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Flashcards in SIRS/Sepsis Deck (45)
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1

In regards to sepsis, explain the role/method of fluid resuscitation.

volume resuscitation using crystalloids or colloids should be used initially aiming at: CVP 8-12 mmHg, mean arterial pressure 65 mmHg, urine output 0.5ml/kg, central venous oxygen saturation 70%

2

Discuss the role of vasopressors and inotropes in the management of sepsis.

vasopressor support with norepinephrine may be considered even before optimal fluid loading has been achieved. Low dose vasopressin can be added to reduce requirement for high dose norepinephrine alone; inotropes are added to volume resuscitation and vasopressors, if there is evidence of continued low cardiac output despite adequate cardiac filling and fluid resuscitation

3

At what point should further IV fluid administration be stopped?

when filling pressures are high and no further improvement is seen in tissue perfusion

4

What happens to the MAC of inhalational anesthetics during severe sepsis?

reduction in MAC requirement

5

What is the goal of mechanical ventilation in patients with severe sepsis?

to use sufficiently high FiO2 concentration to maintain adequate oxygenation; strong evidence supports the use of low tidal volume strategy to minimize overall impact of positive pressure ventilation on lung tissue..... and venous return.... and cardiac output

6

What % of patients with sepsis will develop septic shock?

~50%

7

What is the relationship between sepsis and SIRS?

sepsis is defined as SIRS in response to an infectious process; sepsis is a potentially fatal whole body inflammation caused by severe infection that is now in the blood stream; sepsis can continue even after the infection is gone

8

What are the 3 levels of sepsis?

SIRS, severe sepsis, septic shock

9

What is the criteria for SIRS?

manifestation of 2 or more of the following: abnormal temp (>38 or 90, RR >20 or PaCO2 12,000 or 10% immature (band) forms

10

What is sepsis?

sepsis is a systemic inflammatory response (SIRS) in response to an insult to a host.... in association with infection; manifestations are the same as those described for SIRS; so you must have a DOCUMENTED INFECTION in conjunction with 2 or more: abnormal temp, tachycardia, tachypnea or hyperventilation, or abnormal WBC (>12 or 10% immature "band" forms)

11

What is severe sepsis?

in simple terms: sepsis complicated by organ dysfunction

severe sepsis is sepsis that is associated with organ dysfunction or hypotension; hypoperfusion and perfusion abnormalities may include lactic acidosis, oliguria, or acute alteration in mental status

may see hypoxemia 1.5, hyperglycemia in absence of diabetes (stress response)

12

What is septic shock?

sepsis complicated by high lactate level or by shock that doesn't improve after fluid resuscitation

13

What is MODS?

multiple organ dysfunction syndrome that may occur with severe sepsis or septic shock; perfusion is compromised, ischemia and hypoxia of organs

14

What are organ system specific indicators of MODS?

Cardio: heart failure (need for inotropes despite fluid resuscitation), Neuro: change in LOC, Pulmonary: ARDS, Renal: ARF, Metabolic: acidosis, Hepatic: liver failure, Hematologic: disseminated intravascular clotting

15

What are potential stimuli for activation of an inflammatory response?

trauma, surgery, organ dysfunction, infection with microorganisms or viruses

16

With SIRS there is an activation of inflammatory response: cytokines, TNF-alpha, IL-1, IL-6, IL-8, PAF, prostaglandins, leukotrienes, neutrophil activation, complement system, vascular endothelial cells, activation of clotting and kinin cascades, thromboxane, prostacylin, prostaglandin.
What are clinical manifestations seen after this response?

vasodilation, increased capillary permeability, cellular activation, coagulopathy

17

What is lactic acid?

it is the end point of anaerobic breakdown of glucose in the tissues

18

Why is there an increase of lactate level in sepsis?

in sepsis, the adrenergic state and cytokine storm changes glucose metabolism, lactate metabolism, and lactate use; the heart and brain can take up lactate and use it for energy.... so lactate generation is probably an adaptive response to stress situations

Basic thinking is as oxygen to the tissues decreases, lactate increases... but this isn't entirely true b\c in sepsis there may be good global oxygen delivery

19

What is a normal lactate level value?

normal in unstressed patients is 0.5-1 mmol/L; in critically ill patients it can be considered normal if less than 2; 2-4 is mild to moderate; lactic acidosis is considered if >4 or 5 in association with metabolic acidosis

20

What are anesthetic considerations in regards to the disease state, in patients with sepsis?

examination should focus on the severity of SIRS, state of intravascular hydration, presence of shock or MODs, and adequacy of hemodynamic resuscitation

21

What benefits are derived from the insertion of a central venous catheter in septic patients?

measurement of CVP, mixed venous oxygen saturation, administration of IV fluids, and vasopressor medication

22

What does SvO2 represent?

mixed saturated venous oxygen: a result of oxygen consumption at the tissue level; demonstrates the balance between oxygen delivery and oxygen demand; measured by the oxygen extraction ratio (normal 24-28%---- calculated by O2ER= SaO2- SvO2/SaO2); normal SvO2 alone does not show the status of specific organ perfusion and may not be an adequate representation of tissue perfusion in patients with sepsis; SvO2 has inverse relationship to oxygen utilization in fully saturated blood and a direct relationship to cardiac output and Hgb

23

The first _______ hours of resuscitation of septic patients are referred to as the "golden hours"; crucial and frequently coincide with the time for emergency surgery.

6 hours

24

What are some signs and symptoms of sepsis?

high fever, hot, flushed skin, tachycardia, hyperventilation, AMS, swelling, hypotension

25

What is bacteremia?

the presence of viable bacteria in the bloodstream

26

What is septicemia?

presence of large numbers of bacteria in the bloodstream often associated with systemic signs (fever, rigors, h/a)

27

What is the difference between sever sepsis and septic shock?

severe sepsis involves organ dysfunction, hypotension, or hypoperfusion..... however when hypotension continues despite fluid resuscitation it is classified as septic shock

28

Explain the difference between SaO2 and SvO2?

SO2 represents the % of oxygen bound to Hgb; whereas PO2 represents the tension or pressure exerted on Hgb when dissolved in plasma; SaO2 is usually high 95-08% when being adequately oxygenated---> a resting individual uses approximately 25% oxygen, leaving ~75% that will return in venous system; so SvO2 is approx 60-80% depending on the metabolic oxygen requirements of the body

29

Discuss the oxyhemoglobin dissociation curve and the relationship of PO2 to SaO2.

The association segment of the curve, or upper portion, is essentially flat and represents oxygen uptake in the lung. In this portion of the curve, changes in PO2 levels between 60 and 100 mm Hg cause only small changes in oxygen saturation. For example, at a normal arterial PO2 of 90 mm Hg, the hemoglobin is 97% saturated. Even with a significant decrease in PO2 to 60 mm Hg, the saturation only falls to 90%. This is advantageous in the lung where fluctuations in alveolar PO2, and subsequently arterial PO2,do not affect oxygen loading until PO2 falls significantly lower than normal.

30

Discuss the lower portion of the oxyHgb Dissociation curve and how it relates to venous saturation and tissue delivery.

The lower portion of the curve (below 45 mm Hg)
corresponds to the PO2 levels of venous blood.
This steep part of the curve is referred to as the dissociation segment and represents the release of
oxygen to the tissues. In this low range of PO2 values, even small changes in oxygen tension produce large alterations in oxygen saturation. This is advantageous to the tissue because large quantities of oxygen can be extracted from the
blood for relatively small decreases in PO2. For example, at a PO2 of approximately 40 mm Hg, hemoglobin remains 75% saturated and a large oxygen reserve remains; however, below a PO2 of 30 mm Hg, the oxygen reserve is rapidly depleted.