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Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
Rhythm Strip Review
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Rhythm Strip Review

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Basic ECG Rhythm Interpretation.

Basic ECG Rhythm Interpretation.

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  • How to Read an EKG Strip EKG paper is a grid where time is measured along the horizontal axis. Each small square is 1 mm in length and represents 0.04 seconds. Each larger square is 5 mm in length and represents 0.2 seconds. Voltage is measured along the vertical axis. 10 mm is equal to 1mV in voltage.
  • An easier and quicker way to estimate the heart rate. As seen in the diagram below, when QRS complexes are 1 box apart the rate is 300 bpm. 2 boxes apart...150 bpm, etc. So if you memorize these simple numbers you can estimate the heart rate at a glance!
  • Normal Sinus Rhythm Impulses originate in the SA node regularly at a rate 60-100 per minute in adults and at faster rates in older children (90-110), small children (100-120) and infants (120-160).  P waves upright in L2 and negative in AVR and of uniform size and contour from beat to beat.  PR interval 0.12-0.20 sec and constant when A-V conduction normal; PR prolonged and/or variable when A-V block present.  Each P followed by QRS with resulting P:QRS ratio 1:1 QRS ratio 1:1.  QRS less than 0.11 sec or QRS wide and bizarre when bundle branch block present.  RR intervals may be slightly irregular especially in the young and elderly. Heart Rate 60 - 100 bpm Rhythm Regular P Wave Before each QRS, identical PR Interval (in seconds) 0.12 to 0.20 QRS (in seconds) < 0.12
  • Sinus Arrhythmia Similar to normal sinus rhythm except that PP and RR intervals are irregular because the SA node discharges at a variable frequency.  In children and young adults the irregularity is cyclic or related to respiration with the rate increasing during inspiration and decreasing during expiration.  A cyclic sinus arrhythmia disappears upon exercise or breath holding and is accentuated by deep breathing.  In elderly subjects the irregularity is frequently due to organic heart disease.
  • Sinus Tachycardia Impulses originate in the SA node at a rate 100-160/min in adults (and up to 200 or more in children).  P upright in L2 and negative in AVR with identical or slightly different size and contour from beat to beat.  At very rapid rates P superimposed on preceding T.  When P recognizable, P:QRS ratio 1:1.  Tachycardia usually appears and subsides gradually.  Vagal stimulation produces gradual slowing which reverses when pressure is released.  Exercise further increases the rate. Heart Rate > 100 bpm Rhythm Regular P Wave Before each QRS, identical PR Interval (in seconds) 0.12 to 0.20 QRS (in seconds) < 0.12 Common causes are anxiety; physiological stress such as hemorrhage, dehydration, sepsis, and fever; and hyperthyroidism. Correction of the underlying cause, if necessary, is recommended.
  • Sinus Bradycardia Similar to normal sinus rhythm except that the rate is less than 60/min in adults and older children or less than 80 in younger children.  The PR interval may be slightly prolonged and/or P wave abnormally wide.  Physiological bradycardia occurs in healthy individuals (usually athletes) with increased vagal tone.  Exercise or atropine always increase the rate to normal.  Pathological bradycardia occurs in subjects with acute myocardial infarction (especially inferior) or other heart disease involving the SA node, in subjects taking drugs such as digitalis or beta blockers and in elderly subjects.  Exercise or atropine often fail to increase the rate to normal. Heart Rate < 60 bpm Rhythm Regular P Wave Before each QRS, identical PR Interval (in seconds) 0.12 to 0.20 QRS (in seconds) < 0.12     This rhythm differs from normal sinus rhythm only in that the rate is below 60 beats per minute (bpm). This can be a normal finding in young patients, particularly in athletes. It can be caused by medications, including as beta blockers, some calcium blockers such as diltiazem, aldomet, and perhaps digitalis. If there is any concern about this rhythm, consultation with a Cardiologist is recommended.
  • Sinus Pause (SP) Heart Rate N/A Rhythm Irregular P Wave Before each QRS, identical, Dropped beat PR Interval (in seconds) 0.12 to 0.20, The P to P interval is undisturbed. QRS (in seconds) < 0.12
  • Sinus Arrest (SA) Heart Rate N/A Rhythm Irregular P Wave Before each QRS, identical, New rhythm begins after a pause PR Interval (in seconds) 0.12 to 0.20, The P to P interval is undisturbed. QRS (in seconds) < 0.12 Sinus arrest      This rhythm results from failure of the sinus node to activate the atria. When it is of short duration (less than one to two seconds), it is usually benign. When it is of long duration (greater than or equal to three seconds), it can be life-threatening because of the potential for longer periods of sinus arrest with asystole. It can be caused by medications, including as beta blockers, some calcium blockers such as diltiazem, aldomet, and perhaps digitalis. It can also be part of the sick sinus ("tachy-brady") syndrome, which is one of the leading indications for implantation of permanent pacemakers in this country. If there is any concern about this rhythm, consultation with a Cardiologist is recommended.
  • Atrial Fib. Impulses originate in multifocal atrial pacemaker at a rate 300-600/min but only some of them are conducted to the ventricles.  The atrial activity is represented by numerous, irregularly spaced small deflections of varying configuration (f waves) best seen in L2, L3 AVF and V1.  Occasionally, f waves may be prominent ("coarse" fibrillation) resembling atrial flutter or no atrial activity is discernible ("fine" fibrillation).  Only some f waves pass through the AV junction and activate ventricles in a completely irregular fashion.  Vagal stimulation may have no effect or may slow the ventricular rate by increasing the AV block.     This is a supraventricular rhythm resulting from multiple reentrant circuits within either the right or left atria, or both. It is characterized by an irregularly irregular ventricular rate that is usually rapid in young patients, but may be normal or even bradycardic in elderly patients or patients taking medications that can cause atrioventricular nodal blockade. It can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, or congestive cardiomyopathy. The new onset of either rhythm is seen in about 5% of cases of acute myocardial infarction. The clinician may also want to check for congestive heart failure, since worsening CHF can present with these rhythms. Digitalis toxicity is suggested by a regular ventricular response (Accelerated junctional rhythm) in combination with atrial fibrillation. In the presence of an accessory atrioventricular pathway, atrial fibrillation can manifest as a rapid, irregularly irregular wide complex tachycardia that can resemble ventricular tachycardia closely. It should be suspected particularly in young patients with very rapid tachycardia that is well tolerated hemodynamically. Close examination of the ECG will reveal irregularly irregular RR intervals. In this case: It is important to obtain a 12-lead ECG before cardioversion because the location of the pathway, and therefore the risks of a subsequent curative catheter-mediated radiofrequency ablation procedure, can be estimated fairly accurately from the 12-lead ECG. DO NOT give digitalis or verapamil to try to slow ventricular response if an accessory pathway is suspected . These drugs can accelerate conduction over accessory pathways, resulting in even more rapid ventricular activation which can, in turn, induce ventricular fibrillation. There are four issues related to care of patients with this rhythm: control of the rate of the ventricular response, conversion of the atrial rhythm to sinus rhythm, maintenance of sinus rhythm following conversion, and prevention of embolic stroke from thrombi that form in the fibrillating left atrium. Consultation with an Internist or Cardiologist is recommended for advice on these issues.
  • Atrial Flutter Impulses originate in an atrial pacemaker at a rate 240-340/min but some of them are blocked regularly at the AV junction.  Atrial activity is represented by sawtooth-like deflections (F waves) not separated by an isoelectric segment and best seen in L2, L3 and AVF.  Usually only every second F is conducted to the ventricles (2:1 AV block) with the resulting ventricular rate half the atrial rate; rarely the AV conduction is 3:1, 4:1, 1:1 or variable.  Vagal stimulation may have no effect or slow ventricular rate by increasing AV block or terminate flutter.  Exercise increases HR by decreasing the block. Atrial flutter      This is a supraventricular rhythm resulting from a reentrant circuit that lies within the right atrium. It is characterized by an atrial rate of 250 to 350 beats per minute, and a ventricular response that is usually about 75, 150, or 300 beats per minute. Flutter waves are best found in ECG leads II, III, aVF, and V1. Sometimes they are located at the onset or offset of the QRS complex, and are best found by comparison with the QRS morphology in a 12-lead ECG recording obtained during sinus rhythm. Even if flutter waves are not found, this rhythm should be suspected when the ventricular rate ranges from 140 to 160 beats per minute and there is no clear evidence of atrial activity. It can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, or congestive cardiomyopathy. The new onset of either rhythm is seen in about 5% of cases of acute myocardial infarction. The clinician may also want to check for congestive heart failure, since worsening CHF can present with these rhythms. For emergency treatment of this rhythm, when the patient has hypotension, angina, or acute congestive heart failure, synchronized cardioversion with appropriate anesthesia is indicated. For short-term pharmacologic control of this rhythm, drugs that decrease AV nodal conduction (beta blockers, calcium blockers, and digoxin) may be considered. For long-term treatment of this rhythm, consultation with a Cardiologist is recommended.
  • Atrial Tachycardia (AT) Impulses originate in an atrial pacemaker at a rate 140-250/min.  Atrial activity may be represented by upright P in L2 or by P superimposed on T or ST segment of the preceding beat.  At very rapid rates only every second P may be followed by QRS (2:1 AV block) with the resulting ventricular rate half the atrial.  QRS usually less than 0.11 sec; wide and bizarre QRS mat be due to preexisting BBB or WPWS or due to aberrancy common at rapid rates.  Onset and termination of AT is often abrupt.  Vagal stimulation frequently terminates AT. Atrial tachycardia      This is a supraventricular rhythm resulting from either an atrial automatic focus or a reentrant circuit that lies entirely within the atrium. It is characterized by a rate more than 100 beats per minute, and a P wave morphology that is usually different from that of the sinus P wave. It can be intermittent or incessant (present more than 50% of the time). When it is incessant, it can cause symptomatic dilated cardiomyopathy that is reversible with control of the tachycardia. This is an abnormal rhythm that can result from digitalis toxicity , particularly when it occurs in combination with Atrioventricular nodal block, second degree, Mobitz type I (Wenckebach) . For emergency treatment of this rhythm, when the patient has hypotension, angina, or acute congestive heart failure, synchronized cardioversion with appropriate anesthesia is indicated. For short-term pharmacologic control of this rhythm, drugs that decrease AV nodal conduction (beta blockers, calcium blockers, and diltiazem) may be considered. For long-term treatment of this rhythm, consultation with a Cardiac Electrophysiologist is recommended.
  • Atrial Premature Beat (APB) The impulse is discharged prematurely by some irritable focus in the atria giving rise to a distorted P wave (wide, narrow, notched, inverted or superimposed on the preceding T wave).  The further from the SA node the ectopic focus is, the more abnormal will be P' configuration.  PR interval normal or slightly prolonged.  Premature P followed by QRS less than 0.11 sec except when very premature P is not conducted; occasionally QRS may be wide with RBBB configuration due to aberrancy.  The pause between APB and the next sinus beat is usually noncompensatory, i.e., the RR interval between two QRS enclosing APB is less than twice the normal RR interval. Premature Atrial Contractions (PAC) Heart Rate N/A Rhythm Irregular P Wave Premature & abnormal or hidden PR Interval (in seconds) < 0.20, The P to P interval is undisturbed. QRS (in seconds) < 0.12
  • Wandering atrial pacemaker      This is a supraventricular rhythm resulting from multiple ectopic foci in the atria. It is characterized by three or more P wave morphologies and a rate less than 100 beats per minute. It itself is benign, but reflects electrical abnormalities in one or both atria that increase the likelihood of multifocal atrial tachycardia or other atrial arrhythmias.
  • Junctional rhythm      This is a slow rhythm, with rates ranging from 40 to 60 beats per minute, with QRS complexes that have the patient's normal morphology. Usually, no P waves are seen. When P waves are present, they follow closely after the QRS complexes. This rhythm results from the backup pacemaker capability of the atrioventricular node during sinus arrest. Junctional escape complex      This is a QRS with normal morphology for the patient that is not preceded by a P wave and occurs later than would be expected from the sinus rate. Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as is sinus arrest . Junctional premature complex
  • Junctional Premature Beats (JPB) The impulse prematurely discharged from an irritable focus in or near the AV junction spreads backward (retrograde) to the atria and forward (antegrade) to the ventricles.  An inverted P wave may precede QRS by less than 0.12 sec ("upper" junctional beat ) or inverted P wave may follow QRS ("lower" junctional beat) or P wave may be buried in QRS ("middle" junctional beat).  Premature QRS is less than 0.22 sec but often slightly distorted; occasionally QRS is wide and has RBBB configuration due to aberrancy.  The pause following JPB is noncompensatory as explained for APB. Junctional premature complex      This is a QRS complex that occurs earlier than would be expected from the sinus rate, and that usually has a normal morphology for the patient. It can fail to conduct retrograde through the atrioventricular node, in which case it results in a compensatory pause. That is, the next P wave occurs at the same time as would be expected had the VPC not occurred. More usually, it does conduct through the atrioventricular node, so that the following P wave may occur either sooner or later than would be expected. Junctional premature complexes are relatively uncommon. They can be seen with increased frequency during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter cold remedies. They can also be misdiagnosed when the P wave of an atrial premature complex is obscured by the preceding T wave.
  • Accelerated junctional rhythm      This is a supraventricular rhythm resulting from a focus in or near the atrioventricular junction. The rate ranges from 60 to 100 beats per minute. This is an abnormal rhythm that can result from digitalis toxicity , particularly when it occurs in combination with atrial fibrillation . It can also result from physiologic stress and other causes of increased sympathetic nervous system tone.
  • Junctional Tachycardia Impulses originate in the AV junctional pacemaker at a rate 140-220/min and are conducted retrograde to the atria and antegrade to the ventricles.  P waves are negative in L2 and positive in AVR and may closely precede, follow or coincide with normal QRS complexes.  When P waves precede QRS complexes, the PR interval is less than 0.12 sec; when P waves follow QRS complexes, they appear as splinters deforming the ST segment; when P waves coincide with QRS complexes, they are not discernible.  The paroxysmal form of tachycardia is characterized by a ventricular rate 140-220, sudden onset and offset and sudden termination or no change upon vagal stimulation; the nonparoxysmal form is characterized by a ventricular rate 100-140, gradual onset and gradual slowing or no change upon vagal stimulation.
  • Supraventricular Tachycardia Impulses originate in a supraventricular pacemaker (above the bifurcation of the the common bundle) at a rate 150-250.  P waves cannot be positively identified either because they merge with preceding T waves or because they are buried in QRS complexes so the the differentiation between atrial and junctional tachycardia is impossible.  QRS complexes are less than 0.11 sec; occasionally QRS are wide and have RBBB configuration due to aberrancy. Vagal stimulation may have no effect or may terminate tachycardia abruptly. Supraventricular tachycardia.      This is a generic name for a variety of specific supraventricular rhythms, including Atrioventricular Reentrant Tachycardia, Atrioventricular Nodal Reentrant Tachycardia, and Atrial Tachycardia. It is also used in reference to any narrow complex rhythm to distinguish it from wide-complex rhythms that could arise in the ventricle. In addition to the specific rhythms mentioned above, this use of the term includes atrial fibrillation, atrial flutter, junctional tachycardia, accelerated junctional rhythm, and multifocal atrial tachcyardia.
  • First Degree AV Block Impulses originating in the SA node are conducted abnormally slow through the AV junction to the ventricles.  The rhythm pattern is similar to normal sinus rhythm except that the PR interval is prolonged beyond 0.20 sec in adults and 0.18 sec in children.  With a severe (i.e. greater than 0.5 sec) lengthening of the PR interval or with a rapid rate, the P wave may be superimposed on the preceding T wave.  Occasionally the rate may be slower than 60/minute.  Frequently associated with vagotonia (in which case it disappears after exercise or atropine). Atrioventricular nodal block, first degree This refers to an excessively long PR interval only. All P waves are conducted through the atrioventricular node to the ventricle. By itself, it is a benign condition, but may result from disease in the atrioventricular node, high vagal tone, or medication that reduces conduction through the atrioventricular node .
  • Second Degree AV Block Type I (Wenckebach, Mobitz I) Rhythmic impulses originating in the SA node are conducted through the AV junction at progressively slower (decremental) speed.  P waves are positive in L2 and negative in AVR and occur regularly at a rate 60-100.  A blocked P wave occurs after 2-5 conducted P waves and this so-called Wenckebach cycle or period is repeated.  The P:QRS ratio of 3:2, 4:3, 5:4 may be constant in all cycles or may vary from cycle to cycle.  The PR interval immediately following a dropped QRS complex is the shortest and may be normal or prolonged; with each successive beat the PR interval becomes progressively longer until a P wave is blocked.  QRS complexes may be normal or wide and bizarre if BBB is present. Atrioventricular nodal block, second degree, Mobitz Type I (Wenckebach)      This refers to a gradual prolongation of the PR interval, with occasional failure to conduct a P wave through the atrioventricular node to the ventricle. By itself, it is a benign condition, but may result from disease in the atrioventricular node, high vagal tone, or medication that reduces conduction through the atrioventricular node . It is commonly seen in atheletic young patients, particularly during sleep. This is an abnormal rhythm that can result from digitalis toxicity , particularly when it occurs in combination with Atrial tachycardia . It is distinguished from Second degree Atrioventricular nodal block, Mobitz type II by the fact that the PR interval of the P wave that follows the non-conducted P wave is at least 10 msec shorter than the PR interval of the P wave that precedes the non-conducted P wave. Typically, the QRS complex is unchanged from the patient's normal QRS morphology. By contrast, the PR interval does not change in Mobitz type II block. Mobitz type II block is dangerous because it can progress to complete heart block and death without warning .
  • Second Degree AV Block Type II (Mobitz II) Rhythmic impulses originating  in the SA node are intermittently blocked at the AV junction.  P waves are positive in L2 and negative in AVR and occur regularly at a rate 60-100.  Only every second (or rarely third, fourth, etc.) P wave is followed by a QRS complex resulting in the P:QRS ratio 2:1, 3:1, 4:1, etc. and the ventricular rate 20-60.  Rarely the AV conduction and the P:QRS ratio may be 3:2, 4:3, 5:2 or other and may vary in the same tracing.  The PR interval of the conducted beats is normal or prolonged and usually constant.  QRS complexes are frequently wide and have RBBB configuration because the lesion extends below the AV junction. Atrioventricular nodal block, second degree, Mobitz type II      This refers to occasional failure to conduct a P wave through the atrioventricular node to the ventricle without a change in the PR interval after the nonconducted P wave compared with before the nonconducted P wave. This is a dangerous condition because it can progress to complete heart block and death without warning . Immediate consultation with a Cardiologist for placement of a temporary pacemaker is advisable. Placement of an external pacemaker may be lifesaving if a temporary pacemaker cannot be placed immediately. This condition, while dangerous, is very unusual. The QRS complex is usually wide, due to extensive disease of the His-Purkinje system, although a narrow QRS complex does not exclude the diagnosis. The clinician should measure the change in PR interval carefully, as described for Second degree Atrioventricular nodal block, Mobitz type I . 2:1 Atrioventricular nodal block      This rhythm is diagnosed when the entire rhythm strip shows only conduction of every other P wave to the ventricle. Because the record does not show two consecutive P waves that conduct to the ventricle, it is not possible to measure prolongation of the PR interval, so that it is not possible to distinguish between Mobitz type I and the dangerous Mobitz type II Second degree Atrioventricular nodal block. By convention, recordings obtained at other recent times are used to make this distinction. This degree of block is usually considered pathological when the atrial rate is less than 150 beats per minute or so, because the normal AV node should be able to conduct 1:1 from the atrium to the ventricle at this rate.
  • Third Degree (Complete) AV Block Impulses originate in the SA node or in an atrial pacemaker but none of them is conducted through the AV junction to the ventricles.  P waves are positive in L2 and negative in AVR and occur regularly at a rate 60-100; rarely atrial activity is represented by inverted (ectopic) P waves, F waves of f waves.  Since all P waves are blocked, the ventricles are activated by impulses activated by impulses arising (through escape mechanism) in pacemaker cells below the bifurcation of the common bundle.  The resulting QRS complexes are wide, slurred, frequently of RBBB configuration and occur regularly at a rate 20-40 (the so-called idioventricular rhythm).  P waves occurring at a faster rate are completely unrelated to QRS complexes (AV dissociation). Third degree (complete) heart block      This rhythm is characterized by failure of conduction from the atria through the atrioventricular node to the ventricles. The atrial rhythm is independent of the ventricular rhythm, unless an accessory pathway that conducts antegrade is present. It is most easily distinguished from high-grade atrioventricular nodal block when the atrial and ventricular rhythms are regular but have different rates. Because of weak coupling between the chambers by the autonomic nervous system, these rates can be very close to each other and in fact can oscillate around each other. Complete heart block is one of three forms of atrioventricular dissociation . The other two forms are: sinus arrest or sinus bradycardia with junctional rhythm or Idioventricular rhythm . ventricular tachycardia . Of these three forms, only Complete Heart Block results from antegrade conduction block from the atria to the ventricles.
  • Premature Ventricular Complexes (PVCs) A. Etiology -- an irritable focus in the ventricle discharges before the arrival of the next anticipated impulse from the sinus node. Because the impulse arises in either the right or the left ventricle it does not travel down the normz;l conduction pathway (normally the right and left ventricles are depolarized simultaneously). This produces an abnormal, bizarre-looking complex. B. Characteristics 1. Premature, occurring before & next expected beat. 2. No P wave before the PVC. 3. Compensatory pause 4. QRS widened (0.12 or wider) 5. T wave is usually oppositely directed from QRS complex. C. Clinical significance 1. May be a stable, benign finding in many patients 2. May be a precursor to other more dangerous dysrhvthmias. 3. Patient may feel "palpitations". 4. May lose significant amount of stroke volume with PVCs, precipitating angina, hypotension. C. Clinical significance 1. May be a stable, benign finding in many patients 2. May be a precursor to other more dangerous dysrhvthmias. 3. Patient may feel "palpitations". 4. May lose significant amount of stroke volume with PVCs, precipitating angina, hypotension. D. When to treat PVCs 1. When they Occur at the rate of greater than 6 per minute. 2. Multifocal PVCs 3. R - on - T PVCs 4. Bigeminy PVCs (every other beat is a PVC) 5. Runs of two (2) or more PVCs in a row. E. Treatment 1. Determine the underlying cause a. rnyocardial ischemia b. hypoxemia c. digitalis toxicity, epinephrine, aminophyline d. hypokalemia e. anemia f. CHF g. fever h. acidosis i. bradycardia j. anxiety k.caffeine 2. Treatment a. If PVCs are occurring with bradycardia or AV block, it may help to speed up the heart rate with Atropine b. Treat the underlying cause. c. Lidocaine IV 1. Initial IV bolus of 1 - 1.5 mg/kg. 2. If not suppressed, repeat hdocaine, 0.5 - 1.5mg/kg, until no ectopy, or up to 3mg/kg is given. d. Procainamide 1. Used primarily when hdocaine has been ineffective. 2. Bolus with too mg. every 5 minutes at a rate of 20-30 mg/min. until: a) dysrhytbmia is suppressed b) patient becomes hypotensive c) QRS is widened by 50 d) Until 17 mg/kg has been given 3. Maintenance infusion of I-4mg/min. 4. Precautions - hypotension, widened QRS, lengthened PR or QT interval, AV blocks e. Bretyhum 1. Used when lidocaine and procainamide are ineffective. 2. Give 5-10mg/kg. over 8-10 minutes. 3. Maintenance infusion: 500 mg. in 250 or 500cc DSW infuse at a rate of 1-2 mg/min. 4. Side effects: Initial rise in heart rate and BP, Postural hypotension, nausea and omitting, if given too rapidly. 3. Once ectopy is resolved, follow by an infusion of 2 Gm. In 500cc D5W to infuse at 1-4 mg/min. 4. If patient continues to have PVCs, the drip rate may be increased (up to 4mg/min), but only after repeating the bolus again (Do Not exceed 400-500 mg/hr). 5. Onset of action is 45-90 seconds and the duration of action is 10-20 minutes. 6. Primarily metabolized by the liver; very little excreted by kidneys. 7. Side effects: drowsiness, disorientation, decreased hearing ability, parathesias, muscle twitching, grand mal seizures. Ventricular premature complex This is a wide QRS complex that occurs earlier than would be expected from the sinus rate, and that almost always has an abnormal morphology. It fails to conduct retrograde through the atrioventricular node in half of patients, in which case it results in a compensatory pause. That is, the next P wave occurs at the same time as would be expected had the VPC not occurred. When it does conduct through the atrioventricular node, the following P wave may occur either sooner or later than would be expected. Ventricular premature complexes are a normal finding in adults of all ages. They cause symptoms of palpitations or "skipping" in some people. Their frequency can be increased during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter cold remedies. The frequency is also increased in patients with a tendency to develop ventricular tachycardia .
  • Ventricular Bigeminy An abnormal but usually harmless rhythm characterized by occurrence of one ventricular premature complex (VPC) after each normal QRS complex. This rhythm usually does not progress to dangerous forms of fast ventricular rhythms. Note that in this rhythm, two VPCs never occur one right after the other. Trigeminy An abnormal but usually harmless rhythm characterized by occurrence of one ventricular premature complex (VPC) after every two normal QRS complexes. This rhythm usually does not progress to dangerous forms of fast ventricular rhythms. Note that in this rhythm, two VPCs never occur one right after the other.
  • Ventricular tachycardia, General This rhythm is diagnosed when three or more premature ventricular complexes occur in a row at a rate of 100-120 beats per minute or faster. The major clinical distinctions are between hemodynamically unstable versus stable ventricular tachycardia and between sustained versus unsustained ventricular tachycardia. Hemodynamically unstable ventricular tachycardia is a life threatening emergency for which the ACLS protocol should be initiated immediately. Synchronized cardioversion is usually the treatment of choice. Awake patients should be sedated heavily before cardioversion if at all possible. Sustained ventricular tachycardia is defined as having a duration of 30 seconds or more, or being hemodynamically unstable. The immediate treatment is specified by the ACLS protocol. For long-term treatment, it is important to realize that these patients have a 20% to 40% sudden death mortality, when untreated, over the 12 months following initial presentation. Empiric treatment with antiarrhythmic drugs does not reduce this mortality. Effective treatment with drugs and/or an implantable cardioverter defibrillator reduces the sudden death mortality over the next 12 months to 0-2%. Therefore, consultation with a Cardiac Electrophysiologist is recommended during the initial hospital stay to ensure adequate evaluation and treatment before discharge from the hospital. Ventricular Tachycardia (Vtach, VT) Impulses originating in the SA node control the atria but fail to reach the ventricles; the latter are activated by their own pacemaker firing 100-250/min; rarely ventricle-borne impulses are also conducted to the atria.  P waves are frequently indiscernible or may appear as notches at various points on the QRS-T complexes; if P waves are recognizable, they are usually of normal configuration, occur regularly at a rate 60-100 and bear no fixed relation to the QRS complexes (AV dissociation).  Rarely, when the atria are controlled by the ventricular pacemaker, the P waves are inverted and follow QRS complexes at a constant RP interval.  When the rate is less than 150, the SA-borne impulse may be occasionally conducted through the AV junction and it can activate the ventricles thus producing a QRS complex whose configuration and width are intermediate between the normal and abnormal complexes (fusion beat or partial capture).  QRS complexes are usually wider than 0.12 sec and bizarre.  RR intervals are usually regular but may vary up to 0.03 sec.  Vagal stimulation has no effect on the rate.  An ECG prior to tachycardia showing premature beats of identical configuration favors ventricular origin of the tachycardia. Characteristics Three or more consecutive bizarre, premature beats, each with 1 width of at least 0.12 seconds and the 1. T wave in the opposite direction fiom the QRS. 2. Ventricular rate 100-250/min. 3. Rhythm is essentially regular, but may vary slightly. 4. May occur as a single isolated basf may recur paroxsysmally or may persist for a long run. Clinical Significance 1. Usually indicative of significant underlying cardiovascular disease. 2. Most patients are not able to maintain an adequate blood pressure with persistent V-tach and will quickly become hypotensive. 3. V-tach often degenerates into Ventricular Fibrillation. (V-Fib, VF). Treatment 1. Prevention - treat malignant PVCs before V-tach develops. 2. Hemodynamicallv stable - (Normal B/P, No chest pain) a. Lidocane 1mg/kg. IV bolus (May give precordial thump). b. Lidocaine 1 - 1.5mgkg. every 8 minutes until V-tach resolves or up to 3mg/kg. has been given. c. If V-tach persists give Procainamide, 20 mg/min. Until V-taeh resolves or up to 17mg/kg. has been given. d. If V-tach persists, cardiovert as in unstable patients. e. After normal rhythm is restored, the patient should remain on antiarrhythmic infusion, until stable. 3. Hemodvnamicallv unstable - a. Check oxygen saturation, IV access, Consider sedation. Have suction and intubation equipment available. b. Cardiovert with 100 joules. c. Cardiovert with 200 joules. d. Cardiovert with 300joules. e. Cardiovert with up to 360 joules. f. If recurrent, add Lidocaine and Cardiovert at starting level. If unsuccessful then procainamide or bretylium. 4. Pulseless V-tach - treat a V-fib.
  • Ventricular Flutter (VF) A. "Extreme" V-tach. B. Resembles a sine wave, a helix or a stretched, coiled spring. C. Regular, large oscillations at a rateof 150-300/min D. Requires immediate defibriilation or cadioversion
  • Ventricular Fibrillation (V-Fib, VF) This is a lethal rhythm, characterized by absence of both organized electrical and organized mechanical activity. This rhythm is equivalent to cardiac death. If you see this, you should initiate Cardiopulmonary Resuscitation immediately. A. Ventricles do not beat in any coordinated fashion, but twitch asynchronously and ineffectively; no ventricular contraction. B. Clinical significance - There is no cardiac output . The patient becomes unconscious and perfusion to all parts ofthe body ceases . C. Characteristics - rapid, repetitive, chaotic waves; no uniformity; cannot identify PQRST waves. Treatment 1. Check pulse. If V-fib witnessed on monitor, give precordial thump. 2. CPR until defibriiiator is available. 3. Defibriliate with 200 joules. 4. If no response, defibrillate with 200-300 joules. 5. Defibrillate with up to 360 joules. 6. If patient is still in V-fib VT, Intubate at once. Start IV access. Give Epinephrine 1 mg. IV which should convert fine V-fib to coarse V-fib which is more susceptible to defibrillation. 7. If patient 61l not redcitated, Intubate and continue CPR. 8. Defibrillate with up to 360 joules. 9. Lidocaine 1-1.5 mg/kg. IV push. Repeat in 3-5 min. to total loading dose of 3mg/kg. 10. Defihrillate with up to 360joules.
  • Asytole and Ventricular Standstill Asystole/Ventricular Standstill A. No ventricular activity. No ventricular contraction. B. Clinical significance - no cardiac output. C. Characteristics 1. usually a straight line 2. may have atrial activity (P waver) 3. may have occasional QRS complexes (escape heats) Ventrlcular Standstill Treatment 1. CPR, Intubate at once, N access, confirm. in more than one lead a. Consider causes: hypoxemia, hyperkalemia, hypokalemia, drug overdose, MI, hypothermia 2.. Consider immediate Transcutaneous Pacemaker 3. Drugs- epinephrine, atropine Primary Ventricular standstill This is diagnosed when only ventricular escape complexes are present, and they occur very slowly. This is an agonal rhythm that is not consistent with life. "Primary" means that the condition arose on its own and is the immediate source of difficulty. If you see this, you should initiate Cardiopulmonary Resuscitation immediately. Secondary Ventricular standstill   This is diagnosed when only ventricular escape complexes are present, and they occur very slowly. This is an agonal rhythm that is not consistent with life. "Secondary" means that the condition is caused by another factor, such as severely low oxygen levels, which must be fixed before the rhythm abnormality can be stabilized. If you see this, you should initiate Cardiopulmonary Resuscitation immediately.
  • Sinus Arrest / Sinus Block A. The sinus node fails to function for a prolonged period. In sinus block, the sinus node functions,but the impulse is not conducted to the ventricles. B. Chnical Significance - will led to cardiac arrest with asystole unless another pacemaker takes over. 1. Junctional pacemaker - inherent pacemaker of 40-60/min. 2. Ventricular pacemaker – 20-40/min. C. Characteristics 1. In sinus arrest, there are no P waves; QRS waves will present only if an escape pacemaker has taken over. Treatment 1. Atropine 2. CPR if episode is prolonged and patient becomes hemodynamicdly unstable. 3. Transcutaneous or transvenous pacemaker.
  • Ventricular escape complex      This is a QRS that is wide and occurs later than would be expected from the sinus rate. Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as is sinus arrest .
  • Idioventricular rhythm      This is diagnosed when only ventricular escape complexes are present, and they occur at 20 to 40 beats per minute. This rhythm is barely consistent with life. If you see this, you should consider initiating Cardiopulmonary Resuscitation immediately, and should move the patient to an intensive care unit as soon as possible. DO NOT give lidocaine or any other antiarrhythmic medication for this rhythm. You could cause asystole and death by inhibiting the only spontaneous rhythm the patient's heart is able to generate.
  • Asystole      This is diagnosed when no ventricular escape complexes are present. This is an agonal rhythm that is not consistent with life. To confirm the diagnosis, you should check another ECG lead, because fine (low amplitude) ventricular fibrillation can appear as a flatline in one lead, but should be treated with immediate countershock. If you see these rhythms, you should initiate Cardiopulmonary Resuscitation immediately.
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