1. An arrhythmia is a disruption in the normal events of the cardiac cycle.

2. INTRA ATRAL PATHWAYS

3. COMMON DYSRHYTMIAS Ventricular Premature ventricular contractions Ventricular bigeminy Ventricular fibrillation Ventricular tachycardia

4. VENTRICULAR ARRHYTHMIAS VENTRICULAR ESCAPE RHYTHM Ventricular Escape Rhythms/ Idioventricular Rhythms  Failure of SA node and AV node to fire  results in the Ventricles assuming the role as Pacemaker

5. VENTRICULAR ESCAPE RHYTHM Rate: 20–40 bpm Rhythm: Regular P Waves: None or, if visible, have no consistent relationship to the QRS complex. PR Interval: None QRS: Wide (0.10 sec), bizarre appearance ♥ Clinical Tip: Idioventricular rhythm may also be called agonal rhythm.

7. VENTRICULAR ARRHYTHMIAS PREMATURE VENTRICULAR CONTRACTION (PVC) is a relatively common event where the heartbeat is initiated by the heart ventricles rather than by the sinoatrial node a dysrhythmia that is produced by an ectopic beat originating in a ventricle and being discharged at a rate faster than that of the next normally occurring beat.

8. PVC’s of 6 /minute or more is life threatening  Premature Ventricular Complex,  Ventricular Premature Contraction (or complex or complexes) (VPC),  Ventricular Premature Beat (VPB), or  EXTRASYSTOLE

9. PREMATURE VENTRICULAR CONTRACTION be perceived as a "skipped beat" or felt as palpitations in the chest NORMAL:  the ventricles contract after the atria have helped to fill them by contracting this way the ventricles can pump a maximized amount of blood both to the lungs and to the rest of the body. PVC, the ventricles contract first which means that circulation is inefficient Single beat PVC arrhythmias do not usually pose a danger and can be asymptomatic in healthy individuals

10. PREMATURE VENTRICULAR CONTRACTION Premature ventricular contraction can occur in a healthy person of any age Becomes more frequent in the elderly more commonly found in men PVC frequently occurs spontaneously with no cause.

11. ETIOLOGY Ischemia Certain medicines such as digoxin which increases heart contraction Myocarditis Cardiomyopathy, hypertrophic or dilated Myocardial contusion Hypoxia Hypercapnia (CO2 poisoning) Sarcoidosis Mitral valve prolapse Smoking Alcohol Drugs such as cocaine Caffeine Tricyclic antidepressants Magnesium and potassium deficiency Calcium excess; Thyroid problems Chemical (electrolyte) problems in the blood Heart attack; Adrenaline excess; Lack of sleep/exhaustion Stress

13. PREMATURE VENTRICULAR CONTRACTION Usually PVCs result from an irritable ventricular focus. ■ PVCs may be uniform (same form) or multiform (different forms). ■ The pause following a PVC may be compensatory or noncompensatory.

14. PREMATURE VENTRICULAR CONTRACTION Rate: Depends on rate of underlying rhythm Rhythm: Irregular whenever a PVC occurs P Waves: None associated with the PVC PR Interval: None associated with the PVC QRS: Wide (0.10 sec), bizarre appearance Clinical Tip: Patients may sense the occurrence of PVCs as skipped beats. Because the ventricles are only partially filled, the PVC frequently does not generate a pulse.

17. PREMATURE VENTRICULAR CONTRACTION: UNIFORM (SAME FORM)

18. PREMATURE VENTRICULAR CONTRACTION: MULTIFORM (DIFFERENT FORMS)

20. PREMATURE VENTRICULAR CONTRACTION PATHOLOGY Normally impulses pass through both ventricles almost simultaneously the depolarization waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels in one direction therefore there is no neutralization effect which results in the high voltage QRS wave in the electrocardiograph.

23. PREMATURE VENTRICULAR CONTRACTION VENTRICULAR BIGEMINY a PVC where every other beat is a ventricular complex abnormal heart beats occur every other concurrent beat. Following the PVC there is a pause and then the normal beat returns only to be followed by another PVC. The continuation of this pairing of beats is an example of bigeminy.

24. PREMATURE VENTRICULAR CONTRACTION:VENTRICULAR BIGEMINY  (PVC EVERY OTHER BEAT)

28. PREMATURE VENTRICULAR CONTRACTION:VENTRICULAR TRIGEMINY  (PVC EVERY 3RD BEAT)

30. PREMATURE VENTRICULAR CONTRACTION:VENTRICULAR QUADRIGEMINY  (PVC EVERY 4 TH BEAT)

31. PREMATURE VENTRICULAR CONTRACTION: COUPLETS (PAIRED PVCS)

32. PREMATURE VENTRICULAR CONTRACTION: TRIPLETS (3 SUCCESSIVE PVC’S)

34. PREMATURE VENTRICULAR CONTRACTION SYMPTOMS Chest pain Faint feeling Fatigue Hyperventilation (after exercise) Frequent episodes of continuous PVCs becomes a form of ventricular tachycardia (VT), which is a rapid heartbeat because there is an extra electrical impulse causing an extra ventricular contraction.

35. PREMATURE VENTRICULAR CONTRACTION TREATMENT: Isolated PVCs with benign characteristics require no treatment. In healthy individuals, PVCs can often be resolved by restoring the balance of MAGNESIUM, CALCIUM and POTASSIUM within the body. The most effective treatment is the elimination of triggers  particularly the cessation of the use of substances such as caffeine and certain drugs

36. PREMATURE VENTRICULAR CONTRACTION PHARMACOLOGICAL agents ANTIARRHYTHMICS: these agents alter the electrophysiologic mechanisms responsible for PVCs LIDOCAINE / IV PUSH, DRIP Initial bolus dose: 75 – 100mg then 50 – 100 mg. within 10 – 15 min. as needed. Continuous IV drip bolus dose: 300 mg. PROCAINAMIDE IV PUSH, drip bolus dose: 300mg. BRETYLIUM continuous infusion if lidocaine and procainamide are ineffective.

37. PREMATURE VENTRICULAR CONTRACTION ELECTROLYTES REPLACEMENT Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.) Potassium supplements LIFESTYLE MODIFICATION Frequently stressed individuals should consider therapy, or joining a support group Heart attacks can increase the likelihood of having PVCs

38. PREMATURE VENTRICULAR CONTRACTION RADIOFREQUENCY CATHETER ABLATION TREATMENT (RF)  electrophysiology study to remove cells that are issuing abnormal electrical activity leading to arrhythmia used to destroy abnormal electrical pathways in heart tissue or normal parts that are contributing to a cardiac arrhythmia  medical procedure where part of the electrical conduction system of the heart, tumor or other dysfunctional tissue is ablated using high frequency alternating current to treat arrhythmias

39. Schematic view of a pulmonary vein ablation. The catheter reaches (from below) through the inferior vena cava, the right atrium and the left atrium, to the orifice of the left upper pulmonary vein.

43. PRACTICE EXERCISE: IDENTIFY THE FOLLOWING PVC’S

44. VENTRICULAR BIGEMINY

47. VENTRICULAR TRIGEMINY

49. VENTRICULAR QUIADRIGEMINY

50. SINGLE PVC

52. VENTRICULAR BIGEMINY

53. VENTRICULAR TRIGEMINY

57. VENTRICULAR ARRHYTHMIAS VENTRICULAR TACHYCARDIA a life threatening dysrhythmia that originates for an irritable focus within the ventricle It is an emergency catastrophe Can degenerate into Ventricular Fibrillation Almost always occur in diseased hearts VENTRICULAR PACEMAKER It is an ineffective rhythm for maintaining cardiac output. Associated hypotension

60. Ventricular Tachycardia (VT): Monomorphic Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram(ECG).

61. Rate: 100–250 bpm Rhythm: Regular P Waves: None or not associated with the QRS PR Interval: None QRS: Wide (0.10 sec), bizarre appearance

62. ♥ Clinical Tip: It is important to confirm the presence or absence of pulses because monomorphic VT may be perfusing or nonperfusing. ♥ Clinical Tip: Monomorphic VT will probably deteriorate into VF or unstable VT if sustained and not treated.

65. Ventricular Tachycardia (VT): Polymorphic QRS complexes in polymorphic VT vary in shape and amplitude. ■ The QT interval is normal or long. Rate: 100–250 bpm Rhythm: Regular or irregular P Waves: None or not associated with the QRS PR Interval: None QRS: Wide (0.10 sec), bizarre appearance

66. Clinical Tip: It is important to confirm the presence or absence of pulses because polymorphic VT may be perfusing or nonperfusing. ♥ Clinical Tip: Consider electrolyte abnormalities as a possible etiology.

67. Torsades de Pointes *from the French for “twisting of the points” demonstrates a rapid, POLYMORPHIC VENTRICULAR TACHYCARDIA with a characteristic twist of the QRS complex around the isoelectric baseline

68. Torsades de Pointes The QRS reverses polarity and the strip shows a spindle effect. ■ This rhythm is an unusual variant of polymorphic VT with normal or long QT intervals.

69. Rate: 200–250 bpm Rhythm: Irregular P Waves: None PR Interval: None QRS: Wide (0.10 sec), bizarre appearance Clinical Tip: Torsade de pointes may deteriorate to VF or asystole. ♥ Clinical Tip: Frequent causes are drugs that prolong QT interval and electrolyte abnormalities such as hypomagnesemia.

70. Torsades de Pointes The pattern is called "twisting" because when the peaks are at their smallest in one lead, they are generally at their largest in another, as if a vibrating string were having its plane of vibration slowly rotated about the long axis of the string.

72. CAUSES: Class IA antiarrhythmics Class III antiarrhythmics Hypomagnesemia Hypokalemia Hypocalcemia Hypoxia Acidosis Heart failure Slow heart rate Female gender Hypothermia Subarachnoid hemorrhage Torsades de Pointes

76. TORSADES DE POINTES CLINICAL MANIFESTATIONS: SIGNS AND SYMPTOMS OF ↓ CARDIAC OUTPUT: Hypotension Exercise limitations Syncope Dizziness Restlessness ↓ LOC

77. TORSADES DE POINTES TREATMENT Treatment is directed at withdrawal of the offending agent 1. Infusion of MAGNESIUM SULFATE 2. ANTIARRHYTHMIC DRUGS - Lidocaine 3. Treat Ischemia 4. Electrical therapy as needed. DEFIBRILLATION Because of the polymorphic nature of TORSADES DE POINTES, synchronized cardioversion MAY NOT BE POSSIBLE, and the patient may require an unsynchronized shock or defibrillation

78. TORSADES DE POINTES DEFIBRILLATION consists of delivering a therapeutic dose of electrical energy to the affected heart with a device called a defibrillator. This depolarizes a critical mass of the heart muscle, terminates the arrhythmia, allows normal sinus rhythm to be reestablished by the body's natural pacemaker  SA NODE can be external, transvenous, or implanted, depending on the type of device used or needed

79. TORSADES DE POINTES CARDIOVERSION  a medical procedure by which an abnormally fast heart rate or cardiac arrhythmia is converted to a normal rhythm, using electricity or drugs SYNCHRONIZED ELECTRICAL CARDIOVERSION  uses a therapeutic dose of electric current to the heart, at a specific moment in the cardiac cycle PHARMACOLOGIC CARDIOVERSION AKA chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock

80. SYNCHRONIZED ELECTRICAL CARDIOVERSION a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R WAVE of the QRS complex on the ECG. Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation

89. DIRECT CURRENT

94. VENTRICULAR TACHYCARDIA

97. VENTRICULAR FIBRILLATION a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart making them quiver rather than contract properly. characterized by the random and chaotic discharging of impulses within the ventricle at rates that exceed 300 beats per minute. While there is activity, it is undetectable by palpation (feeling) at major pulse points of the carotid and femoral arteries especially by the lay person. Such an arrhythmia is only confirmed by ECG.

98. VENTRICULAR FIBRILLATION It produces clinical death and must be reversed immediately Ventricular fibrillation is a medical emergency that requires prompt Basic Life Support interventions because should the arrhythmia continue for more than a few seconds, it will likely degenerate further into asystole ("flatline"). This dysrhythmia results in the absence of cardiac output. Almost always occurs with serious heart disease, especially acute MI.

99. VENTRICULAR FIBRILLATION The condition results in cardiogenic shock, cessation of effective blood circulation, and sudden cardiac death (SCD) will result in a matter of minutes. If however the patient is revived after a sufficient period (at room temperature, roughly 5 minutes) of cerebral hypoxia, the patient could sustain irreversible brain damage and possibly be left brain dead death often occurs if normal sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole

100. VENTRICULAR FIBRILLATION Rateunattainable P wave may be present, but obscured by ventricular waves QRSnot apparent Conductionchaotic electrical activity Rhythmchaotic electrical activity

101. VENTRICULAR FIBRILLATION Chaotic electrical activity occurs with no ventricular depolarization or contraction. ■ The amplitude and frequency of the fibrillatory activity can be used to define the type of fibrillation as coarse, medium, or fine. Clinical Tip: There is no pulse or cardiac output. Rapid intervention is critical. The longer the delay, the less the chance of conversion.

108. VENTRICULAR FIBRILLATION CLINICAL MANIFESTATIONS: 1. PULSE DISAPPEARS WITH ONSET OF VF 2. SYNCOPE, UNCONSCIOUSNESS NO CARDIAC OUTPUT 3. RAPID DETERIORATION OF PHYSIOLOGIC STATUS

112. VENTRICULAR FIBRILLATION TREATMENT: 1. Defibrillation Electric defibrillator The condition can often be reversed by the electric discharge of direct current from a defibrillator Although a defibrillator is designed to correct the problem, and its effects can be dramatic, it is not always successful. Implantable electric defibrillator In patients at high risk of ventricular fibrillation, the use of an implantable cardioverter defibrillator has been shown to be beneficial.

114. VENTRICULAR FIBRILLATION Precordial thump If no defibrillator is available, a precordial thump can be delivered at the onset of VF for a small chance to regain cardiac function. However, research has shown that the precordial thump releases no more than 30 joules of energy. This is far less than the 200–360 J typically used to bring about normal sinus rhythm. Consequently, in the hospital setting, this treatment is not used.

115. VENTRICULAR FIBRILLATION Antiarrhythmic agents AMIODARONE OR LIDOCAINE can help, but, unlike atrial fibrillation ventricular fibrillation rarely reverses spontaneously in large adult mammals. Drug therapy with antiarrhythmic agents in ventricular fibrillation does not replace defibrillation and is not the first priority but is sometimes needed in cases where initial defibrillation attempts are not successful.

116. Pulseless Electrical Activity (PEA) Monitor shows an identifiable electrical rhythm, but no pulse is detected. ■ Rhythm may be sinus, atrial, junctional, or ventricular in origin. ■ PEA is also called electromechanical dissociation (EMD).

117. Rate, rhythm, P waves, P-R interval, and QRS: Reflect underlying rhythm. Clinical Tip: Potential causes of PEA are pulmonary embolism, MI, acidosis, tension pneumothorax, hyper- and hypokalemia, cardiac tamponade, hypovolemia, hypoxia, hypothermia, and drug overdose (i.e., cyclic antidepressants, beta blockers, calcium channel blockers, digoxin).

121. ASYSTOLE a state of no cardiac electrical activity hence no contractions of the myocardium and no cardiac output or blood flow. Asystole is one of the conditions required for a medical practitioner to certify death In asystole, the heart will generally not respond to defibrillation because it is already depolarized the treatment of choice is an injection of EPINEPHRINE and ATROPINE (VASOPRESSIN may also be used) and chest compressions

122. ASYSTOLE Electrical activity in the ventricles is completely absent.

123. Rate: None Rhythm: None P Waves: None PR Interval: None QRS: None Clinical Tip: Always confirm asystole by checking the ECG in two different leads. Also, search to identify underlying ventricular fibrillation. ♥ Clinical Tip: Seek to identify the underlying cause as in PEA.

126. CAUSES

132. NON-SHOCKABLE RHYTHMS 1. PEA 2. AYSTOLE

133. DRUGINITIALSUBSEQUENTINTERVALMAXIMUM EPINEPHRINE1 mg 3-5 min.None VASOPRESSI N 40 unitsNone 40 units AMIODARON E 300 mg150 mg10 min 2.2 G in 24 Hours LIDOCAINE1-1.5 mg/kg0.5-0.75 mg/kg 5-10 min.3 mg/kg VENTRICULAR FIBRILLATION AND PEA

134. DRUGINITIAL SUBSEQUEN T INTERVALMAXIMUM ADENOSINE6 mg12 mg2 min3 rd dose AMIODARONE150 mg15010 min 2.2 G in 24 Hours LIDOCAINE 1-1.5 mg/kg 0.5-0.75 mg/kg 5-10 min.3 mg/kg PROCAINAMIDE20 mg/min 0.5-0.75 mg/kg 5-10 min.3 mg/kg VENTRICULAR TACHYCARDIA WITH PULSE