Cardiovascular System Ettinger: ECG Flashcards

Question

Abnormal ventricular repolarization may create an additional ECG deflection called a U wave, which is observed only rarely in dogs and cats. It follows, or is superimposed on the latter part of, the T wave, and is most likely to be observed in patients with severe ......................

Answer 1

Hypokalemia. Alterations in repolarization of the His-Purkinje system are thought to be at least partly responsible for U waves, and the comparatively low density of such fibers in canine ventricles helps to explain the rarity of U waves even in markedly hypokalemic dogs

Answer 2

An Osborn wave or J wave is an ECG wave observed as a typically positive deflection in lead II, occurring at the end of the QRS complex. Classically it is associated with severe hypothermia, which was demonstrated experimentally in canine myocardium but is not routinely recognized in naturally occurring hypothermia in dogs and cats. Because it is a nonspecific indicator of abnormal repolarization, the Osborn or J wave could also occur with advanced cardiac disease, such as severe subaortic stenosis. Hypothermia alters initial repolarization, especially in the epicardial region of myocardium (greater magnitude of transient outward current, Ito) creating an Osborn or J wave on the electrocardiogram (ECG)

Answer 3

The mean electrical axis represents the sum total of electrical forces generated during a heartbeat (Figure 235-13). In the dog, the normal range of ventricular MEA is between +40° and +100°. In cats, the normal range is much larger (from 0° to ±180°) such that the clinical utility of MEA is very limited in the cat.

Answer 4

The usual amplitude setting is 1 cm = 1 mV,

Answer 5

At birth, the ventricular MEA of the normal canine ECG is directed rightward, cranially, and ventrally. Over the first 3 months of life this orientation slowly changes in the normal dog to leftward, caudal, and ventrad. A similar pattern of evolution exists for kittens. Thus, the criteria used for establishing a “normal” ECG are not the same for a dog younger than 12 weeks of age as they are for an adult dog

Answer 6

Artificially increasing a patient's vagal tone has potential value both diagnostically and therapeutically. Diagnostically, slowing the heart rate and increasing AV nodal refractoriness through vagal maneuvers may slow a rapid tachycardia, allowing some of its features to be more apparent and facilitating the ECG diagnosis (Figure 235-14). Therapeutically, an increase in vagal tone that interrupts macro reentrant circuits can terminate such arrhythmias as AV nodal reentrant tachycardia and orthodromic AV reciprocating tachycardia

Answer 7

Carotid sinus massage is one type of vagal maneuver. It involves the simple application of gentle, sustained digital pressure by the clinician to one or both of the patient's carotid sinuses, located just caudal to the dorsal aspect of the larynx (sometimes to the point of eliciting a gag reflex), for 5 to 10 seconds, while the ECG tracing is being recorded. Such a maneuver should be tolerated by the patient, and signs of discomfort, resentment, or a marked change in heart rate warrant immediate termination of the maneuver. Because dogs and cats very rarely suffer from carotid artery atherosclerosis, concern for thromboembolic consequences of carotid sinus massage as expressed in human cardiology is unlikely to be relevant to small animal practice.

Answer 8

Ocular pressure over closed eyelids is another form of vagal maneuver. It consists of applying firm but controlled gentle digital pressure to both globes through closed eyelids. The distance of retropulsion of the globes depends on the shape of the orbit, and subjectively, the amount of pressure applied is the best guide: it should not exceed the digital pressure one would place on a ripe grape without rupturing it. Ocular pressure is contraindicated in patients with ocular problems. There appears to be interindividual variation in response to vagal maneuvers, with some individuals demonstrating a stronger effect during carotid sinus massage and others ocular pressure.

Answer 9

Atropine Response Test Administration of atropine sulfate 0.02 mg/lb (0.04 mg/kg) intravenously can be used diagnostically to evaluate bradycardias. It allows the differentiation between physiologic bradycardias that are purely of vagal origin (atropine increases the heart rate) and pathologic bradycardias that are caused by intrinsic disturbances of impulse formation or conduction (atropine has no effect). The response occurs within seconds to minutes (within 15 minutes) after injection.[3] Unfortunately, a positive response to atropine is poorly predictive of response to oral vagolytic drugs such as propantheline bromide in dogs with sinus node dysfunction (sick sinus syndrome, SSS).

Answer 10

(1) disturbances of impulse formation (cardiac excitability), (2) disturbances of impulse transmission (cardiac conduction) (3) complex disturbances involving abnormalities both of excitation and conduction. Some rhythm disturbances fit poorly into any category. Some disturbances of cardiac excitability are secondary to conduction disturbances (e.g., junctional or ventricular escape rhythms). Disturbances are listed according to the anatomic level of their origin (i.e., atrial, junctional, or ventricular).

Answer 11

Excitation disturbances can cause either excessive or inadequate contraction of the heart or its parts. Increased excitability produces extrasystoles (if intermittent) and tachycardia (if sustained). Ectopy is the term that describes spontaneous production of impulses anywhere in the heart. Decreased excitability leads to loss of impulse formation with electrical quiescence, resulting in bradycardia or asystole.

Answer 12

Conduction disturbances within the heart are all called blocks. Their categorization depends on the anatomic location of the block and its extent or degree. First-degree block refers to a slowing of conduction, second-degree block implies complete but intermittent interruption, and third-degree block involves complete and sustained interruption of conduction. Block can occur at the SA node (rarely identified), the AV node, or in branches of the His bundle (BBBs); in the BBBs, block is not subdivided into degrees but is simply said to be present or, in the normal heart, absent.

Answer 13

Finally, disturbances combining excitability and conduction abnormalities are discussed. Serum electrolyte abnormalities commonly have repercussions on the rhythm of the heartbeat, which may involve alterations in excitation, conduction, or both. In preexcitation, accessory conduction pathways bypass part of the normal AV conduction pathway. Sinus node dysfunction, formerly called sick sinus syndrome (SSS), generally involves periods of bradycardia and tachycardia caused by dysfunction of the sinus node and supraventricular and ventricular conductive tissues.

Answer 14

In the dog, disturbances of excitability, especially extrasystoles and AFib, are more common than are disturbances of conduction, the majority of which are AV blocks.

Answer 15

Because repolarization follows directly in the wake of the wave of depolarization, a QRS complex of abnormal shape should also have a T wave of abnormal or different shape. If the T wave is normal, the possibility of artifact, rather than a truly abnormal QRS, should be considered as the explanation for a wide, bizarre deflection

Answer 16

Even in the hospital setting, the balance between the sympathetic and parasympathetic inputs to the heart generally tilts in favor of the parasympathetic system in most resting dogs. In the veterinary clinic, this characteristic is in contrast to the average cat. Vagal predominance in the dog produces two particular features of sinus rhythm on the canine ECG: (1) RSA and (2) WP.

Answer 17

RSA is the result of vagal effects that occur within the thorax during each respiratory cycle. RSA is first noted in the puppy after 4 weeks of age.

Answer 18

The return of RSA is due to the reduction of sympathetic tone associated with resolving CHF; an additional benefit of digitalization is reactivation of baroreceptors, which otherwise remain downregulated (“exhausted”) by the ongoing sympathetic stimulation of heart failure.

Answer 19

WP is a normal, physiologic phenomenon in dogs that is not associated with pathologic conditions and requires no treatment. On the ECG the result is variation in the P wave amplitude, with a constant P-R interval and QRS complexes that retain a normal, supraventricular appearance. This variability in the P wave is often cyclic and often associated with RSA. In this situation the amplitude of the P wave increases with an increased heart rate (inspiration) and decreases with decreased heart rate (expiration), sometimes to the point of disappearance (isoelectric P wave) or, rarely, negativity in leads II, III, and aVF. The ECG differential diagnosis for WP includes morphologic abnormalities (e.g., P pulmonale) and supraventricular extrasystoles. In some individuals with marked resting vagal tone (e.g., brachycephalic dogs), an exaggerated but normal RSA and WP may be difficult to differentiate from a pathologic arrhythmia, namely PACs (supraventricular extrasystoles). Both PACs and the combination of WP and RSA produce a P wave of different morphology, a shorter R-R interval, and QRS complexes of normal morphology. Differentiation rests on the degree of prematurity (WP and RSA should not occur so prematurely as to produce a P wave inside the preceding T wave), heart rate (WP and RSA do not occur at a rate above 150/minute), and the appearance of a series or “paroxysm” of such beats closely coupled to each other (corresponding to multiple supraventricular extrasystoles [i.e., supraventricular tachycardia], not RSA). If none of these characteristics is apparent, a Holter monitor can be used for assessing a large number of heartbeats (see previous discussion).

Answer 20

The occurrence of SB as part of sinus node dysfunction, where indeed SB may be a primary, pathologic bradycardia, in which case it is typically accompanied by AV block and/or extrasystoles (see sinus node dysfunction [sick sinus syndrome] later).

Answer 21

The causes of STach are diverse and are all marked by sympathetic predominance over parasympathetic inputs. STach is almost invariably a result of, rather than a cause of, a patient's problems. Therefore it can be expected to resolve (return to NSR) when the causative disorder, such as hypovolemia, congestive heart failure, anemia, or pain, has been treated appropriately. Deliberate suppression of STach, especially in an acutely ill patient, may be catastrophic because in many instances STach is a compensatory response; in these cases, suppression of STach using beta-blockers or calcium-channel blockers reduces an essential determinant of adequate cardiac output (heart rate) and may cause hypotension, circulatory collapse, and cardiac arrest.

Answer 22

Identification of PACs is based on a combination of the first two, and often all five, of the following ECG features: (1) prematurity of the P-QRS-T sequence; (2) QRS complexes that have a supraventricular appearance, in that they are narrow and comparable in shape to the sinus QRS complexes (rarely, QRS complexes may be absent or widened in cases of PACs that are exceptionally early and thus occur during the total or partial refractory period, respectively); (3) a P wave of different amplitude than sinus P waves, including negative, biphasic, or positive P waves, but always preceding the QRS complexes; (4) a P-R interval that may be slightly different from the sinus P-R interval, be it shorter or longer[2]; and (5) a postextrasystolic pause that most often is noncompensatory

Answer 23

Possible for PAC, virtually never for PVC

Answer 24

Usually non compensatory for PAC, Usually Usually compensatory for PVC PAC: Same as sinus T wave PVC: Different from sinus T wave

Answer 25

Differentiation between sustained atrial tachycardia and “high” ventricular (i.e., originating near the AV node) tachycardia can therefore be helped by exteriorizing the P waves, which can be elicited with a vagal maneuver (see previous discussion) and subsequent slowing of the tachycardia or even sinus capture (resumption of sinus rhythm). The same goal may also be reached pharmacologically using graded doses of such intravenous agents as propranolol, esmolol, edrophonium, or phenylephrine.

Answer 26

Atrial flutter is characterized by a rapid and regular series of atrial depolarizations, without a rest phase between them. Identification of this arrhythmia is therefore based on the occurrence of (1) rapid, rhythmic waves of atrial electrical activity referred to as flutter (F) waves, usually occurring at a very high rate (280 to 400/min); (2) absence of a return to baseline between F waves, giving a “saw tooth” baseline appearance; (3) QRS complexes of a normal, supraventricular appearance; and (4) a variable, irregularly irregular R-R interval if some atrial impulses are blocked, as is usually the case.

Answer 27

Atrial flutter is different from other atrial tachycardias in that no return to the isoelectric baseline occurs after each atrial depolarization in atrial flutter.

Answer 28

(1) supraventricular-appearing QRS complexes (narrow, upright, and of only slightly variable amplitude in lead II, unless ventricular aberrancy/BBBs are concurrent); (2) an irregularly irregular rhythm, with a ventricular rate that may be low, normal, or most commonly without treatment, high; and (3) no visible P waves (replaced by a fine undulation of the isoelectric line, termed f waves).

Answer 29

During diastole, ventricular filling is optimized by atrial contraction, which can account for up to 30% of total ventricular filling. Its absence therefore can reduce ventricular volume to suboptimal levels, producing overt clinical signs during peaks of cardiac activity such as intense physical exercise. Furthermore, the rapid overall ventricular rate commonly resulting from AFib can limit diastolic filling when insufficient time has occurred during diastole before the ventricles are triggered to depolarize again. For these reasons, some contractions intermittently may be ineffective, and one or more ausculted heartbeat may occur without a corresponding palpable arterial pulse (i.e., pulse deficit).

Answer 30

The explanation for this apparent contradiction lies in the fact that atrial myocytes and the SA node have markedly different responses to cholinergic inputs such as high vagal tone: In the SA node, cholinergic stimulation decreases the amplitude, rate of increase, and duration of the action potential, slowing the rate of SA node depolarization and therefore the heart rate. Increased activity of a potassium current, IkACh, is one of the most important mechanisms. Interestingly, cholinergic stimulation of the same potassium channel, IkACh, in atrial tissue, actually accelerates repolarization of the atrial cells. If atrial cells can repolarize more quickly, then they have a shorter refractory period and are sooner able to depolarize again. The shorter refractory period also can cause heterogeneity of repolarization, and this combination of faster, less organized (heterogeneous) repolarization predisposes to AFib. The reason that activity of the same current, IkACh, has different, essentially opposite effects in the SA node versus the atria relates to the relative resting membrane potentials of the cells in each tissue type. In SA nodal cells, activation of IkACh channels pushes the resting membrane potential to a more negative level, inducing hyperpolarization. In contrast, atrial cells are already at maximum negative membrane potential in their natural state. Therefore in the atria, IkACh activation mainly affects repolarization.

Answer 31

Paroxysmal AFib usually is of short duration and often will resolve spontaneously in

Answer 32

(1) managing the underlying heart disease and (2) maximizing cardiac output by controlling (slowing) the rate of conduction through the AV node if needed

Answer 33

Atrial dissociation The occurrence of two organized but independent atrial rhythms, one of which traverses the AV node normally and triggers ventricular activity while the other is constantly confined to the atria, is referred to as atrial dissociation (Figure 235-28). This uncommon, apparently benign, incidental finding is characterized electrocardiographically by two populations of P waves, one of which (generally the larger P waves) is followed consistently by QRS complexes, and the other of which shows exit block—the smaller P waves (called P’ waves) do not activate the ventricles. The resulting appearance is a superimposition of normal sinus rhythm and an independent atrial rhythm, either of which may or may not be influenced by autonomic inputs (altering the P-P and/or P’-P’ intervals). No disease link is known to exist between atrial dissociation and any other cardiac disorder, and no treatment or intervention is required

Answer 34

By their short R-R interval (prematurity), the wide QRS complexes they generate, which have a different morphology (shape) than normal sinus QRS complexes. Most ventricular extrasystoles have a wide, often bizarre-appearing QRS complex (>0.07 second in dogs), without an associated P wave, and a different (often very large) associated T wave

Answer 35

Single PVCs are usually followed by a compensatory pause but may be interpolated instead

Answer 36

In cats, ventricular extrasystoles are associated predominantly with myocardial disease.

Answer 37

The causative lesion is a degeneration of myocytes predominantly in the outflow tract region of the RV, as supported by histopathologic studies and the typical, left BBB-like appearance of the PVCs indicating their RV origin

Answer 38

ARVC of Boxers can produce overt clinical signs that are the patient's chief complaint. Overt arrhythmic manifestations range from aborted syncope (intermittent episodes of stumbling or “drunken” appearance) to true syncope with or without seizures (due to cerebral hypoxia), sudden cardiac death, or both. These clinical manifestations may be triggered in some cases by intense sympathetic activity, including excitement and physical exertion, and thus are managed by avoiding circumstances that elicit such behavior. The presence of PVC pairs, or of VT, in the absence of any other identifiable systemic or cardiac problem, strongly supports the diagnosis of ARVC

Answer 39

Accelerated idioventricular rhythm: In a typical medium-sized dog, the rate of AIVR by definition is between 70 and 160 beats/min, which places it between idioventricular (i.e., escape) rhythms (

Answer 40

Ventricular tachycardia: An increasingly rapid tachycardia, for example, will cross a threshold of ventricular rate beyond which a greater number of beats will not translate into greater cardiac output. This “point of diminishing returns,” which varies according to the variables described previously, exists because diastolic filling time is most compromised at high heart rates. Thus very rapid VT, like any other very rapid tachycardia, can produce overt clinical signs of reduced cardiac output.

Answer 41

The typical appearance is one or several series of QRS complexes that are widened widened (>0.07 second in the dog, >0.04 second in the cat), do not resemble the sinus QRS complexes, are associated with different-looking, often giant T waves, are not linked to P waves, and may include capture beats (sinus P-QRS complexes after the paroxysm of VT) and fusion beats (QRS complexes with a morphology that is intermediate, between sinus QRS complexes and ectopic QRS complexes)

Answer 42

In VT, P waves are present (the atria depolarize, but the impulse is blocked at [or just after] the AV node because the more rapid rhythm [VT] dominates the ventricles) but are often engulfed by the wide, bizarre QRS complexes and T waves. Thus the presence of P waves at regular intervals but not fixedly associated with QRS complexes is consistent with VT. The atria are not “aware” of VT

Answer 43

. The ECG diagnosis can become more challenging when VT is continuous, particularly if it is of septal or RV origin and thus produces QRS complexes that are fairly narrow and that may resemble supraventricular complexes.

Answer 44

Ventricular flutter Ventricular flutter is a rapid and prefibrillatory stage of VT. The ECG appearance of this rhythm is a tight, tall sinusoidal wave in which it is impossible to separate QRS complexes and T waves. This intermediate stage between VT and VF is rare, brief, and generally precedes cardiac arrest. It must be differentiated from motion artifact. Artifact masquerading as ventricular flutter still shows evidence of coordinated ventricular activity (normal QRS complexes within the “flutter” impostors) on close inspection (see Figure 235-8). Ventricular flutter is considered a severe ventricular arrhythmia and warrants immediate correction of predisposing causes, intravenous antiarrhythmic treatment, and possibly electrical defibrillation.

Answer 45

VF is a disorganized, chaotic pattern of ventricular depolarizations involving complete desynchronization of ventricular electrical activity. Hemodynamically, it produces circulatory collapse and arrest. Therefore it is a preagonal state leading to death within minutes. Indeed, the cardiac rhythms that define cardiac arrest are VF, asystole, and pulseless electrical activity. The ECG appearance of VF consists of erratic, patternless waves of variable morphology, amplitude, and frequency

Answer 46

(1) applying isopropyl alcohol to the skin-ECG lead interface to improve conductivity (help rule out artifact) (2) assessing that the arrhythmia is present in multiple leads, not just lead II; and (3) noting that the patient is unconscious, because VF is inconsistent with adequate cerebral perfusion. VF is often preceded, and therefore heralded, by ventricular extrasystoles (possibly demonstrating the R-on-T phenomenon), then sustained VT, then possibly ventricular flutter. Unfortunately, treatment of PVCs/VT with antiarrhythmic drugs does not reliably reduce the risk of VF, and rather, the underlying cause and other inciting factors that can be arrhythmogenic (hypokalemia, anemia, etc.) must be addressed. When the rhythm has reached VF, treatment (cardiopulmonary resuscitation), though often unrewarding, must be instituted immediately and generally involves electrical defibrillation if available (antiarrhythmic treatments to consider: electrical defibrillation, Class III).

Answer 47

(1) the rhythm immediately prior to onset of TdP is slow, and the Q-T interval is prolonged (>0.25 second in the dog); (2) the onset of TdP involves an R-on-T ventricular extrasystole (e.g., depolarization [R wave] occurs during the vulnerable part of the T wave); (3) the ensuing rapid (>180 beats/min) ventricular rhythm has QRS complexes that are more regular than in VF but that are continuously changing in amplitude and polarity

Answer 48

The total duration of a self-resolving paroxysm of TdP is usually very brief (5 to 10 seconds), but it may persist for longer; in those instances it often evolves lethally into VF. TdP is not commonly recognized in the dog but may be caused by any disorder that prolongs the Q-T interval: congenital long QT syndrome (Dalmatian), hypokalemia, hypocalcemia, and overdose or toxicity due to antiarrhythmic drugs, particularly class 1A antiarrhythmics such as quinidine. The treatment is highly specific and requires discontinuation of all antiarrhythmic drugs and institution of intravenous magnesium sulfate (10 to 30 mg/lb slow intravenous administration).

Answer 49

Ventricular parasystole Ventricular parasystole (“two hearts beat as one”) is a complex arrhythmia that results from the concurrent and independent activity of two pacemakers, one being a normal supraventricular pacemaker and the other existing in a protected site in a ventricle. By definition, parasystole has (1) a ventricular focus with independent, abnormal automaticity and a rate that is greater than an escape focus and (2) a unidirectional (entry) block that shields this focus from sinus depolarizations. Parasystole is most often benign, does not warrant antiarrhythmic treatment, and regardless is usually refractory to antiarrhythmic therapy

Answer 50

Atrioventricular Block AV blocks are defined as delays or stoppages of conduction between the atria and the ventricles. Most commonly it is normal and is due only to high vagal tone. First-degree AV block does not progress to second-or third-degree AV block except in cases of drug toxicity.

Answer 51

Second-degree AV blocks involve the complete (but transient) interruption of AV conduction. Therefore a P wave exists for every QRS complex, but a QRS complex does not exist for every P wave.

Answer 52

The first, Mobitz type I second-degree AV block, is characterized by a progressive lengthening of the P-R interval until ultimately a P wave is blocked (P wave without QRS complex), an entity known as the Wenckebach phenomenon. Anatomically, Mobitz type I second-degree AV block originates high in the AV node and is said to carry a good prognosis because it is closely related to first-degree AV block and virtually never causes clinical signs

Answer 53

The second, Mobitz type II second-degree AV block, by contrast, demonstrates perfectly regular P-R intervals for all beats, until suddenly one or more P waves is/are blocked (Figure 235-36). Mobitz type II second-degree AV block arises from the AV bundle and is said to carry a more guarded to poor prognosis because it more closely resembles third-degree AV block. .

Answer 54

In “simple” Mobitz type II second-degree AV block, more conducted P waves occur than blocked P waves, whereas in “advanced” or “high-grade” Mobitz type II second-degree AV block, more blocked P waves occur than conducted P waves.

Answer 55

Stokes-Adams seizures: true convulsions caused by critical, bradycardia-induced cerebral hypo perfusion, even with minimal exertion.

Answer 56

Third-degree AV block is a complete and sustained interruption of AV conduction. The ventricles depolarize according to a slow, regular, independent rhythm, called an escape rhythm (junctional or ventricular; see following) . It is important to recognize the lifesaving salvage function of a ventricular escape rhythm because it prevents asystole. Therefore even though ventricular escape QRS complexes are wide and bizarre, ventricular antiarrhythmic therapy is absolutely contraindicated

Answer 57

In third-degree AV block, electrical communication between the atria and ventricles is nonexistent (complete AV dissociation). Therefore the ECG diagnosis is based on the complete absence of P wave conduction (P waves occur regularly but are not followed immediately and consistently by QRS complexes; no consistent PR interval) and slow ventricular rhythm, where the QRS complexes are usually of a uniform, but wide, bizarre morphology (shape) and usually occur with near-perfect regularity. Third-degree AV blocks typically produce marked exercise intolerance, weakness, and syncope. Even so, it is possible to encounter older animals, not very active by nature, who have “asymptomatic” third-degree AV blocks, or individuals (especially cats) with third-degree AV block and a rapid ventricular escape rhythm in which the block is an incidental finding. The causes of AV blocks are diverse.

Answer 58

First-degree AV and Mobitz type I second-degree AV blocks often are functional (high vagal tone in healthy individuals, negative dromotropic effects of digitalis, antiarrhythmics, or alpha 2–stimulating anesthetics) and thus are normal physiologic variants or resolve with drug discontinuation. Less commonly, cardiac disease with atrial dilation and AV nodal lesions may be present as a cause of first-degree or Mobitz type I second-degree AV block. Mobitz type II second-degree AV block and third-degree AV block are sometimes functional (hyperkalemia, digitalis toxicity, alpha 2–stimulating anesthetics) but are more commonly associated with a structural lesion, be it inflammatory (endocarditis, Lyme myocarditis, traumatic myocarditis) or degenerative (physical disruption of the AV node arising from cardiomyopathy, endocardiosis, or fibrosis)

Answer 59

In clinically overt, advanced, Mobitz type II second-degree AV blocks or third-degree AV blocks, response to parasympatholytic or sympathomimetic drugs tends to be fairly disappointing and potentially dangerous. Pacemaker implantation is a better choice.

Answer 60

BBBs are slowings or interruptions of conduction involving one or more of the ventricular branches of the His bundle. Blocks may be functional (transient interruptions due to the depolarizations occurring during the refractory period) or structural (permanent interruptions due to a physical disturbance). The duration of the QRS complexes is greater than 0.07 second in dogs with BBB (greater than 0.04 second in cats with BBB), and the polarity is positive in lead II for left BBBs and negative in lead II for RBB blocks. It is a rhythm, not an arrhythmia.

Answer 61

The causes of BBB are many because BBBs may be due to a variety of pathologic changes including concentric hypertrophy (as seen in hypertrophic cardiomyopathy), dilation (as seen in dilated cardiomyopathy), and inflammation (endocarditis, traumatic myocarditis). In the dog, RBB block is often a completely normal, unnecessarily worrisome ECG finding. Clinical manifestations of BBBs alone generally do not occur. These disturbances therefore do not warrant specific treatment beyond that of their underlying problem if one exists. The importance of recognizing BBB lies in the fact that they could be the first indicators of underlying cardiac disease, which itself warrants further diagnosis and treatment, and that they can—and should not—be misinterpreted as ventricular arrhythmias

Answer 62

(1) moderate to marked hyperkalemia (K+ > 7.5 mEq/L; see later discussion), (2) atrial myopathy, and (3) ECG artifact (P waves too small, or isoelectric, preventing them from being seen properly). Although hyperkalemia is the most common cause of atrial standstill (and the only reversible one), atrial standstill may occur due to marked atrial stretch, as occurs particularly in cats with various forms of cardiomyopathy, or atrial parenchymal hypoplasia, as is seen in association with a dystrophic form of neuromyopathy, particularly in the Springer Spaniel. Regardless of cause, the ECG appearance is of a regular rhythm, usually with QRS complexes that are of a supraventricular appearance, and with a low or normal rate but without detectable P waves in any lead on the ECG. Differentiating between the two main causes of this rhythm using the ECG alone is difficult, and immediate measurement of serum electrolytes is warranted

Answer 63

Refers to the failure of conversion of an electrical rhythm into the mechanical forces of systole and diastole. The ECG therefore may show virtually any rhythm, and the diagnosis rests on the combination of a hemodynamically collapsed patient with an ECG that shows any rhythm but asystole. The pulse is usually barely perceptible or absent, the patient typically is unconscious, and EMD most commonly is a prearrest or terminal condition. Treatment requires correction of underlying causes if possible and then is aimed at increasing circulation to improve myocardial perfusion. Because EMD generally indicates profound myocardial hypoxia, the prognosis is grave even with treatment.

Answer 64

Purple top tubes contain tripotassium EDTA, which produces an artifactual test result incompatible with life, and red top tubes allow coagulation, a process that, during platelet activation and aggregation, releases potassium and may artifactually raise the measurement by small but clinically significant levels.

Answer 65

1. It makes the resting membrane potential increasingly negative (see Figure 235-41) which decreases myocyte excitability. This effect is a result of the greater difference between intracellular and extracellular potassium concentrations in hypokalemia compared with normokalemia (hyperpolarization) and in cardiomyocytes is generally mild and transient. 2. Hypokalemia prolongs repolarization, increasing action potential duration. Myocyte repolarization depends principally on the activity of potassium currents, notably the delayed rectifiers Ikr and Iks. With hypokalemia, these currents function more slowly. This prolongation of repolarization lengthens the normally very brief period of repolarization during which the diastolic membrane potential is near the threshold potential. Therefore hypokalemia-induced prolongation of repolarization opens a window of increased excitability during which spontaneous ectopic activity (such as atrial or ventricular extrasystoles) can occur based on the threshold being reached after the absolute refractory period by a slowly repolarizing cell.

Answer 66

Clinically, the second (arrhythmogenic) effect predominates over the first (suppressive), and the dominant cardiovascular effect of a serum potassium concentration

Answer 67

Can include evidence of prolonged, abnormal repolarization in the form of U waves (see previous discussion), Q-T interval prolongation, and AV dissociation.

Answer 68

Because class I antiarrhythmics (e.g., lidocaine, mexiletine, quinidine) act on sodium channels that require normal serum potassium concentrations to function, hypokalemia is also important as a cause of antiarrhythmic drug refractoriness: a patient whose PVCs are caused by hypokalemia will generally return to normal sinus rhythm with potassium supplementation alone, whereas treatment with lidocaine during hypokalemia is unlikely to alter the ventricular arrhythmia but may still cause lidocaine toxicosis (neurologic disturbances such as seizures) if dosing is readministered repeatedly for lack of conversion to sinus rhythm. This important observation has wide-ranging implications in patients with dilutional hypokalemia (e.g., gastric dilatation-volvulus patient with large-volume fluid resuscitation) or potassium-wasting metabolic illness (e.g., chronic renal disease) when PVCs/VTs occur and the question “When should I treat this arrhythmia with an antiarrhythmic?” arises. An important initial step toward answering this question should always be to ensure that normokalemia is present before considering antiarrhythmic therapy.

Answer 69

Hyperkalemia Mildly elevated serum potassium levels (5.6 to 6.5 mEq/L) are associated with greater cell membrane permeability to potassium during repolarization. These repolarization effects predominate over depolarization effects shown in Figure 235-41, and such mild hyperkalemia has been described as a rhythm-stabilizing condition. Thus mild hyperkalemia in dogs may be reflected on the ECG as faster ventricular repolarization (i.e., a shorter than normal Q-T interval and an abnormally narrow, often peaked or “tented” T wave). It is a common but serious mistake to think that tented T waves must always equal hyperkalemia

Answer 70

Because hyperkalemia decreases the activity of normal pacemaker tissue. Specifically, it decreases the slope of phase 4 of diastolic depolarization, which slows the heart rate. However, naturally occurring hyperkalemia also routinely coexists with abnormalities in acid-base status or other serum electrolytes, pain, fear, sepsis, hypovolemia, and other disorders, all of which tend to cause the opposite—sinus tachycardia. The routine observation that many cats and dogs with even severe hyperkalemia have elevated heart rates makes heart rate unreliable for inferring a patient's serum [K+].

Answer 71

The atria are more sensitive to hyperkalemia than are the ventricles, and within the atria, the myocardium is more sensitive to the effects of hyperkalemia than are the internodal tracts (see Introduction, preceding). The result when severe hyperkalemia occurs is a sinoventricular rhythm, so named because the heartbeat originates in the SA node as usual, crosses the atria through the internodal tracts (but the impulse does not spread outward—no atrial activation, no P wave), and then passes through the AV node and His-Purkinje system in the usual sequence. The ECG appearance is a regular rhythm with normal or slightly widened QRS complexes and no P waves

Answer 72

Very high serum potassium concentrations (>8.5 mEq/L) can be lethal. So many other factors influence the rhythm in these catastrophically ill patients that an exact cutoff for lethality cannot be established for serum potassium concentration alone. With rising concentrations comes further widening of the QRS complex and also the T wave, and these may blend into a sine-wave type of regular but poorly functional or nonfunctional rhythm, or a ventricular-type of escape rhythm at a very low rate (both likely preagonal rhythms). If not corrected immediately, critical hyperkalemia that has produced these dramatic ECG changes can cause cardiac arrest (ventricular fibrillation, escape rhythm with pulseless electrical activity) within minutes.

Answer 73

Altered calcium concentrations affect the threshold of a myocyte's action potential, rather than the resting membrane potential. Hypocalcemia lowers the threshold, facilitating depolarization. The clinical expression is fine muscle fasciculations progressing to generalized tremors if calcium is not normalized. This effect is minimal in cardiomyocytes. Hypocalcemia also prolongs the initial phase of ventricular repolarization, which can manifest as a prolongation of the Q-T interval on the ECG. These effects help explain why intravenous calcium infusions are considered “cardioprotective” in severe hyperkalemia, even though they do not change the circulating potassium concentration. Hyperkalemia raises the resting membrane potential (see Figure 235-41), and providing additional calcium raises the threshold for depolarization, reestablishing a more normal ionic gradient across the cell membrane. Considering that 75% of cats with urethral obstruction concurrently have mild, moderate, or severe hypocalcemia, IV calcium gluconate appears to be the preferred first-line treatment for severe hyperkalemia in these patients.

Answer 74

Grounds for stopping the infusion: A sudden slowing of the heart rate, Ahortening of the Q-T interval, or Appearance of ventricular extrasystoles

Answer 75

Similarly, hypercalcemia generally is of greater concern for its extracardiac effects than for any alterations in cardiac rhythm. Severe hypercalcemia raises the threshold of the cardiomyocyte, which should hinder depolarization. It also shortens early ventricular repolarization, making the Q-T interval shorter. These consequences of severe hypercalcemia are of secondary concern compared with dystrophic mineralization of the kidneys and other soft tissues, for example.

Answer 76

In preexcitation, the normal impulse originating from the SA node is split at the end of atrial depolarization, with part of the impulse traveling normally through the AV node and another part of the impulse traveling simultaneously through an abnormal shaft of rapidly conductive fibers that links the atria and the ventricles (also called an accessory pathway or bypass tract), thus bypassing the AV node. The result is partial, premature, immediate activation of the ventricles through the bypass tract, without the benefit of a pause in the AV node; hence the term preexcitation. With one major exception (see later), the effect of this abnormal pattern of activation is minimal because only a part of the atrial contribution to ventricular filling is lost. The ECG demonstrates that the normal delay through the AV node was preempted by conduction through the bypass tract (i.e., little or no segment separates the P wave from the QRS complex) and that conduction through the bypass tract caused asynchronous activation of the ventricles (the bypass tract and the normal AV nodal conduction ultimately each activate their share of the ventricles), resulting in a notched QRS complex. The size and location of the QRS complex's notch, the delta wave, depends on the distance that separates the bypass tract and the AV node in the individual's heart (i.e., on the amount of myocardium that the His bundle and the bypass tract can each depolarize before the impulses collide with each other;

Answer 77

Under usual circumstances, preexcitation is an incidental, clinically silent finding. However, in individuals with preexcitation, a premature atrial depolarization may initiate a type of reentry cycle that can produce extreme tachycardias. Although bypass tracts conduct impulses rapidly, their refractory period is typically longer than that of the AV node. Therefore the timing of a premature supraventricular depolarization may fail to conduct through the bypass tract but be able to conduct through the AV node, depolarizing the ventricles normally. As the impulse completes the depolarization of the ventricles, the bypass tract has repolarized and is able to conduct. Bypass tracts can often conduct impulses in either direction, such that the ventricular impulse conducts retrograde through the bypass tract to the atria, then again through the AV node in the normal direction and again through the bypass tract, initiating an endless loop of conduction. This type of self-perpetuating circuit is a macroreentry circuit, and it may produce a potentially very rapid and clinically overt (apparent discomfort, exercise intolerance, lethargy, syncope) tachycardia called orthodromic (the impulse travels in a normal, “normograde” direction through the AV node) AV reentrant tachycardia (OAVRT), the main form of clinically manifested ventriculoatrial macroreentry, or Wolff-Parkinson-White syndrome, in the dog.[70,75,124] Dogs with this syndrome may have unrelenting heart rates above 300 beats/min. Initial treatment can involve vagal maneuvers that, through slowing of AV conduction (i.e., negative dromotropic action), break the cycle of reentry.

Answer 78

Sinus node dysfunction (sick sinus syndrome [SSS], bradycardia-tachycardia syndrome) involves a complex disturbance of the cardiac conductive tissues, producing simultaneous defects in sinus activity (SB and sinus arrest), AV conduction disturbances (first-degree and second-degree AV blocks), and disturbances in supraventricular and ventricular excitability (see Figure 235-17). Therefore the disturbance is not a problem involving only the SA node, as the name SSS suggests, but rather is an illness that affects cardiac pacemaking and conductive tissues at all levels.

Answer 79

SB (often with first- or second-degree AV block), prolonged sinus pauses with variable escape beats, and bursts of supraventricular tachycardia or ventricular extrasystoles at various rates (Figure 235-43). In some cases only SB occurs. Because these features occur intermittently, the diagnosis often is only made by obtaining an ECG during an episode of syncope, stumbling, or ataxia (near syncope), which are the most common overt clinical manifestations of this arrhythmia. Vagolytic drugs may acutely improve the situation by reducing the impact of bradycardia episodes and pauses, but definitive treatment when episodes are recurrent generally requires the implantation of a pacemaker.

Answer 80

Electrical activity that travels directly toward the positive pole of a lead creates a strong positive deflection (wave) above the baseline on the ECG for that lead (see Web Figure 235-1). Similarly, electrical activity that travels directly away from the positive pole of a lead registers a strong negative ECG wave, below the baseline. All leads register the amount of positivity or negativity generated by that impulse relative to their positive pole and record a wave in proportion to that. The lead that is almost 90 degrees away from the direction of the electrical activity will record little to no activity (i.e., almost isoelectric line; see Web Figure 235-3, lead [aVL]), and the positive pole of the lead that is closest to 180 degrees away from the direction of electrical activity will register a very large, negative complex (see Web Figure 235-3, lead [aVR]).

Answer 81

First, the leads directly and proportionally perceive the amount of energy (i.e., number of cells depolarizing, the smoothness of conduction) involved in depolarization. Thus left ventricular (LV) hypertrophy may be suspected when QRS complexes are abnormally tall in lead II, for example, because the amount of energy transmitted in the normal direction (toward the LV) is greater due to the increased myocardial mass. Right ventricular (RV) hypertrophy can be suspected when the bulk of ventricular electrical activity is directed abnormally toward the right side of the heart (see discussion of right axis deviation later). Second, having multiple leads solves the problem of any single lead's “blindness” to perpendicularity. Posting numerous observers at regular stations around the heart (i.e., having multiple leads) ensures that some leads inevitably will perceive the heart's electrical energy better than others and therefore will show larger, more easily interpreted waves and complexes (see Web Figure 235-3). Therefore on any ECG that shows multiple leads, the clinician will usually find it easiest to interpret the rhythm by first scanning the different leads to see which ones offer the clearest (i.e., largest and with the least artifact) P waves, QRS complexes, and T waves.

Answer 82

The sum total of electrical energy for all the depolarizations in one beat of the ventricles represents the final tally of individual depolarizations, with impulses headed in the same direction adding to each other and impulses headed away from each other canceling each other out. Therefore in a normal heart, the sum total of electrical energy expended for one beat of the ventricles has an overall thrust that is leftward (because the left ventricle [LV] is larger than the right) and caudal (because more energy is directed toward the apex of the heart during initial activation than travels back toward the base at the end of ventricular activation). This sum total, or overall thrust, of electrical energy, is also called the mean electrical axis (MEA)

Answer 83

In normal individuals, the MEA, as just mentioned, points leftward and caudally because that is the overall direction in which the normal ventricles point (see Web Figure 235-3). However, the sum total of electrical energy for one beat of the ventricles (the MEA) may change if the heart changes in shape. For example, if a patient's RV becomes pathologically enlarged to a sufficient degree, the bulk of electrical energy for ventricular depolarization may be directed to move toward the right instead of the left. This is called a right axis shift or right axis deviation.

Answer 84

(1) RV hypertrophy and (2) RBB block. In a case an ECG with multiple leads in a clinical patient could show QRS complexes that were more positive than usual in the right-sided leads (aVR, III) and QRS complexes that were more negative than usual in the left-sided leads (aVL, I, and II) (Web Figures 235-5 and 235-6). This simple ECG finding would increase the suspicion of disorders that cause RV enlargement. Hampered conduction through the RBB, a phenomenon called RBB block, redirects the electrical impulse, a variation that is visible on the ECG (see Bundle Branch Blocks; see Figure 235-39). As a result of RBB block, the incompletely depolarized RV is depolarized late, and incompletely so. Together with unopposed electrical forces depolarizing the LV, the resulting overall thrust of electrical energy for that beat is directed to the right, creating a right axis deviation.

Answer 85

Left axis deviations occur uncommonly because the bulk of electrical activity already is directed toward the left in the normal heart. Therefore LBBB causes a wider (conduction is slower) but otherwise similarly shaped QRS complex compared to normal (see Figure 235-38). LV hypertrophy does not alter the direction of thrust of overall electrical activity from the left-caudal direction but often will increase its magnitude (e.g., taller R waves in lead II). Left anterior fascicular (LAF) block is an example of a conduction abnormality within the ventricles that is compensated for with a thrust of energy in the left dorsal direction, which can cause a left axis shift.

Answer 86

Using vectorial enhancement, the ECG machine uses the three electrode wires connected to patients undergoing an ECG (the fourth is an electrical ground) to assess electrical activity from three additional perspectives (aVR, aVL, and aVF) in addition to I, II, and III, for a total of six different perspectives. The six positions, or leads, are evenly spaced 30 degrees apart and are called the limb leads

Answer 87

The concept of designing ECG leads to “survey” the electrical activity of the heart from multiple angles is a sound one, but even with a lead at every 30 degrees, a major shortcoming still exists. The six limb leads (I, II, III, aVR, aVL, aVF) may cover the entire frontal plane of the body (see Figure 235-13), but electrical energy traveling through a three-dimensional structure like the heart may travel “outward” or “inward” (i.e., in a dorsal or ventral direction). In such a situation, none of the six leads perceives the electrical activity as going clearly toward or away from any positive pole; electrical activity is perpendicular to all of them and therefore is invisible to all. The solution to this problem is the precordial leads (chest leads, thoracic leads, V leads). With precordial leads the ability to perceive electrical activity of the heart extends to three dimensions because the ECG clips for precordial leads are placed circumferentially around the chest. Thus the precordial leads (rV2, V2, V4, and V10) assess electrical activity in the transverse (lateral and ventral-dorsal) plane. Precordial leads provide essential information that may not be apparent in the limb leads (frontal plane) (see Figure 235-5), but they are more susceptible to artifact caused by chest wall motion

Answer 88

From the explanations given previously, it should be seen as logical that lead II is routinely used for evaluating the ECG in small animals. This is because the positive pole of lead II (i.e., the point from which a lead II “observer” detects electrical activity) is at +60 degrees, or in the left caudal region. This is in the middle of the normal range of MEA for healthy dogs and cats. The LV receives more energy than the right, and the overall thrust of electrical energy is caudal, so the positive pole of lead II is likely to perceive a large thrust of electrical energy toward it in normal small animals and thus display a clear ECG with large, visible QRS complexes. The same can be said for atrial activity and the P waves. However, interindividual variation reveals the limitation of using only lead II. Certain patients may fail to provide the desired information in a specific lead

Answer 89

Normal MEA is +30 degrees clockwise to +110 degrees for the dog, and zero degrees clockwise to +160 degrees for the cat.

Answer 90

Those with pulmonic stenosis (right axis deviation in 19 of 21 patients [90%]), right-to-left patent ductus arteriosus (right axis deviation in 8 of 8 patients [100%]), and cor pulmonale.

Answer 91

Changes in position of the limbs[50] and of the position of the heart within the chest (e.g., pericardial effusion), peritoneopericardial diaphragmatic hernia, intrapericardial mass, or body motion in ambulatory ECG) change the perspective from which ECG leads perceive the heart's electrical activity, often causing the false appearance of changes in the MEA.

Cardiovascular System Ettinger: ECG Flashcards

(115 cards)