricular tachycardia,with the risk of transforming into ventricular fibrillation) or in chronic phase (monomorphic ventricular tachycardia);
• Cardiomyopathy: primitive (dilated, hypertrophic) or secondary (hypertension, mitral regurgitation, aortic regurgitation, aortic strenosis, mitral stenosis);
• Arrhythmogenic right ventricular dysplasia;
• Long QT syndrome;
• Iatrogenic: digoxin toxicity after high-dose of  anti-arrhythmic drugs or after surgery (especially after aorto-coronary bypass).

Ventricular Tachycardia

Classification of ventricular tachycardia, is made after:

1. Length: sustained ventricular tachycardia (lasting over 30 seconds) and unsustained ventricular tachycardia (duration less than 30 seconds).
2. After QRS complex morphology: monomorphic (constant aspect of QRS complexes in all derivations), polymorphic (aspect of QRS complexes is polymorphic ) and bidirectional (QRS complexes, although from the same source, change their morphology, either alternatively either regularly – in digoxin toxicity).
3. After origin: ventricular tachycardia of the right ventricle or ventricular tachycardia of the left ventricle.

Ventricular Tachycardia

Diagnosis:

The diagnosis of ventricular tachycardia is based on the symptoms, on physical examination and on ECG interpretation.

Symptoms may differ, depending on the type of ventricular tachycardia. In unsustained forms of ventricular tachycardia, symptoms are minimal, as palpitations or may be absent, and in sustained forms of ventricular tachycardia may appear palpitations, crisis of angina pectoris, paroxysmal dyspnea, syncope.

Physical examination shows the following: peripheral pulse is regular, fast, sometimes is slow and retrieval. Heart sounds are regular and tachycardic. Ventricular tachycardia can sometimes have the appearance of acute pulmonary edema or cardiogenic shock.

ECG in ventricular tachycardia has four important aspects:

1. QRS complexes with abnormal morphology, with increased length, have the aspect of right bundle branch block, if the ventricular tachycardia has the origin from the left ventricle or left bundle branch block aspect if ventricular tachycardia has the origin on the right ventricle. Heart rate is 140-250 beats / minute, the rhythm can be regular or slightly irregular.
2. Atrio-ventricular dissociation: in general the atrial and ventricular electrical activity are independent of each other.
3. Ventricular capture: from time to time may appear thin QRS complexes, which are preceded by P waves, meaning ventricular  “capture” by the supraventricular stimulus.
4. Fusion beats: QRS complex has a morphology intermediate between complexes of ventricular origin and those of supraventricular origin.

Ventricular Tachycardia ECG

Treatment:

The objective of therapy in ventricular tachycardia is rapid conversion to sinus rhythm.

Sustained ventricular tachycardia and well tolerated hemodynamically, is treated with antiarrhythmics from class IA (procainamide), class III (amiodarone) or lidocaine, all administered intravenously. In case of failure of drug therapy is switched to electric conversion.

In the case of sustained ventricular tachycardia with low hemodynamic tolerance but with evolution to acute pulmonary edema or to cardiogenic shock, are made the following maneuvers : oxygen therapy on the mask or on the nasal tube and electric conversion, initially with 50 joules, then with 100 joules, 200 joules, up to 360 joules.

In the case of ventricular tachycardia with very sever hemodynamic deterioration is done electric conversion starting with 200 joules, up to 360 joules.

Prevention of recurrence of ventricular tachycardia is done by taking beta blockers, amiodarone, class IC antiarrhythmic agents, implantable defibrillator or ablation by radiofrequency current (is done only in some forms of ventricular tachycardia).

Ventricular Tachycardia Treatment algorithm

Special types of ventricular tachycardia:

Torsades de pointes is an atypical form of ventricular tachycardia, initiated only in the presence of long QT interval. Production of the latter is favored by the presence of major chronic bradycardia (grade III atrioventricular block), myocardial infarction, mitral valve prolapse, certain antiarrhythmic drugs (quinidine, procainamide), electrolyte disorders (hypokalemia, hypomagnesaemia), intracranial pathological processes.

On ECG are recorded the following aspects:

• Started with a ventricular extrasystole, with phenomena R / T (which appears in a terminal period of large and extended T wave) in the presence of an elongated QT interval.
• The succession of ventricular complexes, with frequency between 240-300 beats / minute with unequal amplitude, with spindle aspect, consisting of a rapid phase with a sharp point and a slow phase, of opposite direction, with rounded tip.
• Progressive reduction of amplitude of QRS complexes, with sens reversal, a phenomenon that occurs cyclically, creating the appearance of oscillations around the isoelectric line.
• Presence of atrioventricular dissociation.

The treatment of torsades de pointes is achieved by intravenous administration of magnesium sulfate or by atrial or ventricular electrical stimulation.

Torsades de points

Accelerated idioventricular rhythm starts generally gradually, ventricular rate is lower, between 60 and 120 beats / minute, appears in accesses, usually short, but repetitive. Occurs trough the increase automatism of an outbreak which is located in the intraventricular conduction system, which compete with the stimuli that are coming from the sinus node.

The main causes are: myocardial infarction, digoxin toxicity, grade III atrioventricular block, cardiomyopathy or rheumatic fever.

On ECG are recorded the following aspects:

• Enlarged and deformed QRS complexes, with frequencies between 60 and 120 beats / min, each QRS complex can be followed by a negative P wave, due to retrograde conduction.
• May be present ventricular captures and ventricular fusion beats.

Accelerated idioventricular rhythm treatment should first treat the cause that triggered the arrhythmia and to increase the heart rate by intravenous administration of atropine or by electrical stimulation.

Ventricular Extrasystoles

In terms of position in the cardiac cycle, ventricular extrasystoles are  premature ventricular depolarizations, which originates from a source which is located distal to the bifurcation of His fascicle.

Causes:

• On a healthy heart, ventricular extrasystoles occur in the following situations: excessive consumption of coffee, tobacco abuse, emotions, stress;
• On a diseased heart: coronary artery disease, cardiomyopathy, mitral regurgitation, left ventricular arrhythmogenic dysplasia;
• Iatrogenic, ventricular extrasystoles appear: in digoxin toxicity, after initiation of fibrinolytic therapy in myocardial infarction and in hypokalaemia.

Ventricular Extrasystole

Diagnosis:

The diagnosis of ventricular extrasystoles is based on the symptoms, on the physical examination and on the ECG interpretation.

Symptoms include palpitations, chest discomfort, feeling of heart stopping, followed by a stronger beat, faintness, syncope.

Physical examination may reveal the following: can be collected an early beat, which is followed by a pause (compensatory pause). In case of frequent ventricular extrasystoles, hypotension may occur.

ECG shows the following:

• Early QRS complex with abnormal configuration and an increased length, which are not preceded by P waves and are followed by ST segment with a T wave which is opposite to the QRS complex. Right ventricular extrasystoles, are generally look like left bundle branch block and left ventricular extrasystoles have the appearance of right bundle branch block.
• The interval between ventricular extrasystoles and the previous QRS complex is constant (fixed coupling interval).
• Post ventricular pause is usually fully compensatory, rarely are interpolated ventricular extrasystoles.

Ventricular extrasystole ECG

The degree of premature ventricular extrasystoles is variable and can occur at any time in the diastole. Sometimes it is a very short coupling interval which will make that the ventricular extrasystoles to be registered on top of previous T wave, a phenomenon name by the  R / T term. In these circumstances there is  the danger of triggering a ventricular fibrillation.

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Ventricular extrasystoles can be:

• Unifocal, QRS morphology is identical in all leads;
• Polifocal, QRS morphology is different in ECG leads, which means that the QRS complexes originate in one or more ectopic outbreaks;
• Isolated, characterized by the occurrence of a single ventricular extrasystole;
• Systematized: the appearance of two or more ventricular extrsistoles under the form of bigeminy, trigeminy, etc..

Based on Holter monitoring, Lown proposed the following classification of ventricular extrasystoles:

1. Class 0: absence  ventricular extrsistoles at least 3 hours;
2. Class I: premature ventricular extrasistoles, monomorphic and occasional, the occurrence is less than one ventricular extrasistole per minute or less than 30 ventricular extrasystoles per hour.
3. Class II: frequent monomorphic ventricular extrasystoles, more than one ventricular extrasistole per minute or more than 30 ventricular extrasystoles per hour.
4. Class IIIa: polymorphic ventricular extrasystoles (multifocal).
5. Class IIIb:  systematized ventricular extrasystoles (bigeminy, trigeminy).
6. Class IVa: coupled repetitive ventricular extrasystoles (2 ventricular extrasystoles).
7. Class IVb: repetitive triplets of ventricular extrasystoles (3 ventricular extrasystoles).
8. Class V:  R/T phenomena.

Ventricular extrasystole

Treatment:

Ventricular extrasystoles that appear on a healthy heart require the removal of trigger factors and in the case of  important symptoms, is recommended the administration of beta blockers and sedatives.

In the case of organic ventricular extrsistoles, the treatment is based on the Lown classification, as follows:

• Classes I and II benefit from treatment of the disease that lead to the appearance of extrasistoles;
• Classes III, IV and V: monitoring, determining of pathological substrate, correcting electrolyte and acid-base disorders, myocardial ischemia and other factors incriminated that are causing the ventricular extrasistoles. Administration of beta blockers, amiodarone or lidocaine, all intravenously.

Sources

1.https://restore-my-blood-pressure.com/

2. https://www.ncbi.nlm.nih.gov/pubmed/2427001

3.  https://restore-your-blood-sugar.com

4. https://medical-dictionary.thefreedictionary.com/ventricular+extrasystole

Atrial Flutter

Atrial flutter is a regular and monomorphic atrial arrhythmia, with a atrial rate of 250-350 beats / minute and regular or irregular ventricular activity, in relation to the variability and the degree of atrioventricular block. Ventricular rhythm is usually regular, with a frequency of 150 beats / minute, corresponding to a heart block 2 / 1.

Atrial flutter may be paroxysmal, or rarely, permanent, and if the arrhythmia persists for more than a week, there is a tendency to pass into atrial fibrillation.

Atrial Flutter

Causes:

Atrial flutter, appears in the following situations:

• In heart disease: myocardial infarction, coronary artery disease, mitral stenosis, aortic stenosis, mitral regurgitation, aortic regurgitation, hypertrophic cardiomyopathy, dilated cardiomyopathy, hypertensive cardiomyopathy, myocarditis, pericarditis, chronic pulmonary heart disease;
• Other medical conditions: hypoxia and hypercapnia, in chronic hyperthyroidism, electrolyte disturbances, hypotension, cardiogenic shock, acute alcoholism, coffee and tobacco abuse and stress.

Atrial Flutter

Diagnosis of atrial flutter:

The diagnosis of atrial flutter is based on the symptoms, on the physical examination and on the ECG interpretation.

Symptoms. Severity of symptoms depends on the ventricular rate and heart condition. May be present: palpitations, dizziness, anxiety, faintness, shortness of breath, attacks of angina pectoris (especially in form with atrioventricular block 2 / 1) especially if it is a severe cardiomyopathy. Atrial flutter with ventricular rate of 75 beats / minute may be asymptomatic.

Physical examination may reveal the following aspects:

• Heart sounds are usually tachycardic and regular, but sometimes may be irregular, when exist a variable atrioventricular block.
• Effort can double the ventricular rate ( from 75 beats / minute increase to 150 beats / minute or from 150 beats / minute increase to 300 beats / minute), or can have no effect.
• Vagal stimulation maneuvers produce an increasing in atrioventricular block with ventricular rate which will be temporarily decreased, which will return to the baseline value after the cessation of the maneuver.

ECG examination shows the following:

• The absence of P waves, the P waves are replaced by “F” waves of flutter, between which are no isoelectric intervals.
• F waves have a frequency of 250-350 beats / minute, are monomorphic, regular and have the appearance of “saw tooth”.
• QRS complex has a normal aspect, it may have a longer duration than usual, if there is a branch block or a ventricular preexcitation syndrome.
• In the absence of atrioventricular accessory pathways, driving trough ventricles is the most common, with block 2 / 1 ( can be met atrioventricular block  3 / 1 or 4 / 1). Atrioventricular driving 1 / 1, although rare, is possible and occurs when the atrial rate is lower (about 200 beats / minute), in ventricular preexcitation syndromes, in hopertiroidism and in children.
• When driving is variable, QRS complexes occur at irregular intervals, and F waves are well evidenced in the ECG.

Atrial flutter ECG

Treatment of atrial flutter:

Treatment of atrial flutter consists of: electrical conversion, rapid atrial electrostimulation (overdriving) or pharmacological conversion.

• Electrical conversion is currently recommended in forms of atrial flutter with hemodynamic deterioration or in combination with Wolf-Parkinson-White syndrome. After sedation, is applied an external electric shock, synchronous with low energy (20-50 joules), which can be repeated if necessary. Anticoagulant therapy should be considered in case of atrial flutter with a length greater than 48 hours.
• Rapid atrial electric stimulation (overdriving) shall be done in atrial flutter occurred after open heart surgery or after the onset of a myocardial infarction, especially in patients who are treated with digoxin.
• Pharmacological treatment is aimed at patients with atrial flutter who are hemodynamically stable:

1. First will be tempt the decrease of ventricular rate with atrioventricular blockers: verapamil, diltiazem, digoxin, esmolol. Sometimes digoxin can converse a atrial flutter into a atrial fibrillation.
2. Pharmacological conversion of atrial flutter is done with antiarrhythmic from class I and class III, in particular: flecainide, propafenone, sotalol, amiodarone, dofetilide, ibutilide, which are intravenously administered. They will be used, only if the treatment to decrease ventricular rate was effective because the decrease only of  the atrial rate with antiarrhythmics from class I and class III will induce the appearance of atrioventricular block.
3. For prevention of recurrence of atrial flutter, are used antiarrhythmics from class IA, class IC and class III, but with limited effectiveness. Failure of atrial flutter recurrence prevention requires the radiofrequency current ablation.

Atrial Fibrillation

Atrial fibrillation is defined by an anarchic atrial electrical activity with a frequency of 350-600 beats / minute, with the cancellation of atrial mechanical function. Ventricular rhythm is completely irregular, usually with a frequency between 100 and 150 beats / minute. Irregular ventricular rhythm is due to a hidden driving trough atrioventricular junction.

Clinical classification of atrial fibrillation is done according to guidelines proposed by the American Heart Association, in the following types:

• Paroxysmal atrial fibrillation: lasts several minutes, hours or up to 7 days and resolves spontaneously;
• Recurrent atrial fibrillation: the patient had repeated episodes of atrial fibrillation, remitted either spontaneously or with treatment;
• Persistent atrial fibrillation: lasting more than seven days and dose not resolves spontaneously;
• Permanent atrial fibrillation (chronic),  which can not be remitted with treatment.

Atrial Fibrilation Causes:

Paroxysmal atrial fibrillation may occur in a healthy heart in the following situations:

• Acute alcoholism;
• Coffee and tobacco abuse;
• Stress.

In a diseased heart, paroxysmal atrial fibrillation occurs in the following situations:

• Myocardial infarction;
• During invasive investigations and during interventions: cardiac catheterization, coronary arteriography, surgical interventions;
• In other situations: acute hypoxia, hypercapnia, electrolyte disturbances, hypotension, cardiogenic shock, etc.

Permanent atrial fibrillation, appears in the following situations:

• In heart disease: coronary artery disease, mitral stenosis, aortic stenosis, mitral regurgitation, aortic regurgitation, hypertrophic cardiomyopathy, dilated cardiomyopathy, hypertensive cardiomyopathy, myocarditis, pericarditis, chronic pulmonary heart disease;
• Other medical conditions: hypoxia and hypercapnia, in chronic hyperthyroidism;
• In 15% of cases, permanent atrial fibrillation is idiopathic, especially in men.

Atrial fibrillation

In terms of pathophysiology, atrial fibrillation, causes the following changes:

1. Reduced cardiac output by atrial systole loss, cardiac output is reduced by 20-30% and by shortening of  the diastole, cardiac output is reduced in proportion to the increase of ventricular rate;
2. Worsening of hemodynamic status, particularly in patients with heart failure, mitral stenosis and ventricular diastolic dysfunction;
3. The occurrence of angina pectoris, in cases of atrial fibrillation with increased ventricular rate by increasing the myocardial oxygen consumption and by the shortening of diastole, will appear the reduction of coronary perfusion.
4. Atrium thrombus formation, with the risk of systemic embolism and of pulmonary embolism.

Atrial Fibrilation Diagnosis

Symptoms of atrial fibrillation are polymorphic. The patient may feel palpitations, anginal pain, the worsening of heart failure symptoms, syncope (if ventricular rate is very high or very low). Atrial fibrillation with ventricular rate close to normal may be asymptomatic.

Physical examination may reveal the following aspects:

• Total irregular heart rhythm, usually with an accelerated rate (100-160 beats / minute) and heart sounds unequal in intensity;
• Peripheral arterial pulse is irregular and unequal in amplitude. At accelerated ventricular rates is present a pulse deficit, due to excessive shortening of diastole, with reduction of the end diastolic volume and therefore will appear a reduce in systolic flow, so that aortic valve does not open. So, not all cases of atrial fibrillation have pulse deficit, but only the forms with marked tachycardia. The effort accentuates the  symptoms and signs of atrial fibrillation.
• ECG shows the following: absence of P waves, atrial electrical activity is replaced by  “f” waves, with small amplitude, irregular and with a frequency between 350-600 beats / minute.  Ventricular rhythm is irregular, with a rate between 100 and 150 beats / minute. QRS complex has a shorter duration than normal.

Sino-carotid massage may cause a transient reduction in heart rate and is useful in the differentiation of atrial fibrillation form atrial flutter.

ECG with Atrial Fibrillation

The prognosis of atrial fibrillation, depends  in particular on:

1. Ventricular myocardium state, which is dependent on the underlying disease, will dictate the degree of hemodynamic deterioration.
2. The presence of atrial thrombus, which is leading to an increased incidence of thromboembolic accidents, of which 75% are cerebrovascular accidents (strokes).

Atrial Fibrilation Treatment

Treatment of atrial fibrillation has the following objectives:

1. Conversion to sinus rhythm (electric or medication), when is indicated and possible;
2. Relapse prevention;
3. Prevention of thromboembolic complications;
4. Control of ventricular function when converting and maintaining of sinus rhythm are not possible.

The choice of therapeutic methods, in the treatment of atrial fibrillation is individualized and should consider the etiologic substrate of atrial fibrillation.

Treatment for paroxysmal atrial fibrillation access:

• Treatment of paroxysmal atrial fibrillation with hemodynamic deterioration associated with myocardial ischemia or Wolff-Parkinson-White syndrome, is electric conversion to sinus rhythm.
• In the case of hemodynamically stable atrial fibrillation, are performed the following:

1. Rate control is the main therapeutic target that can be achieved rapidly by intravenous administration of beta-blockers (metoprolol, bisoprolol) or calcium channel blockers (diltiazem).
2. Pharmacological conversion to sinus rhythm can be achieved by administration of antiarrhythmic agents from  class III (amiodarone, sotalol), class IA (disopyramide) or class IC (propafenone, flecainide).
3. Electric conversion is performed if pharmacological conversion attempt failed for 24 hours.

Atrial Fibrillation Drug Treatment

In the case of electrical or pharmacological conversion of atrial fibrillation, is required the prevention of thromboembolic complications, by the following measures:

• In patients with atrial fibrillation which was installed in less than 48 hours and the patients will be subjected to conversion to sinus rhythm, anticoagulation therapy management is optional, depending primarily on the associate risk of embolism.
• If the occurrence of atrial fibrillation happened in more than 48 hours, and the patient has a higher risk for embolism, then the treatment with oral anticoagulants is required at least with 2 weeks before conversion and must be continued 2 weeks after conversion to sinus rhythm.
• Emergency defibrillation involves anticoagulation with intravenous heparin, initially in bolus and then in continuous infusion in a dose that prolongs the APTT with 1.5-2 times compared to its reference value. After defibrillation, oral anticoagulation therapy should be continued for a period of 2 weeks.

Prevention of recurrence of atrial fibrillation:

Prevention of atrial fibrillation recurrence is performed by administering antiarrhythmic drugs from class IA, class IC and class III. An alternative therapy to prevent relapse of atrial fibrillation, is represented by atrial pacemaker implant, with the anti-tachycardia function.

Treatment of permanent atrial fibrillation:

Atrial Fibrillation

This type of atrial fibrillation has low chances of conversion to sinus rhythm, especially if left atrial diameter exceeds 5 cm.

Heart rate control in permanent atrial fibrillation is performed, electively, with digoxin, which may be associate with low-dose of beta-blocker, verapamil or amiodarone. Optimal therapeutic effect is considered to be obtained when heart rate reaches 60 to 80 beats / minute.

In the case of bad tolerated chronic atrial fibrillation, is practice atrio-ventricular node ablation or ablation of His fascicle by radiofrequency current, followed by permanent pacemaker implantation.

Salmonella Infection

Genus Salmonella belongs to the family Enterobacteriaceae, together with Escherichia coli. Are gram-negative, motile, aerobic or facultative anaerobic bacilli, meaning that they can develop in the absence of oxygen.

Are bacteria that are isolated from soil, water, plants, human and animal intestine. Are part of the body’s normal flora, some species of Salmonella having exclusively human habitat (Salmonella typhi). In terms of pathogenicity, bacteria of the genus Salmonella are highly pathogenic and conditioned pathogenic.

Genus Salmonella germs are resistant in the environment. Salmonella can survive about 5-6 months in polluted water and faeces, survives and multiply at room temperature in wet environments, in food and infusion solutions. The possibility of spreading in the community and in hospitals is very high. Salmonella is destroyed by heat (in 30 minutes at temperatures of 55-60º  Celsius degrees and instantly at boiling temperature), antiseptics and disinfectants.

Salmonella Infection

With modern methods of molecular taxonomy in the Salmonella genus two species are described:

• Salmonella enterica, with 6 subspecies: enterica, salamae, arizonae, diarizonae, houtenae and indica;
• Salmonella bongori.

99.5% of Salmonella strains, involved in human pathology are belonging to Salmonella enterica species.

On the basis of somatic O antigen (antigen-specific group), were described several serological groups, denoted with large letters of the alphabet, from humans being isolated strains belong mainly to A-E groups. H antigen allows individualization in the same group (Salmonella enterica) of the serotypes: Salmonella typhy (the etiologic agent of typhoid fever), Salmonella typhimurium and Salmonella enteritidis.

Pathogenesis and symptoms:

All serotypes of Salmonella enterica are pathogenic to humans and mammals, while serotypes of Salmonella bongori are typically found in birds and cold-blooded animals.

The two major sources of infection, human and animal, are responsible for pollution of soil and water, in which Salmonella can live for a long time.

Germs of the genus Salmonella are highly pathogenic bacteria. The entrance gateway is represented by the digestive tract (small intestine epithelium) that all species of Salmonella can penetrate it.

Salmonella Infection Pathogenesis

Three clinical types of salmonellosis have been described in humans:

Enteric fevers or systemic salmonellosis (typhoid fever and paratyphoid fever), are caused by Salmonella typhi (typhoid fever) and Salmonella paratyphi A, B and C (paratyphoid fever). Are clinical entities distinct from other salmonellosis, with characteristic clinical development and followed by lasting immunity. Contamination is made orally, by eating infected food or by drinking infected water. After an incubation period of about 14 days, the disese begins with lethargy, malaise, fever and generalized pain (during the first week). Constipation is a rule along this period. In the second week the microorganism is back into circulation (bacteremia) and will cause high fever, sensitive stomach and possibly pink macules on the abdominal skin. Diarrhea occurs at the end of the second week or at the beginning of the third week.

The disease is self-limiting, but severe complications are possible (intestinal perforation, severe bleeding due to disseminated intravascular clotting, thrombophlebitis, cholecystitis, cardio-vascular disorders, pneumonia, abscesses).

Enteric salmonellosis are food poisoning (acute gastroenteritis) and represent the common form, widespread in all countries. They are caused most frequently by Salmonella enteritidis and Salmonella typhimurium. Symptoms appear in 10-24 hours after eating contaminated food or drinking contaminated water. Characteristic symptoms are diarrhea, abdominal pain, vomiting, fever, which disappear within 2-4 days.

Enteric salmonellosis in infants, elderly or immunosuppressed may be complicated by bacteremia with secondary localization in the meninges, joints, bone, with a mortality rate of 10-20%.

Bacteremia, with or without the existence of enteritis outbreaks, is caused by Salmonella typhimurium, Salmonella paratyphi A and B and by Salmonella choleraesuis. Mainly affect two age groups. In young children is manifested by fever and gastroenteritis, and in adults is manifested by transient bacteremia during episodes of gastroenteritis, or signs of sepsis without gastroenteritis (in the immunosuppressed).

Chronic carriers, asymptomatic are represented by a rate of 1-5% of patients with typhoid fever or paratyphoid fever. The germs are located in the gallbladder and are excreted continuously or intermittently through feces. This porting condition can be stopped by antibiotics or cholecystectomy.

Salmonella Food Poisoning

Transmission and prophylaxis:

Enteric fevers may evolve endemo-epidemic. Source of infection is represented by patients or carriers, and transmission occurs through fecal-oral mechanism, by consuming water or, less commonly, by contaminated food. Responsiveness is general and is conditioned by the absence of specific immunity.

Food poisoning are often produced by animal pathogens that are transmitted to humans through contaminated food (eggs, meat, milk, mayonnaise, pate), from chickens, turkeys, ducks. It was noted that tools such as knives, bowls, wood chippers, used in the preparation of contaminated food can contribute to the spread of germs on other foods. It is considered that the dose of bacterial contamination is 1.000.000 bacteria or less. The incidence of these infections is higher in summer months.

Salmonella infections are prevented by adequate sanitation and especially by immunization of domestic animals kept for meat consumption. Meat control  in slaughterhouses and proper thermal preparation of food are designed to reduce the risk of infection.

Indiscriminate use of antibiotics to promote animal breeding should be avoided to prevent emergence of resistant strains of Salmonella. Healthy carrier detection is important, but does not replace  the local igena measures.

Specific prophylaxis by anti-typhoid vaccine is recommended for people who work in the sectors of water supply or in slaughterhouses, and those traveling to endemic areas, or population to natural calamities areas (earthquakes, floods).

Anti-Thyroid Vaccine

Treatment:

The enteric fevers in forms with sepsis and enteric salmonellosis in infants and young adults, are treated by using antibiotics with intracellular action: ampicillin, cotrimoxazole, chloramphenicol, ciprofloxacin, fluoroquinolones, third generation cephalosporins.

Food poisoning are treated symptomatically. Antibiotic treatment does not shorten the clinical manifestations and, moreover, extend the porting state.

Pulmonary Heart Disease

Pulmonary heart disease is defined as a dilation of the right ventricle, with or without right ventricular hypertrophy produced due to pulmonary diseases, from vascular or parenchymatous nature.

Pulmonary Heart Disease Causes

1. The main causes of acute pulmonary heart disease are: pulmonary embolism, which interest more than 50% of the pulmonary vascular network.
2. Chronic pulmonary heart disease of parenchymal nature cause are: chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, large pleural fibrosis (post-tuberculosis, the most common), cifo-scoliosis, morbid obesity, sleep apnea, polycythemia vera.
3. Chronic pulmonary heart disease of vascular nature cause are: recurrent pulmonary embolism and primary pulmonary hypertension.

Pulmonary Heart Disease Classification

After the rapidity of installation, pulmonary heart disease is classified as acute pulmonary heart disease and chronic pulmonary heart disease. In its turn, chronic pulmonary heart disease is classified as follows :

According to the type of lung disease:

1. Chronic pulmonary heart disease of vascular nature;
2. Chronic pulmonary heart disease of parenchymal nature.

After the absence or presence of signs of right heart failure:

1. Compensated chronic pulmonary heart disease;
2. Decompensated chronic pulmonary heart disease.

The link between lung disease and heart disease is represented by pulmonary hypertension, defined by pulmonary arterial systolic pressure values over 30 mmHg (normal 22-30 mmHg) and mean pulmonary arterial pressure over 20 mmHg (normal 13 -18 mmHg). Pulmonary hypertension results from the following mechanisms:

• Pulmonary arterial vasoconstriction, caused by hypoxia;
• Increased blood viscosity;
• Thickening, with lumen reduction of pulmonary vessels.

Pulmonay heart disease

Pulmonary Heart Disease Symptoms

Clinical manifestations are nonspecific for pulmonary heart disease. They differ in acute pulmonary heart disease from chronic pulmonary heart disease.

Acute pulmonary heart disease

The onset of acute pulmonary heart disease is suddenly and can occur in the suggestive context of thrombophlebitis of the lower limbs. Nonspecific symptoms are:

• Extremely severe polipnea, without changes in physical examination;
• Unexplained anxiety;
• Chest pain;
• Syncope.

Physical examination may reveal:

• Skin changes: cyanosis, pallor, sweating;
• Signs of cerebral hypoperfusion: agitation, confusion and even coma;
• Tachypnea;
• Tachycardia, gallop rhythm of the right ventricle,systolic murmur of tricuspid regurgitation;
• Signs of decompensation of the right ventricle: jugular turgor, hepatomegaly, often painful, hepato-jugular reflux, lower limb edema.
• Hypotension.

Chronic pulmonary heart disease:

Onset is insidious, clinical manifestations are dominated by the respiratory disease.

Symptoms are also nonspecific: dyspnea, fatigue, chest pain, cough, hemoptysis and in severe forms, dysphonia.

Physical examination may reveal:

• Mixed type of skin cyanosis, sometimes jaundice;
• Changes in cardiac examination: left parasternal impulse given by right ventricular hypertrophy, tachycardia, atrial or ventricular gallop, right systolic murmur of tricuspid regurgitation, systolic ejection murmur at pulmonary focus, diastolic murmur of pulmonary regurgitation.
• Signs of decompensation of the right ventricle: jugular turgor, hepatomegaly, hepato-jugular reflux, edema.

Pulmonary Heart Disease

Paraclinical examination

Chest radiography may reveal:

• Increased transverse diameter of heart;
• Increased inferior branches of pulmonary artery;
• Specific changes that caused pulmonary heart disease.

ECG shows the following changes:

1. In acute pulmonary heart disease: right axial deviation, complete or incomplete right bundle branch block, sinus tachycardia, reversal of T waves in right chest leads.
2. In chronic pulmonary heart disease: right ventricular hypertrophy, right bundle branch block, P wave of pulmonary type, sinus tachycardia, atrial or ventricular arrhythmias.

Two-dimensional echocardiography shows the existence of the right ventricle dilatation. Doppler ultrasound allows measurement of systolic pressure of pulmonary artery and will confirm the pulmonary or tricuspid regurgitation.

Biological tests:

• Increased hematocrit and hemoglobin (secondary to chronic hypoxia or polycythemia vera);
• Changes in blood gases: decreased  oxygen partial pressure, carbon dioxide partial pressure is normal or decreased.

Other tests: respiratory function tests, pulmonary ventilation and perfusion scintigraphy, right heart catheterization, pulmonary angiography, chest CT.

Positive diagnosis is established on history, clinical signs and paraclinical investigations. It is often uncertain for acute pulmonary heart disease.

Pulmonary Heart Disease Echography

Pulmonary Heart Disease Evolution And Prognosis

In acute pulmonary heart disease, short-term prognosis is reserved. Mortality exceeds 25%, death occurring usually within 2 hours after pulmonary embolism. Those who survive this period, will develop cardiogenic shock in the next period. If this period is also exceeded, the evolution is favorable, the recovery is, most often, complete. But there is the risk of pulmonary embolism recurrence and the risk of development of chronic pulmonary heart disease in time.

In chronic pulmonary heart disease, evolution is long, slow and progressive. On this background there is a possibility of decompensation caused by hypoxia, consecutive to intercurrent respiratory infections. Over-addition of atrial fibrillation or atrial flutter, aggravates the prognosis.

Pulmonary Heart Disease Treatment

Acute pulmonary heart disease:

1. Supportive measures: oxygen therapy, on the tube or mask, appropriate parenteral hydration, inotropic support to maintain blood pressure over 90 mmHg.
2. Anti-coagulation treatment is designed to prevent the increasing in size of the emboli. In the absence of contraindications, anti-coagulation therapy should be started even if the diagnosis is uncertain, but is likely. It begins with heparin or fractionated heparin, according to known protocols. The heparin treatment is continued with oral anticoagulants administered so that INR is maintained between 2 and 3.
3. Thrombolytic therapy is designed to dissolve the blood clots. It is established in patients with pulmonary embolism who have signs of hemodynamic instability, being more efficient if is given earlier.
4. Surgical embolectomy or catheter suctioning of the emboli is a last resort solution,  in patients who continue to deteriorate despite conservative treatment which is properly administered.

Cardiac Catheterization

Chronic pulmonary heart disease:

Treatment is aimed, primarily, to solve the lung disease that is generating the chronic pulmonary heart disease (COPD, pulmonary embolism). Improved lung function leads, by increasing the oxygen partial pressure, to lower pulmonary artery pressure.

Diuretics are used for fluid retention. These drugs are administered only after the improvement of respiratory function. Caution must be employed to avoid electrolyte disturbance which, in conditions of hypoxia, can lead to severe ventricular arrhythmias.

Digoxin is not indicated in case of sinus rhythm, because it has no positive inotropic effect on the right ventricle and may promote ventricular arrhythmias. It is recommended for heart rate control, in case of atrial fibrillation.

Other therapeutic methods are the vasodilatory medications (calcium channel blockers, prostacyclin, endothelin receptor antagonists), chronic anticoagulation therapy (in chronic pulmonary heart disease of vascular nature), provoked bleeding (300-400 ml) if the hematocrit is above 55% and lung transplantation.

 Rheumatoid Arthritis

Rheumatoid arthritis is a chronic disease, which is affecting peripheral joints. Given that rheumatoid arthritis is an inflammatory disease, in which the pathogenic immune process causes cartilage destruction and bone erosion, the treatment of rheumatoid arthritis has the following objectives:

1. Fighting the articular and extra-articular inflammatory process of rheumatoid arthritis.
2. Interfering with the pathogenic chain of rheumatoid arthritis by using disease modyfing anti-rehumatic drugs (DMARDs).
3. Maintain or restore the  morphological and functional integrity of the joints.                                                                                                                                                                                                                                                                    
   Fighting the articular and extra-articular inflammatory process, in rheumatoid arthritis using anti-inflammatory medications (non-steroidal and steroidal).

Rehumatoid Arthritis

Non-steroidal anti-inflammatory drugs (NSAIDs):

Considering the selectivity for the inducible cyclooxygenase (COX2), NSAIDs used to treat rheumatoid arthritis are:

• Classic NSAIDs:  inhibit COX1 and COX2 approximately equal (aspirin, diclofenac, ketoprofen, tenoxicam, indomethacin, ibuprofen);
• COX2 – selective: predominantly inhibit COX2 compared to COX1, which causes high antiinflammatory activity and few adverse effects (meloxicam, nimesuluid);
• COX2 – specific: only inhibit COX2. They have an antiinflammatory efficiency comparable to diclofenac in optimal dose, but with fewer side effects (celcoxib, etoricoxib).

Adverse effects of NSAIDs are upper gastrointestinal bleeding, gastroesophageal reflux, anal heartburn (especially if using suppositories), mucocutaneous manifestations (rash, itching, bronchospasm, allergic rhinitis).

In usual doses, therapeutic response to NSAIDs is individualized, meaning that the same drug have varied effects from case to case.

Corticosteroid therapy:

Corticosteroid therapy is used in rheumatoid arthritis, in situations where inflammation is not controlled by NSAIDs. There are three ways of administering cortisone preparations:

Oral use (prednisone). In severe cases of rheumatoid arthritis (acute multiple arthritis, pyrexia, profound alteration of general condition): prednisone in doses of 60-80 mg / day or 1 mg / kg / day or 30-40 mg / day for 1 – 2 weeks. The dose is reduced by 5 mg per week, and when it comes to doses of 15-20 mg / day, is switched to alternate administration (eg., one day is administered 15 mg of prednisone and the next day 5 mg of prednisone or pause) . The total duration of treatment is 3-4 weeks or months.

In medium forms of rheumatoid arthritis, it is recommended taking prednisone at a dose of 5-7.5 mg / day for a long time (months). This is active management is minimizing the adverse effects of corticosteroid therapy.

Intravenous administration of methylprednisolone is an indication in an exacerbation of rheumatoid arthritis. Is recommended pulse therapy and consists in daily administration, in intravenous infusion, of 1 g of methylprednisolone in 200 ml of NaCl 9° or glucose 5% for 3 days, consecutive. Antiinflammatory effects occurs rapidly and lasts 30-40 days. Efficiently is the mini-pulse therapy, consisting of 100-200 mg of methylprednisolone administration by intravenous infusion for 3 consecutive days, especially recommended in situations of rebound occurred during the reduction of prednisone dose.

Administration of intra-articular corticosteroids is recommended when the inflammatory process persists at 1 or 2 joints. Is recommended a maximum of 3-5 injections.

Methylprednisolon

Disease modyfing anti-rehumatic drugs (DMARDs):

Methotrexate (2.5 mg tablets), a folic acid antagonist, has become the most widely used DMARDs agent because it has a not very late onset, after 4-6 weeks, ease of administration and good tolerance. Therapy with methotrexate is indicated for patients with active form of rheumatoid arthritis and poor prognosis, and the dose ranges from 7.5-25 mg / week in three doses at intervales of 12 hours. Stomatitis, alopecia and mild abdominal discomfort, arising from the antagonism of folic acid and can be improved by supplementation with folic acid (1mg/day). Fortunately, most serious complications of methotrexate therapy (liver cirrhosis, pulmonary fibrosis, severe mileosuppression) are rare. Routine monitoring of toxicity is mandatory and includes complete blood count, weekly and then monthly, dosage of AST, ALT, serum albumin and serum creatinine at intervals of 4-8 weeks. Duration of treatment depends on results and side effects emerged, but anyway, is extended to several months or years.

Methotrexate

Sulphasalazine (500 mg tablets) in doses of 2-3 g, is the first DMARDs used in patients with mild rheumatoid arthritis and negative rheumatoid factor. Although it is well tolerated, at only a limited number of patients with rheumatoid arthritis induces complete remission. Duration of therapy is similar to that of methotrexate.

Gold salts (Tauredon, ampoules of 10 mg and 50 mg), intramuscular injections are used in rheumatoid arthritis as follows: 10 mg in the first week, 20 mg in the second week and then 50 mg / week until the achievement of a therapeutic response or up to a total dose of 1 g. The treatment may prolong until the total dose of 2500-3000 mg.

Leflunomide (Arava tablets 10 mg, 20 mg and 100 mg) became available as an DMARDs agent in rheumatoid arthritis from 1998, is a effective imunosupersor similar to methotrexate, representing an alternative for unresponsive patients with rheumatoid arthritis at therapy with methotrexate or patients with methotrexate intolerance. The action of this drug is installed after 4-8 weeks. To achieve an optimal therapeutic concentrations is required a loading dose of 100 mg / day for 3 consecutive days, followed by a maintenance dose of 20 mg / day. Therapy monitoring is done by determining of complete blood cell counts and transaminases, every 2 weeks during the first month and then monthly.

Leflunomide

Inhibitors of tumor necrosis factor alpha used in rheumatoid arthritis are :

• Etanercept (Enbrel), a protein similar to a human monoclonal antibody that binds tumor necrosis factor alpha and inhibit its activity. It is available in ampoules of 25 mg and is injected subcutaneously 2 times a week. Therapeutic effect will appear after 1-2 weeks of treatment.
• Infliximab (Remicade) is a genetically engineered monoclonal antibody that binds with high affinity and specificity the tumor necrosis factor alpha and inhibits it. In combination with methotrexate, inhibits the progression of disease in patients with moderate or severe rheumatoid arthritis who have inadequate or no response to methotrexate therapy. The first dose is 3 mg / kg, administered intravenously, followed by a dose of 3 mg / kg after 2 or 6 weeks after the first dose, then intravenous infusion every 8 weeks in combination with oral methotrexate for at least 1 year or as long as the disease is active.

Other chemotherapy medication use in rheumatoid arthritis: azathioprine, phosphamide, cyclosporin A, in normal doses are used for patients with aggressive forms of rheumatoid arthritis or forms of rheumatoid arthritis with extra-articular manifestations such as systemic vasculitis.

Infliximab

Maintain or restore the  morphological and functional integrity of the joints:

Synovial destruction, chemical with morurat or isotopic with lithium salts, by intra-articular injections, have very limited indications (one joint which is rebellious to medication).

Surgical procedures in rheumatoid arthritis can be practiced early in the disease or in advanced forms of disease.

When a few joints are interested with major synovial proliferation, synovial destruction is recommended, the procedure will improve the local and general condition. Splenectomy is recommended in rheumatoid arthritis associated with splenomegaly (Felty’s syndrome). In very advanced stages of rheumatoid arthritis, when there are major joint damage, orthopedic surgery can correct them by prostheses use.

In rheumatoid arthritis defined by clinical criteria of American College of Rehumatology, treatment is differentiated according to clinical form and stage of the disease. Obtaining a favorable response to one drug requires to continue the therapy, while inadequate response require the addition of other drugs.