ECG

Intrinsic asthma

Rackemann described this as asthma caused by substances from “within the body.”  These patients usually have a negative allergy skin test, and therefore do not have allergies and do not benefit from allergy shots or allergy medications.

Rackemann believed a common cause of intrinsic asthma was colds, and treating the asthma was as simple as avoiding getting a cold. One suggested remedy here was vaccination.2 Other than colds, he suggested sinus infections, chronic sinusitis, teeth infections, gum infections, and throat infections, as probable causes of asthma. The likely treatment would be treatment of the infection, or avoiding it altogether

The  electrocardiogram  (ECG  or  EKG) is a special type of graph that represents cardiac electrical activity from one instant to the next. Specifically, the ECG provides a  time-voltage chart  of the heartbeat. The ECG is a key component of clinical diagnosis and management of inpatients and outpatients because it may provide critical information. Therefore, a major focus of this book is on recognizing and understanding the “signature” ECG findings in life-threatening conditions such as acute myocardial ischemia  and  infarction, severe hyperkalemia or hypokalemia, hypothermia, certain types of drug toxicity that may induce cardiac arrest, pericardial (cardiac) tamponade, among many others. The general study of ECGs, including its clinical applications, technologic aspects, and basic science underpinnings, comprises the field of electrocardiography. The device used to obtain and display the conventional (12-lead) ECG is called the  electrocardiograph, or more informally, the  ECG  machine.  It records cardiac electrical currents (voltages or potentials) by means of sensors, called  electrodes, selectively  positioned  on  the  surface  of  the  body.a Students and clinicians are often understandably confused by the basic terminology that labels the graphical recording as the electrocardiogram  and the recording device as the electrocardiograph! We will  point  out  other  potentially confusing  ECG semantics as we go along. Contemporary ECGs are usually recorded with disposable paste-on (adhesive) silver–silver chloride electrodes.  For  the  standard  ECG  recording,  electrodes are placed on the lower arms, lower legs, and across  the  chest  wall  (precordium).  In  settings  such as  emergency  departments,  cardiac  and  intensive care units (CCUs and ICUs), and ambulatory (e.g., Holter) monitoring, only  one or two “rhythm strip” Please go to  expertconsult.inkling.com  for additional online material for this chapter. aAs discussed in Chapter 3, more precisely the ECG “leads” record the differences  in potential between pairs or configurations of electrodes. leads may be recorded, usually by means of a few chest and abdominal electrodes. ABCs  OF CARDIAC ELECTROPHYSIOLOGY Before the basic ECG patterns are discussed, we review a few simple-to-grasp but fundamental principles of the heart’s electrical properties. The central function of the heart is to contract rhythmically and pump blood to the lungs (pulmonary  circulation)  for  oxygenation  and  then  to  pump this oxygen-enriched blood into the general (systemic) circulation. Furthermore, the amount of blood pumped has to be matched to meet the body’s varying metabolic needs. The heart muscle and other tissues  require  more  oxygen  and  nutrients  when  we are  active  compared  to  when  we  rest.  An  important part of these  auto-regulatory  adjustments is accomplished by changes in heart rate, which, as described below, are primarily under the control of the autonomic (involuntary) nervous system. The signal for cardiac contraction is the spread of synchronized electrical currents through the heart muscle. These currents are produced both by  pacemaker cells  and  specialized conduction tissue  within the heart and by the working  heart muscle  itself. Pacemaker  cells are  like  tiny clocks  (technically called  oscillators)  that  automatically  generate  electrical stimuli in a repetitive fashion. The other heart cells, both specialized conduction tissue and working heart  muscle,  function  like  cables  that  transmit  these electrical signals.b Electrical Signaling in the Heart In simplest terms, therefore, the heart can be thought of  as  an  electrically  timed  pump.  The  electrical 

Fig.  1.1  Normally, the cardiac stimulus (electrical signal) is generated in an automatic way by pacemaker cells in the  sinoatrial  (SA) node, located in the high  right atrium (RA).  The stimulus then spreads through the  RA  and  left atrium (LA).  Next, it traverses the atrioventricular (AV)  node and the  bundle of His, which comprise the  AV junction.  The stimulus then sweeps into the  left  and  right ventricles (LV  and  RV) by way of the  left  and  right bundle branches, which are continuations of the  bundle of His. The cardiac stimulus spreads rapidly and simultaneously to the left and right ventricular muscle cells through the  Purkinje fibers.  Electrical activation of the atria and ventricles, respectively, leads to sequential contraction of these chambers (electromechanical coupling). “wiring” of this remarkable organ is outlined in  Fig. 1.1. Normally, the signal for heartbeat initiation starts in the pacemaker cells of the  sinus  or  sinoatrial (SA) node. This node is located in the right atrium near the opening of the superior vena cava. The SA node is a small, oval collection (about 2  ×  1  cm) of specialized cells capable of automatically generating an electrical  stimulus  (spark-like  signal)  and  functions as  the  normal  pacemaker  of  the  heart.  From  the  sinus node, this stimulus spreads first through the right atrium and then into the left atrium. Electrical stimulation of the right and left atria signals the atria to contract and pump blood simultaneously through the tricuspid and mitral valves into the right and left ventricles, respectively. The electrical stimulus then spreads through the atria and part of this activation wave reaches specialized conduction tissues in the  atrioventricular (AV) junction.c cAtrial stimulation is usually modeled as an advancing (radial) wave of excitation originating in the sinoatrial (SA) node, like the ripples induced by a stone dropped in a pond. The spread of activation waves between the SA and AV nodes may also be facilitated by so-called internodal “tracts.” However, the anatomy and electrophysiology of these preferential internodal pathways, which are analogized as functioning a bit like “fast lanes” on the atrial conduction highways, remain subjects of investigation and controversy among experts, and do not directly impact clinical assessment. The AV junction, which acts as an electrical “relay” connecting the atria and ventricles, is located near the lower part of the  interatrial  septum and extends into the  interventricular septum  (see  Fig. 1.1).d The upper (proximal) part of the AV junction is the AV node. (In some texts, the terms  AV node  and AV junction  are used synonymously.) The lower (distal) part of the AV junction is called the  bundle of His. The bundle of His then divides into two main branches: the right bundle  branch, which distributes the stimulus to the right ventricle, and the left bundle branch,e  which distributes the stimulus to the left ventricle (see  Fig. 1.1). The electrical signal spreads rapidly and simultaneously down the left and right bundle branches into the  ventricular myocardium  (ventricular muscle) by way of specialized conducting cells called  Purkinje f ibers  located in the subendocardial layer (roughly the  inside  half  or  rim)  of  the  ventricles.  From  the f inal branches of the Purkinje fibers, the electrical signal spreads through myocardial muscle toward the epicardium (outer rim). dNote the potential confusion in terms. The muscular wall separating the ventricles is the  interventricular septum, while a similar term—intraventricular conduction delays (IVCDs)—is used to describe bundle branch blocks and related disturbances in electrical signaling in the ventricles, as introduced in Chapter 8. eThe left bundle branch has two major subdivisions called  fascicles. (These conduction tracts are also discussed in Chapter 8, along with abnormalities called fascicular blocks or hemiblocks.)

The bundle of His, its branches, and their subdivisions  collectively  constitute  the  His–Purkinje system. Normally, the AV node and His–Purkinje system provide the only electrical connection between the atria  and  the  ventricles,  unless  an  abnormal  structure called a  bypass tract  is present. This abnormality and its consequences are described in Chapter 18 on Wolff–Parkinson–White preexcitation patterns. In contrast, impairment of conduction over these bridging structures underlies various types of AV heart block (Chapter 17). In its most severe form, electrical  conduction  (signaling)  between  atria  and ventricles  is  completely  severed,  leading  to  thirddegree (complete) heart block. The result is usually a  very  slow  escape  rhythm,  leading  to  weakness, light-headedness or fainting, and even sudden cardiac arrest and sudden death (Chapter 21). Just as the spread of electrical stimuli through the atria leads to atrial contraction, so the spread of stimuli through the ventricles leads to ventricular contraction, with pumping of blood to the lungs and into the general circulation. The  initiation of  cardiac contraction  by electrical stimulation is referred to as  electromechanical coupling. A key part of the contractile mechanism involves the release of calcium ions inside the atrial and ventricular heart muscle cells, which is triggered  by the spread of electrical activation. The calcium ion release process links electrical and mechanical function (see Bibliography). The ECG is capable of recording only relatively large currents produced by the mass of working (pumping) heart muscle. The much smaller amplitude signals generated by the sinus node and AV node are invisible with clinical recordings generated by the surface ECG. Depolarization of the His bundle area can only be recorded from inside the heart during specialized cardiac  electrophysiologic  (EP)  studies. CARDIAC AUTOMATICITY AND CONDUCTIVITY: “CLOCKS   AND CABLES” Automaticity  refers to the capacity of certain cardiac cells to function as  pacemakers  by spontaneously generating  electrical  impulses,  like  tiny  clocks.  As mentioned earlier, the sinus node normally is the primary (dominant) pacemaker of the  heart because of its inherent automaticity. Under special conditions, however, other cells outside the sinus node (in the atria, AV junction, or ventricles) can also act as independent (secondary/ 

subsidiary) pacemakers. For example, if sinus node automaticity  is  depressed,  the  AV  junction  can  act as a backup (escape) pacemaker. Escape rhythms generated by subsidiary pacemakers provide important physiologic redundancy (safety mechanisms) in the vital function of heartbeat generation, as described in Chapter 13. Normally, the relatively more rapid intrinsic rate of SA node firing suppresses the automaticity of these secondary (ectopic) pacemakers outside the sinus node. However, sometimes, their automaticity may be abnormally increased, resulting in competition with, and even usurping the sinus node for control of, the heartbeat. For example, a rapid run of ectopic atrial beats results in  atrial tachycardia (Chapter 14). Abnormal atrial automaticity is of central importance in the initiation of atrial fibrillation (Chapter 15). A rapid run of ectopic ventricular beats results in ventricular tachycardia (Chapter 16), a potentially life-threatening arrhythmia, which may lead to ventricular fibrillation and cardiac arrest (Chapter 21). In  addition  to  automaticity,  the  other  major  electrical property of the heart is  conductivity. The speed with which electrical impulses are conducted through different parts of the heart varies. The conduction is  fastest  through the Purkinje fibers and  slowest through the AV node. The relatively slow conduction speed through the AV node allows the ventricles time to fill with blood before the signal for cardiac contraction  arrives.  Rapid  conduction  through  the His–Purkinje system ensures synchronous contraction of both ventricles. The more you understand about normal physiologic stimulation of the heart, the stronger your basis for comprehending the abnormalities of heart rhythm and conduction and their distinctive ECG patterns. For example, failure of the sinus node to effectively  stimulate the atria can occur because of a failure of SA automaticity or because of local conduction block that prevents the stimulus from exiting the sinus node (Chapter 13). Either pathophysiologic mechanism can result in apparent  sinus node dysfunction  and sometimes  symptomatic sick sinus syndrome  (Chapter 19). Patients may experience lightheadedness  or  even  syncope  (fainting)  because of marked  bradycardia  (slow heartbeat). In contrast, abnormal conduction within the heart can lead to various types of  tachycardia  due to reentry,  a  mechanism  in  which  an  impulse  “chases its tail,” short-circuiting the normal activation 

pathways.  Reentry  plays  an  important  role  in  the genesis of certain paroxysmal supraventricular tachycardias (PSVTs), including those involving AV nodal  dual pathways  or an AV  bypass tract, as well as in many variants of ventricular tachycardia (VT), as described in Part II. As  noted,  blockage  of  the  spread  of  stimuli through  the  AV  node  or  infranodal  pathways  can produce various degrees of AV heart block (Chapter 17), sometimes with severe, symptomatic ventricular bradycardia or increased risk of these life-threatening complications, necessitating placement of a permanent (electronic) pacemaker (Chapter 22). Disease of the bundle branches themselves can produce right or left bundle branch block. The latter especially is a cause of  electrical dyssynchrony, an important contributing mechanism in many cases of heart failure (see Chapters 8 and 22). CONCLUDING NOTES: WHY IS   THE ECG SO USEFUL? The ECG is one of the most versatile and inexpensive clinical tests. Its utility derives from careful clinical and experimental studies over more than a century showing its essential role in: •  Diagnosing dangerous cardiac electrical disturbances causing brady- and tachyarrhythmias. •  Providing immediate information about clinically important problems, including myocardial ischemia/infarction, electrolyte disorders, and drug toxicity,  as  well  as  hypertrophy  and  other  types of chamber overload. •  Providing clues that allow you to forecast preventable catastrophes. A major example is a very long QT(U) pattern, usually caused by a drug effect or by hypokalemia, which may herald sudden cardiac arrest due to  torsades de pointes. PREVIEW: LOOKING AHEAD The  first part  of this book is devoted to explaining the basis of the normal ECG and then examining the major conditions that cause abnormal depolarization (P and QRS) and repolarization (ST-T and U) patterns. This alphabet of ECG terms is defined in Chapters 2 and 3. Some Reasons for  the Importance  of   ECG “Literacy” •  Frontline medical caregivers are often required to make on-the-spot, critical decisions based on their ECG readings. •  Computer readings are often incomplete or incorrect. •  Accurate readings are essential to early diagnosis and therapy of acute coronary syndromes, including ST elevation myocardial infarction (STEMI). •  Insightful readings may also avert medical catastrophes and sudden cardiac arrest, such as those associated with the acquired long QT syndrome and torsades de pointes. •  Mistaken readings (false negatives and false positives) can have major consequences, both clinical and medico-legal (e.g., missed or mistaken diagnosis of atrial fibrillation). •  The requisite combination of attention to details and integration of these into the larger picture (“trees and forest” approach) provides a template for critical thinking essential to all of clinical practice. The  second part  deals with abnormalities of cardiac rhythm generation and conduction that produce excessively fast or slow heart rates (tachycardias and bradycardias). The  third part  provides both a review and further extension of material covered in earlier chapters, including an important focus on avoiding ECG errors. Selected publications are cited in the Bibliography, including  freely  available  online  resources.  In  addition, the online supplement to this book provides extra material, including numerous case studies and practice questions with answers.