Proatrial natriuretic peptide (1-98), but not cystatin C, is predictive for occurrence of acute renal insufficiency in critically ill septic patients.

INTRODUCTION: N-terminal prohormone of atrial natriuretic peptide ((proANP(1-98)) has been extensively analyzed in patients with chronic renal failure. It has been found to be closely related to the renal function and to interdialytic hydration status. The clinical relevance of proANP(1-98) and cystatin C, a novel marker of glomerular filtration, has not been investigated in the subgroup of critically ill septic patients with no history of chronic renal impairment. METHODS: We measured plasma level ofproANP(1-98) and cystatin C in 29 critically ill septic patients on admittance to the surgical intensive care unit and correlated it with the occurrence of acute renal failure. RESULTS: The proANP(1-98) plasma level was significantly higher in the group of patients who developed renal failure (12,722 +/- 12,421 vs. 2,801+/- 2,023 fmol/ml, p < 0.05). Multiple regression analysis shows that proANP(1-98) on the first day in the intensive care unit has a superior predictive value for the occurrence of renal failure to diuresis, calculated creatinine clearance or cystatin C (r = 0.42, p < 0.039). proANP(1-98) is also higher in non-survivors (9,303.8 +/- 11,053 vs. 2,448.5 +/- 1,803 fmol/ml, p < 0.018). CONCLUSION: proANP(1-98) is possibly a better predictor of acute renal failure to calculated creatinine clearance or diuresis among critically ill septic patients. Cystatin C was not correlated with occurrence of acute renal failure in this subgroup of patients.

Hemodynamically unstable pericardial effusion in the Intensive Cardiac Unit: prospective study.

The authors have conducted a prospective investigation on 15 patients with hemodynamically unstable pericardial effusion (main criteria: echocardiographic signs of various degrees of right ventricular diastolic collapse and clinical instability) hospitalized in the Intensive Cardiac Unit (1.97% of all patients) for one year and have compared the results with literature data. The causes of pericardial effusion were neoplasms, infections, rupture of heart of aorta and hypothyroidism. Investigation revealed the most frequent findings: symptoms (dyspnea, retrosternal pain, loading intolerance, nonproductive cough), clinical signs (soft heart sounds, changes in pulmonal findings, fever, jugular venous distention, tachycardia, arterial hypotension and hepatomegaly), laboratory changes (elevated erythrocyte sedimentation rate, leukocytosis), ECG changes (ST-T abnormality, microvoltage, tachycardia) and chest X-rays changes (enlarged cardiac silhouette, pleural effusion). Echocardiography found an average width of pericardial effusion of 2.5 cm (+/- 1.2), frequently thickened pericardium and changes in heart motions. The most used drugs in therapy were indomethacin, antibiotics, analgesics and corticosteroids. In three patients pericardiocentesis, and in two pericardiectomy were performed. Two patients died, 13 patients were discharged from the ICU with an improved health condition. Literature data on this condition are either lacking, or differ from the above findings.

Dominant right ventricular infarction: is angioplasty the optimal therapeutic approach?

Approximately 30% of all acute inferior myocardial infarctions (AIMI) are accompanied by acute right ventricular infarction (ARVI) as a consequence of proximal right coronary artery (RCA) occlusion. Fifty per cent of all patients with ARVI manifest hypotension, jugular venous distension, and dyspnoea with clear lung fields, which is then considered as dominant acute RVI (ARVI). The in hospital mortality rate of patients with ARVI who are treated traditionally is very high. Thrombolytic therapy is relatively ineffective, while primary angioplasty is a more recent approach yet to be established as optimal treatment for patients with ARVI. Thirty-eight patients with dominant ARVI were admitted to our CCU over a period of 24 months. The patients were retrospectively divided into 3 groups according to treatment: Group I (n = 16): traditional treatment; Group II (n = 12): thrombolytic therapy (streptokinase); Group III (n = 10): angioplasty after urgent coronarography. We tested the difference in the number of deaths in all groups by the Fisher exact test. There was a significant difference in the number of deaths between Group I and Group III (P < 0.05). Mortality reduction was also noted between Group II and Group III, which, however, proved to be statistically insignificant.

[Pathophysiologic mechanisms of cardiac decompensation]. / Patofizioloski mehanizmi srcane dekompenzacije.

Heart failure is a complex clinical syndrome in whose manifestations and prognosis compensatory mechanisms have a prominent role as a response of the organism to an elementary disturbance. There are five basic compensatory mechanisms: the Frank-Starling mechanism, structural changes of the heart, activation of neuroendocrine mechanism, adaptation to hypoxia and anaerobic metabolism. The interaction between the two main neurohumoral mechanisms, namely vasodilatation and vasoconstriction, has been drawing much of the attention recently. Vasoconstriction which evolved into maintaining cardiac output in hypovolemic state, leads to a number of deleterious hemodynamic and metabolic disturbances in heart failure. The organism tends to diminish this negative effects by changing beta adrenergic pathway and by activating vasodilative mechanisms. Once heart failure becomes severe, vasoconstriction predominates due to a loss of normal baroreceptor activity. It is considered that too marked activity of neurohumoral mechanisms is a significant cause of disease progression. By use of contemporary drugs (ACE inhibitors, beta blockers, digitalis), excessive vasoconstrictive mechanisms are tried to be diminished and prognosis of the disease improved.