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Terms in this set (3)

Definition of Shock
Shock is circulatory insufficiency caused by tissue oxygen delivery that is insufficient to meet oxygen demands. The result of shock is global hypoperfusion or tissue hypoxia and is manifested by ? venous oxygen content and a metabolic acidosis (lactic acidosis).

Types of Shock
Hypovolemic shock: a volume problem most commonly due to hemorrhage or other fluid losses from vomiting, diarrhea, polyuria, or excessive sweating.
Cardiogenic shock: a pump problem most commonly due to a damaged myocardium secondary to a myocardial infarction or cardiomyopathy.
Distributive or Vasodilatory shock: due to vascular dilatation. This is a resistance problem. The etiology may be the release of vasoactive mediators, or the vasodilatory effect of medications in an overdose. Anaphylactic shock: a form of distributive shock observed in severe allergic reactions secondary to vasoactive mediators
Septic shock: a form of distributive shock in which inflammatory mediators cause increased ?, all of which contribute to the shock state.
Neurogenic shock is another form of distributive shock due to the loss of ?
Obstructive shock: due to a mechanical obstruction to flow. Examples are the cardiovascular collapse that accompanies ?.

Scope of the problem: Sepsis is responsible for 210,000 deaths (9%) per year in the United States, more than lung or breast cancer (200,000 deaths per year) or acute myocardial infarction (180,000 deaths per year). Sepsis consumes over $50 billion in health care resource consumption each year, the most expensive diagnosis among patients admitted to hospitals. The mortality rates from sepsis, severe sepsis and septic shock are ? respectively.

Definitions and Pathophysiology: An organism enters the body and triggers a systemic response that creates a systemic inflammatory response syndrome (SIRS). This reaction may eliminate the pathogen, or may create a generalized response. This process leads to the release of ? mediators and activates the ?. The damaged endothelium inhibits adequate tissue oxygenation. The combination of ? is by definition: sepsis. When the process of inflammation and inadequate tissue oxygenation progresses to ?, this is by definition: severe sepsis. As multiple organs are affected irreversible shock ensues and this is by definition: septic shock (Figure 1 and Table 1 ).

SIRS criteria -- page 16
Clinical Features:
Risk factors for sepsis include ?
Vital Signs: The patient can be hypotensive, tachycardic, tachypneic, and either febrile or hypothermic. The blood pressure can be normal, however. Pulse pressure (systolic minus diastolic) can be ? early in shock. A shock index (?) > 1 should increase suspicion for sepsis. Head and neck: Infections can be present in the soft tissue of the face, periorbital area, sinuses and throat. IV drug users are at risk for ? in the cervical or other areas of the spine.
Pulmonary: Increased minute ventilation is often a compensatory response to a metabolic acidosis. Patient may have crackles or wheezes if a pneumonia or adult respiratory distress syndrome (ARDS) is present.
Cardiovascular: An S3 may be heard in the high cardiac output state of distributive shock. Myocardial ischemia can result in dysrhythmias and poor cardiac function with signs of heart failure including jugular venous distention.
Abdomen: An abdominal exam can give clues to the source of sepsis in cases of cholecystitis, diverticulitis and mesenteric ischemia. Decreased or absent bowel sounds can be indicative of ?, evidence of organ dysfunction.
Genitourinary: CV A tenderness can indicate pyelonephritis, a common source of sepsis. Tenderness or purulent discharge on pelvic exam could represent a ?. In men, ? have been associated with sepsis. A tender fluctuant mass on rectal exam represent a rectal abscess.
Extremities and soft tissue: Warm tender joints with effusion could represent a septic joint. Soft tissue infections, cellulitis, and abscesses can lead to sepsis. ? is a severe form of cellulitis caused by gas-forming organisms.

Diagnostic Tests:
-CBC with differential: Identifies a possible SIRS criteria (WBC or bandemia), indicates need for transfusion (Hgb/Hct), and marker of organ dysfunction ( ?).
-Electrolytes: Gives organ dysfunction variables (BUN/Cr and hyperglycemia), elevated anion gap can be indicative of metabolic acidosis
LFTs and Coagulation studies: markers of organ dysfunction (hepatic) CXR: Identify pneumonia or ARDS
Urinalysis, Urine culture and Blood cultures: Identify source of infection
AAS: Identify ileus or other findings consistent with abdominal source of infection
CT and LP: Identify source of infection
ABG: Identify lung injury or signs of impending respiratory failure Lactic Acid: Important test to quantify the extent of anaerobic metabolism secondary to tissue hypoperfusion.

Treatment: The ABCs should be applied to patients who are septic in the emergency department. Patients who are unable to protect their airway or who have greatly increased work of breathing should be intubated (i.e. a patient with altered mental status and suspected pneumonia or a patient with impending respiratory failure). Supplemental oxygen should be given to patients and their rate and work of breathing should be assessed. Most patients will require volume resuscitation when circulation is assessed. A ? ml/kg fluid bolus of crystalloid should be initiated in septic patients, especially those that are initially hypotensive (SBP <90mmHg). Source control needs to be initiated with antibiotics and/or surgical consult. For patients with an initial lactic acid level >? mmol/liter or whose hypotension (SBP <90mmHg) does not respond to the 20-40 ml/kg fluid bolus, early goal-directed therapy (EGDT) is indicated.
Lactic Acid
Lactic acid is a product of anaerobic metabolism. Lactic acidosis is most commonly a product of exercise and can also be a side effect of some medications. However, in the setting of an infection, serum lactate is a predictor of mortality in emergency department patients. Serum lactate levels of >? mmol/liter in the setting of sepsis are associated with an approximate 30% mortality in hospitalized patients. This high mortality rate is seen in patients with normal blood pressure. Therefore, it is a valuable screening tool used to identify patients with high mortality necessitating an escalation of care. In the setting of sepsis, patients who have a serum lactate >4mmol/liter or who have hypotension (SBP <90 mmHg) which does not respond to a 20-40 ml/kg crystalloid fluid bolus should be treated with early goal-directed therapy.

Early Goal-Directed Therapy Evidence: Early goal-directed therapy (EGDT) is a treatment algorithm from a study in 2001 published in the New England Journal of Medicine showing an 18% absolute risk reduction in the mortality of patients with severe sepsis and septic shock, when compared with standard treatment. Stated in other terms, for every 6 patients who meet criteria for treatment and are treated with EGDT, 1 life is saved. EGDT does not involve novel therapy; it involves applying the principles of ICU care in a standardized method using endpoints to high-risk patients within the first 6 hours of a patient's emergency department visit. The mortality reduction of this protocol has been verified in several other independent studies.

Algorithm: EGDT starts with the application of ?, if indicated. This is in effort to increase oxygen delivery to tissues and decrease oxygen consumption in cases of patients with increased work of breathing requiring intubation. In addition, ? should be treated to decrease oxygen consumption. A central line should be place in the ? and IV fluid, usually normal saline, is infused to get a goal central venous pressure (CVP) of ? mmHg in an effort to increase preload and cardiac output. Albumin or other colloid can also be administered to reach this goal. If a target mean arterial pressure (MAP) of ? mmHg is not achieved rapidly with IV fluids, ? should be used to reach this goal. When the CVP and MAP goals are achieved, then look at central venous oxygen saturation. If the central venous oxygen saturation (Scv02) of 70% is not achieved, look at hemocrit. If hematocrit is <? %, ? . If this does not achieve the ScvO2 goal, ?agents are used increase cardiac output and oxygen delivery to tissues (Figure 2).

Scv02: In a normal person the central venous oxygen saturation (Scv02), measured via a central line with its tip in the superior vena cava near the right atrium, is approximately ?%. In the setting of severe sepsis and septic shock, Scv02 is much lower, putting the heart and brain, the two most oxygen dependent organs at risk of injury.

Vasopressors and Inotropes: ? is generally the vasopressor of choice to increase blood pressure in the setting of hypotension as its effects are primarily alpha receptor medicated vasoconstriction of arterial vessels. ? is the inotrope of choice in conjunction with norepinephrine as its effects are primarily beta receptor mediated increased cardiac stimulation. However, this medication will increase ?

Corticosteroids: Patients who remain on vasopressors to maintain blood pressure, should receive a dose of steroids (i.e. ? 10 mg) and a cortisol stimulation test should be performed to detect the ?

Sepsis Bundle: The elements of the treatment of sepsis, severe sepsis and septic shock are summarized in the sepsis bundle (Figure 3).
sepsis bundle? -- within the first 6 hours