Partial Heart Block Research Articles

An extraordinary degree of partial heart-block: Report of a case in which the P-R interval exceeded the R-R interval

A case of extreme degree of partial heart-block is reported on which observations were made over a period of seven years. The P-R interval on one occasion reached 0.80 second, actually exceeding the R-R interval.

Gallop rhythm: Bramwell, Crighton: Quart. J. Med. 4: 149, 1935

An extreme tachycardia, thought at first to be paroxysmal auricular tachyeardia, persisted for four weeks and led to advanced congestive cardiac failure in an otherwise healthy man forty years of age. After the usual methods of interrupting an attack of paroxysmal tachycardia had failed, an attempt was made to terminate the rapid heart action by exposing the vagus nerves in the neck and stimulating them electrically. There was, however, no demonstrable effect upon the heart. Subsequently, partial heart-block, due to digitalis, resulted in slowing of the ventricles and was followed by improvement. Eventually, the auricles gradually slowed, the heart-block disappeared, the cardiac response to vagal activity returned, and the patient recovered. This course of events strongly suggests that the tachycardia was in reality an extreme sinus tachycardia due to failure of vagus inhibition.

Unusual sinus tachycardia with observations on vagal activity: Direct electrical stimulation of the vagus nerves in man

An extreme tachycardia, thought at first to be paroxysmal auricular tachyeardia, persisted for four weeks and led to advanced congestive cardiac failure in an otherwise healthy man forty years of age. After the usual methods of interrupting an attack of paroxysmal tachycardia had failed, an attempt was made to terminate the rapid heart action by exposing the vagus nerves in the neck and stimulating them electrically. There was, however, no demonstrable effect upon the heart. Subsequently, partial heart-block, due to digitalis, resulted in slowing of the ventricles and was followed by improvement. Eventually, the auricles gradually slowed, the heart-block disappeared, the cardiac response to vagal activity returned, and the patient recovered. This course of events strongly suggests that the tachycardia was in reality an extreme sinus tachycardia due to failure of vagus inhibition.

Partial bundle-branch block: A theoretical consideration of transient normal intraventricular conduction in the presence of apparently complete bundlebranch block

1. 1. Eight cases of partial bundle-branch block of varying degrees are presented with abstracts of their clinical histories, complete physical and laboratory data and electrocardiographic studies. 2. 2. Three unusual cases of transient Type II, intraventricular or bundle-branch block are recorded with sudden transition from complete bundle-branch block to normal intraventricular conduction times in response to respiratory maneuvers. The possible mechanical or nervous factors concerned in the production of the changes are considered to be anoxemia as well as fatigue. Vagus effect may be contributory. 3. 3. We have stressed especially the importance of the recognition of this transient type of disturbance because of its better prognostic outlook. When present it must be relieved by therapeutic rest before necessary surgical or intravenous procedures are to be undertaken. 4. 4. The increased risk assumed in submitting patients, in the presence of bundle-branch block, to a procedure that may apparently only slightly effect the blood pressure and the heart is emphasized. 5. 5. The theories of partial heart-block with special reference to and the intraventricular counterparts of the accepted Types I and II of auriculoventricular types are discussed at some length. 6. 6. The theoretical reasons for the danger of precipitating fatal ventricular fibrillation in the presence of bundle-branch block are given.

Myxedema Heart With Report of One Case

Article1 January 1931Myxedema Heart With Report of One CaseJAY C. DAVIS, M.D.JAY C. DAVIS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-7-733 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMyxedema heart is now a recognized clinical entity. In the last few years cases have been reported from various parts of the world. I have been able to collect 21 authentic cases from the literature with teleröntgenograms and electrocardiograms revealing the condition of the heart before and after thyroid therapy.The slides shown here are from a previously unreported case now on the medical service at the Minneapolis General Hospital. I am greatly indebted to Dr. G. Fahr, Chief of the Medical Service, for the privilege of reporting this case. The patient is a female, 48 years of age, with...1 ZONDEK : Műchen, Med. Wchnschr., 65: 1180, 1918. Google Scholar2 FAHR G: Myxedema Heart. M. A. M. A., 84:345, 1925. CrossrefGoogle Scholar3 FAHR G: Myxedema Heart. Am. Heart J., 3:14, 1927. CrossrefGoogle Scholar4 HOLZMAN JE: Myxedema Heart. Am. Heart J., 4:351, 1929. CrossrefGoogle Scholar5 ZISKEN T: Angina Pectoris Associated with Myxedema Heart. U. S. V. Bureau Med. Bull., 6:24, 1930. Google Scholar6 HERRICK : Combination of Angina Pectoris with Severe Anemia. Amer. Heart J., Vol. 351, 1927. Google Scholar7 BARRON M: Personal Communication. Google Scholar8 DUDEN C: Myxedema with Cardiac Decompensation and Hypertension Which Disappeared under Thyroid Medication. J. Missouri M. A., 26:25-27, January 29th. Google Scholar9 FAHR G MUELLER FPersonal communication to from , Munich, Germany. Google Scholar10 FELIX K: The Effect of Thyroxin and Thyroid Extracts on the Isolated Frog Heart. Proc. of Staff Meetings of the Mayo Clinic, 4:285, 1929. Google Scholar11 CHRISTIAN H: Myocardial Disturbances Due to Abnormal Thyroid Function and Their Management. Penn. Med. Jour., 32:70, 1928. Google Scholar12 STURGISWHITING CW: The Treatment and Prognosis in Myxedema. J. A. M. A., 85:2013, 1925. CrossrefGoogle Scholar13 STURGIS C: Angina Pectoris as a Complication in Myxedema and Exophthalmic Goiter. Boston M. S. J., 195:351, 1926. CrossrefGoogle Scholar14 MEANSWHITEKRANTZ JPC: Observations on the Heart in Myxedema. Boston M. S. J., 195:455, 1926. CrossrefGoogle Scholar15 LUTEN D: Myxedema with Partial Heart Block, and Severe Anemia, Both of Which Disappeared Under Thyroid Therapy. J. Missouri M. A., 26:73-77, February, 1920. Google Scholar16 AMORGOS A: Clinical Aspects of Myxedematous Cardiac Insufficiency. An. de Foi de med., Montevedio, 13:339-437, May-June, 1928. Google Scholar17 DOXIADES LB: Importance of Cardiovascular Examination in Mongolism and Myxedema. Klin. Wchnsehr., 6:1326, July 9, 1927. CrossrefGoogle Scholar18 MACKENZIE GM: Anemia in Hypothyroidism. J. A. M. A., 86:462, 1926. CrossrefGoogle Scholar19 STONE CT: The Occurrence of Anemia in Myxedema. Ann. Int. Med., 2:215, 1928. LinkGoogle Scholar20 GOLDBERG S: Changes in Organs of Thyroidectomized Sheep and Goats. Quart. J. Exp. Physiol., 17:15, 1927. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Minnesota and Minneapolis General Hospital Minneapolis PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited BySystemic Diseases and Heart BlockReversible Atrioventricular Block in MyxedemaChanges in the Electrocardiogram and Achilles Reflex Test during Treatment of HypothyroidismDas Herz bei Myxödem und HypothyreoseComplete auriculoventricular block in myxedema with reversion to normal sinus rhythm on thyroid therapyMYXOEDEMA WITH PERICARDIAL EFFUSIONPericardial effusion in myxedemaBIBLIOGRAPHIEReversible cardiac enlargement in a case of congenital cavernous hemangiomaAngina pectoris and myocardial infarction as complications of myxedemaThe heart in myxedema, with a report of two casesThe Heart in Myxedema*†Electrocardiograms and Roentgen-Ray Measurements before and after TherapyJ. LERMAN, M.D., R. J. CLARK, M.D., J. H. MEANS, M.D., F.A.C.P.Myxedema heartMyxedema A Case Report*HENRY B. GOTTEN, M.D. 1 January 1931Volume 4, Issue 7Page: 733-741KeywordsElectrocardiographyHeartMedical servicesThyroid Issue Published: 1 January 1931 PDF DownloadLoading ...

Congenital aneurysm of the interventricular septum: Cannell, D. E.. Am. J. Path. 6: 477, 1930

1.1. Eight cases of partial bundle-branch block of varying degrees are presented with abstracts of their clinical histories, complete physical and laboratory data and electrocardiographic studies.2.2. Three unusual cases of transient Type II, intraventricular or bundle-branch block are recorded with sudden transition from complete bundle-branch block to normal intraventricular conduction times in response to respiratory maneuvers. The possible mechanical or nervous factors concerned in the production of the changes are considered to be anoxemia as well as fatigue. Vagus effect may be contributory.3.3. We have stressed especially the importance of the recognition of this transient type of disturbance because of its better prognostic outlook. When present it must be relieved by therapeutic rest before necessary surgical or intravenous procedures are to be undertaken.4.4. The increased risk assumed in submitting patients, in the presence of bundle-branch block, to a procedure that may apparently only slightly effect the blood pressure and the heart is emphasized.5.5. The theories of partial heart-block with special reference to and the intraventricular counterparts of the accepted Types I and II of auriculoventricular types are discussed at some length.6.6. The theoretical reasons for the danger of precipitating fatal ventricular fibrillation in the presence of bundle-branch block are given.

Dissociation and interference in partial heart-block: Dressler, Wihelm: Ztschr. f. klin. Med. 111: 23, 1929

Dissociation and interference in partial heart-block: Dressler, Wihelm: Ztschr. f. klin. Med. 111: 23, 1929

The “latency theory” of heart-block and interpolated ventricular premature beats

Experimental evidence has been presented which shows that the fundamental postulates of the “latency theory” of partial heart-block are not valid for conduction in the turtle heart. From an examination of interpolated ventricular premature beats it is concluded that the observed phenomena do not compel us to accept that theory for the human heart.

The treatment of Adams-Stokes syndrome due to auriculoventricular block

1. A. The pathogenesis of Adams-Stokes syndrome due to auriculoventricular block is described. 2. B. The primary aim and the rationale appertaining to any therapeutic measure is discussed. These are shown to be an increase in the ventricular rate, brought about in one or more of the following ways: (1) the resolution of the lesion, as, for example, in gummatous infiltration and acute inflammatory changes; (2) the counteraction of any possible vagal overactivity; (3) the increase directly of stimulus production, of excitability and of contractility of the heart muscle. 3. C. The rationale and the comparative value of various therapeutic measures are discussed. Antisyphilitic treatment is indicated in Adams-Stokes syndrome due to auriculoventricular block when this is the result of gummatous infiltration. Potassium iodide may even aggravate the complaint when the cause is other than syphilis. Thyroid appears to be sometimes of value and may even be completely effective. Atropine, administered between the attacks, in order to prevent their recurrence, is indicated in cases of partial heart-block in which there is vagal overactivity. Digitalis is contraindicated in partial heart-block. It may be of value in complete heart-block. Caffeine and theobromine are of no clinical value. Of reported eases, the nitrites were found to be only of doubtful value in one case. Adrenalin is of value in the great majority of cases. It is not often effective in preventing the recurrence of the attacks. When employed for this purpose, it may be administered either subcutaneously or intramuscularly. It is, however, the only potent therapeutic measure during an attack. When employed for this purpose, intracardiac injection is necessary, except in the rare cases in which the attacks are due to a merely temporary increase in the grade of an existing partial heart-block, in which event it may be given either hypodermically or intramuscularly. Further investigation of ephedrin, administered by mouth, is advisable. Barium chloride, given by mouth, should invariably be tried for the prevention of the recurrence of the attacks in cases of Adams-Stokes syndrome due to auriculoventricular block. If ineffective alone, the drug should be employed with adrenalin, the latter administered either hypodermically or intramuscularly.

Experimental Treatment of Cardiac Arrhythmias.

Since weakening of the heart muscle leads to incomplete emptying and progressive dilatation, which in turn results in impaired conduction, arrhythmias, and auricular fibrillation, it is conceivable that these conditions would be improved by increasing the force of the heart and slowing its rate by digitalis, or by relieving its load. In order to accomplish the latter we have bled 5-10 cc. per kg. or changed the distribution of the blood in the active circulation by snake venom (Lachesis colatitudes), histamine, peptone and nitrites. These drugs were injected into the femoral vein of cats previously anesthetized with urethane. Respiration and blood pressure curves were taken and checked up by simultaneous electrocardiograms. After a normal tracing and electrocardiogram were taken, cardiac arrhythmias were produced by chloral or aconitine, mostly the former because of its more uniform results. Fifty mg. of chloral hydrate per kg. was the initial dose used. Occasionally this was sufficient to cause an irregular heart, but as a rule it had to be repeated 2 or 3 times. As soon as the tracing showed an irregularity, an electrocardiogram was taken, and then the therapeutic drug was injected. The electrocardiograms before the injection revealed numerous right and left ventricular extra-systoles, auricular extra-systoles, nodal rhythm, or partial heart block. Some of these electrocardiograms showed a single irregularity, while others showed combinations of several irregularities. In untreated animals the arrhythmia lasted for 15 to 45 minutes. A few animals died within 15 minutes, the irregularity persisting till death. The first drug used was Lachesis lanceolatus, 0.025 mg. per kg., and, as a rule, in about one minute the heart became regular, as shown by the tracing and the electrocardiogram. Histamine 0.03 mg. per kg., peptone 100 mg. per kg., nitroglycerine 0.4 mg. per kg., withdrawal of about 10 cc. of blood per kg., or pressure on the Inferior Vena Cava gave similar results.

IMPAIRED AURICULOVENTRICULAR CONDUCTION IN RHEUMATIC FEVER

It is now well known that auriculoventricular conduction is frequently impaired in the course of rheumatic fever and that this disturbance affords valuable evidence of myocardial involvement. 1 In a number of instances of partial or complete heart block 2 and in one case showing only prolonged auriculoventricular conduction, 3 postmortem examination of the heart has disclosed characteristic rheumatic lesions involving the auriculoventricular node or bundle. Such lesions have consisted of cellular infiltration and edema during the acute stages of the disease, or of scar tissue after healing has taken place. The transitory nature of conduction disturbances in many cases indicates that the inflammatory process may subside without graphic evidence of permanent damage to the heart muscle. In following a series of cases of rheumatic fever in which frequent electrocardiograms were made, the diagnostic importance of disturbances in auriculoventricular conduction became apparent. The present study covers a period of nine years. Most of

Heart-block with convulsive syncope: Case report and pathological findings in a patient unsuccessfully treated with barium chloride

A case of partial heart-block is reported in the course of which there occurred frequent attacks of syncope with convulsive seizures (Adams-Stokes' syndrome). During the period of observation barium chloride, epinephrin and atropine were administered,—all without appreciable effect. The patient died during an attack of ventricular asystole. Postmortem examination showed a lesion involving junctional tissues and consisting of a fatty and lymphocytic infiltration of the atrioventricular node and the first part of the bundle of His together with a fibrotic process involving both left and right bundle-branches. The bundle fibers showed degeneration. That this degeneration was active, was evidenced by the finding of endotheliocytes which were phagocyting the degenerating Purkinje fibers. We suggest that our failure to establish an idioventricular rhythm might have been due to the presence of extensive destruction of junctional tissues in a patient in whom the lower pacemaker had never been dominant.

NOTE ON THE USE OF EPINEPHRIN IN HEART BLOCK

Phear and Parkinson 1 recently reported a case of complete heart block in which the sudden ventricular standstill responsible for syncopal attacks was entirely prevented by the subcutaneous injection of epinephrin. The heart block and the auricular and ventricular rates remained unchanged. Their review of the continental literature discloses only two cases, one of partial (2:1) block, the other of complete block, in which heart block was reduced or abated by epinephrin. In no case was partial heart block increased in degree, but in nearly all instances the auricular and ventricular rates were accelerated. Experimentally, however, it was shown by Kahn that complete auriculoventricular block may be produced in dogs by the intravenous injection of epinephrin. The paradoxical results reported by Routier, who describes a deblocking effect of epinephrin in dogs in which complete block had been produced by crushing the auriculoventricular bundle, failed of confirmation in the hands of

OBSERVATIONS ON SINO-AURICULAR HEART BLOCK

Heart block is ordinarily understood to be a condition in which there is impairment in the conduction of impulses from auricles to ventricles. The first stage of this process is represented by a mere delay in the conduction time recognized by an increase in the a-c interval in jugular tracings and in the P-R time in electrocardiograms. In this condition all impulses reach the ventricle; but if the delay is sufficient or if the heart rate is rapid, an impulse may occasionally fail to reach the ventricle, giving partial heart block. Finally, there is a condition in which none of the auricular impulses reach the ventricle, and the auricles and ventricles each beat of their own rhythm and independently of one another. These three stages may be termed, first,<i>delayed conduction, second, partial heart block, and third, complete heart block</i>. The cause of this disturbance in

TRANSIENT AURICULOVENTRICULAR DISSOCIATION WITH VARYING VENTRICULAR COMPLEXES CAUSED BY DIGITALIS

In 1913, Cohn 1 and Oppenheimer and Williams 2 described cases of heart-block in which the form of the ventricular complex showed frequent change. In Cohn's case the heart-block was transient. On Aug. 22, 1910, the patient showed partial heart-block with a 3-2 rhythm as shown by polygraphic tracings. On Feb. 10, 1911, this patient was studied again and showed a partial heart-block with a 2-1 rhythm. On February 11 and 13 there was a complete auriculoventricular dissociation. At this time electrocardiographic tracings were made and it was found that successive ventricular complexes changed their outline so that no two were precisely alike. Two general types, however, could be distinguished, the one resembling the type of beat arising from stimuli originating in the wall of the right ventricle and the other those arising in the wall of the right ventricle and the other those arising

Case of Acute Partial Heart-block

Case of Acute Partial Heart-block

A PATHOLOGICAL STUDY OF TWO CASES OF HEARTBLOCK WITH ADAMS-STOKES' SYNDROME

In a recent very interesting report of a case of terminal heart-block, Pardee1demonstrates that an extensive anatomical lesion of the auriculoventricular bundle may be present without disturbance of its function. He then gives three lists : (1) ten cases, in which complete destruction of a transverse section of the bundle was invariably accompanied by complete heart-block; (2) six cases,2with varying degree of block, in which no lesion of the bundle existed; (3) ten cases, (six of complete and four of partial heart-block) accompanied by very slight pathological changes. The intermediate degrees of bundle involvement he has not considered. That is, though it has been firmly established that lesions of the conductive system may cause partial and complete heart-block, it seems also true that such lesions may exist (even though of considerable extent) without block; and further that partial or complete block may exist without

VISUAL METHODS IN DIAGNOSIS OF HEART-BLOCK.II. A REPLY.

In availing myself of the opportunity of making a rejoinder to Dr. Hirschfelder's criticism of my recent communication I wish first to say that I think his criticism is partly right and partly wrong. The diagnosis of complete heart-block with the auricle beating four or five times as fast as the ventricle can undoubtedly, as he says, be made without instruments of any kind. In partial heart-block, however, which probably always precedes the complete form, the problem is entirely different. We may not have bradycardia in these cases, but only an irregularity caused by an occasional "block" of the auricular impulse. These cases, the recognition of which is so important, can scarcely be detected without the aid of suitable instruments. It might, of course, be possible in favorable cases to<i>feel</i>an omission of the radial pulse or apex beat and<i>see</i>that a conspicuous venous pulsation continued without interruption.