Cardiovascular
Classic disease descriptions
Through the exploration of classical books and writings of old-time clinicians, this growing database aims to provide categorized, detailed characterizations of diseases, including finely detailed signs and symptoms.
Description 1
The attack begins suddenly, with pain, usually intense and excruciating, in the region of the heart. The pain radiates into the neck, the left shoulder, and down the arm to the fingers, sometimes to the right arm and down the body. There is also a sense of cardiac construction, often with coldness and numbness of the praecordium and the fingers. The face is pale or ashy gray and betrays a feeling of intense anxiety. The face and body are often covered with drops of cold perspiration.
A sense of impending death is a usual and characteristic symptom. There may or may not be dyspnoea, sometimes associated with wheezing or asthmatic breathing. The arterial tension is usually increased, and while the action of the heart may be arrhythmic, it is often regular and normal. The patient may be restless, but more commonly holds himself quiet and passive in fearful expectation of what may happen. The attack lasts from a few seconds to two minutes, and often terminates with eructations, nausea and vomiting, or the voiding of a large quantity of clear pale urine.
Butler, G. R. (1902). The Diagnostics of internal medicine: a clinical treatise upon the recognised principles of medical diagnosis. New York: Appleton. Pg. 894-895.
Entered by: Erin Choi, 6/17/2020
Edited by: Sonia Y. Khan, 8/4/2020
Description 2
Angina pectoris is never the outcome of an acute affection; it is invariably led up to by a long period of gradual exhaustion. The onset is, in the majority of cases, induced by some extra effort on the part of the heart. This need not be an effort of unusual severity; it occurs more frequently when the individual is using his powers in a way which formerly required no very marked strain. The cause may be of the nature of bodily exertion, mental excitement, exposure to cold air, or anything that calls for more work on the part of the heart. In most cases the attack does not come on at once, unless the effort is per sisted in, as in walking up a hill, and the first warnings of heart exhaustion are ignored. The attack of pain may not come for some minutes or even hours after the causal exertion has ceased, and when the patient has been resting in bed. In some severe cases the attack of pain may come on at intervals when the patient has been exposed to no exertion, particularly in cases where the attacks have been frequent, and a tendency to them has been established [...] The attacks may be so slight at first as to pass almost unnoticed, and it is only after they become more frequent and severe that the patient's attention is called to the fact that he had previously experienced some discomfort. In the more simple cases the pain may not be very severe, and, appearing after some violent exertion, may never again show itself. Instead of pain it may be but a slight sensation of constriction across the chest, that calls for a deep inspiration to relieve the tension. The more severe attacks imperatively command a cessation of all efforts, and here all degrees of suffering may be experienced. During the attack the patient may stand still in a position of rigid immobility, afraid to move or to speak, scarcely daring to breathe, or he may kneel down and rest his head on a chair, or roll on the floor in an extremity of agony, or the patient may become unconscious and, in rare cases, may die. If the pain is located in the arm, he may nurse it across his chest, rocking backwards and forwards. The face may become pale or flushed, and beads of perspiration may roll down the forehead. The attack may terminate with the expulsion of air from the stomach, unconsciously sucked into the stomach during the attack. In most cases the attack lasts for a few seconds, but it may continue with great severity for several hours, yielding only to large doses of opium. Such severe cases may die during the suffering [...] The chief symptom is pain: there may be also a sense of constriction across the chest, a sense of suffocation, and a sense of impending death. Occasionally other reflexes may be present, such as a flow of saliva from the mouth, and an increased secretion of urine. These symptoms are not all present in every attack, nor are they always present in the same degree. There may be a slight pain or a slight sense of constriction across the chest. Or the pain may be of the utmost severity, with constriction of the chest so violent that the patient feels as if his breast bone was about to break [...] Pain is usually referred to some portion of the distribution of the upper four left dorsal nerves in the chest and arm. Sometimes the pain may be felt as low as the distribution of the sixth dorsal nerves in the epigastrium, and as high as the eighth and seventh cervical in the ulnar border of the forearm and hand. It is rarely felt in similar areas on the right side, and sometimes it is felt in the neck and back of the head, in the upper cervical nerves, whose roots are in close association with the vagus. The pain is usually felt across the chest, and may remain stationary there, or it may radiate in a very definite manner into the axilla, and down the arm to the ulnar border of the forearm and hand. When it does this it may stop for a brief period in the upper arm or forearm, and be felt there most violently. On the other hand, the pain may start in the arm and radiate to the chest, where it remains with great severity for a time. Constriction of the Chest. – Arising along with the pain, or following it, or quite independent of the sensation of pain, is a sense of constriction, which I have reasoned is due to the reflex stimulation of the intercostal muscles. It may be so slight as to be felt only as a mere tightness across the chest following exertion, or it may grip the chest so firmly that the patient has to stand still and take a great deep inspiration to relieve the spasm of the muscles. In its most violent form it adds greatly to the suffering of the patient when pain is also present. Thus a man aged forty-eight, who had violently exerted himself, felt a pain in his chest come on gradually some minutes after the exertion. As the pain increased he called on me, and I asked him if he felt his chest constricted. He said ' No '. A few hours later, the pain increased in severity; then suddenly he felt his chest gripped with a violence so great that it added, he said, indescribably to the terror of his suffering. It was only relieved by large doses of opium. Next day he felt for a short time when in bed as though that 'awful gripping were coming on', and he lay for ten minutes with perspiration pouring off him, in the dread of its return. Feeling of impending dissolution. — This, I presume, is the result of violent stimulation of the nervous system comparable to what happens when any other viscus is violently stimulated, as after a blow in the epigastrium, or on the testicle. On rare occasions the patient faints during an attack, and in one instance a patient of mine never recovered, but died during the faint.
Mackenzie, J., Sir. (1908). Diseases of the Heart. (pp. 47-49). London: Henry Frowde; Hodder & Stoughton.
Created by: Sara Ahmed, 06/16/2021
Entered by: Rachel Johnson, 07/09/2021
An aneurysmal tumor extending from the anterior or antero-lateral aspect of the artery, after having attained to a certain size, is perceived by manual examination of the abdomen. It is beneath or to the left of the median line. It is not depressed by a deep inspiration, nor moved laterally by pressure with the fingers. It has usually a strong pulsation. In most cases a systolic murmur is perceived by means of stethoscope, and sometimes also a diastolic murmur. In certain proportion of cases a vibration or thrill is perceived when pressure over the tumor is made with the fingers. Pain more or less intense is felt in the seat or neighborhood of the tumor. […]
As regards to pulsation, the distinctive character of aneurysm is an expansile movement not alone upward, but also marked on the lateral aspect of the tumor. If the tumor be not aneurysmal, the pulsation may sometimes be arrested by lifting it from the artery, or pushing it to one side. Inclining the body forward may notably diminish the force of the impulse. A well-marked thrill is highly diagnostic of aneurysm, if not indeed pathognomonic. aneurysmal tumors rarely have an irregular or nodulated surface, which other tumors often have. The femoral pulse in cases of aneurysm is retarded, that is, occurring after the radial pulse. […] An aneurysm arising from the posterior aspect of the aorta, causes erosion of the vertebra, accompanied by constant pain localized in the spine, and by pains in the course of the lumbar nerves and their branches. […] Taking this direction, the aneurysm leads to a pulsating tumor on the left side of the spinal column.
Flint, A. (1879). Clinical medicine: a systematic treatise on the diagnosis and treatment of diseases; designed for the use of students and practitioners of medicine. London: Churchill. Pg. 242-243.
Entered by: Erin Choi, 6/12/2020
"In this lesion the left ventricle tends to be overextended, and dilation precedes hypertrophy. So long as the compensation is efficient there may be no cardiac symptoms; but in certain proportion of cases, even though compensation is maintained, there may be dull praecordial aching and oppression, or more frequently a sharper pain which radiates to the neck and the arms, the left shoulder and arm in particular. Paroxysms of true angina pectoris may occur. Dyspnoea, praecordial distress, and palpitation often result from slight exertion, and vertigo, faintness, flashes of light before the eyes, tinnitus aurium, and a throbbing headache may be manifest, especially if the patient gets up quickly from a recumbent posture. Occasionally there is redness and a feeling of heat in the skin followed by copious sweating. When the heart begins to fail dyspnoea, sometimes orthopnea, rarely with cyanosis, appears, especially at night. […] oedema of the lower extremities may be an early symptom, and is favoured by the marked anaemia which is commonly associated with aortic incompetency. Cough, pulmonary congestion or oedema, and perhaps haemoptysis, may be present. […] The carotids and other accessible arteries are seen to pulsate violently, and there is epigastric throbbing. […] The impulse of the heart, unless dilation predominates over hypertrophy, is strong and heaving, and a diastolic thrill is occasionally felt. The apex beat is palpable in the 6th or 7th interspace outside the mammillary line. The pulse has the water-hammer character, ‘Corrigan’s pulse’. […] Upon auscultation a diastolic murmur is heard over the aortic area (pg. 356), soft, blowing, rarely harsh, and often almost inaudible. […] Double murmurs may at times be heard in the carotid, subclavian, and femoral arteries, and a short systolic flapping sound is common in the same and even smaller arteries.” - Pg.879-880
* “It is a soft, long drawn out, sometimes almost inaudible murmur beginning with the 2nd sound and replacing the artic closure sound more or less completely. Its point of maximum intensity may be either at the artic cartilage over the left half of the sternum on a level with the 3rd rib or interspace. It is transmitted to the lower end of the sternum, and in some cases is very distinctly audible at the apex.” - Pg. 356
Butler, G. R. (1902). The Diagnostics of internal medicine: a clinical treatise upon the recognised principles of medical diagnosis. New York: Appleton.
Entered by: Erin Choi, 6/15/20
““So long as the hypertrophy compensates for the obstruction the disease is latent.
The earliest symptom of beginning muscular failure are vertigo and faintness, due
to cerebral anaemia with praecordial oppression or anginal pain and palpitation after
exertion. In the later stages the mitral and subsequently the tricuspid valves may
become relatively insufficient because of cardiac dilation, with the usual indirect
evidences of general venous stasis. Embolic phenomena and Cheyne-Stokes respiration
may become manifest. The apex beat is carried to the left and downward, and, unless
hypertrophic emphysema coexists, is strong and forcible. A systolic thrill, often
of marked intensity, is apt to be felt over the aortic area. The area of heart dullness
is increased, provided the oftentimes associated emphysema does not mask it. The aortic
second sound is usually weak, and a systolic murmur (described at page 355)* is heard
over the aortic area. The rather characteristic pulsus tardus is present.” - Pg. 880-881
* “[…] the murmur coincides with the 1st sound, is harsh, accompanied by a thrill,
heard with maximum intensity at the 2nd right interspace or cartilage, transmitted
into the carotids, possible into the axillary artery, and the 2nd aortic sound is
frequently abolished because the valve cusps are too stiff to vibrate and the aortic
pressure is lowered.” - Pg. 355
Butler, G. R. (1902). The Diagnostics of internal medicine: a clinical treatise upon the recognised principles
of medical diagnosis. New York: Appleton.
Entered by: Erin Choi, 6/15/20
Increased Tension - […] A high-tension pulse may exist with very little arterio-sclerosis; but as a rule, when the condition has been persistent, the sclerosis and high tension are found together. […] It may be very difficult to obliterate the pulse, and the firmest pressure on the radial or the temporal may not be sufficient to annihilate the pulse wave beyond the point of pressure. […]
Hypertrophy of the Heart - […] peripheral resistance and increased work of the left ventricle increases in size […]. The apex beat is dislocated in advanced cases an inch or more beyond the nipple line. The impulse is heaving and forcible. The aortic second sound is clear, ringing, and accentuated. […] For years the patient may maintain good health, and be in a condition analogous to a person with a well-compensated valvular lesion. There may be no renal symptoms, or there may be the passage of a larger amount of urine than normal, with transient albuminuria, and now and then hyaline tube-casts. […]
Cardiac - The involvement of the coronary arteries may lead to […] thrombosis with sudden death, fibroid degeneration of the heart, aneurysm of the heart, rupture, and angina pectoris. Angina pectoris is extremely common […]. The patient then presents all the symptoms of cardiac insufficiency - dyspnea, scanty urine, and very often serous effusions.
Cerebral symptoms […] those of many degenerative processes, acute and chronic (which follow sclerosis of the smaller branches), and cerebral hemorrhage, which is usually associated with the miliary aneurysms. Transient hemiplegia, monoplegia, or aphasia may occur in advanced arterio-sclerosis. […]
Renal symptoms supervene in a large number of the cases. […] It is seen in a typical manner in the senile form, and not infrequently develops early in life […]. It is often difficult to decide clinically […] whether the arterial or the renal disease has been the primary.
[…] gangrene of the extremities, due either to endarteritis or to the dislodgement of thrombi. Respiratory symptoms are not uncommon, particularly bronchitis and the symptoms associated with emphysema.
Osler, W. (1892). The Principles and Practice of Medicine. New York: D. Appleton & Company. Pg. 668-669.
Entered by: Ayushi Chintakayala, 6/26/2020
The symptoms of left sided cardiac failure differ from those of the right side [...]. Failure of the left ventricle is seen in its severest forms in the abrupt death stroke of angina pectoris, in the sudden faints with sweats and heart pain of fatty or fibroid hearts, or in the fainting and convulsive attacks of Stokes-Adams disease. Less severe failure may be seen in athletes after a hard race, when vomiting and a feeling of dissolution are present—a type which is sometimes seen in angina, when it is liable to be mistaken for a gastro-intestinal upset. The milder degrees show themselves in an inability to take much exercise or to do much mental work without the sense of great fatigue. Sudden and slow types are also seen in failure of the right side. Subjected to a slight strain, great hyperpnoea and distress may come on, and one form of cardiac dyspnoea which attacks the patient at night is of this nature. The severer forms show an increasing inability to undergo slight extra exertion, such as mounting stairs, or hyperpnoea even when at rest in bed, in both of which there is usually some oedema of the feet, especially at night, if the patient is on his feet most of the clay.
Grouped under their special systems the symptoms complained of by patients with cardiac failure are as follows: (a) Cardio-vascular system: Pain in the cardiac area or extending to the shoulders and down the arms, a sense of weight in the praecordium; palpitation is seldom complained of (b) Respiratory system: Dyspnoea at rest or on exertion, or orthopnoea, Cheyne-Stokes respiration, cough, loss of voice from pressure of a dilated left auricle on the left recurrent laryngeal nerve, hemoptysis (from lung infarcts). (c) Central nervous system; sleeplessness, mental symptoms, delusions, melancholia, and especially toward the end stupor and drowsiness, (d) Cyanosis, pallor, (edema, and occasionally purpura in the lower limbs. (e) Alimentary system: The stasis in the abdominal organs in right heart failure produces loss of appetite, indigestion, flatulence, vomiting, constipation, diarrhea, abdominal pain, hemorrhoids, etc. (f) Renal system: The urine is scanty, high colored, and contains a slight amount of albumin.
Physical examination of the heart may reveal an apex-beat which is feeble, outside the nipple line, diffuse, and whose maximum intensity is not easily localized. The pulsation may be marked on inspection and cover a very wide area; arterial pulsation in the neck in the left heart failure may be great; in right heart failure the jugular veins may be very dilated. On percussion the cardiac area may be much increased to the right or to the left, or both. On auscultation the sounds may be difficult to hear, or feebler than normal; murmurs, usually soft, may be present at both apex and base. Gallop rhythm may be present. The pulse may show great variations [...]. No one sign or combination of signs is significant of cardiac failure. A heart may be insufficient and yet perhaps nothing can be detected by physical examination except feeble sounds and a low tension pulse. The myocardial lesion is not always proportionate to the intensity of the symptom [...]. Shortness of breath on exertion is an early feature in many cases [...].
Osler, W. (1892). The Principles and Practice of Medicine. New York and London: D. Appleton and Company. Pg. 785-786.
Entered by: Sonia Y. Khan, 6/22/2020
The condition may be quite latent. Angina pectoris and a weak, irregular, often slow pulse (50 to 30), are somewhat characteristic; and when the sclerosed heart is slowly failing and dilating, dyspnea, cardiac asthma, palpitation, precordial constriction, and evidences of general venous stasis appear. There may be recurring sometimes fatal, pseudo-apoplectic seizures, which may be preceded by occasional vertigo and syncopal attacks; or true apoplexy may terminate life or cause a hemiplegia. Chronic mania or other form of psychosis may develop. On auscultation, often a systolic murmur at the apex and a galloping rhythm may be heard.
Butler, G. R. (1902). The Diagnostics of internal medicine: A clinical treatise upon the recognised principles of medical diagnosis. New York: Appleton.
Entered by: Bernardo Galvan, 6/28/2020
Symptoms of congenital cardiac disease are usually manifested soon after birth, although
this is not always the case. […] The most striking objective symptom is cyanosis.
Cyanosis maybe slight and noticed only upon exertion, as upon coughing or crying or
it may be intense and constant, giving the skin a dark, leaden color, and the mucous
membrane of the mouth a raspberry hue. […] Cyanosis is of much value in diagnosis,
as it is rarely seen in acquired cardiac disease. The degree of cyanosis and its constancy
are of some importance in determining the gravity of the lesion, although these alone
are not to be depended upon. Another frequent symptom is the enlargement of the terminal
phalanges known as clubbing of the fingers and toes. […] Occasionally there are seen
dyspnoea, oedma of the lower extremities, dropsy of the serous cavities, and haemorrhages,
particularly haemoptysis and epistaxis. […] The murmurs are usually loud, rough, and
often out of proportion to the other signs present. […] In a young child, a very loud
murmur with cyanosis is almost diagnostic of congenital disease.
Holt, L Emmett. The Diseases of Infancy and Childhood: for the Use of Students and Practitioners of
Medicine. Appleton and Co, 1897. Pg. 565-567.
Entered by: Erin Choi, 6/23/2020
Description 1
Simple Acute— The great majority of the cases are latent and there is no indication whatever of cardiac mischief […] The patient, as a rule, does not complain of any pain or cardiac distress. […] Palpitation may be a marked feature […] At first there may be only a slight roughening of the first sound, which may gradually increase to a distinct murmur. The apex systolic bruit is probably more often the result of a myocarditis. It may not be present in the endocarditis of such chronic maladies as tuberculosis and carcinoma, since in them the muscle involvement is less common. Reduplication and accentuation of the pulmonic second sound are frequently present. It is difficult to give a satisfactory clinical picture of malignant endocarditis because the modes of onset are so varied and the symptoms so diverse […] In a majority of the cases there are present certain general features, such as irregular pyrexia, sweating, delirium, and gradual failure of strength. Embolic processes may give special characters, such as delirium, coma, or paralysis from involvement of the brain or its membranes, pain in the side and local peritonitis from infarction of the spleen, bloody urine from implication of the kidneys, impaired vision from retinal haemorrhage and suppuration, and even gangrene in various parts from the distribution of the emboli […] The septic type is met with usually in connection with an external wound, the puerperal process, or an acute necrosis or gonorrhoea. There are rigors, sweats, irregular fever, and all of the signs of septic infection. The heart symptoms may be completely masked by the general condition, and attention called to them only on the occurrence of embolism. In many cases the features are those of a severe septicaemia […] Optic neuritis is not uncommon, and […] recurrent retinal haemorrhages were present. The typhoid type is by far the most common and is characterized by a less irregular temperature, early prostration, delirium, somnolence, and coma, relaxed bowels, sweating, which may be of a most drenching character, petechial and other rashes, and occasionally parotitis. The heart symptoms may be completely overlooked, and in some instances the most careful examination has failed to discover a murmur […] In what may be termed the cerebral group of cases the clinical picture may simulate a meningitis […] The fever is not always of a remittent type, but may be high and continuous. Petechial rashes are very common […] Erythematous rashes are not uncommon. The sweating may be most profuse […] Diarrhea is not necessarily associated with embolic lesions in the intestines. Jaundice has been observed […] The heart symptoms may be entirely latent and are not found unless a careful search be made […] The course is varied, depending largely upon the nature of the primary trouble. Except in the disease grafted upon chronic valvulitis the course is rarely extended beyond five or six weeks.
Subacute Bacterial— Organisms of the Streptococcus viridans group are often found. A special feature is that the patients may become bacteria-free. The prominent features given by Libman are: (1) Marked progressive anemia, (2) brown pigmentation of the face, (3) marked renal disease, (1) marked splenic enlargement and (5) endocarditic symptoms, such as fever, embolism, arthritis and petechiae. The cardiac features may be (1) those of any form of valvular disease and (2) those due largely to embolism. The renal changes are especially in the glomeruli end are often embolic. Renal insufficiency is a common cause of death. The anemia is of the secondary type and usually the leucocytes are normal or diminished. Tenderness over the sternum is a special feature and may be most marked in the bacteria-free stage. The course may be prolonged, the blood may become bacteria-free and some patients recover. In such cases the splenic enlargement may lead to an error in diagnosis.
Chronic Infective— This is almost always engrafted on an old, sometimes an unrecognized, valve lesion. At first fever is the only symptom; in a few cases there have been chills at onset or recurring chills may arouse the suspicion of malaria. The patient may keep at work for months with a daily rise of temperature, or perhaps an occasional sweat, the heart features may be overlooked. The murmur of the old valve lesion may show no change, and even with the most extensive disease of the mitral cusps the heart's action may be little disturbed. For months […] fever and progressive weakness may be the only symptoms […] With involvement of the aortic segments the signs of a progressive lesion are more common. Embolic features are not common, occurring only toward the close. Ephemeral cutaneous nodes, red raised painful spots on the skin of hands or feet and lasting a few days, rarely occur except in this form. Postmortem a remarkable vegetative endocarditis has been found, involving usually the mitral valves, sometimes with much encrusting of the chordae tendineae, and large irregular firm vegetations quite different to those of the ordinary ulcerative form. In some cases, the aortic and tricuspid segments are involved, and the vegetations may extend to the walls of the heart.
Osler, W. (1892). The Principles and Practice of Medicine. New York and London: D. Appleton and Company. Pg. 796-798.
Entered by: Sonia Y. Khan, 6/17/2020
Edited by: Bernardo Galvan, 9/7/2020
Description 2
The only direct evidence of acute endocarditis is the presence of murmurs at one or other orifice of the heart. For practical purposes there are only two murmurs which need to be considered here, viz. a mitral systolic murmur and an aortic diastolic. It is not always easy to tell whether the appearance of a murmur during a febrile attack is due to involvement of the mitral valve in an endocarditic process or to the relaxation of the muscle supporting the orifice. A diastolic aortic murmur is , as a rule, diagnostic of the involvement of the aortic valve in some destructive process. At first this murmur is so faint that one is simply conscious of the fact that the sound does not end with sufficient abruptness. Gradually, however, this passes into a very soft short whiff at the end of the second sound, becoming day by day more marked. In the vast majority of cases the murmurs due to endocarditis are not definitely recognized until sometime after the subsidence of the fever—when the sclerosis sets in. This is particularly the case with presystolic mitral murmurs, which are never recognized during the acute condition that induces the lesion, unless there is narrowing of the mitral orifice on account of vegetations. The formation of vegetations at the mitral and aortic orifices may give rise to murmurs indistinguishable from those due to destruction of the cusps. The presence of a musical murmur may generally be assumed, particularly in acute cases, to be due to a vegetation. An attack of hemiplegia during an acute febrile condition may generally be ascribed to an infarct from a valvular vegetation, and infarcts in any other organ may be assumed to arise from the same cause.
Mackenzie, J., Sir. (1908). Diseases of the Heart. (pp. 219-220). London: Henry Frowde; Hodder & Stoughton.
Created by: Sara Ahmed, 06/16/2021
Entered by: Rachel Johnson, 07/09/2021
In the routine examination of patients we meet occasionally with some, usually middle-aged, sometimes young, who show considerable fluctuations in blood -pressure. Periods of high arterial pressure (hyperpiesis of Clifford Allbutt 58) may be associated with some discomfort, as mental dullness, headache, &c. These periods can be cut short by a smart purge, bodily exercise, &c., or they disappear from no ascertainable cause. It is possible the periods of high arterial pressure are due to faulty metabolism, but they will be found to recur in spite of the greatest care in diet. It is said by some that these periods of high blood -pressure are the cause of arterial degeneration, but, with an imperfect knowledge of all the factors we are not in a position to decide.
Mackenzie, J., Sir. (1908). Diseases of the Heart. (pp. 102). London: Henry Frowde; Hodder & Stoughton.
Created by: Sara Ahmed, 06/16/2021
Entered by: Rachel Johnson, 07/09/2021
As a rule the condition – almost invariably conservative – is subjectively latent until the hypertrophied muscle can no longer respond to the demands upon it and ruptured compensation becomes manifest. The earlier symptoms of well-marked hypertrophy, especially of the left ventricle, consist of an indefinite sense of precordial discomfort or fullness, most marked when lying upon the left side. The sensation is seldom that of pain, and palpitation or a consciousness of the overaction of the heart is usually not perceived except when the patient is neurasthenic or addicted to the overuse of tobacco. There may be a sense of fullness or throbbing in the head, headache, flushing of the face, carotid throbbing, vertigo, tinnitus aurium, flashes of light, exophthalmos, and epistaxis. General arteriosclerosis is a frequent concomitant event, either as a cause or result of the hypertrophy, and broncho-pulmonary or cerebral hemorrhage, due to rupture of the sclerotic smaller vessels by the increased force of the heart may occur.
(1) Physical Signs of Left Ventricular Hypertrophy – The precordium may be prominent, especially in children, and an extensive impulse is visible. On palpation the impulse is characteristically slow, heaving, and forcible (unless a notable degree of dilatation coexists, when it is rather more sudden), and the apex beat is displaced downward, perhaps to the 7th or 8th interspace, and to the left even as much as 3 inches outside of the mammillary line. But in the more common degrees of hypertrophy the apex lies in the 6th space, in or a little outside of the mammillary line. The percussion dullness is increased downward, to the left, and vertically (Fig. 109, p. 356). In simple hypertrophy without valvular lesions there are no murmurs, but the first sound is loud, prolonged, and booming, often with a clicking or murmurish quality; if the dilatation coexists it is shorter and sharper. Aortic closure is accentuated and clear or ringing, and the second sound is often reduplicated, especially in the hypertrophy of the chronic nephritis; if the ventricle is also dilated, or the heart action weak, the second sound is less clear and intense. If the hypertrophy is due to valvular defects there will be the physical signs of the special lesions present. If the hypertrophy is unaccompanied by dilation, the pulse is large, strong, regular, of increased tension, and often not more frequent than normal; if with dilatation, it is softer and as a rule of greater frequency.
(2) Symptoms and Physical Signs of Right Ventricular Hypertrophy – There are no symptoms while compensation is maintained, except moderate dyspnea following unusual muscular exertion; or precordial discomfort, cough, and dyspnea, when the hypertrophy is a sequence of emphysema or chronic interstitial pneumonia. In course of time, when dilatation and relative tricuspid incompetency occur, there will be persistent dyspnea, bronchitis, pulmonary congestion or oedema, cyanosis, hemoptysis, and evidence of systemic venous stasis. The physical signs are (perhaps) an unusual prominence of the lower sternum and the 6th and 7th left cartilages, with a visible somewhat diffuse impulse over the same area, often also in the epigastrium. Unless the chest walls are thick, pulsation is frequently present in the 3rd and 4th interspaces to the right of the sternum, particularly if there is much dilatation. The apex beat is carried to the left usually with but slight downward displacement, and is diffuse, lacking the well-defined thrust of the left ventricular hypertrophy. The cardiac dullness is increased mainly to the right, perhaps an inch or more beyond the sternal margin. The first sound over the tricuspid area is louder than usual, and on account of the increased tension in the pulmonary artery the pulmonary second is accentuated, and reduplication of the second sound may occur. The radial pulse is of small volume, and if dilatation is present may be frequent and arrhythmic.
(3) Signs of Auricular Hypertrophy – The physical signs of hypertrophy, always combined with dilatation, of the left auricle, are few and indefinite. There may be dullness to the left of the sternum in the 3rd or 2nd interspaces, with a presystolic impulse or wave in the 2nd space. The presence of left auricular enlargement may always be inferred if the presystolic murmur of mitral stenosis is heard, or if mitral incompetency exists.
Hypertrophy, never without dilatation, of the right auricle is secondary to incompetency or stenosis of the tricuspid valve with associated right ventricular hypertrophy and dilatation. There is dullness in the 3rd and 4th interspaces to the right of the sternum, often with a presystolic wavy pulsation in the same area, systolic jugular pulsation, and evidences of general venous engorgement.
Butler, G. R. (1901/1909). The Diagnostics of Internal Medicine A Clinical Treatise Upon the Recognised Principles of Medical Diagnosis, Prepared for the Use of Students and Practitioners of Medicine (3rd ed., pp. 971-973).
Created by: Taha Jilani, 06/14/2021
Entered by: Rachel Johnson, 10/05/2021
During development of the lesion, unless the insufficiency comes on acutely in consequence of rupture of the valve segment or of ulceration, the compensatory changes go hand in hand with the defect, and there are no subjective symptoms. So, also, in the stage of perfect compensation, there may be the most extreme grade of mitral insufficiency with enormous hypertrophy, yet the patient may not be aware of the existence of heart trouble, and may suffer no inconvenience except perhaps a little shortness of breath on exertion. It is only when the compensation has not been perfectly effected, or, having been so, is broken that the patients begin to be troubled. The symptoms are dived into two groups:
(a) The minor manifestations while compensation is still good. Patients with extreme insufficiency often have a congested appearance of the face, the lips and ears have a bluish ting, and the venules on the cheeks may be enlarged – signs in many cases very suggestive. In long standing cases, particularly in children, the fingers may be clubbed, and there is shortness of breath on exertion. This is one of the most constant features and may exists for years, even when the compensation is perfect. Owing to the congested condition of the lungs these patients are liable to attacks of bronchitis or hemoptysis. There may also be palpitation. As a rule, however, in well balanced lesions in adults, this period of full compensation is not associated with symptoms which call the attention to an affection of the heart, and with care the patient may reach old age in comparative comfort without being compelled to curtail seriously his pleasures or his work.
(b) Sooner or later comes a period of broken compensation, in which the most intense symptoms are those of venous engorgement. There are palpitations, weak, irregular action of the heart, and signs of fibrillation. Dyspnea is an especial feature, and there may be cough. A distressing symptom is the cardiac “sleep-start,” in which, just as the patient falls asleep, he wakes gasping and feeling as if the heart were stopping. There is usually slight cyanosis, and even slight jaundice. The most marked symptoms are those of venous stasis. The overfilling of the pulmonary vessels accounts in part for the dyspnea. There is cough, often with bloody or watery expectoration, and the alveolar epithelium containing brown pigment-grains is abundant. Edema usually sets in, beginning in the feet and extending to the body and the serous sacs. Right sided hydrothorax may recur and require repeated tapping. The urine is usually scanty and albuminous, and contains casts and sometimes blood cells. With judicious treatment compensation may be restored and all the serious symptoms pass away. Patients usually have recurring attacks of this kind, and die with a general dropsy; or there is progressive dilatation of the heart. Sudden death in these cases is rare. Some cases of mitral disease – stenosis and insufficiency – reach what may be called the hepatic stage, when all the symptoms are due to the secondary changes in the liver.
In children the precordia may bulge and there may be a large area of visible pulsation. The apex beat is to the left of the nipple, in some cases in the sixth interspace, in the anterior axillary line. There may be a wavy impulse in the cervical veins, which are often full, particularly when the patient is recumbent. The force of the impulse depends largely upon the stage. In full compensation it is forcible and heaving; when the compensation is disturbed, usually wavy and feeble. The dullness is increased, particularly in a lateral direction. […] It does not extend so much upward along the left margin of the sternum as beyond the right margin and to the left of the nipple line. At the apex there is a systolic murmur which wholly or partly obliterates the first sound. It is loudest here, and has a blowing, sometimes muscular character, particularly toward the latter part. It is transmitted to the axilla and may be heard at the back, in some instances over the entire chest. There are cases in which, as pointed out by Naunyn, the murmur is heard best along the left border of the sternum. Usually at the apex the loudly transmitted second sound may be heard. Occasionally there is also a soft, sometimes a rough or rumbling presystolic murmur. As a rule, in cases of extreme mitral insufficiency from valvular lesion with great hypertrophy of both ventricles, there is heard only a loud blowing murmur during systole. A murmur of mitral insufficiency may vary a great deal, according to the position of the patient. An important sign is the accentuated pulmonary second sound. The pulse, during the period of full compensation, may be full and regular, often of low tension. With the first onset of symptoms it may become irregular, a feature which then dominates the case throughout. Often after the disappearance of the symptoms of failure of compensation the irregularity persists. This usually due to auricular fibrillation.
The three important physical signs of mitral regurgitation are: (a) Systolic murmur of maximum intensity at the apex, propagated to the axilla and heard at the angle of the scapula; (b) accentuation of the pulmonary second sound; (c) evidence of enlargement of the heart, particularly increase in the transverse diameter, due to hypertrophy of both ventricles.
Osler, W. & McCrae T. (1892/1925). The Principles and Practice of Medicine: Designed for the Use of Practitioners and Students of Medicine (10th ed, pp. 834-835). New York: D. Appleton & Company.
Created by: Taha Jilani, 06/14/2021
Entered by: Rachel Johnson, 10/05/2021
Stenosis of the mitral valve may for years be efficiently compensated by the hypertrophy of the right ventricle. Many persons with this lesion present no symptoms. They may for years be short of breath on going upstairs, but carry on ordinary activity without discomfort. The pulse is smaller in volume than normal, and very often irregular (auricular fibrillation). A special danger is the recurring endocarditis. Vegetations may be whipped off into the circulation and, blocking a cerebral vessel, cause hemiplegia or aphasia, or both. This is not an uncommon sequence in women.
[…] There is often a flush on the cheeks, and clubbing of the fingers is common. The lower sternum and the fifth and sixth left costal cartilages are often prominent, owing to hypertrophy of the right ventricle. The apex beat may be ill defined. Usually it is not far beyond the nipple line, and the chief impulse is over the lower sternum and adjacent costal cartilages. Often in thin chested persons there is pulsation in the third and fourth interspaces close to the sternum. When compensation fails, the impulse is much feebler, and in the veins of the neck there may be marked pulsation or the right jugular near the clavicle may stand out as a prominent tumor. In the later stage there is great enlargement with pulsation of the liver. Palpation reveals in a majority of the cases a characteristic, well defined thrill, which is best felt, as a rule, at the apex or a little inside it. It is of a rough, grating quality, often peculiarly limited in area, most marked during expiration, and terminates in a sharp, sudden shock, synchronous with the impulse. This most characteristic of physical signs is pathognomonic of narrowing of the mitral orifice, and is perhaps the only instance in which the diagnosis of a valvular lesion can be made by palpation alone. It is often variable and may be brought out by exercise. The cardiac impulse is felt most forcibly over the lower sternum and in the fourth and fifth left interspaces. The impulse if felt in the third and fourth interspaces, or in a rare cases even in the second, and it has been thought that here it is due to pulsation of the auricle. It is always the impulse of the conus arteriosus of the right ventricle; even in the most extreme grades of mitral stenosis there is never such tilting forward of the auricle as would enable it to produce an impression on the chest wall. Percussion gives an increase in dullness to the right of the sternum and along the left margin; not usually a great increase beyond the nipple line, except in extreme cases. There may be dullness in the left interscapular region.
The findings are varied and puzzling combination of sounds and murmurs may be heard. At the apex or a little inside it, often in a very limited region, there is heard a rough, vibratory or purring murmur, cumulative or crescendo in character, often of short duration, which terminates abruptly in the loud snapping first sound. This murmur is synchronous with thrill and the loud shock with the first sound. The murmur may occupy the entire period of diastole, or the middle or only the latter half. A difference can often be noted between the earlier and later parts of the murmur, when it occupies the entire time. In some cases a soft diastolic murmur is heard after the second sound at the apex. This may increase and merge into the presystolic murmur. Often there is a peculiar rumbling or echoic quality, which in some instances is heard only over a single bell-space of the stethoscope. […] A systolic murmur may be heard at the apex or along the left sternal border, often of extreme softness an audible only when the breath is held. Sometimes the systolic murmur is loud and distinct and is transmitted to the axilla. The second sound in the second left interspace is loudly accentuated, and often reduplicated. It may be transmitted far to the left and be heard with great clearness beyond the apex. With good compensation the second sound is heard at the apex; its disappearance suggests the approach of decompensation. […] These signs of characteristic only of the stage in which compensation is maintained. The murmur may be soft, almost inaudible, and only brought out of exertion. Finally there comes a period in which, with the establishment of auricular fibrillation, the signs change. Thus a presystolic murmur may disappear as there is not the usual difference in pressure in the auricle and ventricle at the time when the auricle should be contracting. With the auricle paralyzed the murmur is more likely to be heard early in diastole. Difference in rate may cause marked changes in the time and character of the murmur. Sometimes in the apex region a sharp first sound or gallop rhythm may be heard. The systolic shock may be present after the disappearance of the thrill and the characteristic murmur. […] Pressure of the enlarged auricle on the left recurrent laryngeal nerve, causing paralysis of the vocal cord on the corresponding side, has been described and the diagnosis of aneurism of the arch of the aorta may be made.
Osler, W. & McCrae T. (1892/1925). The Principles and Practice of Medicine: Designed for the Use of Practitioners and Students of Medicine (10th ed, pp. 837-839). New York: D. Appleton & Company.
Created by: Taha Jilani, 06/16/2021
Entered by: Rachel Johnson, 10/05/2021
[...] applied to a sudden increase in the heart's rate, usually followed by an equally sudden reversion to the normal. It is due to the starting of the heart's contraction at some part other than the normal. The most common form is really a transient nodal rhythm. There is also a rarer form, where the stimulus arises in the auricle. I therefore restrict the term to the increased frequency of the heart's action due to the temporary inception of an abnormal rhythm.
Mackenzie, J., Sir. (1908). Diseases of the Heart. (pp. xix). London: Henry Frowde; Hodder & Stoughton.
Created by: Sara Ahmed, 06/16/2021
Entered by: Rachel Johnson, 07/09/2021
Description 1
Occasionally there may be heard, particularly if the inflammation is anterior, a pleuritic friction sound which is increased with the systole of the heart. The pulse may be weak during inspiration, and there may be an increased area of cardiac dullness. […] It may produce oedema of the face or the lower extremities, ascites, enlargement of the liver and spleen, but rarely albuminuria. […] The symptoms are few, and many of them are equivocal. As this disease is nearly always secondary, the physician should be on their watch for it in infants with pleurisy or pleuro-pneumonia on the left side, and in older children in the course of articular rheumatism.
Localized pain and tenderness may be present, and also a certain amount of embarrassment of the heart’s action, usually manifested by praecordial distress, palpitation, and slight irregularity of the pulse. There may be dyspnoea, and if there is a large effusion present there may be orthopnoea and cyanosis. Sometimes there is delirium. […] The physical signs in older children resemble those in adults. In dry pericarditis there is usually heard a double friction sound of the praecordial space, the area being generally small and near the base of the heart. The sound is not transmitted, and bears no relation to the respiratory movements. After effusion has taken place the apex beat may be displaced upward, diffused, and somewhat indistinct, or it may not be found at all. There may be bulging of the chest wall.
On palpitation, there is an absence of vocal fremitus over an area usually occupied by the lung. Percussion gives an area of marked dullness or flatness or triangular shape, the base being below and the apex above. The normal area of the cardiac dullness is increased in all directions, and this dullness extends beyond the limits of the heart. On auscultation, the heart sounds are feeble and distant. Friction sounds disappear as serum is poured out, and reappear as it is absorbed. Endocardial murmurs may also be present.
Holt, L Emmett. The Diseases of Infancy and Childhood: for the Use of Students and Practitioners of Medicine. Appleton and Co, 1897. Pg. 571-572.
Entered by: Erin Choi, 6/24/2020
Description 2
Until the introduction of auscultation, dry pericarditis was a disease only discovered on the post -mortem table. The only evidence we have of its presence is the characteristic superficial to - and -fro murmur produced by the movements of the heart. Its discovery is usually accidental, and made when the heart is examined as a matter of routine. There is no other distinctive sign associated with it, and, in marked contrast to dry pleurisy, it is essentially a painless complaint. When pains are associated with its presence it will invariably be found that there is evidence of a myocardial affection. This curious painlessness of pericarditis compared with pleurisy is one that has long puzzled me, and I have only a dim perception of how it may arise. I merely call attention to this fact in passing. Pericarditis may arise in the course of a number of chronic complaints, as in diabetes and Bright's disease, or in the course of an acute disease, as pneumonia or rheumatic fever. Sometimes one comes across it quite accidentally — the patient, not feeling quite well, consults his doctor, and in the course of an examination this is detected. Such patients may go quietly about their occupation for many weeks with a well -marked to -and - fro murmur, and suffer no further trouble. When effusion takes place into the pericardial sac there is an increase in the area of the cardiac dullness, which assumes a somewhat characteristic shape. It reaches up to or above the second rib, and if the area be mapped out it will have a somewhat pear -shaped character. There is an absence of the heart's movements at the lower point to the left, and this should always arouse the suspicion of effusion where there is an increase in the heart's dullness. Ewart describes a small area of dullness behind at the base of the left lung. This is important to remember, for an increase in the size of this area may cause an extensive pericardial effusion to simulate fluid in the pleural cavity. I have tapped a pericardial purulent effusion in mistake for an empyema, and my mistake arose from not ascertaining the position of the heart's movements. Had the case been one of pleural effusion, I should have found the heart beating to the right of the sternum; but the whole left chest was dull, so that the idea of it being pericardial never crossed my mind. The question of pericardial effusion embarrassing the work of the heart has arisen on account of the results of experimentally distending the sac with fluid. I have never found any very serious embarrassment of the heart from extensive pericardial effusion, the reason being probably that while the normal pericardium is a more or less inelastic bag, with the inflammatory invasion it becomes distensile, and therefore able to accommodate an enormous amount of fluid with little embarrassment to the heart.
Mackenzie, J., Sir. (1908). Diseases of the Heart. (pp. 220-221). London: Henry Frowde; Hodder & Stoughton.
Created by: Sara Ahmed, 06/16/2021
Entered by: Rachel Johnson, 07/09/2021
Symptoms similar to those which present themselves in the beginning of a retrobulbar phlegmon accompany thrombosis of the cavernous sinus. The lids and the conjunctiva swell up with oedema, and the eyeball protrudes and becomes difficult to move. The veins of the retina are seen, upon ophthalmoscopic examination, to be distended enormously. At the same time there is doughy oedema in the mastoid region. These symptoms are referable to the fact that the veins of the orbit discharge the greater part of their blood through the ophthalmic veins into the cavernous sinus; hence thrombosis of the latter produces stasis in the veins of the orbit, and especially if the thrombotic process is continued on from the sinus into these veins. The stasis leads to protrusion of the eyeball and also to venous hyperemia of the retina. The oedema of the mastoid region depends upon the fact that in this region an emissary vein of Santorini (the emissarium mastoideum) empties into the transverse sinus, and hence when the thrombosis is carried along from the cavernous to the transverse sinus, the mastoid region also shares in the venous stasis. When this oedema is present (which, to be sure, is not always the case), it forms an important diagnostic sign between sinus thrombosis and retrobulbar phlegmon in which latter it is absent. A further difference is that sinus thrombosis frequently passes over to the other side, so that the same complex of symptoms develops there also, while, on the contrary, a bilateral orbital cellulitis would be one of the greatest rarities. Finally, sinus thrombosis is associated with a very severe cerebral symptoms, terminated at last by the onset of the fatal issue.
Fuchs, E. & Duane, A. (1889/1919). Text-book of Opthamology: Authorized Translation from the Twelfth German Edition (6th ed., pp. 812-813). Philadelphia: J. B. Lippincott Company.
Created by: Taha Jilani, 06/14/2021
Entered by: Rachel Johnson, 10/04/2021
[…] It is met with in conditions of the lungs which cause obstruction to the circulation such as fibrosis and emphysema, particularly with chronic bronchitis. The symptoms are those of obstruction in the lesser circulation with venous congestion in the systemic veins. The signs are:
(a) Systolic regurgitation of the blood into the right auricle and the transmission of the pulse wave into the veins of the neck. If the regurgitation is slight or the contraction of the ventricle is feeble there may be no venous throbbing, but in other cases there is marked systolic pulsation in the cervical veins, both in the internal and external vein, particularly in the latter. Marked pulsation in these veins occurs only when the valves guarding them become incompetent. Slight oscillations are not uncommon, even when the valves are intact. The distention is sometimes enormous, particularly in the act of coughing, when the right jugular at the root of the neck may stand out, forming an extraordinarily prominent ovoid mass. Occasionally the regurgitant pulse wave may be widely transmitted and be seen in the subclavian and axillary veins, and even in the subcutaneous veins over the shoulder, or in the superficial mammary veins. The regurgitant pulsation may be transmitted to the inferior cava, and so to the hepatic veins, causing pulsation of the liver. This is best appreciated by bimanual palpation. The pulsation may be readily distinguished, as a rule, from the impulse from the ventricle or transmitted from the aorta.
(b) the second important sign is the occurrence of systolic murmur of maximum intensity over the lower sternum. It is usually a soft, low murmur, often distinguished from a coexisting mitral murmur by differences in quality and pitch, and may be heard to the right as far as the axilla. Sometimes it is very limited in its distribution. In addition, the percussion usually shows increase in dullness to the right of the sternum, and the impulse in the lower sternal region is forcible. In the great majority of cases the symptoms are those of associated lesions. In fibrosis of the lung and chronic emphysema the failure of the right ventricle with tricuspid insufficiency may lead to gradual failure with cardiac dropsy.
Osler, W. & McCrae T. (1892/1925). The Principles and Practice of Medicine: Designed for the Use of Practitioners and Students of Medicine (10th ed, pp. 839-840). New York: D. Appleton & Company.
Created by: Taha Jilani, 06/14/2021
Entered by: Rachel Johnson, 10/04/2021
The diagnosis if not often made; extreme cyanosis and dyspnea are common, and toward the end the ordinary signs of cardiac failure. Among the important physical signs are presystolic pulsation in the jugular veins and in the enlarged liver. A presystolic thrill may be felt at the tricuspid area with marked systolic shock. The cardiac dullness is increased to the right, a rumbling presystolic murmur may be present over the lower sternum with an extension the right border.
Osler, W. & McCrae T. (1892/1925). The Principles and Practice of Medicine: Designed for the Use of Practitioners and Students of Medicine (10th ed, pp. 840). New York: D. Appleton & Company.
Created by: Taha Jilani, 06/14/2021
Entered by: Rachel Johnson, 10/04/2021
Gouty irritation indubitably aggravates varix, and may, therefore it has been supposed, generate it. Chronic hyperemia of the capillaries is one of the causes of dilatation [...]. Excessive stimulation of a part or organ, [...] enlargement of the spermatic, scrotal, vesical, and hemorrhoidal veins comes under this category. [...] “The dilatation of the veins” says Mr. Hodgson, “is frequently attended by excruciating pain, and sometimes with inflammation of the skin [...] superficial veins are greatly exposed to contusion [...].” [...] varicose enlargement of the branches of both saphenae, below the knee and across the patella, in numerous instances to blows and wounds; several to lesions accompanying fracture of the bones of the leg, or dislocation of the ancle; and not a few to the extension of inflammation from a patch of erythema or eczema, or from an ulcer in close proximity to the vein affected.Many patients [...] refer the commencement of dilatation to repeated attacks of cramp; [...] exposure to cold, too by exciting chronic phlebitis, is most assuredly often productive of varix. [...] may occur directly as an effect of rheumatic inflammation of the external coat of the veins; or secondarily, as a consequence of obstructive phlebitis. [...]
Secondly, varix may originate, consecutively in causes altogether extraneous [..] to the vein itself. Dilatation of the veins of the leg and thigh from the pressure of the gravid uterus upon the iliac veins during pregnancy. The same effect is caused by the presence of tumours of any kind impeding the circulation. [...] It may likewise occur as a result of accumulations in the large intestines in persons of a constipated habit [...]; and may further be produced by tight lacing in women, and in men by wearing riding belts buckled too tightly. [...] “The veins become elongated and their course very tortuous. Their canal is wide and narrow by turns; now simply deviating, now throwing out pouch-like appendices, until the whole vessel has assumed an unwonted aspect, reminding us at one moment of the seminal vesicles, at another of the convolutions of the intestines.” [...] Without first bandaging his legs, the sense of distension becomes so acutely painful that he is totally unable to stand. [...] pain endured, especially at night, [...] with inflammation of the skin, accompanied by extreme irritation and itching. In this state the slightest abrasion, - a mere scratch, it may be, during sleep, - at all times difficult to heal on the leg, is sure to degenerate into a chronic ulcer, which may cripple the exertions of the patient for months or even for years. [...] congestion of the integuments predisposes to various cutaneous disorders [...] risk of serious hemorrhage from a slight wound of veins [...].
Chapman, H.T. (1864) Varicose Veins: Their Nature, Consequences, and Treatment, Palliative and Curative. John Churchill. Pg. 13-33.
Entered by: Ayushi Chintakayala, 7/2/2020