Basic Arrhythmia Review L E AV I T T, 2 0 2 0 Coronary circulation (plumbing) (epicardial arteries, detail) Systole & Diastole Mechanical contraction occurs with electrical depolarization Systole: contraction=ejection of blood ◦ Atrial systole: contraction of atria ◦ Ventricular systole: contraction of ventricles The word SYSTOLE usually refers to VENTRICULAR SYSTOLE or CONTRACTION Diastole: relaxation= ventricles fill with blood SA Node Bundle of pacemaker cells located in the upper right atrium Discharges impulses at rate of 60-100/minute Dominant pacemaker of the heart Most automaticity (ability to generate its own impulses) AV Node & Bundle of His Located in lower right atrium, near septum 2 Functions ◦ Slows impulse conduction from atria to ventricles (gatekeeper) ◦ Back-up pacemaker of heart, if SA node fails Discharges impulses at rate of 40-60/minute The AV Node and Bundle of His together are known as the A-V Junction & Bundle of His Bundle Branches & Purkinje Fibers At Bundle of His, conduction pathways split into the right and left bundle branches to conduct to each ventricle. Bundle branches end in tiny conduction network called Purkinje Fibers Ventricles can be a back-up pacemaker at rate of 2040/minute Purkinje Fibe Purkinje Fibers Note that the general direction of the flow of electrical impulses is from the right arm towards the left foot Eintoven’s Triangle & waveforms Electrical current moving toward a positive electrode will result in a positive deflection Electrical current moving toward a negative electrode will result in a negative deflection Biphasic deflections are both positive and negative • Vertical axis = voltage • One small box is 0.1 mV & 1mm. • Elevation or depression is measured in millimeters EKG graph paper • Horizontal axis = time • One small box is .04 seconds • One large box is .20 seconds • Tic marks on EKG paper occur every 3 seconds The cardiac cycle waveform One complete heartbeat KNOWLEDGE CHECK Electrical impulses moving toward a positive electrode will have a ________ deflection. a. Negative b. Positive c. Biphasic d. Neutral P wave: atrial depolarization QRS complex: ventricular depolarization T wave: ventricular repolarization P wave: atrial depolarization • Starts in SA node and travels through atrium to AV node • Smooth, round and positive deflection in lead II • PR interval is the time of atrial depolarization to ventricular depolarization • .12-.20 seconds (3-5 small boxes) QRS complex: ventricular depolarization • Large wave because it is passing through large ventricular muscle • May have up to 3 deflections • Q wave: negative wave before R wave • R wave: 1st positive deflection • S wave: negative wave after R wave • QRS may not have all components • .06-.10 seconds (1½ - 2½ small boxes) ST segment: early ventricular repolarization • Line btwn end of QRS and beginning of T wave. Look for change in slope. • May be elevated or depressed • J point: place where QRS meets ST and the place we look for ST elevation or depression T wave: ventricular repolarization • Begins at change in slope after ST segment • Ends when wave returns to baseline • Don’t measure T wave, but can measure Q-T interval for some medication effects • Peaked in hyper K+ and hypo Mg++ K+ and Mg++ are monitored closely after cardiac surgery U Wave: Prolonged repolarization Sometimes noted in hypokalemia How to analyze a strip 5 steps to rhythm analysis 1. Determine regularity? ◦ Measure R wave to R wave 2. Calculate the rate? 3. Examine P waves? ◦ P wave for each QRS? ◦ How is the morphology of the P wave? 4. Measure the PR interval ◦ .12-.20 seconds (3-5 small boxes) 5. Measure the QRS interval ◦ .06-.10 seconds (1.5-2.5 small boxes) Then you can name the UNDERLYING rhythm and any abnormalities Determine regularity Using calipers or paper, look at the distance between each complex. (between R waves or any other constant point on the cardiac cycle) What is the rate? Methods to determine rate First method: Rapid rate calculation: Count the number of R waves in a 6-second strip and multiply by 10 (Example 6 sec X10 =60 HR per Minute) ◦ ◦ ◦ ◦ Approx HR in beats per minute, is fast and simple Can be used for both regular and irregular rhythms Each 3 sec equals 15 boxes of.20 sec Each small box is .04 in the EKG paper Look at the P waves One P wave for every QRS? Are they upright? Are they the same size and shape? SHAPE = MORPHOLOGY Measure the PR interval Measure from beginning of P wave to the beginning of the QRS .12-.20 seconds 3-5 small boxes Measure the QRS complex Measure from where the beginning of the QRS leaves the iso-electric line until the ST segment starts. Less than 3 small boxes (1½-2½ small boxes) KNOWLEDGE CHECK This time interval represents the onset of atrial depolarization to the onset of ventricular depolarization: a. P-R interval b. QRS interval c. ST segment d. J Point KNOWLEDGE CHECK This time interval represents ventricular depolarization: a. P-R interval b. QRS interval c. ST segment d. T wave KNOWLEDGE CHECK This time interval represents ventricular repolarization: a. P-R interval b. QRS interval c. ST segment d. T wave Sinus Rhythm Rhythm: Regular Rate: 60-100 P waves: normal size & shape PR interval: normal (.12-.20) QRS complex: Normal (.06-.10) Sinus Bradycardia Rhythm: Regular Rate: < 60 P waves: normal size & shape PR interval: normal (.12-.20) QRS complex: Normal (.06-.10) Sinus Tachycardia Rhythm: Regular Rate: 101-150/min P waves: normal size & shape PR interval: normal (.12-.20) QRS complex: Normal (.06-.10) Sinus Arrhythmia Rhythm: irregular (at least 2 small boxes) Rate: 60-100 or <60 P waves: normal in size and shape PR interval: normal (.12-.20) QRS complex: Normal (.06-.10) Sinus Arrhythmia CAUSES Normal phenomenon, usually associated with phases of respiration ◦ SA node speeds up with inspiration ◦ SA node slows with expiration Common in infants & children, but may occur at any age TREATMENT None required unless very slow rate causes symptoms Atrial Arrhythmias Originate from ectopic sites in the atria ◦ WAP: Wandering Atrial Pacemaker ◦ PAC: Premature Atrial Contraction ◦ Conducted ◦ Non-conducted ◦ PAT or SVT: Paroxysmal Atrial Tachycardia or Supraventricular Tachycardia ◦ A Flutter: Atrial Flutter ◦ A Fib: Atrial Fibrillation Premature atrial contraction (PAC): Ectopic atrial foci Premature Atrial Contraction (PAC) CAUSES • Ectopic pacemaker cells in atrium fire faster than sinus node and the beat comes in EARLY and moves down the normal conduction pathways • Increased vagal tone • Increased automaticity of ectopic atrial cells • Anxiety or excess caffeine • Key word is Premature TREATMENT • No treatment needed if they are rare • Check and correct underlying cause • May be a clue that patient is going into another atrial arrhythmia, such as atrial fibrillation Premature Atrial Contraction (PAC) Rhythm: irregular Rate: same as underlying rhythm P wave: premature, positive, shape is different, may be hidden in previous T wave PR interval: normal or maybe longer QRS interval: normal. QRS looks the same as other complexes KNOWLEDGE CHECK The P wave in a PAC looks different from the sinus P wave – Why? a. Impulse originates in a different part of the atria b. P waves always look different c. Respiratory variation causes the change d. It is rate-dependent Paroxysmal Atrial Tachycardia (PAT or SVT) Paroxysmal Atrial Tachycardia (PAT or SVT) characteristics Rhythm: regular Rate: 150-250 /min P waves: often hidden in previous T wave PR interval: may not be measurable QRS: normal – narrow complex Patients may feel palpitations Paroxysmal Atrial Tachycardia -> SR • PAT: Paroxysmal means “a burst” • Has a start and stop • If sustained, may be called SVT = SUPRAVENTRICULAR TACHYCARDIA Paroxysmal Atrial Tachycardia (PAT or SVT) CAUSES Hyperthyroidism, COPD, valvular heart disease Medications: albuterol treatments Caffeine, alcohol, tobacco SYMPTOMS Palpitations Anxiety Hypotension, SOB, chest pain, syncope – signs of decreased cardiac output…WHY? Heart rate is too fast to allow for adequate filling during diastole PAT/SVT treatment TREATMENT Decrease heart rate ◦ Vagal maneuvers: Cough, bear down, other Valsalva maneuvers ◦ Medications: Adenosine, Diltiazem, Beta blockers ◦ Synchronized cardioversion if unstable Atrial Flutter Atrial Flutter characteristics Rhythm: regular or irreg, depending on conduction ratios Rate: Atrial: 250-400/min Ventricular: whatever the AV node allows through. May be constant or variable P waves: none. Sawtooth “F” flutter waves are baseline. DOES NOT RETURN TO ISOELECTRIC LINE PR interval: not measurable QRS: normal – narrow complex Patients may feel palpitations if rate is fast Atrial Flutter – variable conduction • AV node does not let all the impulses from flutter waves conduct through to ventricles. • Rate of conduction can be constant (2:1, 4:1) or variable, as seen below Sawtooth “F” flutter waves are the baseline. They do not return to isoelectric line Atrial Flutter CAUSES Re-entry, due to valvular heart disease Post-op CV surgery CAD TREATMENT Control rate of ventricles Check hemodynamic effects of loss of atrial contraction (fatigue, hypotension, SOB, CP?) Medication to control rate or convert to SR ◦ Diltiazem, amiodarone, beta-blocker Antigoagulation: because blood pools in atria ◦ Heparin (acute), Coumadin, Pradaxa, Xarelto, Eliquis Synchroniczed Electrical Cardioversion ◦ Anticoagulation or TEE prior (if >48 hours duration) Atrial Fibrillation characteristics Rhythm: ALWAYS irregularly irregular Rate: Atrial: usually >400/min. Atria are quivering Ventricular: whatever the AV node allows through. P waves: wavy baseline (fibrillatory waves) PR interval: not measurable QRS: normal – narrow complex If ventricular rate is 60-100, the rhythm is called “A fib with controlled ventricular response.” A Fib = atrial chaos Atrial Fibrillation with RVR or SVR If rate >100/min., Atrial fibrillation with rapid ventricular response If rate <60/min, Atrial fibrillation with slow ventricular response Atrial Fibrillation A fib is very common. Some causes are… ◦ Post op CV surgery ◦ CAD, Htn, HF, COPD May be transient May be controlled with medication Loss of “atrial kick” causes decreased cardiac output ◦ Fatigue, SOB, chest pain Patients are at risk for stroke, due to stasis of blood in atria ◦ Atria are “quivering” and not contracting, so blood swirls and clots Physiology of Stroke Risk in Atrial fib & Atrial flutter Rapid impulses cause the atria to quiver instead of contracting regularly producing irregular wavy deflections. Stasis of blood can lead to clot formation. Clot (thrombus) is most likely to form in the atrial appendages. Clot in the left atrial appendage is particularly important since the left side of the heart supplies blood to the entire body. Clot that dislodges from left atrial appendage can embolize to the brain BIG STROKE! Atrial Flutter/Fibrillation & Risk of Stroke Coronary Sinus Vein Pulmonary Veins Left Atrial Appendage Clot formation in Left Atrial Appendage Atrial Fibrillation TREATMENT Anticoagulation: because blood pools in atria ◦ Heparin (acute), Coumadin, Pradaxa, Xarelto, Eliquis Medication to control ventricular rate or convert to SR ◦ Diltiazem, amiodarone, beta-blocker, ibutilide (Corvert) Synchronized electrical cardioversion ◦ Anticoagulation or TEE prior (if >48 hrs duration) EP catheter ablation if medication cannot control Refractory A Fib Management (A Fib that is not responsive to other treatments) EP Catheter ablation of pulmonary veins, source of A fib ◦ Radiofrequency ablation - heat ◦ Cryo ablation – cold Maze procedure: open heart surgery creating atrial scar tissue Mini-maze procedure: minimally invasive surgery, incision between ribs ◦ Encircles pulmonary veins with surgical incisions in left atrium Left atrial appendage (LAA) occlusion ◦ Watchman device Cardiac monitoring is a priority after ALL of these procedures KNOWLEDGE CHECK Which of the following atrial arrhythmias put a patient at risk for stroke? a. Paroxysmal atrial tachycardia b. Atrial flutter c. Atrial fibrillation d. Both b & c Junctional Rhythm Originate in AV junction (area around the AV node and the Bundle of His) 2 Functions ◦ Slows impulse conduction from atria to ventricles (gatekeeper) ◦ Back-up pacemaker of heart, if SA node fails Discharges impulses at rate of 40-60/minute Junctional Rhythm Rhythm: regular Rate: 40-60/min P wave: absent (hidden in QRS), inverted, or after QRS PR interval: if present, it is <.12 QRS: normal absent (hidden in QRS), inverted after QRS Junctional rhythm ◦ Remember that horizontal axis of EKG paper measures time ◦ It takes less time for impulse to move from junctional area to ventricle ◦ (From SA node to ventricle is a longer route!) Accelerated Junctional Rhythm & Junctional Tachycardia Accelerated junctional rhythm 60-100/minute Junctional tachycardia >100/minute KNOWLEDGE CHECK In any Junctional Rhythm, the P wave can be a. Inverted in Lead II b. Occurring just before the QRS c. Occurring just after the QRS d. Hidden in the QRS e. All of the above KNOWLEDGE CHECK This strip is an example of a. junctional rhythm b. accelerated junctional rhythm c. junctional tachycardia d. premature junctional contraction What are Heart Blocks? DELAYED conduction or NO conduction through AV node to ventricles AV node is the bridge between that impulses cross to get from atria to ventricles PR Interval measures the time it takes the impulse to cross that bridge The site of pathology of the AV Blocks may be at the level of the: ◦ AV Node ◦ Bundle of His ◦ Bundle Branches Steps to Interpret Heart Blocks Look for the P wave ◦ Is there one P for every QRS? Measure the P-P interval (atrial rhythm) ◦ Is it regular? LOOK FOR HIDDEN P WAVES Measure the R-R interval (ventricular rhythm) ◦ Is it regular? Measure the PR Interval ◦ Is it CONSISTENT? Or does it CHANGE? Measure the QRS complex ◦ Is it narrow or wide? First Degree AV Block Rhythm: Regular Rate: same as underlying P wave: sinus (normal) PR interval: Consistently prolonged (>.20) QRS: normal Second Degree AV Block Type I (Wenckebach, Mobitz I): block is within the AV node Some of the sinus impulses are not conducted to the ventricles P waves are regular PR interval progressively lengthens...then drops QRS Can be confused with non-conducted PAC or third degree heart block Second Degree AV Block Type I (Mobitz I, Wenckebach) CAUSES Ischemia to AV node Medication effect Increased vagal tone TREATMENT None required Usually temporary and resolves spontaneously Note meds, change if necessary Monitor for further conduction problems Second Degree AV Block Type I (Mobitz I) Second Degree AV Block Type II (Mobitz II) Type 2 (Mobitz II): block below the AV node within His-Purkinje system Some of the sinus impulses are not conducted to the ventricles More P waves than QRS complexes (ratio) P waves are regular PR is fixed with dropped QRS Patient condition related to ventricular rate Second Degree AV Block Type II (Mobitz II) CAUSES Anterior wall myocardial infarct (AWMI) Degeneration of the electrical conduction system in the elderly Assess your PT (Asymptomatic or Symptomatic) TREATMENT May SUDDENLY degenerate into complete heart block or ventricular standstill and will usually require pacemaker implantation Atropine not effective Transcutaneous pacer, Dopamine or Isuprel Drip. Transfer to High Acuity of care ICU. Second Degree AV Block Type II (Mobitz II) Third Degree AV Block (Complete Heart Block) Complete AV block: failure of any atrial impulses to be conducted to the ventricles Block is at AV node or Bundle of His Atria and Ventricles beat independently of each other, which is called… A-V Dissociation: P-P interval is fixed; R-R interval is fixed, but they have no relation to each other P waves are usually sinus at 60-100 bpm QRS complexes are either from AV junction (narrow) at 40-60 bpm or from ventricles (wide) at 20-40 bpm Third Degree AV Block (Complete Heart Block) CAUSES Acute MI Conduction system disease Digoxin toxicity TREATMENT Rhythm can progress to ventricular standstill, so pacemaker needed emergently If patient decompensates, use trancutaneous pacer while awaiting transvenous pacer Third Degree AV Block (Complete Heart Block) QRS complexes are either from AV junction (narrow) at 40-60 bpm or from ventricles (wide) at 20-40 bpm KNOWLEDGE CHECK In which of the following heart blocks will you see a P wave with no QRS complex? a. 1st degree AV block b. 2nd degree, Type I c. 2nd degree, Type II d. b & c KNOWLEDGE CHECK In which of the following heart blocks is there consistently NO ELECTRICAL COMMUNICATION between the atria and ventricles? a. 1st degree AV block b. 2nd degree, Type I c. 2nd degree, Type II d. 3rd degree What is an Escape beat? An escape beat occurs when the primary pacemaker of the heart (the sinus node) does not initiate an impulse and one of the back-up pacemakers (atrium, junction or ventricle) takes over. And escape rhythm is when one of the back-up pacemaker sites takes over for an extended time, not just 1-2 beats. Escape beats always follow a pause ESCAPE BEATS ARE NEVER PREMATURE…THEY ALWAYS OCCUR LATE IN THE CARDIAC CYCLE Atrial escape Junctional escape Ventricular escape Bundle Branches & Purkinje Fibers At Bundle of His, conduction pathways split into the right and left bundle branches to conduct to each ventricle. Bundle branches end in tiny conduction network called Purkinje Fibers Ventricles can be a back-up pacemaker at rate of 2040/minute Purkinje Fibe Purkinje Fibers Bundle Branch Block BBB can occur anywhere in R or L Bundle system The right bundle branch (which distributes the electrical impulse across the right ventricle) and the left bundle branch (which distributes the impulse across the left ventricle). Ventricular depolarization (QRS) is wider, because it takes longer QRS .12 or greater = intraventricular conduction delay Differentiating between a RBBB and LBBB requires a 12 lead ECG Right & Left BBB Bundle Branch Block Rhythm: regular Rate: same as underlying rhythm P waves: sinus (Sinus P wave distinguishes BBB from PVC) PR interval: normal QRS: Wide (>.12) KNOWLEDGE CHECK Bundle branch blocks are a. a block of one of the ventricular conduction pathways b. the same as ventricular escape rhythms c. a result of too much caffeine or alcohol d. all of the above Ventricular arrhythmias Premature Ventricular Contractions Ventricular Tachycardia ◦ Monomorphic ◦ Polymorphic (Torsade de pointes) Ventricular Fibrillation Idioventricular Rhythm Accelerated Idioventricular Rhythm Ventricular Standstill Agonal Rhythm [Pulseless Electrical Activity] PVC PVCs Premature Ventricular Contractions CAUSES CAD, ischemia, MI, hypoxia MVP, CHF, Cardiomyopathy Electrolyte imbalances (hypokalemia) Medication effects (digoxin, epinephrine, dopamine) or substances (caffeine, alcohol, tobacco) TREATMENT No treatment if rare PVCs Anti-arrhythmic meds for significant PVCs (>6/min, VT, R-on-T…but check your MD orders) Treat cause PVC Variations R-on-t PVCs The relative refractory period is an electrically vulnerable interval in the cardiac cycle. R-on-T PVC’s may result in Ventricular Tachy or V Fib. KNOWLEDGE CHECK Following are differences between PVCs and PAC’s: a. PVC’s are initiated in the ventricle, PAC’s are initiated in the atrium b. PVCs usually have wider QRS than PACs c. PVCs and PACs both have premature P waves d. All of the above are true e. Only a & b Ventricular Tachycardia Ventricular rhythm of 140-250/minute No P waves A series of wide QRS complexes in short runs or a continuous rhythm Monomorphic: QRS complexes have same morphology – all complexes look alike Polymorphic: QRS complexes have different morphology ◦ Torsade de Pointes is a form of polymorphic VT ◦ QRS complex changes polarity, twisting around isoelectric line ◦ Treatment is Magnesium, even if Mg++is normal Ventricular Tachycardia Rhythm: regular, or might be slightly irregular Rate: 140-250/min P waves: None PR interval: not measurable QRS complex: WIDE (>.12) Ventricular Tachycardia Monomorphic: QRS complexes have same morphology – all complexes look alike Polymorphic: QRS complexes have different morphology Polymorphic VT -> Sinus rhythm Torsade de pointes ◦ Torsade de Pointes is a form of polymorphic VT ◦ QRS complex changes polarity, twisting around isoelectric line ◦ Only treatment is Magnesium 2 Gm slow IV push to stabilize the cardiac membrane, even if Mg++is normal. Other antiarrhythmics have no effect. Cardioversion if pulse, defib if not. Ventricular Tachycardia CAUSES CAD, ischemia, MI, hypoxia MVP, CHF, Cardiomyopathy Electrolyte imbalances (hypokalemia) Medication effects (digoxin, epinephrine, dopamine) This is a life-threatening arrhythmia! RAPID RATE AND LOSS OF ATRIAL KICK REDUCES CARDIAC OUTPUT! MAY LEAD TO VENTRICULAR FIBRILLATION Ventricular Tachycardia TREATMENT (if patient has a pulse, treat as below – if no pulse, treat like V. Fib) Unstable patient? ◦ Hypotension, chest pain, SOB, skin cool, clammy, LOC change ◦ Cardioversion Stable patient? ◦ Patient BP acceptable ◦ No chest pain or SOB ◦ No LOC decrease ◦ Give Amiodarone 150 mg over 10 min and/or Cardioversion VT variations R on T PVC -> VT, polymorphic VT -> V Fib KNOWLEDGE CHECK The monitor room calls and says your patient is in ventricular tachycardia, rate 155. Which of the following actions are appropriate for the med-surg RN? a. assess patient’s LOC, pulse, BP b. cardiovert immediately c. ask patient to cough or bear down d. call Code Indigo e. all of above f. a, c, d g. a, b, d Ventricular Fibrillation Lethal rhythm! Disorganized, chaotic, electrical activity in the ventricles No organized depolarization/repolarization cycle Results in “quivering” of ventricles with no effective contraction No cardiac output Most common cause of sudden death The only way to save this patient is CPR and DEFIBRILLATION! Ventricular Fibrillation Rhythm: None Rate: None P waves: None PR interval: not measurable QRS complex: none Ventricular Fibrillation Coarse or fine VF? Fine VF may look like asystole… Change the lead to check. Ventricular Fibrillation Videos Heart in Ventricular Fibrillation What is Ventricular Fibrillation? (Play first) Ventricular Fibrillation SR->VT -> shock->VF -------------------> shock -> SR!!! Defibrillation IDIOVENTRICULAR RHYTHM Very slow back-up ventricular rhythm Sinus node and AV node are not initiating and impulse OR are blocked. IVR takes over This is an “Escape rhythm” This may be all the heart has left! May occur in single “escape” beats, in short runs or be sustained IDIOVENTRICULAR RHYTHM Rhythm: regular Rate: 20-40/min P waves: none PR interval: not measurable QRS complex: WIDE ACCELERATED IDIOVENTRICULAR RHYTHM Rhythm: regular Rate: 40-100 P waves: none PR interval: not measurable QRS complex: WIDE Agonal Rhythm If Idioventricular rhythm rate is less than 20, the QRS may widen and continue to slow Deterioration of electrical system Often called a “dying heart” Ventricular Standstill Rhythm: if atrial rhythm present, it may be regular, ventricular rhythm will not be present Rate: no ventricular rate, essentially this is asystole P waves: present if atrial activity PR interval: not measurable QRS complex: none CAUSES Ventricular Standstill (Asystole) Hypovolemia Massive MI Complete heart block Hypoxia Tension pneumothorax Pulmonary embolism Hyper/Hypokalemia Hypo/Hyperthermia Drug overdose Cardiac trauma TREATMENT ACLS protocol: CPR, Epi Pulseless Electrical Activity Monitor shows organized rhythm, but patient has no pulse Most Common causes are Hypoxia and Hypovolemia Same causes and treatment as Asystole ACLS protocol PACEMAKERS Why do we use pacemakers? The body’s intrinsic pacemaker is the Sinus node (SA node) If the SA node is not functioning properly, the patient may need an artificial pacemaker This is a generator (for automaticity) that produces impulses that are conducted through hard-wired leads which are placed in the heart Pacemaker indications ◦ Sinus bradycardia, sinus arrest, sinus exit block ◦ A Flutter or A Fib with slow ventricular response ◦ Mobitz II (Second degree, type II) ◦ Complete Heart Block (Third degree) Pacemakers: temporary or permanent? Temporary pacing ◦ Symptomatic bradycardia ◦ Symptomatic Mobitz II or CHB ◦ Some invasive cardiac procedures ◦ Overdrive pacing to “break” SVT ◦ Post CV surgery Permanent pacing ◦ Symptomatic bradycardia or heart block that is not transient ◦ AV node ablation for tachy-brady syndrome Symptomatic patient: what to do before the pacer is placed If patient is symptomatic, anticipate the use of pharmacologic therapy and transcutaneous pacing while waiting to place a temporary wire If medications are the cause, withdrawal of offending drugs is the first treatment for heart block Be vigilant: time is of the essence Transcutaneous pacing for symptomatic bradycardia and heart blocks Chest leads must be on for pacer to work! EMERGENCY Temporary Pacing Procedure (done in ICU, or Cath Lab) Permanent pacemaker pulse generator & leads Micra pacer: FDA approved 2016 Inserted percutaneously transcatheter Ventricular pacing only 3 functions of pacemakers FIRE ◦ Pulse generator produces energy impulse ◦ Indicated on EKG by a spike CAPTURE ◦ Electrical impulse stimulates the cardiac myocytes, causing depolarization ◦ Indicated on the EKG by the P wave (atrial) or the QRS complex (ventricular) SENSE ◦ Pacer “sees” the patient’s own intrinsic (native) beats and DOES NOT FIRE OR Pacer does not “see” a rhythm, so it DOES FIRE ◦ Indicated on the EKG by patient’s native beat with NO paced beats until the next appropriate interval V-pacing! But Check the pulse! V-pacing: look for the spike! Review: what kind of heart block do you see in Strip A? Intrinsic beats Single and dual chamber Chest PA and LATERAL with implanted device KNOWLEDGE CHECK Dual chamber pacemakers A. Have one lead in the right atrium and one lead in the right ventricle B. Have one lead in the right atrium and one lead in the left ventricle C. Can pace the atrium, the ventricle, or both if needed D. Can pace twice as fast as single chamber pacemakers E. A, C, D F. B & C G. A & C 3 functions of pacemakers any malfunction will be in one of these 3 areas FIRE ◦ Pulse generator produces energy impulse ◦ Indicated on EKG by a spike CAPTURE ◦ Electrical impulse stimulates the cardiac myocytes, causing depolarization ◦ Indicated on the EKG by the P wave (atrial) or the QRS complex (ventricular) SENSE ◦ Pacer “sees” the patient’s own intrinsic (native) beats and DOES NOT FIRE ◦ OR Pacer does not “see” a rhythm, so it DOES FIRE ◦ Indicated on the EKG by patient’s native beat with NO paced beats until the next appropriate interval Failure to fire Failure to capture Failure to sense: undersensing Pacer did not “see” the patient’s native beats Fusion Native Native Fusion Paced Failure to sense: oversensing Pacer “saw” the P wave and treated it as a QRS, so it did not pace KNOWLEDGE CHECK What are the three main functions of a pacemaker? A. Pace, fire, capture B. Fire, capture, fuse C. Pace, sense, fire D. Fire, capture, sense Internal Cardioverter/ Defibrillator (ICD) Implantable device that will act as a pacemaker for SLOW rhythms, but will also cardiovert or defibrillate fast rhythms as needed. The device is therefore capable of correcting most lifethreatening cardiac arrhythmias. ICD Types of defibrillators ICDs can be ◦Single chamber: one lead in ventricle ◦Dual chamber: two leads, one in atrium & one in ventricle) ◦Biventricular: two leads in ventricle; may also have atrial lead Subcutaneous ICD ◦Subcutaneous: no leads delivers enough energy to defibrillate the heart without leads! (no pacing function) - THIS IS NEW! Care of patient after cardiac device implantation VS, pain control Observe heart rhythm: Is pacer capturing and sensing appropriately? Observe for bleeding or hematoma Keep affected arm immobilized 24 hours Patient education: Limit range of motion for 2-4 weeks Electrical & mechanical function of the heart = Cardiac Output!!!! And it is ALL ABOUT the Cardiac Output!!!
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