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Flashcards in SIRS/Sepsis Deck (45)
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1
Q

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

A

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
Q

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

A

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
Q

At what point should further IV fluid administration be stopped?

A

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

4
Q

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

A

reduction in MAC requirement

5
Q

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

A

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
Q

What % of patients with sepsis will develop septic shock?

A

~50%

7
Q

What is the relationship between sepsis and SIRS?

A

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
Q

What are the 3 levels of sepsis?

A

SIRS, severe sepsis, septic shock

9
Q

What is the criteria for SIRS?

A

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
Q

What is sepsis?

A

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
Q

What is severe sepsis?

A

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
Q

What is septic shock?

A

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

13
Q

What is MODS?

A

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

14
Q

What are organ system specific indicators of MODS?

A

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
Q

What are potential stimuli for activation of an inflammatory response?

A

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

16
Q

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?

A

vasodilation, increased capillary permeability, cellular activation, coagulopathy

17
Q

What is lactic acid?

A

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

18
Q

Why is there an increase of lactate level in sepsis?

A

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
Q

What is a normal lactate level value?

A

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
Q

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

A

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

21
Q

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

A

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

22
Q

What does SvO2 represent?

A

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
Q

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.

A

6 hours

24
Q

What are some signs and symptoms of sepsis?

A

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

25
Q

What is bacteremia?

A

the presence of viable bacteria in the bloodstream

26
Q

What is septicemia?

A

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

27
Q

What is the difference between sever sepsis and septic shock?

A

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

28
Q

Explain the difference between SaO2 and SvO2?

A

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
Q

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

A

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
Q

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

A

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.

31
Q

What factors affect the oxyHgb dissociation curve?

A

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.

32
Q

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

A

lactate >3, decreased cap refill, mottling of skin

33
Q

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)?

A

levosimendan

34
Q

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

A

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

35
Q

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

A

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

36
Q

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

A

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

37
Q

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

A

serum lactate 70%

38
Q

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

A

True

39
Q

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

A

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

40
Q

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

A

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

41
Q

Why is CVP not the best indicator of fluid status?

A

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

42
Q

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

A

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

43
Q

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

A

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

44
Q

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

A

> 25 with MODs

45
Q

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

A

<20 with one organ failure