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Editor's Notes

1. Septische shock: Hypoperfusie Hypoxie Multi-orgaanfalen en overlijden ‘Early goal directed therapy’ Ieder uur verdubbeld kans op overlijden Infectie, of verdenkinkg op infectie <36C >38,3C HR >90/min of >2SD Tachypneu Veranderd bewustzijn Oedeem of positieve vochtbalans (>20ml/kg/24) Hyperglycemie en geen diabetes Afwijkende parameters: Inflammatie, hemodynamica of orgaandysfunctioneren
2. Warm shock-the first phase Septic shock can be broken down into two different types of shock: warm (or hyperdynamic) shock and cold (or hypodynamic) shock. Warm shock characterized by high cardiac output and low peripheral vascular resistance occurs first. Vasodilation from the effects of histamine, bradykinins, serotonin, and endorphins dramatically decrease total peripheral vascular resistance. It also makes capillaries more permeable causing leakage and fluid shifting into tissues and physiologic third spaces. Two other factors contribute to vascular fluid loss-fever (caused by endogenous pyrogen released by leukocytes attacking gram-negative bacteria) and the patient's high respiratory rate Mr. DeCristo's postoperative temperature, you'll 102.5ÁF and his respiratory rate was 32. Another sign to look for is profound diuresis. This develops because of the high osmotic load being handled by the kidneys, the result of all those dead and dying bacteria, phagocytie cells, tissue breakdown, and end products of cellular metabolism. To compensate for the patient's profoundly diminished plasma volume, catecholamines increase cardiac output and myocardial contractility. But these effects won't be strong enough to keep his blood pressure up. Eventually, tissue perfusion becomes inadequate resulting in loss of cellular energy and increased lactic acid production. Unusually rapid respirations Let's go back for a minute to Mr. DeCristo's rapid respiration-a veryÄ The patient in warm shock will have an unusually high respiratory rate. He'll undoubtedly have a fever and may be in the early stages of metabolic acidosis, but neither of these signs will be severe enough to explain his rapid respirations. Many authorities believe the rapid respiration result from the effect of the bacterial endotoxins on the medullary respiratory center. Whatever its cause, the high respiratory rate can cause a profound respiratory alkalosis that counterbalances lactic acidemia It may actually shift the patient's pH toward alkalosis. What about arterial blood gas(ABG)analysis? What will that show? Probably two things-both metabolic acidosis and respiratory rate may keep his PaO2 elevated in this early stage of septic shock. And because he won't be using up that muck oxygen saturation of mixed venous blood will most likely of mixed venous blood will most likely be greater than the normal 80%. Clotting factors used up Something else is going on, too-excessive activation of the clotting mechanism, resulting in coagulopathy. The complement system contributes to the damage of the vascular endothelium and to neutrophil aggregation, while the Hageman factor accelerates clotting and causes multiple fibrin clots to form. These clots plug up small capillaries, producing petechiae and altered blood flow, which appears as "creeping" mottling of the legs. The mottling starts in the feet and works its way up to the knees. You'll recall that this sign was noted by Mr. DeCristo's nurse. As clotting factors are used up in the microcirculation serum levels of clotting Factors V, VIII, and XIII, as well as platelet and fibrinogen counts will be below normal. Meanwhile decreased cerebral perfusion may produce signs of impaired mental status-vague delayed responses for example with restlessness and confusion. Some authorities consider this a characteristic early sign of septic shock. Others aren't so sure they point out that many patients are alert and oriented until multisystem failure sets in. The release of endorphins, the body's natural opiates may be responsible for keeping the patient relatively comfortable making it that muck more difficult to recognize the trouble he's going into. Cold shock-ominous late stage Most patient swill remain in warm shock for 6 to 72 hours before entering cold shock (also known as low-output or high-resistance shock). This late and nearly irreversible phase of septic shock is usually indistinguishable from terminal hypovolemic shock. Two ominous signs of could shock are a subnormal temperature and a low white blood cell count (with many immature cells). By the time the patient gets to this stage, his hypotension and hypoperfusion are profound. His skin will be cold and mottled in a more generalized fashion-not just below the knees, as in warm shock. Pulse and respirations will still be rapid because of the continued firing of sympathetic nerves and increased catecholamine levels. Cardiac output, however, decreases during cold shock. The catecholamines casue selective vasoconstriction of the renal, pulmonary, and splanchnic circulations. This effect coupled with conagulopathy in the microcirculations releases myocardial depressant factor from pancreatic cells. More beta endotoxinsÄblock pain impulses but further depresses the myocardium. Eventually, cold shock brings multisystem failure-pulmonary edema, adult respiratory distress syndrome, liver and kidney failure, even hemorrhaging from disseminated intravascular coagulation. The patient's mental status and reflexes deteriorate because of hypoperfusion and cerebral microemboli. His ABGs will show uncompensated hypoxemia, acidemia, and hypoventilation with shunting.
3. A, Shock reversal from resuscitative efforts by community hospital physicians resulted in 96% survival versus 63% survival among patients who remained in persistent shock state. B, Resuscitation consistent with the new ACCM-PALS Guidelines resulted in 92% survival versus 62% survival among patients who did not receive resuscitation consistent with the new ACCM-PALS Guidelines. *P < .001 versus shock reversed; †P < .001 versus resuscitation consistent with ACCM-PALS Guidelines.
4. Vaatvulling (soms tot 200ml/kg) Cave ARDS en hersenoedeem, let op hepatomegalie Totdat er crepitaties of hepatomegalie optreden
5. Het belang van intubatie: Afname O2-consumptie 15-30% Ondanks bradycardie of vasodilatie netto positief effect! Neonaten en zuigelingen: lagere functionele residuele capaciteit Zekeren luchtweg Rapid Sequence Induction -> anesthesioloog icc
6. Dopamine increases MAP and cardiac output, primarily due to an increase in stroke volume and heart rate. Norepinephrine increases MAP due to its vasoconstrictive effects, with little change in heart rate and less increase in stroke volume compared with dopamine. Norepinephrine is more potent than dopamine and may be more effective at reversing hypotension in patients with septic shock. Dopamine may be particularly useful in patients with compromised systolic function but causes more tachycardia and may be more arrhythmogenic than norepinephrine [148]. It may also influence the endocrine response via the hypothalamic pituitary axis and have immunosuppressive effects. However, information from five randomized trials (n = 1,993 patients with septic shock) comparing norepinephrine to dopamine does not support the routine use of dopamine in the management of septic shock [136, 149– 152]. Indeed, the relative risk of short-term mortality was 0.91 (95 %CI, 0.84–1.00; fixed effect; I2 = 0 %) in favor of norepinephrine. A recent meta-analysis showed dopamine was associated with an increased risk [RR, 1.10 (1.01–1.20); P = 0.035]; in the two trials that reported arrhythmias, these were more frequentwith dopamine thanwith norepinephrine [RR, 2.34 (1.46–3.77); P = 0.001] [153
7. The role of glucocorticoid supplementation in septic shock remains contentious. In septic shock, the driver for steroid therapy is the premise that there is relative adrenal insufficiency (based on reduced plasma cortisol and blunted cortisol response to corticotropin). The uncertainty arises from the inability of current tests to clearly identify patients who are truly corticosteroid "deficient" at a cellular level, and hence require supplemental glucocorticoid administration. We hypothesise that plasma measurements (total plasma cortisol level and the response to corticotropin) do not consistently reflect the functional adrenal response to stress. Published evidence indicates that there are cellular adaptations in stress, such as pre-receptor upregulation of cortisol, altered receptor density and gene transcription changes, none of which are reflected by plasma cortisol level. This leads us to postulate that the lack of a clearly defined plasma response in severe stress and the presence of an adequate response at the cellular level suggest it is a "sick euadrenal state", analogous to the sick euthyroid state, and not a sick adrenal indicating adrenal insufficiency.