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Flashcards in Cardiac Arrhythmias Deck (43)
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1
Q

Sinus Bradycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Results from slowing of the SA Node.

Etiology: May result from;
Increased Parasympathetic (Vagal) Tone.
Intrinsic disease of the SA Node
Drug Effects (digitalis, beta-blockers, calcium channel blockers)
Normal Finding in Healthy Well Conditioned Persons

Rules of Interpretation: (Lead II) Rate: <60, Rhythm: R-R Regular, Pacemaker Site: SA Node
P Wave: Normal and Upright
PR Interval: Normal 0.12-0.2 second and constant
QRS Complex: Normal 0.04-0.12 second

Clinical Significance: Decreased rate can cause decreased cardiac output, hypotension, angina, or CNS symptoms. Especially true for rates lower than 50bpm. Slow rate may also lead to atrial or ventricular ectopic rhythms. In a healthy athlete this may be normal.

Treatments: Generally unessecary unless signs of poor perfusion (acute altered mental status, hypotension, ongoing chest pain, or other signs of shock). Oxygen. If there are signs of poor perfusion prepare for transcutaneous pacing. Consider 0.5mg bolus of Atropine, repeat every 3-5min until you have achieved a satisfactory rate or have given 3.0mg total. If atropine fails consider transcutaneous cardiac pacing, dopamine or epi infusions.

2
Q

Sinus Tachycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Results from an increased rate of SA node discharge.

Etiology: May Result from;
Exercise, Fever, Anxiety, Hypovolemia, Anemia, Pump failure, Increased Sympathetic Tone, Hypoxia, Hyperthyroidism

Rules of Interpretation: (Lead II)
Rate: >100, Rhythm: Regular, Pacemaker Site: SA Node, P waves: Normal/Upright, PR Interval: Normal, QRS: Normal

Clinical Significance: Often benign. In some cases it is a compensatory mechanism for decreased stroke volume. If greater than 140bpm cardiac output may fall due to ventricular filling time (preload) is inadequate. Increased rates=increased O2 demand for the heart and thus increase possible ischemia or infarct in diseased hearts. Prolonged sinus tach accompanying Acute Myocardial Infarction is often an ominous sign suggesting cardiogenic shock.

Treatments: Directed at underlying cause. Hypovolemia, fever, hypoxia, or other causes should be corrected.

3
Q

Sinus Arrhythmia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Sinus arrhythmia often results from a variation in the R-R Interval.

Etiology: It is often a normal finding and is sometimes related to the respiratory cycle and changes in intrathoracic pressure. Common in children. Pathologically it can be caused by enhanced vagal tone.

Rules of Interpretation: Rate: 60-100 (Varies w/Respirations), Rhythm: Irregular, Pacemaker site: SA Node. P Wave: Upright and Normal, PR Interval: Normal, QRS: Normal

Clinical Significance: It is a normal variant, particularly in the young or elderly.

Treatment: Typically Non-required.

4
Q

Sinus Arrest: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Occurs when the SA Node fails to discharge for a brief period resulting in short periods of cardiac standstill. One or more of the PQRST complexes will be missing. Can persist until pacemaker cells lower in the system discharge (escape beats) or until the SA node resumes discharge. Because the node fails to fire the R-R interval following the dropped beat will vary ie. the pause will not be a multiple of the previous R-R interval.

Etiology: Ischemia of the SA Node, Digitalis toxicity, Excessive Vagal tone, Degenerative Fibrotic Disease

Rules of Interpretation: Rate: Normal to Slow Depending on the Frequency & Duration of the arrest. Rhythm: Irregular, Pacemaker Site: SA Node, P Wave: Upright & Normal, PR Interval: Normal, QRS: Normal

Clinical Significance: Frequent/Prolonged episodes may compromise cardiac output resulting in syncope and other issues. Always the danger of complete cessation of the SA Node activity. Usually, an escape rhythm develops; occasionally cardiac standstill can result.

Treatment: If asymptomatic: observe until changes occur. If signs of poor perfusion (Altered mental status, chest pain, hypotension or other signs of shock) prepare for transcutaneous pacing. Consider bolus of 0.5mg Atropine. Repeat every 3-5min to a max of 3mg. If atropine fails consider transcutaneous pacing or a dopamine or epi infusion.

5
Q

Sinus Block: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Also called Sinus Exit Block occurs when the sinus node fires on time but the impuse 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 the R-R intervals after the last beat will be constant ie. the pause will be a multiple of the previous R-R interval.

Etiology: Ischemia of the SA node, Digitalis Toxicity, Excessive Vagal Tone, Degenerative Fibrotic Disease.

Rules of Interpretation: Rate: Normal to Slow Depending on the Frequency & Duration of the arrest. Rhythm: Regular, Pacemaker Site: SA Node, P Wave: Upright and Normal, PR Interval: Normal, QRS: Normal

Clinical Significance: Frequent/Prolonged episodes may compromise cardiac output resulting in syncope and other issues. Always the danger of complete cessation of the SA Node activity. Usually, an escape rhythm develops; occasionally cardiac standstill can result.

Treatment: If asymptomatic: observe until changes occur. If signs of poor perfusion (Altered mental status, chest pain, hypotension or other signs of shock) prepare for transcutaneous pacing. Consider bolus of 0.5mg Atropine. Repeat every 3-5min to a max of 3mg. If atropine fails consider transcutaneous pacing or a dopamine or epi infusion.

6
Q

Sinus Pause: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Occurs when the sinus node fails to discharge for a brief period resulting in a missing PQRST. Differs from sinus arrest in that only ONE beat is missing. Because the node fails to fire the R-R interval following the dropped beat will vary ie. the pause will not be a multiple of the previous R-R interval.

Etiology: Ischemia of the SA Node, Digitalis Toxicity, Excesive Vagal Tone, Degenerative Fibrotic Disease.

Rules of Interpretation: Rate: Normal to Slow Depending on the Frequency & Duration of the arrest. Rhythm: Irregular, Pacemaker Site: SA Node, P Wave: Upright & Normal, PR Interval: Normal, QRS: Normal.

Clinical Significance: Frequent/Prolonged episodes may compromise cardiac output resulting in syncope and other issues. Always the danger of complete cessation of the SA Node activity. Usually, an escape rhythm develops; occasionally cardiac standstill can result.

Treatment: If asymptomatic: observe until changes occur. If signs of poor perfusion (Altered mental status, chest pain, hypotension or other signs of shock) prepare for transcutaneous pacing. Consider bolus of 0.5mg Atropine. Repeat every 3-5min to a max of 3mg. If atropine fails consider transcutaneous pacing or a dopamine or epi infusion.

7
Q

Sick Sinus Syndrome: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Technically not an arrhythmia but a combination of arrhythmias. Occurs when the SA Node is ischemic or diseased. Characterized by wild swings in HR often moving from profound Brady to severe Tachycardia and back. Sinus blocks are also commonly seen with SSS. Because the node fails to fire the R-R interval following the dropped beat will vary ie. the pause will not be a multiple of the previous R-R interval.

Etiology: Ischemia of the SA Node, Digitalis Toxicity, Degenerative Fibrotic Disease.

Rules of Interpretation: Rate: Extremely Variable, Rhythm: Irregular, Pacemaker Site: SA Node, P Wave: Upright & Normal, PR Interval: Normal, QRS: Normal.

Clinical Significance: Frequent/Prolonged episodes may compromise cardiac output resulting in syncope and other issues. Always the danger of complete cessation of the SA Node activity. Usually, an escape rhythm develops; occasionally cardiac standstill can result.

Treatment: If asymptomatic: observe until changes occur. If signs of poor perfusion (Altered mental status, chest pain, hypotension or other signs of shock) begin transcutaneous pacing or a dopamine or epi infusion.

8
Q

What are the Arrhythmias Originating in the SA Node

A
Sinus Bradycardia
Sinus Tachycardia
Sinus Arrhythmia
Sinus Arrest
Sinus Block
Sinus Pause
Sick Sinus Syndrome
9
Q

What are the Arrhythmias Originating in the Atria?

A
Wandering Atrial Pacemaker
Multifocal Atrial Tachycardia
Premature Atrial Contractions
Paroxysmal Supraventricular Tachycardia
Atrial Flutter
Atrial Fibrillation
10
Q

Wandering Atrial Pacemaker: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Is also called Ectopic Tachycardia. Is the passive transfer of pacemaker sites from the sinus node to other latent pacemaker sites in the atria and AV junction. Often more than one pacemaker site will be present causing a variation in the R-R interval and P wave morphology.

Etiology: A variant of sinus arrhythmia, a normal phenomenon in the very young or elderly, Ischemic Heart disease, Atrial Dilation.

Rules of Interpretation: 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, P waves may dissapear. PR interval: Varies; maybe less than 0.12, normal or greater than .20, QRS: Normal

Clinical Significance: Usually has no detrimental effects. Occasionally it can be a precursor of other atrial arrythmias such as A-Fib. Sometimes it indicated digitalis toxicity.

Treatment: If asymptomatic; observe for changes. If symptomatic consider Adenosine.

11
Q

Multifocal Atrial Tachycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Usually seen in acutely ill patients. It is a wandering pacemaker rhythm with a rate greater than 100. Significant pulmonary disease is seen in ~60% of these patients. Certain meds used to treat pulmonary disease (beta agonists/theophylline) may worsen the arrhythmia. Three different P waves are noted, indicating various ectopic foci.

Etiology: Pulmonary disease, Metabolic Disorders (Hypokalemia), Ischemic heart disease, Recent Surgery.

Rules of Interpretation: Rate: >100, Rhythm: Irregular, Pacemaker Site: Ectopic Sites in Atria. P Wave: Organized, discrete non-sinus P waves w/atleast 3 different forms. PR Interval: Varies, QRS: Maybe .2 depending on the AV node’s refractory status when the impulse reaches it.

Clinical Significance: Frequently these patients are acutely ill. This arrhythmia may indicate a serious underlying illness.

Treatment: Treatment of underlying medical issue usually resolves the arrhythmia. Specific antiarrhythmic therapy is usually not required.

12
Q

Premature Atrial Contractions: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Result from a single electrical impulse originating in the atria outside the SA Node which inturn causes a premature depolarization of the heart before the next expected sinus beat. Because it depolarizes the atrial syncytium, this impulse also depolarizes the SA Node interrupting the normal cadence. This creates a noncompensatory pause in the underlying rhythm.

Etiology: Use of caffeine, nicotine or alcohol. Sympathomimetic Drugs. Ischemic Heart Disease, Hypoxia, Digitalis Toxicity, Idiopathic Causes.

Rules of Interpretation: Rate: Depends on Underlying Rhythm. Rhythm: Depends on the Underlying Rhythm, usually regular except for the PAC. Pacemaker site: Ectopic Focus in the Atrium. P Wave: The P wave of the PAC differs from the P wave of the underlying 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 PRI of .12 or more. Ectopic foci near the AV node will have a PRI of .12 or less. QRS: usually Normal. Maybe greater than .12 if 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 maybe absent.

Clinical Significance: Isolated PAC’s are of minimal significance. Frequent PAC’s may indicate organic heart disease and may precede other atrial arrhythmias.

Treatment: If asymptomatic: Observe. If patient is hypoxic and symptomatic administer O2 to correct hypoxia. Contact medical direction as needed.

13
Q

Paroxysmal Supraventricular Tachycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Occurs when rapid Atrial depolarization overrides the SA Node. Often occurs in paroxysm w/ sudden onset, may last minutes to hrs, terminates abruptly. May be caused by increased automaticity of a single atrial focus or by reentry phenomenon at the AV node. Paroxysmal means it starts and stops. Often they are not seen on the rhythm strip. In order to diagnose PSVT the paroxysms must be seen.

Etiology: May occur at any age, NOT associated w/ heart disease. May be precipitated by stress, overexertion, smoking or caffeine. It is sometimes associated with atherosclerotic cardiovascular disease and rheumatic heart disease. PSVT is rare in patients w/ MI. It can occur w/ accessory pathway conduction such as Wolf-Parkinson-White syndrome.

Rules of Interpretation: Rate: 150-250 Rhythm: Regular except at onset and termination. Pacemaker Site: In the Atria outside SA Node. P Wave: Atrial P wave differs slightly from sinus P waves. May be buried in preceding T Waves. PR Interval: Usually Normal, however it can vary w/ length of ectopic pacemaker. Ectopic pacemakers near SA node have PRI close to .12. Ectopic pacemakers near the AV node will have PRI of .12 or less. QRS: Normal

Clinical Significance: Young pts. w/ good cardiac reserves may tolerate PSVT well for short periods. Patients often sense PSVT as palpitations. Rapid rates can cause reduction in cardiac output due to inadequate ventricular filling. The reduced diastolic phase can also compromise coronary artery perfusion. PSVT can precipitate angina, hypotension or congestive heart failure.

Treatment: If pt. is stable obtain a 12 lead and IV access.
Asymptomatic: Obtain a 12ld, Observe
Symptomatic with NO signs of hypo-perfusion: Vagal Maneuvers. Medications (Adenosine)
Symptomatic WITH signs of hypo-perfusion: Synchronized Cardioversion

14
Q

Supraventricular Tachycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Refers to tachycardias that originate above the ventricles. Pacemaker site is often difficult to determine due to rate. The rapid rate often makes P waves indiscernible. Pacemaker site can be in the SA node, the atria or the AV junction.

Etiology: Use of caffeine, nicotine, or alcohol. Cocaine. Sympathomimetic Drugs, Ischemia heart disease, Hypoxia, Digitalis Toxicity, Idopathic causes.

Rules of Interpretation: Rate: 150-250, Rhythm: Regular except at onset/termination. Pacemaker site: in Atria outside SA node. P Wave: May be impossible to see due to rapid rate. PR Interval: Usually normal but can vary depending on Pacemaker location. Closer to SA .12 closer to AV less than .12. QRS: Normal

Clinical Significance: Young pts. w/good cardiac reserves may tolerate STV for short periods. May feel palpitations. Rapid rates can cause reduction in cardiac output. Reduced diastolic phase can compromise coronary artery perfusion. SVT can precipitate angina, hypotension, or CHF.

15
Q

Atrial Flutter: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

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

Etiology: It may occur in normal hearts but it is usually associated w/ organic disease. It rarely occurs as the direct result of an MI. Atrial dilation which occurs w/ CHF is a cause of A. Flutter.

Rules of Interpretation: Rate: Atrial Rate is 250-350, Ventricular rate varies w/ the ratio of AV conduction. Rhythm: Atrial Rhythm is regular, Ventricular rhythm is usually regular but can be irregular if the block is variable. Pacemaker Site: In the atria outside the SA node. P Waves: Flutter (F) waves are present reselmbling a saw tooth or picket fence pattern. The pattern is often difficult to id in a 2:1 flutter. However, if the rate is ~150 suspect 2:1 flutter.

Clinical Significance: A. Flutter w/normal ventricle rates is normally well tolerated. Rapid ventricular rates may compromise cardiac output and result in symptoms. A. Flutter often occurs in conjunction with A. Fib and is referred to as A. Fib-Flutter.

Treatment: If stable obtain 12lead and IV access.
1. Pharmacological Therapy: Consider rate control w/ Diltiazem or Beta-blockers if the patient is unstable, ie. chestpain, altered mental status, hypotension or shock.

  1. Electrical Therapy: Syncronized cardioversion if rate is more than 150. If time allows sedate patient and apply syncronized DC countershock of 50-100 joules (or biphasic equivalent).
16
Q

Atrial Fibrillation: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Results from multiple areas of reentry within the atria or from ectopic foci bombarding the AV node that physiologically cannot handle all of the incoming impulses. AV conduction is random and highly variable.

Etiology: May be chronic and is often associated with underlying heart disease such as rheumatic heart disease, atherosclerotic heart disease or CHF. Atrial dialtion occurs with CHF and often causes atrial fibrillation.

Rules of Interpretation: Rate: Atrial rate is 350-750bpm (cannot be counted). Ventricular rate varies greatly depending on conduction through the AV node. Rhythm: Irregularly regular. Pacemaker site: Numerous ectopic foci in the atria. P Waves: none discernible. Fibrillation (f) waves are present indicating chaotic atrial activity. PR Interval: None QRS: Normal

Clinical Significance: In A. Fib the atria fail to contract and the atria kick is lost. Thus reducing cardiac output by 20-25%. There is frequently a pulse deficit (a difference between the apical and peripheral pulse rates). If ventricular response is normal and the patient is on digitalis A. Fib is usually well tolerated. If the ventricular rate is less than 60 cardiac output can fall. Suspect digitalis toxicity in patients taking digitalis w/ A Fib and ventricular rates less than 60.

Treatment: If pt. is stable obtain a 12 lead ECG and establish IV access.

  1. Pharmacological Therapy: Consider rate control with diltazem or beta blockers.

If patient is unstable, altered mental status, hypo tension, chest pain, other signs of shock.

  1. Electrical Therapy: Used synchonized cardioversion if the rate is greater than 150. If time allows sedate and apply DC countershock of 50-100 joules or biphasic equivalent.
17
Q

Which Arrhythmia is associated with Pulmonary disease?

A

Multifocal Atrial Tachycardia

18
Q

What are the Regular Rhythms?

A

NSR, NSR w/PAC’s, Sinus Arrest, Sinus Block, Sinus Pause, WAP, Sinus Tach, SVT, PSVT, Atrial Tach, A-Flutter

19
Q

What are the Irregular Rhythms?

A

SSS, Sinus Arrhythmia, A-Fib, A-Flutter, MAT

20
Q

What is the difference between Sinus Arrest, Block and Pause?

A

Sinus Arrest is Irregular where as Sinus Block and Pause will both be regular before and after the missing PQRST. Sinus Pause will only have one missing PQRST and will be regular before and after, Sinus Block may be missing more than one PQRST and will remain regular before and after.

21
Q

What is the main characteristic of SSS?

A

Wild swings from bradycardia to tachycardia.

22
Q

What is characteristic of WAP and MAT? What does differentiates MAT from WAP?

A

They need to have 3 different P Waves, one of those can be a missing P Wave but 3 different morphologies are required.

The different between MAT and WAP is that MAT has a rate greater than 100.

23
Q

What is MAT often mistaken for?

A

A-Fib

24
Q

How many beats do you need to have a rhythm?

A

3

25
Q

What do you need to have to diagnose PSVT?

A

A sudden start to the tachycardia and a sudden stop. Rate will be between 150-250 after it starts and before it stops.

26
Q

What is the “rule” regarding a rhythm that is regular at 150bpm?

A

It should be considered to be Atrial Flutter with 2:1 conduction, unless there is evidence otherwise.

27
Q

What are the two problems that can arise from the AV junction?

A
  1. AV Block- in which the impulse is either blocked completely or slowed as it passes through the AV Node
  2. Arrhythmia’s from a malfunction of the AV Junction cells themselves
28
Q

Why is the AV node or AV junction Important? What purpose does it serve?

A

It slows the impulse from the SA Node to allow for both Atrial emptying as well as Ventricular filling.
Serves as a backup pacemaker site in case the SA Node fails. (rate is 40-60 bpm)
Serves as a junction between the Atria and Ventricles.

29
Q

What does the AV bundle or bundle of His become?

A

The Right and Left Bundle Branches

30
Q

What are common causes of AV Blocks?

A
  1. AV Junctional Ischemia
  2. AV Junctional Necrosis
  3. Degenerative disease of the conduction system
  4. Drug toxicity (Digitalis-most common)
31
Q

What are the AV Block Classifications?

A
  1. First Degree AV Block (a.k.a. 1st AV Delay)
  2. Second Degree AV Block Type I
    - Mobitz Type I
    - Wenkebach
  3. Second Degree AV Block Type II
    - Mobitz Type II
    - Infranodel
  4. 2:1 AV Block
  5. Third Degree AV Block
32
Q

First Degree AV Block: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: First Degree AV Block is actually delay of the impulse, NOT a complete block
First Degree AV Block is not a true “rhythm” itself, but rather an arrhythmia that is in conjunction with another. (Sinus Bradycardia with a 1st Degree AV Block)
Etiology: AV Blocks can occur in a healthy heart, but AV Junction Ischemia is the most common cause.
Rate: depends on underlying rhythm
Rhythm: usually regular
Pacemaker Site: SA Node or Atria
P Waves: normal in appearance
PR Interval: MUST be greater than .20 seconds
QRS Width: usually within normal limits BUT can be wide if there is conduction system disease of the ventricles
Treatment: limited to observation in the pre-hospital setting.
Avoid drugs that slow AV conduction:
Liodcaine
Procainamide

33
Q

Second Degree Type 1: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Is an intermittent block at the level of the AV Node:
Characterized by pattern or rhythmic PR Intervals in which they get progressively longer until an entire QRS is dropped.
P to P is constant, the PR Interval varies as the it takes longer and longer for an impulse to get through to stimulate the ventricles.
Etiology: most common causes of “low grade” (1st and 2nd Deg. Type 1) can occur in healthy hearts, but have other causes:
Ischemia at the AV Junction (most common)
Increased Parasympathetic Tone
Drugs/Medications
Rate: Atrial rate is normal (unaffected) the ventricular rate may be “normal” BUT most often is slow.
Rhythm: Atrial rate is normal (P to P march) the overall rhythm is irregular because of the dropped/missed/non conducted QRS complex
Pacemaker Site: SA Node or Atria
P Waves: Normal in appearance, BUT not every P wave will have a QRS complex.
PR Interval: Will progressively get longer, until a QRS is not conducted, the following PR Interval MUST be shorter than the PR Interval PRIOR to the missed QRS complex. (PR Interval are patterned)
QRS Width: May be normal, OR wide if there is conduction system disease present in the ventricles.
Treatments: Will depend on the symptoms as well as signs or symptoms of Hypo-Perfusion. If your patient is stable, observation and transport are all that is needed. IF, the patient is symptomatic consider the following:
Atropine: is the first line treatment for ALL symptomatic bradycardia patients
Transcutaneous Pacing (TCP)
Chronotropic Infusions

34
Q

Second Degree Type II, Mobitz II, Infranodal Block: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Is an intermittent block characterized by P waves that are not conducted to the ventricles.
It is unlike Second Degree Type I as there is NO progressive lengthening on the PR Interval
Rate of conduction can be constant or variable.
If the rate of conduction is 2:1, it is nearly impossible to distinguish between 2:1 AV Block and Second Degree Type II
Etiology: Second Degree AV Block Type II is usually associated with Acute MI’s or Septal Necrosis
Rate: Atrial is normal, BUT the ventricular rate is usually bradycardiac
Rhythm: Regular (R to R) if the rate of impulse conduction through the AV Junction (AV Node) is constant, Irregular (R to R) if the conduction rate is not constant.
Pacemaker Site: SA Node or Atria
P Waves: P to P are constant, but not all P waves have a QRS complex.
PR Interval: Constant for the conducted QRS complexes with a P wave. (NO progression in PR Interval)
QRS Width: May be normal, but can be wider because of abnormal ventricular depolarization sequence.
Clinical Significance: Second Degree Type II can progress to Complete Heart Block.
Treatments: Based on patient’s symptoms and signs of Hypo-Perfusion:
AHA Guidelines
Atropine maybe ineffective with “high degree” blocks

35
Q

2:1 AV Block: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: 2:1 AV Block is a type of 2nd Degree AV Block. There is 2 P waves per QRS complex. The first P wave (impulse) cannot be conducted. The block is constant, and is NOT intermittent like 2nd Degree Type II
Etiology: 2:1 AV Block is usually associated with Acute Myocardial Infarction or Septal Necrosis
Rate: Atrial rate is normal (unaffected) and Ventricular rate is slow (for every 2 impulses only 1 is conducted)
Rhythm: R to R is regular, P to P is regular
Pacemaker Site: SA Node or Atria
P Waves: 2 P waves per QRS complex. The morphology of the P waves are normal
PR Interval: is constant for the conducted impulses, it may be greater than .20 seconds
QRS Width: Can be normal, BUT is usually wide as a result of Abnormal Ventricular Depolarization Sequence.
Treatment: Identical to 2nd Degree AV Blocks. Mostly observing for worsening in condition, follow AHA Guidelines as needed.

36
Q

3rd Degree AV Block (Complete Heart Block): Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Complete Heart Block is the absence of conduction between the Atrium and Ventricles as a result of complete electrical block at or below the AV Node.
Etiology: Can occur from Acute Myocardial Infarction, Digitalis Toxicity, or Degeneration of the conduction system (occurs in elderly)
Essentially the Atrium cannot get any impulses to the Ventricles, so a backup pacemaker site for the ventricles takes over the ventricular rate.
Rate: Atrial rate is normal, Ventricular rate depends on the pacemaker site for the ventricles. (AV Junction or Lower in the Ventricles)
Rhythm: Both Atrial and Ventricular rhythms are regular
Pacemaker Site: SA Node AND EITHER the AV Junction or the Ventricles.
P Waves: Normal P wave morphology. (* most often there is more than 1 P wave per QRS*)
PR Interval: Varies, there is NO correlation between “P” Waves and “QRS” complexes.
QRS Width: Depends on the location of the Ventricular Pacemaker Site. (AV Node or Ventricles)
Treatments: AVOID the use of Lidocaine or Procainamide in the presence of 3rd Degree AV Block.
Treatments will depend on clinical presentation: Most often its monitoring and rapid, safe transport.
Refer to AHA Guidelines, realize Atropine may not be effective and 3rd Degree AV Block may require TCP.

37
Q

What are the Junctional Arrhythmias?

A
Premature Junctional Contraction (PJC)
Junctional Escape Complex
Junctional Escape Rhythm
Junctional Tachycardia
Accelerated Junctional Rhythm
38
Q

What are the characteristics of AV Junctional Rhythms?

A
“P” Waves:
Inverted P Waves
After the QRS Complex
Hidden in the QRS Complex
PR Interval will be less than .12 seconds
39
Q

Premature Junctional Contractions (PJC): Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Is not a “rhythm” but is an ectopic beat. A PJC is a “single” electrical impulse originating in the AV Node that occurs before the next expected sinus beat.
Description of PJC’s: They can have a “compensatory” or “non-compensatory” pause.
Compensatory Pause- Occurs if the SA Node discharges before the premature impulse reaches it
Non-Compensatory Pause- Occurs if the premature beat depolarizes the SA Node and interrupts the heart’s normal cadence.
Premature Junctional Contractions (PJC) can occur as a single contraction, or in patterns of Bigeminy or Trigeminy.
Etiology: Can result from any of the following:
Use of Caffeine, Tobacco, or Alcohol
Sympathonimetic Drugs
Ischemic Heart Disease
Hypoxia
Digitalis Toxicity
Idiopathic
Rate: Depends on underlying rhythm
Rhythm: Usually regular, with the exception of the PJC (‘s)
Pacemaker Site: Ectopic Foci in the AV Node (V Junction)
P Wave: (PJC) invert, hidden, behind QRS complex
PR Interval: if present, less than .12 seconds
QRS Width: Usually normal
Treatment: Observation is likely all that is needed. If the patient is symptomatic-treat the underlying cause or look for other more common causes.

40
Q

Junctional Escape Complexes Junctional Escape Rhythm: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Junctional Escape Complex or Junctional Escape Rhythm occurs when the primary pacemaker (SA Node) is slower than the AV Junction (AV Node) and as a result the AV Node takes over the pacemaker functions until the SA Node pacemaker rate takes over again
This serves as a safety for the heart
AV Junction (AV Junction) Rate is 40-60 bpm
Etiology: Junctional Escape Complexes or Junctional Escape Rhythm can be the result of the following:
Increased Vagal Tone
Pathological Slow SA Node discharge
Heart Block
Rate: Ventricular is 40-60 bpm, may not be able to measure, “P” waves may be hidden, inverted, or after QRS complexes.
Rhythm: A single Junctional Escape Complex will have an irregular rhythm, if it’s a Junctional Escape Rhythm it will be regular.
Pacemaker Site: AV Junction
P Waves: May be inverted, hidden in the QRS, appear after the QRS complex
PR Interval: if it’s before the QRS complex, it will measure less than .12 seconds
QRS Width: Normal
Treatment: Includes looking at the clinical picture and treating it much like any other symptomatic bradycardia (per AHA Guidelines)

41
Q

Junctional Bradycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Junctional Bradycardia has an intrinsic heart rate of less than 40 bpm.
It has the same Etiologies as Junctional Escape Complexes and Junctional Escape Rhythm
Rules:
Are the same as the Junctional Escape Complexes and Junctional Escape Rhythm
Treatments:
Are the same as any other symptomatic bradycardia

42
Q

Accelerated Junctional Rhythm: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Accelerated Junctional Rhythm results from increased automaticity in the AV Junction causing the AV Junction (AV Node) to discharge faster than the intrinsic rate of the AV Junction (AV Node)
If the rate becomes fast enough it can overtake the SA Node as the pacemaker site. (the rate is faster than 60 bpm)
Etiology: Results from Ischemia of the AV Junction (AV Node)
Rate: Ventricular rate is between 60-100 bpm
Rhythm: Regular
Pre-Hospital Treatment:
“generally unnecessary”

43
Q

Juctnional Tachycardia: Give Description, Etiology, Rules of Interpretation, Wave Descriptions, Clinical Significance and Treatments

A

Description: Junctional Tachycardia is technically considered a form of Supraventricular Tachycardia.
Because of the ventricular rate it is nearly impossible to determine if the P wave is preceding or following the QRS complex, as well as at times not being able to determine the presence of a “P” Wave.
Rules: Follow the same rules as any other Junctional Rhythm, look for P waves that are inverted, hidden, absent, following the QRS complex or which have a PR Interval of less than .12, with a ventricular rate of greater than 100 bpm
Heart Rate must be between 101-150 bpm, anything faster than 150 bpm maybe considered a Supraventricular Tachycardia
Treatment: Same as with any other Tachycardia: assess the clinical picture, treatments are based on symptoms and signs of impaired cardiac function.