The pathophysiology of shock

The pathophysiology of shock

119 The petbophysiolegy of shock Skowronski, G.A. Intensive Care unit, Flinders Medical Centre, Bedford Park, SA 5042, Au&a&z MED. J. AUST., 148(l) (1...

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119 The petbophysiolegy of shock Skowronski, G.A. Intensive Care unit, Flinders Medical Centre, Bedford Park, SA 5042, Au&a&z MED. J. AUST., 148(l) (19881676-583 Shock describes a group of circulatory syndromes, all of which result in generalized cellular hypoxia. This leads to the depletion of adenosine triphosphase, the failure of the sodium-potassium pump, mitochondrial dysfunction, and ultimately, the release of a variety of toxic substances. Eventually, these give rise to irreversible cardiovascular collapse because of their effects on the microcirculation. Shock may arise due to a failure of preload (hypovolaemic shock), myocardial contractility (cardiogenic shock), afterload (septic shock) or combinations of these (for example, anaphylactic shock, traumatic shock and neurogenic shock). During shock, important physiological changes occur in the nervous, respiratory, renal and gastrointestinal systems, as well as in intermediary metabolism. Hypotension is not synonymous with shock, and emphasis should be placed on the detection of more subtle, early signs. Management requires a systematic approach in which diagnostic and therapeutic processes take place in parallel. Particular attention must be paid to ventilation, oxygenation, fluid and electrolyte therapy, haemodynamic monitoring and, where appropriate, inotropic drugs. Corticosteroid and opioid antagonist agents probably do not have a role, but other rf agents, such as thyroid hormones, are under investigation. Resllscitetion artefact Leadbeatter, S., Knight, B. Institute ofPathology, Royal Infirmary, Cardiff CF2 HZ, U.K. MED. SCI. LAW, 28(31(19881200-204 This article provides a selective review of the literature concerning pathological lesions attributed to resuscitation and considers their medico-legal implications. Illustrative cases of interpretational problems are cited. The importance of the pathologist’s awareness prior to autopsy of an attempt at, and the nature of, resuscitation is emphasized. HLW-Breitenausbildung: else Lanze ftir den Diagnostiscben Block resuscitation: The diagnostic sequence Bahr, J., Busse, C. Zentrum Anuesthesiologie der Universitat Gottingen, D-9400 Gottinge% F.R.G. NOTFALL MED.. 14(61(19881456- 460 Extended training in cardiopulmonary

Neue Endobroncbiale Apptiationssonde fiir die Reanimation A new catheter for endobroncbial drug administration for cardiopulmonary Schmidt, C., Schon, FL, Russ, J. Medisinische Poliklinik der Rheinishcen



D-5300 Bonn 1, F.R.G.

NOTFALL MED., 14(81(19881673-674 Anti-shock effect of ACTH_(l-24): Influence of subtotal hepatectomy Guarini, S., Ferrari, W., Bertolini, A. Institute of Pharmacology, University of Modena, 41100 Modena, Italy PHARMACOL. RES. COMMUN., 20(51(19881395- 403 Subtotally hepatectomized or sham-operated rats were bled to hypovolemic shock (mean arterial pressure = 18-25 mmHg1and then treated with an intravenous bolus injection of ACTH-(l-241,160 pg/kg. The treatment caused a prompt and sustained reversal of hypotension, with survival of all sham-operated animals, at least for the first 2 h, while in hepatectomized rats the arterial pressure increase was negligible and there was a 50°Eomortality within 2 h after treatment. Moreover, the blood volume which could be drained from an arterial catheter prior to death, measured 15-20 min after ACTH injection, was 1.51 f 0.12 and 0.64 f 0.11 ml/100 g.b.w. in sham-operated and hepatectomized rats, respectively. These results further support the idea that the effect of ACTH in haemorrhagic shock is due to the mobilization of blood pooled in peripheral reserve organs.