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Boards: Shock/Ischemia/CPR > Shock > Flashcards

Shock Flashcards

1
Q

List types of shock

A

circulatory shock:
- hypovolemia
- maldistributive
- cardiogenic
- obstructive
anemia
hypoxemia
impaired cellular oxygen utilization and energy production

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2
Q

What is the broad definition of shock?

A

the VO2 exceeds DO2 and utilization –> leading to a cellular energy debt and measurable organ dysfunction

other more common now: impaired cellular energy production

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3
Q

DO2 is a function of ____ and ____

A

DO2 is a function of CO and CaO2

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4
Q

CaO2 = ___ x ___ x ___ + ___

A

CaO2 = 1.34 x Hb x SO2 + 0.003 PaO2

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5
Q

Fill in the blanks

A
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6
Q

Explain how the delivery-independent Oxygen cosumption can be maintaned

A
  1. DO2 in excess of VO2
  2. Oxygen extraction only 25% under normal circumstances. Can be increased to 70-80% if DO2 is decreased
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7
Q

When does oxygen consumption become delivery dependent?

A

When the DO2 drops to a point when oxygen extraction cannot be increased enough to compensate and VO2 will drop with further decline in DO2

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8
Q

what are the intracellular consequences of decreased O2 delivery and consumption?

A

decreased DO2 and VO2 –> decreased oxidative phosphorylation/electron transport chain in the mitochondria to produce ATP

–> cells respond by reducing metabolic activity

eventually switch to anaerobic metabolism –> lactate production

–> intracellular acidosis: denaturation of proteins, decreased enzyme function, disruption of transport mechanisms

inadequate cellular energy –> intracellular systems fail (ion pumps fail, oxygen free radical formation, loss of adenine nucleotides) –> tissue injury

ion pumps fail –> membrane integrity of cells fail –> fluid shifts into cells –> cellular edema

–> cellular necrosis or triggering of apoptosis

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9
Q

What are the 3 stages of shock?

A
  • compensated shock
  • decompensated shock
  • terminal/irreversible shock
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10
Q

Explain the pathophysiology of compensated shock

A

the body is attempting to maintain core tissue/organ perfusion

  • baroreceptors sense decreased vessel wall tension
  • chemoreceptors sense hypoxia/hypercapnia/acidemia

► cathecholamine release

► tachycardia, increased cardiac contracility, peripheral vasoconstriction

► restores mean arterial perfusion pressure ► preserves perfusion of core organs

also: activation of RAAS system and increased release of vasopressin ► additional vasoconstriction + decreased urinary water loss
also: decrease in hydrostatic pressure (if applicable) ► water movement from itnerstitial into intravascular compartment

May happen at the expense of peripheral and splanchnic circulation ► hypoxic damage happens here already in compensated phase of shock

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11
Q

Explain the pathophysiology of decompensated shock

A

compensatory mechanisms are overwhelmed/exhausted

► impaired core perfusion

  • hypotension ► hypoperfusion ► hyperlactatemia ► metabolic (lactic) acidosis ► progressive catecholamine insensitivty

► vasodilation/ loss of vasomotor tone ► impaired venous return ► decrease in CO

► bradycardia ► decrease in CO

► irreversible/terminal shock

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12
Q

List 5 groups of complications arising from shock

A
  1. Systemic inflammatory response
  2. Coagulopathy
  3. Mitochondrial dysfunction
  4. Microcirculatory dysfunction
  5. Multiple organ dysfunction syndrome
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13
Q

What are the causes for systemic inflammation in shock?

A
  1. upregulation and release of inflammatory cytokines, e.g., IL-6, G-CSF
  • IL-6 and G-CSF serve as chemotactic factors ► neutrophil infiltration into affected tissues ► diapedesis
  • ► neutrophils release reactive oxygen and nitrogen species and proteolytic enzymes
  • ► vasodilation, increased capillary permeability, dectruction of extracellular matrix
  • ► tissue edema ► decreased O2 and metabolite exchange ► cellular dysfunction
  • neutrophil plugging on endothelium ► vessel obstruction ► disruption of microcirculatory blood flow
  1. activation of the complement system
  • tissue injury ► release of split products, e.g., C3a, C5a (i.e., anaphylactoxins)
  • lead to
  • ► increased vascular permeability
  • ► histamine and arachidonic acid product release
  • ► cytokine production and release,
  • ► promote aggregation and adherence of granulocytes to endothelium

increased activity of phospholipases A2 and C

  • stimulates production of prostaglandins and leukotrienes
  • ► further recruitment of inflamamtory cells
  • ► alterations in vascular permeability
  • ► impaired vasomotor tone
  • ► enhanced platelet activity and aggregation

“shock gut”

  • decreased intestinal perfusion ► increased intestinal permeability ► bacterial translocation

after reperfusion ► release of toxic metabolites and reactive oxygen species

  • hypoxanthines accumulate during ischemia
  • reperfusion ► O2 reintroduced ► formation of ROS
  • lipid peroxidation, membrane disruption, DNA damage
  • ► further cell damage ► necrosis and apoptosis
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14
Q

Explain how shock leads to coagulopathy

A

shock ► systemic inflammation

  • inflammatory cytokines (IL-1, IL-6, TNF-alpha, arachidonic acid metabolites) ► procoagulant
  • increased expression of tissue factor on endothelium and monocytes
  • consumption and downregulation of natural anticoagulants (protein C, antithrombin
  • increased activity of Plasminogen-activator-inhibitor (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI)

► hypercoagulable state ► microthrombi

  • arterial clots ► impairs tissue perfusion
  • venous clots ► impairs venous return and oxygenation (if PTE)

►consumption of clotting factors + platelets ► hypocoagulable state

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15
Q

Explain how shock causes mitochondrial damage

A
  • inflammatory cytokines (e.g., TNF-alpha) ► uncoupling of oxidative phosphorylation, increased mitochondrial permeability and apoptosis
  • increased production of reactive oxygen and nitrogen species and decreased ability to scavange free radicals
  • reperfusion injury (increased free radicals)
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16
Q

During shock, what leads to microvascular derangements, other than decreased perfusion?

A
  • endothelial edema from ischemic injury ► increaed wall thickness decreases diameter
  • increased permeability
  • damage from inflammatory mediators ► inflammation ► endothelial activation ► leukocyte adhesion and capillary plugging
  • arterial microthrombi ► impaired blood flow
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17
Q

Explain how the gastrointestinal tract is compromised during shock

A

►splanchnic and peripheral circulation is first to be compromised during compensatory vasoconstriction to preserve perfusion of vital organs ► ischemic injury

►epithelial injury and loss of mucosal barrier ► bacterial translocation

► reperfusion injury ► shown to cause dysmotility

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18
Q

Briefly describe the pathophysiology of ARDS

A
  • ARDS involves inflammation-induced diffuse alveolar-capillary injury and subsequent severe accumulation of proteinaceous edema in the pulmonary interstitium and alveoli
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19
Q

List 3 examples of DAMPs released during cell death from shock

A

mitochondrial DNA
histones
heat shock proteins

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20
Q

List 8 compensatory mechanisms being initiated during shock

A
  • baroreceptors (sense decreased stretch) - decreased inhibition of sympathetic tone - increases vasoconstriction, HR and contractility
  • peripheral chemoreceptors (sense increased CO2, decreased pH and O2) - vasoconstriction and increasing HR
  • central chemoreceptors (medulla oblongate, senses pH/CO2) - increased RR and TV
  • decreased capillary hydrostatic pressure causes reabsorption of volume from interstitium
  • increased circulating catecholamines and endorphine - vasoconstriction and decreases pain perception
  • hyperglycemia - from upregulated hepatic gluconeogenesis
  • RAAS upregulation
  • ADH synthesis and release - secondary to hypothalamus sensing decreased ECV
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21
Q

What causes neurogenic shock?

A

abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscles

typically TBI or spinal cord injuries

causes distributive shock

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22
Q

What is a normal CVP in a well-perfused patient?

A

0-6 cm H2O

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23
Q

What can cause decreased SvO2

A
  • decreased DO2 (
  • increased VO2 (e.g., hyperthermia, fever, seizures)
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24
Q

What can cause an increased SvO2?

A

hyperdynamic stage of sepsis
cytotoxic tissue hypoxia (e.g., cyanide toxicity)

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25
Q

Compare SvO2 and ScvO2 in critically ill patients with circulatory failure versus in health

A

health
* SvO2 > ScvO2 - higher oxygen extraction ratio of the brain, lowest OER of the kidneys

critically ill
* SvO2 < ScvO2 - blood preferentially diverted to brain and heart, splanchnic contraction - higher OER due to less perfusion

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26
Q

What part of the hypothalamus senses plasma osmolality?

A

supraoptic and paraventricular nuclei

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27
Q

Describe the ROSE principle

A

Resuscitation
Optimization
Stabilization
Evacuation

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28
Q

What is the Mark-Phillips curve?

A

Curve showing changes in extravascular lung water in response to increases in preload
can be used superimposed to the Frank-Starling’s curve, showing how fluid unresponsive patients have significant increases in lung water compared to preload increases

29
Q

What is the Passive Leg Raise?

A

Leg raise in people - equivalent to a mini fluid bolus as it distributes fluids to the central circulation - patient can then be assessed for signs of fluid overload or fails to respond - this can be reversed

equivalent in dogs would be a mini bolus of 3-5 mL/kg

30
Q

What is the equation for venous return?

A

Venous return = (MCFP - RAP) / venous resistance

31
Q

What was the sensitivity of chest radiographs to detedct hypovolemia in traumatized cats?

A

only 19%

look for cardiac size, CVC and pulmonary vessel diameter

32
Q

List the disadvantages of using CVP for intravascular volume assessment

A
  • static parameter
  • poor surrogate for RAP, cardiac filling pressure, or preload changes (ventricular pressure-volume curve is not linear)
  • affected by cardiac, lung, and intrathoracic pressures
  • invasive
  • expensive
  • technically demanding
  • associated with complications
33
Q

List 3 sites for caudal vena cava diameter measurements

A
  • suprailiac (kidney)
  • right intercostal (transhepatic)
  • subxiphoid (diaphragmatic)
34
Q

Which view for caudal vena cava diameter measurements has the lowest inter-rater variability?

A

subxiphoid view

35
Q

Of the cardiac POCUS measurements, which is the most sensitive to detect volume status changes?

A

LA size (this is just the authors opinion, not referenced)

36
Q

How does the Marik-Philips curve change in a septic patient?

A

towards the left
i.e., same preload causes more increase in extravascular lung water

37
Q

Fluid responsiveness is indicated by a PPV or SPV of greater than XX to XXX %

A

greater than 10-15%

38
Q

What are influences that could falsely alter the PPV or SPV?

A
  • spontaneous breathing effort agaisnt vent
  • altered chest wall compliance
  • cardiac disorders like arrhythmias
  • right heart failure
  • altered intrabdominal pressure
39
Q

How do you calculate PPV?

A

(P max - P min) / [(P max + Pmin)/2] x 100

40
Q

How do you calculate the CVC collapsibility index?

A

CVCCI = (CVC d max - CVC d min) / CVC d max

41
Q

What CVC collapsibility cutoffs describes fluid responsiveness?

A

> 50%

42
Q

What is VTI AO?

A

volume time integral in the left ventricular outflow tract

can be used to calculate CO

43
Q

List adverse effects from crystalloid fluid resuscitation (6)

A
  • pulmonary edema and acute lung injury from fluid overload
  • GI: decreased motility and increased permeability - risk of bacterial translocation and abdominal compartment syndrome
  • Heart: ventricular arrhythmias, decreased contractility, decreased CO (if reaching past point of fluid responsiveness on the Starling’s curve)
  • Coagulation: dilution of coag factors and decreased viscosity can cause coagulopathy
  • Inflammation: D-lactate (LRS) can cause neutrophil stimulation; decreased osmolality&raquo_space; cell swelling&raquo_space; phospholipase A2 activation, TNFalpha and interleukin production
  • Glycocalyx damage
44
Q

List 3 definitions of massive transfusion

A
  • patient blood volume or greater over 24 hours
  • 50% patient blood volume over 3 hours
  • 1.5 mL/kg/min over 20 min
45
Q

What is the current evidence for synthetic colloid induced AKI in dogs and cats?

A

dogs:
* inconsistent results - some show increased risk of AKI proportionate to the dose and duration, others showed no difference
* marginal increase in biomarkers for tubular injury or renal inflammation

cats:
* 2 studies, neither found increased risk of AKI or mortality

No randomized controlled trials atm

46
Q

Which clotting factors are mostly affected by synthetic colloid induced coagulopathies?

A

FVIII
vWF

47
Q

Besides increasing intravascular volume, what are benefits of hypertonic saline administration?

A
  • immunomodulatory effects - decreases neutrophil activation/adherence, decreases lymphocyte proliferation, inhibits inflammatory cytokine production
  • decreases intracranial pressure
  • reduces endothelial cell swelling
  • improves myocardial function and causes coronary vasodilation
48
Q

Why could PaCO2 potentially increase in a state of shock?

A

Increased H+ production&raquo_space; intracellular buffering&raquo_space; increased CO2 production

usually compensated for though by hyperventilation

49
Q

How is RAAS activated during shock and what are its effects?

A

activated by:
* sympathetic innervation
* decreased afferent arteriolar stretch
* decreased Cl delivery to the macula densa

effects:
* peripheral vasoconstriction
* efferent arteriolar vasoconstriction&raquo_space; maintains GFR
* increased NaCl absorption
* aldosterone release from adrenal cortex (zona glomerulosa)&raquo_space; increased NaCl absorption
* ADH release triggered

50
Q

Why do patients with decompensated shock develop bradycardia and decreased contractility?

A
  • progressive intracellular acidosis&raquo_space; reduces IC Ca++ cc&raquo_space; decreased contractility
  • intracellular acidosis&raquo_space; impairs conduction system&raquo_space; bradycardia
51
Q

Waht could be used as a surrogate for arterial BP waveforms when trying to assess pulse pressure variations?

A

Pulse oximeter plethysmograph

52
Q

In hypovolemic shock, what may change on the ECG?

A

R wave amplitude decreases

53
Q

What does Pv-aCO2 indicate?

A

increased values indicate tissue CO2 production

indicator for cardiac output

54
Q

What can you assess by dividing Cv-aCO2 by Ca-vO2?

A

indicator of anaerobic metabolism by tissues

55
Q

Why is LRS theoretically a better choice than Norm-R/Plasmalyte to treat hypovolemic shock?

A

acetate may cause vasodilation

56
Q

What is the definition of Cardiogenic shock and how is it clinical diagnosed?

A

decreased cardiac output and tissue hypoxia despite adequate intravascular volume

hypotension (SAP<90, MAP<65) with severely decreased CI and elevated end-diastolic LV pressure (>18 mm Hg)

57
Q

How does glucagon help in cardiogenic shock?

A

Has positive inotropic effects

adjunctive tx option for patients that are unresponsive to other inotropic gent

58
Q

How do you calculate the oxygen extraction ratio?

A

OER (%) = (CaO2 - CvO2) / CaO2

CvO2 = mixed venous O2
calculate CvO2 with same formula as CaO2 formula but need mixed venous O2 saturation

59
Q

In metanalyses, was lactate clearance or SvO2 correction as treatment guidance better at improvig survival?

A

lactate clearance-driven algorithms

60
Q

Describe Near-Infrared Spectroscopy

A
  • measures light absorption according to the Beer-Lambert law
  • can measure tissue oxygen saturation (StO2)
  • assuming status SaO2 - drop if StO2 indicated reduced perfusion
  • can detect perfusion derangements before oximetry, palsma lactate, or physical exam can
  • associated with disease severity but not survival in dogs
61
Q

List 3 methods of microvascular visualization

A
  • orthogonal polarized spectroscopy imaging
  • sidestream dark field imaging
  • Incident Darl Field imaging
62
Q

How does transcutaenous O2 and CO2 monitoring work and what is its utility in critically ill dogs?

A
  • approximately O2 and CO2 tension in tissues
  • measures gas tension via polarography
  • heats skin to 43-45 degrees C&raquo_space; increases transcutaenous gas diffusion

in critically ill dogs&raquo_space; overestimates PaO2 and PaCO2&raquo_space; don’t use in these patients

63
Q

What is regional capnography?

A

tonometer measuring PCO2 in tissues
» used to establish tissue-to-arterial PCO2 gradient

64
Q

By what percentage can splenic contraction increase the RBC mass?

A

up to 20 %

65
Q

At what percentage blood loss is irreversible shock and death imminent?

A

above 40-50%

66
Q

What defines massive hemorrhage?

A

blood loss of total blood volume within 24 hours

or half blood volume within 3 hours

67
Q

How effective are transcapillary fluid shifts at restoring blood volume?

A

up to 50% of plasma volume can return

68
Q

What is Claudin-3?

A

intestinal tight junction protein - lost after hemorrhagic shock - needed to maintain the mucosal barrier

Boards: Shock/Ischemia/CPR (15 decks)

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