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Results for “Cardiac Output, High”

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At least 19 recordsLinked to original sources
PubMed1985

A model of ovine endotoxemia characterized by an increased cardiac output.

High cardiac output sepsis is a major clinical problem. We have designed a sheep endotoxin model to simulate this condition and have evaluated how closely it approximates the clinical situation. The animals were prepared for chronic study by the implantation of cardiopulmonary catheters. One week later, endotoxin (0.75 microgram/kg/30 min) was administered following baseline measurements, and the animals were studied for an additional 15 hr. From 6-15 hr after the administration of endotoxin, there was a statistically significant twofold increase in cardiac output. Simultaneously, the total peripheral vascular resistance and mean arterial pressure was reduced. Eicosanoid measurements made at this time indicated that the vasodilator prostanoid, prostacyclin, was not elevated. A high cardiac output (hyperdynamic) model of sepsis has thus been established by the 30 min infusion of a small quantity of endotoxin. Prostacyclin is not a mediator of this response.

Animals↗
PubMed1990

Unilateral megalencephaly associated with neonatal high output cardiac failure.

High-flow cerebral arteriovenous fistulae are well known to present in the neonatal period with macrocephaly, cranial bruits and high-output cardiac failure. This report describes a newborn infant with such a clinical presentation, who had unilateral megalencephaly without macroscopic arteriovenous shunts. Ultrasound Doppler examination of the carotid and cerebral vessels showed diastolic flow, or a decreased pulsatility index, consistent with decreased intracranial vascular resistance. The ipsilateral cerebral arteries and veins were markedly enlarged at angiography and at post-mortem examination, but there was no arteriovenous malformation. The infant expired from high-output cardiac failure and hypoglycemia. It is postulated that the high-output cardiac failure was due to increased blood flow through the enlarged, dysplastic cerebral hemisphere.

Brain↗
PubMed1991

High cardiac output as a paraneoplastic syndrome.

A high cardiac output (17 1 min-1) was recorded in a young man suffering from lymphoplasmatocytotic lymphoma. The evolution of the blood disease was characterized by two relapses, during which clinical signs of heart failure were prominent but resolved with efficient blood chemotherapy. The known aetiologies of high cardiac output were excluded. The complete normalization of the cardiac parameters with blood remission suggests that the high cardiac output represented an unusual paraneoplastic syndrome, the pathogenesis of which still remains unknown, although several hypotheses were tested.

Adult↗
PubMed1987

[Early changes in the circulation of the humeral artery in borderline arterial hypertension].

The brachial artery diameter and blood flow rate were measured by pulsed Doppler velocimetry in 9 healthy subjects and 24 patients of the same age group with borderline hypertension. To evaluate the results, the patients were divided into two groups according to their cardiac output: high cardiac output group (i.e. patients whose cardiac output was superior to the mean +/- 2 S.D. value in the control population), and normal cardiac output group (i.e. cardiac output lower than that value). Patients in both groups were of the same age and had the same level of blood pressure. The brachial artery diameter and blood flow rate values were the same in the normal cardiac output group and in the control population. However, these values were significantly higher in patients with high cardiac output than in controls (P less than 0.05 and P less than 0.001) and in patients with normal cardiac output (P less than 0.01). These results suggest that the haemodynamic profile in the brachial artery is not the same in all patients with borderline hypertension: there was a tendency to vasoconstriction in patients with normal cardiac output, whereas the brachial artery was clearly dilated in patients with high cardiac output.

Adult↗
PubMed1988

Transition from high cardiac output to elevated vascular resistance in hypertension.

The early phase of hypertension (borderline hypertension) is characterized by a hyperkinetic circulation caused by excessive sympathetic drive and decreased parasympathetic inhibition to the heart. In later phases the cardiac output becomes normal, but the hypertension is still neurogenic, as demonstrated by the fact that continued pharmacologic parasympathetic, beta- and alpha-adrenergic inhibition normalizes the blood pressure. In both of these phases of the process, plasma norepinephrine values are elevated. These patients also show characteristic behavioral patterns; they are outward oriented, submissive, but experience unexpressed anger and frequently harbor hostile feelings. In late phases of hypertension the cardiac output is normal and the total peripheral resistance is elevated. This hemodynamic transition can be explained by a secondary response to elevated blood pressure. The heart becomes less responsive as a result of altered receptor responsiveness and decreased cardiac compliance, whereas the responsiveness of arterioles increases because of vascular hypertrophy, which leads to changes in the wall-to-lumen ratio. However, one observation eludes explanation: the absence of plasma norepinephrine elevation in later phases of hypertension. We propose a new conceptual framework to explain the disappearance of elevated plasma norepinephrine in the course of hypertension. The concept is based on a wide range of observations with the use of various receptor-blocking agents during neurogenic pressor responses. Invariably, the blood pressure response is preserved, but the hemodynamic pattern can be altered from a high cardiac output to high total peripheral resistance or vice versa.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1990

Prevalence and clinical characteristics of a high cardiac output state in patients with multiple myeloma.

PURPOSE: This study was undertaken to define the prevalence and clinical characteristics of patients with a high cardiac output state associated with multiple myeloma. PATIENTS AND METHODS: Specifically, we evaluated clinical, laboratory, and two-dimensional and Doppler echocardiographic data in 36 patients with multiple myeloma. Cardiac output was determined noninvasively by a pulsed Doppler technique. RESULTS: A high cardiac output state, defined as a cardiac index greater than or equal to 4.0 L/minute/m2, was present in eight of 34 (23.5%) subjects in whom cardiac output was measurable. None of the known causes of high output states could be identified in these patients. Four patients developed high output congestive heart failure, two of whom died. Age, sex, degree of anemia, serum calcium level, immunoglobulin type, or disease stage did not differ significantly between subjects with or without high output states. However, severe bone involvement was significantly more frequent in those patients with high cardiac output states, occurring in all eight patients with high cardiac indexes compared with nine of 26 patients with low or normal cardiac indexes (p = 0.001). CONCLUSION: These data demonstrate that high cardiac output states are relatively common in patients with multiple myeloma and are associated with the presence of extensive bone disease.

Bone and Bones↗
PubMed1992

High output cardiac failure caused by multiple giant cutaneous hemangiomas.

A 59-year-old Chinese woman had multiple giant cutaneous cavernous hemangiomas on her right upper limb which resulted in high output heart failure because they presented as a large peripheral arteriovenous (A-V) fistula. Selective right subclavian arteriography showed extremely hypertrophic arteries of the patient's right arm with a tremendous blood supply to the soft tissues; neither superselective embolization nor surgery seemed applicable to this patient. The patient's heart failure was not satisfactorily controlled by conservative treatment.

Angiography↗
PubMed1989

High-output cardiac failure in fetuses with large sacrococcygeal teratoma: diagnosis by echocardiography and Doppler ultrasound.

With two-dimensional echocardiography and Doppler ultrasound, we demonstrated high-output cardiac failure in three fetuses with large sacrococcygeal teratomas. All fetuses had normal cardiac structure, dilated ventricles maintaining a normal fractional shortening index, a dilated inferior vena cava reflecting the increased venous return from the lower body, pericardial and pleural effusions as a manifestation of fetal hydrops, and a markedly thickened placenta. When fetal hydrops was present, the combined ventricular output was very high (mean 1280 ml/min/kg; normal 553 +/- 153 (SD)). Descending aortic flow was also sharply increased (mean 930 ml/min/kg; normal 184 +/- 20), as was placental flow (mean 480 ml/min/kg, normal 110 +/- 26). High-velocity arterial flow signals were also found within the tumor. In one fetus studied serially, placental thickness and tumor diameter increased rapidly; placental flow as a percentage of descending aortic flow decreased, indicating a further increase of flow to the tumor. These abnormal hemodynamic changes were reversed after the fetus's teratoma was surgically removed. We conclude that the sacrococcygeal teratoma acts as a large arteriovenous fistula, which causes high-output cardiac failure. Surgical removal of the teratoma in a previable fetus with such hemodynamic findings may prove to be the most effective treatment.

Echocardiography↗
PubMed1990

Death due to high-output cardiac failure in fetal sacrococcygeal teratoma.

Fetal sacrococcygeal teratoma (SCT) is being recognized with increasing frequency. Placentomegaly and hydrops fetalis are preterminal events, and it has been suggested that fetal death may be due to high-output cardiac failure from arteriovenous shunting through the tumor. We had a chance to examine this hypothesis when a 21-week fetus presented with a huge sacrococcygeal teratoma. There were marked placentomegaly, cardiomegaly, hyperdynamic ventricles, and a pericardial effusion. Doppler studies showed tremendous flow through the SCT with extreme enlargement of the inferior vena cava, consistent with congestive heart failure from increased flow through the tumor. Hydrops developed, and the fetus was delivered because of placental abruption. This case provides supportive evidence that the teratoma acts as a large arteriovenous shunt, causing high-output cardiac failure. We have now collected 18 more cases of sacrococcygeal teratoma diagnosed in utero. Of the total 45 cases of fetal SCT, 9 had placentomegaly and/or fetal hydrops and all 9 fetuses died in utero or shortly after birth. We conclude that the only hope for survival in these severely affected fetuses is to reduce blood flow to the tumor before birth.

Cardiac Output↗
PubMed1985

High-output cardiac failure as a presenting symptom of plasma cell leukemia.

A patient presented with high-output cardiac failure and was found to have plasma-cell leukemia. No cause for the cardiac failure was found, and there was no response to treatment with diuretics and thiamine. Chemotherapy for the leukemia resulted in resolution of the cardiac failure, suggesting that the latter was caused by the leukemia--a hitherto unreported association.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1989

Renal arterial stenosis as a cause of high output cardiac failure.

A patient is described in whom renal arterial stenosis in a functionally solitary kidney led to arterial hypertension and high output cardiac failure. The pulmonary oedema was resistant to conventional drug therapy but showed prompt regression after percutaneous transluminal angioplasty. This case report demonstrates the usefulness of cardiac output measurement in selected patients presenting with hypertension and pulmonary oedema.

Aged↗
PubMed1992

High cardiac output of advanced liver disease persists after orthotopic liver transplantation.

This study measured cardiac output before and 1 or 2 yr after orthotopic liver transplantation in 23 patients. Cardiac output was measured by thermodilution before transplantation and by first-pass radionuclide angiocardiography at follow-up. Study patients were selected as those doing well clinically and by standard laboratory tests at 1-yr and 2-yr reevaluations with no evidence of rejection: six had mild recurrent hepatitis shown on biopsy samples. Hepatocyte function was normal at the time of the study as shown by galactose elimination capacity of 442 +/- 90 mg/min. Medications were cyclosporine and prednisone in all patients, azathioprine in 10 patients and a combination of antihypertensive therapy to maintain diastolic blood pressure less than 90 mm Hg in 20 patients. Mean (+/- S.D.) pretransplantation cardiac output was 9.1 +/- 3.1 L/min and remained elevated at 8.3 +/- 2.1 L/min 1 yr, and 9.6 +/- 2.6 L/min (n = 13) 2 yr after transplantation. A significant (p less than 0.001) correlation was found between pretransplant and follow-up cardiac output. End diastolic, end systolic and stroke volumes are all increased in a pattern similar to that seen in end-stage cirrhosis. These data show that the high cardiac output of the hyperdynamic state of advanced liver disease persists after liver transplantation. The mechanisms and consequences of this require further study.

Cardiac Output↗
PubMed1989

Congenital arteriovenous malformation of the scalp with high output cardiac failure: a case report.

A 19-year-old man was diagnosed with a rapidly enlarging arteriovenous malformation of the scalp and a mild degree of cardiomegaly. Operation to excise the large fistula took place under general anesthesia. Both external carotid arteries and their branches were controlled to prevent intraoperative hemorrhage, and dissection took place down to the periosteum. A split skin graft from the thigh was applied to the scalp defect. The patient recovered well with no further evidence of dyspnea or high output cardiac failure.

Adult↗