Vasopressin therapy in cardiac surgery.

BACKGROUND: Arginine vasopressin (AVP) is a naturally occurring peptide with diverse effects mediated through selective V1 and V2 receptors. About 10% of patients undergoing cardiopulmonary bypass develop postoperative vasodilatory shock requiring high-dose catecholamines. We sought to examine the role of AVP therapy in cardiac surgery. METHODS: A search of Medline was conducted through September 2018 using key words and medical subject headings (MeSH) relating to AVP, copeptin, and cardiac surgery. A systematic review was performed on articles as they pertained to AVP for use as a vasopressor after cardiovascular surgery complicated by vasodilatory shock. RESULTS: A relative or absolute deficiency of Arginine vasopressin is associated with vasodilatory shock after cardiopulmonary bypass. Physiologic replacement with exogenous Arginine vasopressin results in significant increases in systemic vascular resistance and mean arterial pressure with decreased requirements of catecholamines. At doses of <0.1 U/min Arginine vasopressin is safe with very few adverse effects. CONCLUSION: Post-cardiopulmonary bypass vasodilatory shock is largely due to a relative deficiency of Arginine vasopressin. Exogenous administration of low-dose Arginine vasopressin alone or in combination with traditional catecholamines is a safe and effective way to manage this type of vasodilatory shock.

Multidisciplinary mechanical supports improve outcome in a shock patient with cardiac amyloidosis: a case report.

Shock patients with restrictive cardiomyopathy due to cardiac amyloidosis are refractory to medical treatment. Here, we report a case of early initiation of intra-aortic balloon pumping (IABP) in a patient with cardiac amyloidosis who developed postoperative shock. Continuous hemodiafiltration was also applied to control circulating fluid volume. The mechanical treatments allowed reduction of the doses of catecholamine and diuretics and resulted in full recovery. It is reasonable to initiate IABP and hemofiltration dialysis during the early stages for the appropriate control of hemodynamics and fluid in shock patients with cardiac amyloidosis.

Occult hypoperfusion--should the military surgeon care?

The treatment of traumatic shock has changed unrecognizably over the past decade as the combination of targeted research and lessons learnt from conflict have combined with a common goal. The term damage control resuscitation has emerged as the most likely strategy to treat the underlying cause, restore normal physiology and ultimately return to normal function. However, there is still a great deal that we do not understand as to the underlying mechanisms which control the traumatic shock process. Military surgeons have an integral part to play at every step of this process. Their role does not end once the initial damage control surgery is complete and indeed the decisions that are made during the initial resuscitation will have an effect on all future stages of care. The patient's physiology is delicately balanced with the possibility that a wrong treatment decision may be a fatal one. It is essential that the surgeon has an understanding of these underlying processes so that an informed decision can be made at the right time.

Antidiuretic hormone replacement therapy to prevent or ameliorate vasodilatory shock.

Vasodilatory shock is a syndrome with high mortality. It is becoming evident that depletion of antidiuretic hormone (ADH) after cardiac surgery or during sepsis plays an important role in the pathogenesis of this condition. Established vasodilatory shock responds well to exogenous ADH infusion. It is possible that preventing ADH depletion at an earlier stage may abrogate the onset of vasodilatory shock, or at least reduce its severity. This paper examines the evidence supporting this concept, and the potential areas of concern in considering this particular type of hormone replacement therapy.

Vasopressin in the cardiac surgery intensive care unit.

Although nearly 10% of patients experience profound vasodilatory shock after cardiopulmonary bypass, some patients remain refractory to traditional resuscitation. Among this subset are patients who have inappropriately low levels of endogenous vasopressin. Thus, vasopressin replacement is an intuitively attractive intervention. The purposes of this review are to outline the pathophysiology of vasodilatory shock after cardiopulmonary bypass, to discuss the physiological role of endogenous vasopressin, to explore the clinical basis for vasopressin replacement, and to review the pharmacology and dosing guidelines.

Xanthine oxidase inactivation attenuates postocclusion shock after descending thoracic aorta occlusion and reperfusion in rabbits.

"Declamping shock" is observed after aortic crossclamping, with hypovolemia, hypotension, and metabolic acidemia invariably present. We hypothesized that oxidants derived from xanthine oxidase influence the resuscitative interventions required to maintain baseline hemodynamic and acid-base status after aortic occlusion and reperfusion in rabbits. We also hypothesized that inactivation of xanthine oxidase with sodium tungstate could reduce systemic injury as assessed by the release of lactate dehydrogenase and alkaline phosphatase. To test these hypotheses, we established aortic occlusion in rabbits (n = 10, standard diet; n = 8, tungstate diet) for 40 minutes by inflation of a 4F Fogarty catheter in the descending thoracic aorta followed by 2 hours of reperfusion. Sham-operated rabbits (n = 10, standard diet; n = 9, tungstate diet) served as controls. Tungstate-pretreated rabbits required significantly less Ringer's solution (28%), phenylephrine (68%), and sodium bicarbonate (30%) during reperfusion (p < 0.005). Lactate dehydrogenase and alkaline phosphatase release during reperfusion was significantly attenuated by tungstate pretreatment (p < 0.05). Tungstate pretreatment resulted in plasma xanthine oxidase activities significantly lower than those in the sham group administered a standard diet (p = 0.007). Resuscitation requirements and systemic injury were reduced by inactivation of xanthine oxidase in a rabbit model that simulates the situation of human thoracic aorta operations.

Disturbances of hemostasis during declamping shock.

The aorta, above or below renal arteries was clamped for 60 minutes, in a canine model. The blood was taken for testing from above the aorta bifurcation before clamping, after 30 minutes of its duration, directly after declamping and every 30 minute during next 4 hours. Irrespective of clamping level, the platelet count, clot retraction and prothrombin consumption do not undergo significant changes. However, the activity of platelet factor 4 is increased. Prothrombin time, recalcination time, kaolin-kephalin time and the activities of factors V, VII, XI and XII do not differ as well. Thrombin time is prolonged and antithrombin III activity is reduced. Euglobulin fibrinolysis time undergoes prolongation and antiplasmin content is increased. The observed changes show a variable tendency, regardless of clamping level and increase with the passage of experiment time. An increase in the coagulation activity and a decrease in the fibrinolytic activity of the blood plasma may be a resultant of the changes. Finally it may promote thrombus formation and indicates the preventive use of heparin.

Hemostatic activity of organs in declamping shock.

The aim of the study was to determine the haemostatic components activity of organs in declamping shock. The abdominal aorta was cross-clamped below or above renal arteries. No significant changes in tromboplastic and antithrombin activities were found in the kidney, liver, lung, heart and skeletal muscle. Renal cortex and medulla as well as the lungs show higher plasminogen activator activity and considerably higher antiplasmin activity. Diminished fibrinolysis in the kidney and the lung may promote thrombotic complications.

Acute adrenal insufficiency presenting as shock after trauma and surgery: three cases and review of the literature.

Profound nonhemorrhagic shock developed in one postoperative and two trauma patients. Cardiovascular collapse was characterized by severe hypotension (systolic blood pressure less than 80 mm Hg), hyperdynamic cardiac indices (CI greater than 4 L/min/m2), low systemic vascular resistance (SVR less than 500 dyne.sec/cm5.m2), and multiple organ failure. Sepsis was not found by culturing of specimens or visual inspection at laparotomy. Screening cortisol levels were low (less than 2 micrograms/dL in two patients) and did not respond appropriately to synthetic ACTH (cosyntropin) challenge. Administration of exogenous glucocorticoids promptly and dramatically reversed shock and organ failure in two patients. Oral glucocorticoid and mineralocorticoid supplementation were required at hospital discharge. Acute adrenal insufficiency is rare after trauma, but may produce life-threatening cardiovascular collapse, mimicking the "septic" shock state. Cosyntropin stimulation testing confirms the diagnosis and is accurate in traumatized patients. Outcome is dependent upon early recognition and exogenous glucocorticoid administration. Appropriate endocrine evaluation prevents unnecessary use of steroids in a population of trauma patients who are already in a state of immunosuppression.

Oxygen transport measurements to evaluate tissue perfusion and titrate therapy: dobutamine and dopamine effects.

BACKGROUND: Increased cardiac index, oxygen delivery (DO2), and oxygen consumption (VO2) patterns were shown to characterize the physiologic status of surviving high-risk surgical patients, and indicate increased metabolic needs; relatively normal DO2 and VO2 values were found to characterize the sequential pattern of nonsurvivors who developed an early oxygen debt followed by lethal organ failure. The cardiac index, DO2, and VO2 values empirically determined from survivors' patterns were shown to improve outcome in prospective randomized trials. The present study considers these criteria to evaluate the tissue perfusion status as well as the effects of therapy on tissue perfusion and oxygenation. OBJECTIVE: To summarize new information on the temporal patterns of DO2, VO2, and oxygen debt on outcome and the effects of fluids and inotropes on these patterns in a wide range of clinical, temporal, and physiologic conditions. DESIGN: Descriptive analysis based on data gathered prospectively using a specified protocol. PATIENTS: High-risk patients with accidental or elective surgical trauma, and patients with or without sepsis or septic shock and organ failure. SETTING: University-run county hospital with a large trauma service. INTERVENTIONS: Fluids, dobutamine, and dopamine at various times and at various doses throughout critical illness of postoperative, posttraumatic, septic, and hypovolemic patients with and without lethal and nonlethal organ failure. MEASUREMENTS AND MAIN RESULTS: The pattern of DO2 plotted against the corresponding VO2 values in 437 consecutive critically ill surgical patients showed a wide variability and poor correlation probably because complex clinical conditions may obscure the supply-dependent and supply-independent VO2 relationships observed in normal dogs bled or given bacterial infusions. However, the use of specific therapy by well-defined protocols was shown to provide objective evidence of efficacy. Significant increases in DO2 and VO2 were previously shown after whole blood, packed red cells, and colloid administration, but not after crystalloid administration. Dobutamine administration in 715 circumstances in postoperative, traumatic, septic patients and patients with adult respiratory distress syndrome, renal failure, and multiple organ failure significantly improved DO2 and VO2. Dopamine under comparable conditions produced less improvement in DO2 and VO2 than that of dobutamine; most of the VO2 changes were not significant. CONCLUSIONS: The monitored patterns of cardiac index, DO2, and VO2 may be used to evaluate the adequacy of tissue perfusion as well as the relative effectiveness of alternative therapies. Second, these physiologic criteria may be used to titrate therapy in order to achieve optimal outcome. Third, after colloids optimally expand the plasma volume, dobutamine may be used to enhance flow and the distribution of flow in order to improve tissue oxygenation. Vasodilators may be used when hypertensive episodes occur or there is an inadequate response to inotropic agents. Vasopressors are used as a last resort, usually in the terminal or preterminal state.

[Mediators and their antagonists in shock therapy]. / Mediatoren und ihre Antagonisten in der Schocktherapie.

The list of shock mediators currently comprises more than 150 candidates. A careful analysis using the criteria of Koch-Dale together with decision trees for exclusion of bias revealed that only histamine, C5a, beta-endorphin, tumor necrosis factor (TNF) thromboxane B2, platelet-activating factor (PAF), and oxygen free radicals are shown to be causally associated with shock symptoms. Although experimental studies with inhibitors of these mediators were convincing, there is still a lack of evidence under clinical conditions (exception histamine: anaphylactic shock). Combinations of antagonists against different causal mediators are the most promising future approaches.

Pulmonary microembolization in experimental aortic surgery.

Pulmonary dysfunction frequently follows major surgery and has many features identical to "shock lung'. A porcine model of aortic surgery is described in which 111In-labelled platelet kinetics were related to subsequent pulmonary function. In 14 pigs, standardized aortic surgery resulted in reproducible shock and a 50 per cent mortality at 3 days. Cardiac output fell from 2.3 +/- 0.2 to 1.0 +/- 0.1 litres min-1 following removal of the aortic clamp and mean platelet and leucocyte counts fell from 437 +/- 48 to 252 +/- 39 x 10(9) litres-1 and 21.7 +/- 1.5 to 12.9 +/- 1.2 x 10(9) litres-1 respectively (P less than 0.01). Aggregate levels in inferior vena caval blood were maximal at this time and radiolabelled platelets accumulated in the lung with a rise in pulmonary vascular resistance. Alveolar-arterial oxygen difference subsequently increased from initial values of 13.7 +/- 2.0 to 23.4 +/- 3.5 mmHg (P less than 0.01) following resuscitation and to 32.5 +/- 3.4 mmHg at 3 days following surgery (P less than 0.01). This clear sequence suggests that pulmonary platelet microembolization occurs during surgical shock and may be responsible for subsequent pulmonary dysfunction.

Circulatory mechanisms of shock and their mediators.

Traditional concepts of shock therapy have been based on conventional monitoring. However, the availability of invasive monitoring systems has provided the means to describe the patterns of oxygen transport in various acute life-threatening illnesses. Surgical trauma provides a useful model for investigation of other shock syndromes, because measurements may be made in the preoperative control period, during the hemodynamic crisis intraoperatively, and sequentially throughout the postoperative period for survivors and nonsurvivors. This provides a time-related pattern of physiologic events that may form the basis for the physiologic evaluation of mechanisms operative in survivors and nonsurvivors. Physiologic alterations which are compensatory may be identified from the survivor pattern and differentiated from decompensations associated with the lethal course. The DO2 pattern reflects circulatory functional changes which may limit body metabolism as reflected by VO2. The body compensates for tissue hypoxia and increased metabolic needs by increased flow and DO2 in sepsis and trauma, and by increased oxygen extraction in hemorrhagic and cardiogenic shock where flow is limited. The interactions of survivors' hemodynamic and oxygen transport patterns define compensatory responses which primarily are increased cardiac output, DO2, and VO2. Inadequate compensations and decompensations of shock are clearly manifest by the nonsurvivor pattern. Therapeutic goals may be defined by the values of the survivor patterns; reduced mortality and morbidity result when these goals are vigorously applied prospectively (17-19).