Fig. 1-17. Ventricular escape beats. On EKG, how would the QRS of a ventricular escape beat look? Normally the QRS is narrow since the electrical im pulse is conducted rapidly to both ventricles via the Purkinje fibers, and depolarization of the muscle then proceeds uniformly. If some isolated ventricular cells produce an escape beat, the depolarization will spread in a less organized fashion, resulting in a widened QRS. #151 | | |
Fig. 1-18. Rhythm strips of first-, second-, and third degree heart block. How would AV block manifest on EKG? The PR interval represents the time that the impulse travels through the AV node. In first-degree heart block, the PR interval is lengthened (criteria for diagnosis is > 0.2 seconds). #152 | | |
Second-degree heart block is further divided into two types of blocks. In Mobitz type I (also called Wencke bach), the PR interval progressively increases until fi nally an atrial impulse is not conducted at all. This leads to a pause, followed by a normally conducted beat, and then the cycle repeats. In Mobitz type II, the AV node does not conduct some proportion of incoming atrial impulses to the ventricles. This causes ventricu lar beats to be intermittently dropped entirely. In third-degree heart block, there is no conduction at all from the atria to the ventricles. Since the SA node's signal does not reach the ventricles, the cells around the AV node start firing at their own intrinsic rate, which is around 30-50 beats per minute. Since the atria and ventricles then function totally inde pendently of each other in third-degree heart block, this is a form of AV dissociation. . #153 | | |
In summary, bradycardia can be caused by a slow #154 | | |
SA node or decreased conduction. #155 | | |
Treatment ofBradycardia. To increase heart rate, #156 | | |
treatment can either increase rate directly (beta ago nists such as isoproterenol or implantation of a pace maker) or decrease inhibition (anticholinergics such as atropine, which decrease parasympathetic stimu- #157 | | |
lation of the heart). Implantation of a pacemaker is usually necessary for second-degree Mobitz type II or third-degree heart block. #158 | | |
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Tachyarrhythmias are classified by whether they origi #160 | | |
nate above or within the ventricles. Arrhythmias origi nating in the atria or AV node are called supraventricular (i.e., above the ventricle) tachyarrhythmias. #161 | | |
Supraventricular Tachyarrhythmias #162 | | |
Fig. 1-19. Supraventricular Tachyarrhythmias. Sinus tachycardia is simply an increase in the SA #163 | | |
node firing rate above 100 (See Fig. 1-15C). This can happen as the sympathetic nervous system's response to either a physiologic state (e.g., exercise, fight/flight) or a pathophysiologic condition (e.g., fever, pulmonary embolus). #164 | | |
In multifo cal atrial tachycardia (MAT) , multiple sites in the atria take on very fast rhythms. This can occur in patients with pulmonary disease. What would the EKG look like? If multiple sites in the atria fire, there will be multiple P wave morphologies: the P waves will have several different appearances and can occur at irregular intervals. #165 | | |
Atrial flutter and atrial fibrillation are common ar rhythmias that have similar underlying pathophysiol ogy, both involving reentrant circuits. Reentrant circuits are circular pathways in which electrical im pulses can travel around the circle, reactivate the starting point, and create an endless loop. #166 | | |
In atrial flutter, a reentrant circuit in the atrium al lows electrical impulses to spin around the loop at very high speed instead of following the normal conduction pattern. If you imagine this current looping around the atrium, you can also imagine the EKG: a saw-tooth ap pearance to the P waves. In atrial flutter, the atrial rate is typically between 200-400 beats per minute. #167 | | |
In atrial fibrillation, there are many reentrant cir cuits spinning around in the atria. The EKG appears as a wavy, chaotic, disorganized baseline without rec ognizable P waves. Rates in the atria can be over 400 beats per minutes, but due to the refractory period of the AV node, the ventricular rhythm cannot reach this speed. Usually the ventricle gets no faster than 100- 150 beats per minute unless there is an accessory pathway (discussed below). Since the beats that do make it through are essentially random, the ventricu lar rhythm is irregularly irregular. Causes of atrial fibrillation include a variety of heart diseases (e.g., coronary disease, valvular disease, cardiomyopathy, heart failure), pulmonary disease, pulmonary em bolism, hyperthyroidism, and hypertension. Atrial fib rillation can also occur idiopathically. #168 | | |
Because fibrillating atria quiver instead of contract ing, blood flow within them is quite turbulent. This leads to an increased risk of clot formation in the atria. If a clot fo rms in the left atrium, it can pass to the left ventricle and then out the aorta. This could lead to stroke (if it goes up the carotids), mesenteric ischemia (if it lodges in the GI vascular bed), renal ischemia (if it lodges in the renal artery), etc. Patients with atrial fibrillation are thus often given anticoagulants to pre vent clot formation in the atria. #169 | | |
The next two tachyarrhythmias also have reentrant circuits. AV nodal reentrant tachycardia (AVNRT) has a reentrant circuit involving the AV node itself. Atri oventricular reciprocating tachycardia (AVRT) has a reentrant circuit that involves the atrium, AV node, ventricle, and an accessory pathway. #170 | | |
AVNRT develops when the refractory period be comes altered in pathways through the AV node. There are normally two pathways through the AV node, one of which is slower than the other. In AV NRT, a change in the refractory period of the slower pathway allows the electrical impulse to inappropriately come back up to the atrium after its normal path down the AV node. Thus, the EKG can manifest a P wave after the QRS complex, and this P wave may be inverted since the impulse comes backward up through the atria. #171 | | |
In AVRT (e.g., Wolff-Parkinson-White syndrome), there is an accessory pathway that allows impulses to flow to the ventricles directly from the atria and vice versa. If the accessory pathway functions in the retro grade direction (orthodromic), a reentrant loop occurs (from atria to AV node to ventricles back to the atria via the accessory pathway). This cycling of the impulse causes the tachycardia. In orthodromic Wolff-Parkinson White, the impulse travels first normally down the AV node to the ventricles, so the QRS will be normal. If the accessory pathway functions in the anterograde direc tion (antidromic), the atrial impulses bypass the AV node, go directly to the ventricles, and then return to the atria retrogradely via the AV node. What would the antidromic EKG look like? First, there would be a shortened PR interval because the impulse bypasses the built-in delay of the AV node. Second, since part of the ventricle is activated early through the accessory pathway, the QRS can appear abnormal. The upstroke of the QRS reflects this in what is known as a delta wave. A delta wave is a more gradual beginning to the QRS, as opposed to the normal sharp upstroke that oc curs with normally conducted electrical activity. If a patient with an accessory pathway were to develop atrial fibrillation, this rapid rate can be conducted to the ventricles via the accessory pathway, which has none of the built-in delays of the normal system. This can lead to extremely rapid ventricular rates, which can be deadly. #172 | | |
Summary of the supraventricular tachyarrhyth mias. Either the sinus node itself can take on a faster rate (sinus tachycardia); multiple sites in the atria can take on the role of firing (multifocal atrial tachycardia); a large atrial reentrant loop can form in the atria, lead ing to atrial flutter; or multiple reentrant loops in the atria can lead to atrial fibrillation. Reentrant circuits can also involve the AV node itself (AVNRT) and/or an accessory pathway (AVRT, Wolff-Parkinson-White). #173 | | |
Ve ntricular Tachyarrhythmias. In ventricular tachyarrhythmias, the fast rate originates in the ventri cle. If the ventricles depolarize in any way other than by the normal conduction system, this depolarization will spread in a disorganized fashion, resulting in a widened QRS. #174 | | |
Aside from loss of the atrial kick at the end of dias tole, the overall ability of the heart to do its job should not be greatly impaired by atrial arrhythmias (assum ing otherwise normal ventricular function). In marked contrast, sustained ventricular arrhythmias lead to uncoordinated muscular activity in the ventricle, which can suddenly decrease fo rward flow. Thus, sustained ventricular arrhythmias are often emergencies in need of defibrillation. #175 | | |
Fig. 1-20. Ventricular arrhythmias. Ve ntricular tachy cardia can result from a reentrant circuit in the ventri cle or from a group of ventricular cells firing at an increased rate. For example, a myocardial infarction can lead to an area of dead tissue. This area can have abnormal electrical conduction properties, thus creat ing a reentrant circuit, which can result in extremely high ventricular rates. #176 | | |
Ve ntricular fibrillation results from multiple reen trant circuits in the ventricles, just like atrial fibrilla tion results from multiple reentrant circuits in the atria. The electrical (and thus muscular) activity in ven tricular fibrillation is even more uncoordinated than that of ventricular tachycardia because of the multiple circuits, and cardiac output can thus be even more se verely impaired. Without immediate intervention, this can even lead to sudden death. Ventricular fibrillation may result from ischemia or infarcted areas of ventric #177 | | |
ular tissue, similar to the mechanism described above for ventricular tachycardia. Ventricular fibrillation may also result from ventricular tachycardia. #178 | | |
To rsades de Pointes is French for twisting of the points, and describes a specific type of ventricular tachycardia. The name refers to the EKG appearance of this ventricular arrhythmia, since it appears to turn around the horizontal. Causes include anything that can prolong the QT interval, such as certain anti-ar rhythmics (e.g., quinidine, sotalol) and other drugs, hypocalcemia and other electrolyte abnormalities (see endocrine chapter), cardiac ischemia, and congenital long QT syndrome. Torsades can lead to syncope and/or ventricular fibrillation. #179 | | |
Treatment o{Tachyarrhythmia. Tachyarryhthmias are treated with drugs that decrease cardiac my ocytes' rate of firing. This can be accomplished either by decreasing sympathetic stimulation of the heart or by acting at ion channels to alter portions of the car diac action potential, e.g., decreasing upstroke, in creasing threshold, prolonging repolarization. Drugs that decrease sympathetic stimulation of the heart in clude beta-blockers, called Class II antiarrhythmics. Drugs that alter the cardiac action potential include: Class I antiarrhythmics (sodium channel blockers, e.g., quinidine, lidocaine), Class III antiarrhythmics (which act at various ion channels and as beta block ers, e.g., amiodarone, sotalol), and Class IV antiar rhythmics (calcium channel blockers, e.g., verapamil). #180 | | |
If an arrhythmia does not respond to pharmacologic therapy, or in an emergency, electrical defibrillation may be necessary. Additionally, regions of tissue re sponsible for generating the arrhythmia can be ab lated surgically or via catheter techniques. #181 | | |
Review of Arrhythmias #182 | | |
In summary, arrhythmias are abnormal heart #183 | | |
rhythms that can be too slow, too fast, and/or irregu lar. If the rate is too slow, either the SA node (the pacemaker) is firing too slowly (sinus bradycardia), or the SA node is working fine, but there is a block of the signal somewhere along the conduction pathway (heart block). Tachyarrhythmias are heart rates that are too fast, and are generally divided into those which originate in the atria and/or AV node (i.e., supraventricular: sinus tachycardia, MAT, atrial flutter, atrial fibrillation, AV NRT, AV RT, Wolff Parkinson-White) and those that originate in the ventricles (ventricular tachycardia, ventricular fib rillation, torsades de pointes). Atrial tachycardias can be dangerous for two reasons: 1) they can lead to turbulent flow in the atria, which can lead to thrombus formation and embolization (e.g., to the cerebral vasculature leading to stroke) and 2) they can transmit to the ventricle via the AV node (with some holdup) or via accessory pathways (directly), causing very fast ventricular rates. Ventricular tachyarrhythmias are dangerous because ventricu lar function can be so severely compromised as to cause an immediate decrease in forward flow. This can result in sudden death in some cases if immedi ate intervention does not occur. #184 | | |
Diseases of the Heart's Vasculature: Angina and Myocardial Infarction #185 | | |
The coronary arteries provide the heart's blood sup ply. If this blood supply is compromised, oxygen sup ply to the heart can be insufficient, decreasing cardiac function. #186 | | |
Diabetes, smoking, high blood pressure, high choles terol, and many other factors can lead to blood vessel injury and inflammation, which can result in athero sclerotic plaque formation in blood vessels. This nar rows the vessel lumen, hardens the blood vessel, and can predispose to clot formation in the vessel. In the coronary vasculature, this can cause angina and/or myocardial infarction (heart attack). #187 | | |
Angina and Myocardial Infarction #188 | | |
During exertion, the heart beats both harder and #189 | | |
faster to supply oxygen to the muscles. Vasodilation of the coronary vasculature increases blood flow to the cardiac muscle to meet its increased demand for oxy gen. The situation is one of economics in that cardiac function is determined by how the supply (in this case of oxygenated blood) meets the demand (the cardiac muscular demand for oxygen). #190 | | |
Now imagine a heart with bad atherosclerotic dis ease of the coronary vessels. The vessel lumens are narrowed and thus blood supply to the heart is dimin ished. In milder cases, the heart may still be fine at rest. However, increasing exertion can get the heart into trouble because diseased vessels are not only nar row, but they also cannot adequately vasodilate. In economic terms, the vessels cannot supply sufficient #191 | | |
oxygen for the heart's demand, and this can manifest as chest pain/tightness and/or shortness of breath. This situation is known as stable angina. The heart is stable at rest, but with exertion, supply of blood through the narrowed vessels cannot keep up with de mand. The classic story is that a patient has progres sively increased limitations on how much they can exert themselves before they have problems. For ex ample, a patient might say "I was previously able to walk four blocks, then I would have to catch my breath ...now I can only walk two ..." or "I used to have to rest once halfway up the steps in my house, now I have to rest three or four times ..." #192 | | |
With increasing occlusion of the coronary vessel(s), even the demands of the resting heart may be too great for what the diseased vessel(s) can supply. When the pa tient experiences angina even without exertion, or when the level of exertion necessary to cause anginal symptoms decreases, this is unstable angina. Unstable angina is a precipitous state; it means that one or more coronary vessels is nearly totally occluded. If an ather osclerotic plaque ruptures, coronary thrombosis can en sue, causing the occlusion to proceed to 100%. If collateral flow is inadequate, the tissue supplied be comes ischemic. Without oxygen, a portion of the mus cle can die, and this is known as myocardial infarction (or heart attack). Myocardial infarction can present as chest pain unrelieved by rest (sometimes radiating down the left arm or into the jaw or neck), dyspnea, nau sea/vomiting, sweating, fever and/or other signs of dis tress. Myocardial infarction can also be entirely asymptomatic or cause minor symptoms that the pa tient disregards (silent myocardial infa rction). #193 | | |
Va riant, or Prinzmetal's angina occurs secondary to intermittent vasospasm, as opposed to vascular occlu sion. It can thus occur at any time and is not related to the person's activity. #194 | | |
Complications of Myocardial Infarction Depending on which vessel occludes, different regions #195 | | |
of the heart can be affected, causing a variety of con sequences. Ischemia of the conduction system can cause arrhythmias. If a large enough area of muscle infarcts and becomes nonfunctional, heart failure symptoms can occur (ischemic cardiomyopathy). In is chemic cardiomyopathy, there is less effective pump ing because part of the muscular wall has a damaged area that does not move as well as the rest. If the ischemic area is in the left ventricle (e.g., occlusion of the left anterior descending artery), this could lead to left heart failure with pulmonary congestion (back up) and decreased forward flow. If the right coronary artery is the site of occlusion, this can affect the right #196 | | |
ventricle, leading to right heart failure signs (e.g., JVD). Infarction of the papillary muscle can cause it to rupture, leading to acute mitral regurgitation. Infarction of the ventricular wall itself can result in its rupture, either at the septum or in the free wall. A sep tal rupture will lead to a ventricular septal defect and a new systolic murmur. As for ventricular free wall rupture, remember that the heart sits in the pericar dia! sac. If the ventricle ruptures and the heart bleeds into this sac, the blood can quickly surround the heart, preventing it from adequately filling. This is known as tamponade and can be quickly fatal. #197 | | |
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and Myocardial Infarction #199 | | |
Treatment of Angina. Dietary and lifestyle modifi cations are necessary to prevent further progression of atherosclerotic diseases (e.g., reduction in fat intake, quitting smoking, weight loss). In patients with ele vated cholesterol, cholesterol-lowering drugs may also be initiated (Fig. 1-21). Aspirin or other platelet in hibitors can be used to inhibit thrombosis formation. In angina, myocardial demand for oxygen exceeds the ability of the coronary vasculature to supply it. Two treatment angles for remedying this mismatch are possible: decrease the heart's demand fo r oxygen and increase the vasodilation of the coronary vessels. De creasing the heart's demand for oxygen can be accom plished by beta-blockers and calcium channel blockers (both of which decrease both heart rate and contrac tile force). Increased vasodilation is accomplished with nitrates, which dilate the coronary vasculature, and can thus also be used as quick relief for anginal symptoms. Nitrates also dilate veins, decreasing the heart's work by decreasing preload. Calcium channel blockers also increase coronary vasodilatation and de crease coronary vasospasm. For the latter reason, they are also used in the treatment of variant (Prinz metal's) angina. If coronary occlusion is very ad vanced, angioplasty, stenting, or bypass surgery can be performed. The former two procedures seek to open ex isting vessels, while the latter uses vein grafts (usu ally the saphenous vein from the leg), artery grafts (usually from the radial artery), or connection of the blocked coronary artery to the internal mammary ar tery to create an alternate pathway for blood flow, by passing areas of occlusion. #200 | | |
