Cardiovascular Disturbances in Chronic Severe Anemia

Sanghvi, L. M.; Sharma, Ranjan; Misra, S. N.

doi:10.1161/01.cir.15.3.373

Cited by 18 publications

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“…[10][11][12][13][14][15] In this communication we report our observations on the cardiac output and circulatory dynamics in chronic severe anemia and the hemodynamic response to the correction of the anemia. This study was undertaken in an attempt to answer the following three questions: 1.…”

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Hemodynamic Effects of Chronic Severe Anemia

et al. 1963

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Data on the cardiac output and circulatory dynamics obtained by cardiac catheter studies in 51 subjects with chronic severe anemia are presented. Patients are divided into two groups: group A consists of 26 subjects with an average hemoglobin value of 3.0 Gm. per 100 ml. (range 1.5 to 3.8 Gm.); group B, 25 patients with a hemoglobin level of 4.0 to 6.5 Gm., average 4.5 Gm. Group A subjects have a somewhat faster heart rate (99 against 92 a minute), higher cardiac index (8.0 versus 6.3 liters per minute per square meter), and stroke index (88 and 68 ml. per beat per square meter) than group B patients. The oxygen consumption values in both groups are normal (average 158 and 160 ml. per minute per square meter), while more oxygen is extracted by the tissue in group A subjects (61 and 53 per cent) whereas less oxygen is transported to the tissue (261 and 321 ml. per minute per square meter). The stroke volume seems to bear a closer relationship to the high cardiac output than such other parameters as heart rate, right heart filling pressure, and velocity of blood flow. Apparently the presence of slow heart rate does not negate high cardiac output. Data also suggest that systemic vascular resistance may play an important role in the high cardiac output as the two are inversely related, and by increasing the peripheral arterial pressure the output can be significantly reduced. Restudy data after the treatment of the anemia (hemoglobin 10.0 to 12.5 Gm. per 100 ml.) show appreciable reduction in the cardiac output and in the right heart filling pressure, increase in the peripheral vascular resistance and oxygen transport values, and widening of the arteriovenous oxygen differences with concomitant decrease in the oxygen extraction by the tissue.

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Hemodynamic Effects of Chronic Severe Anemia

et al. 1963

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“…Circulation, Volume XXI, June, 1960 The chemical nature of the toxic substance in argemone oil (derived from the seeds of the plant argemone mexicana) is uncertain. Mukherjee and co-workers28 isolated a crystalline free base C19 H15 04 N from the oil and suggested that this represented the toxic fraction.…”

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Cardiovascular Manifestations in Argemone Mexicana Poisoning (Epidemic Dropsy)

1960

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Cardiovascular manifestations have been studied in 11 patients with argemone oil poisoning. Tachycardia, alterations in the heart sounds, cardiac enlargement, or electrocardiographic and ballistocardiographic changes indicated myocardial involvement in every case. The latter was suggestive of a nonspecific type of myocarditis and was considered to be of a minor nature. The prominent manifestations included dyspnea, edema, hepatic enlargement, and pulmonary congestion. The last 3 were probably due to capillary dilatation, whereas the cause of dyspnea was uncertain. These manifestations suggested the presence of cardiac failure, which, however, was considered unlikely except in 1 case.

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Chesler¹

1993

Clinical Cardiology

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Cardiovascular Disturbances in Chronic Severe Anemia

Cited by 18 publications

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Hemodynamic Effects of Chronic Severe Anemia

Hemodynamic Effects of Chronic Severe Anemia

Cardiovascular Manifestations in Argemone Mexicana Poisoning (Epidemic Dropsy)

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