Cardiac Dysrhythmia Final Study Guide Over the past 7 years working on a cardiac telemetry unit, I have found

that the best way to start analyzing a cardiac rhythm strip is to start by looking for the P wave. In many ways it is the key to accurate interpretation. I am going to share with you exactly how I interpret a strip. Keep in mind that you may find another way that works better for you. P waves (atrial depolarization) 1. 2. 3. 4. Is there a P wave? Are the P waves the same shape (morphology) and upright? Are the P waves regular? Is there 1 P wave before EVERY QRS complex?

QRS complex (ventricular depolarization) 1. Are there QRS complexes? (Lets hope so!) 2. Do all of the QRS complexes look the same? 3. Do the QRS complexes occur at a regular interval? T wave (ventricular REpolarization) 1. 2. 3. 4. Are there T waves? Do the T waves all have the same morphology (shape)? Are the T waves all upright? (Shaped like a small camel hump) Is there a T wave after every QRS complex?

Next most important factor: is the rhythm regular? If so, proceed to Timing PR interval .12-.20 (measure from the beginning of the P wave to the beginning of the R wave) QRS complex .06-.12 QT interval <.44 is normal Rate If everything is present that should be present (upright P wave before every QRS & T wave) and the rhythm is regular then its a sinus rhythm, which breaks down to the following: Sinus bradycardia less than 60 bpm Sinus rhythm 60-100 bpm Sinus tachycardia greater than 100 bpm

Sinus bradycardia (SB) Essential information: Everything is present that should be present: P wave before every QRS followed by a T wave. It s regular, but slow Why do I care? Tests are often constructed to give you an opportunity to decide what to do with the information. Do I need to take action, or is this OK? T herefore it is important to always ask What is the significance? Interesting to know: just having a slow rate doesnt mean the patient is in trouble. I had a patient walk onto my floor once with a heart rate of 32! I marveled that he was walking, talking and breathing. He had obviously adjusted to a very slow heart rate. Many athletes have bradycardia too. Significance Sinus brady becomes a problem when it is NOT the patients normal rate. There are many reasons for SB (certain meds, disease, etc.) BUT when the patient has any symptoms (diaphoretic, cool/cold, clammy, nauseated, vomiting, or blue [yikes!]) then you must act. Call the MD, get the crash cart, have pacer pads ready, and of course atropine. Putting on oxygen is also a must since cardiac output is so diminished, supplemental oxygen will help compensate some for the decrease oxygen that accompanies decreased cardiac output. _______________________________________________________________________________________ Sinus arrhythmia (SA) How can you tell its sinus arrhythmia? Essential information: Well, for starters there are upright P waves of the same shape before every QRS. The most distinguishing feature of SA is that it is a regular irregularity. When looking at the strip, its regular but the rate varies. What this means is that there will be several cardiac cycles with a faster rate, followed by several cardiac cycles at a slower rate = faster rate, slower rate, faster rate, slower rate. Interesting to know: If you can observe the patient breathing at the same time you are watching the monitor, youll notice that the rate increases with inspiration and decreases with expiration. Significance Sinus arrhythmia is perfectly OK in infants and young children BUT in adults may be a sign of a diseased SA node (stinks to lose the natural pacemaker of the heart! Therefore patient may need to be evaluated for a pacemaker) or coronary artery disease (CAD) which may require cardiac catheterization.

Sinus block Essential information: the SA node fires, but the impulse is NOT conducted to the atria. Sinus arrest/pause Essential information: the SA node DOES NOT FIRE, but another pacemaker in the heart will How can I tell the difference between these? In the cases of a block, the length of the pause is AN EXACT MULTIPLE of the underlying cardiac cycles. Whether thats 2, 3, or 4 cardiac cycles, the key concept is that it is exactly 2 or exactly 3, or exactly 4. In an arrest/pause, the length of the pause is MORE than 2 times the underlying cardiac cycle. Since the SA node isnt firing, another pacemaker in the heart will (eventually) so after the pause, subsequent complexes may be a P wave from a different site in the atria (therefore the P wave will have a different shape than P waves before the pause), a junctional site (inverted, buried or retrograde P waves), or a site in the ventricles which fire at an inherent rate of 20-40 bpm. Significance These 2 dysrhythmias can be caused by an MI, ischemia ( blood supply to heart) or drugs e.g. digitalis or quinidine. Take action IF the patient is having symptoms: pale, diaphoretic (sweaty) weakness, chest pain, sudden change in blood pressure. _______________________________________________________________________________________ PAC (premature atrial contraction) Essential information: the monitor strip is essentially normal EXCEPT one beat occurs earlier than normal. The way to spot PACs which are isolated occurrences, is to take your calipers and march them out from beat to beat (peak of the R wave to peak of the next R wave is an easy way) of the regular underlying rhythm. As you move your calipers from one R wave to the next, you would expect to see the next R wave right at the other point of your caliper, but the R wave occurs sooner than that. Bottom line: just an early heart beat. Significance A PAC represents increased irritability of the atria. By itself, it is not concerning, BUT it may lead to a more serious dysrhythmia so keep an eye on that patient! Possible causes include: pain, fever, fear, anxiety, sudden excitement, exercise, digitalis, atropine, nicotine, caffeine, and some street drugs. _______________________________________________________________________________________

PAT/PSVT paroxysmal atrial or supraventricular tachycardia Essential information: SUDDEN ONSET of tachycardia WITNESSED ON THE MONITOR, rate >150 Significance Often caused by an irritable site in the atria, it cannot be tolerated for long & leads to cardiac output since the rate is so rapid, the ventricles dont get a chance to fill completely. SVT supraventricular tachycardia Essential information: same as PAT/PSVT BUT the onset was not witnessed on the monitor. The rate is regular and fast > 150. The impulses originate from an irritable site above the bundle of His. The irritability can be caused by stimulants such as caffeine, nicotine and some street drugs. Significance Treat IF the patient becomes medically unstable. This rapid rate wears the patient (and the heart of course) out. Although it is not a lethal dysrhythmia, most people cannot tolerate it for prolonged periods (> 1 hour) Treatment: Adenosine 6 mg IV push, as rapidly as you can push it, followed by 20 mL saline flush. Elevate the extremity Synchronized cardioversion sync button must be pushed on the monitor prior to shocks! Interesting to know: we call this a junk term in cardiology. We call regular tachycardias >150 SVT. We know something above the bundle of His is irritable, but dont know what & usually never find out. Bottom line its regular and fast and we dont know what caused it. _______________________________________________________________________________________ Aflutter Essential information: has a very characteristic saw-tooth pattern of F waves between every QRS. It is generated from one irritable site in the atria. The QRS complexes often occur at regular intervals. Significance Not lethal but often treated because it indicates increased irritability within the atria which may progress to a more serious dysrhythmia. It can be caused by heart disease, MI or drug toxicity. How a patient tolerates it varies from person to person. Interesting to know: although the book states that its important to note whether the pattern is 3:1, 4:1 F waves to QRS complex, on my unit it is considered nice but not necessary. Board certified cardiologists dont need me to tell them the ratio which they can plainly see for themselves. _______________________________________________________________________________________

Atrial fibrillation Essential information: there are P waves, lots of them! There is no rhyme or reason to the shape of the P waves for a very good reason impulses are being simultaneously generated from multiple sites in the atria. All of the cardiac cells in the atria are irritated and that is not a good thing! Since the normal coordinated conduction of nerve impulses (which underpins the efficient flow of blood through the heart) is lost, the end result is that the atria quiver. If the atria dont contract forcefully, the chamber doesnt empty completely and push all of the blood down into the ventricles. Significance Since the blood in the heart isnt moving through the atria efficiently, the blood left behind in the atria due to the weak & incomplete contractions begins to form clots (when blood slows down/sits still it clots). As clots are formed and enter the general circulation, eventually they reach a point in the blood vessels where they are bigger than the diameter of the vessel. If the clot is large enough and lodges in the coronary arteries MI, in the brain stroke, in the lungs pulmonary embolus all of which can kill the patient. How can I tell if its Afib? The hallmark of Afib is that it is irregular. The P waves all look different and the line between QRS complexes may look wavy, flat, have multiple bumpy Ps or any combination of these. When using your calipers, there will not be a regular underlying rhythm. There is NO PR interval (just write zero with a line through it in this section of the strip). When to take action: If its a new onset (theyve never had it before) the answer is ALWAYS TAKE ACTION. The risks associated with possible clot formation are serious and can be life-altering/threatening. Call the doctor and get a 12 lead EKG. If the patient is asymptomatic great! But dont assume that they will stay that way. If the rate is > 150 this is especially concerning and is NEVER ignored. Called Afib RVR (rapid ventricular response) it can progress to more serious dysrhythmias. Call the doctor. If no response within 15 mins., call again. If no response, go up your chain of command. Get ready to start a drip of the calcium channel blocker diltiazem (Cardizem). Signs and symptoms to watch for (ranked from bad to worse): Nausea and/or vomiting Shortness of breath Tachycardia Dizziness, weakness, faintness Pale, cool, clammy skin Diaphoresis (very sweaty) Mild to severe chest pain Dyspnea Confusion, disorientation 5

Cyanosis (blue or grey skin color around mouth, nail beds, or worse all over) Hypotension (low blood pressure) Unresponsive

Interesting to know: atrial fibrillation is one of the most common dysrhythmias. Because of that the general public often equates common with harmless, but nothing could be further from the truth! It is often seen in the elderly. It can be caused by severe heart disease or MI. It can also occur with excessive use of alcohol or caffeine. WPW (Wolff-Parkinson-White Syndrome) pp. 73-75 Essential information: occurs because an electrical impulse follows an additional or abnormal electrical conduction pathway called the bundle of Kent which is an accessory pathway. So there are 2 pathways at play: the normal pathway which functions as usual AND the accessory pathway (bundle of Kent). PR (if P wave present) < .12 QRS is wide > .12 a delta wave is present (extra bump seen in slurred part of QRS) The P-P and R-R intervals vary and tachycardia (>100 bpm) is not unusual Significance Usually not a dangerous rhythm, BUT CAN BECOME LIFE THREATENING if the ventricular rate > 200 The patient may have no symptoms or may complain of palpitations, racing heart, dizziness, weakness, faintness, shortness of breath and/or chest pain __________________________________________________________________________________________ Atrioventricular (AV) Blocks 1st degree AV block p. 110 & figures 5-2 & 5-3 on p. 111 Essential information: PR interval is >.20 not a true block but rather a delay in conduction from the atria and the bundle of His. There is a P wave before every QRS. It can occur in any rhythm where a P wave precedes every QRS (bradycardia, tachycardia, normal rate). Significance Not usually a serious dysrhythmia, BUT if it is a recent change assess the patient carefully since it may indicate damage to the myocardium which may lead to a more serious dysrhythmia. Possible causes: MI (heart attack) or drugs e.g. beta blockers (metoprolol is one) __________________________________________________________________________________________ 2nd degree AV block type I (Mobitz I or Wenckebach) pp. 111-112 & figure 5-5 on p. 113 Essential information: PR interval is LONG, LONGER then a DROPPED QRS. Therefore it is called a progressive heart block. The cycle of a PR interval which is long, longer then followed by a dropped beat repeats itself over and over again. Thats what makes it easy to spot. There is a P wave before every QRS and a QRS follows every P until the QRS (beat) gets dropped. 6

Significance Not a lethal dysrhythmia, but the patient may become unstable if the rate is slow (bradycardia) or there has been a recent injury to the heart (e.g. MI) or the patient has other illnesses (comorbidities). Possible causes: infection, MI, drug toxicity __________________________________________________________________________________________ 2nd degree AV block type II (Mobitz II) pp. 113-114 & figure 5-8 on p. 115 Essential information: PR interval is USUALLY THE SAME; it can be normal or prolonged. So if the PR interval is normal, it will be consistently normal throughout the rhythm (.12, .12, .12). If the PR interval is prolonged, it is consistently prolonged (e.g. .32, .32, .32) Caused by an intermittent interruption in the electrical conduction system near or below the AV junction. Occurs suddenly and without warning. There is a P before every QRS until a QRS (beat) is dropped (there is no PR interval to measure when there is a dropped beat no QRS = no PR interval). Ratio of P waves to QRS: the worse the block, the greater the number of P waves for every QRS 2:1 (bad) 3:1 (worse) 4:1 (worst) The patient may remain in a 2:1 ratio, or it may vary 2:1, then 3:1, 2:1, etc. NO PATTERN IS MORE SERIOUS because it means that the block is irregular and can progress to a more dangerous dysrhythmia. Significance Can be LIFE THREATENING because of irritability of the myocardium if it leads to a more serious dysrhythmia such as a 3rd degree heart block Possible causes: MI, heart disease, drug toxicity __________________________________________________________________________________________ 3rd degree AV block (complete) pp. 114-117 & figures 5-11 & 5-12 Essential information: THIS IS A LIFE THREATENING DYSRHYTHMIA!!!! You must be able to spot this dysrhythmia. The electrical impulse is completely blocked between the atria and ventricles; therefore they will each beat at their own inherent rate. This means that P-P intervals are the same and R-R intervals are the same. However, PR intervals will vary in length. If youre looking at the strip and it just isnt making sense because you cant figure out the PR interval, consider a 3rd degree heart block. The aha! moment usually occurs when you look at all the P-P and theyre all the same, and then look at all the R-R and theyre all the same. Significance Since there is a lack of coordination between the atria and ventricles, blow flow through the heart is not efficient and cardiac output is decreased, especially if the ventricular rate becomes agonal (20-40 bpm). At this point perfusion to the vital organs is no longer sufficient and organs begin to die (including the brain). Possible causes: MI, heart disease, drug toxicity

Treatment: here is one the very few hard and fast rules in cardiology if the patient has a 3rd degree (complete) heart block GET READY TO DO EXTERNAL PACING. __________________________________________________________________________________________ BBB (bundle branch block) pp. 117- 120 & figures 5-15 & 5-16 Essential information: caused by a delay in conduction of the electrical impulse down one of the bundle branches (right or left) that delays depolarization of that ventricle so there is one QRS followed shortly by the other QRS which results in the typical RABBIT EARS. Significance not usually serious unless it is a recent change. Possible causes: heart disease or MI Ventricular Dysrhythmias PVCs pp.133-139 Essential information: appearance is wide & bizarre. They originate from an area below the bundle of His and travel back (retrograde) to the atria, depolarize the atria and then travel to the ventricles. If the PVCs look the same, then they are unifocal because they arise from one site. If they look different, then they are multifocal because they originate from different sites. These are worse because they indicate more irritability in the heart than unifocal PVCs do. Quadrigeminy = every 4 th beat is a PVC Trigeminy = every 3rd beat is a PVC Bigeminy = every other beat is a PVC Ranking from bad to worse: Frequency o Occasional o Quadrigeminy o Trigeminy o Bigeminy o Couplet (2 PVCs in a row) o Runs (3 or more PVCs in a row) Type o Unifocal o Multifocal Possible causes: heart disease, MI, caffeine, nicotine, stress, anxiety Treatment again the maddening answer in cardiology is it depends. If the PVCs are unifocal & occasional and the patient is stable, there is no need for treatment. Many people have unifocal PVCs and are not bothered by them at all. The cardinal rule is always assess your patient first. If the patient is having PVCs that are new/frequent/multifocal AND are symptomatic (fatigued, short of breath, diaphoretic, low blood pressure, etc.) then treatment may be warranted. __________________________________________________________________________________________

VT (ventricular tachycardia) pp. 139-140 often LIFE THREATENING This is another dysrhythmia that you must have down cold. Essential information: looks like wide, bizarre identical QRS complexes, one right after another. There are no P waves. It is fast 101-250 impulses/minute. Possible causes: often from increased irritability from an MI for example, advanced heart disease, severe ischemia, electrical shock, drugs such as epinephrine or digitalis. Treatment: If it is less than 30 seconds (unsustained) treatment may not be necessary o Patient may feel weak o May complain of palpitations or a racing heart If it is greater than 30 seconds (sustained) treatment is often required o If unresponsive with NO pulse CPR first (ALWAYS) followed by shocks within 4 minutes o No DEFIBRILLATION shocks for patients with a pulse! If they have a pulse, they have cardiac output. A shock could send them into asystole (flat line). As always, assess your patient first. I once saw what looked exactly like VT on the monitor. I went into my confused patients room and he was banging repeatedly on the bed rail. He was not really in VT, but it sure looked like it on the monitor! __________________________________________________________________________________________ Torsades pp. 140-141 figure 6-15 on p. 141 LIFE THREATENING Essential information: looks similar to VT, but the fast (>150) wide, bizarre complexes start close to the baseline, increases in size and then decreases again (an undulating, or twisting pattern). The pattern repeats over and over again. It is NEVER a good thing! It is often preceded by a prolonged QT interval. A patient may tolerate short periods of Torsades, but sustained Torsades will result in hypotension, unresponsiveness and loss of pulse. Possible causes: MI, severe heart disease, low magnesium, drugs that prolong the QT interval such as Lidocaine or procainamide. Treatment: Torsades NO PULSE Magnesium sulfate 1-2 grams over 5-20 minutes Torsades WITH PULSE Magnesium sulfate loading dose 1-2 grams over 5-60 minutes *NOTE: We often dont know if its Torsades or Vfib in real life unless we know the patient has a history of Torsades. So treat as Vfib and if that treatment doesnt work, then try Magnesium. __________________________________________________________________________________________ VF (ventricular fibrillation) pp. 141-143 ALWAYS LIFE THREATENING = LETHAL!!!! Essential information: If VT is not treated, it often degenerates into ventricular fibrillation which is definitely worse! There is no organized pattern of any waveforms. It is a wavy line that can be fairly wavy (coarse) or hardly wavy (fine) which is even worse. Vfib represents a dying heart. If you dont intervene IMMEDIATELY, the patient WILL DIE! The heart is now just quivering. There is no cardiac output, therefore no pulse. The patient is not responsive and usually cyanotic (blue). Possible causes: severe heart disease, electrical shock, drug toxicity Treatment: CPR, CPR, CPR!!!! Followed by shocks at 200-360 joules and all of the usual code drugs: epinephrine, amiodarone etc.

*Final note: as always, make sure to check your patient since a loose lead or artifact caused by patient movement (e.g. moving around in bed or coughing) can mimic Vfib. __________________________________________________________________________________________ IVR (idioventricular rhythm) pp. 143-144 LETHAL IMMEDIATE TREATMENT! Essential information: rate is 20-40 QRS complexes are wide & bizarre. There are no P waves. It is the FINAL attempt by the heart to initiate an electrical impulse. It arises from the ventricles since the pacemakers in the atria and bundle of His are no longer functional. Possible causes: end stage advanced heart disease Treatment: IF NO PULSE, CPR, CPR, CPR!!! Followed by shocks at 200-360 joules and all of the usual code drugs. IF PULSE PRESENT: for symptomatic bradycardia, consider atropine, dopamine, epinephrine, and pacing. __________________________________________________________________________________________ Agonal p. 144 LETHAL - IMMEDIATE TREATMENT! Essential information: rate is less than 20 QRS complexes are wide & bizarre. There are no P waves. This is the dying heart. Possible causes: end stage advanced heart disease Treatment: IF NO PULSE CPR, CPR, CPR!!! Followed by shocks at 200-360 joules and all of the usual code drugs. . IF PULSE PRESENT: for symptomatic bradycardia, consider atropine, dopamine, epinephrine, and pacing. __________________________________________________________________________________________ Ventricular standstill pp. 144-145 LETHAL - IMMEDIATE TREATMENT! Essential information: the atria still fire so there are P waves, but NO QRS complexes. Since the ventricles are no longer contracting, there is no cardiac output & no pulse. The patient will be unresponsive. Possible causes: 3rd degree heart block, massive MI, ventricular rupture. Treatment: CPR may be performed, but the patient may still die. If the result of a 3 rd degree block, immediate external pacing may be effective. Outlook is generally bleak. __________________________________________________________________________________________ Asystole pp. 145-146 LETHAL - IMMEDIATE TREATMENT! Essential information: often called flat lining, there is no electrical activity at all and therefore no waveforms of any kind. There may be a slightly wavy line at times. Since it might actually be fine Vfib, make sure to confirm this in 2 different leads. Possible causes: may follow untreated VT or VF Treatment: CPR, CPR, CPR!!! SHOCK IS USELESS IN ASYSTOLE. The various code drugs can be used and circulated with CPR that is hard & fast. (Actually all CPR for any lethal dysrhythmia should be hard & fast). __________________________________________________________________________________________

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Medications (given IV unless otherwise indicated) Adenosine p. 215 ALWAYS PUSH FAST (1-3 seconds) and elevate the extremity Indications: Narrow, complex tachycardia SVT, PAT, PSVT Stable, wide-complex tachycardia Dose: 6 mg followed by a 20 mL saline flush, may repeat with a 12 mg dose one time Note: the heart usually stops for about 6 seconds during which the patient will be unresponsive. The heart resets and restarts usually in a normal rhythm. This drug is always pushed under the direct supervision of a physician or ACLS trained nurse. The crash cart, suction and oxygen should be available right outside the patients door. Amiodarone p. 215 slows conduction, prolongs refractory period therefore slows heart rate down Indications: Vfib VT Pulseless VT Afib Aflutter Dose: 300 mg, no response in 3-5 minutes 150 mg (total 2,200 mg in 24 hours) If amiodarone is the drug that converts the patient to a normal/slower rhythm, then the drip hung is ALWAYS the same drug that was successful in converting the patient into a regular/slower rhythm Atropine pp. 215-216 increases heart rate & sinus node automaticity Indications: Symptomatic bradycardia To increase the heart rate in a bradycardic rhythm with PVCs Dose: 0.5 mg every 3-5 minutes (total dose not to exceed 3 mg) *any single dose less than 0.5 mg may CAUSE bradycardia Calcium Channel Blockers (Diltiazem, Verapamil) p. 216 slows conduction of AV node and refractory period thereby slows heart rate Indications: Narrow complex tachycardia Afib & Aflutter with RVR (rapid ventricular response) Hypertension Dose: Diltiazem initial bolus: 0.25 mg/kg (15-20 mg) over 2 minutes, repeat 0.35 mg/kg (20-25 mg). Give over 2 minutes. Second dose can be given 15 minutes after first dose. Verapamil initial dose: 2.5-5 mg IV over 2 minutes, repeat dose 5-10 mg every 15-30 mins. after first dose total dose not to exceed 20 mg) 11

If diltiazem or verapamil is the drug that converts the patient to a normal/slower rhythm, then the drip hung is ALWAYS the same drug that was successful in converting the patient into a regular/slower rhythm Epinephrine p. 216 increases rate & force of cardiac contractions, increases coronary & cerebral blood flow, increases automaticity Indications: Cardiac arrest Vfib Pulseless VT Asystole PEA Anaphylaxis (severe allergic reaction) Refractory bradycardia or hypotension Dose: 1 mg (1:10,000 dilution) every 3-5 mins. Lidocaine p. 217 decreases automaticity helping to decrease ventricular dysrhythmias. Indicat ions: alternative treatment when amiodarone isnt available PVCs VT pulseless VT Vfib Dose: 1-1.5 mg/kg every 5-10 mins up to a total of 3 mg/kg Magnesium sulfate pp. 217-218 reduces ventricular dysrhythmias that may follow an MI Indications: Treatment of choice for Torsades de Pointes Long QT intervals Dose: 1-2 grams over 5-20 minutes Procainamide p. 218 suppresses ventricular & atrial ectopy, decreases excitability & automaticity Indications: Controls a variety of dysrhythmias Dose: 20 mg/min until dysrhythmia is suppressed, hypotension occurs, QRS complex widens, total of 17 mg/kg Vasopressin p. 218 constricts smooth muscle in blood vessels Indications: Alternative to epinephrine Refractory Vfib pulseless VT asystole PEA Dose: 40 units IV ONE TIME ONLY 12

Funny Looking Beats Escape beats p. 160 figure 7-2 p. 161 Essential information occurs after a sinus arrest (pause) or in bradycardia. An impulse escapes from a site other than the SA node. Whatever complex ends the sinus arrest or slow rhythm is an escape beat. Aberrant conduction pp. 161-162 Essential information: from an electrical impulse generated above the bundle of His so one ventricle depolarizes at a slower rate than the other. The resulting QRS resembles a bundle branch block, but these occur as single complexes instead of an entire rhythm. The QRS complex will look different than the other QRS complexes in the underlying rhythm. PEA pulseless electrical activity pp. 162-163 LETHAL! TREAT IMMEDIATELY Essential information: any dysrhythmia that shows complexes on the monitor without a pulse. The patient has NO pulse and NO blood pressure. The only way to determine if PEA is present is to directly assess the patient to determine if they have a pulse or not. Treatment: CPR, CPR, CPR!!! Then all the normal code drugs. Pacemaker terms & malfunctions pp. 163-171 Temporary outside of the body. Used until a permanent pacemaker can be implanted surgically o Transvenous through the vein o Transcutaneous across the skin (pacemaker pads are positioned on the chest) Permanent surgically implanted when the patients heart cannot maintain a normal rhythm Atrial the lead wire & electrode are inserted into the right atrium Ventricular lead wire & electrode is placed in one of the ventricles Bi-ventricular lead wire & electrodes are placed in both ventricles Sequential pacemakers electrodes & lead wires are placed in one atrium and one ventricle Terms Capture indicates the pacemaker is successfully causing the cardiac cells to depolarize in response to the electrical impulse generated by the pacemaker. A pacer spike will be seen immediately followed by a P wave, or QRS complex depending upon where the lead wires are placed. (Lead wire in atrium spike seen before P wave, lead wire in ventricle spike seen before QRS complex). Electrical impulses are generated, BUT may not result in an actual contraction of the cardiac muscle. Mechanical capture the cardiac muscle actually contracts after the electrical impulse is generated by the pacemaker Loss of capture the pacer spike is NOT followed by a QRS complex Pacing percentage of complexes generated by the artificial pacemaker. Pacemaker rates are deliberately set low so that the patients heart functions on its own to the greatest degree possible. If a patient is completely pacemaker dependent, then you will see a pacer spike for every complex. In most patients with pacemakers, pacemaker spikes are seen occasionally to frequently. Not many patients are completely pacemaker dependent.

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ICDs pp. 171-72 implantable cardioverter defibrillator Essential information: both a pacemaker AND a defibrillator. If the patient does not respond to pacing, then the ICD will deliver shocks to restore heart rate. Most patients describe the shocks like being kicked in the chest by a mule. They are life-saving especially for patients with very low (10-20%) ejection fractions and prevent sudden death. AEDs pp. 172-173 Essential information: happily these are virtually idiot proof. Located in many public buildings, dont ever be shy about using one. Dont worry, it wont shock a person if they dont nee d it! Just put the pads on the upper right chest & below the left nipple (there is usually a diagram inside the lid) turn it on and follow the prompts. Step away from the body so the AED can analyze the rhythm. If a shock needs to be delivered, the AED will say so. ALWAYS make sure to stand clear of the body so you dont get shocked too! Dont put pads directly over a pacemaker. You can tell if the person has a pacemaker because they will have a lump that is approximately 2 inches square beneath the left (and occasionally the right collar bone). __________________________________________________________________________________________ Adult Treatment Guidelines pp. 226-237 These are decent guidelines arranged in a readable format so I will not reproduce them here. Final note: even if youre not sure what the rhythm is on the test, make sure to write out everything you can about what you see: PR interval, QRS interval, regular, irregular, etc. Professor Wilson may not agree with your interpretation, BUT if she can see how you came to the conclusion you did based on writing out all of the factors on the strip, she will give you credit. I wish you the very best of luck on the final!

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