Henry D. McIntosh

P-Wave Analysis in Valvular Heart Disease

Electrocardiographic analysis of the P waves occurring in a series of 113 normal subjects and 100 patients with specifically defined valvular lesions are reviewed. The former methods of analysis showed a marked lack of specificity. By dividing the P wave in lead V1 into initial and terminal portions, a measure designated as the P terminal force has been derived. This measure is of value in two respects: (1) it correctly separates normal subjects from those patients with left-sided valvular lesions in 92 per cent of this series and (2) once a given valve lesion is suspected clinically, this measure enables one to make an estimation of the severity of that lesion from the degree of abnormality of the P terminal force at V1. The P terminal force does not indicate the type of valvular disease present, nor does it correlate with any one specific hemodynamic measure. The abnormality does appear to be related, within each separate type of valve disease, to the specific hemodynamic abnormality of that type of val...

Vasodepressor Syncope Factors Influencing Cardiac Output

Vasodepressor syncope is characterized hemodynamically by a sudden fall in total peripheral resistance with little associated change in cardiac output. The failure of the cardiac output to compensate for the fall in peripheral resistance is a striking feature of the fainting reaction. Possible explanations for this phenomenon are the presence of neurogenic myocardial inhibition or markedly limited volume of blood available to the heart. The effects of atropine injections, inflation of antigravity suit, negative pressure breathing, and albumin infusions on the syncopal reaction were studied. Results favor the causative role of limited venous inflow in the cardiac output response.

Reflex Venomotor Activity in Normal Persons and in Patients with Postural Hypotension

Reflex venomotor activity has been observed and measured in normal subjects by means of the pressures developed within isolated segments of superficial veins. Strong contractions are caused by the Valsalva maneuver, tilting, cold, exercise, and hyperventilation. After the Valsalva and after tilting there is a brief elevation of central venous pressure. Pulmonary vascular pressures are also increased after the Valsalva. This is taken to indicate a widespread venoconstriction with central shifting of blood. Persons with postural hypotension show little or no segment or central venous pressure response to these stimuli, indicating impaired reflex venomotor activity.

Assessment of regional myocardial performance from biplane coronary cineangiograms

Abstract Bifurcations of coronary arteries provide a myriad of natural landmarks on the epicardial surface. With biplane coronary cineangiograms, these bifurcations can be located in space and followed in time. By calculating the spatial distances between bifurcations on successive cine frames, multiple epicardial segment lengths and their dynamic changes during the cardiac cycle can be determined. In 5 animals with epicardial metal markers sutured near the coronary bifurcations, epicardial segment lengths measured from opacified bifurcations correlated closely with those obtained from metal markers (SEE = 2.2%). Epicardial segment lengths were not affected by intracoronary injection of contrast medium in the first 5 to 6 cardiac cycles. Biplane coronary Cineangiograms of 11 patients were analyzed. Measurements of individual segment lengths yielded reproducible curves reflecting various phases of ventricular contraction and filling. These curves allowed quantitation and simultaneous comparison of the onset, duration, extent and rate of segment shortening in multiple and selected areas of the heart. In 5 patients, the extent of shorteing was 1 to 19 percent along the septum, 17 to 27 percent on the free wall and 10 to 15 percent at the base of the left ventricle. Mechanical activation of the left ventricle began from the antereoseptal area at the apex and progressed toward the base and the posterior surface. In 5 of 6 patients with coronary artery disease, localized abnormalities of contraction were found in areas of previous myocardial infarction or at regions supplied by the stenotic arteries. The diseased segments showed either systolic lengthening or marked reduction in rate and extent of shortening. The onset of shortening was frequently delayed. In addition to defining the anatomic details of the coronary circulation, biplane coronary cineangiograms provide a wealth of physiologic information regarding the dynamic changes in geometry, dimensions and movements of the heart. As the first step to utilizing this physiologic information, this study has demonstrated the validity, feasibility and clinical usefulness of this technique in assessing regional myocardial performance in man.

Experience with “cardioversion” of atrial fibrillation and flutter

Abstract Synchronized direct current countershock, “cardioversion,” was used in 70 patients on 94 occasions for reversion of atrial fibrillation or flutter. The method and anesthetic technics are described. A modification of the size and location of the electrode has decreased the incidence of minor discomfort resulting from the procedure and lowered the amount of energy necessary for successful cardioversion. In 90 of 94 episodes, or in 66 of 70 patients, the arrhythmia was restored to sinus rhythm. With a follow-up period of from 1 to 9 months, 52 of 66 patients (79%) remained in sinus rhythm. Fourteen patients (21%) reverted to atrial fibrillation despite multiple cardioversions and maximally tolerated quinidine therapy. Certain factors appear to decrease the chances of maintaining sinus rhythm: duration of fibrillation, type of valvular lesion, functional classification and previous quinidine failure. The advantages anticipated with the restoration of sinus rhythm are discussed. The emergency indication and contraindications are outlined. A broad policy of selection of patients for cardioversion is suggested. The reasons for this approach are the high degree of acute success (94%), the low incidence of complications (5%) and success in maintaining sinus rhythm (79%) for a short follow-up Period.

The Effect of Hypocapnia on Arterial Blood Pressure

In man, hypocapnia induced by hyperventilation causes a drop in arterial pressure. The calculated peripheral resistance is decreased, indicating a net vasodilatation. The forearm blood flow is markedly increased, and the vascular resistance of the forearm is much reduced. Persons with impaired function of the sympathetic nervous system continue to show these effects. The increase in forearm flow is not prevented by brachial block. These results suggest that hypocapnia acts directly on blood vessels to produce a net over-all vasodilatation and fall in blood pressure, and that this effect is not mediated through the nervous system, as usually supposed.

Cardiovascular and blood gas responses to hyperbaric oxygenation

Abstract Ten normal subjects were studied while they breathed air and 100% oxygen at 1 and 3.04 atmospheres. Oxygen inhalation at 3.04 atmospheres was associated with a significant increase in arterial and venous pO 2 and O 2 content. Hemoglobin in the venous circulation was completely saturated in 8 of 10 subjects. Oxygen inhalation at 3.04 atmospheres produced a small but significant increase in venous pCO 2 , presumably due to the loss of the buffering effect of reduced hemoglobin. Heart rate and cardiac output fell significantly with little change in stroke volume during oxygen inhalation at 3.04 atmospheres, indicating that the decrease in cardiac output was rate-dependent. There was little change in mean arterial pressure but an increase in calculated peripheral resistance during oxygen inhalation at 3.04 atmospheres. Two subjects who demonstrated signs of acute oxygen intoxication did not differ significantly from the group as a whole either in terms of blood gas values or patterns of hemodynamic response.

Hereditary nephropathy, deafness and renal foam cells

Abstract A family with hereditary nephropathy and deafness is described. Postmortem examination of one member of the family revealed changes compatible with chronic glomerulonephritis. Large numbers of foam cells were noted in the cortex of the kidneys. The staining characteristics of these cells suggest that they contain neutral fat, mucopolysaccharides, phospholipids, cholesterol and phosphatides. Foam cells may be seen in a variety of renal lesions. A review of the records of 105 consecutive autopsy cases of chronic glomerulonephritis led to the discovery of foam cells in nine patients. Two had hereditary nephropathy and deafness; one had hereditary nephropathy alone; two had a questionable family history of renal disease; three gave no family history of renal disease; and one was thought to be an example of arabinosis. A review of the records of 105 consecutive autopsy cases of pyelonephritis uncovered six patients with renal foam cells. Only one of these had a family history of renal disease. Among this group were patients with xanthogranulomatous pyelonephritis, the de Toni-Fanconi syndrome with cystinosis, and Wegeners granulomatosis with renal abscesses. Although renal foam cells thus are not limited to cases of hereditary nephropathy, their presence should lead to a vigorous search for a family history of renal disease. The basic pathological picture in hereditary nephropathy with deafness is probably quite similar to that of chronic glomerulonephritis, but pyelonephritis may frequently be superimposed. At present there is no explanation for the pathogenesis of hereditary nephropathy or renal foam cell formation.

The mechanism of cough syncope.

Abstract Although described in 1876 by Charcot, 1 the syndrome of cough syncope has until recently been considered a rare form of fainting. However, the excellent reports by Baker, 2 Sharpey-Schafer, 3 and Kerr and Derbes, 4 indicate that the condition may not be uncommon. Despite increasing recognition of the syndrome, the mechanism producing the syncope remains elusive. 4 Earlier investigators have suggested that this form of syncope is an epileptic equivalent 5–7 or the result of a laryngeal reflex. 6,8 These theories, however, have generally been abandoned in favor of a circulatory mechanism producing cerebral anoxia. 9 It has been suggested that the cerebral anoxia might be the result of marked reflex peripheral vasodilation 3 or a decreased cardiac output secondary to a reduced inflow or marked pulmonary vasoconstriction. 10 These theories, though attractive, fail to explain completely certain unique features of this form of syncope. For example, syncope may develop with remarkable rapidity (3 to 5 seconds) after the onset of cough. With the cessation of cough, consciousness is rapidly recovered without vasomotor or other sequelae. The syndrome is rarely observed in women and syncope may occur in the supine or standing subject. The present report, based on observations made on normal individuals and patients with cough syncope, suggests a more acceptable mechanism for this type of fainting.

Demonstration of the dynamic nature of idiopathic hypertrophic subaortic stenosis.

Abstract Isoproterenol infusion converted a patient with potential hypertrophic subaortic stenosis into one with all the hemodynamic features of severe hypertrophic subaortic stenosis in less than 15 minutes. This response was not observed during isoproterenol infusion in 15 patients with left ventricular hypertrophy from a variety of causes. Further study of this drug in patients with left ventricular hypertrophy of unknown etiology is indicated. Infusion of isoproterenol may serve as a provocative test to identify those patients with early or latent forms of hypertrophic subaortic stenosis. Such studies will also allow a more careful examination of the hemodynamic features of the syndrome before the signs and symptoms have become so severe as to preclude extensive investigation.