Is persistent hypotension after transient cardiogenic shock associated with an inflammatory response?

We evaluated the recovery of cardiovascular function after transient cardiogenic shock. Cardiac tamponade was performed for 1 h and post-shock data were collected in 5 domestic large white female pigs (43 ± 5 kg) for 6 h. The control group (N = 5) was observed for 6 h after 1 h of resting. During 1 h of cardiac tamponade, experimental animals evolved a low perfusion status with a higher lactate level (8.0 ± 2.2 vs 1.9 ± 0.9 mEq/L), lower standard base excess (-7.3 ± 3.3 vs 2.0 ± 0.9 mEq/L), lower urinary output (0.9 ± 0.9 vs 3.0 ± 1.4 mL·kg-1·h-1), lower mixed venous saturation, higher ileum partial pressure of CO2-end tidal CO2 (EtCO2) gap and a lower cardiac index than the control group. Throughout the 6-h recovery phase after cardiac tamponade, tamponade animals developed significant tachycardia with preserved cardiac index, resulting in a lower left ventricular stroke work, suggesting possible myocardial dysfunction. Vascular dysfunction was present with persistent systemic hypotension as well as persistent pulmonary hypertension. In contrast, oliguria, hyperlactatemia and metabolic acidosis were corrected by the 6th hour. The inflammatory characteristics were an elevated core temperature and increased plasma levels of interleukin-6 in the tamponade group compared to the control group. We conclude that cardiovascular recovery after a transient and severe low flow systemic state was incomplete. Vascular dysfunction persisted up to 6 h after release of tamponade. These inflammatory characteristics may also indicate that inflammatory activation is a possible pathway involved in the pathogenesis of cardiogenic shock.

N-terminal pro-B-type natriuretic peptide as a marker of disease severity in patients with pericardial effusions

BACKGROUND/AIMS: N-terminal pro-B-type natriuretic peptide (NT-proBNP) has recently been introduced as a useful marker in diagnosing underlying disease in patients with dyspnea and for determining the prognosis of patients with heart failure. The purpose of this study was to evaluate the value of the NT-proBNP as a marker of disease severity in patients with pericardial effusions. METHODS: We enrolled 69 consecutive patients who showed moderate or large pericardial effusion with preserved left ventricular (LV) systolic function; 42 patients finally participated in the study, and 13 (31.0%) of them showed cardiac tamponade. We analyzed the etiologies, the clinical and echocardiographic variables, and the serum NT-proBNP levels in these patients. RESULTS: The mean NT-proBNP level was 751+/-1002 ng/L (range 5 to 5289), and the median level was 385 ng/L (interquartile range 152 to 844). The NT-proBNP levels were higher in those patients with jugular venous distension (p=0.002), pulsus paradoxus (p=0.016), heart rate > or =100/min (p=0.006), cardiac tamponade (p=0.001), large pericardial effusion (p=0.029), exaggerated respiratory variation of the transmitral inflow (p=0.006), or plethora of the inferior vena cava (p=0.01). The NT-proBNP levels showed significant correlation with heart rate (r=0.517, p<0.001) and the diameter of the inferior vena cava (r=0.329, p=0.03). CONCLUSIONS: NT-proBNP may be useful as a marker of disease severity in patients suffering from pericardial effusion, but further prospective studies with more patients will be needed.