Amyl Nitrite Inhalation Research Articles

Echocardiography in coexisting hypertrophic subaortic stenosis and fixed left ventricular outflow obstruction.

Echocardiographic study was done on four pediatric patients with coexisting hypertrophic subaortic stenosis (HSS) and fixed left ventricular outflow (LVO) obstruction. One had valvar aortic stenosis, two had discrete subaortic stenosis and one had coarctation of the aorta. Preoperatively, HSS was not suspected in any of these patients because of the classical findings of fixed LVO obstruction. The echocardiographic examination revealed an abnormal systolic anterior movement (SAM) of the anterior mitral leaflet with ventricular septal hypertrophy in all, but these findings were overlooked or thought to be related to a subvalvar diaphragm. One or two years after the surgical removal of their fixed obstruction, all showed clinical pictures of HSS. Postoperative echocardiographic examination showed an abnormal SAM with asymmetrical septal hypertrophy, and cardiac catheterization revealed mild to severe degrees of resting pressure gradients across LVO tracts. Amyl nitrite inhalation produced a more prominent SAM with increasing pressure gradient, and angiotensin infusion abolished the SAM and reduced the pressure gradient. From our present study, echocardiography has the potential for identification of HSS coexisting with a fixed LVO obstruction. We recommend that all patients with LVO obstruction have an echocardiographic examination along with pharmacological testing. The demonstration of an unusually thickened ventricular septum and especially, abnormal SAM of the mitral valve would require careful evaluation of left heart hemodynamics and the determination of the level of the major obstruction during cardiac catheterization for pre and postoperative management.

Amyl nitrite test using double microphones for differentiation of systolic murmurs in the elderly.

The effects of amyl nitrite on systolic murmurs and hemodynamic alterations in the elderly have been studied with amyl nitrite test using 2 phonocardiographic amplifier channels and 2 microphones of the same frequency response. From the simultaneous recording at the aortic and apical region, the alteration of the amplitude of systolic murmurs in both areas after inhalation of amyl nitrite was checked. In Germany, we named this method with 2 microphones as Doppel Amyl-nitrit Versuch.Mechanocardiographically the time intervals such as HR, Q-I, Q-IIi, ET, ETi, PEPi were checked. The following observations were made: Alterations of systolic heart murmurs were divided in 4 different groups, namely, (1) increased murmurs in both regions, the apex and base (group I), (2) decreased murmurs in both areas (group II), (3) increased murmurs at aortic area and decreased murmurs at the apex (group III), (4) others: i.e. increased murmurs only at the apex, and decreased murmurs only at the apex or base (group IV).The results support the opinion that the effects of amyl nitrite in the elderly is not as conspicuous as in children. Amyl nitrite test using double microphones may be useful to differentiate the origin of some murmurs as the Gallavardin phenomenon.The Gallavardin phenomenon is the more common in the older patients. Furthermore, apical murmurs may also be conducted often to the base of the heart, especially when the left ventricle and ascending aorta are dilated (anti-Gallavardin mechanism). Under some conditions the systolic murmur of mitral incompetence may have its maximum intensity at fourth or third left ICS.

Charge Ballistocardiogram Through Amyl Nitrite and/or Methoxamine

The ballistocardiogram (BCG) or finger plethysmogram (FPG) is one of the bloodless examination methods related to cardiovascular dynamics. The effects of amyl nitrite and methoxamine on BCG, FPG and ECG (electrocardiogram) were studied in order to find out the mechanisms constructing ballistocardiographic waves. Materials and Methods: Seventy healthy persons without cardio-pulmonary diseases were divided into 2 groups: Group I, consisting of 40 young persons less than 35 years of age; and Group 2, consisting of 30 older persons over 50 years of age. The longitudinal BCG through von Wittern's sublow-frequency table, FPG and ECG w, ere recorded simultaneously while holding the breath, before 0.25 ml amyl nitrite inhalation for 15 seconds, and 15, 30, 45, 60 and 90 seconds after the beginning of the inhalation. In 10 minutes after the inhalation, the BCG, FPG and ECG returned to their original levels. Then they were recorded again before the 25-second intravenous injection of 0.08 mg/Kg methoxamine and 30 seconds, 1, 2, 3 and 5 minutes after the beginning of the injection. The effects of the agents were controlled by FPG and ECG. Twenty items (14 items in the longitudinal BCG, 5 items in the FPG and one item in the ECG) were selected from the findings of the records obtained. These items were measured and calculated for the study. The heights of H, I, J, K and N, the amplitudes of HI, IJ, JK and LM, the amplitude ratios of HI/IJ, JK/IJ and LM/IJ, and the times of Q-J and Q-N were measured as usual in longitudinal BCG. Q-J time meant the time from the beginning of the Q wave in the ECG to the tip of J wave in BCG. Q-N time had similar meaning. The tip of the FPG wave was named "B", the incisura named "C", the starting point of the FPG wave on the base line named "S", the amplitude of the wave named "b", and the height of the incisura named "c". The "c/b" was called incisura ratio. "b", "c", "c/b", "SB time" and "SC time" were measured and calculated. R-R time only was measured in ECG.

Measurement of phasic aortocoronary bypass graft blood flow velocity in conscious man

Phasic instantaneous aortocoronary bypass graft blood flow velocity was measured with the Doppler flowmeter catheter in 12 conscious postoperative patients. Graft blood flow velocity is characterized by a large diastolic component with a smaller systolic fraction. Values for systolic flow velocity were uniformly greater at the graft origins when compared with similar measurements at the ostia of bypassed coronary arteries. Graft blood flow velocity decreased in a few subjects who experienced ventricular dysrhythmias. In two patients, inhalation of amyl nitrite resulted in augmented graft blood flow velocity. We conclude that the Doppler flowmeter catheter technique is useful for the direct measurement of aortocoronary bypass graft blood flow velocity in a variety of normal and pathologic states in closed chest conscious subjects.

Pressure-flow studies in man: The nature of the aortic flow pattern in both valvular mitral insufficiency and the prolapsing mitral valve syndrome

In five normal patients and in six patients with various forms of mitral insufficiency, ascending aortic pressure-flow relationships were studied using the pressure gradient technique. Stroke volume, peak flow, mean aortic pressure, and the per cent of aortic flow during the first half of ejection were calculated in the control state, following amyl nitrite inhalation, and following the intravenous injection of 0.4 mg. of phenylephrine. In normal patients, an average of 52 per cent of flow occurred in the first half of ejection both during control and following phenylephrine, and increased to 60 per cent after amyl nitrite. A patient with the prolapsing mitral valve syndrome but without mitral insufficiency had flow curves similar to the normal. Two patients with moderate and severe mitral insufficiency, respectively, and a prolapsing mitral valve had a marked increase in flow during the first half of ejection (68 and 66 per cent) during control; the per cent of flow decreased with amyl nitrite and phenylephrine administration. Patients with mitral insufficiency secondary to either rheumatic heart disease or papillary muscle dysfunction had 58 to 64 per cent of flow during the first half of ejection during control; this pattern did not change significantly with amyl nitrite or phenylephrine.

Influence of the sympathetic system on the pacemaker suppression which follows overdrive.

When ventricular pacemakers are electrically stimulated at a fast rate, the cessation of the drive is followed by a temporary suppression of automaticity ("overdrive suppression"). The role of the sympathetic system in the regulation of this overdrive suppression was studied and the following results obtained: 1) Hypotension induced during overdrive by amyl nitrite inhalation caused a shortening of the pause which follows the drive. 2) Bilateral resection of the stellate ganglia led to the opposite effect. 3) Maximal stellate ganglion stimulation halved the pause duration. 4) Norepinephrine infusion accelerated the idioventricular rate and shortened the pause. 5) Beta adrenergic blockade decreased the idioventricular rate and prolonged the pause. It is concluded that the tonic sympathetic discharge not only controls the basal idioventricular rate but also plays a regulatory role in the suppression of idioventricular automaticity which follows overdrive. This regulatory role can be dissociated from changes in idioventricular rate prior to overdrive.

Electrocardiographic abnormalities and coronary arteriograms in the mitral click-murmur syndrome.

Abstract Ischemic electrocardiographic changes are frequently associated with a mid-systolic click and late systolic murmur. Neither the cause of these electrocardiographic changes nor the natural history of patients with this syndrome has been determined. Five patients with the auscultatory findings of the mitral click syndrome, as well as ischemic electrocardiographic changes, were studied because coronary-artery anomalies or disease was suspected. Phonocardiograms were obtained with patient supine and upright, and during amyl nitrite inhalation, Valsalva maneuver and phasic respiration. Four of five graded bicycle exercise tests were normal, and there were no arrhythmias. At catheterization, prolapsed posterior-mitral-valve leaflets and normal coronary arteriograms were found in all five patients. Repeat catheterizations in two patients spanning five and eight years revealed mild progression in severity of the mitral-valve prolapse. In patients with mitral-valve prolapse the associated ischemic...

Determination of systemic vascular resistance by a noninvasive technic

Measurement of systemic vascular resistance in man currently requires arterial and venous cannulation, so that cardiac output and mean arterial blood pressure may be simultaneously determined. This report describes a noninvasive technic for determining systemic vascular resistance (SVRn), utilizing an ultrasonic method for cardiac output measurement, and a combination of sphygmomanometry and external carotid pulse tracing analysis for determination of mean arterial blood pressure. SVRn was measured by this technic in 18 patients and compared with systemic vascular resistance determined by conventional methods at cardiac catheterization (SVRc). There was excellent correlation, with SVRc = 0.865 SVRn+216 and r = 0.85. The sensitivity of the method was verified in studies on 12 normal subjects in whom SVRn while supine (1235 ± 61 dyne-sec-cm–5, mean ± se) was less than SVRn while standing (1416 ± 81, P < 0.01) and greater than SVRn supine after amyl nitrite inhalation (652 ± 41,P < 0.0001). It is concluded t...

Apex cardiogram in patients with prolapsing mitral valve

The characteristics of the apex cardiogram in patients with a prolapsing mitral valve were investigated. Twenty-four patients having typical echocardiographic evidence of prolapsing mitral leaflets and midsystolic clicks (with or without apical systolic murmurs) were studied. Of the 24 patients, 16 (67 percent) had a sharp systolic retraction on the apex cardiogram occurring simultaneously with the systolic click. Sharp systolic retractions were not observed on the apex cardiogram of normal subjects or patients with rheumatic mitral insufficiency. Eight of the 16 patients had either no or a small systolic retraction at rest, but the systolic retraction was elicited or accentuated by standing or inhalation of amyl nitrite. In patients with the sharp systolic retraction at rest, the click and the systolic retraction occurred earlier in systole during standing or inhalation of amyl nitrite. In 12 patients prolapsing mitral valves were confirmed by left ventricular cineangiograms. Sharp systolic retractions were present in the apex cardiograms in eight of these patients; seven of the eight had moderate to severe prolapse of both mitral leaflets. In the four remaining patients who underwent catheterization no sharp systolic retraction was seen on the apex cardiogram, and there was only mild prolapse of one or both leaflets. Sharp systolic retractions occur on the apex cardiogram in the majority of patients with prolapsing mitral valves, and their presence suggests an abnormal contraction due to the systolic decompression of the left ventricle by the prolapsing mitral leaflets.

Determination of systemic vascular resistance by a noninvasive technic.

Measurement of systemic vascular resistance in man currently requires arterial and venous cannulation, so that cardiac output and mean arterial blood pressure may be simultaneously determined. This report describes a noninvasive technic for determining systemic vascular resistance (SVR n ), utilizing an ultrasonic method for cardiac output measurement, and a combination of sphygmomanometry and external carotid pulse tracing analysis for determination of mean arterial blood pressure. SVR n was measured by this technic in 18 patients and compared with systemic vascular resistance determined by conventional methods at cardiac catheterization (SVR c ). There was excellent correlation, with SVR c = 0.865 SVR n +216 and r = 0.85. The sensitivity of the method was verified in studies on 12 normal subjects in whom SVR n while supine (1235 ± 61 dyne-sec-cm –5 , mean ± se ) was less than SVR n while standing (1416 ± 81, P &lt; 0.01) and greater than SVR n supine after amyl nitrite inhalation (652 ± 41, P &lt; 0.0001). It is concluded that this noninvasive, simple, and safe technic should prove to be a useful bedside method for routine clinical measurement of systemic vascular resistance.

Studies of straingauge kinetocardiogram recording methods and its clinical implication.

1) A new technique of kinetocardiogram (S-KCG) by using straingauge was introduced to measure the absolute precordial movement. 2) The device had constant frequency-response curve within the range lower than 15 Hz, linear relationship between the given displacement and the recorded amplitude and infinite time constant. 3) The influences of intervening soft tissue on the record could be avoided by the pressure (700 gram) on the chest wall applied through the pickup device. 4) The recorded tracings were consisted of 5 main components: atria wave (a), preejection wave and ejection wave (PE and E), midsystolic outward movement (MOM), recoil movement at the time of second heart sound (R), rapid and slow filling wave (rF and sF). A magnitude of wave was expressed as wave ratio to the total maximum deflection (a/TD). 5) Various changes in the configuration of S-KCG in altered hemodynamics which were induced by amyl nitrite inhalation, β-stimulant injection, arrhythmias and various congenital and acquired heart diseases were demonstrated. 6) Absolute amplitude of a wave as well as a/TD increased under the conditions of both pressure, and volume overload in the left atrium. In mitral stenosis, there was significant positive correlation between a/TD and the pulmonary capillary wedge pressure. 7) The direct measurement of isovolumetric contraction time could be possible by measuring the PE-E interval. 8) Several possible mechanism and genesis of MOM wave were discussed. 9) It was concluded that the S-KCG is useful in the evaluation of the synchrony of the contraction.

Hemodynamic effects of amyl nitrite in coronary artery disease

The hemodynamic response to administration of amyl nitrite was studied in 27 patients with coronary artery disease and 6 normal subjects. Amyl nitrite given to 15 patients with coronary artery disease during sinus rhythm resulted in abrupt decreases in brachial arterial pressure (from 124/72 ± 9/4 [mean ± standard error of the mean] to 92/50 ± 5/3 mm Hg) and in left ventricular end-diastolic pressure (from 13 ± 2 to 7 ± 1 mm Hg). Pulmonary arterial mean pressure was reduced from 15 ± 1 to 12 ± 1 mm Hg. Increases occurred in heart rate (from 83 ± 4 to 109 ± 5 beats/min), in cardiac index (from 2.7 ± 0.2 to 4.0 ± 0.4 liters/min per m 2 ) and in maximal rate of rise of left ventricular pressure (dP/dt) (from 1,229 ± 56 to 1,461 ± 105 mm Hg/sec). Right ventricular pressure and tension-time index showed no significant change. Similar changes occurred in the normal subjects. In 12 patients known to experience angina during right atrial pacing, amyl nitrite given 3 minutes before pacing did not prevent angina but did reduce monitored pressures. When administered during pacing-induced angina, amyl nitrite relieved chest pain in 4 of 12 patients and resulted in hemodynamic changes similar to those observed during sinus rhythm. Inhalation of amyl nitrite produced a rise in coronary sinus PO 2 from 22 ± 1 to 32 ± 4 mm Hg at 30 seconds with a return to control values at 3 minutes. The observed hemodynamic response to amyl nitrite would have differing effects on the balance of myocardial oxygen supply and requirements; these variations may explain the unpredictable therapeutic results of use of this agent.

Significance of chronic sinus bradycardia in elderly people.

It may be difficult to evaluate sinus bradycardia in the elderly since sinus rates below 50 beats/min may occur normally with aging. Seven asymptomatic bradycardic subjects (heart rates 41-51 beats/min), ages 67-79 years, with no evidence of impaired cardiac performance and taking no drugs, were compared with four age-matched controls (heart rates 60-84 beats/min). Autonomic function was tested with the Valsalva maneuver, amyl nitrite inhalation, methoxamine infusion, head-up tilt, and atropine intravenously (2 mg). Cardiac index at rest was normal in bradycardic subjects (2.4 ± 0.1 sem ); increased cardiac stroke volume (SV) compensated for the slow heart rate. With supine bicycle exercise, increase in cardiac output per 100 ml increase in oxygen consumption was normal in bradycardics (885 ± 60 ml compared to 907 ± 171 ml in controls). This exercise response was achieved mainly by increased SV in bradycardics and by increased heart rate in controls. Significant increases in cardiac output occurred with both atropine and atrial pacing in bradycardics, but not in controls. Autonomic impairment was not found. Increased vagal tone in bradycardics was suggested by a lesser heart rate response to exercise and passive tilting. Hence, a heart rate below 50 beats/min in elderly people does not necessarily indicate depressed cardiac performance. Further evaluation of the significance of bradycardia in these subjects requires long-term observation.

Effects of amyl nitrite on coronary arterial blood flow velocity in man

Instantaneous coronary arterial phasic blood flow velocity was measured in 21 patients (8 with coronary artery disease) after amyl nitrite inhalation. Measurement was made with use of a Doppler ultrasonic flowmeter catheter positioned at the ostia of the coronary arteries. In all cases, there was an appreciable increase in diastolic coronary arterial phasic blood flow velocity within 10 seconds. Flow velocity increased from 50 to 216 percent over control values after administration of amyl nitrite. Subjects with marked obstructive coronary artery disease had decreased peak coronary arterial phasic blood flow velocity responses when compared with control subjects. Atrial pacing to heart rates attained with amyl nitrite alone resulted in no appreciable increase or decrease in coronary arterial phasic blood flow velocity, thus showing that increase in the latter was not dependent on this action of the drug. Furthermore, increase occurred before appearance of the arterial hypotensive effect of amyl nitrite. The presence of an increase in coronary arterial phasic blood flow velocity after administration of a drug with demonstrable coronary vasodilating action strongly suggests that one of the important attributes of nitrites is their ability to increase coronary arterial blood flow.

Late Systolic Murmur in Coronary Artery Disease

Late systolic murmur with or without a mid-late systolic click has not been reported in patients with coronary artery disease. Eighteen patients are reported with both late systolic murmur and significant coronary artery disease. The latter manifested as either angina pectoris or myocardial infarction. Radiographic confirmation including selective coronary arteriography of obstructive coronary artery disease was obtained in all patients. Left ventriculography revealed systolic prolapse of the posterior and sometimes the anterior mitral leaflets with varying degrees of mitral regurgitation. Differentiation between the late systolic murmur associated with coronary artery disease and the noncoronary “auscultatory-electrocardiographic” syndrome is important, though sometimes difficult. The common denominator in both is an abnormal mitral valve apparatus. Late systolic murmur in coronary artery disease represents a mild form of papillary muscle dysfunction. The discovery of a late systolic murmur in association with chest pain and abnormal electrocardiogram in a middle-aged or older man should not be passed off lightly as “benign”. On the contrary, if it is associated with an accentuated first sound, presystolic and diastolic gallops, becomes softer after an extrasystole, and increases in intensity following inspiration, amyl nitrite inhalation or squatting, it should strongly suggest coronary artery disease and further diagnostic studies, including coronary arteriography, are indicated.

VI. EFFECT OF AMYL NITRITE INHALATION

Acta Medica ScandinavicaVolume 192, Issue S538 p. 89-93 VI. EFFECT OF AMYL NITRITE INHALATION First published: January/December 1972 https://doi.org/10.1111/j.0954-6820.1972.tb03577.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume192, IssueS538January/December 1972Pages 89-93 RelatedInformation

Calibrated low frequency acceleration vibrocardiography. Its hemodynamic determinants and clinical application.

Calibrated low frequency acceleration vibrocardiography (A-VCG) was studied in normal individuals and in patients with coronary heart disease. Experimental studies in anesthetized dogs were also made to look for the hemodynamic determinants of the main waves in the A-VCG, and transmission characteristics of the chest wall over the range of the frequency of the A-VCG. The results were as follows:(1) The S wave of low frequency acceleration vibrocardiography (A-VCG) coincided with the upward slope of the aortic flow rate curve, but showed a reverse phase, and its trough coincided with the vertex of the first derivative of aortic flow rate.(2) The amplitude of the S wave was correlated with the peak value of aortic flow rate, the peak value of the first derivative of aortic flow rate and the peak value of the first derivative of aortic pressure, but was not correlated with aortic pressure, stroke volume and the peak value of the first derivative of left ventricular pressure.(3) In the patients with myocardial infarction, there was a significant increase in A wave amplitude, decrease in S wave amplitude and increased A/S ratio compared with those of normal individuals.(4) In the patients with angina pectoris, there was a significant increase in A/S ratio compared with that of normal individuals with the age of between 30 and 39.(5) In normal individuals, there was tendency for A wave amplitude to increase, S wave amplitude to decrease and A/S ratio to increase with age.(6) During exercise and inhalation of amyl nitrite, increase in S wave amplitude was smaller in the patients with angina pectoris than in normals.(7) These results suggest that the S wave amplitude in A-VCG reflects contractility of the left ventricle, and that the A/S ratio and changes in S wave amplitude during various conditions offer useful means for detecting latent impairment of the functional reserve of left ventricle.(8) The wave form and phase of direct A-VCG from the ventricular wall and those from the chest wall were similar, and the S wave amplitude was about 6dB greater in direct A-VCG.

Carotid pulse tracings in hypertrophic subaortic stenosis

Twenty of 23 patients with the diagnosis of IHSS displayed distinctive carotid pulse tracings. Except for those patients with pure aortic insufficiency, only 5 of the 124 patients with other cardiac disorders had similar abnormalities. These abnormalities were: (1) a UST LVET ratio less than 0.27 before amyl nitrite inhalation, (2) a UST LVET ratio of less than 0.23 after amyl nitrite inhalation, and (3) an increase in LVET greater than 0.06 sec. after amyl nitrite inhalation.

The discharge of sweat in Welsh Mountain sheep

1. Experiments were done on Welsh Mountain sheep to determine whether the sheep can be caused to discharge sweat continuously.2. On administration of sequences of four to eighteen I.V. injections of adrenaline or noradrenaline (200 mug), sheep responded to the first 4-5 injections with decreasing amounts of sweat discharge. Thereafter, the responses were fairly constant at about 10% of the first discharge. Occasionally one injection within a series elicited no sweat discharge but on other isolated occasions large discharges of sweat were induced. The blood pressure response to repeated I.V. injections of adrenaline remained constant.3. Inhalation of amyl nitrite or rebreathing of expired air during I.V. adrenaline injections had little effect on the pattern of intermittent sweat discharges and did not induce a continuous outflow of fluid from the sweat glands.4. Continuous infusions of adrenaline and of carbachol did not cause a change in the rate of continuous water vapour loss from the skin but possibly increased the frequency of intermittent sweat discharges.5. Electrical stimulation of the cervical sympathetic nerve for short (0.5-2 min) or long (20-30 min) periods caused only transient (3-6 min) increases in water vapour loss from the cheek skin.6. None of these experiments indicated that the sweat glands of the sheep can be induced to discharge fluid continuously.

Actions of the Nitrites on the Peripheral Circulation and Myocardial Oxygen Consumption: Significance in the Relief of Angina Pectoris

Myocardial ischemia is best viewed as a discrepancy between myocardial oxygen demands and availability of oxygen to the heart. Although the fundamental action of each nitrite is generalized direct vasodilation, in patients with coronary arterial disease the dynamic factor mediating favorable effects of these agents on angina pectoris appears largely to be reduction of myocardial oxygen requirements. Thus, the salutary effect of sublingual nitroglycerin is most related to venodilation which results in peripheral pooling of blood and reduction of heart size, thereby diminishing systolic wall tension and oxygen consumption of the ischemic left ventricle. With rapid introduction of nitrite into the circulation following inhaled amyl nitrite, marked direct peripheral arteriolar dilation results in decline of systolic tension and oxygen utilization of the heart and relief of myocardial ischemic pain. Thus, a peripheral circulatory mechanism of action of the nitrites is described which is immediately available for improvement of angina pectoris and is operative even in absence of coronary dilation.