1. 10
Introducing the Ventricular Rhythms 1

2. Introducing the Ventricular Rhythms
Objectives
Discuss the origin of the ventricular rhythms
Review specific components of the electrical conduction system of the heart
Identify premature ventricular contractions, including EKG characteristics
Identify idioventricular rhythm, including EKG characteristics
Differentiate idioventricular rhythm and accelerated idioventricular rhythm

3. Introducing the Ventricular Rhythms
Objectives (continued)
Identify ventricular tachycardia, including EKG characteristics
Identify ventricular fibrillation, including EKG characteristics
Identify ventricular asystole, including EKG characteristics
Discuss pulseless electrical activity
Discuss the clinical significance of the ventricular rhythms

4. Origin of the Ventricular Rhythms
The rhythms are classified according to the heart structure in which they begin, or their site of origin
The sinoatrial (SA) node or the AV junctional tissues fails to generate an impulse
If this failure develops, the VENTRICLES will assume the role of pacing the heart

5. Origin of the Ventricular Rhythms
Rhythms that are initiated in the area of the ventricular are called ventricular rhythms
Ventricular rhythms are the least efficient of the heart’s pacemakers; you should recall that patient assessment is the most important indicator of clinical significance

6. Components of Electrical Conduction System of the Heart

7. Origin of the Ventricular Rhythms
Impulses that are ventricular in origin begin in the lower ventricular musculature
Impulse may travel in retrograde (backward) direction to depolarize the atria
Impulse may travel antegrade (forward) to depolarize the ventricles
Either way, the normal conduction pathway is bypassed

9. Origin of the Ventricular Rhythms
Due to bypass, ventricular rhythms will display QRS complexes that are wide (greater than or equal to 0.12 seconds) and bizarre in appearance
Absence of P waves because they are hidden or buried in QRS complex
Remember that QRS complexes of supraventricular rhythms are commonly less than 0.12 seconds in duration

10. Premature Ventricular Complexes (Contractions) (PVC)
Individual complexes rather than an actual rhythm
Single ectopic (out-of-place) complex that occurs earlier then the next expected complex
Arises from an irritable site in the ventricles
The significance of PVCs is based entirely upon the patient’s clinical condition

11. Premature Ventricular Complexes (Contractions) (PVC)
The underlying cadence of SA node is not interrupted by a PVC nor is SA node depolarized
PVC is usually followed by a compensatory pause
Presence of compensatory pause, coupled with wide, bizarre, and premature QRS complex’s are highly suggestive indicators of PVCs

12. Compensatory Pause

13. Premature Ventricular Complexes (Contractions) (PVC)
PVC may fall between two sinus beats without interfering with the rhythm
Referred to as an interpolated beat
PVCs appear in many different patterns and shapes
The morphology, or shape, of the PVC is based on the site of origin of the ectopic focus

14. PVC Patterns of Occurrence

15. Premature Ventricular Complexes

16. Premature Ventricular Complexes - Unifocal

17. Premature Ventricular Complexes - Multifocal

19. Premature Ventricular Contractions (Complexes) OR PVCs
PVCs often indicate myocardial irritability; multifocal PVCs are more serious then unifocal PVCs
Salvos
Runs of ventricular tachycardia
Any indication of increased myocardial irritability dictates that the patient be carefully evaluated and managed

20. Ventricular Bigeminy and Couplet PVCs

22. Ventricular Bigeminy

23. Ventricular Trigeminy

27. R on T

30. Idioventricular Rhythms
Also termed ventricular escape rhythms, considered a last-ditch effort of the ventricles to try to prevent cardiac standstill
Means SA node and AV node have failed
Rate usually less than 40 bpm, and cardiac output is usually compromised

31. Agonal Rhythm
Agonal rhythm is when the idioventricular rhythm falls below 20 bpm
Frequently may be seen as the last-ordered semblance of a heart rhythm when either resuscitation is unsuccessful or after successful defibrillation

32. Idioventricular Rhythms
Causes include extensive myocardial damage, secondary to acute myocardial infarction, or failure of higher pacemakers
Is considered a lethal rhythm and treatment must be immediate and aggressive

33. Idioventricular Rhythms

34. Accelerated Idioventricular Rhythm
May occur when the rate of the ectopic pacemaker exceeds 40 bpm
Commonly accepted rate is bpm
There are no P waves or PR intervals noted

35. Accelerated Idioventricular Rhythm

38. Accelerated Idioventricular Rhythm
May occur in conjunction with myocardial ischemia
Can be mistaken for ventricular tachycardia
Imperative that you remember to always assess and treat the patient, rather than the monitor or EKG strip

40. Ventricular Tachycardia Rhythms
This rhythm is one in which three or more PVCs arise in sequence at a rate greater than 100 bpm
This rhythm commonly overrides the normal pacemaker of the heart
Often occurs rapidly and is initiated by a PVC or by PVCs occurring in rapid succession

41. Ventricular Tachycardia Rhythms
If rhythm is sustained, patient’s clinical condition may rapidly deteriorate
A sustained rhythm is one that lasts for more than 30 seconds
If lasts for less than 30 seconds, it is a nonsustained rhythm,or simply a run of V tach

42. Ventricular Tachycardia

43. Ventricular Tachycardia
Is classified (based on assessment of the patient’s clinical presentation) as either pulseless V tach or V tach with a pulse
Immediate treatment is based on the presence or absence of a palpable pulse
Pulseless V tach
Immediate defibrillation

44. Ventricular Tachycardia
Treatment of V tach with a pulse is based on patient’s clinical picture
Hemodynamically unstable
(Low blood pressure, shortness of breath, etc.) Immediate cardioversion is considered
Hemodynamically stable
( Normal blood pressure, absence of chest pain, and no notable change in mental status ) Drug intervention is appropriate

45. Ventricular Tachycardia
Causes may include
Myocardial ischemia, hypoxia, electrolyte imbalances, increased anxiety or physical exertion, and underlying heart disease

46. Ventricular Tachycardia Rhythm

50. Torsades De Pointes Similar to ventricular tachycardia
Morphology of QRS complexes shows variations in width and shape
Resembles a turning about or twisting motion along base line
May result from
Hypokalemia, hypomagnesemia, tricyclic antidepressant drug overdose, use of antidysrhythmic drugs, or combination of these

51. Torsades De Pointes

53. Torsades De Pointes
Finding and treating the underlying cause of the rhythm is essential
Magnesium is the pharmacologic treatment of choice
Key to recognizing torsades is the variation of QRS morphology, or shape

55. Ventricular Fibrillation
Is a fatal dysrhythmia
Is the most frequent initial rhythm occurrence in sudden cardiac arrest
Tends to occur in the initial hours following an acute myocardial infarction
Occurs as a result of multiple weak ectopic foci in the ventricles

56. Ventricular Fibrillation
Myocardial cells appear to quiver rather than depolarize normally
No coordinated atrial or ventricular contraction, and no palpable pulse
Electrical impulses initiated by multiple ventricular sites; impulses are not transmitted through normal conduction pathway

57. Ventricular Fibrillation
Waveforms appear as disorganized, rapid, irregular waves whose morphology varies vastly
No well-organized QRS complexes
Death will occur if immediate treatment is not established

58. Ventricular Fibrillation
Classified as either
Fine ventricular fibrillation
Ventricular fibrillation waves less than 3 mm of amplitude
Coarse ventricular fibrillation
Ventricular fibrillation waves with amplitudes greater than 3 mm
Course fib is generally more irregular than fine fib

59. Ventricular Fibrillation
Patient assessment is critical in that artifact, or loose leads can resemble ventricular fibrillation
Treat the patient… not the monitor
Causes include
Acute MI, myocardial ischemia, drug toxicity or overdose, hypoxia, and other causes

60. Ventricular Fibrillation

61. Ventricular Fibrillation (Fine)

62. Ventricular Fibrillation (Coarse)

65. Ventricular Asystole The absence of all ventricular activity
Also called cardiac standstill or asystole
Asystole is represented by a flat line, and is the absence of all cardiac electrical activity

66. Ventricular Asystole
It may be difficult to distinguish asystole from fine VF; you must always check two different leads to definitively identify asystole
Often follows unsuccessful resuscitation attempts
May be caused by
Massive MI, cardiac trauma, ventricular aneurysm, and complete heart blocks

67. Ventricular Asystole

68. Ventricular Asystole (Cardiac Standstill, Asystole)

71. Pulseless Electrical Activity
The absence of a palpable pulse and myocardial muscle activity with presence of organized electrical activity on the cardiac monitor
Represents a clinical condition, the patient is clinically dead despite some type of organized rhythm on monitor

72. Pulseless Electrical Activity
Formerly termed electromechanical dissociation, or EMD
Causes include
Profound hypovolemia, massive myocardial damage, ventricular rupture, pulmonary embolism, acidosis, cardiac tamponade, hypothermia, hyperthermia, drug overdose, hypokalemia, hyperkalemia, or tension pneumothorax

73. Clinical Significance of Ventricular Dysrhythmias
Premature ventricular complexes
Little or no significance in patient’s without history of heart disease
May even relate that their caffeine or stress have increased the “palpitations”
Cardiac output may be compromised if PVCs are frequent
Administration of oxygen may abate the PVCs

74. Idioventricular Rhythm
Majority are symptomatic
Due to decreased heart rate, may develop decreased cardiac output, weakness, dizziness, hypotension, and alterations in mental status
A thorough patient assessment is conducted to determine whether rhythm is perfusing

75. Clinical Significance of Ventricular Tachycardia
May be perfusing (producing a palpable pulse) or nonperfusing (producing no palpable pulse)
Due to rapid heart rate, ventricles do not have time to empty and refill = cardiac output compromised
Treatment is based on the absence or presence of a palpable pulse as well as the patient’s clinical picture

76. Clinical Significance of Ventricular Dysrhythmias
If V tach is perfusing and stable
Treatment consists of oxygen administration, IV lifeline, and pharmacologic intervention
If V tach patient becomes clinically unstable (as evidenced by hypotension, SOB, and CP)
Synchronized cardioversion is indicated

77. Clinical Significance of Ventricular Fibrillation
There is no cardiac output, no perfusion
If not treated immediately, patient will not sustain life
The presence of fine V fib
Indicates rhythm has been present for extended period of time

78. Clinical Significance of Ventricular Fibrillation
Treatment includes
CPR, defibrillation (360 J, one shock using monophasic or equivalent biphasic wave forms), airway control, IV lifeline, and drug intervention

79. Clinical Significance of Asystole
Signals a complete termination of ventricular activity
Check in two leads to rule out the presence of fine V fib
Treatment includes
CPR, IV lifelines, endotracheal intubation, and pharmacologic intervention

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