Ventricular Dysrhythmias Chapter 9 Page 197

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1 Ventricular Dysrhythmias Chapter 9 Page 197 Objectives: Identify the EKG characteristics of dysrhythmias that originate in the ventricles Describe the hemodynamic consequences of selected ventricular dysrhythmias. Describe the clinical management of patients with ventricular dysrhythmias. Describe the clinical management of patients with asystole and pulseless electrical activity (PEA). Bundle Branch Block (BBB) Page 198 Figure 3 Presence of BBB can be determined by wide, bizarre complexes in a single monitoring lead Differentiating between right and left bundle branch block requires a 12 lead ECG Bundle Branch Block Characteristics Wide QRS sec or greater Sinus P wave before each QRS with a normal PR interval Characteristics of a Ventricular Beat Page 202 Box 9-2 Wide, bizarre QRS complex with significant voltage (height) Large T wave in the opposite direction of the QRS complex No associated P wave PVC comes early and is followed by a compensatory pause PVC s) Page 199 Figure 9-5 Patterns of PVC s Ventricular Bigeminy Page 200 Figure 9-7 Ventricular Trigeminy Page 201 Figure 9-8 Ventricular Quadrageminy Unifocal (PVC s have the same shape) Page 201 Figure 9-9 Ventricular Coupling-unifocalSame shape Page 201 Figure 9-10 Runs of PVC s (VT) Page 202 Figure 9-11 Multifocal PVC s-different shapes Page 202 Figure 9-12 R-on-T Phenomenon the most dangerous type of PVC! Why? Page 203 Figure 9-14 Causes of PVC s Page 203 Common; more frequent with coronary heart disease Increase in automaticity due to: o Stress (increased sympathetic tone) o Stimulants: caffeine, alcohol, nicotine, cocaine o Ischemia, hypoxia o Drugs: digitalis, epinephrine, norepinephrine Premature Ventricular Contractions (Electrolyte disturbances, esp K + and Mg ++ MI, CHF, Cardiomyopathy Valvular disease Insertion of any catheter into the Ventricle Reperfusion dysrhythmia (GOOD news!) Clinical Significance May be a precursor of more serious ventricular dysrhythmias New 7/12 NAM Page 1

2 Clinical Management Page 203 Determined by the patient s clinical presentation and the cause May not require treatment Significant PVC s Requiring Intervention o more than 6 per minute o multifocal o R on T o Pairs or runs of 3 or more Ventricular Escape Beats Page 203 Figure 9-15 Ventricular Tachycardia Monomorphic Page 204 Figure 9-16 Rhythm: Atrial none Ventricular regular Rate: Atrial none Ventricular - >100 (usually ) P waves none ; PR none QRS sec or greater QT not measured Causes of VT Page 206 Same as PVC s plus: Mechanical stimulation of the myocardium by pacer wires, PA catheters, angioplasty or catheterization leads QT prolongation: caused by many anti-arrhythmics, tricyclic antidepressants; may be congenital Treatment of Monomorphic VT Page 206 Stable: drug therapy o Antiarrrythmic most common is Amiodarone Unstable: synchronized cardioversion and post conversion antiarrhythmic Pulseless: Defibrillation, CPR, epinephrine, antiarrhythmic as necessary Amiodarone Page 206 Actions/Indications: Ventricular dysrhythmias o Stable VT o Pulseless VT o V. Fib Adverse Reactions: o Hypotension o Bradycardia o Prolonged QT interval (proarrhythmia) Amiodarone IV Dosing Page 206 Different for different indications!!! Stable VT : 150 mg IV drip (150 mg in 100mL D5W or NS over 10 minutes) followed by maintenance infusion Cardiac arrest: o 300 mg IVP o May re-bolus with 150 mg Torsades de Pointes Polymorphic V. Tach Page 207 A form of polymorphic VT associated with prolonged QT interval Stable: Drug therapy o Correct electrolyte imbalance or underlying factors New 7/12 NAM Page 2

3 o Most commonly treated with Magnesium Unstable: Defibrillate Pulseless: Defibrillate Magnesium Page 207 Action/Indications: o Rx of choice for Torsades de Pointes o Cardiac arrest associated with low magnesium levels o Life-threatening arrhythmias associated with digitalis toxicity Dose: 1-2 Gms diluted in 10 ml D5W IV Adverse Reactions: o Hypotension o Myocardial depression. Ventricular Fibrillation (V-fib)-Life Threatening Arrhythmia! Page 208 Figure 9-21 No Pulse Present! Fine V-fib Check Your Patient! Page 208 Figure 9-22 No Pulse! Ventricular Fibrillation Page Frequently preceded by PVC s, or VT Most common cause of Death in AMI Other causes of V-fib: myocardial ischemia, hypoxia, dig toxicity, electrolyte imbalance, mitral valve prolapse, cardiac trauma, antiarrhythmics, cardiomyopathy May occur during anesthesia, during insertion of intracardiac catheters or following accidental electrocution Death is imminent unless v-fib is recognized and treated immediately! VF/Pulseless VT: Treatment See Fib Defib Rapid ABC assessment Call a Code CPR if defibrillator is not immediately available Defibrillate, ASAP CPR 2 minutes (5 cycles), IV Epinephrine q 3-5 minutes or Vasopressin x1 to replace first or second dose of epinephrine CPR 2 minutes (5 cycles) Defibrillate Antiarrhythmic Give meds during CPR, minimize interruptions in CPR to 10 seconds or less EPINEPHRINE Page 209 Indication: Any Pulseless Rhythm Dose: 1 mg IVP q 3-5 minutes IV/IO Actions: Aids in achieving primary goal of resuscitation: To improve coronary and cerebral blood flow by causing vasoconstriction and increasing perfusion pressure. Vasopressin Page 209 Indications: Any pulseless arrest Action: vasoconstriction it is an alternative to Epinephrine Dose: 40 Units IV/IO, a single, one time only dose to replace the first or second dose of epinephrine New 7/12 NAM Page 3

4 ELECTRICAL THERAPY Energy Requirements for Defibrillation vary with your equipment o Biphasic (usually J) o Monophasic Defibrillators (360J) Synchronized Cardioversion rhythm specific energy selection (patient has a pulse!) Practice Electrical Safety Clear the patient and bed of all personnel prior to shock delivery! Idioventricular Rhythm (IVR) Page 209 Figure 9-23, Box 9-5 Regular (mostly) Rate: < 40 P waves: absent PRI: not measurable QRS: wide > 0.12 sec QT: Normal for Heart Rate Causes: o Associated with significant heart disease o Often a transient, terminal rhythm immediately preceding asystole. Clinical Significance: o Dramatically reduced cardiac output r/t loss of atrial kick, bradycardia and stroke volume that is low due to poor muscle contractility Clinical Management: o This is a pre-arrest rhythm o Initiate bradycardia management o Call a code Accelerated Idioventricular Rhythm(AIVR) Page 210 Figure 9-25 AIVR Page 211 Box 9-6 Rhythm: usually regular Rate: P waves: absent PRI: not measurable QRS: Wide (> 0.12 seconds) QT: Normal for heart rate Causes: o Common after IWMI o Common reperfusion rhythm o Digitalis toxicity Clinical significance: o Loss of atrial kick but usually no significant impact on cardiac output Clinical Management: None Asystole/Ventricular Standstill Page 212 Figure 9-27 and 9-28 Causes: o Terminal rhythm o Metabolic acidosis o Hypoxia, hyperkalemia, hypokalemia, hypothermia o Overdose Clinical Significance: only 1-2% survival Asystole Treatment Page Rapid ABC assessment Check monitor leads; verify in 2 nd lead New 7/12 NAM Page 4

5 Initiate CPR O2, IV, Intubate Look for reversible causes Epinephrine 1 mg every 3-5 minutes or Vasopressin 40 units IV/IO to replace first or second dose of Epinephrine Pulseless Electrical Activity (PEA) Page 213 PEA is the absence of a detectable pulse in the presence of an ECG tracing that would normally produce a pulse. Electrical activity with no Mechanical Response Causes of PEA/Asystole: H s and T s Hypovolemia Hypoxia Hydrogen ion acidosis Hyper/Hypo-kalemia Hypothermia Tamponade, Cardiac Tablets (OD s) Tension pneumothorax Thrombosis, pulmonary Thrombosis, coronary Clinical significance of PEA: No cardiac output, no perfusion, no myocardial oxygen supply If unable to identify and correct underlying cause, resuscitation efforts will be unsuccessful Treatment of PEA Page 213 Rapid ABC assessment CPR IV, Intubate Epinephrine 1 mg every 3-5 minutes or Vasopressin 40 units IV/IO to replace first or second dose of Epinephrine Identify and treat cause Summary: Ventricular beats: o Are not preceded by a p wave o Have a WIDE QRS (> 0.12 sec) o T wave opposite the QRS Ventricular Beats: o Rate < 40 = Idioventricular Rhythm o Rate = Accelerated Idioventricular Rhythm o Rate > 100 = Ventricular tachycardia o Premature = PVC s o Late = Ventricular escape beats Life-threatening Ventricular Rhythms Ventricular Fibrillation Pulseless VTach Asystole PEA (the ECG may be ANY rhythm) New 7/12 NAM Page 5

6 CHECKPOINT!! Complete the following rhythm strip analysis, give interventions where there is a scenario: Page 219 Strip 9-16 Page 220 Strip 9-21 Page 232 Strip 9-57 Page 218 strip 9-14 Mr.Q s monitor alarm goes off. You find him losing consciousness. BP is 70/50. Page 219 Strip 9-16 Page 220 Strip 9-21 Page 232 Strip 9-57 New 7/12 NAM Page 6