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Alexandria University Faculty of Nursing Critical Care & Emergency Nursing Department Masters program 2nd semester 2011-2012

Supervised by: Prof. Dr/ Amal Kadry Attia.

Prepared & presented by:

Mohamed Mahmoud Awad Sweed. Ahmed Saleh. Ali Elmazaty.

Intended Learning Outcomes of the Course (ILOs) At the end of this seminar, the master student will be able to:1-

Knowledge and Understanding

Describe the electrophysiology of the heart Describe the normal sinus rhythm of the heart Explain the mechanism of cardiac dysrhythmias Explain the causes of atrial dysrhythmias Identify the causes of ventricular dysrhythmias Describe the types of heart block 2- Intellectual capabilities

Calculate the atrial heart rate Calculate the ventricular rate

Differentiate between atrial and ventricular dysrhythmias

Differentiate between type I and II of second degree atrioventricular block

3- Professional and practical skills Evaluate response to therapeutic interventions through systemic and ongoing assessment of patients with cardiac dysrhythmias Evaluate the outcomes of nursing care for individuals with cardiac dysrhythmias Demonstrate proper nursing interventions according to the type of dysrhythmias 4- General and transferable skills

Communicate effectively with family and the patients who is on mechanical ventilator.

Document assessment and intervention in relation to dysrhythmias.

Outline: Introduction o Electrophysiology of the heart o Electrocardiogram Cardiac dysrhythmias o Definition o Mechanism o Types Types of cardiac dysrhythmias I. Sinus node dysrhythmias a) Sinus tachycardia b) Sinus bradycardia c) Sinus dysrhythmia d) Sinus arrest II. Atrial dysrhythmias a) Premature atrial contraction b) Atrial tachycardia

c) Atrial flutter d) Atrial fibrillation III. Ventricular dysrhythmias a) Premature ventricular contraction b) Ventricular tachycardia c) Torsade de pointes d) Ventricular fibrillation e) A systole IV. Atrioventricular and bundle branch blocks a) First degree AV block b) Second degree AV block Type I Type II c) Third degree AV block d) Bundle Branch Block

Effect of serum electrolyte abnormalities on the Electrocardiogram a) b) c) d) Hyperkalemia Hypokalemia Hypercalcemia Hypocalcemia

Management of dysrhythmias

Radiofrequency Catheter ablation Defibrillation and Cardioversion Cardiac Pacemakers

Other management Valsalva maneuver carotid sinus message


ELECTROPHYSIOLOGY Automaticity Arrhythmia interpretation is based on an understanding of the normal anatomy and physiology of electrical conduction in the heart. Myocardial fibers possess highly specialized electrical properties, in addition to the mechanical property of contractility. Automaticity is the ability to generate an electrical impulse independent of stimulation by the nervous system or any other source. This property is unique to certain cardiac cells called pacemaker cells. Excitability and Conductivity Two other electrical properties, excitability and conductivity, are shared by all myocardial cells. Excitability is the ability of cells to respond to electrical stimulation. Conductivity is the ability to pass an electrical impulse from cell to cell through the heart. The hearts electrical conduction system is a network of structures that allows electrical impulses to spread through the heart much faster than if they had to spread through muscle cells alone. The structures of the conduction system, in sequence of normal electrical conduction Sinoatrial (SA) node. This node is the dominant pacemaker of the heart, located in the upper portion of the right atrium. Intrinsic rate is 60100 bpm.

Internodal pathways.

These cells direct electrical impulses between the SA and AV nodes and spread them across the atrial muscle.

Atrioventricular (AV) node. This node is part of an area called AV junction tissue, which includes some surrounding tissue plus the connected bundle of His. Although AV junction tissue contains pacemaker cells, none are thought to exist in the AV node itself. The AV node slows conduction, creating a slight delay before electrical impulses are carried to the ventricles. Intrinsic rate is 4060 bpm. Bundle of His. Located at the top of the interventricular septum, this bundle of fibers extends directly from the AV node and connects the atria and ventricles electrically. Bundle branches. The bundle of His splits into two conduction paths called the right and left bundle branches. These bundles carry electrical impulses at high speed to the tissue of the interventricular septum, and to each ventricle simultaneously. Purkinje system. The bundle branches terminate with this network of fibers, which spread electrical impulses rapidly throughout the ventricular walls. Intrinsic rate is 2040 bpm. The creation of electrical impulses and the spread of impulses through the electrical conduction system occur through a process called depolarization. Chemical pumps in the cell walls alter the precise concentration of electrolytes maintained inside and outside the cell. During depolarization, the electrical charge of a cell is changed by the electrolyte concentration shift on either side of the cell membrane. This change in electrical charge stimulates the muscle

fiber to contract. A resting, or polarized, cell is normally more electrically negative on the inside of the cell wall than on the outside. Electrical stimulation, however, changes the permeability of the cell wall and allows positively charged ions, particularly sodium (Na+), to move into the cell. The rush of sodium, along with the slower influx of calcium (Ca++), causes the inside of the cell to change from negative to positive. The cell is then said to be depolarized. The response of the muscle to this electrical charge is contraction. Because of conductivity, this process of depolarization moves rapidly from cell to cell in the conduction pathway and throughout the muscle cells of the heart. After depolarization, myocardial cells must return to their resting state of internal negativity for further depolarization to occur. The proper distribution of electrolytes is re-established by the cell wall chemical pumps, which pump sodium (Na+) out of the cell and return potassium (K+) into the cell. This

process of reestablishing the internal negative charge of the cell is called repolarization.

The depolarization process (A) A single cell has depolarized. (B) A wave propagates from cell to cell (C) Until all are depolarized. (D) Repolarization than restores each cells normalpolarity.

Progression of depolarization through the heart


The Electrocardiogram The movement of electrolytes across the membranes of myocardial cells (depolarization and repolarization) produces a flow of electrical current and creates an electrical field. Depolarization and repolarization can be seen on the electrocardiogram. Clinical Tip: It is important to keep in mind that the ECG shows only electrical activity; it tells us nothing about how well the heart is working mechanically. The body acts as a giant conductor of electrical current. Electrical activity that originates in the heart can be detected on the bodys surface through an electrocardiogram (ECG). o Component of an ECG tracing: An ECG tracing specifically reflects electrical activity in the heart. A single cardiac cycle inscribes various deflections on the graph paper. This electrical activity is described as:

Wave: A deflection, either positive or negative, away from the baseline (isoelectric line) of the ECG tracing. Complex: Several waves. Segment: A straight line between waves or complexes. Interval: A segment and a wave.

o Clinical Tip:


Between waves and cycles, the ECG records a baseline (isoelectric line), which indicates the absence of net electrical activity.

P Wave: First wave seen. Small, rounded, and upright (positive); indicates atrial depolarization.

PR Interval: Distance between beginning of P wave and beginning of QRS complex. Measures time during which a depolarization wave travels from the atria to the ventricles.

QRS Complex: Three deflections following P wave. Indicates ventricular depolarization

Q WAVE: First negative deflection R WAVE: First positive deflection S WAVE: First negative deflection after R wave

ST Segment: Distance between end of S wave and beginning of T wave. Measures time between ventricular depolarization and beginning of repolarization T Wave: Rounded, upright (positive) wave following QRS complex. Represents ventricular repolarization

QT Interval: Measured from beginning of QRS complex to end of T wave. Represents total ventricular activity.

U Wave: Small, rounded, upright wave following T wave. Indicates repolarization of Purkinje fibers Most easily seen with a slow heart rate

Normal Sinus Rhythm


Normal sinus rhythm is the normal rhythm of the heart. The impulse is initiated at the sinus node in a regular rhythm at a rate of 60 to 100 beats/ minute.

Rate: Normal (60100 bpm) Rhythm: Regular P Waves: Normal (upright, uniform) PR Interval: Normal (0.120.20 sec) QRS: Normal (0.060.10 sec) Clinical Tip: A normal ECG does not exclude heart disease. Clinical Tip: This rhythm is generated by the sinus node and its rate is within normal limits (60100 bpm).

Rhythm strip analysis The following analysis represents a systematic approach to assessment of a cardiac rhythm strip. Whether or not this method is used, it is important to take the time to complete each step because many arrhythmias are not as they first appear. 1. Determine the atrial and ventricular heart rates. Are they within normal limits? If not, is there a relationship between both.


2. Examine the rhythm to see if it is regular. Is there an equal amount of time between each QRS complex (RR interval)? Is there an equal amount of time between each P wave (PP interval)? Are the PP and RR intervals the same? 3. Look for the P waves. Are they present? Is there one or more P wave for each QRS complex? Do all P waves have the same configuration? 4. Measure the PR interval. Is it normal? Is it the same throughout the strip, or does it vary? If it varies, is there a pattern to the variation? 5. Evaluate the QRS complex. Is it normal in width, or is it wide? Are all complexes of the same configuration? 6. Examine the ST segment. Is it isoelectric, elevated, or depressed? 7. Identify the rhythm and determine its clinical significance. Is the patient symptomatic? (Check skin, neurological status, renal function, coronary circulation, and hemodynamic status/blood pressure.) Is the arrhythmia life-threatening? What is the clinical context? Is the arrhythmia new or chronic?


METHODS FOR CALCULATING HEART RATE Heart rate is calculated as the number of times the heart beats per minute (bpm). On an ECG tracing the bpm is usually calculated as the number of QRS complexes. Included are extra beats such as premature ventricular contractions (PVC), premature atrial contractions. Method 1: Count Large Boxes Regular rhythms can be quickly determined by counting the number of large graph boxes between two R waves. This number is divided into 300 to calculate beats per minute.

Method 2: Count Small Boxes The most accurate way to measure a regular rhythm is to count the number of small boxes between two R waves. This number is divided into 1500 to calculate bpm. Method 3: Six-second ECG Rhythm Strip The best method for measuring irregular heart rates with varying R-R intervals is to count the number of R waves in a 6-second strip (including extra beats such as PVCs, PACs, and ) and multiply by 10 .

Electrode placement using a five wire cable A five-wire patient cable is used to monitor the following leads: Standard leads, I, II, and III Augmented leads, aVR, aVL, aVF One chest lead, usually V1

Clinical Tip: Five-wire telemetry units are commonly used to monitor patient in critical care settings.


Definition They are the variation in the normal pattern of electrical stimulation of the heart. It varies from those that are mild, cause no symptoms and requires no treatment to those that require emergency intervention. Their effect on cardiac output and blood pressure determine their clinical significance. Mechanism of dysrhythmias


Abnormal impulse initiation

Abnormal impulse conduction

Both of them

Types of dysrhythmias 1. Sinus node dysrhythmias 2. Atrial dysrhythmias 3. Ventricular dysrhythmias 4. Atrioventricular block

1. Sinus node dysrhythmias A. Sinus tachycardia In sinus tachycardia, the sinus node accelerates and initiates an impulse at a rate of 100 times/ minute or more. Sinus tachycardia usually is caused by factors relating to an increase in sympathetic tone. Stress, exercise, and stimulants such as caffeine and nicotine can produce this arrhythmia. Sinus tachycardia also is associated with such clinical problems as fever, anemia, hyperthyroidism, hypoxemia, heart failure, and shock. Drugs such as atropine, which blocks vagal tone, and the catecholamine (e.g., epinephrine, dopamine) also can produce this rhythm.


Rate: Fast (100 bpm) Rhythm: Regular P Waves: Normal (upright, uniform) PR Interval: Normal (0.120.20 sec) QRS: Normal (0.060.10 sec) Treatment (if symptomatic and not a result of physical exertion):

Treatment for sinus tachycardia usually is directed at eliminating the underlying cause. If heart failure is present specific measures may be used as sedation, oxygen administration, digitalis, and diuretics If the tachycardia is caused by thyrotoxicosis propranolol may be used

B. Sinus bradycardia Sinus bradycardia is defined as a rhythm with impulses originating at the sinus node at a rate of less than 60 beats/ minute Sinus bradycardia is common among individuals of all ages and may be normal in highly trained athletes. It is present in both healthy and diseased hearts. It may be associatedwith sleep, severe pain, inferior wall MI, acute spinal cord injury, and certain drugs (e.g., digitalis, beta-blockers, verapamil, diltiazem.


Rate: Slow (60 bpm) Rhythm: Regular P Waves: Normal (upright, uniform) PR Interval: Normal (0.120.20 sec) QRS: Normal (0.060.10 sec) Treatment: No treatment is indicated unless symptoms are present. If the pulse is very slow and the patient is symptomatic, appropriate measures include: Administration of atropine 0.5 to 1 mg Temporary or permanent pacemaker insertion Dopamine 5 to 20 mg / kg / minute

Epinephrine 2 to 10 mg / minute

C. Sinus dysrhythmia Sinus arrhythmia is a disorder of rhythm that is said to be present if the RR intervals on the ECG, from the shortest RR interval to the longest, vary by more than 0.12second. This arrhythmia is caused by an irregularity in sinus node discharge, often in association with phases of the respiratory cycle. The sinus node rate gradually increases with inspiration and gradually decreases with expiration. Sinus arrhythmia is a normal phenomenon, seen especially in young individuals in the setting of lower heart rates. It also occurs after enhancement of vagal tone (e.g., with digitalis or morphine)


Rate: Usually normal (60100 bpm); frequently increases with inspiration and decreases with expiration; may be less than60 bpm Rhythm: Irregular; varies with respiration difference between shortest R-R and longest R-R intervals is more than0.12 sec P Waves: Normal (upright and uniform) PR Interval: Normal (0.120.20 sec) QRS: Normal (0.060.10 sec) Treatment: Usually no treatment is require Treat the underlying cause if unrelated to respiration Discontinue drug as morphine

D. Sinus arrest and sino atrial block Sinus arrest is a disorder of impulse formation. The sinus node fails to form a discharge, producing pauses of varying lengths because of the absence of atrial depolarization. The P wave is absent, and the resulting PP interval is not a multiple of the basic PP interval. The pause ends either when an escape pacemaker from the junction or ventricles takes over or sinus node function returns.

Rate: Normal to slow; determined by duration and frequency of sinus pause (arrest) Rhythm: Irregular whenever a pause (arrest) occurs P Waves: Normal (upright and uniform) except in areas of pause (arrest) PR Interval: Normal (0.120.20 sec)

QRS: Normal (0.060.10 sec) Treatment (if symptomatic): Identify the cause and maintain cardiac output if there is a mild symptoms. In the presence of serious hemodynamic compromise the goal is to increase the ventricular rate, which may require the use of atropine or a pacemaker Record frequency and duration of pause Asses for signs of decreased cardiac output Document vital signs, how patient feel during pause and what activities the patient was involved and when they occur (valsalva maneuver and vomiting). Obtain serum digoxin and electrolyte level. 2. Atrial dysrhythmias A. Premature atrial contraction A premature atrial contraction (PAC) occurs when an ectopic atrial impulse discharges prematurely and, in most cases, is conducted in a normal fashion through the AV conducting system to the ventricles on the ECG tracing, the P wave is premature and may even be buried in the preceding T wave; it often differs in configuration from the sinus P wave. The QRS complex usually is of normal configuration PACs may occur in healthy individuals as a result of various stimuli, such as emotions, tobacco, alcohol, and caffeine. PACs also may be associated with rheumatic heart disease, ischemic heart disease, mitral stenosis, heart failure, hypokalemia, hypomagnesaemia, medications, and hyperthyroidism. Alternatively, PACs may be a precursor to an atrial tachycardia, atrial fibrillation, or atrial flutter, indicating an increasing atrial irritability.


Rate: Depends on rate of underlying rhythm Rhythm: Irregular whenever a PAC occurs P Waves: Present; in the PAC, may have a different shape PR Interval: Varies in the PAC, otherwise normal (0.120.20 sec) QRS: Normal (0.060.10 sec) Treatment (if symptomatic): No treatment is necessary in many cases unless patient is symptomatic. Frequent monitored the patient for PVC. The patient should be assessed for underlying conditions Documented of premature beats Avoid the underlying causes such as caffeine and alcohol. Teach patient relaxation techniques

B. Atrial tachycardia A rapid atrial rate over rides the SA node and becomes the dominant pacemaker, Some ST wave and T wave abnormalities may be present.

Rate: 150250 bpm Rhythm: Regular P Waves: Normal (upright and uniform) but differs in shape from sinus P waves. PR Interval: May be Less than 0.12 sec) in rapid rates QRS: Normal (0.060.10 sec)

Supraventricular tachycardia (SVT) This arrhythmia has such a fast rate that the P waves may not be seen

Rate: 150250 bpm Rhythm: Regular P Waves: Frequently buried in preceding T waves and difficult to see. PR Interval: Usually not possible to measure QRS: Normal (0.060.10 sec) Clinical Tip: SVT may be related to caffeine intake, nicotine, stress, or anxiety in healthy adults. Clinical Tip: Some patients may experience angina, hypotension, light headedness, palpitations, and intense anxiety. Paroxysmal Supraventricular tachycardia (PSVT) PSVT is a rapid rhythm that starts and stops suddenly. For accurate interpretation, the beginning or end of the PSVT must be seen.


Rate: 150250 bpm Rhythm: Irregular P Waves: Frequently buried in preceding T waves and difficult to see PR Interval: Usually not possible to measure QRS: Normal (0.060.10 sec) but may be wide if abnormally conducted through ventricles. Clinical Tip: The patient may feel palpitations, dizziness, lightheadedness, or anxiety Treatment (depend on type of tachycardia and severity of symptoms): Administer beta adrenergic blockers, calcium channels blockers which increase degree of AV block which in turn decrease the ventricular response and slow the heart rate. Start measures to produce vagal stimulation either through valsalva maneuver or carotid sinus message. Cardioversion if other treatment fails or if patient is severely symptomatic. Ablation (permanent damage of the area causing dysrhythmia). C. Atrial flutter Atrial flutter is a rapid atrial ectopic rhythm in which the atria fire at rates of 250 to 350 beats/ minute. The AV node functions as a gatekeeper, preventing too many impulses from reaching the ventricle. If the ventricles are stimulated 250 to 350 times per minute, they are unable to respond with effective contractions, and cardiac output is insufficient to sustain life. The AV node may allow only every second, third, or fourth atrial stimulus to proceed to the ventricles, resulting in what is known as a 2:1, 3:1, or 4:1 flutter block.


The rapid and regular atrial rate produces saw tooth. Atrial flutter often is seen in the presence of underlying cardiac disease, including coronary artery disease, corpulmonale, and rheumatic heart disease. If atrial flutter occurs in conjunction with a rapid ventricular rate, the ventricular chambers cannot fill adequately, resulting in varying degrees of hemodynamic compromise.

Rate: Atrial: 250350 bpm; ventricular: variable. Rhythm: Atrial: regular; ventricular: variable P Waves: Flutter waves have a saw-toothed appearance; PR Interval: Variable QRS: Usually normal (0.060.10 sec) Treatment If the patient has been experiencing atrial flutter for more than about 72 hours, anticoagulation may be needed before pharmacological or electrical conversion of the rhythm is attempted. Treatment goals for atrial flutter are to reestablish sinus rhythm or to achieve ventricular rate control. When the ventricular rate is rapid, prompt Drugs may be selected to slow the conduction of the impulses through the AV node, including ibutilide, calcium channel blockers, digoxin, amiodarone, or beta adrenergic blockers. If pharmacological conversion is not successful, electrical Cardioversion can be used. Synchronized Cardioversion is especially useful in the prompt treatment of atrial flutter. Other modes of therapy may be indicated for the long-term management of atrial flutter, such as ablation, pacing, and implantable devices.


D. ATRIAL FIBRILLATION Atrial fibrillation is defined as a rapid atrial ectopic rhythm, occurring with atrial rates of 350 to 500 beats/ minute; it is characterized by chaotic atrial activity with the absence of definable P waves. Like atrial flutter, the ventricular rate and rhythm depend on the ability of the AV junction to function as a gatekeeper. If too many atrial stimuli pass through the AV junction, the ventricular response is rapid. If too few atrial stimuli pass through the AV junction, the ventricular response is slow. The ventricular rhythm is characteristically irregular. This rhythm commonly occurs in the setting of heart failure, ischemic or rheumatic heart disease, pulmonary disease, and after open heart surgery. Atrial fibrillation also is seen in congenital heart disease The immediate clinical concern in patients with atrial fibrillation is the rate of the ventricular response. If the ventricular rate is too fast, end-diastolic filling time is decreased and cardiac output is compromised. If the ventricular rate is too slow, cardiac output may again be decreased. Clinical Tip: Signs and symptoms depend on the ventricular response rate. As in atrial flutter, patients with atrial fibrillation have lost AV synchrony and atrial kick, resulting in a compromised cardiac output.


Patients also are at risk for the formation of mural thrombi and embolic events, such as stroke, MI, and pulmonary embolus.

Rate: Atrial: 350 bpm; ventricular: variable Rhythm: Irregular P Waves: No true P waves; chaotic atrial activity PR Interval: None QRS: Normal (0.060.10 sec) Treatment Administer amiodarone as prescribed Cardioversion is indicated if the patient is hemodynamically unstable due to rapid ventricular rate. Assess sign and symptoms of decreased cardiac output. If a patient has chronic atrial fibrillation, anticoagulant should be given first before Cardioversion because Cardioversion can cause forceful atrial contraction so if atrial thrombus present it may go to systemic circulation and lead to systemic emboli. Ablation, pacing, and implantable devices are among the therapy options. 3. Ventricular dysrhythmias A. Premature ventricular contraction (PVC) A premature ventricular contraction (PVC) is an ectopic beat originating prematurely at the level of the ventricles.


The beat is ventricular in origin and results in no electrical activity in the atria. as a result, no P waves appear. The ventricular depolarization does not travel through the normal rapid ventricular conduction system. Instead, ventricular conduction spreads more slowly through the Purkinje system, resulting in a wide QRS complex with a T wave that is opposite in direction to the QRS complex. A compensatory pause often follows the premature beat as the heart awaits the next stimulus from the sinus node. The pause is considered fully compensatory if the cycles of the normal and premature beats equal the time of two normal heart cycles. The most common of all ectopic beats, PVCs can occur with or without heart disease in any age group. They are especially common in individuals with myocardial disease (ischemia or infarction) or with myocardial irritability (hypokalemia, increased levels of catecholamine, or mechanical irritation with a wire or catheter). The presence of PVCs is a sign of ventricular myocardial irritability and, in some patients, may lead to VT or ventricular fibrillation (VF).

Rate: Depends on rate of underlying rhythm Rhythm: Irregular whenever PVC occurs P Waves: None associated with the PVC PR Interval: None associated with the PVC QRS: Wide (more than 0.10 sec), bizarre appearance.


Premature ventricular contraction: uniform

Premature ventricular contraction: multiform

Premature ventricular contraction: ventricular bigeminy In ventricular bigeminy, the PVC occurs with every other beat.

Premature ventricular contraction: ventricular trigeminy In ventricular trigeminy, the PVC occurs with every third beat.


Premature ventricular contraction: couplets In a rhythm with PVC couplets, the PVCs occur in pairs.

Treatment PVCs may be managed with antiarrhythmic agents. In the emergency setting, amiodarone and lidocaine are the drugs of choice. Correct electrolytes imbalance, if serum potassium is low, potassium replacement may correct the arrhythmia. Correct hypothermia or hypoxia. If the arrhythmia is caused by digitalis toxicity, withdrawal of the digitalis may correct it.

B. Ventricular tachycardia(VT) Ventricular tachycardia is recognized by wide, bizarre QRS complexes occurring in a fairly regular rhythm at a rate greater than 100 beats/minute P waves usually are not seen and, if seen, are not related to the QRS complex. In adults with normal hearts, VT is rare but is a common complication of MI. Other causes are the same as those described for PVCs

monomorphic VT QRS complexes have the same shape and amplitude.

Rate: 100250 bpm Rhythm: Regular P Waves: None or not associated with the QRS complex PR Interval: None QRS: Wide (more than0.10 sec), bizarre appearance Clinical Tip: It is important to confirm the presence or absence of pulses because monomorphic VT may be perfused or non-perfused.

Clinical Tip: Monomorphic VT will probably deteriorate into VF or unstable VT if sustained and not treated. polymorphic VT QRS complexes vary in shape and amplitude.


Rate: 100250 bpm Rhythm: Regular or irregular P Waves: None or not associated with the QRS PR Interval: None QRS: Wide (more than 0.10 sec), with the QRS bizarre appearance Clinical Tip: It is important to confirm the presence or absence of pulses because monomorphic VT may be perfused or non-perfused. Treatment:

Start immediate resuscitation if there is pulseless ventricular tachycardia. If the patient is hemodynamically stable with the arrhythmia, lidocaine may be administered intravenously. If the patient becomes unstable, synchronized Cardioversion is indicated. Long-term treatment for this arrhythmia may involve the use of an implantable cardioverterdefibrillator (ICD).

C. Torsades de pointes In French the term means (twisting of the points) is a specific type of VT. The term refers to the polarity of the QRS complex, which swings from positive to negative and vice versa. The QRS complex morphology is characterized by large, bizarre, polymorphous, or multiform QRS complexes of varying amplitude and

direction, frequently varying from beat to beat and resembling torsion around an isoelectric line. The rate of the tachycardia is 100 to 180 beats/minutes but can be as fast as 200 to 300 beats/minutes. The rhythm is highly unstable; it may terminate in VF or revert to sinus rhythm. This form of VT is most likely to develop in myocardial disease when the underlying QT interval has been prolonged. Torsades de pointes are favored by conditions that prolong the QT interval. Examples include severe bradycardia electrolyte disturbances, such as hypokalemia and hypocalcemia. Other factors that can precipitate this arrhythmia include intrinsic cardiac disease, familial QT interval prolongation, central nervous system disorders, and hypothermia. Torsades de pointes may terminate spontaneously and may repeat itself after several seconds or minutes, or it may transform into VF.

Rate: 200250 bpm Rhythm: Irregular P Waves: None PR Interval: None QRS: Wide (more than 0.10 sec), bizarre appearance

Treatment: Treatment is directed at correcting the underlying problem and may necessitate stopping the offending pharmacological agent or correcting the electrolyte imbalance

Treatment for Torsades de pointes consists of shortening the refractory period (and thus the QT interval) of the underlying rhythm. IV magnesium sulfate, magnesium chloride, or isoproterenol is effective in suppression of the arrhythmia. Overdrive pacing also can be used. Emergency Cardioversion or defibrillation is indicated if the torsades does not revert spontaneously to sinus rhythm. D. Ventricular fibrillation Chaotic electrical activity occurs with no ventricular depolarization or contraction. VF may occur in the following circumstances: myocardial ischemia and infarction, catheter manipulation in the ventricles, electrocution, prolonged QT interval, or as a terminal rhythm in patients with circulatory failure. As in Asystole, loss of consciousness occurs within seconds in VF. There is no pulse and no cardiac output. VF is the most common cause of sudden cardiac death and is fatal if resuscitation is not instituted immediately.

Rate: Indeterminate Rhythm: Chaotic P Waves: None PR Interval: None QRS: None

Treatment: Rapid defibrillation is the management of choice.


The patient should be supported with cardiopulmonary resuscitation and drugs if there is no response to defibrillation. An ICD may be indicated for long-term management of VF. E. Asystole Electrical activity in the ventricles is completely absent.

Rate: None Rhythm: None P Waves: None PR Interval: None QRS: None Clinical Tip: Rule out other causes such as loose leads, no power, or signal gain too low. Treatment: Verify the presence of Asystole by checking different ECG leads. Immediately start CPR as soon as determine that the patient has no pulse 4. Atrioventricular block A disturbance in some portion of the AV conduction system causes an AV block. The sinus-initiated beat is delayed or completely blocked from activating the ventricles. The block may occur at the level of the AV node, bundle of His, or the bundle branches because the AV conduction system contains all of these structures. A. First degree atrioventricular block

In first-degree block, AV conduction is prolonged and equal in time. All impulses eventually are conducted to the ventricles P waves are present and precede each QRS complex in a 1:1 relationship. The PR interval is constant but exceeds the upper limit of 0.2 second in duration. First-degree heart block occurs in individuals of all ages and in healthy and diseased hearts. PR prolongation may be caused by drugs, such as digitalis, beta-blockers, or calcium channel blockers; coronary artery disease; a variety of infectious diseases; and congenital lesions. First-degree block is of no hemodynamic consequence but should be seen as an indicator of a potential AV conduction system disturbance. First-degree block may progress to second- or third-degree AV block.

Rate: Depends on rate of underlying rhythm Rhythm: Regular P Waves: Normal (upright and uniform) PR Interval: Prolonged (more than 0.20 sec) QRS: Normal (0.060.10 sec) Treatment: No treatment is indicated for first-degree heart block. The PR interval should be monitored closely, watching for further block. The possibility of a drug effect also should be evaluated.

Treat the underlying cause. B.Second degree atrioventricular block Mobitz type I (Wenckebach) PR intervals become progressively longer until one P wave is totally blocked and produces no QRS complex. After a pause, during which the AV node recovers, this cycle is repeated. It is usually is associated with block above the bundle of His. Therefore, any drug or disease process that affects the AV node, such as digitalis, myocarditis, or an inferior wall MI. Patients with Mobitz type I second-degree AV block rarely are symptomatic because the ventricular rate usually is adequate.

Rate: Depends on rate of underlying rhythm Rhythm: Atrial: regular; ventricular: irregular P Waves: Normal (upright and uniform), more P waves than QRS PR Interval: Progressively longer QRS: Normal (0.060.10 sec) Treatment (if symptomatic): Administer atropine as prescribed. Prepare for temporary pacemaker.

Constant monitoring and observation for progression

Mobitz type II It occurs usually in or below the bundle of His. Mobitz type II block is characterized by a fixed PR interval when AV conduction is present and a non-conducted P wave when the block occurs. Conduction ratio (P waves to QRS complexes) is commonly 2:1, 3:1, 4:1, or variable. QRS complexes are usually wide because this block usually involves both bundle branches. Mobitz type II pattern is seen in the setting of an anterior wall MI and various diseases of the conducting tissue, such as fibrotic disease. A Mobitz type II block is potentially more dangerous than a Mobitz type I block. Mobitz type II block often is permanent, and it may deteriorate rapidly to third-degree heart block with a slow ventricular response of 20 to 40 beats/ minute.

Rate: Atrial: usually 60100 bpm; ventricular: slower than atrial rate Rhythm: Atrial regular and ventricular may be regular or irregular P Waves: Normal (upright and uniform); more P waves than QRSs PR Interval: Normal or prolonged but constant QRS: May be normal, but usually wide (more than 0.10 sec) Treatment:

Constant monitoring and observation for progression to third-degree heart block are required. Medications, such as atropine or isoproterenol Cardiac pacing may be required if a patient becomes symptomatic Permanent pacing often is indicated for long-term management .

C. Third degree atrioventricular block Complete heart block is another name for this rhythm. In third-degree or complete heart block, the sinus node continues to fire normally, but the impulses do not reach the ventricles because of Conduction between the atria and the ventricles is totally absent, this is known as AV dissociation. . The ventricles are stimulated from escape pacemaker cells either in the junction (at a rate of 40 to 60 beats/minute) or in the ventricles (at a rate of 20 to 40 beats/minute), depending on the level of the AV block. The causes of complete heart block are the same as for lesser degrees of AV block.

Rate: Atrial: 60100 bpm; ventricular: 4060 bpm Rhythm: Usually regular, but atria and ventricles acting dependently. P Waves: Normal (upright and uniform) PR Interval: Varies greatly

QRS: Normal if ventricles are activated by junctional escape focus; wide if escape focus is ventricular. Treatment: A temporary pacing wire is usually inserted immediately, and when the patient is stabilized, a permanent pacemaker is implanted. Administer atropine as prescribed. Assess patient tolerance and the need for treatment to support cardiac output. Minimize patient activities and maintain bed rest.

Bundle branch block (BBB) A bundle branch block develops when there is either a functional or pathological block in one of the major branches of the intraventricular conduction system. As conduction through one bundle is blocked, the impulse travels along the unaffected bundle and activates one ventricle normally. The impulse is delayed in reaching the other ventricle because it travels outside of the normal conducting fibers. The abnormal activation produces a wide QRS complex, representing the increased time it takes for ventricular depolarization.

Rate: Depends on rate of underlying rhythm Rhythm: Regular P Waves: Normal (upright and uniform) PR Interval: Normal (0.120.20 sec) QRS: Wide (more than 0.10 sec) with or without a notched appearance.


Effect of serum electrolyte abnormalities on the Electrocardiogram: Potassium and calcium are probably the two most important electrolytes involved in the proper function of the heart. Because of their effects on the electrical impulse in the heart, an excess or insufficiency of either electrolyte frequently causes changes in the ECG. 1. Hyperkalemia Frequently causes changes in the ECG, the earliest sign of hyperkalemia on the ECG is a change in the T wave. It usually is described as tall, narrow, and peaked or tented in appearance The effect of hyperkalemia on an ECG:


(A) This waveform is produced when the serum potassium level falls within the normal range usually considered to be 3.5 to 5 mEq/L. (B) When the serum potassium level rises above 5.5 mEq/L, the T wave begins to peak. The P wave and QRS complex are normal. (C) When the potassium level exceeds 6.5 mEq/L, the P wave grows wider and its amplitude falls. The QRS complex also widens as intraventricular conduction velocity diminishes. (D) When the potassium level reaches 10 mEq/L, the P wave becomes almost indiscernible; the QRS complex is slurred and widened. (E) When the potassium level ranges from 10 to 12 mEq/L, the P wave is undetectable, because the atria are no longer excitable. (F) When the potassium level exceeds 12 mEq/L, the QRS complex is no longer identifiable. The waves are known as sine waves. Ventricular fibrillation and cardiac arrest



The effect of hypokalemia on an ECG:

(A) When the potassium level is normal usually considered to be 3.5 to 5 mEq/L the T wave is much higher than the U wave (see highlighted area). (B) When the potassium level falls to 3 mEq/L, the T wave and U wave are almost the same height (see highlighted area). (C) When the potassium level falls to 2 mEq/L, the U wave starts rising above the T wave (see highlighted area). (D) As the potassium level reaches 1 mEq/L, the U wave starts to resemble a T wave (see highlighted area). The duration of the QT interval remains the same, but it cannot be measured because the two waves are fusing 3. Hypercalcemia


The effect of Hypercalcemia on an ECG:

Is shortening of the QT interval, the shortened QT interval is a result of shortening of the ST segment (Because the QRS complex and T wave usually are unaffected by changes in serum calcium levels) 4. Hypocalcemia

The effect of Hypocalcemia on an ECG:

Prolong the QT interval because of a lengthening of the ST segment. The T wave itself is not prolonged

MANAGEMENT OF DYSRHYTHMIAS Radiofrequency Catheter ablation Defibrillation and Cardioversion 3. Cardiac Pacemakers
1. 2.



Radiofrequency ablation has an increasingly important role in the management of cardiac arrhythmias. Ablation involves the destruction of re-entry circuits, which are often caused by a myocardial scar or a developmental anomaly. Indications: The main indications for catheter ablation are:

Symptomatic supraventricular tachycardia (SVT) due to atrioventricular nodal reentrant tachycardia (AVNRT), Wolff-Parkinson-White syndrome, unifocal atrial tachycardia, and atrial flutter (especially common right atrial forms). Atrial fibrillation with lifestyle-impairing symptoms, after inefficacy or intolerance of at least 1 antiarrhythmic agent. Symptomatic ventricular tachycardia (VT), especially idiopathic VT.

Other indications for catheter ablation include:

Symptomatic drug-refractory idiopathic sinus tachycardia Lifestyle-impairing ectopic beats Symptomatic junctional ectopic tachycardia.


A cardiac catheter is introduced via the peripheral vascular system. A radiofrequency current is passed through an electrode on the end of the cardiac catheter. The lesions created are small, homogeneous, approximately 5-7 mm in diameter and 3-5 mm in depth. This has no effect on cardiac function. The procedure may take several hours or even longer. The patient may feel slight discomfort during the ablation. Patients appear to be particularly aware of their normal heartbeat after the procedure but this sensation disappears after a period of a few weeks. Patients do not require long-term follow-up if the arrhythmia has been cured.



Left atrial ablation and ablation for persistent atrial flutter should not be performed in the presence of known atrial thrombus. Mobile left ventricular thrombus is a contra-indication to left ventricular ablation. Mechanical prosthetic heart valves are generally not crossed with ablation catheters.


Death (0.1-0.2% of all procedures) Cardiac complications, e.g. high-grade atrioventricular (AV) block, cardiac tamponade, coronary artery spasm or thrombosis, pericarditis, valve trauma Vascular complications, e.g. retroperitoneal bleeding, hematoma, vascular Injury, transient ischemic attack or stroke, hypotension, thromboembolism or air embolism Pulmonary complications, e.g. pulmonary hypertension, pneumothorax Other complications include left atrial-esophageal fistula, acute pyloric spasm or gastric hypo motility, phrenic nerve paralysis, radiation or electrically induced skin damage, infection at access site, inappropriate sinus tachycardia. Cardiac wall perforation is rare and is usually due to catheter manipulation rather than the lesion created by ablation.

Nursing Management:

The nurse plays a vital role in the care of the patient undergoing radiofrequency ablation. In collaboration with the physician, the nurse provides information to the patient and family about what to expect before, during, and after the procedure. The psychosocial support provided by the nurse may be crucial in helping the patient and family cope with the uncertainties of dysrhythmia management.


The nurse participates in educating the patient and family about radiofrequency ablation guide for patient and family education.

During the preablation period, the nurse records a 12-lead ECG, continuously monitors the patients cardiac rhythm, and treats any dysrhythmias per the physicians orders. Other baseline data obtained include vital signs, breath sounds, fluid status, serum chemistries, prothrombin time, and complete blood counts. Antidysrhythmic drugs are usually stopped 2 to 3 days before the procedure. The patient receives nothing by mouth for about 8 hours before the procedure. Because of x-ray exposure during the test, it is important to verify that a female patient is not pregnant.


The nurse in the electrophysiology laboratory is responsible for monitoring of the patient throughout the procedure and assisting the physician with necessary interventions. The nurse must be competent in advanced cardiac life support so that an emergency situation can be handled appropriately. Once the patient arrives in the laboratory, the nurse explains all procedures to the patient and helps to put the patient at ease. The nurse connects the patient to an automatic external defibrillator, a grounding pad, physiological recorder, cardiac monitor, automatic blood pressure device, and pulse oximeter. Oxygen is provided by a nasal cannula. If not already in place, an IV line is inserted. IV conscious sedation is administered to ensure patient comfort. A urinary catheter is inserted if the procedure is anticipated to be lengthy. Both groins and the right subclavian vein sites are shaved and the skin prepared. A lead apron is placed under the patients lower back to block fluoroscopy radiation from penetrating the reproductive system. Throughout the procedure, the nurse monitors hemodynamic status, activated clotting time (ACT) if heparin is used, sedation level, and patient comfort. Communication with the patient is essential so that the patient is kept informed about the progress of the procedure, and anxiety and fear are minimized.

The nurse also warns the patient that a burning sensation may be felt for a very brief time during the actual ablation.


Thorough assessment and monitoring of the patient are continued after the ablation procedure. Essential components of the assessment include vital signs, cardiac rhythm, catheter insertion sites, peripheral pulses, and level of consciousness. The patient may remain drowsy for several hours and experience nausea and vomiting as a result of the medications. When an arterial site has been used, leg immobilization and bed rest are maintained for about 6 hours. If only venous sites were used, the patient may begin ambulation in about 4 hours. The nurse assesses the patient for any pain or discomfort and provides comfort measures if indicated. Fluid volume status is checked, and when stable, the urinary catheter is removed. During the post ablation period, the nurse carefully assesses the patient for any evidence of complications.

Defibrillation and Cardioversion


Electrical counter shock therapy is useful in converting supraventricular and ventricular dysrhythmias to sinus rhythm, especially when the patient becomes hemodynamically unstable or does not convert to a normal rhythm with pharmacological agents. As opposed to defibrillation, this delivers an unsynchronized current to the heart through the chest wall in an attempt to convert pulseless ventricular tachycardia or fibrillation to sinus rhythm. Cardioversion delivers a shock that is synchronized with the hearts activity. By setting the defibrillator to the synchronized mode, the device detects the patients R wave and delivers the shock during ventricular depolarization. Hemodynamically unstable cases should be converted immediately using synchronized electrical Cardioversion. Although recommendations are made for the number of joules needed to convert various rhythms, the actual energy needed varies with the duration of the dysrhythmia, rate, morphology, and underlying cause of the dysrhythmias, as well as transthoracic impedance. Procedure: Nursing role in Cardioversion:

Before Cardioversion:

Restrict the patients food and water for 6 to 8 hours before Cardioversion, unless emergency Cardioversion is required. If the patient is on chronic digitalis, confirm that digoxin levels are therapeutic. Patients with digitalis toxicity should not undergo elective Cardioversion until levels are normalized. Explain the procedure to the patient, and obtain informed consent. Record a 12-lead ECG and vital signs. Establish an IV line, and ready all necessary resuscitation equipment.

During Cardioversion:

Turn on the defibrillator and monitor, and attach the monitoring electrodes to the patients chest. Avoid placing the electrodes in the area where the defibrillation paddles will be positioned.

Turn on the synchronizer mode button. The size of the R wave or the monitored lead may need to be adjusted until the synchronization marker appears on each R wave.

Sedate the patient, and maintain an adequate airway. Remove paddles and apply a generous amount of electrode jelly to them, or apply gel pads to the chest wall. This is done to prevent skin burns and decrease electrical resistance. When using patches, be sure that there are no air pockets by applying the patches firmly from the center to the periphery. Air pockets can cause skin burns. Apply paddles, one just below the right clavicle and the other over the apex of the heart. If anterior-posterior patches are used, place the anterior patch over the left precordium and the posterior one behind the heart in the left infrascapular location. Make sure the paddles/ patches are away from electrode wires or from an implanted pacemaker or implantable cardioverterdefibrillator generator. Set the desired energy level. Press the charge button. A light will flash until paddles are fully charged. Reconfirm the synchronization markers on the R waves on the monitor. Call out clear to make sure no one is touching the patient or the bed. Discharge the paddles while applying firm pressure. Push and hold both paddle discharge buttons until the defibrillator discharges. Maintain contact on the chest wall until the machine has delivered the shock. There will be a momentary delay from the pressing of the discharge button to delivery of the shock because of the synchronization with the R wave. Failure to keep the paddles on the chest can result in failure to cardiovert and burns to the chest.


o Clinical Tip: The sync mode delivers energy just after the R wave to avoid stimulation during the refractory, or vulnerable, period of the cardiac cycle when a shock could potentially produce VF. Remove the paddles, and assess the patients rhythm and vital signs. Subsequent shocks may need to be delivered. If so, be certain to select the synchronized mode. o If the patients rhythm deteriorates to ventricular fibrillation, turn off the synchronizer and immediately defibrillate the patient, starting with 200 J and increasing to 360 J as needed.

After Cardioversion:

Observe the patient for changes in rhythm, blood pressure, and respirations. Patients with atrial fibrillation with slow ventricular rates in the absence of AV nodal blocking agents may have underlying sinus node dysfunction. Be prepared for transcutaneous pacing if needed, or have atropine sulfate readily available. Further Antidysrhythmic agents may need to be administered to maintain sinus rhythm. Monitor the patients respiratory status and level of consciousness because sedation was delivered before the procedure. Inspect the chest wall for any signs of burns and treat appropriately.


Implantable Cardioverter Defibrillator (ICD) An implantable cardioverter-defibrillator (ICD) is a small battery-powered electrical impulse generator which is implanted in patients who are at risk of sudden cardiac death due to ventricular fibrillation and ventricular tachycardia. The device is programmed to detect cardiac arrhythmia and correct it by delivering a jolt of electricity. Defibrillation or Cardioversion may be accomplished by an implantable cardioverter-defibrillator (ICD). Electrical treatment of dysrhythmia also includes cardiac pacing. Temporary pacing may be necessary for reversible causes of very slow heartbeats, or bradycardia. A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover.


OTHER MANAGEMENT VALSALVA MANUEVER: The Valsalva maneuver or Valsalva maneuver is performed by moderately forceful attempted exhalation against a closed airway, usually done by closing one's mouth and pinching one's nose shut. The Valsalva maneuver works by decreasing preload to the heart. A complementary maneuver for differentiating disorders is the Handgrip maneuver, which increases afterload. The Valsalva maneuver alters heart rate through sympathetic stimulation (i.e. the accelerator nerve). Neuro-muscular junctions at the sinoatrial node (SAN) release the neurotransmitter norepinephrine (noradrenaline), which increases the SAN's depolarization rate. These effects decrease the time between pacemaker action potentials, which results in a faster heartbeat. In later phases of the Valsalva maneuver (phases II and III), heart rate is reduced due to parasympathetic interplay.

Carotid sinus massage Indications: Can increase vagal nerve stimulation and slow SVT, or even convert SVT to NSR, without severe hemodynamic compromise Method: Place the patient in a supine position, head tilted to either side with the neck hyperextended. Place your index and middle fingers over the carotid artery just below the angle of the jaw, as high on the neck as possible. Massage the artery for 510 sec by pressing it firmly against the vertebral column and rubbing Contraindications: Unequal carotid pulses, carotid bruits, cervical spine injury, or history of cerebrovascular accident or carotid atherosclerosis.

Side Effects: Slow HR or AV block, PVCs, VT, VF, syncope, seizure, hypotension, nausea or vomiting, stroke. Precautions: Be sure the patient is receiving oxygen and an IV is in place. Never massage both arteries simultaneously. Clinical Tip: Each carotid artery should be palpated and auscultated before the procedure to maintain safety measures. Clinical Tip: Alternate vagal maneuvers include encouraging the patient to cough, bear down, or hold his or her breath.


ACLS Cardiac Arrest Circular Algorithm


Bradycardia Algorithm


Tachycardia Algorithm




1. Morton P.U, Fontaine D.K, Hudak C.M., Gallo B.M. Critical care nursing: A holistic approach, 9th ed., Philadelphia, Lippincott Williams & Wikins.