Pericarditis- Causes and Pathological relations, sign and symptoms, diagnosis and treatment by Edwin hale in his book diseases of heart….

Part II

GENTLEMEN: I shall call your attention in this and following lectures to the


Inflammation of the heart may affect one or more of the structures which compose that organ. The investing serous membrane may be alone inflamed, constituting the disease known as pericarditis. When the membrane lining the cavities, or the endocardium, is the seat of inflammation, the affection is called endocarditis. Inflammation of the muscular tissue, or substance of the heart, is designated myocarditis or carditis.

Although these different inflammatory affections may exist each independent of the others, they are often associated. In many cases of pericarditis, carditis co-exists. Myocarditis very rarely occurs except in connection with inflammation of either the investing or lining membrane of the heart.

The importance of these diseases cannot be overrated, and their study is of the highest importance. They are seated in the great vital organ of the body. They involve great suffering and danger to life. Their remote consequences are very grave. All organic affections of the heart have their origin in the inflammatory. Too many physicians neglect to study this class of affections, greatly to their own detriment and that of their patients. The homoeopathic treatment of inflammatory cardiac affections, if skillfully applied, is vastly superior to the ordinary methods. The late improvements in physical examination greatly facilitate correct diagnosis, and enable us to combat these diseases with the happiest results.


Acute pericarditis – Anatomical characters – Morbid changes – Causes and pathology – Connection with rheumatism – With albuminuria – With Bright’s Disease, pyaemia, etc. – Symptoms – Of the heart – Of the circulation – Of the respiratory symptoms – Digestive organs – Brain and spinal cord – Physical signs of pericarditis – Signs furnished by auscultation, percussion, palpation, inspection, and mensuration – Summary – Diagnosis – Prognosis – Treatment.

Inflammation of the investing membrane of the heart is less common than endocarditis, but it is a more serious affection as regards immediate danger.

This membrane is like the serous tissues in other portions of the body, and inflammation results in the same changes in this, as in the pleural and peritoneal membranes. It is more dangerous than the other serous inflammations, because of the small size of the pericardial sac, and the fact that the heart-substance consists of muscular tissue, also because of the important function of the organ and its physiological relations.

In treating of pericarditis the following points will be considered: 1. The morbid changes incident to the disease. 2. Its causes and pathological relations. 3. The symptoms, signs diagnosis, prognosis, and treatment.

Like other inflammatory affections, this has an acute, sub- acute, and chronic form.


The inflammation is seldom diffuse, and is generally limited to single spots. The membrane at first looks injected, opaque, sometimes spotted, in consequence of slight extravasations. Acute inflammation speedily leads to exudation of lymph. This exudation takes place, in most cases, probably within a few hours from the commencement of the inflammation. It is at first of a jelly-like consistence, and adheres slightly to the membrane, forming a thin layer, either limited to the base of the organ and about the roots of the large vessels, or extending more or less over the pericardial surface. The heart, at this stage, is said to present an appearance like that of hoar frost, or to a “layer of liquid gelatine spread upon the parts with a camel’s hair pencil.” The exudation goes on, and generally, but not invariably, more or less liquid effusion varies in quality and quantity. It may amount to a few ounces or to a several pints. the exudation either consists of plastic lymph, mixed or not with serum, or blood, very seldom of serum alone.

The first stage extends to the time when the accumulation of lymph is sufficient to be determined during life by symptoms and physical signs.

The second stage embraces the period during which an appreciable amount of liquid continues.

The third stage comprises the duration of the disease after the resorption of the liquid.

These stages have been called stages of exudation, of liquid effusion, and of adhesion.

If the disease do not prove fatal, the liquid is gradually absorbed, and adhesion follows; or absorption occurs without adhesions; or a membrane may be formed from the plastic exudation; or the effused fluid may be changed to pus. The adhesions may be firm and extensive, or delicate and thread-like.

A liquid effusion sufficient to be manifested by physical signs may take place at a period of the disease, varying from one to four days from the date of the attack.

Death usually occurs during the period of liquid effusion.

The effusion is sometimes absorbed quite rapidly, in other cases slowly. In the latter instance, a condition obtains which has been called dropsy of the heart.


Acute pericarditis is rarely an idiopathic or primary disease. In the great majority of cases it is a secondary affection. There are many cases of which it is an occasional concomitant, but in the larger proportion of instances it occurs either in the course of acute articular rheumatism, or the renal affection known as Bright’s disease.

Of 847 cases of rheumatism, collected from various sources, and analyzed by Dr. Fuller, it existed in 142, or about one to every six cases.

Of 50 cases collected by Dr. Flint, it existed in 19, or more than one-third.

Rheumatism is more likely to become complicated with pericarditis in the young than in the aged, and occurs oftener in females than in males.

The more acute the rheumatic affection, the greater the liability to pericarditis; and it occurs oftener during first attacks than in subsequent.

That there is an intimate relation between acute rheumatism and pericarditis admits of no doubt, but the common notion that there is a metastasis from the joints to the heart is erroneous, although some cases appear to support the supposition. The facts are that pericarditis often precedes the affection of the joints, and the inflammation of the joints does not usually subside when the heart is affected.

The true explanation of the apparent transfer of the disease, and of the relation existing, is, that the pericarditis and affection of the joints depend upon the same condition of the blood. The analogy of structure between the pericardium and the synovial membranes will account for the liability of the former to become inflamed when the latter are affected.

The connection between pericarditis and albuminuria and uraemic phenomena is now quite definitely ascertained.

Of 35 cases of pericarditis analyzed, with respect to causation, by Dr. Taylor, renal disease existed in 13.

Of 50 cases collected by Dr. Flint, renal disease was present in 7. Of 292 cases or renal disease analyzed by Fredrichs, pericarditis occurred in 13. Of 135 fatal cases of pericarditis analyzed by Dr. Chambers, the kidneys were diseased in 36.

Renal disease existed in a larger proportion of the cases of pericarditis which end fatally than of those ending in recovery. The explanation of this is, pericarditis developed in connection with Bright’s disease usually ends fatally; whilst in connection with acute rheumatism recovery takes place in a large proportion of instances.

What is the relation between pericarditis and certain renal affections? It is well known that serous inflammations are apt to become developed in connection with Bright’s disease. These inflammations are attributed to the accumulation of urinary principles in the blood, from faulty excretory function in the kidneys. the excess of urea, or the decomposition of its products in the blood, act as poisonous agents, giving rise to inflammation of the pericardial and other serous membranes.

Pericarditis may be associated with pleurisy or pneumonia. It must not be supposed, however, that it obtains by means of extension, but results from the same pathological cause.

Pyaemia frequently co-exists with pericarditis. Wounds, and surgical operations, in tissues remote from the heart, sometimes give rise to pericarditis. The explanation is, the blood becomes poisoned so as to cause serous inflammations.


The symptoms of pericarditis vary with the three periods of the disease. They are modified by the amount of fluid effused during the second period, and again during the absorption of the fluid in the third stage. The intensity of the inflammation may be in ratio to the severity of the pain.

In some cases, however, pericarditis may run its course with but little pain or febrile movement attendant. But this is equally true of inflammation in any organ, especially in the serous tissues.

The symptomatology of pericarditis is best treated of by taking it up in the following order, namely: The symptoms relating to the heart, and afterwards those referable to the circulatory, respiratory, and nervous system.

Symptoms referable to the heart, (1) pain, (2) tenderness, (3) palpitation.

Pain referred to the praecordia is a prominent symptom in some cases. It is generally burning, lancinating, and often accompanied by a sense of constriction. It is aggravated by inspiration and the movements of the body. The pain is sometimes felt in the epigastrium, or to the right side, or the centre of the sternum. It may extend to the back, to the left shoulder, and down the left arm, as in angina pectoris. The pain much resembles the pain of pleurisy, with which pericarditis may be confounded. The two diseases may, however, exist at the same time; so also may pleurodynia and intercostal neuralgia. But pain in pericarditis may be very slight, or altogether wanting. Dr. Flint says, in the larger number of cases observed by him, the pain was very slight.

It is a disputed question on what the pain depends. Bouilland attributes it to co-existing pleuritis. Flint refers it to the nerves of the heart. Inman says it is a myalgia of the thoracic muscles.

Tenderness on pressure is generally present, but, like pain, varies in degree, and is rarely very marked. Hope says it may be discovered by pressing on the epigastrium beneath the cartilages of the ribs, in a direction toward the heart, when it is not apparent directly over the heart. Flint asserts that in order to constitute a symptom of pericarditis it must be limited to the region of the heart. If tenderness is diffused, it indicates the presence of pleurisy, or pleurodynia. It is only when taken in connection with other symptoms, that tenderness is of positive value. It is well known that in peritonitis tenderness is sometimes absent; so in pericarditis. Why this is so has not been explained.

Increased action of the heart occurs in pericarditis in the early part of the disease. The contractions are violent, and sometimes irregular, and the patient is conscious of an unnatural beating of the heart. This symptom, however, is by no means constant, and of itself is of little value, because it is found in functional disorder and organic disease.

If, during the occurrence of rheumatism, tumultuous action of the heart is noticed, it should lead to a careful examination.

In the stage of liquid effusion, palpitation cannot occur to any degree, and if the effusion is absent the heart is so weakened in the second stage as to make palpitation almost impossible.


The pulse alone, in this disease, does not furnish positive diagnostic information, but when the diagnosis is made, it aids us in judging of the condition of the heart. At the outset of the disease it corresponds to the increased muscular action of the organ, and is strong, quick, and vibratory, more or less frequent, and sometimes irregular.

As the heart becomes weakened the pulse becomes enfeebled; and when, together with a certain amount of paralysis, there occurs liquid effusion, the pulse becomes weak and small, with greater disturbance of rhythm.

Walshe says that the frequency of the pulse “is subject to more sudden variations from the influence of emotional excitement and effort in this than in any other disease.” He adds, that he has known a gentle movement of the trunk to raise the pulse from 80 or 90 to 130 or 140.

But to the above statements there are many exceptions. Even in the first stage it may not be more frequent than in health. Graves says it is often “less frequent.” It may even continue regular, and in no way abnormal.

Lividity of the lips, face, etc., may be due to a weakness of the heart, and belongs to the second stage of the disease, when it denotes serious obstruction. It is attended with feeble and irregular pulse.

Lividity is caused by congestion of the venous radicles, but generally involves some affection of the pulmonary system co- existing with pericarditis. The efficient aeration of the blood by the lungs may in such cases cause lividity. This symptom is not therefore very important as a diagnostic sign of pericarditis.


Respiration is sometimes accelerated in pericarditis in consequence of the inspiratory acts being shortened by the praecordial pain, and, in such cases, dilatation of the alae nasi may be observed, the dyspnoea may be dependent on congestion of the lungs, incident to compression of the heart by liquid effusion, but it may be absent even when the pericardial sac is largely distended. But this symptom is not always present, for the respiration may be unaffected, or only accelerated by the febrile movement.

Cough, dry, hacking, or spasmodic, is common, and may exist independent of any pulmonary disease. It may, however, be absent in all stages. When a dry, short cough is associated with orthopnoea, a frequent and feeble pulse, and lividity of lips and face, it denotes imminent danger.

The voice may be very weak, the patient being unable to speak, except in feeble tones and with great effort. This symptom seems to be connected with copious effusion.


Vomiting is sometimes present and persistent, and may lead us to a faulty diagnosis in mistaking the attack for gastritis.

Dysphagia occasionally occurs, and was first noticed by Testa, an Italian author. It may be a spasmodic affection, or due to pressure of the distended pericardial sac upon the oesophagus.


An expression of anxiety, or apprehension, is often a prominent symptom. The risus sardonicus has been observed in seven cases which terminated fatally. The position of the patient is generally on the back, or diagonally, between that on the back and on the side. It is rarely on the left side, the liver in this position pressing on the heart. In some cases the patient can lie comfortably on the right side. Generally, the patient desires to have the head and shoulders raised. But whatever position the patient selects he is very reluctant to change it, owing to the great increase of the pain or distress, and the excitement of the heart, which gives rise to a feeling of syncope, especially when the sac is filled with fluid. Fatal syncope has been induced by change of position. Flint refers to several cases, and I have observed it to occur in one case of rheumatic pericarditis, and in several cases where cardiac disease was complicated with diphtheria.


In addition to the mental anxiety, depression, and fear of death observed in cases of pericarditis, actual delirium may exist. It has not been considered an element of the disease.

There are, however, cases of pericarditis in which the cerebral symptoms are so marked that they mask the cardiac inflammation. These cerebral symptoms may simulate meningitis, mania, dementia, coma, epilepsy, tetanus, and chorea. In many cases of supposed cerebral disease terminating fatally, autopsy shows no appreciable lesion of the brain and spinal cord. But if the examination had included the heart, pericarditis would have been found to have existed.

Dr. Burrows* *”On Disorders of the Cerebral Circulation and on the Connection between Affections of the Brain and Diseases of the heart.” was the first to call special attention to this connection of cerebral symptoms with cardiac disease. Dr. Flint alludes to several interesting cases of a similar character which came under his observation. These two authors show conclusively that the physician may mistake an inflammation of the pericardium for an inflammation of the brain. In the 16 cases detailed by Burrows there occurred delirium, convulsions, agitation of the limbs resembling chorea, dementia, coma, and seizures resembling apoplexy and tetanic spasms. Flint’s cases had delirium, with wild, staring expression, inability to protrude the tongue, shouting as if from danger, coma, great agitation, blindness of one eye, etc. One patient “ejected saliva with great force, and in all directions.”

Several cases have come under my own observation. One very notably case, in a girl eight years of age. The symptoms all simulated meningitis, and it was only when my attention was called to the heart by the full and very irregular pulse, that physical examination disclosed the presence of pericarditis.

Flint says the delirium is peculiar, “the patient lying in a species of coma vigil, the eyes open and fixed in one direction, not replying to questions, and incapable of being roused; this state was followed by maniacal excitement, the patient shouting, and apparently laboring under fear of harm, with occasional ebullitions of hilarity. A fixed delusion of having committed some crime appears to be a distinguishing feature.”

From the above symptoms – and this peculiar delirium does not occur in meningitis – and also the absence of acute pain in the head, throbbing of the carotids, injection of the eyes and face, we may know that the disease is not cerebral. The delirium resembles somewhat delirium tremens, in which condition the heart is often much disordered. This fact may lead us to understand the curative action of digitalis in mania a potu.

I wish to call attention to a fact which Flint has not mentioned, namely, the disordered action of the heart in idiopathic brain affections. In some cases of meningitis, and nearly all cases of tubercular meningitis, the pulse is at first full and irregular, afterwards soft and fluttering, then intermitting, irregular, full, slow and labored, easily quickened by motion or mental disturbance to double its previous amount of pulsations.

When we reflect that these symptoms also occur in pericarditis, we shall admit that it may be possible for the physician who neglects physical examinations to make a wrong diagnosis. I have seen cases of tubercular meningitis in which the beating of the heart and the character of the pulse simulated pericarditis. The physical signs on percussion were, however, wanting. In such cases the disorder of the heart was functional, or reflex, the nervous irritation being transmitted through the phrenic and pneumogastric nerves, just as in reflex disorder of the brain from pericarditis, but in a contrary direction. I will here remark, that for brain symptoms arising from diseases of the heart, digitalis is generally specific; but if the contrary obtains, it is not indicated.


The symptoms of acute pericarditis above enumerated are not alone sufficient to enable us to diagnose with certainty the presence of that disease. But by means of the physical signs obtained by percussion, auscultation, palpation, inspection, and mensuration, the disease may now be generally recognized with a degree of positiveness which clinical observers, not many years ago, regarded as unattainable.

Instead of entering into a profuse description of these signs occurring in pericarditis, I shall take the liberty to present the admirable summary given by Dr. Flint, in this work on Diseases of the Heart:


“Enlarged area of praecordial dullness; the extent of this area greater in a vertical than in a transverse direction; its shape corresponding to the pyramidal form of the pericardial sac when distended; the dullness within this area, and the sense of resistance on percussion greater than over the praecordial region in health, or in cases of enlargement of the heart. These signs denote an abundant effusion within the pericardial sac.

“Moderate or small effusion denoted by increased width of the area of dullness at the lower and middle portions of the praecordial region. The increase of the area of dullness taking place within a few days or hours, and progressing rapidly; its extent varying on different days during the course of the disease. Dullness from the presence of liquid below the point of the apex-beat of the heart. Diminution of the area of dullness, with more or less rapidity in the progress of the disease toward convalescence, and its final reduction to its normal limits; when convalescence is established.”


“A friction sound developed, usually, soon after the commencement of the inflammation, depending on the exudation of lymph; rarely wanting during the period of the disease which precedes that of liquid effusion; frequently, not invariably, disappearing during the period of effusion; often returning after the absorption of liquid, and sometimes persisting after adhesion of the pericardial surfaces has taken place. Intensification of the heart sounds at the commencement of the disease, or prior to liquid effusion; during the period of effusion, both sounds weakened, but especially the first sound; the element of impulsion in the first sound notably impaired or lost, and this sound, therefore, consisting of the valvular element alone, resembling the second sound as regards quality and duration; the sounds apparently distant, and the apparent distance greater when the patient is recumbent on the back.

“Cessation of respiratory murmur and vocal resonance, concurring with the results of percussion, in determining the enlarged area of praecordial dullness dependent on distension of the pericardial sac.”

Edwin Hale
Edwin Moses Hale 1829 – 1899 was an orthodox doctor who converted to homeopathy graduated at the Cleveland Homoeopathic Medical College to become Professor Emeritus of Materia Medica and Therapeutics at Hahnemann Medical College, editor of the North American Journal of Homeopathy and The American Homeopathic Observer and a member of the American Institute of Homeopathy. Hale was also a member of The Chicago Literary Club.

Hale wrote Lectures On Diseases Of The Heart, Materia medica and special therapeutics of the new remedies Volume 1, Materia Medica And Special Therapeutics Of The New Remedies Volume 2, Saw Palmetto: (Sabal Serrulata. Serenoa Serrulata), The Medical, Surgical, and Hygienic Treatment of Diseases of Women, New Remedies: Their Pathogenetic Effects and Therapeutic Application, Ilex Cassine : the aboriginal North American tea, Repertory to the New Remedies with Charles Porter Hart, The Characteristics of the New Remedies, Materia Medica and Special Therapeutics of the New Remedies, The Practice of Medicine, Homoeopathic Materia Medica of the New Remedies: Their Botanical Description etc.