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Surgical biology and methods > Shock > Flashcards

Shock Flashcards

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1
Q

What factors determine tissue oxygen delivery (DO2)?

A

DO2 = CO x CaO2

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2
Q

What factors determine cardiac output?

A

Heart rate and stroke volume

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3
Q

What are the different classifications of shock?

A

Hypovolemic, cardiogenic, distributive, hypoxic.

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4
Q

What are some causes of the common classifications of shock?

A
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5
Q

What is the oxygen-hemoglobin dissociation curve?

A
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6
Q

How is cardiac output acutely increased during shock?

A

Increased heart rate

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7
Q

How is cardiac output chronically increased during shock?

A

Increased stroke volume

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8
Q

What determines stroke volume?

A

Preload, afterload and contractility

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9
Q

What determines arterial oxygen content?

A

CaO2 = Hb x SaO2 x 1.34 x PaO2 x 0.003.
The hemoglobin concentration (Hb) and oxygen saturation of hemoglobin (SaO2) are the primary determinants of CaO2. PaO2 x 0.003 represents the proportion of dissolved oxygen in blood, which is very low.

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10
Q

If hemoglobin is maximally saturated with oxygen does increasing the FiO2 increase CaO2?

A

No - because the proportion of dissolved oxygen in the blood is very low.

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11
Q

What are the the three main categories that can result in reduced CaO2?

A
  1. Anemia
  2. Altered hemoglobin function
  3. Hypoxemia
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12
Q

What are the ATLS classes of hemorrhage?

A
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13
Q

What is the Frank-Starling mechanism?

A

Increase in end-diastolic volume augments the strength of cardiac contractions

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14
Q

What is oxygen uptake?

A

The rate at which oxygen leaves hemoglobin in the systemic capillaries:
VO2 = CO x (CaO2 - CvO2): Fick equation

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15
Q

What should the oxygen saturation of hemoglobin in venous blood (SvO2) be if oxygen delivery is adequate?

A

70%

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16
Q

What are five conditions that may result in normal SvO2 levels but inadequate tissue oxygenation?

A
  1. Diffusional shunting
  2. Diffusional resistance
  3. Arteriovenous shunting
  4. Perfusion/metabolism mismatch
  5. Cytopathic hypoxia
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17
Q

What is the DO2/VO2 curve?

A
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18
Q

Why does lactate accumulate under conditions of tissue hypoxia?

A

During hypoxia pyruvate is unable to enter the Krebs cycle, and energy production instead relies on anaerobic glycolysis. To avoid accumulation of byproducts pyruvate is converted to lactate, which regenerates NAD a necessary coenzyme for ATP production. In the absence of O2, lactate cannot be metabolized in the liver or kidneys and accumulates.

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19
Q

What is the mechanism behind metabolic lactic acidosis?

A

ATP degrades to ADP and produces H+. Under anaerobic conditions these cannot be consumed by mitochondria and accumulate in parallel with lactate production.

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20
Q

Describe the major physiologic responses to shock.

A
  1. Baroreceptors in the large thoracic arteries and low pressure stretch receptors in the atria and pulmonary arteries cause an increase in sympathetic activity.
  2. This is augmented by a detection of decreased O2 at chemoreceptors in the carotid and aortic bodies.
  3. Sympathetic activation is enhanced by release of angiotensin and vasopressin. Lead to water retention and vasoconstriction.
  4. Activation of the hypothalamic-pituitary-adrenal axis
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21
Q

What are the three main hypotheses to explain acute coagulopathy of trauma?

A
  1. A fibrinolytic variant of disseminated intravascular coagulation.
  2. Enhanced thrombomodulin-thrombin protein C pathway
  3. A neurohumeral response
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22
Q

How does shock enhance the effects of tissue trauma and promote a anticoagulant and hyperfibrinolytic state?

A

Ischemia induced endothelial release of tissue plasminogen activator, inhibition of plasminogen activator inhibitor, increased activation of protein C.

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23
Q

How does inflammation affect coagulation?

A

Cytokines activate platelets resulting in a systemic procoagulant effect. Downregulation of major anticoagulant pathways also occurs.

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24
Q

What are the clinical stages of shock?

A
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25
Q

What are the clinical signs of hypovolemic shock?

A
26
Q

What is the shock organ in the dog?

A

GI tract

27
Q

What is the shock organ in the cat?

A

Lungs

28
Q

What is arterial blood pressure?

A

Cardiac output x systemic vascular resistance

29
Q

How is MAP calculated?

A

DAP + 1/3 x [SAP-DAP]

30
Q

What are the BP ranges for healthy perfusion of the kidneys, heart, and brain in dogs?

A

Renal: 70 - 130 mmHg
Myocardial: 60-140 mmHg
Cerebral: 50-180 mmHg

31
Q

Is low arterial pressure a sensitive or insensitive measure of shock?

A

Insensitive and late marker of shock. Can have normal BP but impaired oxygen delivery through compensatory vasoconstriction.

32
Q

What are the minimum blood pressures needed to maintain perfusion of major body systems?

A

MAP > 60 mmHg, SAP > 90 mmHg

33
Q

What are the two methods of BP measurement in dogs and cats?

A

Direct and indirect

34
Q

What is the normal physiologic central venous pressure in the dog and cat?

A

0 - 5 cm H20

35
Q

How is CVP measured?

A

Catheter placed into the cranial or caudal vena cava at the junction with the right atrium

36
Q

What does a high degree of arterial pulse pressure variation during mechanical ventilation indicate?

A

Low intravascular volume

37
Q

CVP can be seen as a surrogate for preload, afterload or contractility?

A

Preload

38
Q

Is cardiac output measurement commonly performed?

A

No - requires placement of a pulmonary artery catheter and is associated with significant morbidity.

39
Q

Is lactate and early or late marker of hypoperfusion?

A

Late and insensitive marker

40
Q

What could cause elevated lactate despite normal perfusion?

A

Impaired metabolism through severe renal or hepatic disease.

41
Q

What are the two types of lactic acidosis?

A

Type A: caused by inadequate oxygen delivery to tissues
Type B: Caused by mitochondrial dysfunction

42
Q

Is decreased SvO2 an early marker of tissue hypoxia?

A

Yes, SvO2 will decrease before a supply dependent oxygen mechanism is established

43
Q

What can be used as a surrogate for SvO2 due to difficulties in pulmonary artery catheter placement?

A

Central venous oxygen saturation (ScvO2) measured in the cranial vena cava. ScvO2 consistently overestimates SvO2 in shock states.

44
Q

What are some markers of regional perfusion?

A
  1. Rectal temperature
  2. Gastric tonometry/sublingual capnometry
  3. Near-infrared spectroscopy
  4. Microvascular imaging techniques
  5. Pulse oximetry and PaO2
  6. Ultrasonography
45
Q

At what level of circulating deoxygenated hemoglobin does cyanosis or blue mucous membranes occur?

A

> 3 to 5 g/dL

46
Q

What does SpO2 measure?

A

Oxygen saturation of hemoglobin in arterial blood

47
Q

Is SpO2 an early or late marker of respiratory failure?

A

Late - it is a poor indicator of oxygen exchange in the lungs especially during oxygen therapy

48
Q

What is the best indicator of respiratory gas exchange?

A

PaO2

49
Q

What is the normal PaO2 at room air?

A

> 90 mmHg

50
Q

For patients receiving supplemental oxygen what should the PaO2/FiO2 ratio be?

A

500 (PaO2 should be approximately 5 x the percent of inspired oxygen)

51
Q

What are the suggested targets of resuscitation?

A
52
Q

What FiO2 is achieved with flow-by nasal oxygen, oxygen cage, and nasal/nasopharyngeal catheters?

A

Flow-by: 25-40% at a rate of 2-3 L/min
Oxygen cage: >60%
Nasal catheter: 40% and 60% for unilateral and bilateral catheters at a rate of 100 ml/kg/min

53
Q

When does oxygen toxicity occur?

A

If patients are exposed to an FiO2 of greater than 60% for longer than 24 hours

54
Q

What is the difference between hypotensive and limited fluid volume resuscitation?

A

Hypotensive aims for mean arterial pressure of 60 mmHg. Limited fluid resuscitation aims for physiologic endpoints (MAP 70 mmHg, SAP 90 mmHg) with restoration of intravascular volume using smallest possible volume of fluids

55
Q

What is the normal PaO2 in the dog?

A

> 80mmHg

56
Q

Describe the uses and types of fluids for the treatment of shock.

A
57
Q

Describe the MOA of various vasoactive and inotropic agents.

A
58
Q

What are the SIRS criteria for dogs and cats?

A
59
Q

What are the diagnostic criteria for ARDS?

A
60
Q

How does sepsis impact coagulation?

A

Tissue factor is expressed by damaged endothelial cells leading to widespread activation of the coagulation cascade. Additional alterations in the fibrinolytic and anticoagulant systems leads to an initial hypercoaguable state followed by consumptive coagulopathy.

61
Q

What are the clinical signs of septic shock?

A
62
Q

When might low dose glucocorticoid administration be considered in a septic patient?

A

In volume resuscitated patients with vasopressor refractory hypotension (possible critical illness-related corticosteroid insufficiency)

Surgical biology and methods (11 decks)

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