SIRS/Sepsis

Question 1

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

Answer 1

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%

Question 2

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

Answer 2

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

Question 3

At what point should further IV fluid administration be stopped?

Answer 3

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

Question 4

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

Answer 4

reduction in MAC requirement

Question 5

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

Answer 5

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

Question 6

What % of patients with sepsis will develop septic shock?

Answer 6

~50%

Question 7

What is the relationship between sepsis and SIRS?

Answer 7

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

Question 8

What are the 3 levels of sepsis?

Answer 8

SIRS, severe sepsis, septic shock

Question 9

What is the criteria for SIRS?

Answer 9

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

Question 10

What is sepsis?

Answer 10

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)

Question 11

What is severe sepsis?

Answer 11

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)

Question 12

What is septic shock?

Answer 12

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

Question 13

What is MODS?

Answer 13

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

Question 14

What are organ system specific indicators of MODS?

Answer 14

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

Question 15

What are potential stimuli for activation of an inflammatory response?

Answer 15

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

Question 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?

Answer 16

vasodilation, increased capillary permeability, cellular activation, coagulopathy

Question 17

What is lactic acid?

Answer 17

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

Question 18

Why is there an increase of lactate level in sepsis?

Answer 18

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

Question 19

What is a normal lactate level value?

Answer 19

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

Question 20

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

Answer 20

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

Question 21

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

Answer 21

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

Question 22

What does SvO2 represent?

Answer 22

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

Question 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.

Answer 23

6 hours

Question 24

What are some signs and symptoms of sepsis?

Answer 24

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

Question 25

What is bacteremia?

Answer 25

the presence of viable bacteria in the bloodstream

Question 26

What is septicemia?

Answer 26

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

Question 27

What is the difference between sever sepsis and septic shock?

Answer 27

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

Question 28

Explain the difference between SaO2 and SvO2?

Answer 28

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

Question 29

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

Answer 29

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.

Question 30

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

Answer 30

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.

Question 31

What factors affect the oxyHgb dissociation curve?

Answer 31

An increase in hydrogen ion concentration (↓pH), PCO2, temperature, or 2,3 DPG (a byproduct of red blood cell metabolism) will decrease hemoglobin-oxygen affinity, thereby shifting the oxyhemoglobin curve to the right.This shift results in a higher P50 value, indicating that a higher PO2 will be required to saturate 50% of the hemoglobin. Under these conditions, there is a decrease in oxygen saturation for any given PO2, but hemoglobin will release oxygen more readily to the tissues. However, since the amount of oxygen in the blood is decreased, the total amount of oxygen that can be released to the tissues is limited.

Question 32

What are some clinical signs (parameters) to identify/assess tissue hypoperfusion?

Answer 32

lactate >3, decreased cap refill, mottling of skin

Question 33

What drug can be used as an adjunct to conventional inotropic therapy in cases of refractory myocardial dysfunction in sepsis (however is currently unlicensed for use in the US)?

Answer 33

levosimendan

Question 34

What is the MOA for the inotropic and systemic/pulmonary vasodilator effect of levosimendan?

Answer 34

its inotropic effect is attributable to increased cardiac troponin C sensitivity to calcium; the systemic and pulmonary vasodilator effect is attributable to its opening of ATP-dependent K channels; it is a calcium sensitizer

Question 35

What are some generalized anesthetic considerations regarding the induction and maintenance of anesthesia.... in regards to anesthetics and opioids.... in the sepsis patient?

Answer 35

choice of induction agent or narcotic is less important than the care with which it is administered; deliberate step wise process; most IV or inhalation anesthetic agents are going to cause some degree of vasodilation or impaired ventricular contractility; with exception of remifentanil, the effects and duration of action of IV opioids may be increased by impaired hepatic and renal perfusion

Question 36

In regards to the ability to guide intraoperative fluid resuscitation, what measuring device or guide is the most useful?

Answer 36

changes in dynamic markers such as pulse pressure variation and stroke volume variation have been shown to predict volume responsiveness MORE ACCURATELY than pressure based estimates like CVP or pulmonary artery occlusion pressure; if in NSR and mechanically ventilated; TEE is also useful

Question 37

What are two parameters useful for the assessment of adequate global oxygen delivery?

Answer 37

serum lactate 70%

Question 38

T/F? Increasing cardiac output and oxygen delivery in patients with adequate organ perfusion serves no useful purpose.

Answer 38

True

Question 39

What is the reason for a fluid challenge in a septic patient?

Answer 39

to increase stroke volume (volume responsiveness)... if this serves no benefit, then further fluid bolus could be harmful; usually 500mL to 1000mL bolus for sepsis

Question 40

Describe the Frank Starling principle in relation to the heart. (primarily stroke volume and preload)

Answer 40

according to the frank starling principle, as preload increases..... left ventricular stroke volume increases until the optimal preload is achieved, at which point the stroke volume remains relatively constant; this optimal preload is related to the maximal overlap of the actin-myosin myofibrils; it is important to note that in an intact heart the actin myosin links cannot be disengages and hence there is no descending limb of the Frank Starling curve.... once the left ventricle is functioning near the flat part of the frank starling curve, fluid loading has little effect on the SV. In normal physiologic conditions, both ventricles operate on the ascending portion of the frank starling curve; this mechanism provides a functional reserve to the heart in situations of acute stress; in normal individuals, an increase in preload (with volume challenge) results in a significant increase in SV

Question 41

Why is CVP not the best indicator of fluid status?

Answer 41

many studies have been done showing no relationship b\w CVP and fluid responsiveness in various settings; it does not the patients position on the frank starling curve and therefore does not reflect preload reserve; it is a good approximation of RA pressure, but d\t changes in venous tone, intrathoracic pressures, RV and LV compliance, and geometry occurring in severely ill patients... there is a poor relationship b\w CVP and RV end diastolic volume; pulse pressure variation (PPV) and stroke volume variance (SVV) have been closely linked to volume responsiveness

Question 42

What effect does mechanical ventilation have on preload and afterload of the Right side of the heart?

Answer 42

decreases preload (decrease venous return from increased pleural pressure) and increases afterload (inspiratory increase in transpulmonary pressure).... both lead to a decrease in RV stroke volume... leads to a decrease of LV filling... thus LV preload reduction and possible decrease in LV stroke volume

Question 43

If the patient has adequate oxygenation, permissive hypercarbia may be allowed in all cases except?

Answer 43

avoid in patients with increased ICP, compensated metabolic acidosis, or later stages of pregnancy

Question 44

What APACHE score with severe sepsis is associated with high risk of death?

Answer 44

>25 with MODs

Question 45

What APACHE score is associated with low risk of death in sepsis patients?

Answer 45

<20 with one organ failure