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At least 37 records · Page 2Linked to original sources
PubMed2002

Antenatal diagnosis and treatment of a case of fetal goitrous hypothyroidism associated with high-output cardiac failure.

A case of fetal goitrous hypothyroidism associated with high-output cardiac failure is presented. At 32 weeks of gestation, the antenatal diagnosis of goiter was made based on ultrasound examination, and the fetal thyroid function was examined by amniocentesis and cordocentesis. Color and pulsed Doppler examinations demonstrated a high vascular flow pattern in the goiter and marked elevation of the maximum velocity in the common carotid artery at the level of the neck. It was suspected that arteriovenous shunting through the large goiter resulted in high-output cardiac failure with cardiomegaly and pleural effusion. The fetus was treated by injection of levothyroxine sodium into the amniotic fluid at 33 weeks of gestation and the goiter thereafter decreased in size, with subsequent improvement of the high-output cardiac failure. The maximum velocity in the common carotid artery fell rapidly before the shrinkage of the fetal goiter and in parallel with the fetal level of thyroid stimulating hormone.

Adult↗
PubMed1997

[High cardiac output in myeloma patients. Its prevalence and clinical characteristics. The Castile-León Cooperative Group for the Study of Monoclonal Gammapathies].

BACKGROUND: The study determines the prevalence of high cardiac output status in patients with multiple myeloma (MM) and its relationship with the more significant clinical and biological characteristics of the disease. PATIENTS AND METHODS: Cardiac output was determined in 28 patients with multiple myeloma by pulsed Doppler echocardiography. Patients with any other identifiable cause of high cardiac output were excluded. Mean age was 70 +/- 8 SD years (53-84). A stepwise regression with the cardiac output as dependent variable and age, performance status (ECOG), clinical stage (Durie and Salmon), scale of bone lesions, serum calcium, serum creatine, bone involvement (percentage), and M protein quantity as independent variables showed the following results. RESULTS: A high cardiac output state, defined as a cardiac index higher than 4.6 l/min/m2 was present in five patients (17.8%), four of them with severe bone involvement. Two patients developed heart failure. The stepwise regression revealed the scale of bone lesions was the unique variable associated with the risk of developing a high cardiac output status. CONCLUSIONS: A high cardiac output status may be fairly common in patients with multiple myeloma. The syndrome is associated with severe bone involvement, being the scale of bone lesions the only risk factor for this complication.

Aged↗
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↗
PubMed1983

[Mechanisms of regulation of high cardiac output in patients with hypertension (angiocardiographic study)].

To identify mechanism conditioning high cardiac output, an angiocardiographic study was conducted in 39 patients with essential hypertension. Increased stroke and cardiac output was found to be due to increased venous inflow, with inotropic condition of the hypertrophic myocardium being reduced in spite of enhanced general pumping function of the left ventricle. As arterial hypertension tended to stabilize and cardiac output declined, total peripheral resistance assumed the principal responsibility for its regulation, whereas at earlier stages of the disease it shows either normal, or even reduced levels, and venous inflow is the principal factor controlling cardiac and stroke output.

Adult↗
PubMed1996

Circuit factors in the high cardiac output of sepsis.

PURPOSE: The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (Cv), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized. METHODS: Pigs were anesthetized and mechanically ventilated. We measured CO by thermodilution, mean circulatory filling pressure (MCFP) by inflating a balloon in the right atrium, blood volume by dye dilution, and Cv by rapid blood infusions. RVR was calculated from MCFP-Pra/CO). After baseline measurements, we infused 10 micrograms/(kg x h-1) of Escherichia coli endotoxin. Eight animals also received 30 mL x kg-1 of dextran over the 2 hours (volume treated), and seven did not (no volume). After 2 hours we injected 25 mg x kg-1 of the NO synthase inhibitor, L-NAME, and repeated the measurements. RESULTS: In volume-treated animals, CO increased from 3.9 +/- 0.7 to 5.4 +/- 0.8 L x min-1 (P < .05), and blood pressure (BP) fell from 118 +/- 9 to 76 +/- 12 mmHg. MCFP rose, and there was no change in RVR or Cv, whereas capacitance increased (ie, right shift of pressure-volume curve). Cardiac function (ie, Starling curve) did not change. In no-volume animals, CO fell from 4.47 +/- 0.64 to 2.50 +/- 0.86 L x min-1, BP from 114 +/- 10 to 9 +/- 13 mmHg and MCFP fell. Systemic vascular resistance did not change. Cardiac function was markedly depressed, and the heart rate increased from 143 +/- 13 to 203 +/- 30 beats x min-1. L-NAME restored BP in both groups but also increased RVR and depressed cardiac function. CONCLUSION: Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.

Analysis of Variance↗