The following post is a paper written by Matthew Cohen, a senior majoring in Biology, Society, and Environment at the University of Minnesota, in the spring semester of 2015 for Dominique Tobbell’s class HMED 3075. In a recently published pair of articles in the Bulletin of the History of Medicine, Dominique Tobbell and Lois Hendrickson described their use of historical artifacts (from the Wangensteen Historical Library) in their history of medicine courses. Mr. Cohen’s paper is the first of three papers offered as examples of the work students have done in their classes.
The electrocardiogram’s ability to observe the conduction of the heart, changed medical practice for diphtheria in the early 20th century. My paper will argue that the implementation of the electrocardiogram by physicians changed the diagnosis, monitoring and treatment of diphtheria infected patients in American from 1900-1938. I will be using the electrocardiogram from the Wangensteen historical library collection. This paper will discuss how the electrocardiogram functions, and the implications and clinical relevance of using the electrocardiogram to diagnose the infectious disease diphtheria.
To understand the impact and effects of the electrocardiogram, it must first be defined as a medical technology. The electrocardiogram (ECG) is a medical technology that is used to record the electrical signals of the heart. According to Joel Howell’s definition of technology, the ECG is medical technology by virtue of being a physical object, the activity it performs, and the technological know-how needed to use it.[1] The ECG is relatively easy to use and produces an accurate recording of the heart’s electrical signals however, the scientific know-how to understand the results is what makes the ECG a medical technology. The information recorded by the ECG must be interpreted by a person skilled to equate the physical tracing to the physiological functions of the heart. This means that an anatomical and physiological understanding of the heart is required to accurately understand the results.
The heart has two main components that must be considered, the physical heart and its electrical system. The heart is a muscle, comprised of specialized cardiac cells which, under the influence of an electrical current, contracts to force blood throughout the body.[2] The heart has four anatomically distinct regions. The upper portion of the heart is divided into two openings called the atria and the lower portion of the heart is divided into two openings called the ventricles. These openings are filled with blood, which is expelled from the heart to the body during systolic contracting. This is the physical pumping system of the heart, which must work in conjunction with the electrical system.
The coordinated contraction of the atria and ventricles is controlled by the heart’s electrical system. The ECG records this electrical current, which is a representation of the heart’s physical functioning. The electrical signal passes through a well-established pathway inside of the heart. Cardiac tissue has unique properties, which allow it to generate its own electrical impulses. These electrical impulses, under normal cardiac function, originate in a specific cluster of cardiac cells, called the Sinoatrial (SA) node. The electrical impulses then travel via the intra atrial pathway to the Atrioventricular (AV) node.[3] This results in the contraction of the left and right atria. The electrical impulse then travels through the bundle of His and down the purkinje fibers, resulting in the contraction of the left and right ventricle.[4] This is the normal pathway of the heart’s electrical activity, called a normal sinus rhythm. Since all cardiac cells have the potential to generate an electrical impulse, abnormal conductive pathways can also occur.
The invention of the ECG is credited to Willem Einthoven in 1901.[5] Einthoven developed the standardized ECG pattern, which displayed the electrical pathway discussed previously. Einthoven’s work led him to develop the 3 limb lead placement, now known as precordial leads. The 3 limb lead placement creates an equilateral triangle which is used to capture the hearts electrical activity and is still used today.[6]
The essentials of the electrocardiogram have remained largely unchanged since its development. Einthoven’s early ECG was enormous- weighing over 600 pounds, required two rooms and five people to operate.[7] Einthoven’s ECG measured fluctuation in electrical current in a wire that was suspended between electromagnetics.[8] The results were recorded onto a photographic plate. The electrocardiogram in the Wangensteen historical library collection was made by the Cambridge Instrument Company and it was given the name “Simpli-Scribe Portable Model”.[9] This ECG was designed to be portable, with an exterior made of wood and a metal carrying handle.[10] This version of the ECG did not have a date of manufacture but Cambridge produced the Simpli Scribe from 1945-1960.[11] The Simpli Scribe is approximately one foot cubed in size, and is powered by a two prong electrical cord. The five leads on the ECG are attached to the patient via a strap placed on the chest. The resulting electrical fluctuations are recorded by an electrically heated metal needle that scorches the reading into the paper.[12] While the Simpli-Scribe, is smaller and more refined than the earliest electrocardiogram’s designed by Einthoven, the basics still remained unchanged. Both required electromagnets, recorded fluctuation in electrical activity, and used wires attached to a patient at the same locations.
The use of the ECG in recording cardiac activity was well known by the mid 1910s. The electrocardiogram was hailed as an unquestionable way to determine if one was sick or well.[13] The clinical application of the ECG for monitoring cardiac rhythms such as auricle fibrillation and extra systole beats were well documented.[14] In 1916, the British army adapted the electrocardiogram as a means to screen army recruits, in conjunction with X-rays, to determine their cardiac health and fitness to serve.[15] By this time period, the ECG was already recognized for its ability to determine cardiac health. The electrocardiogram was so prevalent, that by 1924, Willem Einthoven was awarded the Nobel Prize for Physiology and Medicine for his discovery.[16] While the electrocardiogram was well known for its ability to record the heart’s electrical activity, its use in medicine during the time was limited to routine physical exams. However, the importance of the ECG changed when the electrocardiogram was used to monitor and diagnose cardiac issues in infectious diseases such as diphtheria.
Diphtheria is an infectious disease caused by the bacteria Corynebacterium diphtheriae that is spread from person to person through respiratory droplets.[17] The disease targets the mucus membranes of the mouth and nose where they can travel to the respiratory system. Diphtheria will produce symptoms similar to a common cold, such as weakness, sore throat and low grade fever.[18] A thick coating will build up in the mouth and nose, making it difficult to breathe. While these respiratory symptoms cause difficulty breathing, the majority of deaths associated with diphtheria are the result of the toxin produced by the bacteria.[19] The diphtheria toxin (DT) can travel into the blood stream, where it will damage internal organs such as the heart, lungs and kidneys.[20] The damage caused to the heart is called myocarditis. Myocarditis is an inflammation of the heart tissue, which results in mortality as high as fifty percent if left untreated in patients.[21]
Diphtheria was a widespread infectious disease in the United States in the early 20th century. In 1921 there were 206,000 confirmed cases of diphtheria which resulted in 15,520 deaths.[22] The population of the United States in 1921 was 108,538,000 according to the United States Census Bureau.[23] This means that 0.18% of the U.S. population in 1921 was infected with diphtheria. There was still a strong prevalence of diphtheria in the U.S., even after the introduction of a vaccine in 1923.[24] The vaccine provided an effective means of prevention but treatments for the afflicted remained the same. The strong presence of diphtheria is shown by specialized hospital wards dedicated to diphtheria patients, fifteen years after the vaccine was introduced.[25]
By the mid to late 1920s the effects of the diphtheria toxin on the neuro-musculature and fatty degeneration of the heart were well known, and understood by physicians to be longer lasting than previously thought. Jenner Hoskin, a doctor at the Philadelphia Hospital conducted a study on the effects of diphtheria on the heart in 1926. Hoskin discovered that upon admission to the hospital, 72% of patients had no cardiac complication with the exception of tachycardia, but several days later 28% of patients were found to have abnormal pulses which degenerated into grave heart trouble.[26] While it was not clear what Hoskin defined as “grave heart trouble” the implications were clear; diphtheria had deadly effects on the heart. Hoskin noted that virtually all patients admitted for diphtheria initially had tachycardia that persisted for 36-48 hours after initial treatment was given.[27] The continued presence of tachycardia following the first 36-48 hours was an indication of myocarditis, a result of the diphtheria toxin damaging the heart.[28] Hoskin’s use of persistent tachycardia over the treatment interval was common practice at the time. Hoskin argues for the importance of electrocardiograms in identifying myocarditis secondary to diphtheria and monitoring the patient’s heart even after their hospital stay.[29] Close monitoring of the heart can result in early recognition of cardiac complications and reduce mortality rates. Physicians in the early 20th century recognized that death as a result of diphtheria typically occurred on the 10th day of infection from acute myocarditis, or on the 3rd week from fatty degeneration of the heart muscle.[30] This highlights the importance of having an effective way to monitor the cardiac function of the heart, which the electrocardiogram does effectively.
Prior to the wide spread use of the ECG in monitoring heart function, a physician would assess heart health through auscultation of the heart, palpation of pulses, physical appearance of the patient and subject statements from patient.[31] Auscultation of cardiac sounds using the stethoscope was the preferred method.[32] The physician would listen to cardiac sounds at specific points on the chest to determine the health of the patient’s cardiac valves. The strength of the heart would also be assessed by feeling the pulse, typically at the wrist, to determine the regularity and strength of the heart.[33] The physical appearance of the patient was noted, pallor or a pale appearance was considered a sign of poor perfusion and attributed to cardiac insufficiency.[34] These assessments were subjective and depended on the knowledge of the individual physician to be able to identify these abnormalities.
Even in patients that survived the disease, lasting cardiac abnormalities were found. Cardiac abnormalities such as premature beats, diminished cardiac reserve, heart enlargement and tachycardia were observed. Hoskin stated that the lasting effects of diphtheria on the heart can be seen in the “slurring of the Q.R.S. complex” visible on ECG.[35] The Q.R.S. complex represents the depolarization of the ventricles and the corresponding contraction. Cardiac abnormalities that resulted from the infection would need to be monitored over the patient’s life to ensure detection of worsening cardiac issues. Hoskin stated that it is of the “utmost importance that patients in whom cardiac symptoms and abnormalities have been discovered be thoroughly examined both clinically and electrocardiographically” and that these examinations must continue until it is resolved or reaches a stable condition.[36] The ECG can be utilized to monitor and diagnose diseases that have an impact on the heart but are not cardiac in nature, such as diphtheria. Diphtheria may have no effect on the electrical conduction system of the heart, but it will result in physical changes to the heart tissue which can be seen on the ECG tracing, such as Q.R.S. complex slurring.
The shift in prevalence of the ECG in cardiac monitoring can be seen in a 1938 article by Mason Leete in which he states it is “presumptuous to enter such a field [diphtheria] armed only with fingers, stethoscope and sphygmomanometer.”[37] This displays an attitude shift during the late 1930s in which the subjective information gathered by the physician decreased in importance and the objective information created by medical technology such as the ECG increased in significance. The importance of the ECG in heart health was noted but traditional measures of obtaining pulses, heart sounds and more recently blood pressures were still valued.[38] The combined use of subjective information obtained by the physician and unbiased technologically obtained data, such as from the electrocardiogram and sphygmomanometer, are valued as the most effective way to monitor patient’s disease progress. A careful comparison of clinical and electrocardiographic findings are required to thoroughly assess the patient’s health and provide an accurate prognosis.[39]
In treating diphtheria and monitoring the progress of infected patients, the use of the electrocardiogram became the standard. The importance of the ECG in diphtheria patients is emphasized in Harries’s 1932 article titled “Auxiliary treatment of toxic Diphtheria,” when he states that “obtaining repeat electrocardiograms from the cases under treatment . . . provid[es] the most valuable evidence as to progress.”[40] This statement displays the value placed on ECG’s in diphtheria patients as the most valuable tool to monitor progress, even over the physical observations of the physician. This shift in preference is mirrored in a 1935 article on electrocardiogram in diphtheria in which the author states that “although there is much agreement between electrocardiographic and clinical signs the former usually proceeds the later and change in the curves may demonstrate lesions which cannot be discovered by other means.”[41] This is an important shift from years prior when the ECG was seen as the primary tool for not only monitoring patients but also diagnosing previously unseen or unobservable lesions of infection. The instrument is sensitive enough and its accuracy is trusted to the point that the information displayed by the ECG is more accurate than what the physician can observe. The importance of the ECG was shown in an 1937 article by Norman Begg in which he states that “Survival depends upon the amount and distribution of undamaged or lesser damaged myocardial tissue,” the severity of which could be determined by the ECG.[42] The value of the ECG to monitor the patient’s progress and prognosis was well known by this time period, but the ECG also influenced treatment of diphtheria.
The medicine used to treat diphtheria remained relatively unchanged from 1899 to the late 1930s. Early treatment of diphtheria consisted of the use of antitoxin for the diphtheria bacteria, although the dosages varied significantly based on the preference of the physician providing care.[43] Additionally, the use of mercurial was advocated for, which was mercury in a solution, generally in a topical form placed on to the lesions of infection and oxygen therapy as needed to treat difficulty breathing.[44] There is no mention of using electrocardiograms to monitor cardiac health. This picture changed dramatically in the mid 1920s with the prevalence of the ECG. While many of the medicines used to treat diphtheria remained unchanged, such as the use of antitoxin, the use of digitalis became prevalent to control the tachycardia that resulted from the diphtheria toxin.[45] This led to the prevalence of the ECG as a tool to determine when certain medicines are indicated to treat the patient.
The electrocardiogram was also important in its influence on treatments given to diphtheria patients. The ECG was used to determine the extent of cardiac toxicity from the diphtheria infected patients and excluded the use of certain drugs, that in milder cases of diphtheria would have been indicated. Digitalis is an example of when an ECG would be used to rule out the use of digitalis for that patient due to cardiac damage.[46] The drug digitalis is well known for its effects on decreasing heart rate, increasing strength of contractions, and increasing blood pressure.[47] Digitalis was generally indicated for use to treat tachycardia in moderate to severe diphtheria infections, determined by electrocardiograph, was contraindicated due to its increased cardiac demand.[48] The ECG was used to not only determine abnormal conduction of the heart but also as a clinical tool to determine if a medicine such as digitalis is safe for the patient.
The ECG was widely used in monitoring diphtheria patients and had a strong influence on treatments rendered. The cases of diphtheria rapidly decreased in the late 1940s with the widespread use of the diphtheria vaccine, even though the vaccine was developed in 1923.[49] After the 1940s, the prevalence of diphtheria dropped sharply from approximately 19,000 in 1945 to 1 in 1998.[50] The diphtheria vaccine resulted in the eradication of new cases of the disease in the United States. The treatment for those infected, with the addition antibiotics such as penicillin in the late 1940s, remains the same.[51]
In conclusion, the electrocardiogram had widespread use in the medical field as a tool for assessing cardiac function. The utilization of the electrocardiogram in monitoring cardiac condition had profound impacts on the diagnosis and treatment of diphtheria during the early 20th century. The ECG became the standard for assessing the severity of infected patients, monitoring their progress, determining patients’ prognosis and which medicines could safely be used. The success of the ECG in diphtheria infected patients redefined the ECG as a medical technology for diagnosing infectious diseases as well as cardiac diseases. The ECG is currently used to monitor a wide variety of infectious diseases including HIV, rubella, typhoid, rheumatic fever and diphtheria.[52] The electrocardiogram changed medical practices in diphtheria and is still actively used in infectious disease care today.
Bibliography
Primary Sources:
Andersen. “The electrocardiogram in diphtheria” The Lancet (1935) 689.
Begg, Norman “Diphtheritic Myocarditis, an electrocardiographic study” The Lancet (1937).
Harries, E. “Auxiliary treatment of toxic diphtheria” The Lancet (1932).
“Heart Diagnosis in British Army.” New York Times (1916).
Hoskin, Jenner. “The after effects of diphtheria on the heart.” The Lancet (1926), 1141-1143.
Leete, Mason. “The Heart in Diphtheria.” The Lancet (1938).
McClanahan, H. “Treatment of Diphtheria.” The Lancet (1899).
Simpli-Scribe EKG, Wangensteen historical library collection. University of Minnesota- Twin Cities.
“Sure way to finding out how sick or well you are by measuring electricity in your body” The Washington Post (1914).
Williams, James. “Electrocardiogram in Clinical Medicine.” American Journal of the Medical Sciences (1910) 644-668.
Williamson, Bruce. “The rational use of Digitalis.” The Lancet (1928).
Secondary Sources:
Anatomy of the Heart National Heart, Lung and Blood Institute, National Institute of Health (November 2011), accessed November 22, 2015.
Barold, S.S. “Willem Einthoven and the birth of clinical electrocardiography a hundred years ago.” Cardiac Electrophysiology Review (2003): 99-104.
“Definition of Penicillin History” MedicineNet (2012).
Diphtheria Centers for Disease Control (2013).
“Historical National Population Estimates.” United States Census Bureau (2000), accessed November 22, 2015.
Howell, Joel, D. Technology in the Hospital, Transforming patient care in the early twentieth century (Baltimore: Johns Hopkins University Press, 1995), 9
Nalmas, Sandhya. “ Electrocardiographic Changes in Infectious Diseases” Hospital Physician (2007), 3.
“Simpli-Scribe” Edward Hand Medical Heritage Foundation, accessed November 22, 2015.
Vaccine, Diphtheria Center for Disease Control, accessed November 22, 2015.
Endnotes
[1] “Anatomy of the Heart” National Heart, Lung and Blood Institute National Institute of Health (November 2011) accessed November 22, 2015.
[2] “Anatomy of the Heart” National Heart, Lung and Blood Institute
[3] “Anatomy of the Heart” National Heart, Lung and Blood Institute
[4] “Anatomy of the Heart” National Heart, Lung and Blood Institute
[5] S.S. Barold, “Willem Einthoven and the birth of clinical electrocardiography a hundred years ago.” Cardiac Electrophysiology Review (2003), 99-104.
[6] “Anatomy of the Heart” National Heart, Lung and Blood Institute
[7] “Simpli-Scribe.” Edward Hand Medical Heritage Foundation, accessed November 22, 2015.
[8] “Simpli-Scribe.” Edward Hand Medical Heritage Foundation
[9] Simpli-Scribe EKG, Wangensteen historical library collection. University of Minnesota- Twin Cities.
[10] Simpli-Scribe EKG, Wangensteen historical library collection.
[11] “Simpli-Scribe.” Edward Hand Medical Heritage Foundation
[12] “Simpli-Scribe.” Edward Hand Medical Heritage Foundation
[13] “Sure way to finding out how sick or well you are by measuring electricity in your body” The Washington Post (1914)
[14] James Williams, “Electrocardiogram in Clinical Medicine.” American Journal of the Medical Sciences (1910), 644-668.
[15] “Heart diagnosis in British army.” New York Times (1916), 21.
[16] Barold, “Willem Einthoven”, 99-104.
[17] Diphtheria Centers for Disease Control (2013) accessed November 22, 2015.
[23] “Historical National Population Estimates.” United States Census Bureau (2000), accessed November 22, 2015.
[26] Jenner Hoskin, “The after effects of diphtheria on the heart.” The Lancet (1926), 1141.
[27] Hoskin, “The after effects of diphtheria on the heart.”, 1142.
[28] Hoskin, “The after effects of diphtheria on the heart.”, 1142.
[29] Hoskin, “The after effects of diphtheria on the heart.”, 1142.
[30] Hoskin, “The after effects of diphtheria on the heart.”, 1142.
[31] Mason Leete, “The Heart in Diphtheria.” The Lancet (1938)
[32] Leete, “The Heart in Diphtheria.”
[33] Leete, “The Heart in Diphtheria.”
[34] Leete, “The Heart in Diphtheria.”
[35] Hoskin, “The after effects of diphtheria on the heart.”, 1142.
[36] Hoskin, “The after effects of diphtheria on the heart.”, 1143.
[37] “The Heart in Diphtheria.”
[38] “The Heart in Diphtheria.”
[39] “The Heart in Diphtheria.”
[40] E. Harries, “Auxiliary treatment of toxic diphtheria” The Lancet (1932).
[41] Andersen “The electrocardiogram in diphtheria” The Lancet (1935), 689.
[42]Norman, Begg. “Diphtheritic Myocarditis, an electrocardiographic study” The Lancet (1937).
[43] H. McClanahan, “Treatment of Diphtheria.” The Lancet (1899).
[44] McClanahan, “Treatment of Diphtheria.”
[45] Bruce Williamson, “The rational use of Digitalis.” The Lancet (1928).
[46] Williamson, “The rational use of Digitalis.”
[47] Williamson, “The rational use of Digitalis.”
[48] “The Heart in Diphtheria.”
[49] Vaccines Center for Disease Control, accessed November 22, 2015.
[51] “Definition of Penicillin History” MedicineNet (2012), accessed November 22, 2015.
[52] Sandhya Nalmas, “ Electrocardiographic Changes in Infectious Diseases” Hospital Physician (2007), 3.
Recommended Dose 