Hyperkinetic Shock Research Articles

Multi-organ failure secondary to an aortocaval fistula-when should it be suspected?

Spontaneous aortocaval fistula (ACF) is a rare, life threatening complication of abdominal aortic aneurysms (AAA) which is seldom suspected clinically. We report a case of progressive multi-organ failure secondary to an ACF wherein a delayed diagnosis was followed by a successful outcome. A 67-year-old man presented with dyspnoea on exertion, cough, and night sweats for three weeks. Initial investigations showed type 1 respiratory failure and mild renal impairment. He was treated for a suspected respiratory tract infection and fluid overload but antibiotic and diuretic therapies were ineffective. Within the following 36 hours he developed progressive azotemia and acute liver failure. He had physical signs of predominantly right-sided heart failure with preserved left ventricular systolic function on echocardiogram. Abdominal ultrasound and a non-contrast computed tomography (CT) revealed mild hepatomegaly, a 10 cm AAA with no evident leak and unremarkable kidneys. Oliguria and metabolic acidosis ensued with rapid deterioration of renal function and hypotension necessitating continuous veno-venous hemofiltration with inotropic support. Hepatic and renal function improved within a week of intensive care therapy but signs of volume overload persisted. A contrast abdominal CT demonstrated an ACF, which was successfully managed by endovascular stent-grafting. This case highlights the importance of being alert to the haemodynamic consequences of aortocaval rupture particularly in the presence of a large AAA in a patient presenting with unexplained organ failure and hyperkinetic shock. Optimisation of supportive care impacts favourably on the perioperative course and overall prognosis of this rare condition.

Nitric oxide involvement in the hemodynamic response to fluid resuscitation in endotoxic shock in rats

Fluid loading is an essential part of cardiovascular resuscitation in septic shock. We hypothesized that fluid administration increases blood flow velocity and thus endothelial shear stress, causing the release of nitric oxide by the vascular endothelium. Because of endothelial dysfunction in sepsis, this mechanism would be less effective in septic animals. Fluid loading may have different effects in septic compared with control animals. Prospective, randomized, controlled study. Animal research laboratory. Male Sprague-Dawley rats. We tested the involvement of nitric oxide in the fluid-induced cardiovascular response after administration of lipopolysaccharide (5 mg/kg, n = 10) or vehicle (control, n = 10) in rats subsequently randomized after 165 mins to receive L-N(G)-nitroarginine (7.5 mg/kg) or saline (n = 5 in each group). At 180 mins, all animals received hydroxyethyl starch (fluid loading, 15 mL/kg in 15 mins). Reversal of L-N(G)-nitroarginine was studied with an intravenous bolus of L-arginine (300 mg/kg). Lipopolysaccharide injection induced a hypokinetic shock (low blood pressure: -30% +/- 9%, p < .05), low cardiac output (aortic pulsed-Doppler probe: -20% +/- 8, p < .05), and unchanged systemic conductance, which turned into a hyperkinetic shock by fluid loading. Pretreatment with L-N(G)-nitroarginine totally abolished this fluid loading-induced vasodilation in control rats but only partially in lipopolysaccharide-treated rats, suggesting an altered endothelial response after lipopolysaccharide injection. Maximal aortic blood flow acceleration was used as an index of left ventricular systolic function. The improvement of maximal aortic blood flow acceleration observed during fluid loading in lipopolysaccharide-treated or control animals was blunted by L-N(G)-nitroarginine pretreatment, suggesting the involvement of nitric oxide in the myocardial response to fluid loading. These results suggest that the endothelium participates in the hemodynamic response to fluid loading in control rats, but less in rats with septic shock, secondary to an altered nitric oxide-dependent vasodilation.

Choc initial du brûlé. Physiopathologie : principes thérapeutiques

Widespread destruction of the skin induces a large necrotic mass and a break of the skin barrier. It also leads to an intense inflammatory reaction. This activates keratinocytes, endothelial cells and neutrophils. Certain mediators (e.g. endothelin, histamine, bradykinin, serotonin, catecholamines, vasopressin, prostaglandins, cytokines and nitrogen monoxide) are thus released in large quantities and act both at the site of the burns and at a distance. The abnormally high level of albumin in the capillary wall and the increased capacity of absorption of the interstitial areas around the burns are the main abnormalities observed. This results in a hypovolemia associated with a hemoconcentration, hyponatremia, hypoalbuminemia, systemic vasoconstriction and myocardial malfunction, which is difficult to evidence. During the initial phase, the major risk is the appearance of hypovolemic shock, which is rapidly irreversible if early treatment is not administered. Vascular filling with iso- or hyper-osmolar sodium crystalloids, associated with buffer solutions, is the first line. There is still debate regarding the best moment at which to give albumin. A hyperkinetic shock may occur after several hours and despite the filling. The symptoms are tachycardia, increased heart rate and a dramatic decrease in systemic vascular resistance. This may lead to metabolic acidosis and multi-organ failure. Study of the hemodynamic profile of the patient allows the rational use of pressor amines and haemodialysis.

In vivo evidence of enhanced guanylyl cyclase activation during the hyperdynamic circulation of acute liver failure

Nitric oxide and atrial natriuretic peptides are the main activators of guanylyl cyclases, which transform GTP into cyclic GMP and thereby contribute to the decrease of vascular tone. To investigate the increase, if any, of plasma cyclic GMP concentrations in human patients with hyperdynamic circulation resulting from acute liver failure and to ascertain whether guanylyl cyclase activation is involved in the decline of systemic vascular resistance that occurs in this pathophysiological condition, we simultaneously recorded hemodynamic data and cyclic GMP levels in patients with fulminant liver failure before and after liver transplantation and in normokinetic patients undergoing abdominal nonseptic surgery. We also compared these data with those recorded in patients with hyperkinetic shock resulting from gram-negative sepsis or nitric oxide-independent vasomotor agent (carbamate) over-dose. In all these patients we simultaneously studied kidney function, platelet counts and atrial natriuretic peptides. Patients with fulminant liver failure had higher cyclic GMP concentrations than did control patients undergoing abdominal surgery (11.02 +/- 1.55 pmol.ml-1 vs. 1.77 +/- 0.18 pmol.ml-1, p < 0.001). At similar heart-loading conditions these concentrations were lower than those in gram-negative septic shock (18.2 +/- 1.35 pmol.ml-1, p < 0.05) but higher than those in carbamate-induced shock (3.6 +/- 0.7 pmol.ml-1, p < 0.01). In addition, cyclic GMP concentrations significantly decreased from the fulminant liver failure period to the posttransplantation period, although atrial natriuretic peptide levels did not change significantly and kidney function worsened.(ABSTRACT TRUNCATED AT 250 WORDS)

Choc hyperkinétique et accès pernicieux palustre

Two cases of cerebral malaria with hyperkinetic shock are reported. The first case concerned a 39-year-old european male who was not taking any prophylactic anti-malarial drugs. After having had headache and fever for a week, he was admitted to the intensive care unit (ICU) in coma and with jaundice. His initial systolic blood pressure was 60 mmg, with a central venous pressure (CVP) of — 3 cmH 2O. Five-hundred ml of modified fluid gelatin increased the CVP without raising the blood pressure. Haemodynamic investigations revealed a cardiac index (CI) = 5.21 · min −1 · m −2, peripheral arterial resistances (Rsa) = 290 dyn · s · cm −5, oxygen consumption (V̇O 2) = 120 ml · min −1 · m −2. Despite treatment with dopamine and dobutamine, the patient died 3 h after his admission, with a CI of 1.91 · min −1 · m −2. The second patient was a 14-year-old senegalese girl, admitted in circumstances similar to the first case. Initial haemodynamic investigations gave the following figures: CI 6.51 · min −1 · m −2, Rsa = 476 dyn · s · cm −5, V̇O 2 = 174 ml · min −1 · m −2. Recovery was obtained with fluid replacement therapy and dopamine. In the absence of another associated infectious disease, the plasmodial origin of the septic shock would seem to be the most likely in both cases. Pathophysiological mechanisms of these algid forms of malaria remain enigmatic. Various factors are discussed: cytoadherence of erythrocytes infected with Plasmodium falciparum, immunological disturbances, or a specific endotoxin.

Hyperkinetic shock in viral and pneumococcal pneumonias

Ten patients, suffering from severe viral or bacterial pneumonia had circulatory shock, characterised haemodynamically by normal or high cardiac output (CI = 4.1 +/- 1.2 1/min/m2) and low systemic resistance (SVR = 14 +/- 3.7 mm Hg/1/min/m2). Existence of such a hyperkinetic state greatly complicates the management of patients. Plasma volume expansion, performed in five cases of initial hypovolaemia, and Dopamine infusion (five patients) increased markedly the intra-pulmonary shunting. High level PEEP ventilation was not tolerated, despite the improvement of blood gases it produced. Extra-corporeal membrane lung oxygenation (three cases), whilst giving an initial decrease of shunting and restoring SVR, produced no long term surviors. All ten patients died from intractable shock and severe hypoxaemia. Spontaneous ventilation with positive expiratory pressure (CPAP) is believed to be an attractive alternative, due to its absence of deleterious haemodynamic effects.