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Flashcards in shock Deck (51):
1

shock

condition in which the total body cellular metabolism is malfunctional

2

what happens if shock goes untx

cellular death, organ damage, and eventual death of person

3

Tissue injury and the associated inflammatory response result in the production or activation of cellular molecules (i.e., cytokines, superoxide radicals, prostaglandins, adhesion molecules) that promote local cellular activation, tissue repair, and host defenses. However, sometimes this local response incites similar responses in cells that are distant from the primary insult which results in

systemic inflammation that can cause organ malfunction and shock

4

main causes of shock

hypoperfusion and inflammation

5

what must be assed in a pt w total body cellular malfunction

circulation of oxygen delivery and state of inflammation for cell toxicity

6

determinants of ventricular function

preload, after load, contractility, heart rate

7

preload

magnitude of myocardial stretch; stimulus to muscle contraction described by Frank-Starling mechanism

8

inc myocardial stretch leads to inc contraction which leads to

muscle being overstretched

9

preload is most appropriately measured as

end diastolic volume

10

after load is determined by

resistance to ventricular ejection that is present in either the pulmonary (pulmonary vascular resistance) or systemic arterial tree (systemic vascular resistance); inc by obstruction or vascular constriction

11

what is heart rate directly proportional to

cardiac output

12

initial response to tissue damage by trauma

bleeding and coagulation

13

hypoperfusion

dec in total body or regional blood flow that is sufficient to result in cellular malfunction or death

14

neurohumoral response to hypoperfusion

tachycardia (epinephrine, norepinephrine, dopamine), vasoconstriction (norepinephrine, arginine vasopressin, angiotensin), diaphoresis (norepinephrine), oliguria with sodium and water conservation (adrenocorticotropic hormone [ACTH], Cortisol, aldosterone, arginine vasopressin), and hyperglycemia (epinephrine, glucagon, Cortisol, insufficient insulin)

15

reperfusion injury

myocardial impairment, usually with arrhythmia, following the opening of arterial blockage and considered to be due to oxygen derived free radicals

16

classic effect of hypo perfusion on cellular metabolism

anaerobic metabolism caused by an oxygen deficit

17

primary etiologies of hypo perfusion states in surgical patients

dec venous return and dec myocardial function

18

mc cause of dec venous return secondary to dec MSP

hypovolemia (inflam, infx, trauma, pancreatitis, burns, vomiting,diuresis, inad oral intake)

19

s/sx of hypovolemic hypoperfusion

agitation, tachypnea, peripheral vasoconstriction

20

labs for hypovolemic hypoperfusion

serum electrolytes, arterial blood gases, blood lactic acid concentration; BUN/Cr

21

tx hypovolemic hypoperfusion

control of bleeding;

IV fluids:
-crystalloid (isotonic: ringer's lactate or 0.9%saline) (hypertonic saline)
-Colloid( rbc, ffp, albumin, processed human protein, LMW dextran, hydroxyethyl starch)

dopamine

22

mc causes of tamponade

chest trauma and bleeding after cardiac surgery

23

s/sx and test results tamponade

depending on the size; hypo perfusion, distended neck veins, muffled heart sounds, inc paradoxical pulse; low voltage on elf, CVP elevated, cxr enlarged heart

24

tx tamponade

removal of fluid surrounding the heart; iv fluid

25

tension pneumothorax

reduces venous return by producing an extracavitary inc in CVP and inc venous resistance in chest

26

causes of tension pneumo

spontaneously from rupture of bleb or penetrating/blunt trauma

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s/sx tension pneumo

dec perfusion, dec breath sounds, tympani over affected thorax, tracheal deviation away from affected side, distended neck veins

28

tx tension pneumo

14gauge needle into chest to release tension; closed thoracostomy; IV fluids

29

when a clinician decides not to administer fluid to a hypotensive pt what are they making the dx of

cardiogenic shock; makes it worse

30

s/sx cardiogenic shock

hypotension, tachycardia, tachypnea, peripheral vasoconstriction, distended neck veins, agitation, confusion, +/- murmurs

31

dx cardiogenic shock

cxr showing hydrostatic pulmonary edema, metabolic acidosis (lactic acidosis), inc CVP and PAOP, elev BUN/Cr; cardio gram shoing ischemia/infarct/arrhythmias; echo

32

what can be used to determine if sufficient oxygen is being provided to the tissues

pulmonary artery catheter (PAC) or central venous catheters

33

systemic inflammatory response syndrome (SIRS)

2 or more:
1. temp >38.5 or 90bpm
3. resp rate >20br/min or Paco2 12000 or 10% immature forms

34

mc etiology of inad cardiac output during inflammation

dec venous return which results from both loss of intravasc fluid and vasodilation

35

primary effect of third space fluid accumulation

deplete plasma volume and impair venous return

36

third space

accumulation of extracellular and intracellular fluid in response to regional or total body cellular or tissue injury; accumulation in excess of the volume of fluid that normally occupies these regions; sequestration decreases intravascular fluid volume.

37

cytopathic hypoxia

cells behave as if there is too little oxygen because of an inflammation-induced alteration in cellular function, not because there is too little oxygen provided for cells to function properly

38

s/sx of severe inflammation

temp/hypothermia, tachycardia, tachypnea, hypotension w warm or cold extremities, change in mental status, respiratory insuff, ileum, oliguria, inc urine protein, elev hemoglobin, thrombocytopenia, leukocytosis, leukopenia, inc serum glucose, dec ionized calcium

39

pts at risk for severe inflammation

recently acquired a ds (pancreatitis) or injury; underlying condition or recently underwent a procedure; sig episode of hypoperfusion

40

characteristics of the pt who is at risk for shock

trauma or burn, vascular catastrophe (ruptured aneurysm), acute cardiac ds, acute abdominal ds, severe extra abdominal infx

41

bedside exam indicators of shock

hypotension, tachycardia, tachypnea, hyperthermia/hypothermia, peripheral vasoconstriction and cool extremities, hypotension w warm extremities, agitation and altered mental status, oliguria

42

common lab abnorm w shock

metabolic acidosis, elev BUN/Cr, leukocytosis or leukopenia, elevated blood glucose, dec platelet count, dec ionized calcium

43

the hypotensive supine adult who does not have a cardiogenic process most often has lost how much intravasc fluid and what is the tx

30% (1500ml in 70kg); placement w isotonic cystalloid solution; 3:1 ratio to begin plasma volume

44

if dec venous return is cause of hypo perfusion what should be done

dx eval of cause while simultaneously restoring circulation w fluid infusion

45

bedside indicators of excellent circulation

normal blood pressure and pulse; normal mental status, warm extremities, urine output >0.5, resolution of metabolic acidosis

46

monitors of circulation status

cardiac index (>4.5), mixed venous O2 sat (>70%), central venous o2 stat (70%), oxygen delivery (>600), oxygen consumption (>170)

47

A 65-year-old man is severely injured in a dump truck rollover accident. He has sustained bilateral femur fractures, a pelvic fracture, and a pulmonary contusion. A pulmonary artery catheter is placed in order to guide you in the optimization of his hemodynamic status and guide his resuscitation. Correction of which current value will have the most dramatic impact on his oxygen delivery?

A. Measured cardiac output of 2 L/minute

B. Serum hemoglobin of 12 mg/dL

C. Arterial PO2 of 82 mm Hg

D. Arterial oxygen saturation of 93%

E. Pulmonary capillary occlusive pressure of 10 mm Hg (Lawrence 108)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

Answer: A

Oxygen delivery is delineated by the relationship O2D = (CO × CaO2 × 10). 10 is a factor to convert mL O2/100 mL blood to mL O2/L blood. The key components of the relationship are CO (measured cardiac output, which in turn is defined by the relationship CO = HR × stroke volume) and arterial oxygen content (CaO2, defined as CaO2 = 1.39 × Hgb × SaO2 + (PaO2 × 0.0031)). Of the answers listed, the most deranged from baseline is a CO of 2L/minute (average adult normal values are 4.5 L/minute for women and 5 L/minute for men), and, given the mathematical relationship of the O2D equation, it will have the greatest impact on this value when corrected. The values given for hemoglobin (B), arterial oxygen saturation (C), and pulmonary artery occlusive pressure (E) are all near or within normal values. Even relatively dramatic changes in arterial PO2 will have a minimal impact on O2D given the correction factor of 0.0031 as delineated in the CaO2 equation (answer C). (Lawrence 109)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

48

A 75-year-old woman with a history of congestive heart failure underwent elective sigmoid resection for severe recurrent diverticulitis. Postoperatively, she experiences shortness of breath. Physical exam and chest radiography suggest the presence of pulmonary edema. Which of the following parameters is the most accurate determinant of her left ventricular preload?

A. Central venous pressure

B. Pulmonary artery occlusive pressure

C. Systemic vascular resistance

D. Pulmonary venous pressure

E. Left ventricular end-diastolic volume (Lawrence 108)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

Answer: E

Preload is defined as the amount of myocardial stretch prior to myocardial contraction. Increased stretch leading to increased myocardial contraction is described by the Frank-Starling mechanism. Preload is most closely related to end-diastolic volume (answer E). Several other factors, including central venous pressure, pulmonary artery occlusive pressure, and pulmonary venous pressure, may also be used to estimate preload, but they are not as accurate as left ventricular end-diastolic volume for this purpose (answers A, B, and D). Systemic vascular resistance (C) is not mathematically related to preload. (Lawrence 109)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

49

A 22-year-old man is transported emergently to the hospital after sustaining a stab wound to the left chest. On initial survey, his airway is patent and he is breathing spontaneously, but he appears to be in shock. Which of the following findings best supports your working diagnosis of pericardial tamponade?

A. Central venous pressure of 8 mm Hg

B. Crisp S1S2 on cardiac auscultation

C. Paradoxical pulse of 18 mm Hg

D. Left atrial distention

E. Increased QRS voltage on ECG (Lawrence 108)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

Answer: C

As the disease process progresses, pericardial tamponade results in decreased venous return, with resultant decreased stroke volume, hypoperfusion, and shock. Clinical evidence of tamponade includes an increased paradoxical pulse (>15 mm Hg; answer C). Other signs include elevated central venous pressure (rather than normal, answer A), muffled heart sounds (rather than crisp S1S2, answer B), left atrial collapse (rather than distension, answer D), and decreased QRS voltage on ECG (answer E). (Lawrence 109)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

50

Two weeks following a severe motorcycle crash, a 25-year-old woman remains intubated in the surgical ICU. You are called to the bedside to evaluate a change in her condition. On evaluation, her vital signs include temperature of 39°C, heart rate of 110 beats/minute, respiratory rate of 22, blood pressure of 88/50, and arterial oxygen saturation of 96%. Her urine output has been 20 mL over the past 8 hours. On exam, she is in moderate distress and appears confused. She has crackles posteriorly in her left lung fields and her extremities are warm. A bronchoalveolar lavage is performed revealing Gram-negative rods. What is your diagnosis?

A. Atelectasis

B. Septic shock

C. Systemic inflammatory response syndrome

D. Allergic reaction to penicillin

E. Pulmonary embolus (Lawrence 108)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

Answer: B

Although inflammation is a normal response to tissue injury, the patient in the above scenario is displaying evidence of a dysfunctional inflammatory response. The derangements noted are too severe for atelectasis (answer A), which is associated with slight fever and normal blood pressure. Although allergic reactions (answer D) can be associated with cardiovascular collapse, there is no history of recent medication administration given. Pulmonary embolus (answer E) may present as tachycardia and hypotension but is typically also associated with hypoxia.

To meet the definition of the systemic inflammatory response syndrome, or SIRS, a patient must have two or more of the following conditions: (1) temperature >38.5°C or 90 beats/minute; (3) respiratory rate >20 breaths/minute or Paco2 12,000 cells/mm3, 10% immature forms. Although the patient in the scenario meets these criteria (answer C), the additional presence of end-organ dysfunction (hypotension, oliguria) and infection (Gram-negative rods on bronchoalveolar lavage [BAL]) make the diagnosis of septic shock more appropriate (answer B). (Lawrence 109)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

51

A 34-year-old woman is thrown from a horse during a trail ride and brought to the emergency department 60 minutes after the accident. She is awake but appears to be mildly confused. She complains of left chest pain that is worsened with inspiration as well as generalized abdominal pain. On exam, her airway is patent and breathing unlabored. Her pulse is 110 beats/minute. Her blood pressure is 85/62. Her breath sounds are equal bilaterally. Her neck veins are flat and her skin is cool. She is tender over her left lower ribs and left upper quadrant. You suspect that she has sustained an injury to her spleen with resultant hemorrhage. Approximately what percentage of intravascular volume loss has she experienced?

A. 0%

B. 10%

C. 20%

D. 30%

E. 50% (Lawrence 108-109)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.

Answer: D

The patient described in the scenario has suffered a splenic injury and progressive hemorrhage over the course of the hour leading up to presentation. She is demonstrating progressive hemodynamic effects from volume loss as described in Table 5-12, including mild tachycardia and hypotension, altered mental status, and decreased skin perfusion. Blood volume loss of 0% to 10% produces little change in hemodynamics or physical exam (answers A and B). Blood loss of 20% over 1 hour results in increased pulse, but normal blood pressure, mentation, and skin palpation (answer C). Blood loss of 30% is associated with mild hypotension, tachycardia, altered mental status, skin vasoconstriction, and decreased urine output (answer D; correct answer). Loss of 50% of blood volume is associated with severe physiological derangements, including profound hypotension, severe tachycardia, obtunded mental status, and anuria (answer E). (Lawrence 109)

Lawrence. Essentials of General Surgery, 5th Edition. Lippincott Williams & Wilkins, 09/2012. VitalBook file.