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

Abstract

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 CO 2 -end tidal CO 2 (EtCO 2 ) 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.

Reclassifying the spectrum of septic patients using lactate: severe sepsis, cryptic shock, vasoplegic shock and dysoxic shock

“…(21,29) The fact that occult hypoperfusion exists and is not diagnosed is unsurprising. The imbalance between the supply and consumption of oxygen is a characteristic of shock conditions, and other markers such as blood pressure, heart rate, are urine output exhibit a low sensitivity of detecting the presence of shock.…”

<p>Association between inflammation-based prognostic scores and in-hospital outcomes in elderly patients with acute myocardial infarction</p>

“…Systemic inflammation is a well-known risk factor for atherosclerosis12 and plays an important role in atherosclerotic plaque instability.13 On the other hand, inflammation is often a downstream pathological change of AMI, and excessive inflammation can lead to the aggravation of the original diseases, resulting in a vicious circle. In patients with AMI, several severe complications such as cardiac shock,14 heart failure15 and secondary infection can lead to increased inflammatory markers. Hence, higher inflammation-based scores at admission reflect the complex clinical baseline characteristics of patients.…”

Metabolic acid-base adaptation triggered by acute persistent hypercapnia in mechanically ventilated patients with acute respiratory distress syndrome

“…In contrast, in acute critically ill animal models, the acid-base disturbances are marked, especially metabolic acidosis. ( 25 , 26 ) In critically ill patients, metabolic acidosis is relevant, multifactorial, and related to clinical outcomes. ( 27 , 28 ) These patients present reduced sodium and chloride renal excretion, ( 10 , 11 , 29 ) together with chloride shift from the extravascular to the intravascular compartments added to exogenous load during fluid resuscitation, ( 30 ) frequently resulting in hyperchloremia.…”