Quotes from Jean-Louis Vincent

Acute pain is triggered by stimulation of peripheral nociceptors in the skin or deeper structures and is a complex process involving multiple mediators at various levels of the neuraxis (Figure 3-2).

These vascular changes, evident to the clinician by examination of the retina, are mirrored by changes in the kidney, leading to a proliferative arteritis, and in advanced stages of the process, fibrinoid necrosis.

Newer agents for treatment of seizures in critically ill patients include the phenytoin prodrug, fosphenytoin; the anesthetic agent, propofol; and the water-soluble benzodiazepine, midazolam.

Aortic dissection results from an intimal tear in the aortic wall. The primary morbidity and mortality results from extension of the tear. This extension is promoted by factors that increase the rate of change of aortic pressure (dp/dt), including elevation in BP, heart rate, and myocardial stroke volume. Blood pressure should be reduced promptly to near-normal levels. Aggressive control of BP with a vasodilator can trigger reflex tachycardia, leading to increased dp/dt.

On the basis of a recent meta-analysis,25,26 continuous peripheral analgesic techniques provide superior analgesia, reduce opioid consumption, and reduce opioid-related side effects (nausea and vomiting, sedation, pruritus). This technique is not commonly used in the ICU setting, but it opens a wide range of possibilities for the future treatment of acute pain in critically ill

Management essentials in the ICU: FASTHUG F=feeding. A=analgesia. S=sedation. T=thrombo-embolism prophylaxis. H=head of the bed elevated (30–45°). U=ulcer prophylaxis (PPI or H2 antagonists). G=glucose control.

Most commonly, hypertensive emergencies occur in the setting of uncontrolled or unknown chronic hypertension. Hypertensive emergencies also may develop as secondary hypertension in association with such diverse etiologies as renal vascular disease, sleep apnea, hyperaldosteronism, pheochromocytoma, and pregnancy (preeclampsia).

VIP rule Ventilate: give oxygen therapy, endotracheal intubation if required. Infuse: give IV fluids. Pump: use vasoactive agents first to raise arterial pressure if needed, then to increase cardiac output if required.

Although specific treatments for ALI/ARDS have been slow to emerge, the recent development of new strategies for mechanical ventilation that improve mortality, and fluid management strategies that reduce the length of mechanical ventilation, emphasizes the importance of identifying and appropriately treating all patients with ALI/ARDS. Although this point would seem to be straightforward, in practice, ALI/ARDS remains largely underdiagnosed,

These effects result in depletion of cellular adenosine triphosphate (ATP) and potentially severe detrimental effects on cell function. It is important to note that the inflammatory response also causes release of vasoconstrictor substances including thromboxane and endothelins.

7 Severe hemophagocytic syndrome with failure of one or more organs. The choice of cytoreductive regimen depends on the type of malignancy, which is not always precisely known on arrival of the patient in the ICU. For acute leukemias, efforts should be made to characterize the lineage (ALL or AML) before treatment is initiated, but if lineage cannot be determined, a non–lineage-specific

Nicardipine is metabolized by the liver, and excretion can be impaired in patients with abnormal hepatic function.

Whenever possible, at least 10 to 15 mL of blood should be withdrawn and inoculated into 2 or 3 bottles or tubes at a ratio of 1 mL of blood per 5 mL of medium.

Febrile patients with head trauma, subarachnoid hemorrhage, or stroke should receive antipyretics to prevent temperature-related increases in cerebral oxygen utilization.

Some physiologic responses to acute pain and stress are mediated by neuroendocrine activation and increased sympathetic tone. As a consequence, patients develop tachycardia, increased myocardial oxygen consumption, immunosuppression, hypercoagulability, persistent catabolism, and numerous other metabolic alterations.5

Several sedation scales—the Richmond Agitation Sedation Scale (RASS), Adaptation to the Intensive Care Environment (ATICE) tool, and the Minnesota Sedation Assessment Tool (MSAT)—as well as tools for assessment of analgesia in the ICU, such as the visual analog scale, the numeric rating scale, behavioral pain scale,7,8 and critical care pain observation scale, have been developed (Figure 3-1).

The relationship between BP and mortality in patients with stroke may be "U-shaped." According to this notion, systolic BP (SBP) values above or below 140 to 180 mm Hg are associated with increased mortality. In the International Stroke Trial, SBP above 200 mm Hg was associated with an increased risk of recurrent ischemic stroke (50% greater risk of recurrence), while low BP (particularly <120 mm Hg) was associated with an excess number of deaths from coronary heart disease.