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PubMed · 2096861

Postoperative perfusion deficits.

Abstract

The three keys to successful recovery of the critically ill postoperative patient are: (1) in-depth preoperative assessment and risk evaluation; (2) review of intraoperative course and evaluation of risk for perfusion deficit; and (3) diligent postoperative monitoring for early onset of perfusion deficit. Complications arise when metabolic demands exceed the body's ability to supply essential nutrients. The choice of treatment modality is related to the cause of perfusion deficits. Decreased preload and afterload is treated with fluid and vasopressor therapy. Increased preload is best managed by diuretics and venous dilation. Afterload reduction is accomplished with vasodilator therapy and decreases in sympathetic stimulation. Contraction is enhanced with inotropic therapy and management of preload and afterload within normal ranges. Metabolic demands are best managed with tight control of the patient's hemodynamic profile, oxygen consumption, and environmental stimuli. The challenge of managing the critically ill postoperative patient is great, but the rewards of successful recovery are tremendous.

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BibTeXRIS

S L Smith. 1990. Postoperative perfusion deficits.. https://pubmed.ncbi.nlm.nih.gov/2096861/

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Use of levosimendan, a new inodilator, for postoperative myocardial stunning in a premature neonate.

OBJECTIVE: To first report the successful use of the new inodilator levosimendan in a premature infant with congestive heart failure (CHF) following cardiac surgery. Although the calcium sensitizer levosimendan improves hemodynamics in adults with CHF, no data are available on the use of levosimendan in premature infants with CHF. DESIGN: Single case report. SETTING: Twenty-bed postoperative adult and pediatric cardiac intensive care unit. PATIENT: A 32 wks gestational age, 1525-g premature male twin with transposition of the great arteries. INTERVENTIONS: The patient underwent arterial switch operation. MEASUREMENTS AND MAIN RESULTS: Immediately after operation, the patient developed signs of low cardiac output syndrome. Mixed venous saturation was 56%, serum lactate increased to 14.8 mmol/L, systolic arterial pressure was 40 mm Hg, left atrial pressure was 24 mm Hg, and echocardiography showed reduced left ventricular function with a fractional shortening of 10%. There were no signs of reduced coronary perfusion. Milrinone, dobutamine, and epinephrine did not improve hemodynamics. Levosimendan was initiated at a dose of 0.05 mug.kg.min, increased to 0.1 mug.kg.min, and continuously infused for 24 hrs. Within 6 hrs after starting the levosimendan infusion, left atrial pressure decreased to 7 mm Hg and systolic arterial pressure increased to 60 mm Hg; within 24 hrs after initiation serum lactate level normalized to 1.7 mmol/L and mixed venous saturation increased to 81%. Echocardiography revealed improvement of left ventricular function with a fractional shortening of 25%. No side effects were recognized during administration of levosimendan. CONCLUSIONS: In this premature neonate with postoperative low cardiac output syndrome due to failing myocardial function, levosimendan was a potent inotropic agent.

Cardiac Output, Low↗