SINUS BRADYCARDIA

SINUS TACHYCARDIA

PATHOPHYSIOLOGY In sinus bradycardia, a P wave precedes each QRS. A normal P wave and PR interval (0.12-0.20) indicate that the impulse originated in the SA node rather than in another area of the conduction system that has a slower inherent rate. Vagal stimulation decreases the firing rate of the SA node and conduction through the AV node to cause a decrease in the heart rate. Vasovagal responses may be associated with a profound bradycardia due to direct parasympathetic action on the SA node. The combination of the slow heart rate and an associated decline in peripheral vascular resistance is often sufficient to produce presyncope or syncope. Stimuli for vagal activation include pressure on the carotid sinus (as may occur with a tight collar or with the impact of the stream of water in a shower), vomiting, a Valsalva maneuver when straining at stool, or sudden exposure of the face to cold water. Eye surgery can also produce sinus bradycardia and sinus arrest can occur during REM sleep The mechanism of tachycardia is enhanced automaticity related to sympathetic stimulation or withdrawal of vagal tone. Sinus tachycardia is a normal response during fever and exercise and in situations that incite sympathetic stimulation. When the sinus node fires with a frequency rate between 100-180bpm, the term sinustachycardia is used. The maximum heart rate a person can achieve during exercise can be calculatedbe estimated by subtracting the age in years from 210, although it is not uncommon for sinus rates to peak above 200/min during vigorous exercise. Usually it is a physiological reaction to stress (exercise, inflammation, stress). External factors can increase the heart rate like coffee and alcohol or drugs. The term inappropriate sinus

COMMON ETIOLOGY Inferior wall myocardial infarction, toxic or environmental exposure, electrolyte disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased intracranial pressure.

MANIFESTATION Often asymptomatic. However, symptoms may include the following: >Syncope >Dizziness >Lightheadedness >Chest pain >Shortness of breath >Exercise intolerance Cardiac auscultation and palpation of peripheral pulses reveal a slow, regular heart rate. The physical examination is generally nonspecific, although it may reveal the following signs: >Decreased level of consciousness >Cyanosis >Peripheral edema >Pulmonary vascular congestion >Poor perfusion

MANAGEMENT A medication that may be depressing sinus node function. As an example, a -blocker or sympathetic blocker can be replaced in hypertensive patients with drugs that do not affect SA node function, such as an angiotensin converting enzyme inhibitor. The sympatholytic agent should not be discontinued abruptly, since a withdrawal syndrome characterized by severe hypertension may be seen

Hyperthyroidism, Fever, Effective volume depletion, Anxiety,Pheochromocyto ma, Sepsis, Anemia, Hypotension and shock, Pulmonary embolism, Acute coronary ischemia and myocardial infarction, Heart failure, Chronic pulmonary disease, Hypoxia, Exposure to stimulants (nicotine, caffeine) or illicit drugs

Often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease

Usually the sinus tachycardia will pass when the external trigger is removed. If patients have persistent complaints, the trigger cannot be removed or in case of an inappropriate sinus tachycardia a beta-blocker can be administered. Patients with a contra-indication for beta-blockers can use nondihydropyridine calcium-channel blockers.

tachycardia is a persistent increase in resting heart rate or sinus rate unrelated to or an exaggerated response to stress in a person without structural heart disease. SINUS ARRYTHMIA Occurs when the sinus nodes creates an impulse at an irregular rhythm; the rate usually increases with inspiration and decreases with expiration Caused by normal variations in vagal tone. Vagal tone refers to signals from the vagus nerve. Your vagus nerve runs from your brain to your chest and abdomen. Signals from the vagus nerve help regulate your heart rate. Variations in vagal tone are common in children and will lessen, but not disappear, with age. Sick sinus syndrome, Increased vagal tone (athletes), Vagal stimulation (surgery, pain),Inferior myocardial infarction, Myocarditis Sinus arrhythmia does not cause any significant hemodynamic effect. Heart rate speeds up when you breathe in and slows down when you breathe out. If you have sinus arrhythmia and you know how to take your pulse, you may notice a slight change in pulse rate as you breathe in and out. Otherwise, there are generally are no symptoms of sinus arrhythmia. Usually not treated

SA BLOCK

Sino-atrial exit block is due to failed propagation of pacemaker impulses beyond the SA node.The sino-atrial node continues to depolarize normally. However, some of the sinus impulses are blocked before they can leave the SA node, leading to intermittent failure of atrial depolarization (dropped P waves). First Degree SA block - Delay between impulse generation and transmission to the atrium Second Degree SA block, Type I (Wenckebach) - Progressive lengthening of the interval between impulse generation and transmission, culminating in failure of transmission Second Degree SA block, Type II - Intermittent dropped P waves with a constant interval between impulse generation and atrial depolarization Third Degree SA Block - None of the sinus impulses are conducted to the right atrium

The heart rate will slow, and symptoms of low blood pressure or stroke will appear. -The person may feel dizzy, weak, confused, or may have less tolerance for exercise.

Drugs: digoxin, betablockers, calcium channel blockers, amiodarone.

SINUS PAUSE/ ARREST

Sinus arrest refers to failure of the SA node to discharge and results in an irregular pulse. An escape rhythm develops as another pacemaker takes over. This may result in prolonged periods of asystole and often predisposes to other arrhythmias

PREMATURE ATRIAL CONTRACTION

Premature atrial contractions are contractions that originate in the atrial conduction pathways or atrial muscle cells and occur before the next expected SA node impulse. This impulse to contract usually is transmitted to the ventricle and back to the SA node. The location of the ectopic focus determines the configuration of the P wave. The retrograde transmission to the SA node often interrupts the timing of the next sinus beat, such that a pause occurs between the two normally conducted beats.

ATRIAL TACHYCARDIA

Atrial tachycardia (AT) is a tachycardia resulting from fast firing in an ectopic focus or micro re-entry circuit in the atria. It has a rate of 100bpm. In some patients the tachycardia has multiple foci (multifocal atrial tachycardia). This results in different

Increased vagal tone, or carotid sinus hypersensitivity, acute myocardial infarction, sinus node degeneration and fibrosis, cerebrovascular disease, accidents, use digitalis, quinidine, potassium, acetylcholine and other drugs. -Alcohol -Smoking -Drugs such as cocaine; -Caffeine -Tricyclic antidepressants -Magnesium and potassium deficiency -Calcium excess; -Thyroid problems; -Chemical (electrolyte) problems in the blood -Heart attack -Adrenaline excess; -Lack of sleep/exhaustion -Stress -Certain medicines such as digoxin, which increases heart contraction Myocarditis; -Cardiomyopathy, hypertrophic or dilated; -Myocardial contusion; -Hypoxia; -Hypercapnia (CO2 poisoning); -Mitral valve prolapsed >Damage to heart tissues from heart disease >Disease or congenital abnormality of the heart >High blood pressure >Smoking

-patients with a long period of sinus arrest have dizzy, -disturbance of consciousness, or even seriously convulsions.

installation of artificial cardiac pacemakers.

Fortunately (considering that they are so common), in most cases PACs do not cause any symptoms at all. However, some people will experience palpitations with PACs, in which case they usually describe a "skipping" sensation, or an unusually strong heart beat. Experiencing palpitations is much more likely after ingesting alcohol, tobacco, caffeine, or medications containing stimulants, all of which are known to increase the frequency of PACs, and to make them more noticeable.

Medications such as beta blockers or calcium blockers are often used but with mixed result. Most important treatment, after ruling out severe underlying heart conditions, is patient reassurance and teaching of various coping mechanisms.

>Dizziness >Lightheadedness >Rapid heartbeat or "palpitations" >Angina (chest pain)

Vagal manoeuvres or adenosine can be effective in terminating focal AT. If AT persist and is drug-resistant DC cardioversion can be indicated. Recurrent episodes of AT can be prevented with anti-arrhythmic

P-wave morphologies on the ECG during the arrhythmia. Atrial tachycardia can be caused by all the mechanisms of arrhythmia formation. Patients after earlier surgery or catheter ablation usually present with macro re-entry AT located around functional or anatomical sides of block. Atrial flutter is a distinct type of AT, but due to its unique mechanism it is discussed separately.

>Drinking too much alcohol/caffeinated beverages

ATRIAL FLUTTER

Atrial flutter (AFL) is the most common type of atrial tachycardia. The typical AFL is dependent of the cavotricuspid isthmus.The isthmus between the caval vein and tricuspid is an area of slow conduction. Due to this slow conduction counter clockwise re-entry around the tricuspid annulus can exist. This re-entry produces a typical arrhythmia with activates the atria at a rate between 250-350 beats per minute. If the re-entry circuit moves counter clockwise a typical AFL is produced. If the re-entry circuit moves clockwise, a atypical AFL is seen.The causes and risk are comparable with atrial fibrillation.

Atrial flutter may be caused by abnormalities of the heart, by diseases of the heart, or by diseases elsewhere in the body that affect the heart. Atrial flutter may also be caused by consuming substances that change the way electrical impulses are transmitted through the heart. Atrial flutter can occur after open heart surgery. In a few people, no underlying cause is ever found. May occur without evidence of underlying heart disease. This is more common in younger people, about half of whom have no other heart problems. This is often called lone atrial

Some people have no symptoms with atrial flutter. Others describe the following symptoms: Palpitations, A fluttering feeling in the chest, Shortness of breath, Anxiety, Weakness

medication, for instance with betablockers or calcium antagonists. However not all AT are sensitive to medication and success rate of medication is usually low. If these drugs are unsuccessful Class IC in combination with AV-nodal-blocking agents or Class III drugs can be tried. The treatment of choice for symptomatic AT is catheter ablation. In an experienced centre up to 90% of the ATs can be ablated, recurrence rate is relatively high often due to a new focus of AT. Treatment of multifocal atrial tachyardia is difficult and therapy is usually directed at the management of underlying disease. To decrease the heart rate rapidly IV medications or controlled electrical shock (defibrillation) will be performed under anesthesia when chest pain or congestive heart failure related to the ventricular rate occurs. In some people, an invasive procedure called radiofrequency catheter ablation may be provided for long-term successful treatment, and no additional medications may be needed.

ATRIAL FIBRILLATION

The pathophysiology of AF is complex and incompletely understood. In most patients the trigger of AF results from extra beats in from the pulmonary veins.This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (i.e. the autonomic nerve system).These triggers

Symptoms of atrial fibrillation vary from person to person and a number of people have no symptoms.The most common symptom in people with intermittent atrial fibrillation is palpitations, a sensation of rapid or irregular heartbeat. This

Treatment: Most people with atrial fibrillation take a blood-thinning drug called warfarin (Coumadin) to lower this risk of stroke and heart failure. Warfarin blocks certain factors in the blood that promote clotting. Acutely, the initial blood thinner is IV or subcutaneous heparin to thin a

can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change and move through the atria. The ability of the atria to sustain AF is dependable on atrial structural changes (fibrosis/inflammation). AF induces electromechanical changes in the atrium. These changes make it easier for AF to perpetuate; AF begets AF. Due to the fast and rapid activation of the atria, there is no functional mechanical activity left. This results in the most feared complication of AF, namely forming of blood clots (with for instance stroke as a result). During atrial standstill the atria does not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage. The strokes resulting from AF are often more severe than other causes of stroke. Another complication of AF is a tachycardiomyopathy. Due to the constant chaotic activity in the atria, the AV-node can conduct these signals at high rate. The result is an irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.

SUPRAVENTRI

An episode of supraventricular tachycardia

fibrillation. Some of the causes that do not involve the heart include the following: Hyperthyroidism, Alcohol use, Pulmonary embolism, Pneumonia. Heart valve disease, Enlargement of the left ventricle walls:This condition is called left ventricular hypertrophy, Coronary heart disease (or coronary artery disease), High blood pressure, Cardiomyopathy, Sick sinus syndrome, Pericarditis, Myocarditis, Advancing agE, Atrial fibrillation frequently occurs after cardiothoracic surgery or procedures, but often resolves in a few days.For many people with infrequent and brief episodes of atrial fibrillation, the episodes are brought on by a number of triggers. Because some of these involve excessive alcohol intake or skipping medications, this is sometimes called "holiday heart "or "Saturday night heart." Some of these people are able to avoid episodes or have fewer episodes by avoiding their triggers. Common triggers include alcohol and caffeine in susceptible individuals. Disease or congenital

may make some people very anxious. Many people also describe an irregular fluttering sensation in their chests. This irregular fluttering sensation is due to the irregular rapid ventricular response (rvr) of the ventricles to the rapid irregular atrial electrical activity. Some people become light-headed or faint.Other symptoms include weakness, lack of energy or shortness of breath with effort, and chest pain or angina.

patient's blood rapidly. Then a decision is made whether they need oral warfarin; Cardioversion; Catheter ablation; Pacemaker

Palpitations

Treatment for PSVT focuses on

CULAR TACHYCARDIA

occurs when abnormal electrical impulses suddenly start in the upper chambers of the heart, and override the heart's natural rhythm.

abnormality of the heart High blood pressure Smoking Fever too much alcohol too many caffeinated beverages side effect of medications Abuse of recreational drugs, such as cocaineImbalance of electrolytes, mineralrelated substances necessary for conducting electrical impulses hyperthyroidism

Light headedness Dizziness Loss of consciousness Chest pain Shortness of breath

decreasing the heart rate and breaking up the electrical circuits made by the abnormal conducting pathways. Treatment can be divided into two broad categories: halting the acute episode and preventing any new episodes. One of the most important considerations in treating an acute episode of PSVT is how severely the heart function has been affected. >Beta- blockers >Calcium channel blocker >Vagal maneuvers to increase parasympathetic tone and slow conduction through the atrioventricular node should be the first approach. The Valsalva maneuver should be the first vagal maneuver tried and works by increasing intra-thoracic pressure and affecting baroreceptors (pressure sensors) within the arch of the aorta. >Reducing coffee, alcohol or tobacco use or increasing the amount of rest may help to alleviate symptoms. >Cardioversion If the patient is unstable or other treatments have not been effective. An ECG should be performed as soon as possible. Direct current (DC) cardio version. Carotid massage is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this manoeuvre. Oral antiarrhythmic drug tablets are not reliably absorbed during rapid PSVT Adenosine and the non-

PAROXYSMAL SUPRAVENTRI CULAR TACHYCARDIA

The contractions are caused by an electrical signal that begins in an area of the heart called the sinoatrial node. The signal moves through the upper heart chambers (the atria) and tells the atria to contract. After this, the signal moves down in the heart and tells the lower chambers (the ventricles) to contract.

Previous myocardial infarction Mitral valve prolapse Rheumatic heart disease Pericarditis Pneumonia Chronic lung disease Current alcohol intoxication Digoxin toxicity

Anxiety Chest tightness Palpitations (a sensation of feeling the heart beat), often with an irregular or fast rate (racing) Rapid pulse Shortness of breath Dizziness Fainting

JUNCTIONAL RHYTHM

In the atrial part of the fuse, the activation travels in the reverse direction (from right to left on the diagram). We know that when it travels "forward" it produces an upright Pwave. When it travels retrograde (which is a snooty, polysyllabic way of saying "backward"), the P wave is inverted (i.e. upside down, below the isoelectric line). Thus, an inverted P wave strongly indicates that the electrical impulse originated in the AV node or beyond. In addition to being upside-down, the junctional P wave may not be before the QRS. When the sinus fires, the atria are depolarized before the ventricles, and thus the P wave is first. Atrial explosives are lit before those of the ventricles, however, in junctional rhythm; it is hard to predict which set of explosives will be ignited first. Perhaps they will be ignited at the same time. The ignition of the explosives in the atria (i.e. atrial depolarization) is the P wave while the ignition of the ventricular explosives (i.e. ventricular depolarization) is the QRS complex. In a junctional rhythm, the P wave may occur before, during, or after the QRS complex. This depends on the exact location of the pacemaker, which may vary. When two waves occur at the same time, they add together. Anything above the isoelectric line counts as positive, below negative. Because the P wave in this case is negative, it will subtract from whatever the QRS is.

Ischemia of the AVN, especially with acute inferior infarction involving the posterior descending artery, the origin of the AV nodal artery branch. Acutely after cardiac surgery, especially in children within 4 days after surgery for congenital cardiac defects Acute inflammatory processes (eg, acute rheumatic fever, lyme disease), which may involve the conduction system Diphtheria Other drugs (eg, betablockers, calcium blockers, most antiarrhythmic agents) that cause sinus bradycardia Metabolic states with increased adrenergic tone Isoproterenol infusion

Junctional rhythms may be accompanied by symptoms or may be entirely asymptomatic. Palpitations, fatigue, or poor exercise tolerance: These may occur during a period of junctional rhythm in patients who are abnormally bradycardic for their level of activity. Dyspnea: Sudden onset of symptoms and sudden termination of symptoms may occur, especially in the setting of complete heart block. Presyncope (near syncope): The underlying cause of the junctional rhythm is the most significant predictor of symptoms. For instance, AV dissociation with complete heart block, defined as an atrial rate that is faster than the junctional escape rate, is more likely to cause symptoms than AV dissociation with a sinus rate slower than the competing junctional pacemaker. Additionally, syncope or presyncope may occur from an acute decrease in heart rate.

dihydropyridine calcium antagonists verapamil and diltiazem are the intravenous (IV) drugs of choice for termination of PSVT. No pharmacologic therapy is needed for asymptomatic, otherwise healthy individuals with junctional rhythms that result from increased vagal tone. In patients with complete AV block, high-grade AV block, or symptomatic sick sinus syndrome (ie, sinus node dysfunction), a permanent pacemaker may be needed. The junctional rhythm serves as an escape mechanism to maintain the heart rate during periods of bradycardia or asystole and should not be suppressed. Emergency department care can include evaluation of the 12-lead ECG findings, airway protection and oxygenation, and blood pressure support, depending on the cause of the rhythm. If the junctional rhythm is due to digitalis toxicity, then atropine, digoxin immune Fab (Digibind), or both may be necessary. In refractory cases of symptomatic digitalis toxicity that results in junctional tachycardia and causes severe symptoms, then intravenous phenytoin can be used. This should be administered in a monitored setting because of possible hypotension or the need for a pacemaker after resolution of the ectopic junctional rhythm. If junctional rhythm is due to symptomatic sick sinus syndrome, permanent pacemaker implantation is indicated. If ectopic junctional tachycardia,

which usually occurs in the pediatric population, is incessant and symptomatic, then radiofrequency ablation via a percutaneous approach is indicated. ACCELERATED JUNCTIONAL RHYTHM Accelerated junctional rhythm (AJR) occurs when the rate of the AV junctional pacemaker exceeds that of the sinus node. This situation arises when there is increased automaticity in the AV node coupled with decreased automaticity in the sinus node. Junction tachycardias are rare but still seen occasionally among patients with SVT. Their actual incidence and prevalence are unknown. Two forms of junctional tachycardia are recognized, and each has a different mechanism. The permanent form of junctional reentrant tachycardia (PJRT) is a reentrant tachycardia in which an accessory pathway lies very close to the AV node. The tachycardia is slower than AV nodal reentrant tachycardia and is often an incessant. This tachycardia has been associated with the development of a reversible cardiomyopathy that resolves when the tachycardia is successfully terminated. PJRT is usually treated by interruption of the tachycardia circuit by RF ablation. Automatic junctional tachycardia is, as the name suggests, an automatic tachycardia of the AV node. It may be caused by drug toxicity or it may be idiopathic. It is usually controlled with antiarrhythmic drugs. 1 DEGREE AV BLOCK
ST

myocardial ischaemia, digoxin toxicity, cardiac surgery, myocarditis and b eta-agonists (e.g. isoprenaline)

The typical rate of an AJR is 60 130 bpm, in contrast to junctional escape rhythms which have a typical rate of 40 60 bpm

Emergency care; Vital signs monitoring; Cardiac care; Cardiac precautions; Oxygen therapy; Fluid/electrolyte management; Surveillance

JUNCTIONAL TACHYCARDIA

Most commonly it is due to digitalis toxicity,sometime it may be due to AV node block or coronary artery disease. Juctional tachycardia may be precipitated by Hyperkalemia in a patient with conduction system disease.

Palpitations crises with abrupt onset and end, without any triggering element. An oftenfound element is the regularity of the tachycardia. Anxiety depends on the patients degree of acquired tolerance to this tachycardia. An abundant urine output is frequent after the crisis. Sometimes, when the patient is used to these crises, he makes them disappear by achieving some small gestures like the provocation of the nauseating reflex, the compression of the eyeballs or even the massage of the artery localized at the level of the neck, the carotid artery.

The prolonged PR interval indicates delayed AV conduction, but all atrial impulses are conducted to the ventricles. this condition

Possible in healthy persons, inferior-wall MI or ischemia, hypothyroidism,

may not cause any symptoms heart rate and rhythm are usually normal

1 - The well-tolerated junctional tachycardia: Medicines are administered by IV in a specialized environment, permitting to break the tachycardia. The electrocardiogram is recorded non-stop. The ill-tolerated junctional tachycardia: Long-term treatment of the illness; beta-blockers, the verapamil, amiodarone or even digitalics drugs can be used. With these treatments, a spacing of the crises and especially a bigger sensitivity to the vagal manoeuvres are observed. The dangerous junctional tachycardia: The heating emitted by a radiofrequency current destroys the cardiac conductive tissue responsible for the tachycardia. The electrofulguration is still used nowadays. The efficacy of this method is around 90%. More and more often, the junctional tachycardia are treated by this method, permitting to avoid the medicinal treatment. correction of underlying cause - possibly atropine if severe symptomatic bradycardia develops

2 DEGREE AV BLOCK MOBITZ I

ND

usually produces a regular atrial and ventricular rhythm. Clinically significant PR interval prolongation can result from conduction delays in the AV node itself, the His-Purkinje syste, or both. When the QRS complex is normal in contour and duration, the AV delay almost always occurs in the AV node and rarely in the bundle of his. In contrast, when the QRS is prolonged, showing a bundle branch block pattern, conduction delays may be in the AV node or the His-Purkinje system. The electrical signal goes slower and slower as it passes the AV node before entering the ventricles which increases the time of atrial and ventricular electrical signals and contractions until the heart actually skips a beat. After the delay, the ventricles contract and the electrical signals returns to resting phase, then the ventricles relax Some of the electrical signals don't reach the ventricles. However, the pattern is less regular than it is in Mobitz type I. Some signals move between the atria and ventricles normally, while others are blocked. The area that is blocked is lower in the conduction system and is often associated with more severe conduction disease. Normally, electrical impulses within your heart's muscle signal it to beat (contract). These impulses travel along a pathway, including a slender cluster of cardiac fibers of the heart's electrical system. One area of these fibers is called the bundle of His. This bundle divides into two branches the right and the left bundles one for each of your heart's two lower chambers (ventricles). If one or both of these branch bundles become damaged due to a heart attack, for example this change can prevent your

hypokalemia, and hyperkalemia, digoxin toxicity; use of quinidine, procainamide, betaadrenergic blockers, calcium channel, Blockers, or amiodarone

- cautious use of digoxin, calcium channel blockers, and betaadrenergic blockers

- inferior-wall MI, cardiac surgery, acute rheumatic fever, and vagal stimulation - digoxin toxicity; use of propanolol, quinidine, or procainamide

fainting - dizziness or lightheadedness - fatigue - shortness of breath - chest pain

treatment of underlying cause - atropine or transcutaneous pacemaker for symptomatic bradycardia - discontinuation of digoxin, if appropriate

SECONDDEGREE AV BLOCK MOBITZ II

severe coronary artery disease (CAD), anteriorwall MI, and acute myocarditis - digoxin toxicity

fainting - dizziness or lightheadedness - fatigue - shortness of breath - chest pain - slow heart rate

temporary or permanent pacemaker - atropine, dopamine, or epinephrine for symptomatic bradycardia - discontinuation of digoxin, if appropriate

Bundle Brach Block

BBB occurs when one of the bundle branches becomes diseased or damaged, and stops conducting electrical impulses; that is, one of the bundle branches becomes "blocked." The chief effect of a bundle branch block is to disrupt the normal, coordinated and simultaneous

In most people, bundle branch block doesn't cause any symptoms. Fainting (syncope) Feeling as if you're going to faint (presyncope) Having a slow heart rate (bradycardia)

Artificial pacemakers For some people with bundle branch block and a history of fainting, doctors may recommend implanting an artificial pacemaker. This pacemaker is a compact device that is implanted under the skin of your upper chest (internal pacemaker). Cardiac resynchronization treatment (CRT) may be used.

heart from beating normally. The heart's electrical impulses that make your heart beat may be slowed down or blocked. When this occurs, your heart's ventricles no longer contract in perfect coordination with one another. 3rd Degree AV Block In the heart, normal impulse initiation begins in the sinoatrial node. The excitation wave then travels through the atrium. During this time, surface ECG recordings show the P wave. Following intra-atrial conduction to the area of the lower intra-atrial septum, this wavefront reaches the inputs to the AVN. The AVN then conducts the impulse to the His bundle. The His bundle divides into the right and left bundles, which distribute this impulse to the ventricles. During atrial, AVN, and His-Purkinje conduction, the PR segment is observed. Heart block occurs when slowing or complete block of this conduction occurs. Traditionally, AV block can be divided into first-, second-, and third-degree block. No atrial impulses reach the ventricle in third degree or complete heart block (waveform 1The block can exist in the AV node or in the infranodal specialized conduction system A His-bundle electrocardiographic study can determine the site of block quite accurately, but the escape rhythm provides important clues

contraction of the two ventricles. The contraction of one ventricle (the one whose bundle branch is blocked) occurs slightly after the contraction of the other. Degenerative diseases Lengre disease, noncompaction cardiomyopathy, nailpatella syndrome, mitochondrial myopathy Infectious causes - Lyme borreliosis (particularly in endemic areas),Trypanosoma cruzi infection, rheumatic fever, myocarditis, Chagas disease, Aspergillus myoc arditis, varicella-zoster virus infection, valve ring abscess Rheumatic diseases Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, scleroderma Neuromuscular disorders Becker muscular dystrophy, myotonic muscular dystrophy Chemical changes or imbalances in the body Certain medications, including common asthma medications Alcohol or illegal drugs Increased levels of

Chest pain, Palpitations, difficulty breathing, excessive sweating, severe fatigue, nausea, vomiting, fainting

external pacing and atropine for acute, symptomatic episodes and permanent pacing for chronic complete heart block.

Premature Ventricular Complex

Your heart is made up of four chambers two upper chambers (atria) and two lower chambers (ventricles). The rhythm of your heart is normally controlled by the sinoatrial node (SA node) or sinus node an area of specialized cells located in the right atrium. This natural pacemaker produces

Premature ventricular contractions often cause no symptoms. But you may feel an odd sensation in your chest, such as: Flip-flops, Fluttering, Pounding or jumping, Skipped beats or missed beats Increased

Pharmacological agentsAntiarrhythmics: these agents alter the electrophysiologic mechanisms responsible for PVCsBeta blockersCalcium channel blockers Electrolytes replacementMagnesium

the electrical impulses that trigger the normal heartbeat. From the sinus node, electrical impulses travel across the atria to the ventricles, causing them to contract and pump blood out to your lungs and body. Premature ventricular contractions are abnormal contractions that begin in the ventricles. These extra contractions usually beat sooner than the next expected regular heartbeat. And they often interrupt the normal order of pumping, which is atria first, then ventricles. As a result, the extra, out-ofsync beats are usually less effective in pumping blood throughout the body. PREMATURE VENTRICULAR COMPLEX Premature ventricular contractions Uniform reflect activation of the ventricles from a site below the atrioventricular node (AVN). Suggested mechanisms for PVCs are reentry, triggered activity, and enhanced automaticity. Reentry occurs when an area of 1-way block in the Purkinje fibers and a second area of slow conduction are present. Reentry can produce single ectopic beats, or it can trigger paroxysmal tachycardia. riggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. With ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI). Premature ventricular contractions Multiform are beats which are initiated in the ventricles or lower chambers of the heart, prematurely. As opposed to PACs, when the SA node gets interrupted, do not interrupt the SA node. However, with PVC Multiform the ventricles contract, which normally causes the impulse from the atria to be blocked from reaching the ventricles. During ventricular activation, the area of slow conduction activates the blocked part

adrenaline in the body that may be caused by caffeine, exercise or anxiety Injury to the heart muscle from coronary artery disease, congenital heart disease, high blood pressure or infections (myocarditis)

awareness of your heartbeat.

supplements (e.g. magnesium citrate, orotate, Maalox, etc.)Potassium supplements Radiofrequency catheter ablation treatment Lifestyle modificationFrequently stressed individuals should consider therapy, or joining a support group.Heart attacks can increase the likelihood of having PVCs.

PVC MULTIFORM

Chemical changes or imbalances in the body Certain medications, including common asthma medications Alcohol or illegal drugs Increased levels of adrenaline in the body that may be caused by caffeine, exercise or anxiety Injury to the heart muscle from coronary artery disease, congenital heart disease, high blood pressure or infections (myocarditis) Caffeine, Alcohol, Tobacco, Exercise Hypertension, Anxiety Underlying heart disease, including congenital heart disease, coronary artery disease, heart attack, myocarditis and cardiomyopathy

Palpitations at night or when they are relaxing. Feeling dizzy or lightheaded Experience chest pain Asymptomatic

Lifestyle changes. caffeine or tobacco Medications. Beta blockers calcium channel blockers, or antiarrhythmic drugs, such as amiodarone

palpitations in the chest weakness dizziness fainting

Perform telemetry Secure intravenous (IV) access. Administer oxygen. Complex ectopy in the setting of myocardial ischemia or causing hemodynamic instability should be suppressed. Use lidocaine for patients with myocardial ischemia

PVC VENTRICULAR BIGEMINY

of the system after the rest of the ventricle has recovered, resulting in an extra beat. Known to Lown grading system of grade 3. A premature ventricular contraction or ventricular ectopic beat is a cardiac contraction that is generally premature or occurs before the expected sinus QRS complex and arises out of the ventricular tissue. And when PVC follows every atrial beat, it is called bigeminy.

Drug or metabolic cause on non-invasive investigations Symptomatic, complex ectopy in a patient having an MI Symptomatic ectopy in patient with prolonged QTc as most other agents such as amiodarone tend to further lengthen the QTc. ischemia, hypoxia, hypokalemia, hypomagnesemia, hypercalcemia, digoxin, cocaine, alcohol, tobacco, cardiomyopathy, MI, mitral valve prolapse

Dyspnea Acute myocardial ischaemic event Hypertension Could there be a drug overdose, in particular, digoxin toxicity or theophylline and methylxanthine poisonings and overdoses

Check electrolytes K+, Mg++ Beta adrenergic blockers may be considered if haemodynamically stable. Anti-arrhythmic agents should be avoided Premature ventricular contractions in slow rhythms; they may be an escape focus. Do NOT give lignocaine in this scenario.

PVC TRIGEMINY, QUADRIGEMIN Y, COUPLET

Premature ventricular contractions (PVCs) are beats which are initiated in the ventricles or lower chambers of the heart, prematurely. As opposed to PACs, when the SA node (the natural pacemaker of the heart) gets interrupted, PVCs do not interrupt the SA node. However, with a PVC the ventricles contract, which normally causes the impulse from the atria to be blocked from reaching the ventricles.

Abnormal EKG, Irregular heart beat, Shortness of breath, Dizziness, Feeling your heart beat (palpitations), Feeling of occasional, forceful beats, Increased awareness of your heart beat

VENTRICULAR TACHYCARDIA

cardiac output is reduced due to the rapid heart rate and lack of a properly timed or coordinated atrial contraction which results in diminished myocardial perfusion, worsening inotropic response and degeneration to VF, resulting to sudden death

anti- arrhythmic medications, change in blood chemistry, changes in pH, lack of enough oxygen

light headedness or dizziness, palpitations ( skipping, fluttering or pounding in the chest), fatigue, chest pressure or pain, shortness of breathfainting spells ETIOLOGY: antiarrhythmic medications, change in blood chemistry, changes in pH, lack of enough oxygen palpitation

Pharmacological agents: Antiarrhythmics, Beta blockers, Calcium channel blockers, Electrolytes replacement, Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.), Potassium supplements, Radiofrequency catheter ablation treatment, Lifestyle modification, Frequently stressed individuals should consider therapy, or joining a support group, CPR, electrical fibrillation or cardioversion, antiarrhythmic medications, ablation procedure

VENTRICULAR

In ventricular monomorphic, all the

myocardial infaction,

ICD, endocardial catheter ablation

TACHYCARDIA MONOMORPHI C

beats look the same because the impulse is either being degenerated from increased automaticity of a singlr point in either the left or right ventricle, or due to a re-entry circuit within the ventricle During VT, cardiac output is reduced due to the rapid heart rate and lack of a properly timed or coordinated atrial contraction. Ischemia and mitral insufficiency may also contribute to hemodynamic intolerance. Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or with very rapid rates. Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response and degeneration to VF, resulting in sudden death. The abnormality underlying both acquired and congenital long QT syndromes is in the ionic current flow during repolarization, which affects the QT interval. A variety of changes in ionic current can result in the common effect of decreased repolarizing current, reflected in a long QT, and these changes can secondarily lead to subsequent depolarizing currents and sometimes action potentials, termed afterdepolarizations. This leads to a further delay in repolarization and causes early afterdepolarization (EAD), the triggering event for torsade. Repolarization has 3 phases. During the initial upstroke of action potential in a normal cardiac cell, a rapid net influx of + ++ positive ions (Na and Ca ) occurs, which results in the depolarization of the cell membrane. This is followed by a rapid, transient outward potassium current (Ito), + while the influx rate of positive ions (Na , ++ Ca ) declines. This represents the initial part of the repolarization, or phase 1.

VENTRICULAR TACHYCARDIA POLYMORPHIC

cardiomyopathy, right ventricular dysplasia, right and left ventricular outflow, surgical scar, hypertrophy, muscle degeneration, Idiopathic, sodium channel gene mutation abnormalities of ventricular muscle repolarization, drug toxicity, electrolyte abnormalities, ischemia, myocarditis

sudden death

magnesium, isoproterenol, pacing, phenytoin, lidocain

TORSADE DE POINTES

Prolongation of the QT interval may be congenital, as seen in the Jervell and Lange-Nielsen syndrome (ie, congenitally long QT associated with congenital deafness) and the Romano Ward syndrome (ie, isolated prolongation of QT interval). Both of these syndromes are associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.

rapid pulse, low or normal blood pressure, or transient or prolonged loss of consciousness. This could be preceded by bradycardia or premature ventricular contractions (leading palpitations). Pallor and diaphoresis may be noted, especially with a sustained episode.

Pharmacologic therapy Magnesium is the drug of choice for suppressing EADs and terminating the arrhythmia. Magnesium achieves this by decreasing the influx of calcium, thus lowering the amplitude of EADs. Mexiletine also may be helpful in suppressing torsade. In one study, it was used in patients with HIV who had acquired long QT interval and torsade. It effectively suppressed the torsade on a long-term basis. Patients with congenital long QT syndromes are thought to have an abnormality of sympathetic balance or tone and are treated with betablockers. If the patient experiences breakthrough torsade, a short-acting beta-blocker, such as esmolol, can be tried. Isoproterenol can be used in bradycardia-dependent torsade that usually is associated with acquired

Phase 2 is characterized by the plateau. The positive currents flowing inward and outward become almost equal during this stage. Phase 3 of repolarization is mediated by activation of the delayed rectifier potassium current (IK) moving outward while the inward positive current decays. If a slow ++ + inactivation of the Ca and Na currents occurs, this inward "window" current can cause single or repetitive depolarization during phases 2 and 3 (ie, EADs). These EADs appear as pathologic U waves on a surface ECG, and, when they reach a threshold, they may trigger ventricular tachyarrhythmias.

long QT syndrome (pausedependent). It should be administered as a continuous IV infusion to keep the heart rate above 90 bpm. Isoproterenol accelerates AV conduction and decreases the QT interval by increasing the heart rate and reducing temporal dispersion of repolarization. Beta-adrenergic agonists such as isoproterenol are contraindicated in the congenital form of long QT syndrome (adrenergic-dependent). Because of precautions, contraindications, and adverse effects associated with its use, this drug is used as an interim agent until overdrive pacing can be started. Loss of consciousness or fainting is the most common sign of ventricular fibrillation. Early ventricular fibrillation symptoms Chest pain Rapid heartbeat (tachycardia) Dizziness Nausea Shortness of breath Abnormal automaticity Cardiopulmonary resuscitation (CPR). Defibrillation.

VENTRICULAR FIBRILLATION

PULSELESS ELECTRICAL ACTIVITY

VF occurs in a variety of clinical situations but is most often associated with coronary artery disease (CAD) and as a terminal event. VF may be due to acute myocardial infarction or ischemia, or it may occur in the setting of chronic infarct scar. Intracellular calcium accumulation, the action of free radicals, metabolic alterations, and autonomic modulation are some important influences on the development of VF during ischemia. Thrombolytic agents reduce the incidence of ventricular arrhythmias and inducible ventricular tachycardia (VT) after myocardial infarction (MI). nsion, drugs, metabolic disturbances) has been proposed to be the precipitator of VF. Pulseless electrical activity (PEA) is a clinical condition characterized by unresponsiveness and lack of palpable pulse in the presence of organized cardiac electrical activity. Pulseless electrical activity has previously been referred to as electromechanical dissociation (EMD). While a lack of ventricular electrical activity

Pulseless electrical activity (PEA) occurs when a major cardiovascular, respiratory, or metabolic derangement results in the inability of cardiac muscle to generate

PEA does not mean mechanical quiescence. Patients may have weak ventricular contractions and recordable aortic pressure (pseudo-PEA). True PEA is a condition in which cardiac contractions are absent in the presence of coordinated

Cardiopulmonary resuscitation is initiated immediately. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. relieving a tension pneumothorax The mainstay of drug therapy for PEA is epinephrine Sodium bicarbonate 1meq per kilogram may

always implies a lack of ventricular mechanical activity (asystole), the reverse is not always true. In other words, electrical activity is a necessary, but not sufficient, condition for mechanical activity. In a situation of cardiac arrest, the presence of organized ventricular electrical activity is not necessarily accompanied by meaningful ventricular mechanical activity. The qualifier meaningful is used to describe a degree of ventricular mechanical activity that is sufficient to generate a palpable pulse.

ASYSTOLE

Asystole can be primary or secondary. Primary asystole occurs when the heart's electrical system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (ie, sclerosis) of the sinoatrial (SA) node or atrioventricular (AV) conducting system. Primary asystole is usually preceded by a bradydysrhythmia due to sinus node block-arrest, complete heart block, or both. Reflex bradyasystole/asystole can result from ocular surgery, retrobulbar block, eye trauma, direct pressure on the globe, maxillofacial surgery, hypersensitive carotid sinus syndrome, or glossopharyngeal neuralgia. Episodes of asystole and bradycardia have been documented as manifestations of left temporal lobe complex partial seizures. These patients experienced either dizziness or syncope. No sudden deaths were reported, but the possibility

sufficient force in response to electrical depolarization. PEA is always caused by a profound cardiovascular insult (eg, severe prolonged hypoxia or acidosis or extreme hypovolemia or flowrestricting pulmonary embolus). Additional etiologic factors: Hypovolemia, Hypoxia Hydrogen ion (acidosis), Hypokalemia/hyperkalemi a, Hypoglycemia, Hypothermia, Toxins, Cardiac tamponade Tension pneumothorax Thrombosis (coronary or pulmonary), Trauma Primary asystole, severe ischemia-pacemaker cells cannot transport the ions necessary to affect the transmembrane action potential. Implantable pacemaker failure may also be a cause of primary asystole. Proximal occlusion of the right coronary artery can cause ischemia or infarction of both the sinoatrial (SA) and the atrioventricular (AV) nodes.

electrical activity. PEA encompasses a number of organized cardiac rhythms, including supraventricular rhythms (sinus versus nonsinus) and ventricular rhythms (accelerated idioventricular or escape). The absence of peripheral pulses should not be equated with PEA, as it may be due to severe peripheral vascular disease

be considered in this rhythm. Signs and symptoms PEA is usually noticed because a person loses consciousness and stops breathing spontaneously. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds.

adequate airway management Treat with sodium bicarbonate, regular insulin, dextrose, calcium chloride, Kayexalate, and furosemide. If these measures fail or if the patient experiences complications, use dialysis. Treat with potassium IV Treat by maximizing oxygen and ventilation, correcting the underlying problem, and, if the pH is low, administering sodium bicarbonate. If the patient is intubated, use hyperventilation. Treat by re-warming the patient

exists if asystole were to persist. The longest interval was 26 seconds. Secondary asystole occurs when factors outside of the heart's electrical conduction system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia with metabolic acidosis. Asystole or bradyasystole follows untreated ventricular fibrillation and commonly occurs after unsuccessful attempts at defibrillation. This forebodes a dismal outcome.