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P wave; atrial depolarization.
QRS complex; ventricular depolarization.
T wave; Repolarization of the ventricles.
U wave; may be present. Follow T waves May be associated w/electrolyte abnormalities or maybe normal.

PR interval (PRI) or P-Q interval (PQI) 0.12-0.20sec.
The time the Impulse takes to travel from the atria to the ventricles. If the R wave is absent it’s called PQ interval. A prolonged PRI longer than 0.20 seconds indicates a delay in the AV node.
QRS interval The time necessary for ventricular depolarization.
ST segment usually an iso electric line it may be elevated or depressed in certain disease states such as ischemia.
QT interval represents total duration of ventricular depolarization. 0.33-0.42sec. QT intervals and heart rate have inverse relationship> Increases in HR usually decrease QT interval; decreases in HR usually prolong QT interval. Generally the QT interval is expressed as corrected QT(QTc) by taking QT interval and dividing it by the square root of the RR interval (interval between vent depolarizations).
Normal QTc is <0.44 sec.

Refractory period two parts:
Absolute Refractory period stimulation produces no depolarization whatsoever. Usually last from the beginning of the QRS complex to the apex of the T wave.
Relative refractory period A sufficiently strong stimulus may produce depolarization. This usually corresponds to the tea waves down slope.

ST segment changes usually in isoelectric line. Myocardial infarctions which are caused by lack of blood to part of the heart produce changes in this line.
In the sequence;  ischemia>injury>necrosis.
ST depression = ischemia
inverted T-wave = Ischemia
ST elevation = injury (often early MI)
Q waves/significant (at least one small square wide 0.04 sec) or more than 1/3 height of the QRS complex. Q waves may also indicate extensive transient ischemia.

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Identify:
Rate
Rhythm
P waves
PR intervals
QRS complex

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Rate;
B<60, N 60-100, T >100.
Count complexes in 6 sec strip x 10.
Or
RR Interval; Measure duration between our waves in seconds divide the number to 60 give me the heart rate per minute.
Or
Count Lg squares divide into 300.
Or
Count Sm squares divide into 1500.

Only regular rhythms: triplicate method.
Start dark line: (each dark line)
300,150,100,75,60,50.

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Measure RR intervals;
If irregular;
Occasionally irregular? (one or two are our intervals on one strip irregular)?
Regularly irregular? (pattern irregularity or group beating?
Irregularly irregular? (no pattern)

P waves; atrial depolarization
P waves Present?
P waves regular?
P waves for each QRS complex?
P waves upright or inverted(compared to the QRS complex)?
P waves look like?

PR interval (PRI); Time needed for atrial depolarization and conduction of impulse to the AV node.
0.12-0.20 sec (3-5 sm boxes). Any deviation is abnormal.
PR interval consistent across the strip?

QRS complex; ventricular depolarization.
QRS complexes all look alike?
QRS duration? Norm 0.04-0.12 sec.
Anything longer than 0.12 seconds
(>3 small boxes is abnormal).

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Bradycardia results from slowing of the SA node.
Causes:
•Increased parasympathetic (vagal) tone.
•Intrinsic disease of the SA node.
•Drug affects (digitalis, beta blockers,
calcium channel blockers).
•Normal finding in well conditioned people; athletes.

Rules of interpretation;
Rate; <60
Rhythm; regular
Pacemaker site; SA Node
P waves; upright and normal
PR interval; normal (0.12-0.20 sec.)
QRS complex; normal (0.04-0.12 sec)

Clinical significance: can cause decreased cardiac output, hypotension, angina or CNS symptoms (especially if rates are slower than 50 BPM). Slow rates may also lead to atrial ectopic or ventricle ectopic rhythms.
And healthy athletes sinus bradycardia can be normal.

Tx: generally a necessary unless signs of poor perfusion; acute altered mental status, ongoing chest pain, hypotension and other signs of shock.

Signs of poor perfusion:
prepare for transcutaneous pacing.

Consider:
Atropine sulfate 0.5mg bolus
Repeat 3-5 min.
Max dose 3.0mg
*Book states/Not MAS protocol>If Atropine fails> TCP transcutaneous pacing. Or Catecholamine infusion)

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Increased rate of SA node discharge.
Cause:
• Exercise
• Fever
• Anxiety
• Hypovolemia
• Anemia
• Pump failure
• Increased sympathetic tone
• Hypoxia
• Hyperthyroidism

Rules of interpretation lead ll/monitoring:
Rate: >100
Rhythm: Regular
Pacemaker site: SA Node
PR interval: Normal
QRS complex: Normal

Clinical significance;
often benign. Sometimes a comp and Cerri mechanism for decreased stroke volume.
If rate >140 bpm cardiac output may fail because ventricle filling time is inadequate. Can precipitate ischemia or infarct in diseased hearts.
Prolonged sinus tachycardia accompany acute myocardial infarction (AMI) is often an ominous finding. Suggesting cardiogenic shock.

Tx: treatment directed at underlying cars. Hypervolemia, fever, hypoxia or other causes should be corrected.

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Sinus arrhythmias often result from a variation of the RR interval.

Etiology; often a normal finding, sometimes related to respiratory cycle changes in intrathoracic pressure. Very common in children. Can be caused by enhanced vagal tone.

Rules of interpretation/ lead ll monitoring:
Rate: 60-100 BPM (varies w respirations)
Rhythm: irregular
Pacemaker site: SA Node
P waves: upright and normal
PR interval: normal
QRS complex: normal

Clinical significance; normal especially in The young and the aged.

Tx: typically none required.

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Sinus node fails to discharge for a brief period, resulting short periods of cardiac standstill. One or more PQRST complexes will be missing. This standstill can persist until pacemaker cells lower in the conductive system discharge (escape beats) or until the sinus node resumes discharge. Because the node fails to fire the RR interval following the dropped beat will vary (e.g., pause will NOT be a multiple of previous RR intervals).

Etiology: sinus arrest can result from any of the following conditions:
• ischemia of the SA node
• digitalis toxicity
• Excessive vagal tone
• Degenerative fibrotic disease

Rules of interpretation/ lead ll monitoring:
Rate: normal to slow depending on frequency and duration of arrest.
Rhythm: irregular
Pacemaker site: SA Node
P waves: upright and normal
PR interval: normal
QRS complex: normal

Clinical significance: frequent or prolonged episodes may compromise cardiac output resulting in syncope (fainting) and other problems. Always a danger of complete cessation of SA node activity. Usually an escape for them develops; however cardiac standstill occasionally can result.

Tx: if patient is asymptomatic, observation is all that is required unless there is signs of poor perfusion/AMS/i’m going chest pain, hypotension, or other signs of shock.

Poor perfusion> TCP transcutaneous pacing.

Consider:
Atropine Sulfate 0.5mg bolus
Repeat 3-5 min.
Max dosage 3.0mg
If Atropine fails>TCP transcutaneous pacing or Catecholamine infusion.

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Sinus block also called sinus exit block, occurs when sinus node fires on time but the impulse is blocked before it exits the sinus node. This results in a pause that varies in length depending on how many sinus beats are blocked. Because the SA node fires that are our intervals after the last beat will be consistent (e.g., The paws will be a multiple of the previous RR interval).

Etiology: resulting from conditions:
• Ischemia of the SA node
• Digitalis toxicity
• Excessive vagal tone
• Degenerative fibrotic disease

Rules of interpretations/ Lead ll monitoring:
Rate: normal to slow, depending on frequency and duration of the arrest.
Rhythm: regular
Pacemaker site: SA Node
P waves: upright and normal
PR interval: normal
QRS complex: normal

Clinical significance; frequent or prolonged episodes may compromise cardiac output, resulting in syncope fainting and other problems. There is a danger of complete cessation of the SA node activity. Usually an escape rhythm develops however cardiac standstill occasionally can result.

Tx: If patient is asymptomatic, observation is all that is required unless there is signs of poor perfusion (AMS, ongoing chest pain, hypotension, other signs of shock).
Signs of poor perfusion prepare for TPC transcutaneous pacing.
Consider:
Atpropine sulfate 0.5mg
Repeat: 3-5 min.
Max dose 3.0mg
* if atropine fails consider TCP or catecholamine and fusion.

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Sinus pause occurs when the sinus node fails to discharge for a break. Resulting in a missing single PQRST complex. Sinus pause differs from a sinus arrest in that only a single beat is messed with a sinus pause whereas multiple beats may be missed with sinus arrest. Because the node fails to fire the RR interval following the dropped B will very (e.g., The Paws will not be a multiple of the previous RR interval).
Etiology: sinus pause can result from any of the following conditions;
• Ischemia of the SA node
• Digitalis toxicity
• Excessive vagal tone
• Degenerative fibrotic disease

Rules of interpretation/ lead ll monitoring;
Rate: normal to slow, depending on the frequency and duration of the arrest.
Rhythm: irregular
Pacemaker site: SA Node

P waves: upright and normal

PR interval: normal

QRS complex: normal

Clinical significance; frequent or prolonged episodes may compromise cardiac output, resulting in syncope fainting and other problems. There is always a danger of complete cessation of the SA node activity. Usually an escape rhythm develops however cardiac standstill occasionally can result.

Tx: If patient is asymptomatic, observation is all that is required unless there is signs of poor perfusion (AMS, ongoing chest pain, hypotension, other signs of shock).

Signs of poor perfusion prepare for TPC transcutaneous pacing.

Consider:

Atpropine sulfate 0.5mg

Repeat: 3-5 min.

Max dose 3.0mg

* if atropine fails consider TCP or catecholamine and fusion.

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Technically sick sinus syndrome is not an arrhythmia per se, but a combination of arrhythmias. Sick sinus syndrome occurs when the sinus node is diseased or ischemic. It is characterized by wild swings in the heart rate – often moving rapidly from a profound bradycardia to a severe tachycardia and back. Sinus blocks are also commonly seen with sick sinus syndrome. The sinus node fails to discharge for a brief period, resulting in missing a single PQRS complex. Because the node fails to fire, the RR interval following the dropped B will vary (e.g., The paws will NOT be a multiple of the previous RR interval).

Etiology: sick sinus syndrome can result from any of the following conditions:
• Ischemia of the SA node
• Digitalis toxicity
• Degenerative fibrotic disease

Rules of interpretation/ lead ll monitoring;
Rate: extremely variable
Rhythm: your regular
Pacemaker site: SA node
P waves: upright and normal
PR interval: normal
QRS complex: normal

Clinical significance:

Pacemaker site: SA Node

P waves: upright and normal

PR interval: normal

QRS complex: normal

Clinical significance; frequent or prolonged episodes may compromise cardiac output, resulting in syncope fainting and other problems. There is a danger of complete cessation of the SA node activity. Usually an escape rhythm develops however cardiac standstill occasionally can result.

Tx: If patient is asymptomatic, observation is all that is required unless there is signs of poor perfusion (AMS, ongoing chest pain, hypotension, other signs of shock).

Signs of poor perfusion prepare for TPC transcutaneous pacing.

Signs of poor perfusion: begin TCP transcutaneous pacing
or catecholamine and infusion.

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Arrhythmias originating in the atria

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Wandering atrial pacemaker also called ectopic tachycardia is the passive transfer of pacemaker sites from the sinus node to either latent pacemaker sites in the atria in the AV junction. Often more than one pacemaker site will be present, causing variation in the RR interval and P wave morphology.

Etiology: May result from any of the following conditions;
• A variant of sinus arrhythmia
• A normal phenomenon in the very Young or the aged
• Ischemic heart disease
• Atrial dilation

Rules of interpretation/lead ll monitoring;
Rate: usually normal
Rhythm: slightly irregular
Pacemaker site: varies among the SA node, atrial tissue, and the AV junction.
P-wave: morphology changes from beat to beat; pee waves may disappear entirely.
PR interval: varies;  maybe less than 0.12 seconds, normal, or greater than 0.20 second.
QRS complex: normal

Clinical significance; wandering atrial pacemaker usually has no detrimental effects. Occasionally it can be a precursor of other atrial arrhythmias, such as atrial fibrillation. It sometimes indicates digitalis toxicity.

Tx: if the patient is asymptomatic observation is all that is required. If the patient is symptomatic consider adenosine.

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Multifocal atrial tachycardia (MAT) he’s usually seen in acutely ill patients. Basically, MAT is a wandering pacemaker rhythm with a rate >100. Significant pulmonary disease is seen in about 80% of these patients. Certain medication‘s used to treat lung disease (such as
beta-agonists and theophylline) May worsen the arrhythmia. Three different P waves are noted, indicating various ectopic foci.

Etiology; multifocal atrial tachycardia can result from any of the following conditions:
• pulmonary disease
• metabolic disorders (Hypokalemia)
• ischemic heart disease
• recent surgery

Rules of interpretation/lead ll monitoring:
Rate: >100
Rhythm: irregular
Pacemaker site: ectopic sites in atria
P-waves: organized, discrete non-sinus P waves with at least three different forms.
PR interval: varies
QRS complex: maybe less than 0.1 to second, normal, greater than 0.20 second, depending on the AV node refractory status when the impulse reaches it.

Clinical significance: frequently these patients are acutely ill; this arrhythmia may indicate a serious underlying medical illness.

Tx: treatment of the underlined medical disease usually resolves the arrhythmia. Specific anti-arrhythmic therapy is not frequently required.

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Premature atrial contractions (PACs) result from a single electrical impulses originating in the atria outside of the SA node, which in turn causes a premature depolarization of the heart before the next expected sinus peak. Because it depolarizes the atrial sync them, this impulse also depolarizes the SA node.  Interrupting the normal cadence. This creates a non-comp and satori pause in the underline rhythm.

Etiology: A premature atrial contraction can result from any of the following conditions:
• Use of caffeine, nicotine, or alcohol
• sympathomimetic drugs
• ischemic heart disease
• Hypoxia
• Digitalis toxicity
• no apparent cause/idiopathic

Rules of interpretation/lead ll monitoring;
Rate: depends on the underline rhythm.
Rhythm: depends on the underlying rhythm usually regular except for the PAC.
Pacemaker site: ectopic focus in the atrium
P waves: The P-wave of the PAC differs from the P waves of the underline rhythm. It occurs earlier than the next expected P wave and may be hidden in the preceding T wave.
PR interval: usually normal can vary with the location of the ectopic focus. Ectopic foci near the SA node will have a PR interval of 0.1 to 2nd or greater. Whereas ectopic foci near the AV node will have a PR interval of 0.12 seconds or less
QRS complex: Usually normal may be greater than 0.12 second at the PAC is abnormally conducted through partially refractory ventricles. In some cases the ventricles are refractory and will not depolarize in response to the PAC. In these cases the QRS complex is absent.

Clinical significance:  Isolated PACs are of a minimal significance. Frequent PACs may indicate organic heart disease and may proceed other atrial arrhythmias.

Tx: if the patient is asymptomatic observation is all that is required in the field. The patient is hypoxic and symptomatic, administer enough oxygen to correct hypoxia. Contact medical direction as needed.

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PSVT proximal atrial Supraventricular tachycardia Occurs when rapid atrial depolarization overrides the SA node. It often occurs in Proxim with sudden onset, May last minutes to hours, and terminates abruptly. It may be caused by increased automaticity of a single atrial focus or by reentry phenomenon in the AV node. Note paroxysmal means that it starts and stops. Often the paroxysms would not be seen on the rhythm strip, to diagnose PSVT, the paroxysms must be seen.

Etiology: Paroxysmal supraventricular tachycardia may occur at any age and often is not associated with underlying heart disease. It may be precipitated by stress, overexertion, smoking or ingestion of caffeine. It is however sometimes associated with underlying Atherosclerotic cardiovascular disease and rheumatic heart disease. PSVT is rare in patients with myocardial infarction. It can occur with a Cesery pathway conduction such as wolf  Parkinson’s white syndrome WPWS.

Rules of interpretation/lead ll monitoring;

Rate: 150-250 BPM

Rhythm: characteristically regular; except at onset and termination

Pacemaker site: in the atria outside the SA node.

P waves: The atrial P waves differ slightly from sinus P waves. The P-wave is often buried in the proceeding T wave. The P-wave may be impossible to see, especially if the rate is rapid. Turning up the speed of the graph paper or the Oscilloscope to 50mm/sec spreads out the complex I can help identify P waves.

PR interval: usually normal however it can vary with location of the ectopic pacemaker. Ectopic pacemaker is near the SA node will have PR intervals close to 0.12 second, whereas ectopic pacemakers near The AV node will have PR intervals of <0.12 seconds or less.

QRS complex: normal

Clinical significance: Young patients with good cardiac reserves may tolerate PSVT well for short periods. Patients often sense PSVT as palpations. However rapid rates can cause a marked reduction in cardiac output because of the inadequate ventricular filling time. The reduced diastolic Phase of the cardiac cycle can also compromise coronary artery perfusion. PSVT can precipitate angina, hypotension, or congestive heart failure.

Tx: it’s a patient is stable obtain a 12 lead ECG, establish IV access and do the following:
Vagal maneuvers; As a patient to perform vagal maneuvers. This is a forced expiration against a closed Gladys or the act of bearing down as if to move the barrels. This results in vagal stimulation which may slow the heart. If this is unsuccessful attempt carotid artery massage, if the patient is eligible. Do not attempt carotid artery massage in patients with carotid bruits or known cerebrovascular or carotid artery disease.
Pharma logical therapy:
Adenosine (Adenocard) Is safe and highly effective and terminating PSVT, especially if it’s ideology is reentry. Administer
Adenosine 6mg rapid IV bolus and flush.
SLAM IT & SLAM FLUSH!!!
(for one to three seconds) through the medication port closest to the patient’s heart or central circulation.
* if patient does not convert after 1-2 minutes; repeat w increased dose:
Adenosine 12mg
SLAM IT & SLAM FLUSH!!!
Repeat ECG
If the spells in the patient has a normal blood pressure> Look again at the width of the QRS. Discerning narrow complex tachycardia from wide complex tachycardia can be difficult. It is sometimes helpful to look at the lead V one or MCL one to determine whether the arrhythmia is actually a narrow or wide complex tachycardia. In many instances a narrow complex tachycardia will be complicated by a bundle branch block, which can be more apparent in these leads. This determination as important as the treatments are considerably different for the two arrhythmias. If the patient has a narrow complex tachycardia and is stable provide supportive care. The patient becomes unstable it is prudent to proceed with synchronized cardioversion.

Unstable (AMS ongoing chest pain hypotension shock):
Electrical therapy; HR >150

Sedate patient if time allows.
Midazolam (versed)
IVP:
2mg-5mg (titrate 1mg every 3/5 min.)
Max dose 20mg
Or
Midazolam (Versed)
IN:
5mg
Max dose 10mg

Fentanyl 25-100mcg IVP
Max dose 400mcg.

*Cardioversion is contradicted if you suspect digitalis toxicity as the PSVTs cause.
Synchronized cardio conversion DC Countershock:
100 J Monophasic/ 50 biphasic
200 J Monophasic/ 100 biphasic
360 J Monophasic/ 150 biphasic
360 J  Monophasic/ 200 biphasic

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Supraventricular tachycardia refers to the tachycardia that originate above the ventricles. The pacemaker site is often difficult to determine because of the heart rate. A rapid heart rate often makes the pee waves and discernible. The pacemaker site can be in the SA node, the atria, or the AV junction.

Etiology: Super ventricular tachycardia can result from any of the following conditions:
• use of caffeine, nicotine or alcohol
• cocaine
• sympathomimetic drugs
• ischemic heart disease
• hypoxia
• digitalis toxicity
• idiopathic; no apparent cause

Rules of interpretation/lead ll monitoring:
Rate: 150 to 250 BPM
Rhythm: characteristically regular, except at onset and termination.
Pacemaker site: In the atria, outside the SA node.
P waves: The P wave may be impossible to see, especially if the rate is rapid, turning up the speed of the graph paper or the oscilloscope to 50 mm/s spreads out the complex and can be helpful to identify P waves.
PR interval: usually normal, however it can vary with the location of the topic pacemaker ectopic pacemaker near the SA node will have the PR interval is close to 0.12 to second, whereas act topic pacemakers near the AV node will have the PR intervals of <0.12 seconds or less.
QRS complex: normal.

Clinical significance: Young patients with good cardiac reserves may tolerate SVT well for short periods. Patients often sense SVT as palpations. However rapid rates can cause a marked reduction in the cardiac output because of inadequate ventricular filling time. The reduced diastolic phase of the cardiac cycle can also compromise coronary artery perfusion. SVT can precipitate angina hypertension or congestive heart failure.

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Atrial flutter results from a rapid atrial reentry circuit and an AV node that physiologically cannot conduct all impulses through the ventricles. The AV junction may allow impulses in a 1:1 (rare), 2:1, 3:1 or 4:1 ratio or greater, resulting in a discrepancy between the atrial and ventricular rates. The AV block may be consistent or variable.

Etiology: atrial flutter may occur in normal hearts, but it is usually associated with organic disease. It rarely occurs as a direct result of an MI. Atrial dilation, which occurs with congestive heart failure, is a common cause of atrial flutter.

Rules of interpretation/lead ll monitoring:
Rate: atrial rate is 250-350 BPM. Ventricular rate varies with the ratio of the AV conduction.
Rhythm: atrial rhythm is regular; ventricular rhythm is usually regular, but can be irregular if the block is variable.
Pacemaker site: sites in the atria outside the SA node.
P waves: flutter (F) waves are present, resembling a sawtooth or picket fence pattern. This pattern is often difficult to identify in a 2:1 flutter. However, if The ventricular rate is approximately 150, suspect 2:1 flutter.
PR interval: usually constant but may vary.
QRS complex: normal

Clinical significance:  atrial flutter with normal ventricular rate is generally well tolerated. Rapid ventricular rates may compromise cardiac output and result in symptoms. Atrial flutter often occurs in conjunction with atrial fibrillation and is referred to as atrial fib-flutter.

Tx: stable patient obtain 12 lead ECG establish IV access and do the following:
Pharmacological therapy: consider rate control with the Diltiazem or beta blockers if the patient is unstable (AMS, ongoing chest pain hypotension or other signs of shock).
Electrical therapy: use synchronized cardio conversion at the rate is greater than 150 BPM. If time allows sedate the patient and apply synchronize DC countershock of
100 Joules/ 50 biphasic.

Sedate patient if time allows.

Midazolam (versed)

IVP: 2mg-5mg (titrate 1mg every 3/5 min.)

Max dose 20mg

Or

Midazolam (Versed)

IN:  5mg

Max dose 10mg

Fentanyl 25-100mcg IVP

Max dose 400mcg.

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Atrial fibrillation results from multiple areas of reentry within the atria from multiple ectopic foci bombarding an AV node that physiologically cannot handle all the incoming impulses. AV conduction is random and highly variable. It is the most common sustain cardiac arrhythmia.

Etiology: atrial fibrillation may be chronic and is often associated with underlying heart disease such as rheumatic heart disease, at Therio sclerotic heart disease, or congestive heart failure. Atrial dilation occurs with congestive heart failure and often causes atrial fibrillation. Atrial fibrillation is often classified as follows:
• First detected episode. The patient has no known history of atrial fibrillation prior to the current episode.
• Recurrent arrhythmia. The patient has a known history of atrial fibrillation prior to the current episode.
• Paroxysmal. The arrhythmia is self terminating.
• Persistent. Continues until medical treatment is provided.
• permanent. continuous are more than a year despite medical treatment.
Rules for interpretation/lead ll monitoring:
Rate: atrial rate is 350 to 750 BPM (cannot be counted). Ventricular rate varies greatly, depending on conduction through the AV node.
Rhythm: irregularly irregular.
Pacemaker site: numerous ectopic foci in the atria.
P-waves: non-discernible. Fibrillation (F) waves are persistent, indicating chaotic atrial activity.
PR interval: none
QRS complex: normal

Clinical significance: an atrial fibrillation, the atria failed to contract and the so-called atrial kick is lost, thus reducing the cardiac output by 20 to 25%. There is frequently a pulse deficit(A difference between the epic apical and the peripheral pulse rates). If the rate of ventricular response is normal, as often occurs in patients with digitalis, the rhythm is usually well tolerated. If the ventricular rate is less than 60, cardiac output can fall. Suspect digitalis toxicity in patients taking digitalis with atrial fibrillation and a ventricular rate less than 60. If the ventricular response is rapid, coupled with a loss of atrial kick, cardiovascular decompensation may occur, resulting in hypotension, angina, infarct, congestive heart failure, or shock. Atrial fibrillation is often characterized by the associated ventricular rate(e.g., atrial fibrillation with a rapid ventricular response).

Tx: if the patient is stable, obtain a 12 lead ECG and establish IV access, and do the following:
Pharma logical therapy: consider rate control with Diltiazem or beta blockers.
If patient is unstable (AMS, ongoing chest pain, hypotension, or other signs of shock)   Do the following:
Used to synchronized cardio conversion. If the rate is greater than 150 Bpm. If time allows sedate the patient and apply synchronize DC countershock of 50 to 100 J.

Sedate patient if time allows.

Midazolam (versed)

IVP:

2mg-5mg (titrate 1mg every 3/5 min.)

Max dose 20 mg

Or

Midazolam (Versed)

IN:

5mg

Max dose 10 mg

Fentanyl 25-100 mcg IVP

Max dose 400 mcg.

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Arrhythmias originating within the AV junction; AV Blocks

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A first degree AV block is a delay in the conduction at the level of the AV node rather than an actual block. First degree AV block is not a rhythm in itself but a condition super imposed on another rhythm. The underlying rhythm must also be identified for example; sinus bradycardia with a first degree AV block.

Etiology: AV block can occur in the healthy heart. However, ischemia at the AV junction is the most common cause.

Rules of interpretation/lead ll monitoring:
Rate: depends on the underlying rhythm.
Rhythm: usually regular; can be slightly irregular.
Pacemaker site: SA node or atria.
P waves: normal
PR interval: greater than 0.20 second (diagnostic)
QRS complex: usually less than 0.12 seconds; maybe bizarre in shape if conductive system disease exists in the ventricles.

Clinical significance: first-degree block is usually no danger and itself. However, a newly developed first-degree block me proceed a more advanced block.

Tx: generally no treatment is required except observation, unless the heart rate dropped significantly. If possible, avoid drugs that slow AV conduction, such as lidocaine and procainamide.

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A type one2° AV block (also called second-degree Mobitz one for Wenckebach) is an intermittent block at the level of the AV node. It produces a characteristic cyclic pattern in which the PR intervals become progressively longer until an impulse is blocked (not conducted). The cycle is repetitive, and the P to P interval remains consistent. The ratio of conduction(P waves to QRS complexes) is commonly 5:4, 4:3, 3:2, or 2:1. The pattern may be constant or variable.
Etiology: Low grade AV block(first degree and second-degree Mobitz one) can occur in the healthy heart. However, ischemia at the AV junction is the most common cause. Increased parasympathetic tone and drugs are also common etiologies.
Rules of interpretation/lead ll monitoring:
Rate: atrial rate is unaffected; ventricular rate maybe normal or slowed.
Rhythm: atrial rhythm is typically regular; ventricular rhythm is irregular because of the nonconducted beat.
Pacemaker site:  SA node or atria.
P waves: normal; some P waves are not followed by QRS complexes.
PR interval: becomes progressively longer until the QRS complex is dropped; the cycle repeats.
QRS complex: usually less than 0.12 second, maybe bizarre in shape if conductive system disease exists in ventricles.

Clinical significance: if beats are frequently dropped, second- degree block can compromise cardiac output by causing problems such as syncope and angina. This block is often a transient phenomenon that occurs immediately after an inferior wall my cardio infarction.

Tx: generally, no treatment other than observation is required. If possible avoid drugs that slow AV conduction, such as lidocaine or procainamide.
If the heart rate falls and the patient becomes symptomatic, administer:
Atropine 0.5 mg IV
Repeat 3-5min. Until you have a satisfactory rate or have given
Max dose 3.0mg.

* if atropine fails: consider TCP transcutaneous cardiac pacing.
Or
Catecholamine infusion.

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A type to 2nddegree AV block(also called second-degree Mobitz 24 infranodal) is an intermittent block characterized by P waves that are not conducted to the ventricles, but without associated lengthening of the PR interval before the dropped beats. The ratio of conduction (P waves to the QRS complexes) is commonly 4:1, 3:1, 2:1. The ratio may be constant or may vary.
A 2:1 Morbitz ll block is often indistinguishable from a 2:1 Mobitz l block.

Etiology: Second degree AV block common Mobitz ll, is usually associated with acute myocardial infarction and septal necrosis.

Rules of interpretation/lead ll monitoring:
Rate: atrial rate is unaffected;  ventricle rate is usually bradycardic.
Rhythm: regular or irregular, depending on whether the conduction ratio is consistent or varied.
Pacemaker site: SA node or atria
P waves: normal; some P waves are not followed by QRS complexes.
PR interval: Constant for conducted beats; May be greater than 0.20 seconds.
QRS complex: maybe normal; however it is often greater than 0.1 to 2nd because of the abnormal ventricular depolarization sequence.

Clinical significance: A Mobitz ll Block can compromise cardiac output, causing problems such as syncope and angina if beats are frequently dropped. Because this block is often associated with cell necrosis resulting from myocardial infarction, it is considered much more serious than Mobitz l.  Many Mobitz ll blocks develop into full AV blocks.

Tx: treatment is generally a necessary unless signs of poor perfusion (e.g., AMS, ongoing chest pain, hypotension or other signs of shock) are present. If there are signs of poor perfusion, prepare for transcutaneous pacing TCP.
Consider:
Atropine sulfate 0.5mg bolus
Repeat 3-5 min.
Max 3.0mg

*If atropine fails consider transcutaneous pacing or catecholamine infusion.

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2:1 AV block is a type of second-degree AV block in which there are 2P waves for each QRS complex. The first P-wave of each pair of people waves is blocked. A 2:1 AV Black can result from either a Mobitz l (Wenckenbach) or Mobitz ll AV block.

Etiology: Second degree 2:1 AV block is usually associated with acute myocardial infarction and septal necrosis

Cause of interpretation/lead ll monitoring:
Rate: atrial rate is unaffected;  ventricular rate is usually bradycardic.
Rhythm: regular
Pacemaker site: SA node or atria
P waves: 2 P waves for each QRS complex
PR interval: Constant for conducted beats; May be greater than 0.20 second.
QRS complex: maybe normal;  however, it is often greater than 0.12 second because of abnormal ventricular depolarization sequence.

Clinical significance: 2:1 AV Black can compromise cardiac output, causing problems such as syncope and angina if beats are frequently dropped this block is often associated with cell necrosis resulting from myocardial infarction. A 2:1 AV block can develop into full AV block (third- degree AV block).

Tx: treatment is generally a necessary unless signs of poor perfusion (e.g., AMS, i’m going chest pain, hypertension or other signs of shock) Are. If there are signs of poor perfusion, prepare for transcutaneous pacing TPC.
Consider: atropine
Atropine sulfate: 0.5 mg IV Bolus
Repat 3-5 min.
Max dose 3.0 mg

*If atropine fails: consider TCP transcutaneous pacing or catecholamine infusion.

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1/3degree AV block or complete walk, is the absence of conduction between the atria and the ventricles, resulting from complete electrical block at or below the AV node. The atria and ventricles subsequently paste the heart independently of each other. The sinus node often functions normally, depolarizing the atrial syncytium, while the escape pacemaker, located below the atria, pieces of ventricle syncytium.

Etiology: third degree AV block can result from acute myocardial infarction, digitalis toxicity or degeneration of the conductive system, as occurs in the elderly.

Rules for interpretation/lead ll monitoring:
Rate: atria rate is unaffected.
Ventricular rate is 40 to 60 If the escape pacemaker is junctional, less <40 if the escape pacemaker is lower in the ventricles..
Rhythm: both atrial and ventricular rhythms are usually regular.
Pacemaker site: SA node and AV junction or ventricle.
P waves: normal. P wave show no relationship to the QRS complex, often falling within the T wave and QRS complex.
PR interval: no relationship between P waves in our waves.
QRS complex: greater than 0.12 second if pacemaker is ventricular;
Less than 0.1 second if pacemaker is junctional.

Clinical significance: third-degree block can severely compromise cardiac output because of decreased heart rate and loss of coordinated atrial kick.

Tx: treatment is generally a necessary unless signs of poor perfusion (e.g., acute AMS, Ongoing chest pain, Ongoing chest pain, or other signs of shock) are present.
If there are signs of poor perfusion prepare for transcutaneous pacing TPC. Consider administration of:
atropine sulfate:
0.5mg IV bolus
Repeat 3-5min
Max dose 3mg

* if atropine fails; transcutaneous pacing TCP or or a catecholamine infusion.

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Arrhythmia sustained or originating in the AV junction.
Arrhythmias can originate within the AV node. The location of the pacemaker site will dictate the morphology of the P-wave. Ischemia hypoxia and other factors have been identified as causes. Arrhythmias originating in AV node include:
• premature junctional contractions
• junctional escape complexes and rhythm
• junctional bradycardia
• accelerated junctional rhythm

All arrhythmias that originate in the AV junction have in common the following ECG features:
• inverted P-wave and lead to, resulting from retrograde depolarization of the atria. The P waves relationship the QRS depolarization depends on the relative timing of atrial and ventricular depolarization. The P waves can occur before the QRS complex if the atria depolarize first
after the QRS complex if the ventricles depolarize first
During the QRS if the atria and the ventricles depolarize simultaneously. Depolarization of the atria during ventricle depolarization masks the P wave. Some atrial complexes that originate near the AV junction can also result in inverted P waves.
• PR interval of < 0.12 second
• normal QRS complex duration

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Premature junctional contractions (PJCs) result from a single electrical impulses originating in the AV node that occurs before the next expected sinus beat. A PJC can result in either a compensatory  pause or a non-compensatory pause, depending on whether the SA node is depolarized. A non-compensatory pause occurs if the premature beat depolarizes the SA node and interrupts the hearts normal cadence. A compensatory Pause occurs only if the SA node discharges before the premature impulse reaches it.

Etiology: A premature junctional contraction can result from any of the following conditions:
• use of caffeine, tobacco, or alcohol
• sympathomimetic drugs
• ischemic heart disease
• hypoxia
• digitalis toxicity
• idiopathic no apparent cause

Rules of interpretation/lead ll monitoring:
Rate: depends on the underlying rhythm
Rhythm: depends on the underline rhythm; usually regular except for the PJC.
Pacemaker site: ectopic focus in the AV junction
P-waves: inverted; May appear before or after the QRS complex. P waves can be masked by the QRS complex or be absent.
PR interval: if the P-wave occurs before the QRS complex, the PR interval will be less than 0.12 to second; if the P wave occurs after the cure X complex then technically it is a R-P interval.
QRS complex: usually normal;  maybe greater than 0.12 second if the PJC is abnormally conducted through partial refractory ventricles

Clinical significance: isolated PJCs are of minimal significance. Frequent PJCs indicate organic heart disease and may be precursors to other junctional arrhythmias.

Tx: if the patient is asymptomatic, only observation is required in the field.

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A junctional escape beat, or junctional escape rhythm, is an arrhythmia that results when the rate of the primary pacemaker, usually the SA node is slower than that of the AV node. The AV node then becomes the pacemaker. The AV node usually discharges at it’s in Stranczek rate of 40 to 60 BPM. This is a safety mechanism that prevents cardiac standstill.

Etiology: Junctional escape rhythm has several etiologies, including increased vagal tone, which can result in SA node slowing, pathological slow as a no discharge, or heart block.

Rules of interpretation/lead ll monitoring:
Rate: 40 to 60 BPM
Rhythm: irregular in Single junctional escape complex; regular and junctional escape rhythm.
Pacemaker site: AV junction.
P waves: inverted; May appear before or after the QRS complex. The P waves can be masked by the QRS orby absent.
PR interval: If a P wave occurs before the QRS complex, the PR interval will be less than 0.12 second.
If the P-wave occurs after the QRS complex, technically it is an RP interval.
QRS complex: usually normal; maybe greater than 0.12 second.

Clinical significance: The slow heart rate can decrease cardiac output, possibly precipitating angina and other problems. If the rate is fairly rapid, the rhythm can be well tolerated.

Tx: treatment is generally unnecessary and less signs of poor perfusion (e.g., acute altered mental status, ongoing chest pain, hypotension or other signs of shock) are present. if there are signs of poor perfusion, prepare for  transcutaneous  pacing TCP.
Consider administering:
Atropine sulfate 0.5 mg
Repeat 3-5 min
Max dose 3.0mg
Until you’ve obtained satisfactory rate or have given Max dose.
If atropine fails consider TCP transcutaneous pacing or catecholamine infusion.

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Junctional bradycardia is a junctional arrhythmia with a heart rate less than D in Stranczek rate of the AV node (40-60 bpm). A slow rate can significantly compromise cardiac output.

Etiology: Junctional bradycardias have several ideologies including increased vagal tone, which can result in SA node slowing, pathological slow SA node discharge, or heart block. Instrinsic disease of the node can also be a cause.

Rules of interpretation/lead ll monitoring:
Rate: less than 40 bpm.
Rhythm: irregular in single junctional escape complexes; regular in junctional escape read.
Pacemaker site: AV junction
P waves: inverted; May appear before or after the QRS complex. The P waves can be masked by the QRS or be absent.
PR interval: if the P wave occurs before the QRS complex, the PR interval will be less than 0.12 second. If the P wave occurs after the QRS complex, technically it is an RP interval.
QRS complex: usually normal; May be greater than 0.12 second

Clinical significance:
The slow heart rate can decrease cardiac output, possibly precipitating angina and other problems.

Tx: treatment is generally a necessary unless signs of poor perfusion(e.g., Acute altered mental status, ongoing chest pain, hypotension or other signs of shock) are present. If there are signs of poor perfusion, prepare for transcutaneous pacing TCP.
Consider administering:
Atropine sulfate
0.5mg IV Bolus
Repeat 3-5min
Max dose 3.0mg
If atropine fails: consider TCP transcutaneous cardiac pacing or
Catecholamine infusion.

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Accelerated junctional rhythm results from increased automaticity in the AV junction, causing the AV junction to discharge faster than it’s in Stranczek rate. If the rate becomes fast enough, the AV node can override the SA node. Technically, the rate associated with an accelerated junctional rhythm is not a tachycardia. However, when compared to the instrument rate of the AV junction or tissue (which is 40-60 bpm) it is considered accelerated.

Etiology: accelerated junctional rhythms often result from ischemia of the AV junction.

Rules of interpretation/lead ll monitoring:
Right: 60-100 bpm
Rhythm: regular
Pacemaker site: AV junction
P waves: inverted; May appear before or after the QRS complex. P waves may be masked by the QRS or be absent.
PR interval: if the P wave occurs before the QRS complex, the PR interval will be less than 0.12 second. If it occurs after the QRS, technically it is an RP interval.
QRS complex: normal

Clinical significance: an accelerated junctional rhythm is usually well tolerated. However because ischemia is often the etiology, the patient should be monitored for other arrhythmias.

Tx: prehospital treatment is generally unnecessary.

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Arrhythmias originating in the ventricles.
Some arrhythmias originate within the ventricles. The pacemaker site will dictate the morphology of the QRS complex. Many factors, including ischemia, hypoxia, and medication, I’ve been identified as causes. Arrhythmias originating in the ventricles include the following:
• ventricular escape complexes and rhythms
• accelerated idioventricular rhythm
• premature ventricular contraction
• ventricular tachycardia
• torsades de points
• ventricular fibrillation
• Asystole
• artificial pacemaker rhythm

ECG features common to all arrhythmias that originate in the ventricles are:
• QRS complexes of 0.12 second or greater
• absent P waves

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A ventricular escape beat (ventricular escape rhythm or idioventricular rhythm) results either when impulses from higher pacemakers fail to reach the ventricles or when the discharge rate of the higher pacemakers become less than that of the ventricles (normally 15-40 bpm). Ventricle escape rhythms serve as safety mechanisms to prevent cardiac stand still.

Etiology: ventricular escape complexes and ventricular rhythms have several etiologies, including slowing of the super ventricular pacemaker sites or high degree AV block. They are frequently the first organized rhythms scene following successful defibrillation.

Rules of interpretation/lead ll monitoring:
Rate: 15 to 40 BPM occasionally less
Rhythm: The rhythm is irregular in a single ventricular escape complex.
Ventricular escape rhythms are usually regular unless the pacemaker site is low in the ventricle conductive system. Such placement makes regularity unreliable.
Pacemaker site: ventricle
P-wave: none
PR interval: none
QRS complex: greater than 0.12 second and bizarre in morphology.

Clinical significance: The slow heart rate can significantly decreased cardiac output, possibly to life-threatening levels. The ventricular escape rhythm is a safety mechanism that you should not suppress. Escape rhythms can be perfusing or non-perfusing.

Tx: treatment is generally a necessary unless signs of poor perfusion (e.g., acute altered mental status, ongoing chest pain, hypotension or other signs of shock) are present. If there are signs of poor perfusion prepare for transcutaneous pacing TPC.
Consider:
Atropine sulfate
0.5 mg IV bolus
Repeat 3-5 min
Max dose 3.0 mg

If atropine fails consider transcutaneous cardiac pacing PCP or a catecholamine infusion. If the rhythm is slow and or non-perfusing, follow the AHA cardiac arrest protocol. Direct treatment at correct in the primary problem:
Hypovolemia, hypoxia, cardiac tapenade, acidosis, or others.
Consider fluid challenge
20ml/kg NS.

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This is an example of a life-threatening Idioventricular rhythm.
The slow heart rate can significantly decrease cardiac output, possibly do a life-threatening level such as this. The ventricular is great for them is a safety mechanism that otherwise should not be suppressed.

Rules of interpretation/lead ll monitoring:
Rate: 15 to 40 BPM or less.
Rhythm: The rhythm is irregular in a single ventricular escape complex. Ventricular escape rhythms are usually regular unless the pacemaker site is low in the ventricular conductive system. Such placement makes regularity unreliable.
Pacemaker site: ventricle
P-wave:  no
PR interval: no
QRS complex: greater than 0.12 second and bizarre in morphology.

Tx: treatment is generally unnecessary and less signs of poor perfusion or ongoing chest pain. Hypotension and other signs of shock are present. If there are signs of poor perfusion prepare for transcutaneous pacing. Consider administration of atropine sulfate.
Atropine sulfate
0.5mg IV bolus
Repeat 3-5 min.
Max dose 3.0 mg.

If atropine fails:
Transcutaneous cardiac pacing TCP
Or a catecholamine infusion.
Follow AHA cardiac arrest protocol.
Treatment should be directed at correcting a primary problem:
Hypovolemia, hypoxia, cardiac tapenade, acidosis, or others.
Consider fluid challenge.
20mg/kg NS.

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Accelerated idioventricular rhythm is an abnormally wide ventricular arrhythmia that usually occurs during an acute myocardio infarction AMI.
It is a some type of ventricular escape rhythm. Typically the rate is 60 to 110 BPM. The patient does not require treatment unless he becomes hemodynamically unstable. If this occurs treat the ventricular focus with atropine or overdrive pacing. The principal action should be aggressive treatment of the underlined myocardial infarction as indicated, including appropriate prehospital care.

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Premature ventricular contractions (PVC, or ventricular ectopic) is a single ectopic impulse arising from an irritable focus in either the ventricle that occurs earlier than the next expected beat. It may result from an increased automaticity in the ectopic cell or a reentry mechanism. The altered sequence of ventricular depolarization result in a wide and bizarre QRS complex and may additionally cause the T wave to occur in the direction opposite of the QRS complex.
A PVC does not usually depolarize the SA node and interrupt its rhythm. That is it does not interrupt the hearts normal cadence. The pause following the PVC is fully compensate Tori. Occasionally, an
Interpol lighted beat occurs when a PVC Falls between two sinus beats without interrupting the rhythm.
If more than one PVC occurs, each can be classified as unifocal or multifocal (see unifocal PVC And multifocal PVCs. Because the PVC morphology depends on the ectopic pacemakers location, two PVCs of different morphologies imply that two different pacemaker sites (multifocal).
PVCs with the same morphology imply one pacemaker site (Unifocal).  If the coupling interval (The distance between the preceding beet and the PVC) is consistent, the PVCs are most likely unifocal.
PVCs often occur in patterns of group meeting. These include:
• Bigeminy-every other beat is a PVC.
• Trigeminy-every third beat is a PVC.
• Quadridgeminy-every 4th feet is a PVC.
These terms can be applied to PACs and PICs as well.
Repetitive PVCs are two consecutive PVCs without a normal complex in between. They can occur in groups of two (couplets) or three (triplets). More than three consecutive PVCs is often considered ventricular tachycardia.
PVCs can trigger lethal arrhythmias such as ventricular fibrillation if they fall within the relative refractory period(The so-called R on T phenomenon). They are often classified by their relationship to the previous normal complex.

Etiologies: etiologies for PVCs include:
• myocardial ischemia
• increased sympathetic tone
• hypoxia
• idiopathic causes
• acid-bass disturbances
• electrolyte imbalances
• normal variant

Rules of interpretation:lead ll monitoring:
Rate: depends on the underlying rhythm and rate of PVCs.
Rhythm: interrupts regularity of the underline rhythm; occasionally irregular.
Pacemaker site: ventricle
P waves: None: however, a normal sinus P-wave (Interpolated P wave) sometimes appears before a PVC.
PR interval: none
QRS complex: greater than 0.12 second and bizarre in morphology.

Clinical significance:
Patients often sense PVCs as skipped beats. In a patient without heart disease, PVCs may be insignificant. In patients with myocardial ischemia, PVCs may indicate ventricular irritability and may trigger lethal ventricular arrhythmias. PVCs are often classified as malignant or benign. Malignant PVCs have at least three of the following traits:
• more than six PVCs per minute
• R on T phenomenon
• couplets or runs a ventricular tachycardia
• multifocal
• associated chest pain

With most PVCs the ventricles do not feel adequately. Because of this, you will usually not feel a pulse during the PVCs themselves. Frequent PVCs may reduced cardiac output.
PVCs can be described in terms of the loan grading system for premature beats. The higher the grade, the more serious the ectopy:
• Grade 0= No premature beats
• Grade 1= occasional (<30 per hr) PVCs
• Grade 2= frequent (>30 per hr) PVCs
• Grade 4= Multi form (multifocal)
• Grade 5= R on T phenomenon

Tx: it’s a patient has no history of cardiac disease and no symptoms, and if the PVCs are non-malignant, no treatment is required. Administer oxygen if the patient is hypoxic and place an IV line. Although it was one common practice to aggressively treat PVCs with antiarrhythmic drugs, research has shown that most treatments were ineffective or harmful. Today PVCs are rarely treated, with the exception of PVCs that occur during reperfusion therapy, when the myocardium is extremely irritable. Even then the use of anti-rhythmic drugs and these cases is extremely limited.

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PVC unifocal  premature ventricular contraction

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See premature ventricular contractions.

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See premature ventricular contractions PVC.

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Ventricular tachycardia VT consists of three or more ventricular complexes in succession at a rate of 100 bpm or more. This rhythm overrides the hearts normal pacemaker, and the atria and ventricles are asynchronous. Sinus P waves may occasionally be seen, disassociated from the QRS complexes.
In monomorphic VT, the complex is all appear the same;
In polymorphic VT they have different sizes and shapes.
One example of a polymorphic VT is torsades de points.

Etiology: as with PVCs, etiologies for ventricular tachycardia include:
• myocardial ischemia
• increased sympathetic tone
• hypoxia
• idiopathic causes
• acid-base disturbances
• electrolyte imbalances

Rules of interpretation/lead ll monitoring:
Rate: 100-250 bpm
Rhythm: usually regular; can be slightly irregular
Pacemaker site: ventricle
P-waves: if present, not associated with the QRS complexes.
PR interval: none
QRS complex: greater than 0.12 second  and bizarre  in morphology.

Clinical significance: ventricular tachycardia usually result in poor stroke volume, which, coupled with rapid ventricular rate, may severely compromised cardiac output and coronary artery perfusion. Whether ventricular tachycardia is perfusing or non-perfusing dictates the type of treatment. Ventricular tachycardia may eventually deteriorate into ventricular fibrillation.

Tx: The treatment of perfusing ventricular tachycardia has changed dramatically in recent years. Refusing to ventricular tachycardia that is causing hypotension, acutely altered mental status, signs of shock, ischemic chest pain, and or acute heart failure should be treated with synchronized cardio conversion.

Ventricular tachycardia that is not accompanied by the findings detailed above should be treated with Adenosine.
(if regular and monomorphic) and/or in a antiarrhythmic infusion (Procainamide, amiodarone, sotalol). If the patient is non-perfusing, follow the protocol for ventricular fibrillation. Treatment includes: defibrillation, Epinephrine , and Amiodarone.
VFib tx:
Insert protocol here.

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Torsades de points is a polymorphic ventricular tachycardia that difference in appearance and cars from ventricular tachycardia in general. It is more common in women than men. Torsades de points is most commonly caused by the use of certain antiarrhythmic drugs, including quinidine (Quinidex), Procainamide (Pronestyl), disopyramide (Norpace), flecainide (Tambocor), sotalol (Betapace) and amiodarone (Cordarone). These agents affects all seem to be exasperated by the coadministration of certain nonsedating antihistamines, and, in addition, the Azole antifungal agents and macrolide antibiotics: Erythromycin, azithromycin (Zithromax), and clarithromycin (Biaxin). Any of these agents increase the likelihood of the patients developing torsades de points.
The morphology of the QRS varies from beat to beat(hence the term torsades de points, which means twisting at a point). In addition, the QT interval is markedly increased, to 600 ms or more. Torsades de points will usually occur in bursts that are not sustained. During these breaks from these bursts you should examine the rhythm strip for a prolonged QT interval. The QRS rate is usually between 166 and 300 bpm, and the RR interval varies in an irregularly irregular pattern. The QRS complexes are wide and change in size over the span of several complexes. Attempting treatment of a torsades de points with antiarrhythmics you usually used for the treatment of ventricular tachycardia can have disastrous consequences. Therefore recognition of torsades de points as a separate arrhythmia is essential.

Tx:
magnesium sulfate
1g to 2g
Given over one to two minutes.
Can be repeated every four hours with close monitoring of the deep tendon reflexes. Ultimately overdrive pacing may be required.
*Correct  any underline electrolyte problems especially in hyperkalemia.

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Ventricular fibrillation is a chaotic ventricular rhythm usually resulting from the presence of many reentry circuits within the ventricles. There is no ventricular depolarization or contraction.

Etiology: A wide variety of causes have been associated with ventricular fibrillation. Most cases result from advanced corner artery disease CAD.

Rules of interpretation/lead ll monitoring:
Rate: no organizer of them
Rhythm: no organized rhythm
Pacemaker site: numerous ectopic foci throughout the ventricles
P waves: usually absent
PR interval: absent
QRS complex: absent

Clinical significance:
Ventricular fibrillation V fib is a lethal arrhythmia. The absence of cardiac output or an organized electrical pattern results in cardiac arrest.

Tx: Beefin and non-perfusing ventricular tachycardia are treated identically:
Rhythm shockable: Yes
V-Fib/PulselessV-Tach>
Shock
CPR 2 minutes IV/IO
Rhythm shockable: Yes
Shock
CPR 2 minutes
Epinephrine every 3-5 min> consider advanced airway. EtCO2
Rhythm shockable: Yes
Shock
CPR 2 min
Amiodarone
Treat reversible causes
———————————
Rhythm shockable: NO
Asystole/PEA
CPR 2 min IV/IO
Epinephrine every 3-5 min
Consider advanced airway. EtCO2.
Rhythm shockable: NO
CPR 2 min > Tx underlying causes
Rhythm shockable: NO
Reevaluate ROSC
-post resuscitation care.

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A systole cardiac standstill is the absence of all cardiac electrical activity.

Etiology: systole may be the primary event in cardiac arrest. It is usually associated with massive myocardial infarction, ischemia, and necrosis. Resulting from heart blocks when no escape pacemaker takes over, systole is often the final outcome of ventricular fibrillation. Often, before all electrical activity is lost, occasional bizarre complexes are seen as the heart dies. This is often referred to as an agonal rhythm

Rules of interpretation/lead ll monitoring:
Rate: no electrical activity
Rhythm: no electrical activity
Pacemaker site: no electrical activity
P-waves: usually absent, but in certain cases only P waves will be seen (no QRS complexes)
PR interval: absent
QRS complex: absent

Clinical significance Asystole results in cardiac arrest. The prognosis for resuscitation is very poor.

Tx: treat a systole as for all types of cardiac arrest. Look for and if possible treat the underlying cause.

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An artificial pacemaker rhythm results from regular cardiac stimulation by an electrode implanted in the heart and connected to a power source. The pacemaker may be implanted in any of the several locations in the heart, although it is most often placed in the right ventricular, ventricular pacemaker or in both of the right ventricle and right atria a dual chamber pacemaker
Fixed rate pacemakers fire continuously at a preset rate, regardless of the hearts electrical activity. Demand pacemakers contain a sensing device that fire only when the natural heart rate drops below a set rate. In these causes the pacemaker acts as an escape rhythm.
Ventricular pacemaker stimulate only the right ventricle, resulting in a rhythm that resembles an idioventricular rhythm. Dual chamber pacemaker’s commonly called AV sequential pacemakers, stimulate the atria first and then the ventricles. They are most beneficial for patients with marginal cardiac output who need the extra atrial kick to maintain cardiac output
Pacemakers are usually inserted into patients Who have chronic high-grade heart block or sick sinus syndrome or who have had episodes of severe sympathetic Bradycardia.

Rules of interpretation/lead ll monitoring:
Rate: varies with the preset rate of the pacemaker
Rhythm: regular if pacing consistently;  irregular if pacing on demand.
Pacemaker site: depends on the electrode placement
P-waves: Nonproduce biventricular pacemaker is. Sinus pee waves may be seen but are unrelated to the paste QRS complexes. Dual chamber pacemaker is produce a pee wave behind each atrial spike. A pacemaker Spike is an upward or downward deflection from the baseline, which is an artifact created each time the pacemaker fires. The pacemaker Spike tells you only did the pacemaker is firing. He reveals nothing about ventricular depolarization.
PR interval: if present it varies
QRS complex: The QRS complexes associated with pacemaker rhythms are usually longer than 0.1 to second and bizarre and morphology. They often resemble ventricular escape rhythm’s. The QRS complex should follow each pacemaker Spike. If so, the pacemaker is said to be capturing. With demand pacemaker some of the patient’s own QRS complexes may appear. A pacemaker Spike should not be associated with these complexes.

Problems with pacemakers: although rare pacemakers can have problems. One causes battery failure. Most pacemaker batteries have a relatively long live the cardiologist can check them and usually replaces them before problems arise. If a battery fails, however no pacing will occur in the patient’s underline rhythms which may be bradycardiac or a systematic may return.
Occasionally, a pacemaker may run away. This condition, rarely seen with new pacemakers, results in a rapid discharge rate. A runaway pacemaker usually occurs when the battery runs low; newer models compensate for this by gradually increasing their rate as their batteries run low.
Demand pacemakers can fail to shut down for the patients extrinsic heart rate exceeds the rate set for the device. That’s the pacemaker competes with the patients natural pacemaker. Occasionally a paste beat can fall in the absolute or relative refractory period, precipitating ventricular fibrillation.
Finally pacemakers can fail to capture if the leads become displaced or the battery fails. In such cases pacemaker spikes are usually present without pee waves or QRS complexes. Bradycardia often results.

Consideration for management: always examine any unconscious patient for a pacemaker. Battery packs are usually palpable under the skin, often in the shoulder or auxiliary region. Treat Brady arrhythmias, a systole and ventricular fibrillation from pacemaker failure as any other patient. Defibrillate patience with pacemakers as usual, but do not discharge the paddles directly over the battery pack. If external cardiac pacing is available, you can use it until definitive care is available. Transport pacemaker failure patients promptly without prolonged field stabilization. Definitive care consists of battery replacement or temporary pacemaker insertion.
Most modern pacemakers can be interrogated for information about the device and patient incidents. These interrogations usually take place in a cardiologist office or in the emergency department. Typically a sensor or computer one is placed over the pacemaker on the skin, allowing communication between the device and the external computer. This provides important information such as battery usage and remaining battery life, as well as how often the pacemaker is used or not used. It also indicates whether the leads are still in the proper position and whether the lead wires are intact. It allows adjustment of the power level and other essential parameters.
Use of a magnet applying a magnet over the pulse generator inhibits all sensing and sets the pacemaker to a predetermined rate usually 70. The patient should carry a card with information about his particular pacemaker, as these rates are men you facture and model dependent. Use a magnet only for short periods to avoid the unlikely development of a serious arrhythmia including ventricular fibrillation. The indicator for magnetic use is a runaway pacemaker.

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PEA pulseless electrical activity essentially means that the electrical complexes are present, with no accompanying mechanical contractions of the heart. PA is a perfect example of why you should treat the patient, not the monitor. Your monitor may show a textbook perfect, normal sinus rhythm, but the patient may be pulseless.
Causes:
• hypovolemia
• cardiac tapenade
• tension pneumothorax
• hypoxemia
• acidosis
• massive pulmonary embolism
• ventricular wall rupture

Tx: administer Epinephrine
Epinephrine
1mg IV
Every 3-5 min. Entry underlying causes.
Hypervolemia> Fluids
Cardiac tapenade> Pericardiocentesis
Tension pneumothorax> Needle thoracostomy
Hypoxemia> intubation/oxygen
Acidosis> Ventilation, consider
NaHCO3 sodium bicarbonate.

Early treatment can potentially reverse some of these conditions therefore prompt recognition and initiation of therapy or essential. Outcomes from PEA are generally poor.

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Arrhythmias resulting from disorders of conduction
Several arrhythmias result from improper conduction through the heart. Three general categories of conductive disorders are:
• atrioventricular blocks
• disturbances of ventricular conduction
• Preexcitation syndromes

Disturbances in conduction of the depolarization impulse or not limited to the AV node. Problems can arise within the ventricles as well.
Aberrant Conduction is a single superventricular be conducted through the ventricles in a delayed manner.
Bundle branch block is a disorder in which all super ventricular beats are conducted through the ventricles in a delayed manner. Either the left or right bundle branch can be involved. If both branches are blocked then 1/ thirddegree AV block exists. These complexes originate above the ventricles and should be distinguished from pure ventricle rhythms, which can have a similar QRS morphology. An incomplete bundle branch block has a normal QRS complex;  A complete block has a wide QRS complex.
One of the two known causes for ventricular Conduction disturbances is ischemia or necrosis of either right or left bundle branch, rendering it in capable of conducting the impulse to the ventricle. The second is either a premature atrial contraction or a premature junctional contraction it reaches the ventricles or one of the bundle branches, usually at the right, when it is still refractory period this often happens in atrial fibrillation because the irregular rhythms varying speed of Repolarization. BBB bundle branch blocks.
The ECG features of ventricular conduction disturbances include a QRS complex longer than 0.1 to 2nd because the block side of the heart is depolarized much more slowly than the unaffected side. The impulse passes much more slowly through the myocardium than through the rapid electrical conduction pathway. The QRS morphology is often bizarre. It could be notched or slurred. Reflecting rapid depolarization through the normal conductive system and slow depolarization through the myocardium on the blocked side.
Ventricular conduction disturbances sometimes complicate ECG Rhythm strip interpretation. In these cases, super ventricular beats and have abnormally wide Urus complexes. If you suspect a conduction system disturbance relating to super ventricular beats ,  then it is prudent to inspect some of the other leads to determine the problems.
Although exceptions do occur superventricular tachycardia is caused by disturbances and conduction usually different several ways from the wide complex tachycardia is originating in the ventricles:
• A change in battle branch blocks suggest superventricular tachycardia SVT with aberrancy.
• A trial of carotid sinus massage may slow conduction through the AV node and may terminate the reentrant SVT or slow conduction with other superventricular tachyarrhythmias. These maneuvers will have no effect on ventricular tachycardia’s.
• AV disassociation, also known as AV block, indicates a ventricular origin of the arrhythmia.
• A full comp and satori pause, usually seen after a ventricular beep, indicates ventricular tachycardia.
• Fusion beats suggest ventricular tachycardia.
• A cure restoration of longer than 0.14 second usually indicates the VT.

Patient sister may also help to differentiate the etiologies of wide complex tachycardia’s.  In older patients with a history of myocardial infarction, congestive heart failure or coronary artery disease, he’s with me is most likely have a ventricle origin.
When in doubt, treat the patient as if he has a more lethal arrhythmia: ventricular tachycardia. In either case use cardioversion if the patient is unstable; it is effective for both ventricular and superventricular tachycardia’s.

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Preexcitation syndrome’s involve premature ventricular excitation by an impulse that bypasses the AV node. The most common of these is wolf Parkinson white syndrome WPW.
WPW occurs in approximately three out of every 1000 persons. It is characterized by a short PR interval, generally less than 0.1 to second, and a long QRS duration, generally more than 0.1 to 2nd. Additionally, the upstroke of the QRS often has a slur, called the delta wave. In WPW, conduction of the depolarization impulse from the atria to the ventricles is abnormal. The bundle of Kent an extra conduction pathway between the atria and the ventricles effectively bypasses the AV node, shortening the PR interval and prolonging the QRS complex. Most WPW patients are asymptomatic, however the disorder is associated with a high incidence of tachyarrhythmias, usually through every entry mechanism. WPW is also frequently associated with organic heart diseases such as atrial septal defects or mitral valve prolapse. Based treatment on the underlying rhythm.

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Electrolyte imbalances can cause arrhythmias that will appear on ECG rhythm strips. The electrolytes most commonly associated with ECG Disturbances are potassium and calcium.
Hypokalemia: hypokalemia is a condition in which the potassium level in the blood is low. Normal potassium levels are 3.5 to 5.0 mEq/L.  Hypokalemia can cars a prominent you wave on the ECG and also tends to flatten the T wave. These changes result from the effect of low potassium levels on phase 3 repolarization of the action potential.
Hyperkalemia: Hyperkalemia is a condition in which the potassium level in the blood is elevated. Normal potassium levels are 3.5 to 5.0 mEq/L.  As potassium levels start to rise, changes in the ECG can be seen. As potassium levels approach 6.0 to 6.5 mEq/L a tall, pointed T wave will be seen. The T-wave will become higher and more peaked as potassium levels approach seven. When levels approach eight the T wave will begin to merge with a QRS forming a very wide QRS complex. Add potassium levels of nine the waveform becomes almost sinus sodium. Potassium levels greater than 10 mEq/L are generally incompatible with life.
Hypocalcemia: hypocalcemia is a low serum calcium level and can be caused by the use of diuretics in certain endocrine conditions. Hypocalcemia prolong Sabree polarization and causes a prolonged ST segment and thus a prolonged QT interval.
Hypercalcemia: Hypercalcemia is an abnormal elevation in serum calcium levels. It can be caused by adrenal insufficiency, hyper parathyroidism, kidney failure, or malignancies. Hypercalcemia shortens the repolarization phase, that’s causing the ST segment to shorten sometimes to the point at which the T-wave seems to be almost on top of the QRS. The concomitant effects of hypercalcemia and digitalis can be quite detrimental.

Digital us(Lanoxin) is sometimes used in the treatment of congestive heart failure and atrial fibrillation. It increases the force of cardiac contraction and slows AV conduction to slow ventricular response in atrial fibrillation. The effects of digital us can often be seen on the ECG as a sagging or scooping of the ST segment. It can also prolong the PR interval because of slowing of the AV conduction.
In hypothermia, The Osborn wave, or Jay wave, is a parent. It is a slow, positive deflection at the end of the QRS complex.
Other ECG changes may include:
• t-wave inversion
• PR, QRS, QT prolongation
• sinus bradycardia
• atrial fibrillation or flutter
• AV block
• PVCs
• ventricular fibrillation
• Asystole

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LITFL ECG library is a free educational resource covering over 100 ECG topics relevant to Emergency Medicine and Critical Care. All our ECGs are free to reproduce for educational purposes, provided:

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Textbooks

Zimmerman FH. ECG Core Curriculum. 2023

Mattu A, Berberian J, Brady WJ. Emergency ECGs: Case-Based Review and Interpretations, 2022

Straus DG, Schocken DD. Marriott's Practical Electrocardiography 13e, 2021

Brady WJ, Lipinski MJ et al. Electrocardiogram in Clinical Medicine. 1e, 2020

Mattu A, Tabas JA, Brady WJ. Electrocardiography in Emergency, Acute, and Critical Care. 2e, 2019

Hampton J, Adlam D. The ECG Made Practical 7e, 2019

Kühn P, Lang C, Wiesbauer F. ECG Mastery: The Simplest Way to Learn the ECG. 2015

Grauer K. ECG Pocket Brain (Expanded) 6e, 2014

Surawicz B, Knilans T. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric 6e, 2008

Chan TC. ECG in Emergency Medicine and Acute Care 1e, 2004

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ECG library and interpretation. Clinical cases, contextual blog posts and high quality EKG images for download from LITFL ECG Library