ECG Interpretation Part 2 Carolyn M. Malone RN,MSN,FNP-C

Review of Rhythms

Atrial Arrhythmia Premature atria contraction or PAC impulse occurs earlier than predicted in the cycle causing the p-wave to look different. Usually does not require any treatment unless the patient is symptomatic

Atrial Flutter Characterized by classis saw-toothed waves instead of classis p-wave. If there is a rapid ventricular response this rhythm is grouped as Narrow Complex Tachycardia.

Atrial Fibrillation

Atrial Fibrillation

Narrow Complex Tachycardia Treatment This term is assigned to tachyarrhythmias with a narrow QRS typically seen with atrial fibrillation or atrial flutter with rapid ventricular responses or A-Fir RVR Assess ABC’S → apply oxygen →place patient on monitor → obtain blood pressure and oximetry → obtain IV access Is the QRS narrow (0.12 seconds)?

Narrow Complex Tachycardia Treatment Is the rhythm regular? If yes attempt vagal maneuvers → administer Adenosine (Adenocard) 6mg rapid IV push prefer IV site at a/c level If not effective may repeat at 12 mg IV rapid push. Adenosine slows conduction time through the AV node and reentrant pathways restoring NSR. If the rhythm does convert continue to monitor the patient. If it does not convert consider other medications.

Narrow Complex Tachycardia Treatment Diltiazem (Cardizem) inhibits calcium from entering the slow channels during depolarization producing a relaxation of vascular smooth muscle and coronary vasodilatation and increases myocardial oxygen delivery in patients with vasospastic angina. Dose is typically 0.25mg/kg typically 20mg bolus over 2 minutes may repeat at 0.35mg/kg, usually 25mg bolus. If patient rhythm is not resolve pt will require drip typically at 5-10mg/hr

Narrow Complex Tachycardia Treatment Verapamil (Calan) Inhibits calcium from entering the slow channels during depolarization, produces relaxation of coronary smooth muscle and coronary vasodilation, increases myocardial oxygen delivery, slows automaticity and conduction of AV node. Dose 2.5-5mg SIVP over 2 minutes second dose at 5-10 mg 15-30 minutes after the first dose.

Narrow Complex Tachycardia Treatment Betablockers Esmolol (Brevibloc). Competitively blocks response to β1 adrenergic stimulation with little or no effect on β2 receptors except at high doses. Dose is 500mcg/kg/min loading dose followed by a 50mcg/kg/min for 4 minutes and continue to increase at 50mcg/kg/min to achieve rate control.

Intro to AV Blocks It is the AV Node that is diseased in atrioventricular blocks. The SA node usually functions normally. Since the SA node is not affected in AV blocks, the P waves occur at regular rhythm.

AV Blocks Since the PR interval reflects the impulse traveling through the AV node this measurement is one of the criteria used to determine the type of AV block that is present. A prolonged PR interval signifies first-degree AV block.

AV Blocks There are three levels of AV block: first-degree, second-degree, and third-degree AV Block. The number and pattern of impulses conducted through the AV node determines the presence and degree of AV block.

First-Degree AV Block

First-Degree AV Block In first-degree AV Block, there is a 1:1 ratio between P waves and QRS complexes. All of the impulses are conducted to the ventricles, but are delayed in the AV node. The delay results in a prolonged PR interval. The occurrence of first-degree AV block will be noted in addition to your interpretation of the patient’s basic rhythm. There is no tx.

ECG Criteria: First-Degree AV Block P waves: similar, 1:1 with QRS Rhythm: Atrial – regular Ventricular - regular Rate: Usually 60-100/minute PR: greater than 0.20 second (prolonged) QRS: 0.04-0.10 second (normal) QT: 0.32-0.44 second (normal)

First Degree AV Block

Possible Causes of First-Degree AV Block Conduction system disease Digitalis administration Antiarrhythmics, such as quinidine and Amiodarone Acute MI

Treatment First-Degree AV Block Treat underlying cause O2, Atropine for symptomatic bradycardia

Second Degree AV Block There are 2 type of second-degree AV block: Mobitz I (also called Type I or Wenckebach) Mobitz II (also called Type II) The PR interval abnormality differentiate the two rhythms. Mobitz II is a more serious dysrhythmia because the causes more often result in permanent changes. Mobitz II is also more likely to develop into complete or third-degree AV block.

Second-Degree AV Block Mobitz I (Wenkebach)

Second Degree AV Block Mobitz I

Mobitz I - Wenckebach With Mobitz I, the PR interval gradually lengthens until an impulse is not conducted. You will see a P wave without a corresponding QRS complex. The R-to-R shortens until a QRS is dropped. It is as though the AV node is warning that soon an impulse won’t get through. The P wave may be buried in another wave.

ECG Criteria Mobitz Type I Second Degree AV Block P waves: similar – more P waves than QRS’s Rhythm: Atrial – regular Ventricular - irregular Rate: Atrial: usually 60-100/minute Ventricular – depends on the number of blocked impulses; will be less than atrial PR: gradually increases until there is a P wave with no QRS; it is a cyclic pattern. QRS: 0.04-0.10 second (normal) QT: 0.32-0.44 second (normal)

Second-Degree AV Block Type I

Possible Causes for Mobitz I Increased vagal stimulation (such as vomiting or straining) Post myocardial infarction (usually inferior wall of left ventricle) Medications (such as digitalis, beta-blockers, Quinidine, Procainamide)

Treatment - Mobitz Type I No treatment is usually needed for Mobitz I as the rhythm is well-tolerated. Assess ABC’S apply oxygen, place the patient on the monitor and oximetry, establish IV access obtain blood pressure monitor for s&s of instability i.e chest pain, SOB, hypotension, chest pain, signs of shock, continue to monitor AV block, such as Mobitz II or third degree.

Second-Degree AV Block Mobitz Type II

Second-Degree AV Block Mobitz II With Mobitz II, the PR interval is constant, but some impulses are not conducted. There are P waves without QRS complexes. Unlike Mobitz I there is no warning that some of the impulses will be blocked.

ECG Criteria: Mobitz II Second-Degree AV Block P waves: similar, more P waves that QRS Rhythm: Atrial – regular Ventricular - irregular Rate: Atrial – usually 60-100/minute Ventricular – depends on the number of blocked impulses; will be less that atrial rate PR: constant for conducted beats QRS: may be normal but often > 0.10 second QT: 0.32-0.44 second (normal)

Second-Degree AV Block Type II

Possible Causes for Mobitz II Acute Myocardial Infarction – usually anterior wall of left ventricle Hypoxia Chronic hypertension Ischemic heart failure Symptoms depend on frequency of dropped beats/ventricular rate The causes of Mobitz II are likely due to irreversible damage to the conduction system

Treatment The physician should be notified as soon as possible when this rhythm develops. Mobitz II is often associated with a poor prognosis since development of complete AV block should be anticipated. A temporary pacemaker may be inserted prophylactically/permanently Assess ABC’S provide oxygen, place on monitor establish rhythm obtain blood pressure, oximetry, obtain IV access Atropine dose is 0.5mg may be repeated up to a total of 3mg prepare to transcutaneous pace Epinephrine 2-10mcg/min Dopamine 2-10mcg/kg/min vasoactive drips

Third Degree AV Block

Third-Degree AV Block Complete (or third-degree) AV block indicated absence of conduction between the atria and ventricles. The block can be in the AV node or in the bundle of His. The atria are paced by the SA Node and an independent pacemaker generates impulses for the ventricles. Thus, the atrial and ventricular contractions are not synchronized.

Third degree AV Block The ECG rhythm is characterized by separate, but regular, atrial and ventricular rhythms and rates. Because of the different rates and because there are two separate pacemakers, there is no correlation between the P waves and the QRS complexes. As a results, there is no true PR interval.

ECG Criteria: Third-Degree AV Block P waves: similar – more P waves than QRS’s Rhythm: Atrial – regular Ventricular - regular Rate: Atrial – usually 60-100/min Ventricular – usually less than 40/min; it can be up to 60/min if the block is high in the AV node PR: varies – no true PR interval since atria and ventricles conducting independently QRS: Greater than 0.10 second QT: may be normal or prolonged

Third-Degree AV Block

Possible Causes for Third-Degree AV Block Extensive myocardial infarction (usually anterior wall of the left ventricle) Acidosis Hypoxia Hyperkalemia Digitalis toxicity Extensive ventricular conduction system disease

Treatment – Third-Degree Block The MD should be notified immediately when third-degree heart block develops. The patient may not tolerate a sudden decrease in cardiac output associated with the slow rate. Because the independent ventricular pacemaker may be unreliable and may result in periods of asystole, third-degree heart block may become a lethal dysrhythmias. A temporary transcutaneous or transvenous pacemaker is usually inserted. A permanent cardiac pacemaker is often necessary.

Treatment – Third-Degree Block Assess ABC’S → administer oxygen → obtain blood pressure, place on ECG monitor oximetry → establish IV access → assess perfusion status i.e. chest pain, mental status, hypotension, signs of shock → prepare for transcutaneous pacing → consider Atropine at 0.5mg IV may repeat for a total dose of 3mg → consider Epinephrine drip at 2-10mcg/min or Dopamine 2-10mcg/kg/min while waiting for pacer or if pacing is ineffective.

Complete HB with Pacer

Modes of Pacing 34-24 Synchronous (demand) pacing 1. Temporary pacing most common 2. Pacemaker's sensitivity set to client's beats 3. If intrinsic rate is  rate set, the pacemaker is inhibited from firing 4. If intrinsic rate is  rate set, pacemaker fires to stimulate depolarization Asynchronous (fixed rate) 1. Used for asystole or profound bradycardia 2. Fires at a fixed rate regardless of client's intrinsic rhythm 3. Complications: pacemaker competition, R-on-T phenomenon

Noninvasive Temporary Pacing (NTP) 34-25 Noninvasive Temporary Pacing (NTP) Two large patch electrodes attached to an external pulse generator Electrical pulses transmitted transcutaneously to stimulate depolarization Used as an emergency measure or prophylactically Complications: discomfort from cutaneous/muscle stimulation, skin irritation and diaphoresis from patches Loss of capture Inappropriate pacing

Figure 34-20A Equipment and electrode placement for external pacing

Figure 34-20B Equipment and electrode placement for external pacing

Invasive Temporary Pacing 34-26 Invasive Temporary Pacing Transvenous pacing Epicardial pacing Complications: 1. Infection/hematoma 2. Ectopic complexes 3. Loss of capture 4. Under-sensing/pacemaker competition/over-sensing 5. Electromagnetic interference 6. Stimulation of chest wall or diaphragm

Figure 34-22A Permanent dual-chamber pacemaker

Figure 34-22B Implanted permanent dual-chamber pacemaker with leads

Figure 34-21 Pacemaker catheter electrode placement/corresponding ECG patterns

Figure 34-19 Modes of pacing

Figure 34-17 AV Blocks: NSR with first-degree AV block (A), second-degree AV block, Type I (B), and second-degree AV block, Type II (C)

Figure 34-18 AV Blocks: third-degree block with regular rates 44 bpm (A), third-degree block with regular rates 38 bpm (B), and NSR with bundle branch block

Asystole Asystole, a lethal dysrhythmia, is characterized by the absence of any ventricular activity. It is also called straight line.

Ventricular standstill In rare instances, there may be P waves. In this case, the rhythm is called ventricular standstill.

Possible Causes of Asystole Severe hemorrhage Air Embolism Heart failure Myocardial Infarction Electrical shock Severe acidosis Ventricular dysrhythmia Cocaine overdose

Treatment Asystole is lethal if not treated immediately often it is lethal even when treated accurately and aggressively. Treatment consisted of initiation of CPR and the cardiac arrest protocols. Assess ABC’S initiate CPR hard and fast assess if shockable rhythm if not resume CPR for 5 cycles administer epinephrine 1mg 10:10,000 q3-5 minutes after or during CPR cycles and consider Atropine 1mg may repeat q3-5 minutes for a total of 3mg. Consider reversible causes 6H’s and 5 T’s

Pulse Electrical Activity (PEA) Formerly termed EMD, or electrical mechanical dissociation, is the term used to describe electrical activity without mechanical contraction. Always assess the patient for a pulse. There may be electrical activity, but if there is no myocardial contraction there will be no pulse, no cardiac output, and no blood pressure.

Treatment – search for underlying causes 6 H’s Hypovolemia Hypoxia Hydrogen Ion (acidosis) Hyper-hypokalemia Hypoglycemia Hypothermia 5 T’s Toxins Tamponade (cardiac) Tension Pneumothorax Thrombosis (coronary and pulmonary) Trauma

Ventricular Dysrhythmias PVC’s can occur with a specific pattern. Characterized as a wide QRS that occurs early in the cycle followed by a compensatory pause. Identify the underlying rhythm, often NSR

Ventricular Dysrhythmias Bigeminy rhythm is characterized as a normal complex followed by a premature beat. Every other beat is a PVC . Identify if the PVC is the same shape, if different it is termed multifocal PVC. Multifocal PVC’s are potentially more lethal than unifocal more irritable sites in the myocardium

Ventricular Dysrhythmias Multifocal PVC occurring with significant frequency. Assess for ABC’S provide oxygen, obtain v/s, I/V access 12 lead EKG place the defibrillator pads on the patient be prepared to act emergently Code CART

Ventricular Dysrhythmias

Ventricular Dysrhythmias Patterned PCV’s are typically characterized by normal followed with abnormal complex. Pulse is irregular, pt can be symptomatic and unstable assess ABC’s oxygen, 12 lead EKG IV access, v/s oximetry, defibrillation pads in place, code cart at bedside

Ventricular Dysrhythmias Trigeminy every third complex is an abnormal complex. These rhythms have the potential to deteriorate into v-tach or v-fib. The more PVC’s that are present the more irritable foci is present.

Ventricular Tachycardia

Ventricular Tachycardia

Ventricular Tachycardia Ventricular Tachycardia characterized by wide QRS complex with the absence of atrial depolarization. Major problem is there is poor cardiac output and hypoperfusion is a concern along with cellular hypoxia to major organs. Assess ABCD’S check for the presence of a pulse. If pulse is absent it is treated the same as ventricular fibrillation. D represents defibrillation not disability

V-Tach Treatment Assess and support ABC’s → give oxygen place on monitor identify rhythm →establish IV access → Is patient stable or unstable? (unstable s&s are chest pain, SOB, hypotension, altered mental status → Unstable patients require immediate Synchronized cardioversion. Provide sedation if the patient is awake Energy selection if monophasic use 100-200J in biphasic wave form use 50-100J

V-Tach Treatment Continued Stable v-tach assess for ABC’S → give oxygen → assess for the presence of pulses → obtain blood pressure → place on monitor identify the rhythm → establish IV access → obtain 12 lead EKG Goal of therapy is to suppress this lethal arrhythmia since it has a high propensity to deteriorate to v-fib and cardiac output is compromise

V-Tach Treatment Continued Goal standard of management is the use of Amiodarone (Cordarone)150 mg IV over 10minutes mixed in 100 ml of D5W. Repeat as needed for a max of 2.2 g/24 hours. Once the rhythm is arrested place the patient on an Amiodarone drip typically at 1mg/min drip. Amiodarone affects Na+, K+ and Ca+ channels. Decreases AV node and Sinus node conduction additionally it has alpha & β adrenergic blocking properties.

Ventricular Fibrillation

Ventricular Fibrillation V-fib characterized by chaotic electrical activity. Absent of coordinated pumping action of the ventricles, each cell is depolarizing independently

V-Fib Continued Goal of treatment is to arrest this rhythm. There is no pulse activity, this is termed Pulseless Arrest. Initiate BLS until an AED is available continue with chest compressions until the AED is in place. Stop chest compressions to allow the AED to analyze the rhythm. Follow the voice prompt and shock the patient when advised by the monitor.

V-Fib Continued Initial energy selection for biphasic monitors is 120J to 200J if monophasic start at 360J → resume CPR immediately for 5 cycles (or 2 minutes). Pump hard and fast to achieve a rate of 100 beats/min → give one shock at 120 to 200J if monophasic 360J → resume CPR immediately after the shock → establish IV or IO access administer Epinephrine 1mg or 1:10,000 concentration and repeat every 3-5 minutes → give 5 cycles of CPR → shock at 120 to 200 J or 360J → resume CPR for 5 cycles

V-Fib Continued Consider antiarrhythmics give during CPR or before or after shock give Amiodarone 300mg IVP → resume CPR for 5 cycles → check rhythm if shockable shock at 120-200J or 360J for monophasic monitors → resume CPR for 5 cycles administer Epinephrine 1mg 1:10,000 IVP q 3-5 minutes and repeat Amiodarone 150mg IV/IO over 3-5 minutes or Lidocaine at 1-1.5mg/kg dose for the first dose then 0.5mg-0.75mg/kg IV/IO maximum of 3 doses or 3mg/kg

V-Fib Continued After 5 cycles check rhythm is it shockable? Shock with 120-200J or 360J for monophasic monitor → resume CPR for 5 cycles consider Magnesium loading dose of 1-2g diluted in 10ml of D5W IV/IO over 5-20 minutes for torsades de pointes assess the rhythm and continue the cycle of CPR for 5 cycles or 2 minutes → shock → CPR and medication → shock etc.