کاردیولوژی - دکتر مددی

NANOBIOTIC TREATMENT FOR REVERSING ATHEROSCLEROSIS

ecg — Fri, 15 Feb 2008 11:23:18 GMT

THE PATHOGENESIS OF VASCULAR

CALCIFICATION, NEW CLINICAL

DIAGNOSTIC MARKERS AND A NEW

CURATIVE NANOBIOTIC TREATMENT

FOR REVERSING ATHEROSCLEROSIS

IN HUMANS.

Kajander EO^{1,2,3, Aho KM1, Maniscalco BS3, Mezo}

^{GS3, 1University of Kuopio, Kuopio, 2Nanobac Oy, Kuopio, Finland; 3NanobacLabs Research Institute, Tampa, USA}

Background: Atherosclerosis is an inflammatory disease stimulated by various infectious agents. Our hypothesis is that nanobacteria (Nanobacterium sanguineum, Ns), a new self-replicating infectious calcifying agent found in human blood, which causes life-long infections and adversely affects human cells, is causing atherosclerosis in the human vasculature. Clinical efficacy of a new targeted nanobiotic medication to reverse calcified atherosclerotic plaques and microvascular disease was evaluated in patients with advanced heart disease.

Methods (1) Ns was screened with immunohistochemical staining in human aortic calcific plaques and with prospective epidemiological survey on Ns markers (Ag and Ab) done by Nyyssönen, Kajander, Ciftcioglu and Salonen. (2) Ns lipid, mineral and protein components and biological interactions were analyzed with focus on atherosclerosis. (3) NanobacTX-ACES Clinical Study was undertaken to document the efficacy of the new nanobiotic, NanobacTX, to reverse coronary artery plaque calcification in 90 patients with well-documented coronary artery disease and high levels of coronary artery calcification. 4-month treatment outcome of NanobacTX was followed with EBCT Coronary Artery Calcification Scoring and with Ns markers in blood. Other medications or diet were not changed during the Study.

Results: Immunohistochemical staining detected Ns in 2 out of 4 aortic calcific plaques verifying results from the Mayo Clinic (Rasmunssen et al. JACC 39 Suppl: 206, 2002) and Puskas (Nanobacteria Minisymposium, http://www.nanobac.com/nbminisymp080301/page13.html). The Epidemiological Study found an association between Ns antigen and risk of MI and stroke. Ns biofilm contains Ca2+, unique lipopolysaccaride (LPS) and prothrombin, known active components of inflammatory and clotting processes. The NanobacTX-ACES Nanobiotic Study showed decreases in Coronary Artery Calcification EBCT scores by an average of 58% in Study subjects. Ns antigen and antibody showed a trend to rise at 2 months and to fall after 4 months.

Conclusions: Immunohistochemical staining showed presence of Ns in human aortic calcific plaques. Ns markers in blood have prognostic value for risk of MI and stroke. Ns contains components capable of stimulating immune cascades leading to local tissue/vascular wall inflammation and are risk factors for arterial and venous thrombus formation. Our earlier animal studies have revealed thrombus formation in large veins and arteries after Ns injection. Nanobiotic treatment with NanobacTX was effective in reversing coronary artery calcification. NanobacTX treatment caused initial increase in Ns markers leading to decline with concomitant improvement of atherosclerotic calcification scores in EBCT. Findings of the study open new insights to pathogenesis, diagnostics and treatment of atherosclerosis. Further research is clearly warranted.

In: XXIV Tampereen Lääkäripäivät 20.–22.3.2003 Luennot XXIV. Eds. Anttila S, Antonen J, Hutri-Kähönen N, Lahtela J, Tomas E, Anttila P. Lege Artis Oy, Tampere. Vammalan Kirjapaino Oy, Vammala 2003, p.330.

Kajander EO, Aho KM, Maniscalco BS, Mezo GS. THE PATHOGENESIS OF VASCULAR CALCIFICATION, NEW CLINICAL DIAGNOSTIC MARKERS AND A NEW CURATIVE NANOBIOTIC TREATMENT FOR REVERSING ATHEROSCLEROSIS IN HUMANS. 24th Tampere Medical Symposium, March 20-22, 2003, Tampere, Finland. The Organizing Committee of Tampere Medical Symposium 2003, Abstract Book, page 330 abstract No.2. Publisher Lege Artis Oy, Tampere.

Mayo Clinic Zooms In On Nanobacteria

ecg — Fri, 15 Feb 2008 11:22:18 GMT

Mayo Clinic Zooms In On

Nanobacteria

TAMPA, Fla.—January 4, 2007 – Nanobac Pharmaceuticals, Inc. (OTCBB: NNBP)announces Scientists at Mayo, working under a collaborative agreement with NanobacPharmaceuticals Inc. have published an article in the Journal of Investigative Medicineregarding successfully isolating nanoparticles from human kidney stones in cell cultures.

The Mayo scientists also isolated proteins, RNA and DNA that appear to be associated with the nanoparticles or CNPs.

Entitled "Mayo Clinic Zooms In On Nanobacteria" the paper describes why the Mayo researchers say the findings could lead to solving the mystery of whether nanoparticles are viable living forms that can lead to disease - in this case, kidney stones. "We are looking at how kidney stones start as very small calcifications inside the kidney and then eventually grow into stones," said Mayo Clinic's John Lieske. "In the laboratory, we have isolated nanoparticles from kidney tissue and kidney stones, and have successfully propagated them in culture. This does not clearly confirm the role of nanoparticles in the formation of kidney stones, but it offers insight not otherwise known."

Intriguingly, the study cites evidence that the calcification process is not driven solely byphysical chemistry, but instead is influenced by specific proteins and cellular responses.

"There are at least two novel hypotheses here in terms of how stones might actually form.

One: an infectious agent. If that was the case, that would point us in the direction of using different kinds of treatments specific to an infectious agent.

Two: the idea that cells drive calcification. That would suggest other alternative therapies," added co-researcher Virginia Miller.

Dr. Maniscalco, co-chair of Nanobac, stated “We believed that CNPs play a major role in one of the most pervasive medical conditions in existence: calcification of arteries and organs. This study conducted by one of the lead medical and research facilities in the United States, lends credence to our beliefs.”

About Nanobac Pharmaceuticals: Nanobac Pharmaceuticals Inc. is dedicated to the discovery and development of products and services to improve human health through the detection and treatment of calcifying nanoparticles (CNPs), formerly known as nanobacteria. The company's pioneering research is establishing the pathogenic role of CNPs in soft tissue calcification, particularly in coronary artery, prostate and vascular disease.

Nanobac's drug discovery and development is focused on new and existing compounds that effectively inhibit, destroy or neutralize CNPs. Nanobac manufactures In Vitro Diagnostic (IVD) kits and reagents for detecting calcifying nanoparticles. IVD products include a line of assays, proprietary antibodies and reagents for uniquely recognizing CNPs. Nanobac's BioAnalytical Services works with biopharmaceutical partners to develop and apply methods for avoiding, detecting, and inactivating or eliminating CNPs from raw materials.

Nanobac Pharmaceuticals Inc. is headquartered in Tampa, Florida. For more information, visit our website at: http://www.nanobac.com.

Investors are cautioned that certain statements in this document, some statements in periodic press releases and some oral statements of Nanobac Pharmaceuticals, Inc. officials are "Forward-Looking Statements" within the meaning of the Private Securities Litigation Reform Act of 1995 (the "Act"). Forward-Looking statements include statements which are predictive in nature, which depend upon or refer to future events or conditions, which include words such as "believes," "anticipates," "intends," "plans," "expects," and similar expressions. In addition, any statements concerning future financial performance (including future revenues, earnings or growth rates),

ongoing business strategies or prospects, and possible future Nanobac Pharmaceuticals, Inc. actions, which may be provided by management, are also forward-looking statements as defined by the Act. Forward-Looking statements involve known and unknown risks, uncertainties, and other factors which may cause the actual results, performance or achievements of the Company to materially differ from any future results, performance or achievements expressed or implied by such forward-looking statements and to vary significantly from reporting period to reporting period. Although management believes that the assumptions will, in fact, prove to be correct or that actual future results will not be different from the expectations expressed in this report. These statements are not guarantees of future performance and Nanobac Pharmaceuticals, Inc. has no specific intention to update these statements.

Contact:

Nanobac Pharmaceuticals, Tampa

Brady Millican, 813-264-2241

Redwood Consultants

Jens Dalsgaard, 415-884-0348

Source: Nanobac Pharmaceuticals Inc.

سايت كتابخانه بيماريهاي مادرزادي قلب در بزرگسالان

ecg — Thu, 06 Sep 2007 07:34:58 GMT

www.achd-library.com

سايت خوب در مورد منحني هاي هموديناميك

ecg — Thu, 06 Sep 2007 07:30:41 GMT

www.westodd.com

بعضی سایت های خوب

ecg — Mon, 06 Aug 2007 10:44:47 GMT

سایت مایو http://www.mayo.edu/cardiologyreview/

مقالاتی از وب لاگ http://heartscanblog.blogspot.com

ecg — Mon, 06 Aug 2007 10:26:18 GMT

کلیک کنید

Heart physical Exam

ecg — Mon, 06 Aug 2007 10:10:18 GMT

برای رجوع به سایت مربوطه می توانید در لینک زیر کلیک کنید

http://medicine.osu.edu/exam/*

* Requires the use of Flash Player ver 6.

A brief history of ECG

ecg — Mon, 06 Aug 2007 09:51:18 GMT

A (not so) brief history of electrocardiography.

Find out how electrocuting chickens (1775), getting laboratory assistants to put their hands in buckets of saline (1887), taking the ECG of a horse and following it to the slaughterhouse (1909), induction of indiscriminate angina attacks (1931), and hypothermic dogs (1953) have helped to improve our understanding of the ECG as a clinical tool. And why is the ECG labelled PQRST (1895)?

17th and 18th Centuries

The harnessing of electricity, observations of its effects on animal tissues and the discovery of 'animal electricity'.

1600

William Gilbert

William Gilbert, Physician to Queen Elizabeth I, President of the Royal College of Physicians, and creator of the 'magnetic philosophy' introduces the term 'electrica' for objects (insulators) that hold static electricity. He derived the word from the Greek for amber (electra). It was known from ancient times that amber when rubbed could lift light materials. Gilbert added other examples such as sulphur and was describing what would later be known as 'static electricity' to distinguish it from the more noble magnetic force which he saw as part of a philosophy to destroy forever the prevailing Aristotlean view of matter. Gilbert W. De Magnete, magneticisique corporibus, et de magno magnete tellure. 1600

1646

Sir Thomas Browne, Physician, whilst writing to dispel popular ignorance in many matters, is the first to use the word 'electricity'. Browne calls the attractive force "Electricity, that is, a power to attract strawes or light bodies, and convert the needle freely placed". (He is also the first to use the word 'computer' - referring to people who compute calendars.)Browne, Sir Thomas. Pseudodoxia Epidemica: Or, enquiries Into Very Many Received Tenents, and Commonly Presumed Truths. 1646: Bk II, Ch. 1. London

1660

Otto Von Guericke builds the first static electricity generator.

1662

Descarte's reflex ©BIU

The work of Rene Descartes, French Philosopher, is published (after his death) and explains human movement in terms of the complex mechanical interaction of threads, pores, passages and 'animal spirits'. He had worked on his ideas in the 1630s but had abandoned publication because of the persecution of other radical thinkers such as Galileo. William Harvey had developed similar ideas but they were never published. Descartes R. De Homine (Treatise of Man); 1662: Moyardum & leffen, Leiden.

1664

Jan Swammerdam, a Dutchman, disproves Descartes' mechanistic theory of animal motion by removing the heart of a living frog and showing that it was still able to swim. On removing the brain all movement stopped (which would be in keeping with Descarte's theory) but then, when the frog was dissected and a severed nerve end stimulated with a scalpel the muscles twitched. This proved that movement of a muscle could occur without any connection to the brain and therefore the transmission of 'animal spirits' was not necessary.

Swammerdam's ideas were not widely known and his work was not published until after his death. However, he wrote many letters and his friend, Nicolaus Steno, did attack the Cartesian ideas in a lecture in Paris in 1665. Boerhaave published Swammerdam's 'Book of Nature' in the 1730s which was translated into English in 1758.

1668

electrical stimulation? ©BIU

Swammerdam refines his experiments on muscle contraction and nerve conduction and demonstrated some to notable figures such as the Grand-Duke Cosimo of Tuscany who was visiting Swammerdam's father's house on the Oude Schans in Amsterdam. One experiment suspended the muscle on a brass hook inside a glass tube with a water droplet to detect movement and 'irritated' the nerve with a silver wire. This produced movement of the muscle and it may have been due to the induction of a small electrical charge - although Swammerdam would have been unaware of this.

In the diagram opposite - a) glass tube, b) muscle, c) sliver wire, d) brass wire, e) drop of water, f) investigator's hand.

1729

Stephen Gray, English scientist, distinguishes between conductors and insulators of electricity. He demonstrates the transfer of static electrical charge to a cork ball across 150 metres of wet hemp thread. Later he found that the transfer could be achieved over greater distances by using brass wire.

1745

Leyden Jar

Dutch physicist Pieter van Musschenbroek discovers that a partly filled jar with a nail projecting from a cork in its neck can store an electrical charge. The jar is named the 'Leyden Jar' after the place of its discovery. Ewald Georg von Kliest of Pomerania invented the same device independently.

Using a Leyden jar in 1746, Jean-Antoine Nollet, French physicist and tutor to the Royal family of France sends an electrical current through 180 Royal Guards during a demonstration to King Louis XV.

1769

Edward Bancroft, an American Scientist, suggests that the 'shock' from the Torpedo Fish is electrical rather than mechanical in nature. He showed that the properties of the shock were similar to those from a Leyden jar in that it could be conducted or insulated with appropriate materials. The Torpedo fish and other species were widely known to deliver shocks and were often used in this way for therapeutic reasons. However, electrical theory at the time dictated that electricity would always flow through conductors and diffuse away from areas of high charge to low charge. Since living tissues were known to be conductors it was impossible to imagine how an imbalance of charge could exist within an animal and therefore animals could not use electricity for nerve conduction - or to deliver shocks. Furthermore, 'water and electricity do not mix' so the idea of an 'electric fish' was generally not accepted. Bancroft, E. An essay on the natural history of Guiana, London:T. Becket and P. A. de Hondt, 1769.

1773

John Walsh

John Walsh, fellow of the Royal Society and Member of Parliament, obtains a visible spark from an electric eel Electrophorus electricus. The eel was out of water as it was not possible to produce the spark otherwise. He used thin strips of tin foil and demonstrated his technique to many colleagues and visitors at his house in London. Unfortunately he never published his eel experiment though he did win the Copley medal in 1774 and 1783 for his work. The observations of Walsh, and Bancroft before him, added to the argument that some form of animal electricity existed. Walsh, J. On the electric property of torpedo: in a letter to Ben. Franklin. Phil. Trans. Royal Soc. 1773;63:478-489

1774

The Rev. Mr Sowdon and Mr Hawes, apothecary, report on the surprising effects of electricity in a case report of recovery from sudden death published in the annual report of the newly founded Humane Society now the Royal Humane Society. The Society had developed from 'The Institution for Affording immediate relief to persons apparently dead from drowning'. It was "instituted in the year 1774, to protect the industrious from the fatal consequences of unforseen accidents; the young and inexperienced from being sacrificed to their recreations; and the unhappy victims of desponding melancholy and deliberate suicide; from the miserable consequences of self-destruction."

A Mr Squires, of Wardour Street, Soho lived opposite the house from which a three year old girl, Catherine Sophia Greenhill had fallen from the first storey window on 16th July 1774. After the attending apothecary had declared that nothing could be done for the child Mr Squires, "with the consent of the parents very humanely tried the effects of electricity. At least twenty minutes had elapsed before he could apply the shock, which he gave to various parts of the body without any apparent success; but at length, upon transmitting a few shocks through the thorax, he perceived a small pulsation: soon after the child began to sigh, and to breathe, though with great difficulty. In about ten minutes she vomited: a kind of stupor, occaisioned by the depression of the cranium, remained for some days, but proper means being used, the child was restored to perfect health and spirits in about a week.

"Mr. Squires gave this astonishing case of recovery to the above gentlemen, from no other motive than a desire of promoting the good of mankind; and hopes for the future that no person will be given up for dead, till various means have been used for their recovery."

Since it is clear she sustained a head injury the electricity probably stimulated the child out of deep coma rather than providing cardiac defibrillation (see also 1788, Charles Kite). Annual Report 1774: Humane Society, London. pp 31-32

1775

Abildgaard shows that hens can be made lifeless with electrical impulses and he could restore a pulse with electrical shocks across the chest. "With a shock to the head, the animal was rendered lifeless, and arose with a second shock to the chest; however, after the experiment was repeated rather often, the hen was completely stunned, walked with some difficulty, and did not eat for a day and night; then later it was very well and even laid an egg." Abildgaard, Peter Christian. Tentamina electrica in animalibus. Inst Soc Med Havn. 1775; 2:157-61.

1786

Luigi Galvani

Italian Anatomist Luigi Galvani notes that a dissected frog's leg twitches when touched with a metal scalpel. He had been studying the effects of electricity on animal tissues that summer.

On 20th September 1786 he wrote "I had dissected and prepared a frog in the usual way and while I was attending to something else I laid it on a table on which stood an electrical machine at some distance from its conductor and separated from it by a considerable space. Now when one of the persons present touched accidentally and lightly the inner crural nerves of the frog with the point of a scalpel, all the muscles of the legs seemed to contract again and again as if they were affected by powerful cramps."

He later showed that direct contact with the electrical generator or the ground through an electrical conductor would lead to a muscle contraction. Galvani also used brass hooks that attached to the frog's spinal cord and were suspended from an iron railing in a part of his garden. He noticed that the frogs' legs twitched during lightening storms and also when the weather was fine. He interperated these results in terms of "animal electricity" or the preservation in the animal of "nerveo-electrical fluid" similar to that of an electric eel. He later also showed that electrical stimulation of a frog's heart leads to cardiac muscular contraction. Galvani. De viribus Electritatis in motu musculari Commentarius. 1791

Galvani's name is given to the 'galvanometer' which is an instrument for measuring (and recording) electricity - this is essentially what an ECG is; a sensitive galvanometer.

1788

Charles Kite wins the Silver Medal of the Humane Society (awarded at the first Prize Medal ceremony of the Society co-judged with the Medical Society of London) with an essay on the use of electricity in the diagnosis and resuscitation of persons apparently dead. This essay is often cited as the first record of cardiac defibrillation but the use of electricity suggested by Mr Kite is much different. For example, on describing a case of drowning from 1785 where resuscitation had been attempted with artificial respiration, warmth, tobacco, "volatiles thrown into the stomach, frictions, and various lesser stimuli" for nearly an hour, he then recalls the use of electricity. "Electricity was then applied, and shocks sent through in every possible direction; the muscles through which the fluid [electricity] passed were thrown into strong contractions." He concluded that electricity was a valuable tool that could determine whether or not a person, apparently dead, could be successfully resuscitated. Annual Report 1788: Humane Society, London. pp 225-244. Kite C. An Essay on the Recovery of the Apparently Dead. 1788: C. Dilly, London.

1792

Alessandro Volta

Alessandro Volta, Italian Scientist and inventor, attempts to disprove Galvani's theory of "animal electricity'" by showing that the electrical current is generated by the combination of two dissimilar metals. His assertion was that the electrical current came from the metals and not the animal tissues. (We now know that both Galvani and Volta were right.) To prove his theory he develops the voltaic pile in 1800 (a column of alternating metal discs - zinc with copper or silver - separated by paperboard soaked in saline) which can deliver a substantial and steady current of electricity. Enthusiasm in the use of electricity leads to further attempts at reanimation of the dead with experiments on recently hanged criminals. Giovani Aldini (the nephew of Galvani) conducts an experiment at the Royal College of Surgeons in London in 1803. The executed criminal had lain in a temperature of 30 F for one hour and was transported to the College. "On applying the conductors to the ear and to the rectum, such violent muscular contractions were executed, as almost to give the appearance of the reanimation". Aldini, J. Essai: Théorique et expérimental sur le Galvanisme, Paris (1804), Giovani Aldini. General Views on the Application of Galvanism to Medical Purposes Principally in cases of suspended Animation (London: J. Callow, Princes Street and Burgess and Hill, Great Windmill Street, 1819). Mary Shelly's Frankenstein was published in 1818. Louis Figuier, Les merveilles de la Science (Paris, 1867), p.653

1800 to 1895

The design of sensitive instruments that could detect the small electrical currents in the heart.

1819

While demonstrating to students the heating of a platinum wire with electricity from a voltaic pile at the University of Copenhagen, Danish physicist Hans Christian Oersted notices that a nearby magnetized compass needle moves each time the electrical current is turned on. He discovers electromagnetism which is given a theoretical basis (with remarkable speed) by André Marie Ampère.

1820

Johann (Johan) Schweigger of Nuremberg increases the movement of magnetized needles in electromagnetic fields. He found that by wrapping the electric wire into a coil of 100 turns the effect on the needle was multiplied. He proposed that a magnetic field revolved around a wire carrying a current which was later proven by Michael Faraday. Schweigger had invented the first galvanometer and announced his discovery at the University of Halle on 16th September 1820.

1825

Leopold Nobili, Professor of Physics at Florence, develops an 'astatic galvanometer'. Using two identical magnetic needles of opposite polarity, either fixed together with a figure of eight arrangment of wire loops (in earlier versions), or one moveable needle with a wire loop and one with a scale (in later versions), the effects of the earth's magnetic field could be compensated for. In 1827, using this instrument, he managed to detect the flow of current in the body of a frog from muscles to spinal cord. He detected the electricity running along saline moistened cotton thread joining the dissected frog's legs in one jar to its body in another jar. Nobili was working to support the theory of animal electricity and this conduction, transmitted without wires, he felt demonstrated animal electricity.

1838

Carlo Matteucci

Carlo Matteucci, Professor of Physics at the University of Pisa, and student of Nobili, shows that an electric current accompanies each heart beat. He used a preparation known as a 'rheoscopic frog' in which the cut nerve of a frog's leg was used as the electical sensor and twitching of the muscle was used as the visual sign of electrical activity. He also used Nobili's astatic galvanometer for the study of electricity in muscles typically inserting one galvanometer wire in the open end of the dissected muscle and the other on the surface of the muscle. He went on to try and demonstrate conduction in nerve but was unable to do so (since his galvanometers were not sensitive enough). Matteucci C. Sur un phenomene physiologique produit par les muscles en contraction. Ann Chim Phys 1842;6:339-341

1840

Dr Golding Bird, a Physician, accomplished chemist and member of the London Electrical Society, opens an electrical therapy room at Guy's Hospital, London treating a large range of diseases. Although the application of electricity was popular it was not considered a subject worthy of serious investigation. Because of Bird's reputation as a researcher electrical therapy achieved popularity amongst London Physicians including his mentor Dr Thomas Addison. Bird G. Lectures on Electricity and Galvanism, in their physiological and therapeutical relations, delivered at the Royal College of Physicians, in March, 1847 (Wilson & Ogilvy, London, 1847)

1843

Emil Du bois-Reymond

German physiologist Emil Du bois-Reymond describes an "action potential" accompanying each muscular contraction. He detected the small voltage potential present in resting muscle and noted that this diminished with contraction of the muscle. To accomplish this he had developed one of the most sensitive galvanometers of his time. His device had a wire coil with over 24,000 turns - 5 km of wire. Du Bios Reymond devised a notation for his galvanometer which he called the 'disturbance curve'. "o" was the stable equilibrium point of the astatic galvanometer needle and p, q, r and s (and also k and h) were other points in its deflection. Du Bois-Reymond, E. Untersuchungen uber thierische Elektricitat. Reimer, Berlin: 1848.

1850

Bizarre unregulated actions of the ventricles (later called ventricular fibrillation) is described by Hoffa during experiments with strong electrical currents across the hearts of dogs and cats. He demonstrated that a single electrical pulse can induce fibrillation. Hoffa M, Ludwig C. 1850. Einige neue versuche uber herzbewegung. Zeitschrift Rationelle Medizin, 9: 107-144

1856

Rudolph von Koelliker and Heinrich Muller confirm that an electrical current accompanies each heart beat by applying a galvanometer to the base and apex of an exposed ventricle. They also applied a nerve-muscle preparation, similar to Matteucci's, to the ventricle and observed that a twitch of the muscle occured just prior to ventricular systole and also a much smaller twitch after systole. These twitches would later be recognised as caused by the electrical currents of the QRS and T waves. von Koelliker A, Muller H. Nachweis der negativen Schwankung des Muskelstroms am naturlich sich kontrahierenden Herzen. Verhandlungen der Physikalisch-Medizinischen Gesellschaft in Wurzberg. 1856;6:528-33.

1858

William thompson (Lord Kelvin), Professor of Natural Philosophy at Glasgow University, invents the 'mirror galvanometer' for the reception of transatlantic telegraph transmissions. A small, freely rotating mirror, with magents stuck to its back is suspended in a fine copper coil and a reflected spot of light from this mirror 'amplifies' the small movements when electrical current is present. The whole apparatus was suspended in an air chamber and the pressure inside could be adjusted to vary the damping seen on the signals. This galvanometer was sensitive enough for transatlantic telegraphy.

1867

Thompson improves telegraph transmissions with the 'Siphon Recorder'. Before d'Arsonval (1880), Thompson uses a fine coil suspended in a strong magnetic magnetic field. Attached to the coil but isolated from it by ebonite (an insulator) was a siphon of ink. The siphon was charged with high voltage so that the ink was sprayed onto the paper that moved over an earthed metal surface. The siphon recorder could therefore not only detect currents it could also record them onto paper.

1869-70

Alexander Muirhead, an electrical engineer and pioneer of telegraphy, may have a recorded a human electrocardiogram at St Bartholomew's Hospital, London but this is disputed. If he had he is thought to have used a Thompson Siphon Recorder. Elizabeth Muirhead, his wife, wrote a book of his life and claimed that he refrained from publishing his own work for fear of misleading others. Elizabeth Muirhead. Alexander Muirhead 1848 - 1920. Oxford, Blackwell: privately printed 1926.

1872

French physicist Gabriel Lippmann invents a capillary electrometer. It is a thin glass tube with a column of mercury beneath sulphuric acid. The mercury meniscus moves with varying electrical potential and is observed through a microscope.

1872

Mr Green, a surgeon, publishes a paper on the resuscitation of a series of patients who had suffered cardiac and / or respiratory arrest during anaesthesia with chloroform. He uses a galvanic pile (battery) of 200 cells generating 300 Volts which he applied to the patient as follows "One pole should be applied to the neck and the other to the lower rib on the left side." Green T. On death from chloroform: its prevention by galvanism. Br Med J 1872 1: 551-3. Although this has been reported as an example of cardiorespiratory resuscitation it is unclear what the exact mechanism seems to be. It is unlikely to be electric cardioversion or external pacing. It seems to be another example of electrophrenic stimulation (See also Duchenne 1872).

1872

An 'electric' smile.

Guillaume Benjamin Amand Duchenne de Boulogne, pioneering neurophysiologist, describes the resuscitation of a drowned girl with electricity in the third edition of his textbook on the medical uses of electricity. This episode has sometimes been described as the first 'artificial pacemaker' but he used an electrical current to induce electrophrenic rather than myocardial stimulation. Duchenne GB. De l'electrisation localisee et de son application a la pathologie et la therapeutique par courants induits at par courants galvaniques interrompus et continus. [Localised electricity and its application to pathology and therapy by means of induced and galvanic currents, interrupted and continuous] 3ed. Paris. JB Bailliere et fils; 1872

1875

Richard Caton, a Liverpool Physician, presents to the British Medical Association in July 1875 in Edinburgh. Using a Thompson 'mirror galvanometer' in animals he shows it was possible to detect 'feeble currents of varying direction ... when the electrodes are placed on two points of the external surface, or one electrode on the grey matter and one on the surface of the skull'. This is the first report of the EEG (or electroencephalogram). Caton was proving another Physician's hypothesis, John Hughlings Jackson, who suggested in 1873 that epilepsy was due to excessive electrical activity in the grey matter of the brain. Caton R: The electric currents of the brain. BMJ 1875; 2:278, Mumenthaler, Mattle Eds. Neurology. 4th Edition. Stuttgart, Thieme: 2004.

1876

Marey uses the electrometer to record the electrical activity of an exposed frog's heart. Marey EJ. Des variations electriques des muscles et du couer en particulier etudies au moyen de l'electrometre de M Lippman. Compres Rendus Hebdomadaires des Seances de l'Acadamie des sciences 1876;82:975-977

1878

British physiologists John Burden Sanderson and Frederick Page record the heart's electrical current with a capillary electrometer and shows it consists of two phases (later called QRS and T). Burdon Sanderson J. Experimental results relating to the rhythmical and excitatory motions of the ventricle of the frog. Proc R Soc Lond 1878;27:410-414

1880

French physicist Arsène d'Arsonval in association with Marcel Deprez, improves the galvanometer. Instead of a magnetized needle moving when electrical current flows through a surrounding wire coil the Deprez-d'Arsonval galvanometer has a fixed magnet and moveable coil. If a pointer is attached to the coil it can move over a suitably calibrated scale. The d'Arsonval galvanometer is the basis for most modern galvanometers. Comptes rendus de l'Académie des sciences, 1882, 94: 1347-1350

1884

John Burden Sanderson and Frederick Page publish some of their recordings. Burdon Sanderson J, Page FJM. On the electrical phenomena of the excitatory process in the heart of the tortoise, as investigated photographically. J Physiol (London) 1884;4:327-338

1887

British physiologist Augustus D. Waller of St Mary's Medical School, London publishes the first human electrocardiogram. It is recorded with a capilliary electrometer from Thomas Goswell, a technician in the laboratory. Waller AD. A demonstration on man of electromotive changes accompanying the heart's beat. J Physiol (London) 1887;8:229-234

1889

Dutch physiologist Willem Einthoven sees Waller demonstrate his technique at the First International Congress of Physiologists in Bale. Waller often demonstrated by using his dog "Jimmy" who would patiently stand with paws in glass jars of saline.

1890

GJ Burch of Oxford devises an arithmetical correction for the observed (sluggish) fluctuations of the electrometer. This allows the true waveform to be seen but only after tedious calculations. Burch GJ. On a method of determining the value of rapid variations of a difference potential by means of a capillary electrometer. Proc R Soc Lond (Biol) 1890;48:89-93

1891

British physiologists William Bayliss and Edward Starling of University College London improve the capillary electrometer. They connect the terminals to the right hand and to the skin over the apex beat and show a "triphasic variation accompanying (or rather preceding) each beat of the heart". These deflections are later called P, QRS and T. Bayliss WM, Starling EH. On the electrical variations of the heart in man. Proc Phys Soc (14th November) in J Physiol (London) 1891;13:lviii-lix and also On the electromotive phenomena of the mammalian heart. Proc R Soc Lond 1892;50:211-214 They also demonstrate a delay of about 0.13 seconds between atrial stimulation and ventricular depolarisation (later called PR interval). On the electromotive phenomena of the mammalian heart. Proc Phys Soc (21st March) in J Physiol (London) 1891;12:xx-xxi

1893

Willem Einthoven introduces the term 'electrocardiogram' at a meeting of the Dutch Medical Association. (Later he claims that Waller was first to use the term). Einthoven W: Nieuwe methoden voor clinisch onderzoek [New methods for clinical investigation]. Ned T Geneesk 29 II: 263-286, 1893

1895 to date

The first accurate recording of the electrocardiogram and its development as a clinical tool.

1895

Einthoven, using an improved electrometer and a correction formula developed independently of Burch, distinguishes five deflections which he names P, Q, R, S and T. Einthoven W. Ueber die Form des menschlichen Electrocardiogramms. Arch f d Ges Physiol 1895;60:101-123

Why PQRST and not ABCDE? The four deflections prior to the correction formula were labelled ABCD and the 5 derived deflections were labelled PQRST. The choice of P is a mathematical convention (as used also by Du Bois-Reymond in his galvanometer's 'disturbance curve' 50 years previously) by using letters from the second half of the alphabet. N has other meanings in mathematics and O is used for the origin of the Cartesian coordinates. In fact Einthoven used O ..... X to mark the timeline on his diagrams. P is simply the next letter. A lot of work had been undertaken to reveal the true electrical waveform of the ECG by eliminating the damping effect of the moving parts in the amplifiers and using correction formulae. If you look at the diagram in Einthoven's 1895 paper you will see how close it is to the string galvanometer recordings and the electrocardiograms we see today. The image of the PQRST diagram may have been striking enough to have been adopted by the researchers as a true representation of the underlying form. It would have then been logical to continue the same naming convention when the more advanced string galvanometer started creating electrocardiograms a few years later.

1897

Clement Ader, a French electrical engineer, reports his amplification system for detecting Morse code signals transmitted along undersea telegraph lines. It was never intended to be used as a galvanometer. Einthoven later quoted Ader's work but seems to have developed his own amplification device independently. Ader C. Sur un nouvel appareil enregistreur pour cables sous-marins. C R Acad Sci (Paris) 1897;124:1440-1442

1899

Karel Wenkebach

Karel Frederik Wenckebach publishes a paper "On the analysis of irregular pulses" describing impairment of AV conduction leading to progressive lengthening and blockage of AV conduction in frogs. This will later be called Wenckebach block (Mobitz type I) or Wenckebach phenomenon.

1899

Jean-Louis Prevost, Professor of Biochemistry, and Frederic Batelli, Professor of Physiology, both of Geneva discover that large electrical voltages applied across an animal's heart can stop ventricular fibrillation. Prevost JL, Batelli F: Sur quelques effets des descharges electriques sur le coeur des mammiferes. Acad. Sci. Paris, FR.: 1899; 129:1267-1268.

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1901

Einthoven invents a new galvanometer for producing electrocardiograms using a fine quartz string coated in silver based on ideas by Deprez and d'Arsonval (who used a wire coil). His "string galvanometer" weighs 600 pounds. Einthoven acknowledged the similar system by Ader but later (1909) calculated that his galvanometer was in fact many thousands of times more sensitive. Einthoven W. Un nouveau galvanometre. Arch Neerl Sc Ex Nat 1901;6:625-633

1902

Einthoven publishes the first electrocardiogram recorded on a string galvanometer. Einthoven W. Galvanometrische registratie van het menschilijk electrocardiogram. In: Herinneringsbundel Professor S. S. Rosenstein. Leiden: Eduard Ijdo, 1902:101-107

1903

Einthoven discusses commercial production of a string galvanometer with Max Edelmann of Munich and Horace Darwin of Cambridge Scientific Instruments Company of London.

1905

Einthoven starts transmitting electrocardiograms from the hospital to his laboratory 1.5 km away via telephone cables. On March 22nd the first 'telecardiogram' is recorded from a healthy and vigorous man and the tall R waves are attributed to his cycling from laboratory to hospital for the recording.

1905

John Hay of Liverpool, publishes pressure recordings from a 65 year old man showing heart block in which AV conduction did not seem to be impaired since the a-c intervals on the jugular venous waves was unchanged in the conducted beats. This is the first demonstration of what we now call Mobitz type II AV block. Hay J. Bradycardia and cardiac arrhythmias produced by depression of certain functions of the heart. Lancet 1906;1:138-143.

1906

Einthoven publishes the first organised presentation of normal and abnormal electrocardiograms recorded with a string galvanometer. Left and right ventricular hypertrophy, left and right atrial hypertrophy, the U wave (for the first time), notching of the QRS, ventricular premature beats, ventricular bigeminy, atrial flutter and complete heart block are all described. Einthoven W. Le telecardiogramme. Arch Int de Physiol 1906;4:132-164 (translated into English. Am Heart J 1957;53:602-615)

1906

Cremer records the first oesophageal electrocardiogram which he achieved with the help of a professional sword swallower. Oesophageal electrocardiography later developed in the 1970s to help differentiate atrial arrhythmias. He also records the first fetal electrocardiogram from the abdominal surface of a pregnant woman. Cremer. Ueber die direkte Ableitung der Aktionstrِme des menslichen Herzens vom Oesophagus und über das Elektrokardiogramm des Fِtus. Munch. Med. Wochenschr. 1906;53:811

1907

Arthur Cushny, professor of pharmacology at University College London, publishes the first case report of atrial fibrillation. His patient was 3 days post-op following surgery on an "ovarian fibroid" when she developed a "very irregular" pulse at a rate of 120 - 160 bpm. Her pulse was recorded with a "Jacques sphygmochronograph" which shows the radial pulse pressure against time - much like the arterial line blood pressure recordings used in Intensive Care today. Cushny AR, Edmunds CW. Paroxysmal irregularity of the heart and auricular fibrillation. Am J Med Sci 1907;133:66-77.

1908

Edward Schafer of the University of Edinburgh is the first to buy a string galvanometer for clinical use.

1909

Thomas Lewis of University College Hospital, London buys a string galvanometer and so does Alfred Cohn of Mt Sinae Hospital, New York. Thomas Lewis publishes a paper in the BMJ detailing his careful clinical and electrocardiographic observations of atrial fibrillation. At one point Lewis identified a fibrillating horse using the string galvanometer's electrocardigram recording. He then followed the horse to the slaughterhouse where he could visually confirm the fibrillating atrium. Lewis T. Auricular fibrillation: a common clinical condition. BMJ 1909;42:1528.

1909

Nicolai and Simmons report on the changes to the electrocardiogram during angina pectoris. Nicolai DF, Simons A. (1909) Zur klinik des elektrokardiogramms. Med Kiln 5;160

1910

Walter James, Columbia University and Horatio Williams, Cornell University Medical College, New York publish the first American review of electrocardiography. It describes ventricular hypertrophy, atrial and ventricular ectopics, atrial fibrillation and ventricular fibrillation. The recordings were sent from the wards to the electrocardiogram room by a system of cables. There is a great picture of a patient having an electrocardiogram recorded with the caption "The electrodes in use".James WB, Williams HB. The electrocardiogram in clinical medicine. Am J Med Sci 1910;140:408-421, 644-669

1911

Thomas Lewis publishes a classic textbook. The mechanism of the heart beat. London: Shaw & Sons and dedicates it to Willem Einthoven.

1912

Einthoven addresses the Chelsea Clinical Society in London and describes an equilateral triangle formed by his standard leads I, II and III later called 'Einthoven's triangle'. This is the first reference in an English article I have seen to the abbreviation 'EKG'.Einthoven W. The different forms of the human electrocardiogram and their signification. Lancet 1912(1):853-861

1918

Bousfield describes the spontaneous changes in the electrocardiogram during angina. Bousfield G. Angina pectoris: changes in electrocardiogram during paroxysm. Lancet 1918;2:475

1920

Hubert Mann of the Cardiographic Laboratory, Mount Sinai Hospital, describes the derivation of a 'monocardiogram' later to be called 'vectorcardiogram'. Mann H. A method of analyzing the electrocardiogram. Arch Int Med 1920;25:283-294

1920

Harold Pardee, New York, publishes the first electrocardiogram of an acute myocardial infarction in a human and describes the T wave as being tall and "starts from a point well up on the descent of the R wave". Pardee HEB. An electrocardiographic sign of coronary artery obstruction. Arch Int Med 1920;26:244-257

1924

Willem Einthoven wins the Nobel prize for inventing the electrocardiograph.

1924

Woldemar Mobitz publishes his classification of heart blocks (Mobitz type I and type II) based on the electrocardiogram and jugular venous pulse waveform findings in patients with second degree heart block. Mobitz W. Uber die unvollstandige Storung der Erregungsuberleitung zwischen Vorhof und Kammer des menschlichen Herzens. (Concerning partial block of conduction between the atria and ventricles of the human heart). Z Ges Exp Med 1924;41:180-237.

1926

A doctor from the Crown Street Women's Hospital in Sydney, who wished to remain anonymous, resuscitates a new-born baby with an electrical device later called a 'pacemaker'. The doctor wanted to remain anoymous because of the controversy surrounding research that artificially extended human life.

1928

Ernstine and Levine report the use of vacuum-tubes to amplify the electrocardiogram instead of the mechanical amplification of the string galvanometer. Ernstine AC, Levine SA. A comparison of records taken with the Einthoven string galvanomter and the amplifier-type electrocardiograph. Am Heart J 1928;4:725-731

1928

Frank Sanborn's company (founded 1917 and acquired by Hewlett-Packard in 1961 and since 1999, Philips Medical Systems) converts their table model electrocardiogram machine into their first portable version weighing 50 pounds and powered by a 6-volt automobile battery.

1929

Sydney doctor Mark Lidwill, physician, and Edgar Booth, physicist, report the electrical resuscitation of the heart to a meeting in Sydney. Their portable device uses an electrode on the skin and a transthoracic catheter. Edgar Booth's design could deliver a variable voltage and rate and was employed to deliver 16 volts to the ventricles of a stillborn infant.

1930

Wolff, Parkinson and White report an electrocardiographic syndrome of short PR interval, wide QRS and paroxysmal tachycardias. Wolff L, Parkinson J, White PD. Bundle branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J 1930;5:685. Later, when other published case reports were examined for evidence of pre-excitation, examples of 'Wolff Parkinson White' syndrome were identified which had not been recognised as a clinical entity at the time. The earliest example was published by Hoffmann in 1909. Von Knorre GH. The earliest published electrocardiogram showing ventricular preexcitation. Pacing Clin Electrophysiol. 2005 Mar;28(3):228-30

1930

Sanders first describes infarction of the right ventricle. Sanders, A.O. Coronary thrombosis with complete heart block and relative ventricular tachycardia: a case report, American Heart Journal 1930;6:820-823.

1931

Charles Wolferth and Francis Wood describe the use of exercise to provoke attacks of angina pectoris. They investigated the ECG changes in normal subjects and those with angina but dismissed the technique as too dangerous "to induce anginal attacks indiscriminately". Wood FC, Wolferth CC, Livezey MM. Angina pectoris. Archives Internal Medicine 1931;47:339

1931

first patented pacemaker

Dr Albert Hyman patents the first 'artificial cardiac pacemaker' which stimulates the heart by using a transthoracic needle. His aim was to produce a device that was small enough to fit in a doctor's bag and stimulate the right atrial area of the heart with a suitably insulated needle. His experiments were on animals. His original machine was powered by a crankshaft (it was later prototyped by a German company but was never successful). "By March 1, 1932 the artificial pacemaker had been used about 43 times, with a successful outcome in 14 cases." It was not until 1942 that a report of its successful short term use in Stokes-Adams attacks was presented. Hyman AS. Resuscitation of the stopped heart by intracardial therapy. Arch Intern Med. 1932;50:283

1932

Goldhammer and Scherf propose the use of the electrocardiogram after moderate exercise as an aid to the diagnosis of coronary insufficiency. Goldhammer S, Scherf D. Elektrokardiographische untersuchungen bei kranken mit angina pectoris. Z Klin Med 1932;122:134

1932

Charles Wolferth and Francis Wood describe the clinical use of chest leads. Wolferth CC, Wood FC. The electrocardiographic diagnosis of coronary occlusion by the use of chest leads. Am J Med Sci 1932;183:30-35

1934

By joining the wires from the right arm, left arm and left foot with 5000 Ohm resistors Frank Wilson defines an 'indifferent electrode' later called the 'Wilson Central Terminal'. The combined lead acts as an earth and is attached to the negative terminal of the ECG. An electrode attached to the positive terminal then becomes 'unipolar' and can be placed anywhere on the body. Wilson defines the unipolar limb leads VR, VL and VF where 'V' stands for voltage (the voltage seen at the site of the unipolar electrode). Wilson NF, Johnston FE, Macleod AG, Barker PS. Electrocardiograms that represent the potential variations of a single electrode. Am Heart J. 1934;9:447-458.

1935

McGinn and White describe the changes to the electrocardiogram during acute pulmonary embolism including the S1 Q3 T3 pattern. McGinn S, White PD. Acute cor pulmonale resulting from pulmonary embolism: its clinical recognition. JAMA 1935;114:1473.

1938

American Heart Association and the Cardiac Society of Great Britain define the standard positions, and wiring, of the chest leads V1 - V6. The 'V' stands for voltage. Barnes AR, Pardee HEB, White PD. et al. Standardization of precordial leads. Am Heart J 1938;15:235-239

1938

Tomaszewski notes changes to the electrocardiogram in a man who died of hypothermia. Tomaszewski W. Changements electrocardiographiques observes chez un homme mort de froid. Arch Mal Coeur 1938;31:525.

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1939

Langendorf reports a case of atrial infarction discovered at autopsy which, in retrospect, could have been diagnosed by changes on the ECG. Langendorf R. Elektrokardiogramm bei Vorhof-Infarkt. Acta Med Scand. 1939;100:136.

1942

Emanuel Goldberger increases the voltage of Wilson's unipolar leads by 50% and creates the augmented limb leads aVR, aVL and aVF. When added to Einthoven's three limb leads and the six chest leads we arrive at the 12-lead electrocardiogram that is used today.

1942

Arthur Master, standardises the two step exercise test (now known as the Master two-step) for cardiac function. Master AM, Friedman R, Dack S. The electrocardiogram after standard exercise as a functional test of the heart. Am Heart J. 1942;24:777

1944

Young and Koenig report deviation of the P-R segment in a series of patients with atrial infarction. Young EW, Koenig BS. Auricular infarction. Am Heart J. 1944;28:287.

1947

Gouaux and Ashman describe an observation that helps differentiate aberrant conduction from ventricular tachycardia. The 'Ashman phenomenon' occurs when a stimulus falls during the relative or absolute refractory period of the ventricles and the aberrancy is more pronounced. In atrial fibrillation with aberrant conduction this is demonstrated when the broader complexes are seen terminating a relatively short cycle that follows a relatively long one. The QRS terminating the shorter cycle is conducted 'more aberrantly' because it falls in the refractory period. The aberrancy is usually of a RBBB pattern. Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34:366-73.

1947

Claude Beck, a pioneering cardiovascular surgeon in Cleveland, successfully defibrillates a human heart during cardiac surgery. The patient is a 14 year old boy - 6 other patients had failed to respond to the defibrillator. His prototype defibrillator followed experiments on defibrillation in animals performed by Carl J. Wiggers, Professor of Physiology at the Western Reserve University. Beck CS, Pritchard WH, Feil SA: Ventricular fibrillation of long duration abolished by electric shock. JAMA 1947; 135: 985-989.
Wiggers CJ, Wegria R. Ventricular fibrillation due to single localized induction in condenser shock supplied during the vulnerable phase of ventricular systole. Am J Physiol 1939;128:500

1948

Rune Elmqvist, Swedish engineer who had trained as a doctor but never practiced, introduces the first ink jet printer for the transcription of analog physiological signals. He demonstrates its use in the recording of ECGs at the First International Congress of Cardiology in Paris in 1950. The machine (the mingograph) was developed by him at the company that later became Siemens. (Luderitz, 2002)

1949

modern 'Holter' Monitor

Montana physician Norman Jeff Holter develops a 75 pound backpack that can record the ECG of the wearer and transmit the signal. His system, the Holter Monitor, is later greatly reduced in size, combined with tape / digital recording and used to record ambulatory ECGs. Holter NJ, Generelli JA. Remote recording of physiologic data by radio. Rocky Mountain Med J. 1949;747-751.

1949

Sokolow and Lyon propose diagnostic criteria for left ventricular hypertrophy i.e. LVH is present if the sum of the size of the S wave in V1 plus the R wave in V6 exceeds 35 mm. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J 1949;37:161

1950

John Hopps, a Canadian electrical engineer and researcher for the National Research Council, together with two physicians (Wilfred Bigelow, MD of the University of Toronto and his trainee, John C. Callaghan, MD) show that a coordinated heart muscle contraction can be stimulated by an electrical impulse delivered to the sino-atrial node. The apparatus, the first cardiac pacemaker, measures 30cm, runs on vacuum tubes and is powered by household 60Hz electrical current. Bigelow WG, Callaghan JC, Hopps JA. "General hypothermia for experimental intracardiac surgery." Ann Surg 1950; 1132: 531-539.

1953

Osborn, whilst experimenting with hypothermic dogs, describes the prominent J (junctional) wave which has often been known as the "Osborn wave". He found the dogs were more likely to survive if they had an infusion of bicarbonate and supposed the J wave was due to an injury current caused by acidosis. Osborn JJ. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175:389.

1955

Richard Langendorf publishes the "rule of bigeminy" whereby ventricular bigeminy tends to perpetuate itself. Langendorf R, Pick A, Winternitz M. Mechanisms of intermittent ventricular bigeminy. I. Appearence of ectopic beats dependent upon the length of the ventricular cycle, the "rule of bigeminy." circulation 1955;11:442.

1956

Paul Zoll, a cardiologist, uses a more powerful defibrillator and performs closed-chest defibrillation in a human. Zoll PM, Linenthal AJ, Gibson P: Termination of Ventricular Fibrillation in Man by Externally Applied Countershock . NEJM 1956; 254: 727-729

1957

long QT syndrome

Anton Jervell and Fred Lange-Nielsen of Oslo describe an autosomal recessive syndrome of long-QT interval, deafness and sudden death later known as the Jervell-Lange-Nielsen syndrome. Jervell A, Lange-Nielsen F. Congenital deaf mutism, functional heart disease with prolongation of the QT interval and sudden death. Am Heart J 1957;54:59.

1958

Professor Ake Senning, of Sweden, places the first implantable cardiac pacemaker designed by Rune Elmqvist into a 43-year-old patient with complete heart block and syncope (Arne Larsson).

1959

Myron Prinzmetal describes a variant form of angina in which the ST segment is elevated rather than depressed. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris. I. A variant form of angina pectoris. Am J Med 1959;27:374.

1960

Smirk and Palmer highlight the risk of sudden death from ventricular fibrillation particularly when ventricular premature beats occur at the same time as the T wave. The 'R on T' phenomenon. Smirk FH, Palmer DG. A myocardial syndrome, with particular reference to the occurrence of sudden death and of premature systoles interrupting antecedent T waves. Am J Cardiol 1960;6:620.

1963

Italian paediatrician C. Romano and Irish paediatrician O. Conor Ward (the following year) independently report an autosomal dominant syndrome of long-QT interval later known as the Romano-Ward syndrome. Romano C, Gemme G, Pongiglione R. Aritmie cardiache rare dell'eta pediatrica. Clin Pediatr. 1963;45:656-83.
Ward OC. New familial cardiac syndrome in children. J Irish Med Assoc. 1964;54:103-6

1963

Excercise ECG

Robert Bruce and colleages describe their multistage treadmill exercise test later known as the Bruce Protocol. "You would never buy a used car without taking it out for a drive and seeing how the engine performed while it was running," Bruce says, "and the same is true for evaluating the function of the heart." Bruce RA, Blackman JR, Jones JW, Srait G. Exercise testing in adult normal subjects and cardiac patients. Pediatrics 1963;32:742
Bruce RA, McDonough JR. Stress testing in screening for cardiovascular disease. Bull. N.Y. Acad Med. 1969;45:1288

1963

Baule and McFee are the first to detect the magnetocardiogram which is the electromagnetic field produced by the electrical activity of the heart. It is a method that can detect the ECG without the use of skin electrodes. Although potentially a useful technique it has never gained clinical acceptance, partly because of its greater expense. Baule GM, McFee R. Detection of the magnetic field of the heart. Am Heart J. 1963;66:95-96.

1966

Mason and Likar modify the 12-lead ECG system for use during exercise testing. The right arm electrode is placed at a point in the infraclavicular fossa medial to the border of the deltoid muscle, 2 cm below the lower border of the clavicle. The left arm electrode is placed similarly on the left side. The left leg electrode is placed at the left iliac crest. Although this system reduces the variability in the ECG recording during exercise it is not exactly equivalent to the standard lead positions. The Mason-Likar lead system tends to distort the ECG with a rightward QRS axis shift, a reduction in R wave amplitude in lead I and aVL, and a significant increase in R wave amplitude in leads II, III and aVF. Eur Heart J. 1987 Jul;8(7):725-33

1966

Torsade de pointes

François Dessertenne of Paris publishes the first case of 'Torsade de pointes' Ventricular Tachycardia. Dessertenne F. La tachycardie ventriculaire a deux foyers opposes variables. Arch des Mal du Coeur 1966; 59:263

1968

Journal of Electrocardiography, the Official Journal of the International Society for Computerized Electrocardiology and the International Society of Electrocardiology, is founded by Zao and Lepeschkin.

1968

Henry Marriott introduces the Modified Chest Lead 1 (MCL1) for monitoring patients in Coronary Care.

1969

Rosenbaum reviews the classification of ventricular premature beats and adds a benign form that arises from the right ventricle and is not associated with heart disease. This becomes known as the 'Rosenbaum ventricular extrasystole'. Rosenbaum MB. Classification of ventricular extrasystoles according to form. J Electrocardiol 1969;2:289.

1974

Jay Cohn, of University of Minnesota Medical School, describes the 'syndrome of right ventricular dysfunction in the setting of acute inferior wall myocardial infarction'. Cohn JN, Guiha NH, Broder MI. Right ventricular infarction. Am J Cardiol 1974:33:209-214

1974

Gozensky and Thorne introduce the term 'Rabbit ears' to electrocardiography. Rabbit ears describe the appearence of the QRS complex in lead V1 with an rSR' pattern (good rabbit) being typical of Right Bundle Branch Block and an RSr' (bad rabbit) suggesting a ventricular origin i.e. ventricular ectopy / tachycardia. Gozensky C, Thorne D. Rabbit ears: an aid in distinguishing ventricular ectopy from aberration. Heart Lung 1974;3:634.

1976

Erhardt and colleagues describe the use of a right-sided precordial lead in the diagnosis of right ventricular infarction which had previously been thought to be electrocardiographically silent. Erhardt LR, Sjogrn A, Wahlberg I. Single right-sided precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction. Am Heart J 1976;91:571-6

1988

Professor John Pope Boineau of Washington University School of Medicine publishes a 30-year percpective on the modern history of electrocardiography. Boineau JP. Electrocardiology: A 30-year Perspective. Ah Serendipity, My Fulsome Friend. Journal of Electrocardiology 21. Suppl (1988): S1-9

1992

Brugada syndrome

Pedro Brugada and Josep brugada of Barcelona publish a series of 8 cases of sudden death, Right Bundle Branch Block pattern and ST elevation in V1 - V3 in apparently healthy individuals. This 'Brugada Syndrome' may account for 4-12% of unexpected sudden deaths and is the commonest cause of sudden cardiac death in individuals aged under 50 years in South Asia. The technology of the electrocardiogam, which is over 100 years old, can still be used to discover new clinical entities in cardiology. Brugada P, Brugada J. Right Bundle Branch Block, Persistent ST Segment Elevation and Sudden Cardiac Death: A Distinct Clinical and Electrocardiographic Syndrome. J Am Coll Cardiol 1992;20:1391-6

1992

Cohen and He describe a new non-invasive approach to accurately map cardiac electrical activity by using the surface Laplacian map of the body surface electrical potentials. He B, Cohen RJ. Body surface Laplacian ECG mapping. IEEE Trans Biomed Eng 1992;39(11):1179-91

1993

Mac 5000, 15-lead ECG

Robert Zalenski, Professor of Emergency Medicine, Wayne State University Detroit, and colleagues publish an influential article on the clinical use of the 15-lead ECG which routinely uses V4R, V8 and V9 in the diagnosis of acute coronary syndromes. Like the addition of the 6 standardised unipolar chest leads in 1938 these additional leads increase the sensitivity of the electrocardiogram in detecting myocardial infarction. Zalenski RJ, Cook D, Rydman R. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 1993;22:786-793

1999

Researchers from Texas show that 12-lead ECGs transmitted via wireless technology to hand-held computers is feasible and can be interpreted reliably by cardiologists. Pettis KS, Savona MR, Leibrandt PN et al. Evaluation of the efficacy of hand-held computer screens for cardiologists' interpretations of 12-lead electrocardiograms. Am Heart J. 1999 Oct;138(4 Pt 1):765-70

2000

Physicians from the Mayo Clinic describe a new hereditary form of Short QT syndrome associated with syncope and sudden death that they discovered in 1999. Several genes have since been implicated. Gussak I, Brugada P, Brugada J, et al. Idiopathic short QT interval: a new clinical syndrome? Cardiology. 2000;94(2):99-102

2005

Danish cardiologists report the successful reduction in the time between onset of chest pain and primary angioplasty when the ECG of patients is transmitted wirelessly from ambulance to the cardiologist's handheld PDA (Personal Digital Assistant). The clinician can make an immediate decision to redirect patients to the catheter lab saving time in transfers between hospital departments. Clemmensen P, Sejersten M, Sillesen M et al. Diversion of ST-elevation myocardial infarction patients for primary angioplasty based on wireless prehospital 12-lead electrocardiographic transmission directly to the cardiologist's handheld computer: a progress report. J Electrocardiol. 2005 Oct;38(4 Suppl):194-8

Sources

Acierno. The History of Cardiology. 1994. New York: Parthenon.
The Bakken Library and Museum
Bibliotheque Inter-Universitaire de Medicine, Paris. Source of the images of 'Descarte's reflex' from De Hominis and Swammerdam's possible electrical stimulation of a nerve-muscle preparation.
Burchell HB. A centennial note on Waller and the first human electrocardiogram. Am J Cardiol 1987;59:979-983
Burnett J. The origins of the electrocardiograph as a clinical instrument. Medical History Supplement 5: 1985, 53-76. Published as a monograph. The emergence of modern cardiology. Bynum WF, Lawrence C, Nutton V, eds. Wellcome Institute for the History of Medicine:1985.
Cobb, Matthew. Exorcizing the animal spirits: Jan Swammerdam on nerve function. Nature Reviews, Neuroscience 2002;3:395-400
On Animal electricity: Being an Abstract of the Discoveries of Emil Du Bios-Reymond (translated). Edited by Dr Bence Jones. 1852. Churchill: London.
Fye WB. A history of the origin, evolution, and impact of electrocardiography. Am J Cardiol 1994;73:937-949
Geddes LA. Supplement. The Physiologist 1984;27(1):S-1
Hewlett-Packard - 'History and Mission'
google.com, altavista.com, excite.com
Berndt Luderitz. History of the Disorders of Cardiac Rhythm. Third Edition. 2002. Blackwell Publishing.
Jaakko Malmivuo & Robert Plonsey: Bioelectromagnetism - Principles and Applications of Bioelectric and Biomagnetic Fields, Oxford University Press, New York, 1995
Nobel Institute. Presentation speech by Professor JE Johansson. The Nobel Prize in Physiology or Medicine 1924.
North American Society of Pacing and Electrophysiology.
Pumphrey S. Latitude and the Magnetic Earth. Icon books, Cambridge: 2002. (see also the William Gilbert website)
Royal Humane Society, Annual Reports. Brettenham House, Lancaster Place, London, WC2 7EP.
Schamroth L. The 12 Lead Electrocardiogram. Blackwell Scientific Publications, Oxford: 1989.
Snellen HA. Willem Einthoven (1860-1927) Father of electrocardiography. Kluwer Academic Publishers, Dordrecht: 1995. with thanks to Kees Swenne
Titomir LI. The remote past and near future of electrocardiography: Viewpoint of a biomedical engineer. Bratisl Lek Listy 2000;101(5):272-279.

ECG Arshive

ecg — Mon, 06 Aug 2007 09:45:18 GMT

The normal electrocardiogram.

Exam of the Heart

ecg — Mon, 06 Aug 2007 09:28:18 GMT

Exam of the Heart

The major elements of the cardiac exam include observation, palpation and, most importantly, auscultation (percussion is omitted). As with all other areas of the physical exam, establishing adequate exposure and a quiet environment are critical. Initially, the patient should rest supine with the upper body elevated 30 to 45 degrees. Most exam tables have an adjustable top. If not, use 2 or 3 pillows. Remember that although assessment of pulse and blood pressure are discussed in the vital signs section they are actually important elements of the cardiac exam.

Observation: Assessment for distention of the right Internal Jugular vein (IJ) is a difficult skill. Its importance lies in the fact that the IJ is in straight-line communication with the right atrium. The IJ can therefore function as a manometer, with distention indicating elevation of Central Venous Pressure (CVP). This in turn is an important marker of intravascular volume status and related cardiac function. The focus here is on simply determining whether or not Jugular Venous Distention (JVD) is present. A discussion of the a, c and v waves that make up the jugular venous pulsations can be found elsewhere. These are quite difficult to detect for even the most seasoned physician.

Why is JVD so hard to assess? The IJ lies deep to skin and soft tissues, which can provide quite a bit of cover. Additionally, this blood vessel is under much lower pressure then the adjacent, pulsating carotid artery. It therefore takes a sharp eye to identify the relatively weak, transmitted venous impulses. A few things to remember:

Think anatomically. The right IJ runs between the two heads (sternal and clavicular) of the sternocleidomastoid muscle (SCM) and up in front of the ear. This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement. The two heads form the sides of a small triangle, with the clavicle making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks. Note, you are trying to identify impulses originating from the IJ and transmitted to the overlying skin in this area. You can't actually see the IJ. The External Jugular (EJ) runs in an oblique direction across the sternocleidomastoid and, in contrast to the IJ, can usually be directly visualized. If the EJ is not readily apparent, have the patient look to the left and valsalva. This usually makes it quite obvious. EJ distention is not always a reliable indicator of elevated CVP as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when CVP is normal. It also makes several turns prior to connecting with the central venous system and is thus not in a direct line with the right atrium.
Take your time. Look at the area in question for several minutes while the patient's head is turned to the left. The carotid artery is adjacent to the IJ, lying just medial to it. If you are unsure whether a pulsation is caused by the carotid or the IJ, place your hand on the patient's radial artery and use this as a reference. The carotid impulse coincides with the palpated radial artery pulsation and is characterized by a single upstroke timed with systole. The venous impulse (at least when the patient is in sinus rhythm and there is no tricuspid regurgitation) has three components, each associated with the aforementioned a, c and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin. In contrast, the carotid causes a single up and down pulsation. Furthermore, the carotid is palpable. The IJ is not and can, in fact, be obliterated by applying pressure in the area where it emerges above the clavicle.
Search along the entire projected course of the IJ as the top of the pressure wave (which is the point that you are trying to identify) may be higher then where you are looking. In fact, if the patient's CVP is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else their will be no identifiable "top" of the column as the entire IJ will be engorged). After you've found the top of the wave, see what effect sitting straight up and lying down flat have on the height of the column. Sitting should cause it to appear at a lower point in the neck, while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
Shine a pen light tangentially across the neck. This sometimes helps to accentuate the pulsations.
If you are still uncertain, apply gentle pressure to the right upper quadrant of the abdomen for 5 to 10 seconds. This elicits Hepato-Jugular Reflux which, in pathologic states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the IJ, making the transmitted pulsations more apparent. Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
Once you identify JVD, try to estimate how high in cm the top of the column is above the Angle of Louis. The angle is the site of the joint which connects the manubrium with the rest of the sternum. First identify the supra-sternal notch, a concavity at the top of the manubrium. Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch. This is roughly at the level of the 2nd intercostal space. The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the right atrium with the patient lying at a 45 degree angle. The sum is an estimate of the CVP. However, if you can simply determine with some accuracy whether JVD is present or not, you will be way ahead of he game! Normal is 7-9 cm.

Bony Structures of the Chest

Finding the Angle of Louis:The wooden Q-tips highlight the different slopes of the sternum and manubrium. The point at which the
Q-tips cross is the Angle of Louis.

Determining the CVP

Video of patient with markedly elevated central venous pressure.

Video simulation and discussion of central venous pressure.

Take some time to look across the left chest and try to identify the transmitted impulse caused by ventricular contraction, which may be apparent when contractions are particularly vigorous.

Palpation: The palm of your right hand is placed across the patient's left chest so that it covers the area over the heart. The heel should rest along the sternal border with the extended fingers lying below the left nipple. Focus on several things:

Palpation of the Precordium to Determine the Location of the PMI

Can you feel a Point of Maximum Impulse (PMI) related to contraction at the apex of the underlying left ventricle? If so, where is it located? After identifying the rough position with the palm of your hand, try to pin down the precise location with the tip of your index finger. The normal sized and functioning ventricle will generate a penny sized impulse that is best felt in the mid-clavicular line, roughly at the 5th intercostal space. If the ventricle becomes dilated, most commonly as the result of past infarcts and always associated with ventricular dysfunction, the PMI is displaced laterally. In cases of significant enlargement, the PMI will be located near the axilla. Occasionally, the PMI will not localize to any one area, which does not necessarily indicate ventricular enlargement or dysfunction. Obesity and COPD may also limit your ability to identify its precise location. Palpating while the patient is in the left lateral decubitus position can make the PMI more obvious.
What is the duration of the impulse? In the setting of hypertension or any other state of chronic pressure overload, the ventricle hypertrophies and the PMI becomes sustained (i.e. you feel the impulse for a longer period of time). This is actually pretty subjective and can be tough to detect. Note that hypertrophy and dilatation are not synonymous. They can exist separately or in conjunction with one another.
How vigorous is the transmitted impulse? Processes associated with ventricular hypercontractility (e.g. compensated mitral regurgitation or aortic insufficiency that result in exceptionally large stroke volumes) generate an impulse of unusual vigor.
Do you feel a thrill, a vibratory sensation produced by turbulent blood flow that is usually secondary to valvular abnormalities? The feeling is similar to that produced when you squeeze on a garden hose, partially obstructing the flow of water. The location of the thrill will depend on the involved valve (e.g. thrills caused by aortic stenosis are best felt toward the right upper sternal border). If a loud murmur is detected during auscultation, you may then go back and reassess for the presence of a thrill. In general, thrills are an uncommon finding.

*Palpation of the precordium of a female patient is best done by placing the palm of your right hand directly beneath the patient's left breast such that the edge of your index finger rests against the inferior surface of the breast. Make sure that you tell that patient what you are about to do (and why) before actually performing this maneuver. Remember that with age tissue turgor often declines, causing the breasts to hang below the level of the heart.
Carotid Artery Palpation: This is of greatest value during the assessment of aortic valvular and out flow tract disease (see below) and should thus be performed after auscultation so that you know whether or not these problems exist prior to palpation. However, for the sake of completeness it will be described here. The carotids can be located by sliding the second and third finger of either hand along the side of the trachea at the level of the thyroid cartilage (i.e. adams apple). The carotid pulsation is palpable just lateral to the groove formed by the trachea and the surrounding soft tissue. The quantity of subcutaneous fat will dictate how firmly you need to push. The pulsations should be easily palpable. Diminution may be caused by atherosclerosis, aortic stenosis, or severely impaired ventricular performance. Do not push on both sides simultaneously as this may compromise cerebral blood flow.

Auscultation: The following anatomic pictures will aid you in understanding the principles of cardiac auscultation.

Become comfortable with your stethescope. There are multiple brands on the market, each of which incorporates its own version of a bell (low pitched sounds) and diaphragm (higher pitched sounds). Some have the diaphragm and bell on opposite sides of the head piece. Others have the bell and diaprhragm built into a single side, with the bell engaged by applying light pressure and the diaphragm engaged by pushing more firmly. Adult, pediatric, and newborn sizes also exist. And some combine adult and pediatric scopes into a single unit. Take the time to read the instructions for your particular model so that you are familiar with how to use it correctly. Several sample stethescopes are pictured below. It's worth mentioning that almost any commercially available scope will do the job. The most important "part" is what sits betwen the ear pieces!

Adult Stethoscope

Adult Stethoscope: Diaphragm and Bell
Incorporated Into Single Side.

Combination Adult & Pediatric Stethoscope

Newborn Stethoscope
Engage the diaphragm of your stethescope and place it firmly over the 2nd right intercostal space, the region of the aortic valve. Then move it to the other side of the sternum and listen in the 2nd left intercostal space, the location of the pulmonic valve. Move down along the sternum and listen over the left 4th intercostal space, the region of the tricuspid valve. And finally, position the diaphragm over the 4th intercostal space, left midclavicular line to examine the mitral area. These locations are rough approximations and are generally determined by visual estimation. In each area, listen specifically for S1 and then S2. S1 will be loudest over the left 4th intercostal space (mitral/tricuspid valve areas) and S2 along the 2nd R and L intercostal spaces (aortic/pulomonic valve regions). Note that the time between S1 and S2 is shorter then that between S2 and S1. This should help you to decide which sound is produced by the closure of the mitral/tricuspid and which by the aortic/pulmonic valves and therefore when systole and diastole occur. Compare the relative intensities of S1 and S2 in these different areas.

Auscultation of the Heart
In younger patients, you should also be able to detect physiologic splitting of S2. That is, S2 is made up of 2 components, aortic (A2) and pulmonic (P2) valve closure. On inspiration, venous return to the heart is augmented and pulmonic valve closure is delayed, allowing you to hear first A2 and then P2. On expiration, the two sounds occur closer together and are detected as a single S2. Ask the patient to take a deep breath and hold it, giving you a bit more time to identify this phenomenon. The two components of S1 (mitral and tricuspid valve closure) occur so close together that splitting is not appreciated.
You may find it helpful to tap out S1 and S2 with your fingers as you listen, accentuating the location of systole and diastole and lending a visual component to this exercise. While most clinicians begin asucultation in the aortic area and then move across the precordium, it may actually make more sense to begin laterally (i.e. in the mitral area) and then progress towards the right and up as this follows the direction of blood flow. Try both ways and see which feels more comfortable.

Univeristy of Utah, Review of Cardiac Physiology
Listen for extra heart sounds (a.k.a. gallops). While present in normal subjects up to the ages of 20-30, they represent pathology in older patients. An S3 is most commonly associated with left ventricular failure and is caused by blood from the left atrium slamming into an already overfilled ventricle during early diastolic filling. The S4 is a sound created by blood trying to enter a stiff, non-compliant left ventricle during atrial contraction. It's most frequently associated with left ventricular hypertrophy that is the result of long standing hypertension. Either sound can be detected by gently laying the bell of the stethoscope over the apex of the left ventricle (roughly at the 4th intercostal space, mid-clavicular line) and listening for low pitched "extra sounds" that either follow S2 (i.e. an S3) or precede S1 (i.e. an S4). These sounds are quite soft, so it may take a while before you're able to detect them. Positioning the patient on their left side while you listen may improve the yield of this exam. The presence of both an S3 and S4 simultaneously is referred to as a summation gallop.

Listening for Extra Heart Sounds
Murmurs: These are sounds that occur during systole or diastole as a result of turbulent blood flow. Traditionally, students are taught that auscultation is performed over the 4 areas of the precordium that roughly correspond to the "location" of the 4 valves of the heart (i.e. aortic valve area ='s the 2nd Right Intercostal Space, pulmonic valve area ='s the 2nd LICS, tricuspid valve area ='s 4th LICS, and mitral valve area ='s 4th LICS in the midclavicular line). This leads to some misperceptions. Valves are not strictly located in these areas nor are the sounds created by valvular pathology restricted to those spaces. So, while it might be OK to listen in only 4 places when conducting the normal exam, it is actually quite helpful to listen in many more when any abnormal sounds are detected. If you hear a murmur, ask yourself:
1. Does it occur during systole or diastole?
2. What is the quality of the sound (i.e. does it get louder and then softer; does it maintain the same intensity throughout; does it start loud and become soft)? It sometimes helps to draw a pictoral representation of the sound.
3. What is the quantity of the sound? The rating system for murmurs is as follows:
  - 1/6… Can only be heard with careful listening
  - 2/6… Readily audible as soon as the stethescope is applied to the chest
  - 3/6… Louder then 2/6
  - 4/6… As loud as 3/6 but accompanied by a thrill
  - 5/6… Audible even when only the edge of the stethescope touches the chest
  - 6/6… Audible to the naked ear
    Most murmurs are between 1/6 and 3/6. Louder generally (but not always) indicates greater pathology.
4. What is the relationship of the murmur to S1 and S2 (i.e. when does it start and stop)?
5. What happens when you march your stethescope from the 2nd RICS (the aortic area) out towards the axilla (the mitral area)? Where is it loudest and in what directions does it radiate? By moving in small increments (i.e. listening in 8 or 10 places along the chest wall) you will be more likely to detect changes in the character of a particular murmur and thus have a better chance of determining which valve is affected and by what type of lesion.

Auscultation over the carotid arteries (see under aortic stenosis for additional information): In the absence of murmurs suggestive of aortic valvular disease, you can listen for carotid bruits (sounds created by turbulent flow within the blood vessel) at this point in the exam. Place the diaphragm gently over each carotid and listen for a soft, high pitched "shshing" sound. It's helpful if the patient can hold their breath as you listen so that you are not distracted by transmitted tracheal sounds. The meaning of a bruit remains somewhat controversial. I was taught that bruits represented turbulent flow associated with intrinsic atherosclerotic disease… and that the disappearance of a bruit which was previously present was a sign that the lesion was progressing (i.e. further encroachment on the lumen of the vessel). However, a number of studies provide evidence that atherosclerotic disease is frequently absent when a bruit is present as well as the reverse situation. This is actually of clinical importance because recent data suggest that it may be beneficial to surgically repair carotid disease in patients who have significant stenosis yet have not experienced any symptoms (e.g. Transient ischemic attacks or strokes. Surgery in these settings has already proven to be beneficial). Thus, it is becoming increasingly important to determine the best way of identifying asymptomatic carotid artery disease... and carotid auscultation may, in fact, not be the mechanism of choice!

	The Auscultation Assistant is an excellent heart sound simulation site developed at UCLA. Press the "Back" button to return to this page.
	Blaufuss Multimedia Heart Sounds Tutorial. Press the "Back" button to return to this page.
	This University of Washington site also provides a variety of simulated heart sounds. Press the "Back" button to return to this page.
	In addition, there is an excellent heart sound tutorial CD ROM called, The Physiological Origins of Heart Sounds and Murmurs available at the OLR.

Identifying the Most Common Murmurs:

1. Systolic Murmurs: In the adult population, these generally represent either aortic stenosis or mitral regurgitation. To distinguish between them, remember the following:

Murmurs of Aortic Stenosis (AS):

Tend to be loudest along the upper sternal borders and get softer as you move down and out towards the axilla. There is, however, a phenomenon referred to at the Gallavardin Effect which can cause murmurs of AS to sound as loud towards the axilla as they do over the aortic region. When this occurs, the shape of the sound should be similar in both regions, helping you to distinguish it from MR (see below).
Have a growling, harsh quality (i.e. get louder and then softer.. also referred to as a crescendo decrescendo, systolic ejection, or diamond shaped murmur). When the stenosis becomes more severe, the point at which the murmur is loudest (i.e. its peak intensity) occurs later in systole, as it takes longer to generate the higher ventricular pressure required to push blood through the tight orifice.
Are better heard when the patient sits up and exhales.
Are heard in the carotid arteries and over the right clavicle. Radiation to the clavicle can be appreciated by simply resting the diaphragm on the right clavicle. To assess for transmission to the carotids, have the patient hold their breath while you listen over each artery using the diaphragm of your stethescope. Carotid bruits can be confused with the radiating murmur of aortic stenosis. In general, carotid bruits are softer. Also, murmurs associated with aortic pathology should be audible in both carotids and get louder as you move down the vessel, towards the chest. In settings where carotid pathology coexists with aortic stenosis, a loud transmitted murmur associated with a valvular lesion may overwhelm any sound caused by intrinsic carotid disease, masking it completely.
Carotid upstrokes refer to the quantity and timing of blood flow into the carotids from the left ventricle. They can be affected by aortic stenosis and must be assessed whenever you hear a murmur that could be consistent with AS. This is done by placing your fingers on the carotid artery as described above while you simultaneously listen over the chest. There should be no delay between the onset of the murmur, which marks the beginning of systole, and when you feel the pulsation in the carotid. In the setting of critical (i.e. very severe) aortic stenosis, small amounts of blood will be ejected into the carotid and there will be a lag between when you hear the murmur and feel the impulse. This is referred to as diminished and delayed upstrokes (a.k.a. parvus et tardus), as opposed to the full and prompt inflow which occurs in the absence of disease. Mild or moderate stenosis does not alter the character of carotid in-flow.
Sub-Aortic stenosis is a relatively rare condition where the obstruction of flow from the left ventricle into the aorta is caused by an in-growth of septal tissue in the region below the aortic valve known as the aortic outflow tract. It causes a crescendo-decrescendo murmur that sounds just like aortic stenosis. As opposed to AS, however, the murmur is louder along the left lower sternal border and out towards the apex. This makes anatomic sense as the obstruction is located near this region. It also does not radiate loudly to the carotids as the point of obstruction is further from these vessels in comparison with the aortic valve. You may also be able to palpate a bisferiens pulse in the carotid artery (see under aortic insufficiency). Furthermore, the murmur will get softer if the ventricle is filled with more blood as filling pushes the abnormal septum away from the opposite wall, decreasing the amount of obstruction. Conversely, it gets louder if filling is decreased. This phenomenon can actually be detected on physical exam and is a useful way of distinguishing between AS and sub-aortic obstruction. Ask the patient to valsalva while you listen. This decreases venous return and makes the murmur louder (and will have the opposite effect on a murmur of AS). Then, again while listening, squat down with the patient. This maneuver increases venous return, causing the murmur to become softer. Standing will cause the opposite to occur. You need to listen for 20 seconds or so after each change in position to really appreciate any difference. Because the degree of obstruction can vary with ventricular filling, sub-aortic stenosis is referred to as a dynamic outflow tract obstruction. In aortic stenosis, the degree of obstruction that exists at any given point in time is fixed.

Murmurs of Mitral Regurgitation (MR):

Sound the same throughout systole.
Generally do not have the harsh quality associated with aortic stenosis. In fact, they sound a bit like the "shshing" noise produced when you pucker your lips and blow through clenched teeth.
Get louder as you move your stethescope towards the axilla.
Will get even louder if you roll the patient onto their left side while keeping your stethescope over the mitral area of the chest wall and listening as they move. This maneuver brings the chamber receiving the regurgitant volume, the left atrium, closer to your stethescope, accentuating the murmur.
Get louder if afterload is suddenly increased, which can be accomplished by having the patient close their hands tightly. MR is also affected by the volume of blood returning to the heart. Squatting increases venous return, causing a louder sound. Standing decreases venous return, thereby diminishing the intensity of the murmur.

Sometimes murmurs of aortic stenosis and mitral regurgitation co-exist, which can be difficult to sort out on exam. Moving your stethescope back and forth between the mitral and aortic areas will allow for direct comparison, which may help you decide if more then one type of lesion is present or if the quality of the murmur is the same in both locations, changing only in intensity (i.e. consistent with a one valve problem).

2. Diastolic Murmurs: Tend to be softer and therefore much more difficult to hear then those occurring during systole. This makes physiologic sense as diastolic murmurs are not generated by high pressure ventricular contractions. In adults they may represent either aortic regurgitation or mitral stenosis, neither of which is too common. While systolic murmurs are often obvious, you will probably not be able to detect diastolic murmurs on your own until you have had them pointed out by a more experienced examiner.

Aortic Regurgitation (AR); a.k.a. Aortic Insufficiency (AI):

Is best heard along the left para-sternal border, as this is the direction of the regurgitant flow.
Becomes softer towards the end of diastole (a.k.a. decrescendo).
Can be accentuated by having the patient sit up, lean forward and exhale while you listen.
Occasionally accompanies aortic stenosis, so listen carefully for regurgitation in patients with AS.
Will cause the carotid upstrokes to feel extraordinarily full as significant regurgitation increases ventricular pre-load, resulting in ejection of an augmented stroke volume. AI can also produce a double peaked pulsation in the carotids known as a bisferiens pulse, which is quite difficult to appreciate. Feeling your own carotid impulse at the same time that you're palpating the patient's may accentuate this finding. In cases of co-existent AS and AI, a bisferiens pulse suggests that the AI is the dominant problem. It may also be present with sub-aortic stenosis (see above), helping to distinguish it from AS.

Mitral Stenosis (MS):

Heard best towards the axilla
Can be accentuated by having the patient role onto their left side while you listen with the bell of your sthethescope.
Associated with a soft, low pitched sound preceding the murmur, called the opening snap. This is the noise caused by the calcified valve "snapping" open. It can, however, be pretty hard to detect.

Auscultation, an ordered approach:
Try to focus on each sound individually and in a systematic fashion. Ask yourself: Do I hear S1? Do I hear S2? What is their relative intensities in each of the major valvular areas? Is S2 split physiologically? Are there extra sounds before S1or after S2 (i.e. an S4 or S3)? Is there a murmur during systole? Is there a murmur during diastole? If a murmur is present, how loud is it? What is its character? Where does it radiate? Are there any maneuvers which affect its intensity? Remember that these sounds are created by mechanical events in the heart. As you listen, remind yourself what is happening to produce each of them. By linking auscultatory findings with physiology, you can build a case in your mind for a particular lesion.

Interrelationship of Cardiac Events & Sounds

This diagram courtesy of Dr. Wilbur Lew, Department of Medicine, San Diego VA Medical Center.

A few final comments about auscultation:

Pulmonic valve murmurs are rare in the adult population and, even when present, are difficult to hear due to the relatively low pressures generated by the right side of the heart.
Tricuspid regurgitation (TR) is relatively common, most frequently associated with elevated left sided pressures which are then transmitted to the right side of the heart (though a number of other processes can cause TR as well). In this setting, both mitral and tricuspid regurgitation often co-exist. The murmur of MR is generally louder then that of TR, again due to the higher pressures on the left side of the heart. It can therefore be difficult to sort out if there is co-existent TR when MR is present. Try to listen along both the low left and right sternal borders (areas where the tricuspid valve is best assessed) and compare this to the mitral area. Move your stethoscope slowly across the precordium and note if there is any change in the character/intensity of the murmur. TR murmurs are also accentuated by inhalation, which increases venous return and therefore flow across the valve.
Patients with COPD (emphysema) often have very soft heart sounds. Air trapping and subsequent lung hyperinflation results in a posterior-inferior rotation of the heart away from the chest wall and causes the interposition of lung between the chest wall and heart. In this setting, heart sounds can be accentuated by having the patient lean forward and fully exhale prior to listening. Furthermore, in any patient with particularly "noisy" breath sounds, it may be helpful to ask them to hold their breath (if they're able) while you examine the heart.
Rubs: These are uncommon sounds produced when the parietal and visceral pericardium become inflamed, generating a creaky-scratchy noise as they rub together. The classic rub is actually made up of three sounds, associated with atrial contraction, ventricular contraction, and ventricular filling. In reality, its rare to hear all 3 components (more commonly, 2 are apparent). They can be accentuated by listening when the patient sits up, leans forward and exhales, bringing the two layers in closer communication. I feel compelled to mention this finding only because a common short hand for reporting the results of the cardiac exam comments on the absence of "Gallops, murmurs, or rubs," implying (incorrectly) that rubs are a frequent finding.
If a patient has an abnormal heart sound due to a structural defect that has been quantified by echocardiography, make sure that you compare your findings to those identified during the study. This is a great way of learning!
Don't get frustrated! Auscultation is a difficult skill to "master" and we are all continually refining our techniques. Take your time. Make sure the room is quiet. Be patient. Ask for help frequently. Read about particular murmurs and their pathophysiology when you encounter them. A number of the more subtle findings (e.g. an S3 or S4) can be very difficult to identify when the patient is tachycardic, a not uncommon scenario as this is one of the compensatory mechanisms for dealing with the dysfunction that has generated these findings in the first place. Re-examination after the patient has made clinical improvement may be more revealing.

In general, many of the above techniques are not used when examining every patient. If the exam is normal, it would be neither efficient nor revealing to put a patient through all of these maneuvers. The goal is to have a "bag of skills" at your disposal that you can reach into and employ to better define abnormalities when they present themselves.

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Heart physical Exam

A brief history of ECG

A (not so) brief history of electrocardiography.

Sources

ECG Arshive

ischaemic heart disease

hypertrophy patterns

atrioventricular (AV) block

bundle branch block

supraventricular rhythms

ventricular rhythms

pacemakers

Wolff Parkinson White syndrome

miscellaneous

other

Exam of the Heart

Exam of the Heart