NURS/ 1-24 Abnormalities of Cardiac Conduction & Rythm | COMPLETE STUDY GUIDE.

A b n o r m a l i ti e s o f C a r d i a c C o n d u c ti o n & R hy t h m • Normal Conduction o Sinoatrial node o Atrioventricular node ▪ Little hiccup of time here ▪ Insulator part that prevents conduction going ...

A b n o r m a l i ti e s o f C a r d i a c C o n d u c ti o n & R hy t h m • Normal Conduction o Sinoatrial node o Atrioventricular node ▪ Little hiccup of time here ▪ Insulator part that prevents conduction going from anywhere other than the AV node o Bundle of His ▪ Right bundle ▪ Left bundle o Purkinje fiber network • Sinoatrial Node (SA) o Pacemaker (60 – 100 BPM) o Sympathetic & parasympathetic innervation ▪ Primarily sympathetic innervation, but there is a good amount of parasympathetic innervation ▪ The sinoatrial (SA) node is the primary site for impulse initiation. Impulses initiated in the SA node are rapidly conducted across the right and left atria, causing them to contract. ▪ The electrical impulse then travels between the fibrous atrioventricular (AV) rings, where it slows down briefly at the AV node. The impulse then continues down the interventricular septum, branching into right and left portions and ending in an even smaller branching network of fibers called the His-Purkinje system. o Perfusion ▪ 60% RCA ▪ 40% L circumflex which comes off L coronary artery • The SA node is located at the junction of the superior vena cava and the right atrium, and is richly innervated by sympathetic and parasympathetic nerve endings. In 60% of individuals, the arterial blood supply to the SA node comes from the right coronary artery; in the remaining 40%, the blood supply is from the left circumflex coronary artery. • Atrioventricular Node o Annula fibrosa – insulator ▪ Insulates the right atrium from right ventricle & from rest of heart ▪ Requires impulse to go through AV node o The AV rings are the tough fibrous frames that support the delicate tissue of the tricuspid and mitral valves. These rings essentially insulate the conduction tissue of the AV node, thus allowing conduction through the normal pathway while preventing aberrant electrical conduction between the atria and ventricles. o Located in septal wall of RA ▪ The AV node is located in the septal wall of the right atrium, anterior to the coronary sinus and above the insertion of the septal leaflet of the tricuspid valve. o Perfusion ▪ 85 – 90 % RCA o Sympathetic & parasympathetic innervation ▪ It is also innervated by both parasympathetic and sympathetic nerves. The blood supply to the AV node comes from the right coronary artery in 85-90% of the population and from the left circumflex coronary artery in the remaining 10-15%. ▪ The AV node slows the conduction velocity of the electrical impulse, which allows time for atrial contraction, the so-called atrial kick, to contribute an additional 20% to filling of the ventricles in late diastole. After a brief slowing of the electrical impulse at the AV node, the impulse continues down the conduction tract along the bundle of His. o Long refractory period ▪ Little bit of pause in the impulse conduction which allows for atrial contraction & ventricular filling primarily ▪ In addition, the AV node has a long refractory period to prevent overstimulation of the ventricles in the event of abnormally rapid atrial impulses. • Bundle of His o Perfusion for LAD ▪ The bundle of His quickly divides into two branches, right and the left bundles, within the interventricular septum. ▪ The right bundle branch (RBB) is a relatively thin bundle of fibers that courses down the right ventricle and then branches near the right ventricular apex. • Because of this late branching, the RBB is more vulnerable to interruption than the left bundle branch (LBB), which branches early and widely. ▪ The LBB divides into two fascicles: the left anterior superior fascicle and the left posterior inferior fascicle. The left and right bundles both receive blood supply from branches of the left anterior descending coronary artery. • Infarction in the territory of the left anterior descending coronary artery can often affect the left anterior superior fascicle and the RBB, but rarely the left posterior inferior fascicle, because that portion receives additional blood supply from the posterior descending coronary artery. • This is why disruption of the more robust LBB in the form of a left bundle branch block (LBBB) usually indicates more extensive cardiac disease or damage than a right bundle branch block (RBBB). • The distal branches of the right and left bundles interlace into a network of Purkinje fibers. o Right bundle ▪ Longer, branches near RV apex • Longer before it branches • Doesn’t branch until it gets near apex of RV ▪ More prone to blocking o Left bundle ▪ Branches early • Very quickly branches; much more quickly than RBB • Branches into posterior/inferior and anterior/superior division ▪ Fascicles • Left anterior superior • Left posterior inferior ▪ LBBB sign of more severe heart disease • Because it branches earlier, does not block as much as RBB. So when a pt does block, they have more cardiac issues. Also a big deal because we care more about LV than RV • Electrophysiology o RMP ▪ Spontaneously depolarizing; upslope instead of flat like we see in most action potentials o Phase 4 ▪ Spontaneous depolarization o Threshold ▪ Fast Na channels opening up o Phase 0 ▪ Ventricular depolarization ▪ QRS complex on EKG o Phase 1-3 ▪ Ventricular repolarization • ECG o P wave ▪ Atrial depolarization • Doesn’t have anything to do with ventricular AP o QRS ▪ Ventricular depolarization o ST segment o T wave ▪ Ventricular repolarization • ECG o PR interval ▪ 0.12 – 0.20 sec ▪ *Need to know all these numbers* ▪ Beginning of P wave to beginning of QRS ▪ Delayed PR interval = something problematic with the conduction from the SA node through the AV node ▪ The time between atrial depolarization and the initiation of ventricular depolarization is the PR interval. The normal reference range for the PR interval is 0.12 to 0.20 seconds. o QRS duration ▪ 0.05 – 0.10 sec ▪ > 0.12 sec abnormal ▪ >.12 = widened QRS • Something problematic occurring with ventricular conduction (after AV node) ▪ The QRS complex corresponds to the wave of depolarization as it emerges from the AV node and moves downward to depolarize the right and left ventricles. The QRS is normally 0.05 to 0.10 seconds in duration. Abnormal intraventricular conduction is suggested by a QRS complex that exceeds 0.12 seconds. o ST Segment (repolarization of the ventricle; should be at isoelectric line [the same level as the reading before & after the P wave]) ▪ Elevation • Less than 1 mm on the standard EKG can be normal ▪ Depression • Almost always indicative of some kind of ischemia ▪ The segment between the end of the S wave (end of ventricular depolarization) and the beginning of the T wave is the ST segment. ▪ The ST segment represents the time between ventricular depolarization and the start of ventricular repolarization. It is normally isoelectric but can be elevated to 1 mm in the absence of any cardiac abnormality. However, it is never normal for the ST segment to be depressed. o QT segment (beginning of Q wave to end of T wave) ▪ Rate dependent • Faster the heart rate, shorter it will be ▪ < 0.47 sec ▪ Less than half of R-R distance • From the peak of one QRS to the peak of another QRS • This is how you would compensate for changes in QT segment associated with changes in HR • Delay in QT = delay in repolarization of the ventricle that can cause a variety of ventricular dysrhythmias that can occur & degenerate into torsades or vfib • QT segment is important to us because some of the drugs we give can prolong this; can cause people that have increased QT segment can cause them to degenerate into torsades ▪ The T-wave deflection should be in the same direction as the QRS complex and should not exceed 5 mm in amplitude in standard leads or 10 mm in precordial leads. Normal values for the QT interval should be corrected for the heart rate (QTc) because the QT interval varies inversely with heart rate. A normal QTc is less than 0.47 seconds. As a general rule, the QT interval is less than one half of the preceding R-R interval. • Abnormalities o Dysrhythmias (usually describe them based on their rate) ▪ Rate • Tachy or brady ▪ Location • Supraventricular or ventricular o Conduction problems ▪ Degree of blockade • 1st, 2nd, 3rd degree ▪ Location o Clinical significance (ask yourself these two things) ▪ Is it a perfusing rhythm? • If perfusing, doesn’t mean you can ignore it, but don’t have to act immediately • If you have a good BP, you have time to think about arrhythmia & what the problem is • If BP 60/20, no time to start thinking about things. Need to do something immediately to change rhythm ▪ Will it lead to something worse? • If perfusing rhythm, but something you recognize that will turn into bad rhythm, you need to address it acutely (ex, starting esmolol or beginning CPR) ▪ Cardiac rhythms that show abnormalities in rate, interval length, or conduction path are referred to as dysrhythmias. Dysrhythmias are usually classified according to heart rate and the site of the abnormality. ▪ The clinical significance of these abnormalities for the anesthesiologist depends on the effect they have on vital signs and the potential for deterioration into life-threatening rhythms. In healthy adults, a wide variation in heart rate can be tolerated, because normal compensatory mechanisms serve to maintain cardiac output and blood pressure. In patients with cardiac disease, however, dysrhythmias and conduction disturbances can overwhelm normal compensatory processes and result in hemodynamic instability, cardiac and other end-organ ischemia, congestive heart failure, and even death. • Tachydysrhythmias o Rhythm with rate > 100 bpm ▪ A cardiac rhythm higher than 100 beats per minute is considered a tachydysrhythmia. ▪ Tachydysrhythmias can result from three mechanisms: (1) increased automaticity in normal conduction tissue or in an ectopic focus, (2) reentry of electrical potentials through abnormal pathways, and (3) triggering of abnormal cardiac potentials due to afterdepolarizations. o Mechanisms ▪ Increase automaticity ▪ Reentry through abnormal pathways usually in the AV node ▪ Triggering of abnormal cardiac potentials due to afterdepolarization • Tachydysrhythmias o Automaticity ▪ The site with the fastest pacemaker sets the rate for the heart (usually the SA node) • Whichever part of the heart has the steepest phase 4 or the lowest threshold rate will set the rate for the heart • The fastest pacemaker in the heart is normally the SA node. The SA node spontaneously discharges at a rate of 60 to 100 beats per minute. ▪ This can be within the conduction system or outside it (ectopic focus) • Will not always be SA node because other things like morphologic changes, acidosis, ischemia, can make other places of the heart more sensitive/irritable, and these can take over rate-setting duties of SA node • If not SA node setting the rate, we say there is an ectopic foci setting the rate • Other pacemakers can be accelerated and overdrive the SA node as a result of disease states or iatrogenic influences such as mechanical or drug stimulation. A sustained rhythm resulting from accelerated firing of a pacemaker other than the SA node is called an ectopic rhythm. ▪ Rate can change by an increase in depolarization rate (Phase 4) or a decrease in threshold potential • Decrease in threshold so that threshold is reached sooner • Can be a combo of both • Abnormal automaticity is not confined to secondary pacemakers within the conduction system. Almost any cell in the heart may exhibit automaticity under certain circumstances. The automaticity of cardiac tissue changes when the slope of phase 4 depolarization shifts or the resting membrane potential changes. Sympathetic stimulation causes an increase in heart rate by increasing the slope of phase 4 of the action potential and by decreasing the resting membrane potential. Conversely, parasympathetic stimulation results in a decrease in the slope of phase 4 depolarization and an increase in resting membrane potential to slow the heart rate. ▪ Usually gradual onset and resolution • Sympathetic response causes an increase in rate of depolarization. Usually happens globally in RA so that every place gets an increase in rate of depolarization, but SA node is still fastest & still maintains responsibility for setting rate for the heart • Paroxysmal = comes on easily, leaves easily • Clinically, dysrhythmias resulting from an ectopic focus often have a gradual onset and termination. Cardiac dysrhythmias caused by enhanced automaticity result from repetitive firing of a focus other than the sinus node. • Tachydysrhythmias o Reentry Pathways (has to be 2 competing pathways; usually happens at AV node) • Normal conduction coming down from SA node, gets to a point where there is a bifurcation/split (usually associated with AV node). One tract goes down one way, the other tract goes down other way. For some reason, one tract gets blocked but the other one doesn’t get blocked. So it conducts down the leg of the fork, through the AV node, through the ventricle, then comes back up, essentially as a short circuit. If the other leg was conducted it couldn’t come through there (if depolarized, can’t come through tissue). Impulse gets sent back up here, by the time it gets here, depolarized, then comes down & sends another impulse through heart. Forms circle. Every time it goes around, it sends an impulse down. So there is retrograde conduction over accessory tract. ▪ Abrupt onset & termination • Paroxysmal = comes on easily, leaves easily. Responsible for more reentry pathways. • Reentrant dysrhythmias tend to be paroxysmal with abrupt onset and termination. ▪ Requires two pathways • Normal • Accessory tract o Reentry or triggered dysrhythmias require two pathways over which cardiac impulses can be conducted at different velocities (Figure 4-3, below). o Extra pathways called accessory tracts can exist around the AV node and can conduct impulses bypassing the AV node and normal infranodal conduction tract. These accessory tracts are usually remnants of tissue left from the embryologic formation of the heart. ▪ Retrograde conduction over accessory tracts • Normally, passage through the AV node is the slowest portion of the conduction system. In a reentry circuit, there is anterograde (forward) conduction over the slower normal conduction pathway and retrograde (backward) conduction over a faster accessory pathway. Pharmacologic or physiologic events may alter the balance between conduction velocities and refractory periods of the dual pathways, resulting in the initiation or termination of reentrant dysrhythmias. ▪ Accounts for most premature beats & tachydysrhythmias • Reentry pathways account for most premature beats and tachydysrhythmias. • FIGURE 4-3. Essential requirement for initiation of reentry excitation is a unilateral block that prevents uniform anterograde propagation of the initial cardiac impulse. Under appropriate conditions, this same cardiac impulse can traverse the area of blockade in a retrograde direction and become a reentrant cardiac impulse. • Extra Picture (below, not in notes) • Afterdepolarizations o “Oscillations” in membrane potential ▪ Afterdepolarizations are oscillations in membrane potential that occur during or after repolarization. ▪ First pic (below) is ventricular depolarization, but there are oscillations in membrane before it becomes repolarized. Instead of repolarizing all the way down like we expect, it gets stuck & oscillates. If one of the oscillations becomes big enough to reach threshold, we create another impulse. ▪ Can have early afterdepolarizations where the potential doesn’t get back to RMP ▪ You can have delayed where it gets back to RMP but fires back again before another impulse should be generated ▪ The after early depolarizations usually occur in phase 2 or 3 • More likely to happen if rate is slow. To get rid of them, you speed the rate up ▪ Delayed afterdepolarizations happen in phase 4 • Tend to be enhanced by fast rates. Opposite of early. Treated by slowing the rate down. ▪ Tachydysrhythmias are either increased automaticity, reentry pathways, or afterdepolarizations ▪ Phase 2/3 (relative refractory period)? ▪ Something is going on in the heart either mechanically or acidosis/ischemia o Can trigger a complete depolarization ▪ Normally, these membrane oscillations dissipate. However, under special circumstances they can trigger a complete depolarization. Once triggered, the process may continue and result in a self- sustaining dysrhythmia. o Early Afterdepolarizations ▪ Phase 2 or 3 ▪ Enhanced by slow rates ▪ Treated by accelerating heart rates ▪ Triggered dysrhythmias associated with early afterdepolarizations are enhanced by slow heart rates and are treated by accelerating the heart rate with positive chronotropic drugs or pacing. o Afterdepolarizations ▪ Phase 4 ▪ Enhanced by fast rates ▪ Treated by slowing heart rates ▪ Conversely, triggered dysrhythmias associated with delayed afterdepolarizations are enhanced by fast heart rates and can be suppressed with drugs that lower the heart rate. • Supraventricular Dysrhythmias o Sinus dysrhythmias o Sinus tachycardia o Premature atrial beats o Supraventricular tachycardia o Multifocal atrial tachycardia o Atrial flutter o Atrial fibrillation • Sinus Dysrhythmias o Irregular sinus rhythm ▪ You have sinus beats but they are irregular ▪ If you did R:R interval, it would not be the same, but every beat is the same (P before QRS, then T wave), but they aren’t regular ▪ Occasionally an ECG will show a sinus rhythm that appears irregular. This normal variant is called sinus dysrhythmia. o Normal response to changes in intrathoracic pressure during respiration (Bainbridge reflex) ▪ Inspiration accelerates HR • Response to Bainbridge reflex. You inspire, decrease intrathoracic pressure, sucks blood back into atrium, stretches atria, body perceives this as an increase in VR, so Bainbridge reflex will increase HR. • The variation in heart rate is in response to intrathoracic pressure changes during inspiration and expiration known as the Bainbridge reflex. • Inspiration accelerates the heart rate and expiration slows it down. • It is a normal variant and carries no risk of deterioration into a more dangerous rhythm. ▪ Expiration slows HR • When you exhale, you increase the intrathoracic pressure, decreasing VR, the body will interpret as a decrease in VR, so the HR will go down. • Bainbridge reflex increases HR as RAP increases to keep blood from backing into RA o Common in youth, declines with age ▪ Usually seen in young, healthy people ▪ Sinus dysrhythmia is common in children and young people but tends to decrease with age. o Seen in OR when using positive pressure ventilation ▪ PPV forces gas into the lungs with inspiration, increasing intrathoracic pressure, decreasing VR, which will slow the HR down via the Bainbridge reflex ▪ Usually if you see this, the patient is a little dry ▪ Usually if euvolemic, this will not happen ▪ Can also see this variation on inspiration/expiration on pulse ox, also another hint they are dry ▪ Benign rhythm, usually at a normal rate • Sinus Tachycardia o “Gradual” increase in HR (100 – 160 bpm) ▪ Really hard to have ST >160 ▪ Gradual increase, as opposed to paroxysmal ▪ Sinus tachycardia occurs at a heart rate of 100-60 beats per minute. o Normal response to sympathetic stimulation ▪ Typically, it is a nonparoxysmal increase in heart rate that speeds up and slows down gradually. ▪ Sinus tachycardia is caused by acceleration of SA node discharge secondary to sympathetic stimulation. ▪ Sinus tachycardia without manifestations of hemodynamic instability is not life-threatening. It can occur as part of the normal physiologic response to stimuli such as fear or pain or as a pharmacologic response to medications or substances such as atropine or caffeine. o In sick heart is an effort to increase CO ▪ If you have a sick ventricle & cannot increase CO, the only way you increase CO is by increase in HR. ▪ Don’t want to beta block these patients as it is their only way to increase CO ▪ Only way a kid can respond to decrease in CO is to increase HR ▪ Sick heart = CHF or ventricular problems ▪ On BB to decrease workload of heart, but still has some ability to increase HR, so if HR in 80s, don’t try to block them to 60 o Commonly seen with MI ▪ Since it does increase myocardial oxygen demand, it can contribute to myocardial ischemia and congestive heart failure in susceptible patients. ▪ Sinus tachycardia can also occur as a compensatory mechanism in the setting of significant heart disease such as congestive heart failure or myocardial infarction (Table 4-1). ▪ In these circumstances, the increased heart rate is usually a physiologic effort to increase cardiac output. Sinus tachycardia is the most common supraventricular dysrhythmia associated with acute myocardial infarction, occurring in 30% to 40% of these patients. o Normal “P” wave in front of each QRS ▪ The ECG during sinus tachycardia shows a normal P wave before every QRS complex. The PR interval is normal unless a co-existing conduction block exists. o Tx ▪ Fix the problem, first!!!!! • If you see sinus tach in OR, don’t reach for esmolol to change it, unless it is nonperfusing or patient is 87 years old & it is sinus tach with ST segment changes, then you can change it • Figure out problem. Light anesthesia, hypovolemia, ETT bouncing on carina which is very stimulating, full bladder, going into malignant hyperthermia, thyroid storm, febrile, hypoglycemic • If tachy to maintain CO, don’t want to slow it down. Can send them into CHF or compound their existing CHF • Treatment of sinus tachycardia is directed toward correcting any underlying causes of increased sympathetic stimulation. • Sinus tachycardia in patients with ischemic heart disease, diastolic dysfunction, or congestive heart failure can lead to significant clinical deterioration because of the increased oxygen demand, increased wall stress, and inability to increase myocardial perfusion in many of these patients. • Many causes of sinus tachycardia such as hypovolemia are clinically obvious, but some of the most serious causes, such as infection, hypoxia, myocardial ischemia, and congestive heart failure, may be less apparent. • If a specific cause of sinus tachycardia can be determined, it should be treated. ▪ Beta blockers • Start w/esmolol o Quick acting, so if you did mistreat it, will wear off quickly • Don’t use if increased HR is sustaining CO!!!!! • Avoidance of vagolytic drugs, such as pancuronium, can aid in management of sinus tachycardia intraoperatively. Although sinus tachycardia is generally well tolerated in young healthy patients, supplemental oxygen should be administered to increase oxygen supply in response to the increased oxygen demand. If a patient is not hypovolemic, intravenous administration of a β-blocker may be employed to lower the heart rate and decrease myocardial oxygen demand. • Caution must be exercised in the use of β-blockers in patients susceptible to bronchospasm. β-Blocker–mediated decreases in heart rate can cause an abrupt and dangerous decrease in blood pressure in patients with impaired cardiac function. Such patients may be unable to increase their stroke volume to compensate for the reduction in heart rate. • Premature Atrial Beats o Arise from ectopic foci in atria ▪ That will either cause an occasional premature beat, or can actually takeover from SA node ▪ Premature atrial contractions (PACs) arise from ectopic foci in the atria. ▪ The occurrence of PACs is not a risk factor for progression to a life-threatening dysrhythmia. o “Fluttering” or “heavy” heart beat ▪ Typical symptoms of PACs include an awareness of a "fluttering" or a "heavy" heart beat. o Causes ▪ Usually things that irritate the heart ▪ Acidosis, too much coffee, methylzenthene (theophylline), dig tox, too much soda, caffeine, a variety of stimulants can cause this ▪ Precipitating factors include excessive caffeine, emotional stress, alcohol, nicotine, recreational drugs, and hyperthyroidism. PACs are common in patients of all ages with and without heart disease. o More common at rest, will decrease w/increased heart rate ▪ As HR increases, SA node takes back over ▪ They often occur at rest and become less frequent with exercise. o Associated with ▪ Lung dz ▪ Ischemic heart dz ▪ Digitalis toxicity ▪ They are more common in patients with chronic lung disease, ischemic heart disease, and digitalis toxicity. ▪ PACs are the second most common dysrhythmia associated with acute myocardial infarction. • Premature Atrial Beats o ECG ▪ Early, abnormal “P” waves • PACs are recognized on the ECG by the presence of early, abnormally shaped P waves. ▪ Variable PR interval • The PR interval is variable. ▪ Usually normal QRS • Because everything is ok before ventricle. Whatever ectopic foci gets through SA node & everything below the SA node will be normal, so normal QRS o Tx • Most often the duration and configuration of the corresponding QRS complex is normal, because activation of the ventricles occurs through the normal conduction pathway. • Aberrant conduction of atrial impulses can occur, resulting in a QRS complex that is widened and may mimic that associated with a premature ventricular contraction (PVC). ▪ No compensatory pause • Like with PVCs • PACs, unlike PVCs, are not followed by a compensatory pause. ▪ Avoid cause • Put down the coffee or crack pipe • Avoidance of precipitating drugs or toxins can reduce the incidence of PACs. • Underlying predisposing conditions should be treated. ▪ Usually benign • Won’t cause a problem • PACs are usually hemodynamically insignificant and do not require acute therapy unless they are associated with initiation of a tachydysrhythmia. In this situation treatment is directed at controlling or converting the tachydysrhythmia. ▪ Anesthetic management of the patient with PACs should include avoidance of excessive sympathetic stimulation and drugs that might induce PACs. Pharmacologic treatment is required only if the PACs trigger secondary dysrhythmias. PACs can usually be suppressed with calcium channel blockers or β-blockers. The secondary dysrhythmias triggered by PACs are treated with drugs or maneuvers that improve heart rate control and/or convert the dysrhythmia to sinus rhythm. • Supraventricular Tachycardia o S&S ▪ Lightheadedness ▪ Dizziness • Because they are lightheaded & CO is down ▪ Fatigue ▪ Chest discomfort ▪ Dyspnea • Common symptoms during an episode of SVT include light-headedness, dizziness, fatigue, chest discomfort, and dyspnea. ▪ Syncope • Really is a bad decrease in CO • 15% of patients with SVT experience overt syncope. ▪ Polyuria • When people are in SVT, their atrium is contracting out of sync with their ventricle, so a lot of time the atria is trying to contract against a mitral or tricuspid valve, increases pressure, increases release of ANP hormone, which makes you pee more. Atrium interprets it as an increase in blood volume so tries to decrease by making more urine • Polyuria can be associated with SVT or any atrial tachycardia that causes AV dyssynchrony. The polyuria is caused by increased secretion of atrial natriuretic peptide. This happens because atrial pressures increase from contraction of the atria against closed AV valves and atrial stretch receptors are activated. o Female > males ▪ SVT occurs most often in the absence of structural heart disease in younger individuals and occurs three times more often in women than in men. • Supraventricular Tachycardia (SVT) o Any tachydysrhythmia created by foci above the AV node ▪ Supraventricular tachycardia (SVT) is a tachydysrhythmia (average heart rate of 160 to 180 beats per minute) initiated and sustained by tissue at or above the AV node. o Usually paroxysmal ▪ PSVT ▪ Comes on abruptly & ends abruptly ▪ Unlike sinus tachycardia, SVT is usually paroxysmal and may begin and end very abruptly. o AV nodal reentrant tachycardia (AVNRT) – usually caused by reentry phenomenon ▪ Normal anterograde conduction • Normal conduction from AV node down, so usually your QRS complexes look normal, as opposed to vtach where you will usually always have a widened QRS complex ▪ Faster retrograde conduction via accessory path ▪ AV nodal reentrant tachycardia (AVNRT) is the most common type of SVT and accounts for 50% of diagnosed SVTs. AVNRT is most commonly due to a reentry circuit in which there is anterograde conduction over the slower AV nodal pathway and retrograde conduction over a faster accessory pathway. Other mechanisms for SVT include enhanced automaticity of secondary pacemaker cells and triggered impulse initiation by afterdepolarizations. Atrial fibrillation and atrial flutter are SVTs, but their electrophysiology and treatment are distinctly different from those of other forms of SVT, so they are discussed separately. • Supraventricular Tachycardia (SVT) o HR ▪ Range 150-250 BPM ▪ Average 160-180 BPM o Usually narrow QRS o P wave ▪ Absent • Usually no P wave or if there is, it is abnormal & does not look like normal P wave • What’s happening is that the SA node is conducting right around to AV node & gets caught in the circle. Every time it goes through cycle, it causes AV node to fire. It gets caught in this cycle. Usually starts abruptly & ends abruptly. • No P wave because atrium is not contracting properly. Ventricles contract by short circuit right above AV node. Essentially ventricle is contracting before atrium can contract, so you see very rapid ventricular contraction that looks normal with no P wave ▪ Abnormal • Supraventricular Tachycardia (SVT) o Treatment ▪ If stable • Vagal maneuvers o If the patient is in hemodynamically stable condition, the initial treatment of SVT can consist of vagal maneuvers such as carotid sinus massage or Valsalva's maneuver. Termination by a vagal maneuver suggests reentry as the causative mechanism. • Used to do carotid maneuvers • Stick kids heads in ice, have them blow up a balloon • Want to kick up parasympathetic stimulation to slow down the rate ▪ Drugs • If conservative treatment is not effective, pharmacologic treatment directed at blocking AV nodal conduction is indicated. Clinical factors guide the choice of drug treatment, but adenosine, calcium channel blockers, and β-blockers are commonly used to terminate SVT. • Adenosine o Adenosine has a unique advantage over other intravenous drugs used to treat SVT because it has a very rapid onset (15 to 30 seconds) and very brief duration of action (10 seconds). Most AVNRT episodes can be terminated by a single dose of adenosine. o Multifocal atrial tachycardia, atrial flutter, and atrial fibrillation do not respond to adenosine. o Heart transplant recipients require a reduction in dosage because of denervation hypersensitivity. o Conversely, patients taking theophylline may require higher dosages of adenosine to produce a therapeutic effect because of competition with adenosine for receptor sites. • Beta blockers o Intravenous β-blockers can also be used to control or convert SVT. o Intravenous digoxin is not clinically useful in acute control of SVT because digoxin has a delayed peak effect and a narrow therapeutic window. • Ca++ channel blocker o Intravenous administration of calcium channel–blocking drugs such as verapamil and diltiazem is also useful for terminating SVT. These drugs offer the advantage of a longer duration of action than adenosine. However, side effects, including peripheral vasodilation and negative inotropy, can contribute to an undesirable degree of hypotension. ▪ Cardioversion if unresponsive to drugs or unstable • Synchronized defibrillation • Electrical cardioversion is indicated for SVT unresponsive to drug therapy or SVT associated with hemodynamic instability. ▪ Long-term medical treatment of patients with repeated episodes of SVT includes calcium channel blockers, digoxin, and/or β-blockers. Radiofrequency catheter ablation may also be used to treat patients with recurrent or recalcitrant AVNRT. ▪ Anesthetic management for a patient with SVT should focus on avoiding factors known to produce ectopy, such as increased sympathetic tone, electrolyte imbalances, and acid-base disturbances. Because SVT is usually paroxysmal, monitoring of vital signs to detect any progression to hemodynamic instability and verbal reassurance (if the patient is awake) is usually all that is needed until an episode of SVT terminates. One should evaluate and treat any potential aggravating factors and anticipate the need for antidysrhythmics and/or cardioversion. • Multifocal Atrial Tachycardia o Irregular rhythm caused by multiple ectopic foci in atria ▪ At least 2 other foci other than AV (?) node ▪ Multifocal atrial tachycardia (MAT) is an irregular rhythm that electrophysiologically reflects the presence of multiple ectopic atrial pacemakers. o ECG ▪ 3 or more different shaped “P” waves • The ECG shows P waves with three or more different morphologies, and the PR intervals vary. ▪ Irregular PR intervals • Because it is coming from different spots ▪ Rate 100 – 180 (slower than a fib) • This rhythm is frequently confused with atrial fibrillation, but unlike atrial fibrillation, the rate is not excessively rapid. • The atrial rhythm is usually between 100 and 180 beats per minute. o Treatment ▪ Fix the cause (lung dz is common) • Very often you can just give them O2 because they get hypoxic, causing hypoxic vasoconstriction so their lungs get constricted & they get pulm HTN, backing blood up into right side of heart. Giving them O2 cures hypoxia, vasodilates lungs, decreases backflow into RA & these go away • MAT is most commonly seen in patients experiencing an acute exacerbation of chronic lung disease. • It can also be associated with methylxanthine toxicity (theophylline and caffeine), congestive heart failure, sepsis, and metabolic or electrolyte abnormalities. • MAT usually responds to treatment of the underlying pulmonary decompensation with bronchodilators and supplemental oxygen. An improvement in arterial oxygenation tends to decrease the activity of the ectopic foci that cause MAT. Pharmacologic treatment of MAT has limited success and is considered secondary. • Magnesium sulfate 2 g IV over 1 hour followed by 1 to 2 g IV per hour by infusion has shown some success in decreasing atrial ectopy and converting MAT to sinus rhythm. Verapamil 5 to 10 mg IV over 5 to 10 minutes slows the ventricular rate and will convert to sinus rhythm in some patients. Likewise, β-blockers such as esmolol or metoprolol can decrease the ventricular rate but at the risk of worsening the situation by provoking bronchospasm in susceptible patients. Theophylline use can exacerbate this condition. Cardioversion has no effect on the multiple sites of ectopy that produce this dysrhythmia. • In summary, patients with MAT who must undergo urgent surgery benefit from optimization of their pulmonary function and arterial oxygenation. Avoidance of medications or procedures that could worsen the pulmonary status and avoidance of hypoxemia are the mainstays of anesthetic management. o FIGURE 4-5 (above, NOT in class PPT). Comparison of the electrocardiogram appearance of multifocal atrial tachycardia (A) and atrial fibrillation (B). Both rhythms are irregular. However, note several distinct P-wave morphologies and varying PR intervals with multifocal atrial tachycardia. There are no distinct P waves with atrial fibrillation. • Atrial Flutter o Organized atrial rhythm w/rate 250-350 ▪ Atrial flutter is characterized by an organized atrial rhythm with an atrial rate of 250 to 350 beats per minute with varying degrees of AV block. o Varying degree of AV block (usually 2:1) ▪ In this case it is 3:1 ▪ The rapid P waves create a sawtooth appearance on ECG and are called flutter waves. The flutter waves are particularly noticeable in leads II, III, aVF, and V1. The flutter waves are not separated by an isoelectric baseline. ▪ The ventricular rate may be regular or irregular depending on the rate of conduction. Most commonly, patients have 2:1 AV conduction so, for example, an atrial rate of 300 beats per minute with 2:1 conduction results in a ventricular rate of 150 beats per minute. Characteristically, the ventricular rate is about 150 beats per minute. o Associated with structural heart dz (atrial dilation) ▪ Dilation of atrium, usually from regurg/a valvular problem ▪ Atrial flutter is usually associated with structural heart disease. It occurs in approximately 30% of patients with atrial fibrillation and may be associated with more intense symptoms than atrial fibrillation because of the more rapid ventricular response. o Commonly seen with atrial fibrillation ▪ Either will progress into a-fib or go back and forth from a-fib to a flutter ▪ Atrial flutter frequently occurs in association with other dysrhythmias such as atrial fibrillation or atrial tachycardia. Reciprocating deterioration of atrial flutter into atrial fibrillation and then reversion of atrial fibrillation into atrial flutter is common. o Hold elective surgery for new onset a flutter ▪ Because they are not optimized ▪ About 60% of patients experience atrial flutter in association with an acute exacerbation of a chronic condition such as pulmonary disease, acute myocardial infarction, ethanol intoxication, or thyrotoxicosis, or after cardiothoracic surgery. In many instances treatment of the underlying disease process restores sinus rhythm. • Atrial Flutter o Treatment ▪ Unstable – cardioversion (~50 J) • If atrial flutter is hemodynamically significant, the treatment is cardioversion. Often less than 50 J (monophasic) is adequate to convert the rhythm to sinus. • Patients with atrial flutter lasting longer than 48 hours should receive anticoagulant therapy and should be evaluated by transesophageal echocardiography for the presence of an atrial thrombus before any attempt at cardioversion is made. ▪ Stable • Pacing (transcutaneous) o In a patient in hemodynamically stable condition, overdrive pacing using transesophageal or atrial electrodes can be used for conversion to sinus rhythm. • Drugs o First priority is to control AV conduction (avoid converting to 1:1 conduction!!!!) ▪ Every time they have a flutter wave, you don’t want it to become ventricular contraction, or else their ventricle will be contracting 200 times a minute which is not sustainable ▪ Pharmacologic control of the ventricular response and conversion to sinus rhythm can be challenging in patients with atrial flutter. Ventricular rate control should be the initial goal of therapy. This is done to prevent deterioration in AV conduction from 2:1 to 1:1, which represents a doubling of the heart rate. Such an increase in heart rate can cause severe hemodynamic instability. If there is 1:1 conduction with a ventricular rate of 300 beats per minute or faster, reentry is the most likely mechanism and procainamide administration should be considered. o Amiodarone o Diltiazem o Verapamil ▪ More commonly, intravenous drug therapy for ventricular rate control includes amiodarone, diltiazem, and verapamil. All of these drugs are helpful in controlling the ventricular rate, but none of these agents is likely to convert atrial flutter to sinus rhythm. o Anticoagulation ▪ Patients with atrial flutter lasting longer than 48 hours should receive anticoagulant therapy and should be evaluated by transesophageal echocardiography for the presence of an atrial thrombus before any attempt at cardioversion is made. • Atrial Fibrillation o S&S (due to loss of atrial kick & decrease in CO) ▪ Fatigue ▪ Generalized weakness ▪ Palpitations ▪ Angina ▪ CHF ▪ Hypotension o Causes ▪ Valve Dz ▪ Ischemic heart dz ▪ Hypertension ▪ COPD ▪ Pericarditis ▪ PE ▪ DM ▪ Atrial hypertrophy o Atrial fibrillation is the most common sustained cardiac dysrhythmia in the general population, affecting 2.2 million people in the United States. The incidence of atrial fibrillation increases with age: it is present in 1% of individuals younger than 60 years of age, increases to 5% in those 70 to 75 years, and exceeds 10% in those older than 80 years. The most common underlying cardiovascular diseases associated with atrial fibrillation are systemic hypertension and ischemic heart disease. Valvular heart disease, congestive heart failure, and diabetes mellitus are independent risk factors for the development of atrial fibrillation. Long-term atrial fibrillation increases an individual's risk of heart failure. o Atrial fibrillation can be a sustained or an episodic dysrhythmia. o Predisposing conditions include rheumatic heart disease (especially mitral valve disease), hypertension, hyperthyroidism, ischemic heart disease, chronic obstructive pulmonary disease, alcohol intake (holiday heart syndrome), pericarditis, pulmonary embolus, and atrial septal defect. o In some instances, treating the underlying disorder eliminates the atrial fibrillation. Increased left atrial size and mass are positive predictors for atrial fibrillation. Atrial fibrillation may be identified on physical examination or ECG in a patient with no associated symptoms. However, most patients are symptomatic. Symptoms may be vague, such as generalized weakness and fatigue, or prominent, such as palpitations, angina pectoris, shortness of breath, orthopnea, and hypotension. • Atrial Fibrillation o Multiple sites in atria depolarize & contract at the same time ▪ Atrial fibrillation occurs when multiple areas of the atria continuously depolarize and contract in a disorganized manner. There is no coordinated depolarization or contraction, only a quivering of the atrial walls. o Results in loss of atrial pumping ability o Greatest danger associated with clot formation ▪ Heart is quivering, does not empty properly, blood sits there for a while with turbulence, creating clots, which can go to brain & cause a CVA o ECG ▪ Chaotic atrial activity ▪ No “P” waves • No organized atrial activity • R:R between QRS is random • Lost atrial kick (responsible for 20% of atrial filling) o Most people do fine with this as long as heart is not taxed. If heart is taxed, they can have big problems • The dysrhythmia is characterized on the ECG by chaotic atrial activity with no discernible P waves. • Atrial fibrillation may be triggered by other atrial tachycardias and commonly occurs in association with atrial flutter. ▪ Variable ventricular response (usually 180 if untreated) • Rapid, disordered atrial activation and irregular electrical input to the AV node result in sporadic AV nodal conduction and irregularly irregular ventricular contraction. Ventricular response rates as high as 180 beats per minute can occur in patients with normal AV node function. Extremely rapid ventricular responses in excess of 180 beats per minute can be seen in patients with accessory AV nodal bypass tracts. In this situation, the QRS complex is often wide, and the ECG can resemble ventricular tachycardia or ventricular fibrillation. • Atrial Fibrillation o Treatment goals ▪ Return to NSR ▪ Control ventricular rate • If cannot get back to NSR • A-fib with RVR. Fairly good conduction between number of atria contractions & ventricular contractions so the atria is conducting fast, not allowing atrial filling or good stroke volume. This taxes ventricle because it demands good CO • If cannot convert to NSR, get ventricular rate close to as normal as you can o Cardioversion ▪ Drugs – amiodarone ▪ Electricity (100 – 200 J – needs sedation!!!) • Give them Versed & then almost an induction dose of Propofol • Not something you do in the OR or intubate anyone for o Rate control ▪ Beta blockers ▪ Ca channel blockers ▪ Digoxin o Loss of coordinated atrial contraction promotes stasis of blood within the left atrium and can lead to the formation of atrial thrombi. Atrial thrombi and the potential for thromboembolic stroke are the most serious clinical dangers of atrial fibrillation. Patients with atrial thrombus are usually treated with anticoagulants. The prophylactic regimen chosen for each patient is determined by risk stratification for thromboembolism based on age and concomitant heart disease. In the acute setting, intravenous heparin is most commonly administered. For long-term anticoagulation therapy, warfarin is most often used. Warfarin is a vitamin K antagonist, with a narrow therapeutic window that necessitates frequent monitoring of clinical effect (international normalized ratio). It also interacts with numerous foods and medications. An alternative to warfarin emerged in 2010 with U.S. Food and Drug Administration (FDA) approval of the first new oral anticoagulant to become available in 50 years. Dabigatran (Pradaxa) is now available for the prevention of stroke and systemic embolization in patients with atrial fibrillation. Dabigatran is a thrombin inhibitor with a half-life of 12 to 17 hours. There is no specific antidote for dabigatran effects. However, transfusion of fresh frozen plasma or packed red blood cells and surgical intervention to control bleeding are supportive therapies recommended for severe hemorrhage associated with dabigatran therapy. o A large proportion of patients with new-onset atrial fibrillation experience spontaneous conversion to sinus rhythm within 24 to 48 hours. Therapy goals for new-onset atrial fibrillation include ventricular rate control and electrical or pharmacologic cardioversion. Control of ventricular response is typically achieved with drugs that slow AV nodal conduction. The most commonly used drugs for this purpose are β-blockers, calcium channel blockers, and digoxin. β-Blockers are useful in the prevention of recurrent atrial fibrillation, provide good heart rate control, and reduce symptoms during subsequent episodes of atrial fibrillation. Potential side effects of β-blocker therapy are hypotension and bronchospasm. Calcium channel–blocking drugs such as diltiazem and verapamil can rapidly reduce the ventricular rate during atrial fibrillation. These drugs have negative inotropic effects and must be used with caution in patients prone to heart failure. Digoxin can be useful to control ventricular rate but is not effective for conversion of atrial fibrillation to sinus rhythm. In the acute setting of rapid atrial fibrillation, the usefulness of digoxin is limited due to the fact that its peak therapeutic effects are delayed by several hours. Side effects associated with digitalis therapy are dose related and most commonly include AV block and ventricular ectopy. o Pharmacologic cardioversion is most effective if initiated within 7 days of the onset of atrial fibrillation. Several drugs are efficacious in converting atrial fibrillation to sinus rhythm, including amiodarone, propafenone, ibutilide, and sotalol. The preferred drug for patients with significant heart disease, including ischemic heart disease, left ventricular hypertrophy, left ventricular dysfunction, and heart failure, is amiodarone. The efficacy of intravenous amiodarone in producing chemical cardioversion ranges from 34% to 69% for a bolus dose and 55% to 95% when the bolus is followed by a continuous drug infusion. Amiodarone also suppresses atrial ectopy and recurrence of atrial fibrillation and improves the success rate of electrical cardioversion. Adverse effects of short-term amiodarone administration include bradycardia, hypotension, and phlebitis at the site of administration. Potential long-term side effects include visual disturbances, thyroid dysfunction, pulmonary toxicity, and skin discoloration. Electrical cardioversion is the most effective method for converting atrial fibrillation to normal sinus rhythm and is indicated in patients with co-existing symptoms of heart failure, angina pectoris, or hemodynamic instability. o If new-onset atrial fibrillation occurs before induction of anesthesia, surgery should be postponed if possible until ventricular rate control or conversion to sinus rhythm has been achieved. Intraoperative management of atrial fibrillation depends on the hemodynamic stability of the patient. If the atrial fibrillation is hemodynamically significant, the treatment is cardioversion. Synchronized cardioversion at 100 to 200 J (biphasic) is indicated. If vital signs are stable, the primary goal should be rate control with a β-blocker or calcium channel blocker if there are no clinical contraindications. The drug of choice for rate control in a patient with a known or suspected electrical accessory pathway and preexcitation is procainamide or amiodarone. Pharmacologic conversion to sinus rhythm with intravenous amiodarone may be attempted if vital signs allow. o Atrial fibrillation is the most common postoperative tachydysrhythmia and frequently occurs early in the postoperative period (first 2 to 4 days), especially in elderly patients following cardiothoracic surgery. Patients with chronic atrial fibrillation should continue to receive their antidysrhythmic drugs perioperatively with close attention to serum magnesium and potassium levels, particularly if the patient is taking digoxin. Careful coordination with the primary care team is needed to manage the transition on and off of intravenous and oral anticoagulation. • Ventricular Rhythms o Ventricular Ectopy (PVCs) o Ventricular Tachycardia o Ventricular Fibrillation • Ventricular Ectopy (PVCs) o Short or sustained episodes ▪ Can have single PVCs or a run of PVCs o More than 3 consecutives PVCs would be a run of PVCs o S&S ▪ Palpitations ▪ Near syncope • They don’t generate the normal SV of a normal ventricular contraction, decreasing CO ▪ Syncope • If sustained more than a few beats, can decrease CO enough to cause syncope o Usually benign o More than 6/min, repetitive or multifocal PVCs indicate increased risk ▪ Unifocal PVC – looks the same every time it occurs because it is coming from the same point in the ventricle ▪ Multifocal – coming from more than one spot & will look different; more than one spot on the heart is irritated, which is something you need to take care of • Increased risk = generate into vtach or vfib, so is something you will have to deal with • Ventricular Ectopy (PVCs) o ECG Findings ▪ Premature, wide QRS complex • Unifocal or multifocal o Premature = occurs before you expect it to happen o Pic below – PVC to the left, multifocal PVC to the right. Because the impulse is originating from two different spots on the ventricle o Ventricular premature beats arise from single (unifocal) or multiple (multifocal) foci located below the AV node. ▪ No “P” wave prior to PVC • Impulse comes from the ventricle itself, is not generated by the SA node • Characteristic ECG findings include a premature and wide QRS complex, no preceding P wave, ST segment and T-wave deflection opposite to the QRS deflection, and a compensatory pause before the next sinus beat. ▪ ST segment & T wave w/opposite deflection • T wave is lost in the depolarization of this strip, so you can’t see a T wave here ▪ Compensatory pause • Ventricular ectopy can occur as short episodes with spontaneous termination or as a sustained period of bigeminy or trigeminy. The occurrence of more than three consecutive PVCs is considered ventricular tachycardia. • The most common symptoms associated with ventricular ectopy are palpitations, near syncope, and syncope. • The volume of blood ejected during a PVC is smaller than that ejected during a sinus beat because of lack of the atrial contribution to ventricular filling during diastole (loss of "atrial kick"). • There is a compensatory pause after a PVC before the P wave of the next sinus beat. The stroke volume of the sinus beat following the compensatory pause is larger than normal. o R on T phenomenon ▪ When PVC occurs in middle third of T wave. Can initiate series of repetitive beats. • Can initiate vtach, then vfib • What you don’t want to happen: the T wave is repolarizing the ventricle, you don’t want a T wave occurring where the ventricle is trying to repolarize, then get stimulated and cause a PVC. Instead of creating PVCs, it can generate sustained vtach, which then can cause vfib • This is why you use synchronized cardioversion • If repetitive or multifocal, you want to take care of it so it doesn’t cause R-on-T phenomenon • PVCs can be benign and self-limiting or progressive and detrimental. The vulnerable period of the ECG complex (corresponding to the relative refractory period of the cardiac action potential) occurs at approximately the middle third of the T wave. PVCs that occur during this time may initiate repetitive beats that can deteriorate into a sustained rhythm such as ventricular tachycardia or ventricular fibrillation. This clinical situation is known as the R-on-T phenomenon. • Ventricular Ectopy (PVCs) o Treat when ▪ Frequent ▪ Polymorphic ▪ Occur in runs of 3 or more • During administration of an anesthetic, if a patient exhibits six or more PVCs per minute and repetitive or multifocal forms of ventricular ectopy, there is an increased risk of development of a life-threatening dysrhythmia. The immediate availability of a defibrillator should be confirmed. • The differential diagnosis of possible causes of PVCs includes acidosis, electrolyte imbalance, use of prodysrhythmic drugs, and mechanical irritation such as from cardiac surgery or intracardiac or intrathoracic catheters. • Treatment should be aimed at elimination of as many of these causative factors as possible. Amiodarone, lidocaine, and other antidysrhythmics are indicated only if the PVCs progress to ventricular tachycardia or are frequent enough to cause hemodynamic instability. β-Blockers are the most successful drugs in suppressing ventricular ectopy. ▪ Risk causing R-on-T • Ventricular premature beats should be treated when they are frequent, are polymorphic, occur in runs of three or more, or exhibit the R-on-T phenomenon, because these characteristics are associated with an increased incidence of progression to ventricular tachycardia and ventricular fibrillation. o Eliminate underlying cause ▪ Many antidysrhythmic drugs have prodysrhythmic effects • If they are on an antidysrhythmic, it may be the origin of their PVCs. This is also why you don’t want to nonchalantly give these people antidysrhythmic drugs for unconcerning PVCs because it can cause more problems than it helps with • With the exception of β-blockers, currently available antidysrhythmic drugs have not been shown in randomized clinical trials to be effective in the primary long-term management of ventricular dysrhythmias. Many antidysrhythmic drugs have prodysrhythmic effects and/or prolong the QT interval. • In fact, prolongation of depolarization (QT interval) can precipitate and increase the propensity for dysrhythmias. Amiodarone, lidocaine, and other antidysrhythmics are not indicated unless PVCs progress to ventricular tachycardia or are frequent enough to cause hemodynamic instability. Drug therapy is not effective in suppression of ventricular dysrhythmias caused by mechanical irritation of the heart. ▪ Drugs that prolong the QT interval • Want to avoid drugs that prolong QT interval. If you prolong T wave, you increase risk of R-on-T • Primary steps in the treatment of ventricular premature beats include elimination or correction of the underlying cause, discontinuation of prodysrhythmic drugs or drugs that prolong the QT interval, and elimination of any iatrogenic mechanical irritation of the heart such as from intracardiac catheters. A defibrillator should be immediately available in case clinical deterioration into a life-threatening dysrhythmia occurs. ▪ Cardiac irritants • A lot of things can cause cardiac irritations, could be something mechanical like a PA catheter or pacing wires or could be ischemia, acidosis o Typically, benign ventricular premature beats occur at rest and disappear with exercise. An increased frequency of PVCs with exercise may be an indication of underlying heart disease. The prognostic significance of ventricular ectopy depends on the presence and severity of co-existing structural heart disease. The incidence of PVCs in a healthy population ranges from 0.5% in those younger than 20 years to 2.2% in those older than 50 years. In the absence of structural heart disease, asymptomatic ventricular ectopy is benign with no demonstrable risk of sudden death even in the presence of ventricular tachycardia. o The occurrence of six or more PVCs per minute and repetitive or multifocal forms of ventricular ectopy, even if asymptomatic, indicate an increased risk of developing a life-threatening ventricular tachydysrhythmia. The most common pathologic conditions associated with this type of dysrhythmia are arterial hypoxemia, myocardial ischemia or infarction, valvular heart disease, cardiomyopathy, QT interval prolongation, digitalis toxicity, and electrolyte abnormalities, especially hypokalemia and hypomagnesemia. Excessive caffeine, alcohol, and cocaine use can also cause PVCs. • Ventricular Tachycardia o Palpitations, near syncope & syncope ▪ When someone is in vtach, they know it. They have a fluttering in their heart ▪ Syncope as it disrupts CO o ECG ▪ No “P” waves • P wave not being conducted through the SA node; it is all ventricular impulses ▪ Sustained, regular, wide QRS complex • If normal vtach, usually the same shape ▪ Rate >120 • Ventricular tachycardia (also called monomorphic ventricular tachycardia) is present when three or more consecutive ventricular premature beats occur at a heart rate of more than 120 beats per minute (usually 150 to 200 beats per minute). ▪ Can be difficult to differentiate from SVT • Usually vtach has wider QRS complexes; SVT usually has narrow QRS complexes • Ventricular tachycardia can occur as a nonsustained, paroxysmal rhythm or as a sustained rhythm. The rhythm is regular with wide QRS complexes and no discernible P waves (Figure 4-6). • SVT can sometimes be difficult to distinguish from ventricular tachycardia, especially if there is aberrant conduction or if the patient has an RBBB or LBBB. • Ventricular tachycardia is common after an acute myocardial infarction and in the presence of inflammatory or infectious diseases of the heart. Digitalis toxicity may also appear as ventricular tachycardia. ▪ Torsade de Points is a distinct form • Ventricular waves oscillate; get bigger & smaller, bigger & smaller • Not regular like to left; look irregular like to right • Not vfib because vfib does not have nearly as much regularity to it • The waves getting bigger/smaller makes it characteristic for torsades • Torsade de pointes (TdP; also called polymorphic ventricular tachycardia) is a distinct form of ventricular tachycardia initiated by a ventricular premature beat in the setting of abnormal ventricular repolarization (prolongation of the QT interval). Drugs that prolong repolarization, such as phenothiazines, tricyclic antidepressants, certain antiemetics, and most antidysrhythmics, predispose to development of TdP. o Ventricular dysrhythmias occur in 70% to 80% of persons older than age 60 and are often asymptomatic. The prognosis depends on the presence or absence of structural heart disease. In the perioperative environment, mechanical ventilation, drug therapy, insertion of central catheters, and other interventions can be iatrogenic causes of ventricular dysrhythmias. The risk of sudden death in patients with structurally normal hearts experiencing ventricular dysrhythmias is low. However, treatment with a β-blocker or calcium channel blocker can suppress the dysrhythmia and alleviate symptoms. Catheter ablation or implantation of a cardioverter or defibrillator are options for treatment of drug-refractory ventricular tachycardia. • Ventricular Tachycardia o Treatment ▪ If unstable – cardioversion • On occasion, it may be impossible to differentiate monomorphic ventricular tachycardia from SVT based on clinical symptoms, vital signs, or ECG findings. • Patients with symptomatic or unstable monomorphic ventricular tachycardia or SVT should undergo cardioversion immediately. • Cardioversion can begin at an output of 100 J (monophasic) and increase in increments of 50 to 100 J as necessary. ▪ Persistent or recurrent (give antidysrhythmic) • Amiodarone o If vital signs are stable but the ventricular tachycardia is persistent or recurrent after cardioversion, then administration of amiodarone 150 mg over 10 minutes is recommended. This may be repeated as needed to a maximum total dose of 2.2 g in 24 hours. • Procainamide o Recommended alternative drugs include procainamide, sotalol, and lidocaine. • Lidocaine ▪ Pulseless V-Tach • CPR/ACLS • Pulseless ventricular tachycardia or polymorphic ventricular tachycardia under any circumstances requires initiation of cardiopulmonary resuscitation (CPR) and immediate defibrillation using 360 J (monophasic). o The occurrence of paroxysmal nonsustained ventricular tachycardia during anesthesia should prompt an investigation into potential causes. A plan to improve reversible factors should be implemented. At any point, episodic ventricular tachycardia can progress to stable ventricular tachycardia or deteriorate into unstable ventricular tachycardia, pulseless ventricular tachycardia, or ventricular fibrillation. The occurrence of sustained ventricular tachycardia with or without a pulse demands immediate action. In addition to electrical therapy and drug treatment, endotracheal intubation and evaluation and correction of acid-base and electrolyte disturbances should be undertaken as clinically appropriate. o FIGURE 4-6 (above, from book, NOT class PPT). Comparison of the electrocardiographic appearance of monomorphic ventricular tachycardia, polymorphic ventricular tachycardia (torsade de pointes), and ventricular fibrillation. • Ventricular Fibrillation o “Irregular ventricular rhythm incompatible with life” ▪ Heart is quivering ▪ Ventricular fibrillation is the most common cause of sudden cardiac death. Most victims have underlying ischemic heart disease. In patients with acute coronary ischemia, those receiving β- blockers, angiotensin-converting enzyme inhibitors, and statins have ventricular tachycardia or ventricular fibrillation less often than those not receiving these drugs. Ventricular tachycardia often precedes the onset of ventricular fibrillation. The gold standard for long-term treatment of recurrent episodic ventricular tachycardia or fibrillation is implantation of a permanent automatic pacemaker-cardioverter-defibrillator with adjuvant drug therapy as a second-line treatment. ▪ Ventricular fibrillation is a rapid, grossly irregular ventricular rhythm with marked variability in QRS cycle length, morphology, and amplitude (see Figure 4-6). This rhythm is incompatible with life because there is no associated stroke volume or cardiac output. A pulse or blood pressure never accompanies ventricular fibrillation. If a patient with presumed ventricular fibrillation is awake or responsive, the ECG must be reevaluated before treatment decisions are made. o Defibrillation is the only treatment ▪ Ventricular fibrillation during anesthesia is a critical event. CPR must be initiated immediately. Electrical defibrillation is the only effective method to convert ventricular fibrillation to a rhythm capable of generating a cardiac output. Defibrillation involves delivery of an electrical current through the heart to depolarize all myocardial cells at once. Ideally, a single pacemaker focus will then restore myocardial synchrony. o Sooner the better (3-5 minutes from onset) ▪ This treatment should be instituted as soon as possible, because cardiac output, coronary blood flow, and cerebral blood flow are extremely low during ventricular fibrillation, even with ideally performed external cardiac compressions. The single most important factor affecting survival in patients experiencing ventricular fibrillation is time to defibrillation. Survival is best if defibrillation occurs within 3 to 5 minutes of cardiac arrest. o Success can be improved with epinephrine or vasopressin ▪ When ventricular fibrillation is refractory to electrical treatment, administration of epinephrine 1 mg IV or vasopressin 40 units IV may improve the response to electrical defibrillation. Adjunctive therapy with amiodarone, lidocaine, or, in the case of TdP, magnesium may be indicated. Standardized advanced cardiac life support (ACLS) algorithms (Figure 4-7) should be followed for electrical, pharmacologic, and adjunctive therapy. ▪ In any pulseless arrest, contributing factors should be sought and treated. The differential diagnosis includes hypoxia, hypovolemia, acidosis, hypokalemia, hyperkalemia, hypoglycemia, hypothermia, drug or environmental toxins, cardiac tamponade, tension pneumothorax, coronary ischemia, pulmonary embolus, and hemorrhage. • Wolff-Parkinson-White Syndrome o Usually asymptomatic ▪ So people don’t know it until they get EKG ▪ Since Wolff-Parkinson-White (WPW) syndrome was first described in 1930, the understanding of WPW syndrome and reentrant tachycardias has improved enormously. WPW syndrome occurs in 1% of the general population. It is more common in patients with Ebstein's malformation of the tricuspid valve, hypertrophic cardiomyopathy, and transposition of the great vessels. There is a bimodal age distribution in initial symptoms, with the first peak in early childhood, then a second in young adulthood. o Symptoms ▪ Paroxysmal palpitation • Sudden onset & sudden resolution • Paroxysmal palpitations with or without dizziness, syncope, dyspnea, or angina pectoris are common during the tachydysrhythmias associated with this syndrome. The initial manifestation of WPW syndrome occurs during pregnancy in some women. • Other patients have the first manifestation of WPW syndrome during the perioperative period. The incidence of sudden cardiac death in patients with WPW syndrome is 0.15% to 0.39% per patient-year, but it is very unusual for sudden death to be the initial manifestation of WPW syndrome. ▪ Dizziness ▪ Syncope ▪ Angina o ECG ▪ Delta wave • Kind of a lazy Q wave • It doesn’t go up as abruptly; has less of a slope • The diagnosis of WPW syndrome is reserved for conditions characterized by both preexcitation and tachydysrhythmia. • Ventricular preexcitation causes an earlier than normal deflection of the QRS complex called a delta wave. Delta waves can mimic the Q waves of a myocardial infarction. ▪ Slightly wider QRS • Wolff-Parkinson-White Syndrome o AV Nodal Reentry Tachycardia (AVNRT) most common dysrhythmia • Usually associated with a reentry tachycardia. • AVNRT is the most common tachydysrhythmia seen in patients with WPW syndrome. It accounts for 95% of the dysrhythmias seen with this syndrome. This tachydysrhythmia is usually triggered by a PAC. AVNRT is classified as either orthodromic (narrow QRS complex) or antidromic (wide QRS complex). • Two kinds: ▪ Orthodromic • Regular anterograde conduction (narrow complex) o Regular anterograde or forward conduction o This is what you would think of as a normal reentry pathway, then you get the retrograde conduction • Accessory retrograde conduction • Most common (90-95%) o Orthodromic AVNRT is much more common (90% of 95% of cases) and has a narrow QRS complex because the cardiac impulse is conducted from the atrium through the normal AV node–His-Purkinje system. o These impulses return from the ventricle to the atrium using the accessory pathway. ▪ Antidromic • Accessory anterograde conduction (wide complex) o Forward conduction goes through an abnormal pathway o In the less common antidromic form of AVNRT, the cardiac impulse is conducted from the atrium to the ventricle through the accessory pathway and returns from the ventricles to the atria via the normal AV node. The wide QRS complex seen in antidromic AVNRT makes it difficult to distinguish this dysrhythmia from ventricular tachycardia on ECG. • Regular retrograde conduction o Conduction that is coming back up & causing problem, goes up back through the regular conduction system • Wolff-Parkinson-White Syndrome o Treatment ▪ Orthodromic (slow or block normal AV conduction) • Vagal maneuvers • Adenosine • Verapamil • Beta blockers • Amiodarone o Treatment of orthodromic AVNRT in conscious patients in stable condition should begin with vagal maneuvers such as carotid sinus massage or Valsalva's maneuver. If vagal maneuvers are unsuccessful, adenosine, verapamil, β- blockers, or amiodarone may be used as clinically appropriate. ▪ Antidromic (do not give drugs that will slow normal AV conduction) • Procainamide • Cardioversion o Treatment of antidromic AVNRT is intended to block conduction of the cardiac impulse along the accessory pathway. Drugs that slow AV nodal conduction, such as adenosine, calcium channel blockers, β-blockers, lidocaine, and digoxin, may increase conduction along the accessory pathway and are contraindicated. Facilitation of conduction over the accessory pathway may produce a marked increase in ventricular rate. Treatment of antidromic AVNRT in patients with stable vital signs includes intravenous administration of procainamide 10 mg/kg IV infused at a rate not to exceed 50 mg/min. Procainamide slows conduction of cardiac impulses along the accessory pathway and may slow the ventricular response rate and terminate the wide-complex tachydysrhythmia. Electrical cardioversion is indicated if the ventricular response cannot be controlled by drug therapy. ▪ Definitive treatment is catheter ablation • Ablate accessory pathways ▪ “I’m not going to ask you anything about treatment for WPW. It’s clearly out of our scope.” o Atrial fibrillation and atrial flutter are uncommon in WPW syndrome but are potentially lethal because they can result in very rapid ventricular response rates and deteriorate into ventricular fibrillation. The mechanism responsible is anterograde conduction from the atria to the ventricles through the accessory pathway. There is no mechanism along the accessory pathway to slow the conduction speed. The result is extremely rapid ventricular rates that often degenerate into ventricular fibrillation and death. Atrial fibrillation in the setting of WPW syndrome can be treated with intravenous procainamide. Verapamil and digoxin are contraindicated in this situation because they may actually accelerate conduction through the accessory pathway, making the situation worse. Electrical cardioversion is preferred in the presence of hemodynamic instability. Long-term management of tachydysrhythmias in patients with WPW syndrome usually involves radiofrequency catheter ablation of the accessory pathway. The procedure is curative in 95% of patients and has a low complication rate. Antidysrhythmic drugs may be used as adjuvant therapy. o Patients with known WPW syndrome coming for surgery should continue to receive their antidysrhythmic medications. The goal during management of anesthesia is to avoid any event (e.g., increased sympathetic nervous system activity due to pain, anxiety, or hypovolemia) or drug (digoxin, verapamil) that could enhance anterograde conduction of cardiac impulses through an accessory pathway. Appropriate antidysrhythmic drugs and equipment for electrical cardioversion-defibrillation must be immediately available. • Prolonged QT Syndrome o Duration of QT interval > 480 milliseconds ▪ Beginning of Q to end of T ▪ By definition, a patient with long QT syndrome (LQTS) has a prolongation of the QTc exceeding 460 milliseconds. ▪ Typically, women have longer QT intervals than men. This difference is more pronounced at slower heart rates. The incidence of congenital and acquired prolonged QT syndromes is higher in women. Not surprisingly, the incidence of TdP is also higher in women. The strongest predictor of the risk of syncope or sudden death in patients with congenital prolonged QT syndrome is a QTc exceeding 500 milliseconds. o Inherited and iatrogenic forms ▪ Can be caused by meds we give ▪ There are two types of LQTS: congenital and acquired. Acquired iatrogenic LQTS is far more common than the inherited forms of LQTS. Acquired LQTS may be caused by many prescription medications such as antibiotics, antidysrhythmics, antidepressants, and antiemetics. Data suggest that TdP occurs in 1% to 10% of patients receiving QT-prolonging antidysrhythmic drugs. However, the incidence of TdP is much lower in patients receiving noncardiovascular QT- prolonging drugs. LQTS can be associated with hypokalemia, hypomagnesemia, severe malnutrition, hypertrophic cardiomyopathy, and intracranial catastrophes such as subarachnoid hemorrhage. o Long QT represents a prolonged repolarization period allowing afterdepolarization ▪ Will also increase risk of R-on-T ▪ The prolongation of repolarization in LQTS results in a dispersion of refractory periods throughout the myocardium. This abnormality in repolarization allows afterdepolarizations to trigger PVCs. o Concern centers around generation of PVCs that can deteriorate into TdP and V fib ▪ Under certain circumstances, the triggered PVCs initiate a ventricular reentry rhythm manifesting as polymorphic ventricular tachycardia, also known as torsade de pointes (TdP). TdP is electrocardiographically characterized by a "twisting of the peaks" or rotation around the ECG baseline. In other words, there is a constantly changing cycle length, axis, and morphology of the QRS complexes around the isoelectric baseline during TdP. This dysrhythmia may be repetitive, episodic, or sustained and may degenerate into ventricular fibrillation. o Treatment ▪ Correct electrolyte problems (Mg, K) • Torsades = Mg • Treatment of LQTS includes correction of electrolyte abnormalities, particularly those of magnesium or potassium. ▪ Stop any drugs that could lengthen QT • Droperidol used to be the big one • Any drugs associated with QT prolongation should be discontinued. • A preoperative ECG to rule out LQTS is useful in a patient with a history of unexplained syncope or a family history of sudden death. • The choice of anesthetic drugs deserves special attention in the case of LQTS, since many common anesthetic drugs cause some prolongation of the QTc. Isoflurane and sevoflurane have been shown to prolong the QTc in otherwise healthy children and adults. Currently, however, there is insufficient information to favor one volatile anesthetic over another. • Droperidol and other antiemetic drugs also increase the QT interval. Events known to prolong the QT interval should be avoided, such as abrupt increases in sympathetic stimulation associated with preoperative anxiety and noxious stimulation intraoperatively, acute hypokalemia due to iatrogenic hyperventilation, and administration of drugs known to prolong the QTc. ▪ Beta blockers • Pacing is usually employed in combination with β-blocker therapy. Studies have shown a considerable reduction in cardiac events and mortality in congenital LQTS patients treated with β-blocker therapy (from 50% to <5% over a 10-year period). • Consideration may be given to establishing β-blockade before induction in patients believed to be at particular risk. A defibrillator should be available, because the likelihood of perioperative ventricular fibrillation is increased. ▪ Pacing • Cardiac pacing is a treatment option in LQTS, because TdP is often preceded by bradycardia. Programming a pacemaker to pace at a higher backup rate than usual can prevent the bradycardia that precedes TdP and abort the dysrhythmia. ▪ Long term – implant a defibrillator • In recent years, implantable cardioverter-defibrillators (ICDs) with pacing capability have emerged as the lifesaving therapy for patients with recurrent symptoms and recalcitrant TdP despite ventricular suppression therapy with β-blockers. o There are several genetic syndromes that manifest a long QT interval. The two most common are the Romano-Ward and Timothy syndromes. These are inherited as autosomal dominant disorders and usually present as syncope in late childhood. Manifestations can occur as early as the first year of life or as late as the sixth decade. A rarer autosomal recessive form of prolonged QT syndrome, called Jervell and Lange-Nielsen syndrome, is associated with congenital deafness. Syncope is the hallmark symptom of the inherited forms of prolonged QT syndrome. These syncopal events are commonly associated with stress, emotion, exercise, or other situations that lead to increased sympathetic stimulation. • Bradycardia o Normal for well-trained athletes ▪ HR <60 normal if involved in athletic activity ▪ Trained athletes often exhibit resting bradycardia, as may normal individuals during sleep. o Abnormal ▪ Inability to increase HR when needed • Peds • Beta blocked patients • Sick sinus syndrome, MI, CHF o Anything that will decrease LV output o Dysfunction of the SA node, also referred to as sick sinus syndrome, is a common cause of bradycardia. Sick sinus syndrome with symptomatic bradycardia is the most common reason for insertion of a permanent cardiac pacemaker. The prevalence of sinus node dysfunction may be as high as 1 in 600 patients older than 65 years of age. Many patients with sick sinus syndrome are asymptomatic; others experience syncope or palpitations. Episodes of SVT may punctuate periods of bradycardia, which accounts for another common name for sinus node dysfunction: tachycardia-bradycardia (tachy-brady) syndrome. In patients with ischemic heart disease, periods of bradycardia may contribute to the development of congestive heart failure, whereas periods of tachycardia can contribute to the development of hypertension and angina pectoris. The rate of progression to second- or third-degree AV heart block in patients with sick sinus syndrome is approximately 1-5% per year. ▪ Resting HR less than 40 is abnormal no matter what athletic ability is • An inability to increase the heart rate adequately during exercise, bradycardia associated with symptoms (such as syncope, dizziness, and chest pain), or a heart rate of less than 40 beats per minute in the absence of physical conditioning or sleep is considered abnormal. ▪ Symptoms • If symptomatic at 62, then that is bradycardic and needs to be addressed o Causes ▪ SA node dysfunction • Usually something else in the atrium will take over & serve as a new or ectopic source of atrial conduction • Bradydysrhythmias are most commonly caused by SA node dysfunction or dysfunction in the conduction system below the SA node. ▪ Conduction block o Often other pacemakers will take over for the SA node • Sinus Bradycardia o Sinus rhythm with a HR <60 BPM ▪ Bradycardia is defined as a heart rate of less than 60 beats per minute. ▪ The ECG during sinus bradycardia demonstrates a regular rhythm with a normal-appearing P wave before each QRS complex and a heart rate of 60 beats per minute or less. The SA node usually fires between 60 and 100 times per minute and overdrives other potential pacemakers in the heart. However, if the SA node does not fire, other slower pacemaker cells may take over primary pacemaker function. There is normally a pause in electrical activity before a secondary slower pacemaker begins to fire. Each group of potential pacemaker cells has an intrinsic rate. Cells near the AV node, so called junctional pacemakers, fire at 40 to 60 beats per minute. Ventricular cells below the AV node can act as an ectopic pacemaker but fire at a very slow rate in the range of 30 to 45 beats per minute. o S&S (if it compromises CO) ▪ Altered mental status ▪ Dizziness ▪ Seizures ▪ Angina ▪ Heart failure ▪ Hypotension ▪ Shock ▪ Syncope • Sinus Bradycardia o Treatment ▪ Asymptomatic • None required but monitor o In asymptomatic patients with sinus bradycardia, no treatment is required. However, these patients should be monitored for worsening bradycardia or hemodynamic deterioration. ▪ Mildly symptomatic • Eliminate contributors o In mildly symptomatic patients, any potential contributing factors such as excess vagal tone or drugs should be eliminated. • Consider pretreatment o If you see a healthy person in OR with resting HR 48-50, you can give Robinul 0.3 mg IV o Don’t want them having a vagal response & bradying down to 35 during laryngoscopy ▪ Severely symptomatic • Pacing (transcutaneous) o In severely symptomatic patients—that is, those with chest pain or syncope— immediate transcutaneous or transvenous pacing is indicated. • Drugs o Atropine (always give at least 0.5 mg IV) (Max dose 3 mg!!!) ▪ If you give <.5 mg, you can have a paradoxical reaction which will slow HR ▪ More than 3 mg, they can become bradycardic on you ▪ Atropine 0.5 mg IV every 3 to 5 minutes (to a maximum of 3 mg) may be given to increase heart rate but should not delay initiation of pacing. It should be noted that small doses of atropine (<0.5 mg IV) can cause a further slowing of the heart rate. o Glycopyrrolate ▪ Usually will start with Robinul o Epi ▪ In the event that cardiac pacing is delayed or pacing capabilities are limited, an epinephrine or dopamine infusion may be titrated to response while cardiac pacing is awaited. o Dopamine o Glucagon (beta blocker & CCB overdose) ▪ If atropine is ineffective, glucagon may be useful if the bradycardia is due to β-blocker or calcium channel blocker overdose. Glucagon stimulates glucagon-specific receptors on the myocardium that increase cyclic adenosine monophosphate (cAMP) levels and increase myocardial contractility, heart rate, and AV conduction. Suggested dosing of glucagon is 50 to 70 mcg/kg (3 to 5 mg in a 70-kg patient) every 3 to 5 minutes until clinical response is achieved or a total dose of 10 mg is reached. To maintain clinical effect, this should be followed with a continuous infusion at 2 to 10 mg/hr. • Bradycardia with Regional Anesthesia o Can occur w/any patient (1.5/10,000 cases) ▪ Some people get bradycardic with spinals ▪ “WON’T TEST YOU ON THIS. I DON’T LIKE IT. ▪ Will talk about next semester ▪ Bradycardia during neuraxial blockade can occur in patients of any age and any American Society of Anesthesiologists (ASA) physical status class, whether or not they are sedated. The incidence of profound bradycardia and cardiac arrest during neuraxial anesthesia is approximately 1.5 per 10,000 cases. By contrast, cardiac arrest during general anesthesia occurs at a rate of 5.5 per 10,000 cases. o Can occur at any time (usually 1 hr into case) ▪ Bradycardia or asystole may develop suddenly (within seconds or minutes) in a patient with a previously normal or even increased heart rate, or the heart rate slowing may be progressive. Bradycardia can occur at any time during neuraxial blockade but most often occurs approximately an hour after anesthetic administration. The risk of bradycardia and asystole may persist into the postoperative period even after the sensory and motor blockade has diminished. o About half the time preceded by S&S of high block o Pretreatment doesn’t prevent it o Treatment ▪ Early recognition • Oxygen saturation is usually normal before the onset of bradycardia. Approximately half of patients who experience arrest during neuraxial anesthesia complain of shortness of breath, nausea, restlessness, light-headedness, or tingling of the fingers and manifest deterioration in mental status before arrest. ▪ Atropine ▪ Epinephrine ▪ CPR o The exact mechanism responsible for bradycardia and asystole during spinal and epidural anesthesia is not known. One proposed mechanism is termed the Bezold-Jarisch response. This is a paradoxical reflex- induced bradycardia resulting from decreased venous return and activation of vagal reflex arcs mediated by baroreceptors and stretch receptors. Another possible mechanism is the unopposed parasympathetic nervous system activity that results from the anesthetic-induced sympathectomy. Blockade of cardiac accelerator fibers originating from thoracic sympathetic ganglia (T1 to T4) may alter the balance of autonomic nervous system input to the heart and lead to relatively unopposed parasympathetic influences on the SA node and AV node, which slows the heart rate. o Bradydysrhythmias associated with spinal or epidural anesthesia should be treated aggressively. Bradycardia can occur despite prophylactic therapy with atropine and/or intravenous fluids. Recalcitrant bradycardia necessitates transcutaneous or transvenous pacing. Secondary factors such as hypovolemia, opioid administration, sedation, hypercarbia, concurrent medical illnesses, and long-term use of medications that slow the heart rate can contribute to the development of bradycardia. In the clinical setting of severe bradycardia, preparation should be made for management of asystole, which is treated with CPR. Pharmacologic management should follow ACLS protocols and include treatment with atropine, epinephrine, and/or vasopressin as appropriate. • Junctional Rhythm o Pacemaker activity from tissue surrounding the AV node ▪ AV node (junction between ventricles & atria) will takeover ▪ Junctional or nodal rhythm is due to the activity of a cardiac pacemaker in the tissues surrounding the AV node. o Rate 40 – 60 BPM (intrinsic rate of AV node) ▪ Junctional pacemakers usually have an intrinsic rate of 40 to 60 beats per minute. o Next location to take over pacemaking if SA fails ▪ The impulse initiated by a junctional pacemaker travels to the ventricles along the normal conduction pathway but can also be conducted retrograde into the atria. The site of the junctional pacemaker determines whether the P wave precedes the QRS complex (with a shortened PR interval), follows the QRS complex, or is buried within the QRS complex and is not visible. The diagnosis of junctional rhythm may be an incidental finding on ECG. Junctional rhythm can be suspected if on physical examination the jugular venous pulsation shows cannon a waves. o Can cause dyssynchrony between atria & ventricle resulting in decrease of CO ▪ Usually the atrium is not doing anything coordinated if you are in a junctional rhythm ▪ No P waves ▪ If the junctional rhythm has an accelerated rate, it is called a junctional tachycardia or accelerated nodal (junctional) rhythm. Junctional tachycardia is a narrow-complex tachycardia at a rate usually lower than 120 beats per minute. Junctional rhythms can cause AV dyssynchrony, loss of atrial kick, and in some circumstances rapid ventricular rates. This can result in symptoms such as fatigue, generalized weakness, angina pectoris, impaired cardiac output, congestive heart failure, pulmonary edema, and hypotension. o Associated with older inhalation agents ▪ 1.5 MAC Halothane used to cause patients to drop into a junctional rhythm. They would still be perfusing, but drop back on the MAC & they will convert o Treat if symptomatic with atropine (0.5 – 1 mg IV) ▪ Kick starts SA Node • Conduction Disturbances o Consider ▪ Site of block • Usually the AV node ▪ Risk of progression to complete block • Risk of progressing from 2nd to 3rd. 3rd is bad. ▪ Likelihood another pacemaker will take over o Causes ▪ MI (RCA) ▪ Dig toxicity ▪ Beta blocker OD ▪ Ca Channel blocker OD ▪ Rheumatic fever ▪ Lyme disease ▪ Sarcoidosis ▪ Amyloidosis o Junctional rhythm can occur in association with many different disorders. It is often an escape rhythm because of depressed sinus node function, SA block, or delayed conduction in the AV node. Junctional tachycardia can result from increased automaticity of junctional tissues in the setting of digitalis toxicity or cardiac ischemia. Junctional rhythm that occurs in association with myocarditis, myocardial ischemia, or digitalis toxicity should be managed by treating the underlying disorder. Junctional rhythms are not uncommon during general anesthesia using halogenated anesthetic vapors and, in this setting, require no treatment. Even in the setting of acute myocardial infarction, junctional rhythms are usually considered benign and require no treatment. However, in certain patients the loss of AV synchrony during a junctional rhythm will result in myocardial ischemia, heart failure, or hypotension. Atropine at a dose of 0.5 mg can be used to accelerate the heart rate if a slow junctional rhythm becomes hemodynamically significant. • First Degree Block o Prolonged PR interval (>0.2 sec) ▪ Instead of the normal pause in the AV node, it is just a little longer than normal ▪ First-degree AV block is defined as a PR interval of longer than 0.2 seconds. Each P wave is conducted and has a corresponding QRS complex of normal duration. o Site of block is the AV node ▪ There is a delay in the passage of the cardiac impulse through the AV node. o Normal result of aging of conduction system ▪ First-degree AV block is often a result of minor degenerative changes in the cardiac conduction system that accompany normal aging. o Other causes ▪ Can be the result of increased parasympathetic activity ▪ Ischemia ▪ Other causes include myocardial ischemia (involving the blood supply to the AV node), inferior wall myocardial infarction, drugs affecting AV node conduction (digitalis and amiodarone), and processes that enhance parasympathetic nervous system activity and vagal tone. First-degree AV block can be found in patients with and without structural heart disease. o Usually asymptomatic ▪ If perfusing, it is no problem ▪ People walk around with it all the time, so no big deal ▪ Patients with first-degree AV block are usually asymptomatic and appear to have no significant increase in mortality compared with matched controls. The Framingham Heart Study followed long-term outcomes of individuals with first-degree heart block, and the results suggested an increased risk of atrial fibrillation in this population. o Perioperative Management ▪ Anesthetic management of the patient with first-degree heart block should be aimed at avoiding any clinical situation or drug that increases vagal tone or slows AV conduction. Atropine administration can speed conduction of cardiac impulses through the AV node. However, in patients with significant heart disease, the increase in heart rate produced by atropine may contribute to myocardial ischemia. In patients with risk factors such as coronary ischemia and systemic infection, these clinical conditions should be treated and medically optimized before surgery. Digoxin levels should be checked before surgery, and serum potassium should be maintained at normal levels in patients receiving digoxin. • Second Degree Block o Mobitz Type I (Wenckebach) ▪ Progressive prolongation of PR interval until a beat is dropped. ▪ Caused by delayed conduction through the AV node ▪ Usually transient & asymptomatic • Although people can have chronic Wenckebach and be fine ▪ Low risk of progressing to complete heart block • Second Degree Block o Mobitz Type II ▪ Complete interruption of conduction at a point below the AV node (in the His-Purkinje fibers) • More concerning than Mobitz Type I • Usually between the AV node and the Bundle of His ▪ Widened QRS ▪ Usually results from damage to the heart ▪ Usually symptomatic • Palpitations • Near syncope o Depending on degree of CO compromise o Picture below: long PR interval, then drop a beat ▪ Much greater risk of progressing to complete heart block • Second Degree Block o Treatment ▪ Type I • Usually not needed • Atropine if CO needs to be increased ▪ Type II • Pacing o Need transcutaneous pacing if it happens emergently on the OR bed • Atropine is usually ineffective o Because it is below the atrium. The atropine will only help with cholinergic innervation. • Bundle Branch Blocks o Conduction problem in the branches of the His – Purkinje portion of the conduction system o QRS longer than 120 milliseconds o Usually associated with significant structural heart dz o Marker of poor prognosis • Right Bundle Branch Blocks o In normal heart R more common than L o Usually asymptomatic for RBBB o Bifascicular block ▪ RBBB w/a block of one of the fascicles of the LBB • With one of the two parts of the LBBB ▪ RBBB + Left anterior hemiblock most common • Right Bundle Branch Blocks o ECG ▪ Wide QRS • Because we are blocking impulse through ventricle, so the depolarization of the ventricle is widened ▪ rSR V1 – V2 • rSR looks like there are 2 R waves; an initial R wave then a 2nd R wave ▪ Deep “S” wave I & V6 o Treatment ▪ Observation ▪ Avoid conduction delay ▪ Have pacing available • Left Bundle Branch Blocks o More ominous ▪ More concerning because of LV o Associated with ▪ Ischemic heart dz ▪ LV hypertrophy ▪ Valvular dz which is causing hypertrophy of LV o During anesthesia, occurrence is a strong indicator of ischemia o Be careful with insertion of central lines!!! ▪ If someone comes in with LBBB, that means the L side of their heart is compromised. If you are putting a central line in them, you can elicit a RBBB when you put PA cath into RV. If you accidentally create a RBBB with a PA cath and the LBBB is already blocked, that really compromises CO output ▪ If someone comes in with a LBBB & needs a central line, it’s time to go to lunch and let the surgical resident do that. • Left Bundle Branch Blocks o ECG ▪ QRS duration >120 milliseconds ▪ No “Q” wave in lead I & V6 o Unifascicular or bifascicular ▪ Left anterior more common • If you have unifascicular the L anterior is more commonly blocked ▪ Left posterior less common • Third Degree Heart Block o Complete disconnect between atria and ventricle ▪ The atrium is contracting in response to the AV node & the ventricle is contracting in response to itself o ECG shows no association between “P” waves and QRS complex o Ventricular rate depends on ectopic pacemaker in the ventricle ▪ Usually about 40 bpm o Loss of atrial kick decreases CO o Stokes – Adams attack ▪ Syncope associated with LOC without warning o Treatment - Pacing