3. Shock Flashcards

(41 cards)

1
Q

<font><span>4 basic categories of shock</span></font>

A

-distrib<br></br>-hypovolemic<br></br>-cardiogenic<br></br>-obstructive

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2
Q

What structure of the cell is primarily effected in shock?

A

mitochondria<br></br>–>hypoxia = cannot provide e

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3
Q

Hemorrhage shock: how does the physiology occur?

A

rapid reduction of IV blood volume from any cause

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4
Q

Hemorrhage shock: rapid hemorrhage causes an incr in which 2 things?<br></br>then ___ activation and peripheral ___

A

HR<br></br>cardiac contraction<br></br>baroreceptor<br></br>vasoconstriction

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5
Q

<span>The base deficit, therefore, crudely represents the physiologic endpoint that distinguishes trivial blood loss from clinically significant hemorrhage</span>

A

<span>A normal base deficit is more positive than −2 mEq/L. The arterial and venous blood base deficit can become more negative early in hemorrhage, even while blood pH and BP remain normal. </span>

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6
Q

<span>Significant traumatic hemorrhage in otherwise normal ED patients, therefore, will generally cause an arterial lactate concentration greater than 4.0 mmol/L, Paco </span>2<span> less than 35 mm Hg, mild hyperglycemia (150 to 170 mg/dL), and mild hypokalemia (3.5 to 3.7 mEq/L).</span>

A
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7
Q

<span>Septic shock causes three primary effects in variable degrees that must be addressed during resuscitation: hypovolemia, cardiovascular depression, and induction of systemic inflammation.</span>

A
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8
Q

<span>Cardiogenic shock results when more than 40% of the myocardium becomes dysfunctional from ischemia, inflammation, toxins, or immune injury. </span>

A
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9
Q

<span>Patients with shortness of breath, abnormal cardiac enzymes, ischemia on the EKG, or lacking fever are more likely to have a cardiac etiology of their shock</span>

A
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10
Q

<span> However, ED patients with shock from acute spinal injury actually manifest a range of HRs and peripheral vascular resistance, most likely due to variable location of injury and the balance between disrupted efferent sympathetic and parasympathetic tone. </span>

A
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11
Q

<img></img>

A
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12
Q

<span>Measurement of urine output, however, requires 30 to 60 minutes for accurate determination of whether output is normal (>1.0 mL/kg/h), reduced (0.5 to 1.0 mL/kg/h), or severely reduced (<0.5 mL/kg/h)</span>

A
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13
Q

shock - <span>More useful is real-time, arterial or venous lactate concentration and the base deficit. </span>

A
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14
Q

<span>Chest radiography, electrocardiography, finger stick glucose measurement, complete blood count (CBC), urinalysis, serum electrolyte levels, and kidney and liver function tests should be obtained for most patients with suspected shock.</span>

A
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15
Q

<span>arterial blood gas determination provides the base deficit and allows correlation of arterial gas tensions (Pao </span>2<span> and Paco </span>2<span> ) with those measured by pulse oximetry and capnography. </span>

A
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16
Q

Sequ Organ Failure Assessment score components

A
  1. resp (pao2/fio2 ratio)<br></br>2. cv<br></br>3. coagulation - plt <br></br>4. renal - cr<br></br>5. liver - total bili<br></br>6.neuro GCS
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17
Q

<span>Septic shock, meanwhile, has be redefined as sepsis plus shock requiring vasopressors and a lactate level greater than 2 mmol/L.</span>

18
Q

<img></img>

19
Q

<span>Patients with cardiac failure or renal failure may benefit from closer measurement of dynamic variables of fluid responsiveness that can be measured from an arterial line (e.g., stroke volume variation or stroke volume index) or a central venous line (central venous pressure [CVP]</span>

20
Q

<span>Alternatively, lactate clearance refers to serial measurements of the venous or arterial lactate level. Lactate clearance has been shown to be equivalent to central venous oxygen saturation as an endpoint of early septic shock resuscitation, though it has not been systematically studied in other forms of shock</span>

21
Q

<span>. If the lactate concentration has not decreased by 10% to 20% 2 hours after resuscitation has begun, additional steps are undertaken to improve systemic perfusion</span>

22
Q

<span>Most patients with shock can be fully resuscitated with peripheral venous access established with at least two 18-gauge catheters</span>

23
Q

<span>A better approach involves the use of clinical response to fluid resuscitation, such as increases in urine output, BP, and decreasing lactate concentrations, either alone or in combination with CVP measurements</span>

24
Q

<span>standard treatment for hemorrhagic shock historically consisted of rapidly infusing several liters of isotonic crystalloid in adults or three successive 20-mL/kg boluses in children. </span>

25
Initial volume replacement consists of the rapid infusion of 20 to 25 mL of isotonic crystalloid per kilogram
26
septic shock:
Persistent hypotension, despite 30 mL/kg of IV fluid, indicates the need to add vasopressors to the resuscitation (see below). If patients require large volumes of crystalloid (>4 L), we recommend adding 5- to 10-mL/kg boluses of a natural colloid (e.g., albumin), rather than additional isotonic crystalloid alone, until further volume fails to improve hemodynamics.
27
in the setting of hemorrhage or a critically low hemoglobin level (<7 g/dL), we recommend transfusion of PRBCs (1 to 2 units in adults or 5 to 10 mL/kg in children) if criteria for shock persist despite crystalloid infusion. 
28
If patients require more than 2 units of PRBCs for hemorrhage, we recommend a balanced resuscitation using PRBCs, fresh-frozen plasma, and platelets in a 1:1:1 ratio, which is associated with better hemostasis and lower death due to exsanguination by 24 hours. 
29
The primary goal of vasopressor support is to increase cardiac output and oxygen delivery to vital organs when crystalloid resuscitation alone is inadequate. To reduce the potential for limb damage from extravasation from a peripheral IV injection, vasoactive medications are optimally administered through a central venous catheter
30
Norepinephrine is the vasopressor of choice for correction of hypotension in septic shock
31
n patients who remain in shock after initial crystalloid boluses, norepinephrine should be initiated at a rate of 0.05 mcg/kg/min, or 3 to 5 mcg/min for most adult patients, and titrated at 3- to 5-minute intervals until the mean arterial pressure is greater than 65 mm Hg
32
septic shock, ne then: Vasopressin or phenylephrine can be a useful adjunct or alternative agent if the patient develops a tachydysrhythmia (e.g., atrial fibrillation with rapid ventricular response), to improve both HR and cardiac output. A
33
Dobutamine may be used with norepinephrine to increase cardiac output and maintain adequate oxygen delivery in both cardiogenic and septic shock
34
One such regimen would include piperacillin-tazobactam, 4.5 g IV every 6 hours or cefepime 2 g IV every 8 hours, and vancomycin, 30 mg/kg (maximum dose, 2 g) given every 12 hours, adjusted as appropriate for trough levels and renal failure. 
35
Addition of another agent (such as levofloxacin, 750 mg IV every 12 hours) is recommended to provide double coverage in patients with risk factors for or in areas of high prevalence of multi-drug resistant bacteria, particularly Enterococcus and Pseudomonas s
36
Due to the nondefinitive results of steroids trials to date, empiric corticosteroids are not routinely recommended in all ED patients with sepsis
37
Rapid sequence intubation is the preferred method of airway control in most patients with refractory shock 
38
Strenuous use of accessory respiratory muscles can increase oxygen consumption by 50% to 100% and decrease cerebral blood flow by 50%. More importantly, if the patient has increased airway resistance (e.g., bronchospasm with anaphylaxis) or a decrease in lung compliance (e.g., pulmonary edema, ARDS), a more negative intrathoracic pressure must be generated to fill the lungs with each inspiration. The greater suction effect is also exerted on the left ventricle, impeding its ability to eject and increasing functional afterload. Positive-pressure ventilation removes this impedance and can improve ventricular function and cardiac output up to 30%. The use of etomidate for airway management in patients with septic shock
39
In the setting of traumatic shock from an injury distal to the renal arteries without evidence of aortic injury, Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is a more recent technology that can maintain cardiac and cerebral perfusion while definitive source control is obtained through the insertion of an intra-aortic balloon via an arterial puncture. 
40
In septic shock related to an abscess, aggressive infection (e.g., necrotizing fasciitis or perinephric abscess; see Chapter 126 ), or wound (e.g., toxic shock syndrome; see Chapter 126 ), removal of the infectious stimulus through surgical intervention should proceed as soon as practical.
41
Outcomes have progressively improved, with emphasis on early diagnosis and treatment. In general, persistent hypotension (refractory shock) is associated with worse outcomes. Patients meeting consensus definitions for hemorrhagic shock have a mortality rate of about 20%, whereas this exceeds 40% in septic and cardiogenic shock.