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Sepsis

Sepsis. RN Strong June 20, 2012. Presep catheter in service video. Insight into the Frank-Starling Curve. Successful fluid optimization has been shown in numerous clinical studies to lead to improved patient outcomes, including reduced morbidity and shorter hospital stays.

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Sepsis

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  1. Sepsis RN Strong June 20, 2012

  2. Presep catheter in service video

  3. Insight into the Frank-Starling Curve • Successful fluid optimization has been shown in numerous clinical studies to lead to improved patient outcomes, including reduced morbidity and shorter hospital stays. • The studies are typically based on the physiological principles outlined by the Frank-Starling curve, which states that an increase in preload or volume will lead to cardiac flow-related improvement (e.g., better stroke volume) up to a certain point, after which the “law of diminishing returns” applies.

  4. Passive Leg Raising (PLR): • In situations where it is not possible to use SVV (i.e., during arrhythmias, when patients are not on control-mode of ventilation, or in patients at risk of complications from fluid loading), simply raising the legs has been proven clinically to act like a “self volume challenge” to indicate the patient’s status on the Frank-Starling curve. If the patient is fluid-responsive, SV will increase substantially.

  5. Why does the level go up and down?

  6. Case Study • Clinical Events • A 78-year-old male (85 kg) was admitted with severe • sepsis secondary to left lower lobe pneumonia. He had • a previous history of pulmonary TB 30 years ago. On • admission his respiratory rate was 42 and he was using • his accessory muscles. Other observations included: • Temp 39.1; MAP 58; HR 135. Urine output had been • 10/20/5 over the last 3 hours. • On physical examination he was cool peripherally • with clammy skin. His GCS was 10. His abdomen • was distended and it was noted that he had not been • absorbing his nasogastric feed. His arterial blood gases • were: PH 7.30; P02 78 on FI02 .70; PC02 41; ABE –10.3; • Lactate 4.2; Na+ 127; K+ 4.7; Cl- 88

  7. Case Study • His treatment included immediate intubation and • ventilation on PSIMV, with an inspiratory pressure of 25, • PEEP of 10 and respiratory rate of 15. He was sedated • on 40 mg propofol 1% and 2 mg of alfentanyl. He made • no respiratory effort during the case study hour. Following • insertion and checking the position of invasive lines (left IJ • CVC and right radial arterial line) along with additional • flow monitoring from the Edwards Vigileo monitor and • Edwards FloTrac sensor, the patient was started on • noradrenaline at 0.5 mg/kg/min and given fluid challenges • to achieve a stroke volume variation (SVV) < 10%.

  8. Case Study • Over the next 7 hours fluids were given in • boluses to maintain a SVV < 10%. In addition, maintenance • fluid at 1.5 ml/kg/hr was given. His urine output picked • up, lactate came down and his ventilation improved. • Subsequent investigations included: bronchoscope & • lavage (gram – cocci); blood cultures; CT abdomen & • pelvis – which was NAD; a blood film which suggested • overwhelming sepsis. Over the next 6 days he was • weaned, then successfully extubated. Antibiotic therapy • was continued for 10 days.

  9. Surveillance and Early Warning Case No. 1: Shivering The patient in Figure 16 maintained a normal SvO2 during an extensive and prolonged operative event, yet in the recovery room SvO2 decreased suddenly to 50%. The logical assumption was that cardiac output had decreased. However, thermodilution cardiac output indicated that cardiac output had actually increased. The patient was examined and found to be shivering. Shivering increased oxygen consumption, which the body attempted to meet by increasing cardiac output. Since this was insufficient, increased amounts of oxygen were extracted from the blood, causing a decrease in SvO2. A paralyzing agent was administered and oxygen consumption returned to normal. This eliminated the need for increased oxygen consumption, therefore, cardiac output and SvO2 returned to normal limits.

  10. The patient in Figure 17 was admitted in profound cardiogenic shock with an SvO2 of only 35%. Various aggressive therapies were initiated without any improvement. Several hours later, SvO2 increased for no identifiable reason. The cause was found when the patient's temperature spiked to 104°F The patient was septic. In this case, the change in SvO2 toward the normal range did not herald the patient's survival. Peripheral shunting involved in septic shock caused large amounts of oxygenated blood to be returned to the heart. Traditionally a high cardiac output and low peripheral vascular resistance have been considered indications of sepis. Perhaps now an unexplained rise in SvO2 may be considered diagnostic for sepsis as well.

  11. In the example shown in Figure 18, a small and then larger drop in SvO2 accompanied turning and suctioning the patient, respectively. The SvO2 remained depressed and preceded cardiac arrest by 15 – 20 minutes. SvO2 monitoring on a continuous basis may signal the clinician when to modify care. In this case, perhaps suctioning should have been delayed until SvO2 returned to normal, and cardiac arrest might have been avoided.

  12. Various therapeutic maneuvers may interfere with the concentration of inspired oxygen. The case illustrated in Figure 19 represents the effects of tracheobronchial suctioning. The fall in SvO2 is profound and prolonged. The clinician, after observing such a change in SvO2, might have elected to preoxygenate this patient prior to repeated bouts of suctioning.

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