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Dysrhythmias EKG DANCE-click here EKG shows electrical activity of the heart. Electrical precedes mechanical (Without electricity…no pump!!) Click here How is the electricity generated? By action potentials (click for animated visuals) Na K pump (animation) Calcium channels Depolarization-contraction RepolarizationThink about this when administering cardiac meds…antidysrhytmics *ECG wave forms- Produced by movement of charged ions across the semipermeable membranes of myocardial cells. Click here- YouTube- How Body Works-A Nerve Impulse Understanding cardiac action potential & meds Electrical system Multimedia Tutorials Each beat that is generated from same pacemaker will look identical. Impulses from other cardiac cells are called “ectopic” (PVC, PAC) This electrical activity produces mechanical activity that is seen as waveforms *Note pattern that occurs with atrial depolarization, repolarization; ventricular depolarization, re-polarization The P wave signifies ventricular activity 1. True 2. False *False- P wave associated with atrial depolarization Cardiac Cycle Intrinsic rates Yellow = isoelectric phase. SA node 60-100 AV node 40-60 Bundle of His; Left and Right Bundle Branch; Purkinge Fibers 15-40 Purple= "P"wave. Purple and yellow split = "PR" interval Red = "Q" wave; Light blue = “R" wave Light green = "S" wave; Black = "ST" segment Orange = "T" wave; Yellow again = isoelectric. Dark blue ="U" wave (seldom seen)* risk for *hypokalemia, med effect, hypercalcemia, . How is rate controlled? Nervous System Control of Heart Parasympathetic nervous system: when? Vagus nerve Dec. rate Slows impulse conduction Dec. force of contraction Sympathetic nervous system: when? Inc. rate Inc. force of contraction Pacemakers other than *SA node •Pacemaker from another site > lead to dysrhythmias; may be discharged in a number of ways. oSecondary pacemakers- may originate from AV node or His-Purkinje system. oSecondary pacemakers can originate when they discharge more rapidly than the normal pacemaker of the SA node. oTriggered beats (early or late) may come from ectopic focus (area outside normal conduction pathway) in atria, AV node, or ventricles. EKG waveforms P wave associated with atrial depolarization (stimulation) QRS complex associated with ventricular depolarization (stimulation) T wave associated with ventricular repolarization (recovery) Atrial recovery wave hidden under QRS wave Stimulus causes atria to contract before ventricles Delay in spread of stimulus to ventricles allows time for ventricles to fill and for atrial kick EKG graph paper Horizontal measures time Vertical measures voltage Helps to determine rate Width of complexes Duration of complexes EKG graph paper Each small square box on the graph paper is equal to: 1. 2. 3. 4. 0.06 sec. 0.08 sec. 0.04 sec. 0.20 sec. If you didn’t know, look at previous slide- 0.04 Cardiac Monitoring- based on 12 lead EKG Each lead has positive, negative and ground electrode. Each lead looks at different area of heart. *Can be diagnostic as in case of an MI RNCEU’s Lead II positive R arm looking to LL neg 3 lead placement: Depolarization wave moving toward a positive lead will be upright. Depolarization wave moving toward a negative lead will inverted. Depolarization wave moving between negative and positive leads will have both upright and inverted components. *Five lead placement allows viewing all leads within limits of monitor Leads to monitor EKG Best- lead II and MCL or V1 leads- lead II easy to see P waves. MCL or V1 easy to view ventricular rhythms. If impulse goes toward positive electrode complex is positively deflected or upright If impulse goes away from positive electrode complex is negatively deflected or goes down form baseline Five lead system- uses all leads shown: three lead system uses only black, white and red leads. Two lead telemetry systems use black and red leads- placement may change depending on what EKG lead (view) is required. Black and white leads are placed on shoulder area; green and red leads placed on lowest rib on both sides of torso, and brown lead (ground) is placed at 4th intercostal space, just to right of sternum. (follow guidelines of facility) Key Characteristics of Cardiac Cells Cardiac cells- either contractile cells influencing pumping action or pacemaker cells influencing electrical activity of heart Automaticity Excitability Conductivity Contractility *Refractoriness Relative Absolute Refractory Period Myocardial cells resistive to stimulation; **dysrhythmias triggered during relative refractory and absolute refractory periods •Absolute refractory period: no depolarization can occur- from Q wave until middle of T wave •Relative refractory period: greater than normal stimulus needed for depolarization (contraction); goes through 2nd half T wave Risk Factors for Dysrhythmia (Arrhythmia) Hypoxia Structural changes Electrolyte imbalances Central nervous system stimulation Medications Lifestyle behaviors Who is/are at Greatest Risk for Dysrhythmia? Patient(s) with 1. COPD 2. MI MI; valvular disease (best two answers3. Valvular disease have high risk for hypoxia (MI) and structural 4. Colon resection chg with valvular) Assessment Calculate rate (know how to do this) Big block Little block Number of R waves in 6 sec times 10 Calculate rhythm-reg or irreg Measure PR interval, <.20 QRS interval .04.12 P to QRS relationship Rate Calculation 1 lg box= .20 5 lg boxes =1 sec 30 lg boxes =6 secs Therefore there are 300 lg boxes in 1 min. Each small box represents 0.04 seconds on horizontal axis and 1 mm or 0.1 millivolt on vertical axis. PR interval-measured from beginning of P wave to beginning of QRS complex; QRS complex -measured from beginning of Q wave to end of S wave; QT interval -measured from beginning of Q wave to end of T wave; and TP interval- measured from end of T wave to beginning of next P wave. If there are 10 small squares between 2 QRS waves, the rate would be: 1. 2. 3. 4. 75 100 150 100 *Rate 150; 1500 / 10 = 150 (see also p. 844 text) Sinus Rhythm Normal P wave PR interval<.20 QRS.04-.12 T wave for every complex Rate is regular 60-100 *Rate >100: Sinus Tachycardia Causes-anxiety, hypoxia, shock, pain, caffeine, drugs Treatment-eliminate cause Sinus Tachycardia Rhythm: Rate: P Waves: PR Interval: QRS Complex: Regular Fast (>/= 100 bpm) “Normal” and upright, one for each QRS “Normal” (0.12-0.20 seconds) “Normal” (0.08-0.12 seconds) •Due to an increase in rate of sinus node discharge. •Common dysrhythmia due to many things as exercise, fever, caffeine, anxiety, smoking, etc. •Treatment : address underlying cause and/or determine if it is even a problem (Medsadenosine, beta blockers). Clinical significance Dizziness and hypotension due to decreased CO Inc. myocardial oxygen consumption may lead to angina Name these rhythms & count rate!! (What you just covered) Sinus Bradycardia- brady heart song Cause-vagal stimulation, athlete, drugs (Beta blockers; digoxin), head injuries, MI Sinus node fires <60 bpm; Normal conduction; rhythm regular; P: QRS: 1:1; PR interval: 0:12 to .20 sec.; QRS complex: 0.04 to 0.12 sec Clinical significance- Dependent on symptoms Hypotension Pale, cool skin Weakness Angina Dizziness or syncope Confusion or disorientation Shortness of breath Treatment- if symptomatic, atropine or pacer Sinus BradycardiaTreatment- if symptomatic, atropine or pacer Patients with bradycardia are likely to display which of these symptoms: 1. 2. 3. 4. Heart rate less than 60 Dizziness Hypertension Confusion 1. 2. 3. 4. Heart rate less than 60 Dizziness Hypertension (all except) Confusion Sinus Dysrhythmias (Arrhythmia) (SA) Rate 60-100 Irregular rhythm- increases with inspiration, decreases with expiration P, QRS,T wave normal Cause- children, drugs (Morphine sulphate), MI Treatment- none Sinus Arrest See pauses May see ectopic beats (PAC’s PVC’s)*don’t treat Cause MI Treatment Atropine Isoproterenol (Isuprel) Pacemaker *synthetic sympathomimetic amine Atrial Dysrhythmias Atria is the pacemaker Atrial rate contributes 25-30% of cardiac reserve Serious in patients with MI- WHY? Medications used to treat the atrial dysrhythmias (if patient symptomatic) Diltiazem (Cardizem) Digoxin (Lanoxin) Amiodarone (Cordarone) Dofetilide (Tikosyn) Verapamil (Calan) ? Atropine Think-rate too slow, too fast?? Premature Atrial Contraction (PAC’s) P wave abnormally shaped PR interval shorter QRS normal Cause-age, MI, CHF, stimulants, dig, electrolyte imbalance Treatment- remove stimulants; watch for SVT, depends upon cause Supraventricular Tachycardia (SVT)/PSVT (paroxysmal SVT) Rate- 150-250 (Very fast!) Atria is pacemaker (may not see p waves) Cause-SNS stimulation, MI, CHF,sepsis SVT/Paroxysmal Supraventricular Tachycardia (PSVT) Clinical significance Prolonged episode and HR >180 bpm may precipitate ↓ CO Palpitations Hypotension Dyspnea Angina •Treatment•Meds: adenosine, digoxin, diltiazem (Cardizem) or verapamil (calcium channel blockers), propranolol (inderal), dofetilide (Tikosyn) •Vagal stimulation Atrial Flutter Rate of atria is 250-300, vent rate varies Regular rhythm P waves saw tooth, ratio 2:1, 3:1, 4:1 Flutter waves- No PR interval Cause-diseased heart, dig Treatment- cardioversion, calcium channel blockers and beta blockers, amiodorone, ablation, warfarin (Coumadin) 3:1 flutter Atrial Flutter Clinical significance High ventricular rates (>100) and loss of the atrial “kick” can decrease CO and precipitate HF, angina Risk for stroke due to risk of thrombus formation in the atria Atrial Fibrillation-**most common Rate of atria 350-600- (disorganized rhythm) Ventricular response irregular No P waves, “garbage baseline” Cause-#1 arrhythmia in elderly, heart disease- CAD, rheumatic, CHF, alcohol Complications- dec. CO and thrombi (stroke) Treatment- *convert if possible); digoxin, calcium channel blockers, beta blockers, amiodorone, pronestyl, cardioversion (TEE ck for thrombus) warfarin - ck PT and INR, *ablation, Maze procedure (involves open heart) or Mini Maze *Thrombus formation, pulse deficit, AR>RR Atrial Fibrillation Atrial Fib YouTube Can result in decrease in CO due to ineffective atrial contractions (loss of atrial kick) and rapid ventricular response Thrombi may form in the atria as a result of blood stasis Embolus may develop and travel to the brain, causing a stroke *Thrombus formation, pulse deficit Dysrhythmias- AV Node AV Conduction Blocks Junctional Rhythm AV node is pacemaker- slow rhythm (40-60) but very regular impulse goes to atria from AV nodebackward) P wave patterns Absent or hidden Short < .0.12 or negative or RP interval P wave precedes QRS inverted in II, III, and AVF P wave hidden in QRS P wave follows QRS QRS normal Often no treatment . First Degree AV Block Transmission through AV node delayed PR interval >0.20 QRS normal and regular Cause-dig toxicity, MI, CAD, vagal, and blocker drugs Treatment- none but watch for further blockage Characteristics of 1st degree block include: 1. Regular rhythm 2. Long PR interval 3. More P’s than QRS’s 4. Rate less than 100 1. 2. 3. 4. Regular rhythm Long PR interval More P’s than QRS’s Rate less than 100 Second Degree AV Block more P’s than QRS’s A. Mobitz I (Wenckebach) YouTube - Diagnosis Wenckebach PR progressively longer then drops QRS Cause- MI, drug toxicity Treatment- watch for type II and 3rd degree B. Mobitz II More P’s but skips QRS in regular pattern 2:1,3:1, 4:1 Constant PR interval Treatment-Pacemaker Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) Clinical significance Usually a result of myocardial ischemia or infarction Almost always transient and well tolerated May be a warning signal of more serious AV conduction disturbance Second-Degree AV Block, Type 2 (Mobitz II) Clinical significance Often progresses to third-degree AV block and is associated with poor prognosis Reduced HR often results in dec. CO with subsequent hypotension and myocardial ischemia Mobitz type 1 or Wenchebach has a constant PR interval. 1. True 2. False Answer: False-Mobitz I (Wenckebach)PR progressively longer then drops QRS 3rd Degree AV Block Atria and ventricles beat independently Atrial rate- 60-100 Slow ventricular rate 20-40 No PR interval Wide or normal QRS (depends on where block is) Cause- severe heart disease, blockers elderly, MI Complications- dec. CO, ischemia, HF, shock, syncope Treatment- atropine, pacemaker Third-Degree AV Heart Block (Complete Heart Block) Clinical significance Decreased CO with subsequent ischemia, HF, and shock Syncope may result from severe bradycardia or even periods of asystole (patient may present with history of fall) Bundle Branch Blocks *not in text- understand concept Left BBB Right BBB QRS.12 or greater Rabbit ears- RR’ No change in rhythm Normal bundle conduction Right Bundle Branch Block Ventricular Arrythmias Most serious Easy to recognize Premature Ventricular Contractions (PVC’s)-ectopic QRS wide and bizarre No P waves T opposite deflection of PVC Cause- 90% with MI, stimulants, dig, electrolyte imbalance Treatment- O2, lidocaine, procainamide (Pronestyl), *amiodarone, *abalation No longer prophylactic Premature Ventricular Contractions Clinical significance In normal heart, usually benign In heart disease, PVCs may dec. CO and precipitate angina and HF **Patient’s response to PVCs must be monitored PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse **Apical-radial pulse rate- assess to determine if pulse deficit exists Premature Ventricular Contractions Clinical significance **Ventricular irritability > Ventricular Fibrillation . May occur After lysis of coronary artery clot with thrombolytic therapy in acute MI— reperfusion dysrhythmias Following plaque reduction after percutaneous coronary intervention PVC’s-unifocal PVC’s multi-focal Multifocal- from more than one foci Bigeminy- every other beat is a PVC trigeminy- every third beat is a PVC Couplet- 2 PVC’s in a row Treat if: >5 PVC’s a minute Runs of PVC’s Multi focal PVC’s “R on T” What is this? Ventricular Tachycardia (VT) Ventricular rate 150-250, regular or irregular No P waves QRS>.12 Can be stable- pulse or unstable –no pulse Cause- electrolyte imbalance, MI, CAD, dig Life- threatening, dec. CO, watch for V-fib Treatment- same as for PVC’s and defibrillate for sustained (if not responsive) Ventricular Tachycardia Clinical significance VT can be stable (patient has a pulse) or unstable (patient is pulseless) Sustained VT: Severe decrease in CO • Hypotension • Pulmonary edema • Decreased cerebral blood flow • Cardiopulmonary arrest Ventricular Tachycardia Clinical significance Treatment for VT must be rapid May recur if prophylactic treatment is not initiated Ventricular fibrillation may develop Polymorphic Ventricular Tachycardia- Torsades de Pointes” (“twisting around a point”) Rhythm: Rate: P Waves: PR Interval: QRS Complexes: Well…irregular…but… 100-250 bpm Usually not seen (buried in QRS if they exist) None Wide, distorted, bizarre, and “rhythmic” – getting smaller, then larger, then smaller, then… AKA: “Torsades de Pointes” (“twisting around a point”) Usually caused by hypo/hyperkalemia, HYPOMAGNESEMIA, TCA OD, and some antidysrhythmic medications. Treatment - includes treating cause(s), medications, and defibrillation or cardioversion. VT- Torsades de Pointes French for twisting of the points Ventricular Fibrillation Garbage baseline-quivering No P’s No QRS’s No CO Cause-MI, CAD, CMP, shock, altered K+, hypoxia, acidosis, and drugs Treatment- code situation, ACLS, CPR, **defibrillate *cannot cardiovert…no rhythm to cardiovert Complications of Arrhythmias Hypotension Tissue ischemia Thrombi- low dose heparin, or ASA Heart failure Shock Death Diagnostic Tests Telemetry- 5 lead (lead II and V1) 12 lead EKG Holter or event monitoring Exercise stress test Electrophysiology studies- induce arrhythmias under controlled situation EKG changes in an acute MI Not linked…but watch EKG changes in evolving MI Nursing Assessment Apical rate and rhythm Apical/radial deficit Blood pressure Skin Urine output Signs of dec. cardiac output Nursing Diagnoses Dec. cardiac output Dec. tissue perfusion Activity intolerance Anxiety and Fear Knowledge deficit Goals- Medications Classified by effect on action potential Class I- fast Na blocking agents-ventricular Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol Class II- beta blockers (esmolol, inderal) SVT, Atrial fibrillation, Atrial flutter Class III- K blocking (sotalol, amiodorone)both atrial and ventricular Class IV- Calcium channel blockers (verapamil, diltiazem(cardiazem) for SVT, Afib, atrial flutter Other- adenosine, dig, atropine, magnesium (correct electrolytes) Antiarrhythmics Remembering that of all anti-arrhythmics “Some Block Potassium Channels" can help you: Class I "Some" = S = Sodium Class II "Block" = B =Beta blockers Class III "Potassium" = Potassium channel blockers Class IV "Channels" = C =Calcium channel blockers Comfort Measures Rest- dec. cardiac demands; careful monitoring!! O2 IV access; Select appropriate therapy Relieve fear and anxiety- Diazepam (valium) Invasive procedures Defibrillation Emergency- start at 200 watt/sec, go to 400 Safety precautions AED’s now Synchronized Cardioversion- ventricular tachycardia or SVT or a- fib, flutter to convert Usually planned Get permit Start at 50 watt/sec Awake, give O2 and sedation Have to synchronize with rhythm http://www.dearnurses.net/ cardioversion To defibrillate a rhythm, it needs to be synchronized to the QRS? True or False? False! No QRS to synchronize with!! Implanted Cardiac Defibrillator (AICD) Senses rate and width of QRS Goes off 3 times, then have to be reset Some combined with pacemaker Pacemaker Permanent- battery under skin Temporary- battery outside body Types Transvenous Epicardial- bypass surgery Transcutaneous- emergency Modes Asynchronous- at preset time without fail Synchronous or demand- when HR goes below set rate Review classifications- (Wikipedia) Pacemaker resources View Pacemaker insertion Pacemakers Transcutaneous - emergency Fig. 36-27 Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc Pacemaker Problems: •Failure to sense •Failure to capture Ablation View video Done in special cardiac procedures lab Use a laser to burn abnormal pathway EKG CHANGES ASSOCIATED WITH ACUTE CORONARY SYNDROME 12-lead ECG - primary diagnostic tool used to evaluate patients presenting with ACS. Definitive ECG changes occur in response to ischemia, injury, or infarction of myocardial cells; seen in leads that face area of involvement. Typical ECG changes seen in myocardial ischemia include STsegment depression and/or T wave inversion. Typical ECG change seen during myocardial injury is STsegment elevation. ST-segment elevation and a pathologic Q wave may be seen on ECG with myocardial infarction. 3 ECG Changes Associated with Acute Coronary Syndrome (ACS)> STEMI Ischemia ST segment depression and/or T wave inversion ST segment depression- significant if at least 1 mm (one small box) below isoelectric line Injury/Infarction ST segment elevation is significant if >1 mm above isoelectric line If treatment is prompt & effective, may avoid infarction • If serum cardiac markers present, an ST-segment-elevation myocardial infarction (STEMI) has occurred Infarction/Necrosis Note: physiologic Q wave is first negative deflection following P wave Small and narrow (<0.04 second in duration) *Pathologic Q wave- deep and >0.03 second in duration EKG changes in an acute MI ECG Changes Associated with Acute Coronary Syndrome (ACS) Typical EKG changes associated with an MI include: 1. 2. 3. 4. Long PR interval Q waves ST segment elevation T wave inversion 1. 2. 3. 4. Long PR interval Q waves (Pathological) ST segment elevation T wave inversion Syncope Brief lapse in consciousness CausesVasovagal Cardiac dysrhythmias Other- hypoglycemia, seizure, hypertrophic cardiomyopathy 1-year mortality rate as high as 30% for syncope from cardiovascular cause QuizzesDiscussionQuestions Casestudies Practice! Prioritization Question A client with atrial fibrillation is ambulating in the hall on the coronary step-down unit and suddenly tells you, “I feel really dizzy.” which action should you take first? A. Help the client sit down. B. Check the client’s apical pulse C. Take the client’s blood pressure D. Have the client breathe deeply Prioritization Question A client with atrial fibrillation is ambulating in the hall on the coronary step-down unit and suddenly tells you, “I feel really dizzy.” which action should you take first? A. Help the client sit down. B. Check the client’s apical pulse C. Take the client’s blood pressure D. Have the client breathe deeply Prioritization question Cardiac rhythms are being observed for clients in the CCU. Which client needs immediate intervention? A client: A. admitted with heart failure who has atrial fibrillation with a rate of 88 while at rest. B. with a newly implanted demand ventricular pacemaker, who has occasional periods of sinus rhythm, rate 90-100. C. who has just arrived on the unit with an acute MI and has sinus rhythm, rate 76, with frequent PVC’s. D. who recently started taking atenolol (Tenormin)) and has a first-degree heart block rate 58. Prioritization question Cardiac rhythms are being observed for clients in the CCU. Which client needs immediate intervention? A client: A. admitted with heart failure who has atrial fibrillation with a rate of 88 while at rest. B. with a newly implanted demand ventricular pacemaker, who has occasional periods of sinus rhythm, rate 90-100. C. who has just arrived on the unit with an acute MI and has sinus rhythm, rate 76, with frequent PVC’s. D. who recently started taking atenolol (Tenormin)) and has a first-degree heart block rate 58. Prioritization question A diagnosis of ventricular fibrillation is identified for an unresponsive 50 year old client who has just arrived in the ED. Which action should be taken first? A. Defibrillate at 200 joules B. Begin CPR C. Administer epinephrine 1 mg IV D. Intubate and manually ventilate. Prioritization questions A diagnosis of ventricular fibrillation is identified for an unresponsive 50 year old client who has just arrived in the ED. Which action should be taken first? A. Defibrillate at 200 joules B. Begin CPR C. Administer epinephrine 1 mg IV D. Intubate and manually ventilate.