Article

Electrocardiographic changes during hyperventilation resembling myocardial ischemia in patients with normal coronary arteriograms

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Abstract

In a series of 238 patients having hyperventilation tests just prior to treadmill exercise and selective coronary arteriography during the same hospital admission, 15 per cent of 46 patients with normal coronary vessels had electrocardiographic changes during hyperventilation that were virtually identical to those of myocardial ischemia. The hyperventilatory ECG changes were the sole basis for “false-positive” interpretation of their stress tests. Patients with normal coronary angiograms who had no ECG alterations during hyperventilation all had negative treadmill tests.In contrast, only 3 per cent of 192 patients with angiographically demonstrable coronary disease had ischemic changes during hyperventilation. Awareness that not all RST alterations seen during hyperventilation are easily distinguishable from those due to myocardial ischemia is of the utmost importance in evaluating treadmill tests, as errors in interpretation may thus be minimized, resulting in fewer “false-positive” readings.Although the number of patients is small, we found that “ischemic” ECG changes seen during hyperventilation (as well as during exercise) in patients with suspicious histories indicate that very probably no coronary artery disease exists. The routine performance of adequate hyperventilation testing prior to exercise is strongly urged.

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... The effects of voluntary hyperventilation on T wave were not consistent. Changes were only evident in 8-57% of subjects and therefore cannot be considered reproducible (Barker et al., 1939;Golden et al., 1975;Joy & Trump, 1981;Kemp & Ellestad, 1968;Lary & Goldschlager, 1974;McCance, 1932;Wasserberger et al., 1956). In addition, many studies did not measure end tidal CO 2 (PetCO 2 ) and so the degree of induced hypocapnia cannot be quantified (McCance, 1932;Thompson, 1943;Christensen, 1946;Scherf & Schlachman, 1947;Wasserberger et al., 1956;Kemp & Ellestad, 1968;Biberman et al., 1971;Lary & Goldschlager, 1974;Joy & Trump, 1981;Jacobs et al., 1974). ...
... Changes were only evident in 8-57% of subjects and therefore cannot be considered reproducible (Barker et al., 1939;Golden et al., 1975;Joy & Trump, 1981;Kemp & Ellestad, 1968;Lary & Goldschlager, 1974;McCance, 1932;Wasserberger et al., 1956). In addition, many studies did not measure end tidal CO 2 (PetCO 2 ) and so the degree of induced hypocapnia cannot be quantified (McCance, 1932;Thompson, 1943;Christensen, 1946;Scherf & Schlachman, 1947;Wasserberger et al., 1956;Kemp & Ellestad, 1968;Biberman et al., 1971;Lary & Goldschlager, 1974;Joy & Trump, 1981;Jacobs et al., 1974). It is possible that ECG changes were caused by inconsistent inflation volumes that occur during voluntary hyperventilation (Rutherford et al., 2005). ...
... This is indicated in studies where changes in T wave amplitude were matched by proportional changes in the R wave (table 1.2) (Barker et al., 1939;Scherf & Schlachman, 1947;Christensen, 1946). (Kemp & Ellestad, 1968;Lary & Goldschlager, 1974;Joy & Trump, 1981;Ardissino et al., 1987). In these studies, clinically significant ECG changes are referred to as ST segment elevation/depression of >0.1mV and T wave inversion (<-0.1mV). ...
... It is well known that patients with MVP often have high levels of catecholamines171819202122. On the other hand, patients with high levels of catecholamines frequently present with ST-segment depression during hyperventilation in the absence of CAD2324252627. We examined whether the presence of ST-segment depression during hyperventilation in patients with MVP leads to false positive ETs. ...
... Jacobs et al. [24] also report that changes associated with hyperventilation are usually related with normal coronary arteries. Propranolol and other beta blockers have been shown to block the ST-segment changes associated with hyperventilation, suggesting an autonomic etiology252627. Mechanisms involving disturbed balance between oxygen demand and supply, decreased level of high-energy phosphate stores, changes in electrolyte contents, intracellular Ca 2+ overload, and oxidative stress play essential role in the pathogenesis of catecholamine-induced myocardial dam- age [32]. Several studies have shown that under stressful conditions high concentrations of catecholamines become oxidized to form aminolutins and generate oxyradicals. ...
... MVP is probably due to excessive amount of catecholamines, increased oxygen demand, and coronary spasm171819202122 33] and may be prevented by beta-adrenergic blockers, which are useful for lowering oxygen consumption and downregulating sympathetic nervous system activity [27]. Considering all these potential pathophysiological mechanisms and that patients with high levels of catecholamines frequently present with ST-segment depression during hyperventilation in the absence of CAD252627, the improvement in diagnostic ability of exercise testing in our study with the use of this novel ECG criterion seems reasonable. ...
Article
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Objectives. Mitral valve prolapse (MVP) is a known cause for false positive exercise test (ET). The purpose of this study was to establish additional electrocardiographic criteria to distinguish the false positive exercise results in patients with MVP. Methods. We studied 218 consecutive patients (53 ± 6 years, 103 males) with MVP (according to echocardiographic study), and positive treadmill ET was performed due to multiple cardiovascular risk factors or angina-like symptoms. A coronary angiography was performed to detect coronary artery disease (CAD). Results. From 218 patients, 90 (group A) presented with normal coronary arteries according to the angiography (false positive ET) while the rest 128 (group B) presented with CAD. ST-segment depression in hyperventilation phase was present in 54 patients of group A (60%) while only in 14 patients of group B (11%), P < .05. Conclusions. Presence of ST-segment depression in hyperventilation phase favors a false positive ET in patients with MVP.
... Thus we observed that ST-segment depression of less than 1mm in inferior or lateral precordial leads during hyperventilation is a nonspecific finding. Previous workers have also observed that hyperventilation can produce ST-segment changed in subjects with or without coronary artery disease [2,5,10,25,27,28]. Exact pathogenesis of these changes is not clear. ...
... The exact significance of ST-segment depression seen during hyperventilation is not clear. These changes can be seen in subjects with or without significant obstruction on coronary angiography [10,13,27]. Some authorities, therefore, feel that hyperventilation does not help in identifying false responders [10]. ...
Article
Electrocardiographic changes on standing from supine position and subsequent hyperventilation were studied in 100 persons. Changes were correlated with any evidence of myocardial ischemia during stress and/or recovery phase of treadmill stress testing. 15 individuals showed electrocardiographic changes on standing from supine position. Increase in heart rate of more than 30 beats per minute without a fall of more than 20 mm Hg in systolic blood pressure was seen in three cases. Two of them developed ischemic changes during exercise. Decrease in R wave amplitude in leads V2 to V6 was seen in one individual who developed ischemic changes during exercise. New inversion of T waves in leads V2 to V4 in a case with pre-existing RBBB and inverted T wave becoming positive in lead V2 were also associated with electrocardiographic evidence of myocardial ischemia during exercise testing. Mild change in QRS axis, decrease in R wave amplitude in leads II, III, aVF and/or V3 to V5 , ST segment depression of less than 1 mm and decrease in amplitude or inversion of T waves in leads II, III, aVF and V1 to V6 did not have any correlation with evidence of myocardial ischemia during exercise. Fourteen persons showed new electrocardiographic changes during hyperventilation after standing. Three cases had decrease in heart rate. All the three had evidence of myocardial ischemia during treadmill testing. Increase in amplitude of R wave in lead V4, normalization of pre-excitation with unmasking of old myocardial infarction and ST segment depression of more than 2 mm in inferior and lateral precordial leads with ST segment elevation in lead aVR were also associated with development of ECG evidence of myocardial ischemia during treadmill testing. Decrease in R wave amplitude in leads II, III, aVF and/or V4 - V6 , ST segment depression of less than 1mm in inferior or lateral precordial leads and inversion of T waves did not have any significant correlation with development of electrocardiographic signs of myocardial ischemia during treadmill stress test.
... Myocardial perfusion defects following hyperventilation are well described in patients with vasospastic angina and anatomically normal coronary arteries by thallium-201 scintigraphy. 12,13 In subjects with coronary artery disease, only poor correlations are reported between sites of perfusion defects and anatomic stenoses, 12,13 which is consistent with our findings of a close, but not precise, association. Possible operating mechanisms could include abnormal vasoreactivity confined to the diseased vessel, release of vasoactive substances within the diseased vessel, local reflex vasoconstriction, and focal coronary vasospasm. ...
... Myocardial perfusion defects following hyperventilation are well described in patients with vasospastic angina and anatomically normal coronary arteries by thallium-201 scintigraphy. 12,13 In subjects with coronary artery disease, only poor correlations are reported between sites of perfusion defects and anatomic stenoses, 12,13 which is consistent with our findings of a close, but not precise, association. Possible operating mechanisms could include abnormal vasoreactivity confined to the diseased vessel, release of vasoactive substances within the diseased vessel, local reflex vasoconstriction, and focal coronary vasospasm. ...
Article
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Forced hyperventilation is simple, safe to perform, and can be used as a provocative test for coronary vasospasm. This study assesses whether a vasospastic component of angina might be detected in patients with angiographically "nonobstructive" coronary artery disease by posthyperventilation technetium-99m (Tc-99m) sestamibi single-photon emission computed tomography (SPECT) cardiac imaging. Eleven patients with angiographically nonobstructive coronary artery disease underwent Tc-99m sestamibi SPECT imaging at rest and after forced hyperventilation. Vessel diameters were measured by quantitative angiography before and after forced hyperventilation, and posthyperventilation SPECT images were compared with dipyridamole Tc-99m sestamibi stress images. Forced hyperventilation resulted in a 15% reduction in coronary artery diameter in stenotic segments (p <0.01), and a 17% reduction in adjacent nonstenotic segments (p <0.001). Myocardial uptake of Tc-99m sestamibi in segments perfused by vessels with angiographically nonobstructive stenoses was reduced by 24% following forced hyperventilation (p <0.001) compared with only 4% following dipyridamole (p <0.02). These findings suggest that posthyperventilation Tc-99m sestamibi SPECT imaging in patients with angina pectoris and nonobstructive coronary artery disease may be useful in identifying a vasospastic component of angina.
... Eighteen other subjects who had an abnormal exercise test before treatment were given stilboestrol , 5 mg daily (Table). Sixteen (89%) 1Usp Discussion Exercise-induced ST segment depression is usually considered evidence of myocardial ischaemia (Detry, 1973), though factors other than ischaemia may also produce these changes (Bruce, 1974; Lary and Goldschlager, 1974). Since most of the subjects in this study had clinically evident coronary heart disease as manifested by angina pectoris or a previous myocardial infarction, the postexercise ST segment changes in this group were probably the result of ischaemia in most instances. ...
Article
The effect of three oestrogens (including an oestrogen-progestogen combination) on the postexercise electrocardiogram was studied in 33 men and 18 women who earlier had shown ST segment abnormalities after exercise. When pretreatment exercise tests were compared with tests after two weeks of treatment, the postexercise ST segments which were abnormal before treatment became even more abnormal in 18 (90%) of 20 subjects treated with conjugated oestrogens 10 mg daily, in 16 (89%) of 18 subjects treated with stilboestrol 5 mg daily, and in 12 (92%) of 13 subjects treated with norethynodrel (9-85 mg) and mestranol (0-15 mg)1 daily. The ST segment abnormalities reverted to pretreatment appearance within 6 weeks of stopping oestrogens. When 10 subjects with normal near-maximal exercise tests were treated for 2 weeks with conjugated oestrogens 10 mg daily, the tests remained unchanged in 9. The hypothesis favoured to explain these findings is that of an oestrogen-induced increase in coronary artery smooth muscle tone. An increase in arterial tone would also account for the increased incidence of myocardial (and cerebral) infarction that has been reported among individuals treated with oestrogen, either alone or in combination with progestogen.
... There is one report associating ST depression with altered cardiac tone during spinal anesthesia [5]. Depression of the ST segment has also been described with hyperventilation [6]. The ECG monitor showing artifactual ST depression, may be in 'fliter' or 'monitor' mode [7] but such monitor will develop continuous ST depression, rather than intermittent as in present and few previous reports [1][2][3]. ...
... Nevertheless, ST-segment shifts are known to be related, not only to ischemia, but also to other physiological parameters, for example body position (upright or supine) 1,2 and hyperventilation. 1,[3][4][5][6][7] Here we present the case of a patient who had an electrocardiographically positive exercise test, in order to illustrate the effect of arm position on the ST-segment during the test. Shifting the patient's left arm to the upright and behind the head position during the recovery period led to normalization of the existing ST-segment depression. ...
Article
Full-text available
ST-segment changes during exercise testing can be attributed mainly to ischemia, but also, in some patients, to other physiological parameters, such as body position or hyperventilation, making ECG exercise test interpretation more complex. Here we describe the case of a patient who had an electrocardiographically positive exercise test, in order to illustrate the correlation between arm position and ST changes during exercise testing.
... Further clouding of the diagnostic and etiologic picture comes from the fact that hyperventilation, a common symptom of panic attacks, induces electrocardiographic (ECG) changes that resemble ischemia in persons both with and without apparent heart disease. [36][37][38][39][40][41][42][43][44][45] While there are some indications that these are typically false-positive ECG changes, 38-40 they may also represent true myocardial ischemia, especially in patients with known coronary artery disease 28,46 or coronary artery spasm. 28,[46][47][48][49] ...
Article
Approximately one quarter of patients who present to physicians for treatment of chest pain have panic disorder. Panic disorder frequently goes unrecognized and untreated among patients with chest pain, leading to frequent return visits and substantial morbidity. Panic attacks may lead to chest pain through a variety of mechanisms, both cardiac and noncardiac in nature, and multiple processes may cause chest pain in the same patient. Panic disorder is associated with elevated rates of cardiovascular diseases, including hypertension, cardiomyopathy, and, possibly, sudden cardiac death. Furthermore, patients with panic disorder and chest pain have high rates of functional disability and medical service utilization. Fortunately, panic disorder is treatable; selective serotonin reuptake inhibitors, benzodiazepines, and cognitive-behavioral psychotherapy all effectively reduce symptoms. Preliminary studies have also found that treatment of patients who have panic disorder and chest pain with benzodiazepines results in reduction of chest pain as well as relief of anxiety.
... Nausea and symptoms consistent with aerophagia and globus hystericus are also commonly associated with the anxiety and rapid breathing. Hyperventilation produces sinus tachycardia and other electrocardiographic changes [8][9][10], most commonly downward shifts of ST segments with flattening of the T waves in the left precordial leads together with an apparent prolongation of the QT interval, changes resembling those of hypokalemia. Isolated T wave inversions and marked ST depressions are less common. ...
... Forced hyperventilation produces hypocapnia, i.e. reduction in arterial pC0 2 and respiratory alkalosis. Furthermore, hyperventilation per se has been shown to induce ST segment depression (Lary and Goldschlanger, 1974). ...
Thesis
Syndrome X is characterised by chest pain on exertion, indistinguishable from that due to myocardial ischaemia, a positive exercise test and unobstructed epicardial coronary arteries on angiography. The underlying mechanism(s) remain unresolved. A body of evidence favours the concept that in many patients myocardial ischaemia occurs due to impaired coronary artery dilator response, caused by prearteriolar vasoconstriction and sympathetic hyperactivity. The main focus of the study was to examine the effect of exercise on the catecholamines, adrenaline and noradrenaline, in patients with syndrome X, compared to a normal control group. In addition, measurements were included for blood lactate, plasma potassium, plasma bicarbonate and creatine kinase. The study population consisted of two groups, thirty patients with chest pain, a positive ECG response to exercise, a normal coronary arteriogram and a normal ventricular angiogram (syndrome X group) and thirty apparently normal non-hospital staff subjects (control group). All subjects underwent formal, symptom-limited treadmill exercise tests, according to the Bruce protocol. The study protocol involved two exercise tests in each group. In syndrome X patients the first exercise test confirmed the presence of a positive test and the second was used in the study. In the control subjects the first exercise test served as a familiarisation procedure and also to establish that the test was normal, and the second test was used for the purpose of the study. Three venous blood samples were taken with the patient supine. The first 20 minutes prior to exercising, the second immediately post-exercise and the third 20 minutes into the recovery period. Samples were analysed for adrenaline and noradrenaline blind at another hospital and for the biochemical markers by the routine hospital laboratory. Resting heart rates were similar in both the control and syndrome X groups. There was no statistical difference between them. (Two-sample t test, P=0.26). Resting blood pressures were also similar in both groups and there was no significant statistical difference between them. (Two-sample t test, systolic P=0.99, diastolic P=0.77). The duration of exercise tests was comparable in both control and syndrome X subjects and there was no significant statistical difference between them. (Two-sample t test, P=0.2). The heart rate achieved immediately after exercise was also comparable in both groups and there was no significant statistical difference between them. (Two-sample t test, P=0.5). The blood pressures achieved immediately post-exercise were again similar in both control and syndrome X groups. There was no significant statistical difference between them. (Two-sample T test, systolic P=0.56, diastolic P=0.84). The main positive finding of this study was that the increase in plasma noradrenaline concentration from pre-exercise to immediately post-exercise was greater in the syndrome X group than the control group. Thus, at the 95% significance level the data is compatible with there being a difference between control and syndrome X in immediately post-exercise plasma noradrenaline concentrations. (Mann-Whitney, P=0.04). Furthermore, there was a statistical difference at the 99% level in delta plasma noradrenaline values (Mann-Whitney, P=0.005) and percentage noradrenaline increases from pre-exercise to immediately post-exercise (Mann-Whitney, P=0.002) between the two groups. Resting, pre-exercise supine plasma catecholamine levels were similar in both control and syndrome X groups. (Mann-Whitney, adrenaline P=0.82, noradrenaline P=0.12). Resting, pre-exercise supine other metabolic levels were also similar in both groups. (Lactate P=0.24, potassium P=0.16, bicarbonate P=0.56, creatine kinase P=0.96). No significant differences were observed between the control and syndrome X groups in values from pre-exercise to immediately post-exercise (delta values) in respect of lactate (Mann-Whitney, P=0.61), potassium (Mann-Whitney, P=0.08), bicarbonate (Mann-Whitney, P=0.63) and creatine kinase (Mann-Whitney P=0.58) concentrations. There was no significant difference in plasma adrenaline increases from pre-exercise to immediately post-exercise (delta values) between the two groups. (Mann-Whitney, P= 0.87) There was also no relation in the syndrome X patients between delta plasma catecholamine concentration changes from pre-exercise to immediately post-exercise (delta values) and immediately post-exercise ST segment depression. (Spearman Rank Correlation Coefficient, adrenaline P[greater-than]0.2, noradrenaline, P[greater-than]0.1). These data show that the catecholamine response to exercise is different in syndrome X, in that patients with this condition increase plasma noradrenaline concentrations to a greater extent compared to apparently normal people without this condition. The data are also consistent with the view that there may be an association between sympathetic overactivity and some patients with this condition and that catecholamines, and possibly other neurotransmitters, might be implicated in the pathogenesis. A hypothesis is therefore advanced, that an enhanced catecholamine response over a period of time may have a deleterious effect on coronary artery endothelium, altering endothelial function and resulting in a susceptibility to true myocardial ischaemia during exercise.
... Many studies have found that anxiety-induced hyperventilation symptoms and non specific electrocardiographic ST and T wave changes were common in patients with chest pain and normal coronary angiography. [15][16][17] Elias and colleagues 18 found negative correlation between the maximum degree of coronary stenosis and measures of neuroticism(anxiety, depression and somatic complaints) in a sample of 136 men and women awaiting coronary arteriography. The more anxious, depressed, or concerned with somatic complaints the person was, the less coronary artery stenosis was demonstrated. ...
... Hyperventilation leading to an alteration in repolarization in ECG has been described [3,4]. T-wave inversion occurs in more than one lead due to hyperventilation and it gets corrected once hyperventilation is corrected [5,6]. ...
Article
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T-wave inversion in ECG is very frequent and concerning finding as it is often associated with life- threatening conditions. There are numerous conditions mentioned in the literature for transient T-wave inversion such as acute coronary syndrome, cardiac memory T-wave, subarachnoid hemorrhage, electroconvulsive therapy, hyperventilation and indeterminate origin. Hyperventilation is already known as a cause of transient T-wave inversion; however, it is often forgotten in modern clinical settings. A 33-year- old doctor working in the same hospital reported to the emergency department during working hours with a history of acute onset breathing difficulties and atypical chest pain involving the retrosternal region. Arterial blood gas analysis (ABG) findings of respiratory alkalosis with transient T-wave inversion, which normalized soon after normal breathing and reassurance along with normal cardiac workup helped us to reach the correct diagnosis of hyperventilation syndrome.
Article
The following conclusions can be drawn : (1) The nervous outflow to the heart may be varied from the baseline to opposite directions by different stressful stimuli. (2) ST-T alterations may be induced and abolished by adrenergic activation and inhibition respectively. (3) These effects are dissociated from or not necessarily associated with an exaggerated responsiveness of the cardiac beta receptors. (4) The adrenergic influences on the ST-T abnormalities of myocardial ischemia and hypertension are limited.
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We determined the effect of alterations in coronary arterial PCO2 on coronary vascular resistance (CVR) at a constant coronary sinus (CS) PO2 and the effect of coronary arterial PO2 variation on CVR at a constant CS PCO2. A linear but opposing effect on CVR was found for both gases. The sensitivity of CVR to O2 change, represented as CVR/CS PO2, was approximately twice that of the ratio CVR/CS PCO2. (0.0852 +/- 0.006 vs. -0.0362 +/- 0.005). The entire range of CVR variation obtainable through CO2 variation was as great as that resulting from O2 variation. During randomized variation of O2 and CO2, CVR can be mathematically related in a multiple linear expression to CS PO2 and CS PCO2.
Article
The value of the exercise stress test in the evaluation of clinically healthy subjects and patients with coronary heart disease is not limited to the isolated interpretation of abnormalities of the S-T segment. Other measurable parameters which are of diagnostic and prognostic importance include: (1) a decrease in systolic blood pressure during exercise; (2) the appearance of complex ventricular arrhythmias of low exercise heart rates; (3) the appearance of inverted U waves during or after exercise; (4) the patient's maximal exercise capacity; and (5) new auscultatory findings postexercise. The reliability of the exercise test as a diagnostic tool is futher enhanced by proper patient selection and careful attention to exercise techniques. Subjects with labile ST-T wave changes during standing hyperventilation, fixed ST-T changes at rest, and intraventricular conduction defects are not ideal candidates for "diagnostic" stress testing and the examining physician must rely more heavily on nonelectrocardiographic findings. The criteria used to define an abnormal S-T response will vary according to the lead system used. However, in both symptomatic and asymptomatic subjects the appearance of marked degrees of S-T depression at low exercise heart rates significantly increases the probability of finding advanced coronary disease, particularly if the S-T depression is seen in multiple monitoring leads and is of prolonged duration postexercise.
Article
Sixteen healthy, active men were studied to determine the effects of severe arterial hypoxemia on the electrocardiograms during exercise. The electrocardiograms were all normal at maximum heart rate while the subject breathed ambient air. During maximal exercise breathing ten percent oxygen (mean arterial oxygen pressure [Po2] of 31 mm Hg), only one of the 16 had ST segment changes suggestive of ischemia. These were not present on a repeated study. The widely held view that systemic hypoxemia causes ischemic changes on the electrocardiogram was not confirmed in this study.
Chapter
Neurowissenschaften revolutionieren unsere Sicht von Körper und Geist. Zu den wichtigsten neueren Erkenntnissen der Neurowissenschaften dürfte die Aufdeckung von Mechanismen der neuronalen Plastizität auf synaptischer und zellulärer Ebene gehören. Damit wird ein »Fenster« zu neuronalen und strukturellen Grundlagen von Lernen, Gedächtnisbildung und Gehirnaktivität eröffnet, durch das man bereits seit einigen Jahren mit Hilfe der revolutionierten bildgebenden Verfahren schauen kann und das einen Brückenschlag zwischen neurobiologischen, lerntheoretischen, medizinischen und psychologischen Krankheitszugängen ermöglicht. Psychologische und insbesondere lerntheoretisch fundierte Behandlungsstrategien lassen sich nun vereinzelt bis in ihre molekularen Bedingungen hinein verfolgen und z. T. bereits sehen, wobei die Hoffnung besteht, dass diese Behandlungsverfahren bei psychischen Störungen im engeren Sinne und ebenso bei somatischen Erkrankungen an Bedeutung gewinnen. An vielen Beispielen konnte bereits gezeigt werden, dass durch syndromorientierte Verhaltenstherapie auch bei rein körperlichen Erkrankungen wesentliche Verbesserungen erzielt werden können (z. B. in der Rehabilitation von Myokard- und Hirninfarkten, bei Parkinson, Asthma oder Diabetes mellitus).
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Numerous disorders can mimic chronic coronary disease either clinically or electrocardiographically. Particularly noteworthy are Wolff-Parkinson-White syndrome, asymmetric septal hypertrophy, floppy mitral valve syndrome, angina pectoris with normal coronary arteries, hyperventilation syndrome, neurogenic T wave abnormalities, vasoregulatory abnormality, cervicoprecordial angina, hyperkalemia or hypokalemia, left ventricular hypertrophy, and left anterior fascicular block.
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This review consists of two parts: (1) discussion of the electrophysiologic mechanisms that are believed to produce ventricular repolarization changes during the electrocardiographic stress test, and (2) clinical assessment of the electrocardiographic changes with stress in patients with an abnormal electrocardiogram at rest. In the first part, the mechanisms of S-T segment elevation, S-T segment depression, T wave changes and linked S-T and T wave changes are reviewed. In the second part, all electrocardiographic abnormalities at rest are grouped into four categories: (1) changes that mask the manifestations of ischemia, (2) changes that stimulate or exaggerate the manifestations of ischemia, (3) changes that have no important effect on the manifestations of ischemia, and (4) changes that reproduce the patterns of acute myocardial infarction after an apparent healing. The reported studies of electrocardiographic stress testing in patients who have abnormal electrocardiogram at rest are summarized.
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The hyperventilation syndrome is a disease affecting children as well as adults. It predominates in female and may be debilitating. It is frequently associated with anxiety. The diagnosis, that is unfortunately often belated, is a diagnosis of exclusion and relies on the anamnesis, various non specific signs, on the Nijmegens score and on a hyperventilation provocation test. A specialized treatment allows, in most cases, a good control of ventilation and the disappearance of symptoms.
Article
The hyperventilation syndrome is very common—an incidence of as much as 10% in the office practice of a primary care physician. The acute form of hyperventilation is easily recognized and is commonly diagnosed in the emergency room and other outpatient settings. With the dramatic findings of overt anxiety, transitory bouts of hyperpnea, carpopedal spasm, and other symptoms of tetany, it is seldom misdiagnosed. However, chronic hyperventilation, the form represented by 99% of patients with the syndrome, can manifest itself by bizarre and often apparently unrelated symptoms that may affect any part of the body and any organ system.1 The pathophysiological effect may be functional cardiac or gastrointestinal disease, chronic nervous exhaustion, atypical fibromyositis or other myalgias, neurocirculatory asthenia, or various other disorders. Even after the physician has diagnosed hyperventilation syndrome and confirmed it with negative laboratory data, he may find it difficult to explain to the patient how anxiety
Article
In two groups of 500 unselected general hospital patients, EKG abnormalities were found in the EEG lab in 7% and 18.6%. While the most common abnormality was premature ventricular contractions, a wide variety of serious and minor abnormalities were seen, in some instances of emergent nature. Cardiac disease was unsuspected in around 40% of these patients and confirmed in a majority of these when looked for. Depending on the EKG abnormality, hyperventilation was shown to have an adverse effect 9--50% of the time in patients with normal EKG's, it tended to produce an increase of heart rate, but this was not invariant and the change in heart rate was not related to air exchange or EEG change. It is easy for any EEG laboratory to record EKG with existing equipment, and the results of this study suggest that it should be incorporated as a routine procedure. Moreover, the data indicated that hyperventilation is not necessarily a benign procedure. It should be undertaken only after control EKG recordings and assessment of the patient's cardiac status, and performed with EKG monitoring.
Chapter
Although it is only since the development of coronary angiography in the 1960’s that the label “chest pain and normal coronary arteries” has been used, accounts of similar patients can be found in the literature up to a century earlier. Most early descriptions emphasize organic abnormalities in explaining the symptoms: but there has been an increasing recognition that psychological abnormalities are also common. Several recent studies, reviewed below, have clearly demonstrated high levels of psychological morbidity, both at the time of angiography, and on follow-up. This observed association could be explained in several ways. The psychological abnormalities observed could simply be reactions to the physical symptoms; or they might cause those symptoms directly, via a range of possible pathophysiological mechanisms. A third model is suggested below, in which psychological and physical factors interact in a variety of ways to precipitate, and especially to maintain, physical symptoms. Such a model indicates a place for psychological approaches in the management of patients with chest pain and normal coronary arteries. The essential elements of a suggested form of psychological treatment are set out below, together with evidence of its efficacy.
Chapter
Neurowissenschaften revolutionieren unsere Sicht von Körper und Geist Zu den wichtigsten neueren Erkenntnissen der Neurowissenschaften dürfte die Aufdeckung von Mechanismen der neuronalen Plastizität auf synaptischer und zellulärer Ebene gehören. Damit wird ein „Fenster“ zu neuronalen und strukturellen Grundlagen von Lernen, Gedächtnisbildung und Gehirnaktivität eröffnet, durch das man bereits seit einigen Jahren mit Hilfe der revolutionierten bildgebenden Verfahren schauen kann und das einen Brückenschlag zwischen neurobiologischen, lerntheoretischen, medizinischen und psychologischen Krankheitszugängen ermöglicht. Psychologische und insbesondere lerntheoretisch fundierte Behandlungsstrategien lassen sich nun vereinzelt bis in ihre molekularen Bedingungen hinein verfolgen und z.T. bereits sehen, wobei die Hoffnung besteht, dass diese Behandlungsverfahren bei psychischen Störungen im engeren Sinne und ebenso bei somatischen Erkrankungen an Bedeutung gewinnen. An vielen Beispielen konnte bereits gezeigt werden, dass durch syndromorientierte Verhaltenstherapie auch bei rein körperlichen Erkrankungen wesentliche Verbesserungen erzielt werden können (z. B. in der Rehabilitation von Myokard- und Hirninfarkten, bei Parkinson, Asthma oder Diabetes mellitus).
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Hyperventilation and Supraventricular Tachycardia. Introduction: Hyperventilation has been demonstrated to alter autonomic function. Sympathomimetic drugs (isoproterenol) and parasympatholytic drugs (atropine) may be needed to facilitate induction of supraventricular tachycardia (SVT). The aim of this study was to test the clinical utility and mechanisms of hyperventilation to facilitate SVT initiation. Methods and Results: Fourteen patients with clinically documented SVT (9 AV nodal reentrant tachycardia and 5 AV reciprocating tachycardia) but noninducible during baseline electrophysiologic study were included. Immediately after hyperventilation test (at least 30 respirations/min) for 2 minutes, systolic blood pressure, sinus cycle length, anterograde and retrograde 1:1 conduction, and induced SVT were measured. Arterial blood gas, pH, and heart rate variability before and after hyperventilation were measured. Seven of nine patients with AV nodal reentrant tachycardia and 3 of 5 patients with AV reciprocating tachycardia could be induced immediately after the hyperventilation test. After hyperventilation, anterograde AV and retrograde VA 1:1 conduction were improved, sinus cycle length was decreased, and heart rate variability were decreased in both groups. Conclusion: Hyperventilation can facilitate induction of SVT. Improvement of conduction properties and changes of autonomic function are the possible mechanisms.
Article
Respiratory alkalosis is the most frequent acid-base disturbance encountered in clinical practice. This is particularly true in critically ill patients, for whom the degree of hypocapnia directly correlates with adverse outcomes. Although this acid-base disturbance often is considered benign, evidence suggests that the alkalemia of primary hypocapnia can cause clinically significant decreases in tissue oxygen delivery. Mild respiratory alkalosis often serves as a marker of an underlying disease and may not require therapeutic intervention. In contrast, severe respiratory alkalosis should be approached with a sense of urgency and be aggressively corrected.
Chapter
A discussion of the electrocardiogram (ECG) must consider that the parameters such as axis and amplitude of the waves on the electrocardiogram are the net result of both the “cardiac generator” and the electrical properties of the surrounding tissues, as recorded at fixed, arbitrary points on the body surface. This interplay of heart and thorax becomes especially prominent in the presence of pulmonary disease, which may produce either (a) heart disease (cor pulmonale) by causing elevation of pulmonary arterial pressure that overloads the right ventricle, and/or (b) thoracic alterations (due to the hyperinflation of emphysema) that modify the electrical signal transmitted to the body surface from the heart. In theory one should be able to distinguish between the changes produced on the ECG by these markedly different factors. The confusion apparent in the literature indicates, however, that such a distinction is quite difficult. This confusion originates from discrepancies in the criteria used for the clinical diagnosis of entities such as emphysema, chronic bronchitis, and cor pulmonale. Even the definitions of these terms vary. Patients commonly do not have a “pure” form of lung disease; therefore, the ECG criteria designed to separate these entities are often derived from patients with mixed disease and are considered to indicate “chronic obstructive pulmonary disease” (COPD). Either emphysema or bronchitis may be the major or sole process initially, but most patients eventually enter the common pathway of airways obstruction and parenchymal destruction, with the resultant air-trapping, hypoxia, acidosis, hypercapnia, and pulmonary hypertension that cause both hyperinflation and cor pulmonale.
Article
Exercise capacity is one of the most powerful predicting factors of life expectancy, both in patients with and without cardiac disease. Cardiopulmonary exercise testing provides a global assessment of the integrative exercise responses involving the pulmonary, cardiovascular, hematopoietic, neuropsychological, and skeletal muscle systems, which are not adequately reflected through the measurement of individual organ system function. This relatively noninvasive, dynamic, physiologic overview allows the evaluation of both submaximal and peak exercise responses, providing the physician with relevant information for clinical decision making. Chronic heart failure is a significant cause of worldwide mortality and morbidity, whose clinical picture is characterized by exercise intolerance and impaired quality of life. The purpose of this review is to provide an update of the role of cardiopulmonary exercise testing in heart failure patients with specific comorbidities. Heart failure patients frequently present concomitant clinical conditions, such as obesity, anemia, lung or kidney disease, diabetes mellitus, cancer, depression, and psychogenic disorders, which could affect length and quality of life, including everyday activities and exercise performance. Poor effort and malingering may be suspected when early discontinuation of the exercise test with irregular breathing occurs.
Chapter
Panic, as an individual experience, is an extreme form of anxiety or terror. Usually panic tends to occur in life-threatening situations, especially when it is unclear whether avenues of escape are available. An informative, subjective account of such intense anxiety was provided by Casey (1978), who described his experience of waking up from general anesthesia while remaining com pletely paralyzed by curare. Such experiences of panic can have profound and long-lasting effects. For example, Campbell, Sanderson, and Laverty (1964) reported a finding, later dramatized in the film Clockwork Orange, that stimuli classically conditioned to brief episodes of Scoline-induced respiratory paralysis produced conditioned anxiety responses that failed to habituate, even after 300 extinction trials extending over several months.
Chapter
It is increasingly obvious that the paradigms that hold sway over cardiology at present are not providing adequate solutions. Risk factor management has been disappointing [1] and coronary artery bypass grafting is not the simple answer to angina pectoris, usually considered to be due solely to the rigid coronary atheromatous narrowings demonstrated at angiography [2].
Chapter
Patients who exhibit morbid concern about their heart yet do not present symptoms suggestive of heart disease are more likely to be referred to the psychiatrist than to the cardiologist. The fear may range from phobic concern, hypochondriacal preoccupation, to delusional conviction.
Article
A. 100 consecutive unselected psychoitc in-patients having ECG monitors during routine EEG revealed 6% with abnormal ECGs. B. In comparison 100 non-psychotic outpatients identically studied revealed a lower percentage (3%) with abnormal ECGs. A reason forthis difference might be the inability of the psychotic patients to make known their physical symptoms. C. The necessity and advantages of ECG monitoring during the performanceof an EEG has been reviewed. They are: 1. Identification of artifactual ECG contamination on the EEG resembling and confused with cerebral spikes, especially when the ECG is of varying voltage and irregularly intermittent. 2. Detection of rhythm disturbance which could preclude some evoking procedures such as carotid compressions. 3. Referral suggestion for cardiac evaluation in patients being studied for cerebral symptoms not exhibiting or not verbalizing cardiac abnormality. 4. Calling attention to the possible influence of certain central nervous system lesions (i.e. floor of the third ventricle) on the ECG complex and rhythm. 5. To recognize StokesAdams Syndrome if it occurs symptomatically and observe the effect on the EEG. This could be a possible reasonto discontinue hyperventilation. D. Additionally, we suggest that hyperventilation as an evoking procedure should be tailored to the achievement of a desired end point rather than a finite period of time. For example, incardiology achieving a heart rate of 150 per minute during any stress test takes precedence over time-span. Itwould seem advisable also in electroencephalography to discontinue any stressful procedure if the heart rate reaches 150 per minute. © 1977, American Medical Electroencephalographic Association. All rights reserved.
Chapter
The views expressed herein are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the U.S. Government. COHb Carboxyhemoglobin CPET Cardiopulmonary exercise testing CXR Chest radiograph DLCO Carbon monoxide diffusing capacity EBCT Electron beam computed tomography ECG Electrocardiogram EELV End-expiratory lung volume (EELV1/4TLC - IC) EILV End inspiratory lung volume (EILV1/4TLV - IRV) EVH Eucapneic voluntary hyperventilation ExtFVL Exercise tidal flow-volume loop f Respiratory frequency FEV1 Forced expiratory volume in first second of exhalation FVL Flow-volume loop FVC Forced vital capacity GERD Gastroesophageal reflux disease GFR Glomerular filtration rate HCO3 Serum bicarbonate HIV Human immunodeficiency virus HR Heart rate HRCT High resolution computed tomography HRR Heart rate reserve IET Incremental cardiopulmonary exercise test IC Inspiratory capacity ILD Interstitial lung disease MEP Maximum expiratory pressure MFVL Maximal volitional flow-volume envelope MIP Maximum inspiratory pressure MVV Maximum voluntary ventilation O2 Oxygen O2 pulse VO2/HR, a noninvasive estimate of stroke volume PAH Pulmonary arterial hypertension PaO2 Arterial partial pressure of oxygen P(A-a) O2 Alveolar-arterial difference in partial pressure of oxygen PETCO2 Partial pressure of end tidal CO2 PETO2 Partial pressure of end tidal O2 PVO2 Venous partial pressure of oxygen RER Respiratory exchange ratio RV Residual volume SaO2 Arterial oxygen saturation SpO2 Noninvasive oxygen saturation measured by pulse oximetry SV Stroke volume TLC Total lung capacity VCD Vocal cord dysfunction CO2 Carbon dioxide output D/T Dead space to tidal volume ratio E Minute ventilation Emax Maximal E achieved during exercise E/CO2 Minute ventilation over carbon dioxide output, a marker of ventilatory efficiency E/O2 Minute ventilation over oxygen uptake, a marker of ventilatory efficiency O2 Oxygen uptake O2/kg Oxygen uptake normalized for body mass O2max Maximal oxygen uptake value O2peak Peak oxygen consumption V/Q Ventilation/Perfusion VR Ventilatory reserve (Emax/MVV; MVV - Emax) V-slope Plot of CO2 vs. O2, used to determine anaerobic threshold T Tidal volume VTE Venous thromboembolism WR Work rate I. Introduction Dyspnea is a common complaint. An estimated 3-25% of the general community has been reported to complain of shortness of breath (1). Dyspnea is the presenting complaint for 3.7% of ambulatory medicine visits (2), 2.7% of emergency department visits (3), and 15-25% of all hospital admissions (4,5).
Article
Background: Hyperventilation is known to cause ST segment changes and QT variability in adults, but this has not been systematically studied in children. Aim: To investigate the effect of hyperventilation on rate corrected QT interval (QTc) in children. Methods and results: 25 children (male=10) with a median age of 14 (range 8.3-17.6) years were asked to hyperventilate for 1 min before exercise testing using the modified Bruce protocol. Mean QTc at rest, after hyperventilation, at peak exercise and at 1 min of recovery was 425(±31), 460(±30), 446(±38) and 420(±32) ms, respectively. Mean increase (95% CI) in QTc after hyperventilation was 35(19 to 51) ms (p<0.001), while there was minimal difference between QT interval at rest and after hyperventilation (mean QT 352(±41) vs 357(±44) ms). In six children, there were abnormalities in T wave morphology following hyperventilation. The QTc increment following hyperventilation was more pronounced in children with resting QTc <440 ms (n=14, mean increment (95% CI): 55 (33 to 78) ms) compared to children with QTc ≥440 ms (n=11, mean increment (95% CI): 9 (-4 to 22) ms) (p=0.001). QTc prolongation following hyperventilation was seen in children with both low and intermediate probability of long QT syndrome (LQTS). Peak exercise and early recovery did not cause a statistically significant change in QTc in either of these groups. Conclusions: Hyperventilation produces repolarisation abnormalities, including prolongation of QTc and T wave abnormalities in children with low probability of LQTS. The likely mechanism is delayed adaptation of QT interval with increased heart rate. Thus, a hyperventilation episode can be misdiagnosed as LQTS, especially in an emergency department.
Article
This study was designed to evaluate whether treadmill stress testing would facilitate selection of patients with advanced coronary artery disease and, specifically, whether markedly abnormal ischemic responses could be used as indicators of severity of disease. Among 59 consecutive patients with documented coronary artery disease having both maximal treadmill testing and coronary angiographic studies, 15 (group 1) had normal responses to exercise, 18 (group 2) showed 1 to 2.9 mm “ischemic” (flat or downward-sloping) ST-segment depression, and 26 (group 3) demonstrated marked (≧ 3 mm) ischemic responses. Group 3 had statistically significant higher incidences of triple-vessel disease (18/26; 69 percent) and proximal lesions of the left anterior descending coronary artery (24/26; 92 percent), compared with group 1 (2/15 and 10/15, respectively) and group 2 (6/18 and 12/18, respectively). Group 3 also manifested more extensive disease than groups 1 and 2 (judged by scoring system of Friesinger et al), with a score of 11 or more in 18 of 26 patients. We conclude that marked depth of “ischemic” ST-segment depression aids in identifying that subgroup of the coronary population with severe coronary artery disease and, therefore, serves as a useful means of culling out patients with a potentially serious prognosis who might benefit from intensive diagnostic or therapeutic interventions.
Article
In the context of stress-internal or external events that threaten the individual's physical or psychological well-being-the human body signals distress along with disruptions in physiological regulation. When stress-related disruptions are extreme or are not limited in time, they may result in a broad range of somatic, behavioral, and cognitive symptoms. This article aims to (1) provide clinicians with a theoretical framework for understanding the body systems that mediate stress-induced somatic symptoms, and (2) illustrate how this framework can be applied clinically. The article begins with a brief overview of the key body systems involved in homeostasis, paying special attention to how those systems take on self-protective functions in the face of stress. Against that background, the focus then turns to a discussion of commonly occurring somatic symptoms and their probable neurophysiological underpinnings. Short vignettes illustrate typical presentations and how potential etiologies can be discussed with patients, be used to co-construct formulations, and be integrated into jointly determined treatment plans.
Article
It has been clearly shown that coronary artery spasm is the cause of Prinzmetal’s variant angina and an important mechanism of acute myocardial ischemia in angina at rest. Moreover, a role for coronary spasm in the pathogenesis of myocardial infarction has been postulated, especially in patients with normal coronary arteries. The diagnosis of vasospastic myocardial ischemia should be based on the direct documentation of ischemic ECG changes during spontaneous attacks. However, in the case of sporadic episodes, these ischemic changes are not easily recorded and so provocative tests for coronary vasoconstriction could play an important diagnostic role. Provocative tests may also be clinically useful in evaluating treatment efficacy in vasospastic angina: It is highly likely that the prevention of ischemic attacks induced by provocative testing is also predictive of a drug’s ability to abolish spontaneous attacks as well. A number of provocative tests for coronary vasospasm have been proposed, but only a few of them have been extensively applied in clinical practice.
Article
Anxiety-induced emergencies such as vasodepressor syncope and hyperventilation are well known to most practitioners. Despite advances in pain control, reconstructive dentistry, and behavior management techniques, the prevalence of dental fear in the general population remains fairly high. Fearful dental patients, who exist in each of our practices, are often expected to submit to dental treatment with little consideration given to their emotional state. Although many are capable of enduring their own high arousal state with various behavioral or cognitive distraction methods, the occasional young adult succumbs to syncope or hyperventilation. The practitioner should be able to prevent the onset of most psychogenic emergencies by amending the medical and dialogue history to include questions that preoperatively explore dental fears. Additionally, a brief physical examination should be incorporated into the initial visit and at the onset of subsequent treatment visits. When a positive history of fainting or panic attack is obtained, the practitioner should consider numerous available modalities to prevent recurrence during dental treatment. Behavioral modification strategies provide the greatest long-term benefit; however, pharmacologic sedation may be necessary to accomplish short-term dental goals. Emergencies that arise out of psychophysiologic responses are rarely lifethreatening and can be managed readily by the alert dental office team. It is imperative, however, to use all available information during the emergency assessment. Inaccurate diagnosis and treatment as a result of confusion between presyncope and hyperventilation may result in an accelerated onset of the emergency episode. Rapid recognition of an impending alteration of consciousness should minimize the progression toward or reduce any period of unconsciousness. If unconsciousness occurs, basic life support and supine positioning with supplemental oxygen should be provided immediately. Finally, the dental team should be prepared to treat other life-threatening emergencies that might initially present as syncope, such as cardiac arrest, stroke, or anaphylactic reactions.
Article
Hyperventilation-induced S-T segment changes that simulate myocardial ischemia have previously been noted, but the origin of this electrocardiographic finding has never been defined. To investigate further the basis for this response, the records were reviewed of 1,678 consecutive patients who underwent forced hyperventilation for 90 seconds and treadmill exercise testing. Twenty-eight patients (1.7 percent) were identified in whom hyperventilation resulted in ischemic-appearing S-T segment changes, and follow-up was possible in 21 (17 women, 4 men). Of the 21 patients, 16 (76 percent), including 15 (88 percent) of the 17 women, had evidence of mitral valve prolapse, 6 on auscultation alone, 2 on echocardiography alone and 6 with a combination of studies. Ten of the 21 patients had a negative exercise test; of the 11 patients who had a positive exercise test, only 1 had angiographic evidence of coronary arterial narrowing. The finding of ischemic-appearing S-T segment changes in response to forced hyperventilation has a high predictive value for the presence of mitral valve prolapse, particularly in women. The possible association of autonomic factors and mitral valve prolapse in the patho-genesis of an abnormal response to hyperventilation is discussed.
Article
In this study we assessed whether various responses to exercise testing could be quantified in order to derive the probabilities of presence of coronary disease, and if present, to assess its severity. A treadmill score based on the exercise response was determined in 405 patients who had both treadmill tests and coronary angiograms. The score was derived using discriminant function analysis, by weighting and combining depth and configuration of ST depression (downsloping, horizontal or slowly upsloping), timing onset and duration of ischemia, grading ventricular arrhythmias, heart rate and blood pressure change, coexistence of exercise-induced chest pain and sex. The treadmill score was effective in detecting coronary disease (lesions with an greater than or equal to 50% narrowing), with a predictive accuracy (PA) (probability that a subject manifesting a positive test has disease) of 87%, a true negative rate (TNR) (probability of a subject with a negative test having no disease) of 80%, and sensitivity of 94%. The treadmill score also detected severe disease (triple-vessel, main left and/or greater than 90% proximal occlusion of the left anterior descending artery), with a PA of 73%, TNR of 79% and sensitivity of 82%. We conclude that the exercise response, expressed numerically as a treadmill score, permits analysis of most of the relevant data from exercise testing, increases test accuracy by 10-15% compared with standard criteria for treatmill test interpretation, and enables the derivation of probability statements for presence and severity of coronary disease. The validity of any prediction on the basis of exercise performance may thus be quantitatively judged.
Article
A group of 305 patients were studied to evaluate the significance of orthostatic and hyperventilative T-wave changes, orthostatic blood pressure changes, and the relationship of ischemic heart disease, as determined by treadmill stress testing, to these observed changes. The results indicate that orthostatic and hyperventilative T-wave changes are not at all an unusual finding in the younger age group and are not related to ischemic heart disease. In patients having ischemic heart disease, a stationary or decreased systolic blood pressure when changing from a sitting to a standing position was seen in the majority studied. The presence of orthostatic and hyperventilative T-wave changes did not confuse the interpretation of the treadmill stress test electrocardiogram when evaluated by our criteria for ischemic abnormality.
Article
Twenty-nine patients with angina-like chest pain and angiographically normal coronary arteries and left ventricle underwent rapid coronary sinus pacing with sampling of coronary sinus and arterial blood for lactate and recording of electrocardiograms and left ventricular pressures. In 25 patients immediate postpacing left ventricular cineangiograms were obtained. Two groups were defined: 9 patients who showed evidence of myocardial lactate production and 20 who did not. The degree of S-T segment depression with pacing provided the only means of separating lactate producers (> 2 mm) from nonproducers (< 1 mm). Left ventricular contractile abnormalities could not be induced by pacing in either group. The ability to elicit electrocardiographic and metabolic changes with pacing suggests that in some of these patients chest pain may be related to myocardial ischemia. The clinical value of identifying patients who exhibit this response remains uncertain.
Article
The maximal heart rate of 190 healthy male subjects was measured during exhausting treadmill exercise. A total of 148 of these men were accustomed to a sedentary or semisedentary life while 48 of them were trained athletes. The influence of age, height, weight, and athletic training on the maximal heart rate was examined.A highly significant negative correlation was found between the maximal heart rate and the age of the subject. No significant influence of height or weight on this relationship was detected by a linear multiple stepwise regression analysis. However, at any given age the athletes had a slightly but significantly slower maximal heart rate than the untrained men. Thus, the regression equations for the two groups: MHR (sedentary) = 205.02 − 0.411 age and MHR (athletes) = 198.19 − 0.411 age, are significantly different by virtue of differences in the intercept value, although the slopes of the lines are identical.From these observations, it is apparent that predictions of maximal heart rate could be improved by making a distinction between trained and untrained subjects.
Article
Myocardial infarction with normal coronary arteriographic findings is rare. Three patients are presented who had typical clinical and laboratory findings of acute myocardial infarction and normal coronary arteriograms. Two patients were male, 16 and 24 years old, respectively, and 1 was female, aged 36 years. None had major predisposing factors to precocious coronary atherosclerosis. Thrombocytosis was considered to be the etiologic factor in 1 male patient; no etiologic factor could be traced in the other male patient; estrogen therapy may be considered as the cause of the myocardial infarction in the female patient.
Article
This report summarizes our experience with the oral potassium-loading test in a group of patients who presented with abnormal T wave inversion on routine resting electrocardiograms. The test empirically normalizes most T wave abnormalities that are unassociated with clinically demonstrable heart disease, particularly the T wave changes induced by brief hyperventilation or by anxiety reactions. The response to the test procedure is dosage-dependent and is not related to a nonspecific osmolar load.
Article
In 11 patients with angina pectoris and abnormal stress electrocardiograms, no narrowing or obstruction of coronary vessels was visible by selective cut film and coronary cinearteriography. One patient showed chemical evidence of myocardial hypoxia despite normal arteriograms. Similar evidence of impaired myocardial oxygen supply was absent in the remaining 10 patients. We found no abnormality in hemoglobin O2 affinity which might jeopardize myocardial O2 supply. The clinical course of these patients, including that during a 1 to 2 year followup period, has not been complicated by myocardial infarction or cardiac failure. In 5 symptoms have decreased.
Article
A group of 40 patients who have "ischemic" electrocardiographic (that is, 1 mm flat S-T segment depression) responses to exercise but who do not fulfill the usual criteria for ischemic heart disease are discussed. These patients have been followed up for a minimum of 3 years and clinical findings of ischemic heart disease have not developed. It is suggested that they have vasoregulatory abnormalities. Vasoregulatory abnormalities include an unusual increase in heart rate on standing, ST-T segment changes on standing, "ischemic" electrocardiographic changes unaccompanied by chest discomfort occurring early in exercise and disappearance of "ischemic" changes as exercise proceeds. Propranolol administration tends to abolish the changes, and the Valsalva maneuver temporarily restores the electrocardiographic changes toward normal. Recognition of this syndrome, its possible causes, and the importance of proper counseling and recommendations in management are discussed briefly.
Article
In a 43 year old man with a well documented inferior myocardial infarction, coronary angiography performed 16 months later revealed a widely patent right coronary artery supplying the infarcted area. Although the fate of the original lesion is unknown, lysis of a previous thrombus seems likely.
Article
A case of posterior myocardial infarction in a 17 year old boy is reported. The unusual features include the age of the patient, the localization of the infarct and the finding of a normal coronary arteriogram 15 weeks after the attack.
Article
This article has no abstract; the first 100 words appear below. BEFORE diagnostic coronary angiography, a relation between ischemic heart disease and coronary obstructive disease was assumed. Recent studies have demonstrated the presence of myocardial ischemia and occasionally subendocardial necrosis in the presence of normal coronary arteriograms.¹²³⁴ This report documents an unusual case of acute transmural myocardial infarction in a young man without coronary obstructive disease. Case Report K.G., a 19-year old college student, was admitted to the Newton-Wellesley Hospital in August, 1967, because of retrosternal chest pain with radiation to the jaw and left arm of 4 hours' duration. He had experienced 4 or 5 similar episodes of exertional pain . . . †From the departments of Medicine, Newton-Wellesley Hospital, Newton, and Tufts University School of Medicine, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Mass, (address reprint requests to Dr. Sidd at the Newton-Wellesley Hospital, 2014 Washington St., Newton, Mass. 02162). Supported by grants from the Heart Research Foundation, Inc., and Women's Aid for Heart Research, Boston, Mass. (Dr. Gorlin is an investigator for the Howard Hughes Medical Institute).
Article
A patient with atypical precordial chest pain demonstrated segmental S-T-segment depression in response to treadmill exercise. Although this finding was very suggestive of the presence of ischemic heart disease, the reproducibility of these S-T-segment changes with hyperventilation and a normal coronary cineangiographic study supported our impression of a false positive response to exercise.Certain characteristic electrocardiographic features observed in patients mainifesting a false positive response to exercise due to hyperventilation are described.
Article
We studied the effects of three types of hyperventilation (HV) on the ECG, arterial blood gases, and plasma electrolyte concentration in twelve patients without heart disease in whom HV produced T-wave abnormalities, and in eleven healthy volunteers. The T-wave abnormalities produced by HV could not be attributed to alkalosis, changes in plasma Na, K, Ca, or Mg concentrations, or changes in heart position. In ten of eleven subjects in whom the T wave became inverted during HV, isoproterenol infusion at a rate of 3 to 6 μg per minute also produced T-wave inversion. In all subjects the T-wave inversion during HV and isoproterenol infusion was transient, occurred at the onset of tachycardia, and was associated with prolongation of the Q-Tc interval, attributed to the hysteresis of the Q-T interval. We have postulated that the transient T-wave abnormalities during HV and isoproterenol infusion may be due to asynchronous shortening of repolarization.
Article
Although coronary arteriograms of a 48-year-old woman with exertional chest pain typical of angina pectoris and an abnormal exercise electrocardiogram were normal, myocardial hypoxia and anaerobic metabolism were demonstrated during induced tachycardia and are proposed as the basis of the angina pectoris. A cause of impaired myocardial oxygen metabolism other than obstructive disease of visible coronary arteries is suggested.
Article
The ECG has been recorded in patients with vasoregulatory asthenia, coronary insufficiency and arterial hypertension, as well as in healthy controls at rest, after hyperventilation, during an orthostatic test and a work test. S-T and T depressions, usually of sympathicotonic type, appeared or were accentuated after hyperventilation, particularly in patients with vasoregulatory asthenia, who also showed similar changes during an orthostatic test. Such ECG changes were uncommon in the other groups. The results sustain the concept that an increased sympathetic autonomic nervous tone provoked by hyperventilation causes the S-T and T depressions, particularly in patients with vasoregulatory asthenia. The diagnostic value of the hyperventilation ECG for analysing functional S-T and T depressions is emphasized, as well as the diagnostic difficulties in the evaluation of ECG changes in patients who hyperventilate, for instance during a hypoxia test.
Article
This article has no abstract; the first 100 words appear below. CINE coronary arteriography affords a means of correlating clinical manifestations of coronary heart disease with responsible vascular abnormality in the living patient.¹²³⁴⁵ Several of the comparative analyses have indicated that obstructing atherosclerosis can be demonstrated in at least 2 major coronary arteries in most patients with angina and abnormal electrocardiograms at rest and after exercise.¹²³⁴ In documenting the wide distribution and severity of the arterial disease in these patients the reports parallel earlier views based on comparisons between clinical and morbid findings.⁶ Obviously, the correlation does not hold when a significant anomaly of the coronary arteries, aortic regurgitation, aortic stenosis . . . *From the Cardiac Section of the Department of Medicine, Hahnemann Medical College and Hospital. Supported by a grant (HE-06368) from the National Heart Institute for the Clinical Cardiovascular Research Center, Hahnemann Medical College and Hospital. Source Information PHILADELPHIA †Professor of medicine and head, Section of Cardiology, Hahnemann Medical College and Hospital. ‡Associate professor of medicine and assistant head, Section of Cardiology, Hahnemann Medical College and Hospital. §Senior instructor in medicine and acting director, Cardiac Catheterization Laboratory, Hahnemann Medical College and Hospital.
Article
Following the taking of 12-lead routine electrocardiograms, three precordial leads were recorded before, during, and after 10 to 15 seconds of voluntary hyperventilation in 296 students, ranging in age from 8 to 17 years. Fifteen per cent of the total group, comprising 212 Caucasians and 84 Negroes, inverted one or more previously upright precordial T waves following hyperventilation. The incidence of T-wave inversion in children 12 years of age and under was nearly four times greater in Caucasians than in Negroes. There was no significant difference when the older Negro and Caucasian students were similarly compared. Sinus tachycardia, T-wave flattening, and "tucking," short of frank inversion, as well as junctional depression of the ST segment, were commonly seen following hyperventilation. The similarity of the hyperventilation-induced T-wave inversion in children to those previously documented in adults is noted, and the clinical implication of this study requires continued cognizance of the occurrence of "nonpathological" T-wave inversion in adults, so as to avoid iatrogenic heart disease.
Article
Summario in Interlingua 1.Intermaio 1952 e maio 1954 le admissiones al Hospital Madison del Administration de Ancian Combattentes includeva 34 casos (24 negre e 10 caucasian) de persistente e inexplicate alterationes del segmento RS-T e del unda T. Nulle de iste patientes monstrava signos de morbo cardiac.2.Le major alterationes electrocardiographic consisteva de concavisation del segmento RS-T e franc inversion del unda T in derivationes precordial central e sinistre.3.Le administration de un agente de blocage vagal (Pro-Banthina) resultava in le prompte normalisation de iste anormalitates electrocardiographic.4.Hyperventilation de durantias de dece a vinti secundas reproduceva uniformemente le alterationes original del segmento RS-T e del unda T. Tamen, iste effecto del hyperventilation esseva “blocate” durante le periodo del activitate maximal de Pro-Banthina.5.Super le base de evalutationes psychosomatic e del resultatos de tests psychologic, il esseva domonstrate que iste patientes habeva un o altere forma de disordine psychiatric o emotional. Sin reguardo a lor categorias diagnostic, le subjectos de iste gruppo esseva characterisate per le manifestation prominente de un combination de instabilitate vasomotor, anxietate, e hypochondriasis.6.Le natura e le frequentia de iste “configuration juvenil” es discutite insimul con le mechanismo e le rolo de stress emotional in anormalitates electrocardiographic de iste typo.
Article
The effect of brief hyperventilation on the precordial T waves of 350 normal adults is described. Evidence is presented that brief hyperventilation initiates a vagal reflex which results in the T-wave inversion. Supportive data are also given to exclude respiratory alkalosis as a possible mechanism. Caution is advised in interpreting isolated T-wave inversions as indicative of organic heart disease. It is proposed that isolated T-wave inversion be deleted as a criterion for a "positive" exercise test.
Article
A study of 433 asymptomatic men emphasizes the value of strenuous exercise testing in the early detection of myocardial ischemia. The sensitivity of the maximal exercise capacity test was nine times greater than that of the double Master's two-step test in eliciting electrocardiographic evidence of myocardial ischemia in 201 “normal” men who were over 34 years of age. Improved detection of potential coronary heart disease by this method is illustrated by comparison with several epidemiologic studies. If the reliability and specificity of this electrocardiographic abnormality in predicting clinical coronary heart disease is confirmed by future follow-up examinations, a method of detection and study of potential coronary heart disease and factors influencing its course will be available.
Article
Plasma potassium concentration was determined in arterial and in portal, hepatic, and peripheral venous blood during acute respiratory alkalemia. It was found that passive hyperventilation produces an increase in plasma potassium, reaching peak values after 15 min. The hyperkalemia is due to potassium release in the prehepatic splanchnic territory. The liver apparently plays no part in producing it, while muscular territories take up potassium.
Myocardial ischemia after maximal exer-Lary and Goldechlager 12
  • A E Doan
  • D Peterson
  • It
  • J R Blackman
  • R A Bruce
Doan, A. E., Peterson, D. It., Blackman, J. R., and Bruce, R. A.: Myocardial ischemia after maximal exer-Lary and Goldechlager 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. perventilation on precordial T waves of children and adolescents, Circulation 36:700, 1967.
Effects of hyperven-tilation on ECG in patients with circulatorv distur-bances, Acta Med. f&and False positive ECG response to exercise secondary to hyperventiiation: Cineangiographic cor-relation, AM
  • C Furberg
  • H Linderholm
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Furberg, C., and Linderholm, H.: Effects of hyperven-tilation on ECG in patients with circulatorv distur-bances, Acta Med. f&and. 185:167,1969. " McHenry, P. L., Cogan, 0. J., Elliott, W. C., and Knoebel, S. B.: False positive ECG response to exercise secondary to hyperventiiation: Cineangiographic cor-relation, AM. HEART J. 79683.1970.
Exe\& electrocardiography and'vasoregmatory abnormalities The effects of alkalosis and of acidosis upon the human electrocardiogram
  • L Biberman
  • R N Sarma
  • B I Surawicz
  • Mason R E Barker
  • P S Shrader
  • E L Ronzoni
Biberman, L., Sarma, R. N., and Surawicz, B.: T-wave abnormalities during hvnerventilation and isonrotere-----no1 infusion, AM.HEART J. 81:166,1971. Friesinaer. G. C.. Biern. R. 0.. Likar. I.. and Mason. R. E.: Exe\& electrocardiography and'vasoregmatory abnormalities, Am. J. Cardiol. 30~733, 1972. Barker, P. S., Shrader, E. L., and Ronzoni, E.: The effects of alkalosis and of acidosis upon the human electrocardiogram, AM. HEART J. 17:169,1939. Blesa, S. B., Gonzalez, N. C., and Cingolani, H. E.: Early increase in plasma potassium in hyperventilation, Am. J. Physiol. 20&537, 1965.
Myocardial function during pacing induced electrocardiographic “ischemia” in patients with angina and normal coronary arteriograms (Abstr.)
  • Abrogast