PubMed · 4092464
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L M Sakhrani, S G Massry. 1985. Hyponatremia.. https://doi.org/10.1159/000411882
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BACKGROUND: Preterm babies are at risk of haemorrhagic and ischaemic brain injury. One controlled trial suggested that prophylactic fresh-frozen plasma (FFP) may reduce that risk but did not clarify whether the reduction in periventricular haemorrhage seen on ultrasonography was due to a haemostatic effect or stabilisation of intravascular volume by FFP. We undertook a trial of 776 babies of gestational age at birth less than 32 weeks to look at the short-term and long-term outcome after early prophylactic FFP. METHODS: The defined primary trial outcome was survival without identifiable major disability 2 years after birth. The babies were randomly allocated, within 2 h of birth, 20 mL/kg FFP followed by a further 10 mL/kg after 24 h; or the same volumes of a gelatin-based plasma substitute; or maintenance infusion of glucose (control). The three groups were similar at trial entry. Outcome at discharge from hospital after birth (reported elsewhere) was similar in the three groups. FINDINGS: No child was lost to follow-up, and all the surviving children underwent neurological and developmental assessment at the age of 2 years. The proportions dying (21.0%, 24.9%, 20.5%), and the proportions of survivors with a severe disability (11.3%, 11.2%, 14.1%) did not differ significantly between the randomised groups. The survivors had similar mean developmental quotients at age 2 (Griffiths' quotients 94, 97, and 95). INTERPRETATION: This trial provides no evidence that the routine early use of FFP, or some other form of intravascular volume expansion, affects the risk of death or disability in babies born more than 8 weeks before term.
BACKGROUND: Congestive heart failure is associated with blood volume expansion caused by stimulation of the renin-aldosterone system and arginine vasopressin. The use of left ventricular assist devices as bridges to heart transplantation has improved the survival of patients during this critical period. In studying heart failure physiology on support devices, we hypothesized that improvement of cardiac function by a left ventricular assist device is associated with normalization of volume load secondary to normalization of its regulatory substances. METHODS AND RESULTS: We studied 15 patients (13 men, 2 women: age 51 +/- 8 years) with end-stage heart failure who were cardiac transplant candidates eligible for HeartMate implantation. We measured plasma volume and plasma levels of atrial natriuretic peptide, aldosterone, renin, and arginine vasopressin sequentially before HeartMate implantation (baseline), after HeartMate implantation (weeks 4 and 8), and after transplantation. Baseline plasma volume was 123 +/- 20% of normal; it was 122 +/- 22% at week 4 and decreased to 115 +/- 14% at week 8. Atrial natriuretic peptide was 359 +/- 380 pg/mL at baseline, 245 +/- 175 pg/mL at week 4, and 151 +/- 66 pg/mL at week 8. Plasma aldosterone fell from 68 +/- 59 ng/dL at baseline to 17 +/- 16 ng/dL at week 4 (P < .05 versus baseline) and was 32 +/- 50 ng/dL at week 8. Plasma renin activity decreased from 80 +/- 88 ng/dL at baseline to 11 +/- 12 ng/dL at week 4 and was 16 +/- 38 ng/dL at week 8 (both P < .05 versus baseline). Arginine vasopressin fell from 5.0 +/- 4.8 fmol/mL at baseline to 1.1 +/- 0.7 fmol/mL at week 4 and 1.2+/-0.8 fmol/mL at week 8 (both P < .05 versus baseline). CONCLUSIONS: The reduction of plasma renin activity, plasma aldosterone, and arginine vasopressin occurred earlier than the reduction of plasma volume and atrial natriuretic peptide after HeartMate implantation, possibly because of decreased pulmonary congestion and improved renal perfusion. The reduction of atrial natriuretic peptide cannot be responsible for the lack of adequate decrease of plasma volume; its reduction can be taken as a marker of improved cardiac pump function and decreased atrial stretch.
In cirrhosis, cardiac contractile function has been extensively documented to be abnormal. At baseline, cardiac output is increased, and this is one of the characteristics of hyperdynamic circulation. However, when cirrhotic patients are challenged by pharmacological or physiological stress, ventricular hyporesponsiveness is revealed. Similar patterns have been noted in cirrhotic animal models. This phenomenon has been termed "cirrhotic cardiomyopathy." Although alcohol abuse may contribute to some cases of cirrhotic cardiomyopathy, it has been clearly documented to occur even in the absence of alcohol ingestion. Diminished myocardial beta-adrenergic receptor signal transduction function, possibly caused by a persistent elevation in norepinephrine content, has been shown to play an important role. Alternation in cardiac plasma membrane properties due to impaired lipid metabolism is also crucial. Other possible pathogenic factors are reviewed, including accumulation of cardiodepressant substances caused by hepatocellular insufficiency, and ventricular overload secondary to increased blood volume and hyperdynamic circulation. Because the cardiac reserve function is borderline in patients with cirrhosis, cardiovascular status should be carefully monitored, especially when patients undergo stresses such as liver transplantation or portosystemic shunting procedures.