Dysrhythmias

This section addresses the likely rhythms that a patient may generate. Each rhythm is described in the same manner, which will coincide with the process described later of how to differentiate between each rhythm. A picture of each rhythm strip is included to illustrate its typical appearance. The treatment plan for a patient exhibiting the rhythm, whose chief complaint can be attributed to being in that rhythm, then follows.

Sinus and Atrial Rhythms

Sinus and atrial rhythms are generated either within the SA node or from the automaticity of the atrial muscle tissue.

Table 4.3 Sinus Bradycardia

Origination Point: SA Node		Differential Causes
P Wave		Athletes (not clinically significant) Increased vagal tone Myocardial infarction (MI) Increased ICP Hypothermia Beta-blocker and calcium channel blocker overdose Hypoxemia Sick sinus syndrome Electrolyte imbalances Hypothyroidism Idiopathic
Shape	Upright
P rate	<60
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	<0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	<60
Treatment Options. The treatment for sinus bradycardia is largely dependent on the hemodynamic stability of the patient and the root cause for the bradycardia. If the patient is stable and has not displayed any change in mentation while in this rhythm, aggressive treatment likely is not indicated. For situations thought to be related to increased vagal tone or parasympathetic stimulation, 0.5–1 mg atropine is the first-line treatment of choice. If this fails and the patient remains symptomatic, transcutaneous pacing (TCP) should be considered and initiated. The TCP procedure is discussed later in this chapter. In cases of acute myocardial infarction (AMI), increasing the rate may have a negative effect on the condition of the patient because of the concurrent increase in myocardial O2 demand. In this case, increasing blood pressure without appreciably increasing the workload of the heart is desirable. This can be accomplished with fluid. For presumed hypoxemia, administer O2. This is particularly important for pediatric patients. An overdose of any of a variety of drugs can cause symptomatic bradycardia. An effort should be made to determine the drug and administer its antidote; in cases of opiate or calcium channel blocker overdose, administer naloxone or calcium, respectively. If unable to determine the specific drug, treat the patient symptomatically and support the ABCs.

Table 4.4 Sinus Tachycardia

Origination Point: SA Node		Differential Causes
P Wave		Exercise (not clinically significant) Fever/hyperthermia Hypoxia (early) Hypotension/dehydration MI Beta-agonist, caffeine, and cocaine CHF Anxiety/stress Hyperthyroidism/thyroid storm Serotonin syndrome
Shape	Upright
P rate	>100
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	<0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	>100
Treatment Options. In many cases, treatment for sinus tachycardia is based on the underlying cause if rhythm-specific treatment is needed. Because tachycardia is the body’s natural response to shock, infection, and stress, among other issues, treatment specific to this rhythm often is limited to fluid bolus. If the patient is in this rhythm as a result of CHF, however, fluid would be inappropriate, and O2 and nitrates would be the best options. See chapter 3 for more information on CHF.

Table 4.5 Sinus Arrhythmia

Origination Point: SA Node		Differential Causes
P Wave		Normal finding if rate accelerates with inhalation and slows with exhalation. If not tied to respiratory rate, it could indicate ischemia of the heart.
Shape	Upright; same shape throughout
P rate	Usually 60–100; could be faster or slower
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	<0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regularly irregular; could be irregularly irregular
Rate	Usually 60–100; could be faster or slower
Treatment Options. The treatment for sinus arrhythmia is limited and should focus on the factors surrounding it. Remember, this is a normal finding in the pediatric population.

Table 4.6 Sinus Arrest and Sick Sinus Syndrome

Origination Point: SA Node		Differential Causes
P Wave		Sinus Arrest Ischemia of SA node Increased vagal tone Digitalis use Quinidine use Idiopathic; only significant if it causes hemodynamic instability Sick Sinus Syndrome Simply a poorly functioning SA node May present as alternating bradycardia and tachycardia
Shape	Upright
P rate	Usually 60–100; could be faster or slower
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	<0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular, except during unpredictable arrest where an entire P-QRS-T cycle is dropped.
Rate	Usually 60–100; could be faster or slower
Treatment Options. Occasional dropped beats are typically not an issue. If they happen frequently enough, essentially resulting in a marked bradycardia, initiate treatment similar to that for sinus bradycardia.

Table 4.7 Wandering Atrial Pacemaker

Origination Point: SA Node and Atrial Muscle, >3 Foci		Differential Causes
P Wave		Respiratory failure COPD Electrolyte imbalances Nicotine and caffeine Alcohol Enlarged atria Treated symptomatically
Shape	May be upright or inverted; notched, biphasic, or have 2 humps depending on foci
P rate	Usually 60–100; could be faster or slower
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	Varied but always <0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Very slightly irregular
Rate	Usually 60–100; could be faster or slower
Treatment Options. Treatment usually is not necessary for the wandering atrial pacemaker. However, the treatment of respiratory problems associated with this rhythm, such as respiratory failure and COPD, often relieve this rhythm.

Table 4.8 Multifocal Atrial Tachycardia

Origination Point: Atrial Muscle, Multiple Foci		Differential Causes
P Wave		Respiratory failure COPD Digoxin toxicity Hypomagnesemia Hypokalemia Nicotine, alcohol, and caffeine
Shape	May be upright or inverted; notched, biphasic, or have 2 humps depending on foci
P Rate	100–150; could reach 250
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	Varied but always <0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Irregularly irregular
Rate	100–150; could reach 250
Treatment Options. Treatment is primarily related to the underlying cause. Because it is most commonly associated with COPD and hypoxia, appropriate treatment of the breathing issues is important. Also, if hypomagnesemia is the suspected cause, give 2–4 g magnesium sulfate.

Table 4.9 Atrial Flutter

Origination Point: Atrial Muscle, Single Focus		Differential Causes
P Wave		MI Atherosclerosis Digoxin Rheumatic heart disease Alcoholism Thyrotoxicosis (hyperthyroidism) Pulmonary embolus Pneumonia Pericarditis—infection of the pericardium
Shape	Absent; F waves present; sawtooth baseline
P Rate	200–400 or higher; rate of 300 most common
P wave for every QRS?	No
QRS complex for every P wave?	Most commonly 2 F waves for every QRS complex (2:1 conduction); 3:1 and 4:1 possible as well
PRI
Duration	Not applicable
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	Usually 60–100; could be faster or slower
Treatment Options. Not commonly treated in the field, unless the patient is showing signs of altered mental status related to hypotension most likely caused by the rate. The rate pictured here would not warrant emergency treatment interventions; however, if the ratio was 2:1 (instead of the 4:1 pictured here), the ventricular rate would be 150 or higher. Treatment in that case would include electrical cardioversion or medications including diltiazem.

Table 4.10 Atrial Fibrillation

Origination Point: Atrial Muscle, Countless Foci		Differential Causes
P Wave		Age Idiopathic Left atrial enlargement MAD RAT PPP MI Atherosclerosis Digoxin Rheumatic heart disease Alcoholism Thyrotoxicosis (hyperthyroidism) Pulmonary embolus Pneumonia Pericarditis
Shape	Absent; course to fine fibrillating baseline
P rate	Not applicable
P wave for every QRS?	Not applicable
QRS complex for every P wave?	Not applicable
PRI
Duration	Not applicable
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Irregularly irregular
Rate	Varies anywhere from <60 to >150; hemodynamic stability based mostly on rate
Treatment Options. People live their daily lives with their heart in an atrial fibrillation rhythm, so treatment of this rhythm is strongly dependent on its underlying ventricular rate. Atrial fibrillation with a rapid ventricular response, (pulse >150) is associated with decreased blood pressure and altered mental status. This needs to be aggressively treated with fluid first, followed by 0.25 mg/kg diltiazem if the rate remains high after fluid and the patient is still showing signs of hemodynamic instability.

Table 4.11 Supraventricular Tachycardia

Origination Point: AV Nodal Reentry Cycle		Differential Causes
P Wave		Idiopathic Caffeine Nicotine Cocaine
Shape	Not visible; if present, typically buried in T wave of preceding cycle
P rate	Unable to be discerned
P wave for every QRS?	Unable to be discerned
QRS complex for every P wave?	Unable to be discerned
PRI
Duration	None
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	>150
Treatment Options. Supraventricular tachycardia (SVT) is a rhythm that is too fast to be able to generate adequate cardiac output for a long period of time. Patients may present initially stable and deteriorate the longer they are in the rhythm. For stable SVT, treatment includes a regimen of 6 mg adenosine followed by a rapid saline flush of at least 10 mL. If that is unsuccessful at converting the rhythm to a sinus rhythm, the dose may be repeated with double the initial dose, 12 mg adenosine, an additional 2 times. If that is unsuccessful, diltiazem can be considered. Unstable SVT, designated as SVT associated with a change in mentation, chest pain, syncope, or other symptoms related to hemodynamic instability, is treated more aggressively than stable SVT. Unstable SVT is treated with synchronized electrical cardioversion—described later in this chapter—at 100 J initially, with sequential doses of 150 J, 200 J, 300 J, and 360 J if the initial cardioversion is unsuccessful.

Junctional Rhythms and AV Blocks

When the SA node and subsequently the atria fail to maintain the pacemaking duties for the heart, the junction, or the AV node, will take over. These are referred to as junctional rhythms. These 3 rhythms are closely related, varying only in rate. In distinguishing these rhythms apart from each other, pay particular attention to the rate.

AV blocks vary by how well the atria successfully communicate with the AV node and therefore the ventricles. For example, in 1st-degree block, there is still a 1:1 ratio of P:QRS, but the PRI is lengthened. In a 2nd-degree Mobitz type I block, the PRI lengthens until 1 entire QRS complex is omitted; then the process begins anew. In a Mobitz type II block, there is a regular ratio of P:QRS, but it is not 1:1. It can be 2:1, 3:1, or even 3:2; it is similar to banging on a door multiple times until it opens. Finally, in 3rd-degree heart block, there is no communication whatsoever between the SA node and the ventricles, and, therefore, no relationship of P waves to QRS complexes; they each just do their own thing at their own rate.

Table 4.12 Junctional

Origination Point: AV Node		Differential Causes
P Wave		Increased parasympathetic tone Digoxin, beta-blocker, or calcium channel overdose Myocardial ischemia or MI Sick sinus syndrome Electrolyte imbalances Increasing ICP Idiopathic
Shape	Typically absent (buried within the QRS); possibly inverted before or after QRS complex
P rate	Unable to be discerned
P wave for every QRS?	Unable to be discerned
QRS complex for every P wave?	Unable to be discerned
PRI
Duration	Not applicable
QRS Complex
Shape	Normal, possibly wide
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	40–60, junction’s intrinsic rate
Treatment Options. Treatment is limited to treating the underlying cause and symptoms. The junctional rhythm, with its rate of 40–60, may require treatment for bradycardia. In that case, 0.5–1 mg atropine should be given initially, followed by TCP if the rate and blood pressure do not improve. Administration of 1 g calcium chloride is recommended if calcium channel blocker toxicity or overdose is suspected.

Table 4.13 Accelerated Junctional

Origination Point: AV Node		Differential Causes
P Wave		Increased parasympathetic tone Digoxin, beta-blocker, or calcium channel overdose Myocardial ischemia or MI Sick sinus syndrome Electrolyte imbalances Idiopathic Recent heart surgery
Shape	Typically absent (buried within the QRS); possibly inverted before or after QRS complex
P rate	Unable to be discerned
P wave for every QRS?	Unable to be discerned
QRS complex for every P wave?	Unable to be discerned
PRI
Duration	Not applicable
QRS Complex
Shape	Normal, possibly wide
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	60–100; faster than the junction’s intrinsic rate but <100
Treatment Options. Treatment is limited to treating the underlying cause and symptoms. Only in the basic junctional rhythm, with its rate of 40–60, would treatment for bradycardia likely be necessary. An accelerated junctional rhythm is likely fast enough to be able to maintain viable cardiac output, therefore focusing on the rhythm is unnecessary. Fluid for hypotension and 1 g calcium chloride for suspected calcium channel blocker toxicity or overdose are recommended treatments.

Table 4.14 Junctional Tachycardia

Origination Point: AV Node		Differential Causes
P Wave		Increased parasympathetic tone Digoxin, beta-blocker, or calcium channel overdose Myocardial ischemia or MI Sick sinus syndrome Electrolyte imbalances Idiopathic Recent heart surgery
Shape	Typically absent (buried within the QRS); possibly inverted before or after QRS complex
P rate	Unable to be discerned
P wave for every QRS?	Unable to be discerned
QRS complex for every P wave?	Unable to be discerned
PRI
Duration	Not applicable
QRS Complex
Shape	Normal, possibly wide
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	>100
Treatment Options. Junctional tachycardia is likely fast enough to be able to maintain viable cardiac output; therefore, focusing on the rhythm is unnecessary. A fluid bolus of 500–1,000 mL may correct hypotension. Calcium is again recommended.

Table 4.15 First-Degree AV Block

Origination Point: SA Node, AV Nodal Delay		Differential Causes
P Wave		Idiopathic Myocardial ischemia or MI Calcium channel blocker or beta-blocker overdose Increased vagal tone Surgery or trauma to the heart Myocarditis Infections Congenital heart diseases
Shape	Upright, normal
P rate	SA nodal rate
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	Prolonged, >0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	>150
Treatment Options. z-degree AV block is rarely treated in the prehospital environment, unless it is associated with severe bradycardia.

Table 4.16 Second-Degree AV Block, Mobitz Type I, Wenckebach

Origination Point: SA Node, AV Conduction Delay		Differential Causes
P Wave		Idiopathic Myocardial ischemia or MI Calcium channel blocker or beta-blocker overdose Increased vagal tone Surgery or trauma to the heart Myocarditis Infections Congenital heart diseases
Shape	Upright, normal
P rate	SA nodal rate
P wave for every QRS?	Yes
QRS complex for every P wave?	No
PRI
Duration	Increasing in sequential cycles until 1 QRS complex is dropped
QRS Complex
Shape	Normal with 1 missing
Duration	0.08–0.12 second
R-R Interval
Regularity	Regularly irregular
Rate	60–100
Treatment Options. Treatment for 2nd-degree AV block, Mobitz type I (Wenckebach), is generally limited to treatment for the bradycardia, which can include atropine and TCP as with earlier bradycardic rhythms. Although this rhythm can result from an active evolving AMI, traditional treatments for AMI, such as morphine and NTG, may not be possible because those medications may be contraindicated in the presence of hypotension. If the patient possibly overdosed on beta-blockers, blood pressure support with pressors and fluid may be indicated in addition to TCP. For calcium channel blocker overdose, calcium also should be considered.

Table 4.17 Second-Degree AV Block, Mobitz Type II

Origination Point: SA Node, AV Conduction Delay		Differential Causes
P Wave		Idiopathic Myocardial ischemia or MI Calcium channel blocker or beta-blocker overdose Increased vagal tone Surgery or trauma to the heart Myocarditis Infections Congenital heart diseases
Shape	Upright, normal
P rate	SA nodal rate
P wave for every QRS?	Yes
QRS complex for every P wave?	No
PRI
Duration	The P waves that have the QRS complex immediately after it usually have a normal PRI (<0.20 second). The PRI is always constant.
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regularly irregular
Rate	<100, dependent on conduction ratio
Treatment Options. Treatment for 2nd-degree AV block, Mobitz type II, is generally limited to treatment for the bradycardia, which can include atropine and TCP as with earlier bradycardic rhythms. Although this can result from an active evolving AMI, traditional treatments for an AMI, such as morphine and NTG, may not be possible because those medications may be contraindicated in the presence of hypotension. If the patient possibly overdosed on beta-blockers, blood pressure support with pressors and fluid may be indicated in addition to TCP. For calcium channel blocker overdose, calcium also should be considered.

Table 4.18 Third-Degree AV Block

Origination Point: SA Node and Ventricular Tissue, Separately		Differential Causes
P Wave		Idiopathic Myocardial ischemia or MI Calcium channel blocker or beta-blocker overdose Increased vagal tone Surgery or trauma to the heart Myocarditis Infections Congenital heart disease
Shape	Upright, normal
P rate	60–100
P wave for every QRS?	No
QRS complex for every P wave?	No
PRI
Duration	Not applicable
QRS Complex
Shape	Wide, bizarre
Duration	>0.12 second
R-R Interval
Regularity	Regular
Rate	<60
Treatment Options. Third-degree heart block, also known as AV dissociation, has no communication from the atria to the ventricles; it is typically treated in the field only if the resultant bradycardia is so severe that the patient is hypotensive and displaying signs of altered mental status. At that point, the best option is TCP because atropine will serve only to accelerate the P rate, leaving the ventricular R rate unchanged.