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Transcript
Arrhythmias: By Kelle Howard From the notes of : Nancy Jenkins The EKG is the electrical activity of the heart. Electrical precedes mechanical (Without electricity, we have no pump!!) How is electricity generated? By action potentials (view on own) Na, K and Ca very important for this • • • • Na K pump Calcium channels Depolarization Repolarization YouTube - How the Body Works : A Nerve Impulse ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells. 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 -25-30% CO Cardiac Cycle Conduction system- Pacemakers • • • • • SA node -- 60-100 bpm AV node -- 40-60 bpm Bundle of His Left and Right Bundle Branch Purkinge Fibers -- 15-40 bpm • Each beat that is generated from the same pacemaker will look identical. • Impulses from other cardiac cells are called _______ and look different (___________, _________) • Primary and secondary pacemakers EKG graph paper • • • • • Horizontal measures time Vertical measures voltage Helps us determine rate Width of complexes- intervals (_______) Duration of complexes- intervals (_________) EKG graph paper Definitions: PR Interval: time the electrical impulse takes to travel from the sinus node to the AV node where it enters the ventricles. The PR interval is a good estimate of AV node function. QRS Complex: depolarization of the right and left ventricles QT Interval: represents electrical depolarization and repolarization of the left and right ventricles. T Wave: absolutely refractory period ST Segment: represents the period when the ventricles are depolarized. Intervals: PR .12-.20 QRS .04-.12 QT .34-.43 Monitoring leads- based on 12 lead EKG • Each lead is either unipolar or bipolar. • Each lead looks at a different area of the heart. • This can be diagnostic in the case of an MI RNCEU’s We monitor using 3 leads or 5 leads Best for arrhythmiaslead II and MCL(if using 3 leads) or V1 leads- easy to see P waves MCL or V1 easy to see ventricular rhythms. If impulse goes toward positive electrode complex is positively deflected or _____________ If impulse goes away from positive electrode complex is negatively deflected or goes __________ from baseline How to place leads HINTS: White is right clouds over grass (white over green) & smoke over fire (black over red) In 5 lead **V1 is 4th ICS right of sternum – brown or ground (most important) Cardiac cells are either: contractile cells pacemaker cells 4 Characteristics of Cardiac Cells • • • • • Automaticity-_____________ Excitability- ______________ Conductivity- _____________ Contractility- _____________ Refractoriness – relative – absolute Refractory Period Risk Factors for Arrhythmias • • • • • • Hypoxia Structural changes Electrolyte imbalances Central nervous system stimulation Medications Lifestyle behaviors Steps in Assessment of Rhythms • **Calculate rate – Big block- big blocks in R-R divide into 300 – Little block - little blocks in R-R into 1500 – Number of R waves in 6 sec times 10 • • • • Calculate rhythm Measure PR interval QRS interval P to QRS relationship How is the rate controlled? Autonomic Nervous System • Parasympathetic nervous system: – i.e. Vagus nerve • Decreases rate • Slows impulse conduction • Decreases force of ____________ • Sympathetic nervous system: • Increases rate • Increases force of _____________ Rate Calculation 1 lg box= .20 5 lg boxes =1 sec 30 lg boxes =6sec Therefore there are 300 lg boxes in 1 min. Sinus Rhythm • • • • • Normal P wave PR interval <.20 QRS .04-.12 T wave for every complex Rate is regular 60-100 What is common to all arrythmias? • Decreased Cardiac Output – Neuro – Cardiac – Respiratory – GI – Renal – Skin Characteristics for ST include: If rate >100: Sinus Tachycardia Causes-anxiety, hypoxia, shock, pain, caffeine, drugs Treatment-eliminate cause 1. 2. 3. 4. Regular rhythm PR interval less than .20 secs. QRS < .12 Rate greater than 100 • Rate<60: Sinus Bradycardia – (can be relative) – Cause-vagal stimulation, athlete, drugs (Blockers and digoxin), head injuries, MI – Watch for syncope and falls – Treatment- if ____________: atropine or pacer Sinus Arrhythmia (SA) • Rate 60-100 • Irregular rhythm- increases with inspiration, decreases with expiration • P, QRS,T wave normal • Cause- drugs (morphine), MI • Treatment- _________ Sinus Arrest • See pauses • May see ectopic beats (PAC’s PVC’s) do not treat • Cause MI • Treatment – Atropine – Isuprel – Pacemaker Atrial Arrythmias • Atria is the pacemaker • Atrial rate contributes 25-30% of cardiac reserve **Medications used to treat the atrial rhythms • Cardizem and Verapamil – calcium channel blockers • • • • Digoxin Amiodarone or dronedarone- (Multaq) Corvert- (ibutilide) Metropolol and Propanalol – beta blockers Premature Atrial Contraction (PAC’s)ectopic • • • • P wave abnormally shaped PR interval shorter QRS normal Cause-age, MI, CHF, stimulants, dig, electrolyte imbalance, stress, fatigue • Treatment- remove stimulants and watch for SVT (Paroxysmal) Supraventricular Tachycardia (PSVT/SVT) • Rate is 150-300, regular, p often hidden • Atria is pacemaker (may not see p waves) reentrant phenomenon • Cause-SNS stimulation, MI, CHF, sepsis • Treatment- vagal stimulation, * ________, digoxin, verapamil, inderal, cardizem, tikosyn, or ____________ • • • • • • Atrial Flutter Rate of atria is 250-300, vent rate varies Regular rhythm- single focus in RA 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, ALSO: __________, __________, __________ 3:1 flutter Atrial Fibrillation – most common • Rate of atria 350-600- (disorganized rhythm) • Problem arises when: – Ventricular response becomes irregular – (RVR) – rapid ventricular response • No P waves, “garbage baseline” • Cause: #1 arrhythmia in elderly – heart disease- CAD, rheumatic fever, CHF, alcohol • Complications: __________________ • Treatment: – ___________________ – Prevent cerebral embolic events – Convert to SR if possible Treatment Afib • Rate control- – start with digoxin, ca channel blockers, beta blockers, (multaq-too many side effects no longer use) • Convert to SR– amiodorone and ibutilide (corvert), pronestyl, cardioversion (TEE to see if clots before) Coumadin- check PT and INR, ablation and Maze • Prevent embolic events– Coumadin, Pradaxa, Xarelto, Lovenox – (ASA if low risk) Atrial Fibrillation Arrhythmias of AV Node **AV Conduction Blocks- important to check HR and hold blockers First Degree AV Block • • • • • • Transmission through AV node delayed Regular rhythm Rate <100 PR interval >.20 QRS normal and regular Cause-dig toxicity, MI, CAD vagal, and blocker drugs • Treatment- none but watch for further blockage, monitor meds (_____________) Second Degree AV Block more P’s than QRS’s • A. Mobitz I (Wenckebach) YouTube - Diagnosis Wenckebach – PR progressively longer then drops QRS (long, longer, longest, drop) – Cause- MI, drug toxicity, ischemia – 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(QRS usually greater than .12-BBB) – Constant PR interval- can be normal or prolonged – Treatment-Pacemaker – Occurs in HIS bundle with bundle branch block 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 a more serious AV conduction disturbance Second-Degree AV Block, Type 2 (Mobitz II) • Clinical significance – Often progresses to third-degree AV block – Associated with a poor prognosispacemaker – Reduced HR often results in decreased CO with subsequent hypotension and myocardial ischemia 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, and syncope • Treatment- __________, _________ 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) 3rd Degree Bundle Branch Blocks • • • • • Left BBB Right BBB QRS .12 or greater Rabbit ears- RR No change in rhythm Right Bundle Branch Block Junctional Rhythm • AV node is pacemaker- slow rhythm (40-60) but very regular impulse goes to atria from AV node- (backward) • P wave patterns – Absent – P wave precedes QRS inverted in II, III, and AVF – P wave hidden in QRS • P wave follows QRS • PR interval – Absent or hidden – Short <.12 – Negative or RP interval • QRS normal • No treatment . 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, amiodarone, lidocaine, pronestyl Premature Ventricular Contractions • Clinical significance – In normal heart, usually benign – In heart disease, PVCs may decrease 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 _________ ___________ • Apical-radial pulse rate should be assessed to determine if pulse deficit exists Premature Ventricular Contractions • Clinical significance – Represents ventricular irritability – May cause HF, angina, and dec CO – May occur • After lysis of a coronary artery clot with thrombolytic therapy in acute MI— reperfusion dysrhythmias • Following plaque reduction after percutaneous coronary intervention PVC’s 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 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 Lifethreatening, dec. CO, watch for V-fib Treatment– same as for PVC’s – __________ for sustained/pulseless – __________ for wide complex Ventricular Tachycardia • Clinical significance – Treatment for VT must be rapid – May recur if prophylactic treatment is not initiated – Ventricular fibrillation may develop • Sustained VT: Severe decrease in CO Ventricular Tachycardia is worse than Ventricular Fibrillation. 1. True 2. False VT- Torsades de Pointes- polymorphic VT (Magnesium) French for twisting of the points Ventricular Fibrillation • • • • • Garbage baseline-quivering No P’s No QRS’s No CO Cause-MI, CAD, CMP, shock, K+, hypoxia, acidosis, and drugs • Treatment- code situation, ACLS, CPR, **__________- if available no delay Complications of Arrhythmias • • • • • • Hypotension Tissue ischemia Thrombi Heart failure Shock Death Diagnostic Tests • • • • Telemetry- 5 lead( lead II and V1) 12 lead EKG Holter monitor- pt. keeps a diary Event monitoring- pt. records only when having the event • Exercise stress test • Electrophysiology studies- induce arrhythmias under controlled situation Nursing Assessment • • • • • • Apical rate and rhythm Apical/radial deficit Blood pressure Skin Urine output Signs of decreased cardiac output Nursing Diagnoses • • • • • Decreased cardiac output Decreased tissue perfusion Activity intolerance Anxiety and Fear Knowledge deficit Medications • Classified by effect on action potential • Class I- fast Na blocking agents-ventricular – Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol • Class II-beta blockers (esmolol, atenolol, inderal) atrial- SVT,Afib,flutter • Class III- K blocking (amiodorone, tikosyn, sotalol, corvert) both atrial and ventricular • Class IV- Ca, channel blockers (verapamil cardizem)SVT,Afib,flutter • Other- adenosine, dig, atropine, magnesium Medications • Classified by effect on action potential • Class I– fast Na blocking agents-ventricular – Quinidine, Pronestyl, Norpace, ___________, Rhythmol • Class II– beta blockers - atrial- SVT,Afib,flutter – esmolol, ________, _________ • Class III– K+ blocking - both atrial and ventricular – _______, _________, sotalol, corvert • Class IV– Ca, channel blockers - SVT, Afib, A flutter – verapamil, __________ • Other- adenosine, dig, atropine, magnesium Comfort Measures • Rest • O2 • Relieve fear and anxiety Invasive procedures • Defibrillation – Emergency- start at 200 watt/sec, go to 400 – Safety precautions – AED’s • Synchronized Cardioversion- for vent. or SVT – – – – – Can be planned- if stable Get permit Start at ________ watt/sec (depending on wide/narrow) Awake, give O2 and sedation Have to synchronize with rhythm cardioversion • Implanted Cardiac Defibrillator (ICD) – Senses rate and width of QRS – Goes off 3 times, then have to be reset – Combined with pacemaker- overdrive pacing or back up pacing Implantable Cardioverter- Defibrillator (ICD) Fig. 36-22 Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. http://www.vmth.ucdavis.edu/cardio/cases/case14/pacemaker.htm 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 Pacemaker Classification Most pacemakers are 1. Atrial 2. Ventricular 3. Dual Pacemakers Fig. 36-27 Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. Pacemaker Problems: Failure to sense Failure to capture Ablation • Done in special cardiac procedures lab • Use a laser to burn abnormal pathway EKG changes associated with an MI or ACS include: • • • Q waves ST segment elevation or depression T wave inversion 3 ECG Changes Associated with Acute Coronary Syndrome (ACS) • Ischemia – ST segment depression and/or T wave inversion – ST segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line ECG Changes Associated with Acute Coronary Syndrome (ACS) • Injury/Infarction- ST elevation – ST segment elevation is significant if mm above the isoelectric line >1 • If treatment is prompt and effective, may avoid infarction –If serum cardiac markers are present, an ST-segment-elevation myocardial infarction (STEMI) has occurred (code stemi) ECG Changes Associated with Acute Coronary Syndrome (ACS) • Infarction/Necrosis- Q wave – Note: physiologic Q wave is the first negative deflection following the P wave • Small and narrow (<0.04 second in duration) – Pathologic Q wave is deep and >0.03 second in duration ECG Changes Associated with Acute Coronary Syndrome (ACS) FYI only Fig. 36-29 A Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. ECG Changes Associated with Acute Coronary Syndrome (ACS) Fig. 36-29 B Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. ECG Changes Associated with Acute Coronary Syndrome (ACS) Fig. 36-30 Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. 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