Shock and tranfusion II Flashcards

1
Q

Da-Nang lung refers to

A. ARDS
B. TRALI
C. Trauma associated cardiac overload
D. Pulmonary Embolism

A

ans A -

Da-nang Lung or shock lung was later identified as ARDS.

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2
Q

Which of the following is most sensitive to the change in intravascular volume

A. Carotid sinus pressure receptors
B. Atrial baroreceptors
C. Aortic arch baroreceptors
D. Chemoreceptors in aorta

A

ans B -

Baroreceptors

  • Atrial baroreceptors are sensitive to change in both chamber pressure and wall stretch.
  • they are activated with low volume hemorrhage or mild reductions in right atrial pressure.

Baroreceptors in aortic arch and carotid bodies respond to alterations in pressure or stretch of the arterial wall, they respond to much larger reductions in intravascular volume or pressure.

Normally - these receptors have a continuous inhibitory outflow to the sympathetic system.
When activated by decrease in intravascular volume they diminish their output and thus allow sympathetic activity to take place.

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3
Q

Which of the following is true regarding the chemoreceptor response -

A. Vasodilation of coronary arteries
B. Vasoconstriction of splanchnic circulation
C. Tachycardia
D. vasoconstriction of skeletal muscle circulations

A

ans C -

Chemoreceptors in aorta and carotid bodies are sensitive to -

  • changes in Oxygen tension
  • changes in H+ ion concentration
  • changes in carbon dioxide levels

Stimulation of these chemoreceptors leads to

  • vasodilation of the coronary arteries
  • slowing down of HR
  • vasoconstriction of splanchnic and skeletal muscle circulation.
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4
Q

Venous capacitance is increased in which of the following etiologies of shock

A. Cardiogenic
B. Septic
C. Neurogenic
D. Cardiogenic

A

ans B -

Hypovolemic shock - 
CO decreases
SVR increases
Venous capacitance decreases
CVP decreases
Septic shock - 
CO increases, 
SVR decreases
Venous capacitance increases
CVP decrease/increase
Cardiogenic shock - 
CO decreases dramatically
SVR increases dramatically
no change in venous capacitance
CVP raised
Neurogenic shock - 
CO increases
SVR decreases
Venous capacitance no change
CVP decreased
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5
Q

Catecholamine levels peak after

A. within minutes
B. 6 hours from injury
C. 12 hours from injury
D. 24 hours from injury

A

ans D -

Catecholamine levels peak within 24 to 48 hours of injury and then return to baseline.

Persistent elevation beyond this point of time suggests ongoing injury or noxious stimulation.

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6
Q

Majority of the norepinephrine produced in sympathetic response to injury is derived from -

A. Adrenal medulla
B. Pituitary
C. Neuroendocrine system
D. Synapses of the sympathetic nervous system

A

ans D-

Epinephrine - majority from the adrenal medulla.

Norepinephrine - from the synapses of the sympathetic nervous system.

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7
Q

T/F

During severe hypovolemia ACTH secretion occurs independently of cortisol negative feedback inhibition.

A

True.

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8
Q

All of the following stimulate the release of ADH except -

A. Hypoglycemia
B. Pain
C. Angiotensin II
D. Epinephrine

A

ans A -

ADH is released in response to -

  • Hypovolemia
  • changes in circulating blood volume sensed by baroreceptors and left atrial stretch receptors
  • increased plasma osmolality (sensed by hypothalamus)
  • Epinephrine
  • Angiotensin II
  • Pain
  • Hyperglycemia
  • proinflammatory cytokines (septic shock)
  • endotoxin
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9
Q

ADH levels usually remain elevated for ——- after injury

A. 12 hours
B. 1 day
C. 3 days
D. 1 week

A

ans D -

ADH levels remain elevated for about 1 week after initial insult.

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10
Q

All of the following are effects of vasopressin except

A. Free water absorption from collecting duct

B. Mesenteric vasoconstriction

C. Hepatic glycogenolysis

D. increased hepatic gluconeogenesis

A

ans C -

ADH acts on distal tubule and collecting ducts of the nephron to increase water permeability.

Potent mesenteric vasoconstrictor.

Increased hepatic gluconeogenesis and Glycolysis. (NOT Glycogenolysis)

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11
Q

Which of the following statements is false :

  1. Endotoxin induces ADH secretion independently of blood pressure, osmotic or intravascular changes.
  2. Chronic therapy with ACE inhibitors increased the risk of developing hypotension and vasodilatory shock with open heart surgery.
  3. Most alterations in cardiac output in the normal heart are related to changes in preload
  4. Sympathetic tone produces a greater decrease in skeletal muscle blood volume compared to the splanchnic blood volume
A

Ans 4.

Increases in sympathetic tone have a minor effect on skeletal muscle beds but produce a dramatic reduction in splanchnic blood volume, which normally holds 20% of blood volume.

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12
Q

All of the following are acute responses to intravascular volume changes except -

A. Change in venous tone
B. Systemic vascular resistance
C. ADH release
D. Change in intrathoracic pressure

A

ans C-

Acute responses in intravascular volume include changes in venous tone, systemic vascular resistance and intrathoracic pressure, with the slower hormonal changes less important in early response to volume loss.

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13
Q

Majority of the afterload is contributed by the -

A. Arterioles
B. Precapillary smooth muscle sphincters
C. systemic arteries
D. Capillaries

A

ans B -

Arterial pressure is the major component of afterload. This vascular resistance is determined by pre-capillary smooth muscle sphincters.

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14
Q

Dysoxia is defined as -

A. Increased alveolar-arterial oxygen gradient.

B. Decreased Oxygen carrying capacity of Hb

C. Failure to sustain oxidative phosphorylation

D. Any of the above

A

ans C -

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15
Q

Complete oxidation produces _______ mol of ATP from 1 mol of glucose

A. 2 mol
B. 30 mol
C. 36 mol
D. 38 mol

A

ans D -

Failure of oxidative phosphorylation, leads to shift to anerobic metabolism and glycolysis to generate ATP.

Glycolysis is a RAPID process but inefficient. Producing only 2 mol of ATP from 1 mol of glucose, compared to complete oxidation of 1mol of glucose that produces 38 mol of ATP.

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16
Q

expression of all of the following genes are increased by shock except -

A. Heat shock proteins
B. VEGF
C. eNOS
D. Heme-oxygenase-1

A

ans C -

Expression of gene products such as heat shock proteins, VEGF, iNOS, Heme-oxygenase-1 and cytokines is increased by shock.

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17
Q

All of the following are DAMPs except

A. Mitochondrial DNA
B. Hyaluronan oligomers
C. Heparan sulfate
D. Extra domain A of fibronectin
E. Interleukin 1-alpha
F. LPS
A

ans F -

Endogenous DAMPs

  • mitochondrial DNA
  • Hyaluronan oligomers
  • Heparan sulfate
  • Extra domain A of fibronectin
  • HSP 60,70
  • gp 96
  • surfactant protein A
  • Beta-defensin 2
  • Fibrinogen
  • Biglycan
  • HMGB-1
  • Uric acid
  • Interleukin 1alpha
  • S-100
  • Nucleolin

DAMPs are intracellular molecules released by broken cells that can have paracrine and endocrine like effects on distant tissues to activate inflammatory and immune responses. This is called Danger signalling.

They are recognized by Pattern Recognition Receptors or PRRs which include Toll Like Receptors and Receptor for advanced glycation end products or RAGE.

LPS is a Pathogen-associated molecular pattern or PAMP.

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18
Q

which of the following cells function as sentinel responders -

A. Macrophages
B. Neutrophils
C.Lymphocytes
D. Monocytes

A

ans A -

Before the recruitment of leukocytes to the site of injury, tissue based macrophages or mast cells act as sentinel responders releasing histamines, eicosanoids, tryptases and cytokines.

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19
Q

TNF-alpha levels peak within

A. 30 min
B. 1 hour
C. 1.5 hour
D. 2 hours

A

ans C-

TNF-alpha is one of the earliest cytokines released in response to injurious stimuli. Monocytes, macrophages and T cells release this potent inflammatory cytokine.

TNF-alpha levels peak within 90 minutes of stimulation and return frequently to baseline levels within 4 hours.

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20
Q

TNF-alpha all are true except -

A. Released by monocytes, macrophages and T cells.

B. Released in response to endotoxins, hemorrhage and ischemia.

C. Increase in TNF-alpha in trauma patients is much higher than that seen in septic patients.

D. Causes peripheral vasodilation, procoagulant activity and cachexia

A

ans C -

TNF alpha is released by monocytes, macrophages and T cells.

Released in response to Bacterial endotoxin in septic shock as well as hemorrhage and ischemia.

The increase in serum TNF-alpha levels reported in trauma patients is far less than that seen in septic patients.

Effects -

  • Peripheral vasodilation
  • release of other cytokines
  • Procoagulant activity
  • muscle protein breakdown
  • cachexia
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21
Q

IL-1 all are true except -

A.Half life is 6 minutes.
B. induces febrile response to injury
C. induces anorexia
D. supresses the release of Beta endorphins

A

ans D -

IL-1 has actions similar to TNF-alpha.
Half life : 6 min.
Primarily paracrine action - local cellular responses.

Systemic action -
- induces febrile response by stimulating PG production in anterior hypothalamus.

  • anorexia by activating satiety centre.
  • augments secretion of ACTH, Glucocorticoids and Beta-endorphins.
  • stimulates release of other cytokines - IL-2, IL-4, IL-6, IL-8, GMCSF, IFN-gamma.
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22
Q

Diffuse alveolar damage and ARDS in shock is mediated largely by -

A. TNF-alpha
B. IL-6
C. IL-1
D. IL-2

A

ans B -

IL6

elevated in - hemorrhagic shock, major surgery and trauma.

Levels correlate with shock

Contributes to Lung, Liver and Gut injury after hemorrhagic shock.

May play a role in development of diffuse alveolar damage and ARDS.

IFN-gamma - also promotes ARDS.

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23
Q

All of the following hepatic acute phase proteins except -

A. C-reactive protein
B. Fibrinogen
C. Albumin
D. Haptoglobin
E. Alpha-1 Anti-trypsin
A

ans C -

IL-6 and IL-1 are mediators of the hepatic acute phase response and they enhance the expression of -

  • Complement
  • CRP
  • Fibrinogen
  • Haptoglobin
  • Amyloid A
  • Alpha-1 antitrypsin
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24
Q

which of the following is correctly matched.

A. IL-1 - induces febrile response by activating prostaglandin in posterior hypothalamus

B. IL-2 Promotes gut barrier integrity

C. IL-4 Increases the production of IL-1, IL-6 and IL-8

D. IL-8 Chemoattractant to monocytes.

A

ans B -

IL-1: Induces fevers through PG activity in anterior hypothalamus, promotes Beta-endorphin release from pituitary and half life <6min.

IL-2 - promotes lymphocyte proliferation, immunoglobulin production, gut barrier integrity

IL-4 - induces B-lymphocyte production of IgG4 and IgE, mediators of Allergic and anti-helminthic response.
Downregulates TNF, IL-1, IL-6 and IL-8

IL-5 - promotes eosinophil proliferation and airway inflammation.

IL-6 - Elicited by virtually all immunogenic cells. Long half life. Prolongs survival of activated neutrophils.

IL-8 - chemoattractant for Neutrophils, basophils, eosinophils, lymphocytes.

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25
Q

which of the following are anti-inflammatory cytokines

A. IL-10
B. IL-15
C. IL-13
D. Both A and B

A

ans D -

IL-10 - Prominent anti-inflammatory cytokine, reduces mortality in animal sepsis and ARDS models.
Inhibits proinflammatory cytokine production, O2 radical production by phagocytes, adhesion molecule expression, lymphocyte activation.

IL-12 - Promotes Th1 differentiation, synergistic action with IL-2.

IL-13 - Promotes B lymphocyte function and structurally similar to IL-4. Inhibits Nitric oxide and endothelial activation.

IL-15 - anti-inflammatory cytokline. Promotes lymphocytic activation, promotes neutrophil phagocytosis in fungal infection.

IL-18 - Similar to IL-12 in function. Levels are increwased in Sepsis, especially Gram positive infections and high levels found in cardiac death.

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26
Q

IL that is found in high levels in cardiac death -

A. IL-13
B. IL-15
C. IL-18
D. IL-17

A

ans C

IL-18 -
produced by macrophages, Kupffer cells, Keratinocytes, adrenal cortical cells and Osteoblasts.

Similar to IL-12 in function, and levels are increased in sepsis, especially in gram positive infections.

High levels of IL-18 are found in cardiac death.

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27
Q

which IL has structural similarity to IL-4

A. IL-5
B. IL-13
C. IL-10
D. IL-12

A

ans B -

IL-13 is structurally similar to IL-4 and it also promotes B lymphocyte function.
Inhibits Nitric oxide and endothelial activation.

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28
Q

All of the following are key mediators in ARDS except -

A. HMGB1
B. IL-6
C. IFN-gamma
D. TGF-Beta

A

ans D -

HMGB1 - high mobility group box chromosomal protein. It is a DNA transcription factor. Late mediator of inflammation leading to ARDS, Gut barrier disruption. Induces “Sickness behavior”

IFN-gamma - Mediates the IL-12 and IL-18 functions. Promotes ARDS. It is usually found in wounds 5-7 days after injury.

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29
Q

Which of the following interleukins is preferentially secreted by Th2 cells -

A. IL-18
B. IL-21
C. IL-13
D. IL-15

A

ans B -

IL-21 is preferentially secreted by Th2 cells. Structurally similar to IL-2 and IL-15. Activates NK cells, B cells and T cells. Influences adaptive immunity.

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30
Q

C3a, C4a and C5a induce all of the following except -

A. Increased adherence of neutrophils to vascular ednothelium.

B. Vascular permeability increased.

C. Smooth muscle cell contraction.

D. Histamine release.

E. All of the above

A

ans E -

Significant complement consumption after hemorrhagic shock.

Trauma pts - degree of complement activation is proportional to the magnitude of injury and may serve as a marker for severity of injury.

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31
Q

First cells to be recruited to the site of injury are -

A. Neutrophils
B. Monocytes
C. Macrophages
D. Lymphocytes

A

Ans A -

Neutrophil activation - early event. First cells to be recruited to the site of injury.

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32
Q

All of the following are true regarding PMNs

A. produce reactive oxygen species that induce lipid peroxidation.

B. Tocopherol and Glutathione are used up reactive oxygen species.

C. Elastase and cathepsin G are proteolytic enzymes released by neutrophils.

D. Ischemia - reperfusion injury also activates PMNs

E. All of the following

A

Ans E -

Activated PMNs generate reactive oxygen species (Superoxide anion, hydrogen peroxide, hydroxyl radical) which cause lipid peroxidation.

Proteolytic enzymes such as elastase and Cathepsin G are released as well as vasoactive mediators - eicosanoids, leukotrienes, platelet activating factor.

Oxygen free radicals also consume glutathione and tocopherol.

Ischemia reperfusion activates PMNs and causes PMN induced organ injury.

In animal models - activation of PMN correlates with irreversibility of shock.

In humans, activation of neutrophils has a role in MODS. Plasma markers of PMN activation - Elastase - correlates with severity of injury.

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33
Q

Which of the following is the plasma marker of neutrophil injury -

A. Elastase
B. Collagenase
C. Neuron Specific Enolase
D. S100

A

ans A -

Elastase is the plasma marker of neutrophil activation.

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34
Q

True regarding - TLR4 mediated cell signalling

A. MyD88 dependent mechanism activates NF-kB.

B. MyD88 independent pathway induces IRF3

C. Both A and B

D. Neither A nor B

A

ans C -

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35
Q

Most common cause of shock in surgical patients?

A. Hypovolemic shock
B. Hypothermic shock
C. Septicemic shock
D. Neurogenic shock

A

ans A -

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36
Q

Average amount of blood loss in class III hemorrhagic shock -

A. <750 mL
B. 750-1500 mL
C. 1500-2000mL
D. >2000 mL

A

ans C -

Blood loss
Class I : <15% or <750mL, HR<100.
Class II : 15-30% or 750-1500 mL. HR > 100.
Class III : 30-40% or 1500-2000 mL, HR > 120.
Class IV : >40% or >2L, HR >140.

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37
Q

Orthostatic hypotension is seen in which stage of hemorrhagic shock

A. Class I
B. Class II
C. Class III
D. Class IV

A

ans B -

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38
Q

Orthostatic hypotension is seen in which stage of hemorrhagic shock

A. Class I
B. Class II
C. Class III
D. Class IV

A

ans B -

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39
Q

Hypotension in trauma patients is defined by

A. SBP <90 mmHg
B. SBP <110 mmHg
C. DBP <60mmHg
D. Both A and C

A

ans B -

Recent data in trauma patients suggest that a systolic BP of less than 110mmHg is a clinically relevant definition of hypotension and hypoperfusion based on an increasing rate of mortality below this pressure.

40
Q

which of the following is false

A. Lactate is a marker of oxygen and severity of hemorrhagic shock

B. Both base deficit and lactic acidosis correlate with extent of shock and patient outcome.

C. Base deficit and Lactate levels are closely correlated with each other

D. Base deficit at admission can predict tranfusion requirements.

A

ans C -

The amount of lactate is an indirect marker of tissue hypoperfusion, cellular oxygen debt and severity of hemorrhagic shock.

Serum lactate at admission and serial serum lactate levels are reliable predictors of morbidity and mortality with hemorrhage.

Both base deficit and lactate correlate with extent of shock and patient outcome, but interestingly do not firmly correlate with each other.

Base deficit upon admission correlates with tranfusion requirement, development of multiple organ failure and death.

41
Q

which of the following is false

A. Lactate is a marker of oxygen and severity of hemorrhagic shock

B. Both base deficit and lactic acidosis correlate with extent of shock and patient outcome.

C. Base deficit and Lactate levels are closely correlated with each other

D. Base deficit at admission can predict tranfusion requirements.

A

ans C -

The amount of lactate is an indirect marker of tissue hypoperfusion, cellular oxygen debt and severity of hemorrhagic shock.

Serum lactate at admission and serial serum lactate levels are reliable predictors of morbidity and mortality with hemorrhage.

Both base deficit and lactate correlate with extent of shock and patient outcome, but interestingly do not firmly correlate with each other.

Base deficit upon admission correlates with tranfusion requirement, development of multiple organ failure and death.

elevated base deficit persists (or lactic acidosis) in trauma patient, ongoing bleeding is often the etiology.

Trauma patients with base deficit greater than 15 mmol/L required twice the volume of fluid infusion and six times more blood transfusion in the first 24 hours compared to patient with mild acidosis.

42
Q

Best predictor of red blood cell tranfusion

A. Tachycardia
B. Hypotension
C. Acidosis
D. Hematocrit at admission

A

ans D -

Although hematocrit changes do not rapidly reflect the total volume of blood loss, admission hematocrit has been shown to be associated with 24 hour fluid and transfusion requirements.

Hematocrit at admission is more strongly associated with packed red blood cell tranfusion than tachycardia, hypotension and acidosis.

Lack of depression in initial hematocrit does not rule out substantial blood loss or ongoing bleeding.

43
Q

Amount of blood that can collect in one pleural cavity

A. 500-1000 mL
B. 1000-1500mL
C. 1500-2000mL
D. 2000-3000mL

A

ans D - each pleural cavity can hold 2-3L of blood.

44
Q

most common source of blood source of blood loss inducing shock

A. External bleeding
B. Intra-peritoneal bleeding
C. Hemothorax
D. Long bone fracture

A

Ans B -

Intra-peritoneal hemorrhage is probably the most common source of blood loss inducing shock.

45
Q

The probability of death increases by 1% for every _____ spent in trauma bay in patients with major injuries requiring emergency laparotomy

A. 1 min
B. 2min
C. 3min
D. 5min

A

ans C

Clarke and colleagues demonstrated that trauma patients with major injuries isolated to the abdomen requiring emergency laparotomy had an increased probability of death with increasing length of time in the emergency department for patients who were in the emergency department for 90 minutes or less. This probability increased approximately 1% for each 3 minutes in the emergency department.

46
Q

Permissive hypotension in damage control resuscitation aims to keep SBP at -

OR

Goal of SBP in penetrating injury

A. <80 mmHg
B. 80-90 mmHg
C. 90-110 mmHg
D. >110mmHg

A

ans B -

Damage control resuscitation begins in the emergency department

47
Q
Damage control resuscitation begins in - 
A. At the scene
B. Emergency department
C. Operative room
D. ICU
A

ans B -

First stage - Emergency department - start fluids and arrange blood.

Second stage - OT - control of hemorrhage.

Third Stage - ICU - Treat hypothermia and coagulation.

48
Q

If closed head injury is suspected in a patient then SBP must be maintained -

A. <80 mmHg.
B. 80-90mmHg
C. 90-110mmHg
D. >110mmHg

A

ans D -

Any delay in surgery for control of hemorrhage increases mortality

With uncontrolled hemorrgage attempting to achieve normal blood pressure may increase mortality especially with penetrating injuries and short transport time.

A goal of SBP of 80-90 mmHg may be adequate in the patient with penetrating injury.

Profound hemodilution should be avoided by early transfusion of red blood cells.

For the patient with blunt injury where the major cause of death is a closed head injury, the increase in mortality with hypotension in the setting of brain injury must be avoided. In this setting, an SBP of 110mmHg would seem to be more appropriate.

Bailey >90 mmHg.

49
Q

Current recommendation for target hemoglobin in stable iCU patients admitted with hemorrhagic shock -

A. 6-8 mg/dL
B. 7-9 mg/dL
C 8-10 mg/dL
D. >10mg/dL

A

ans B -

50
Q

Target Platelet counts in trauma patients are -

A. 5 x 10^10/L
B. 10 x 10^10/L
C. 15 x 10^10/L
D. 50 x 10^10/L

A

ans A -

50 x 10^9/L or 50,000/uL

51
Q

Trauma patients who are most likely to benefit from platelet transfusion -

A. Long bone injury
B. Brain injury
C. Intra-peritoneal hemorrhage
D. External bleeding

A

Ans B -

Increased platelet use appears to improve outcome.
The benefit of platelet transfusion may be most pronounced in trauma patients with brain injury.

Platelets should be transfused to maintain counts above 50000/uL.

52
Q

Trauma patients who are most likely to benefit from platelet transfusion -

A. Long bone injury
B. Brain injury
C. Intra-peritoneal hemorrhage
D. External bleeding

A

Ans B -

Increased platelet use appears to improve outcome.
The benefit of platelet transfusion may be most pronounced in trauma patients with brain injury.

Platelets should be transfused to maintain counts above 50000/uL.

53
Q

Which of the following findings suggests that fibrinogen concentrates or prothrombin complex concentrates should be used in trauma patients

A. Thromboelastography
B. Raised PT
C. Fibrinogen <100mg/dL
D. Both A and C

A

ans D -

There is potential role for other coagulation factor based products such as fibrinogen concentrates and prothrombin complex concentrates. Use of these agents may be guided by a drop in fibrinogen levels to less than 1g/L or less specifically by thromboelastography suggesting of hyperfibrinolysis.

Traditional measures of platelets, INR and PT may not reflect coagulopathy of trauma or response to therapy effectively.

54
Q

Tranexamic acid all are true except -

A. Irreversible inhibitor of plasmin and plaminogen

B. Synthetic lysine analogue

C. CRASH-2 trial suggested that early use can reduce mortality in trauma patients.

D. None of the above

A

Ans A -

Tranexamic acid is a competitive inhibitor of plasmin and plaminogen.

It is a synthetic lysine analogue.

CRASH-II trial suggested early use of tranexamic acid limits rebleeding and reduces mortality.

1g iv over 10 minutes and 1g every 8 hours. Should be given to all trauma patients with SBP <110 mmHg and pulse >110 min.
Needs to administered within 3 hours of injury.

All traumatized patients with signs of shock should recieve tranexamic acid.

55
Q

Acute coagulopathy of trauma occurs within

A. Minutes
B. 1-2 hours
C. 2-6 hours
D. 1-2 days

A

Ans A -

Acute coagulopathy of trauma occurs as an immediate consequence of injury

Abnormal admission coagulation is a predictor of high mortality.

56
Q

Which of the following is true regarding Thromboelastography-

A. Predicts need for red cell tranfusion better than conventional coagulopathy

B. Predicts need for platelet tranfusion better than platelet count

C. Predicts need for plasma transfusion better than fibrinogen levels

D. All of the above

A

Ans D

57
Q

Early total care of trauma patients is a viable option if lactate levels are -

A. <2 mmol/L
B. 2-3 mmol/L
C. >3 mmol/L
D. >5 mmol/L

A

ans A

<2 mmol/L - early total care

2-3 mmol/L - look at the trend - increasing or decreasing

> 3 mmol/L - may be under-resuscitated - either further resuscitation or damage control surgery (If surgery is urgent)

> 5 mmol/L - damage control surgery

58
Q

Which of the following is a cause of vasodilatory shock

A. Hypoxic lactic acidosis
B. Septic shock
C. Post-cardiotomy shock
D. Irreversible hemorrhagic shock
E. All of the above
A

Ans All of the above

The most common form of vasodilatory shock is septic shock.

Others -

  • Pancreatitis
  • Burns
  • Anaphylaxis
  • Acute Adrenal insufficiency
  • Prolonged severe hypotension (Terminal Cardiogenic shock, Irreversible hemorrhagic shock, cardiopulmonary bypass)
  • Hypoxic lactic acidosis
  • Carbon monoxide poisoning
59
Q

All of the following are true regarding septic shock except -

A. Catecholamine levels are decreased.
B. Mortality rate 30-50%.
C. RAAS is activated
D. Peripheral Vasodilation

A

Ans A -

Hypotension results from failure of the vascular smooth muscle to constrict appropriately. Vasodilatory shock is characterized by peripheral vasodilation with resultant hypotension and resistance to treatment with vasopressors.
Despite the hypotension the plasma catecholamine levels are raised and the RAAS is activated.

Despite advances in intensive care, the mortality rate for severe sepsis 30-50%.

60
Q

All of the following are anti-inflammatory interleukins except -

A. IL-10
B. PAF
C. IL-4
D. IL-13

A

Ans B

Anti-inflammatory mediators include -

IL-4, 10 and 13; PGE2; TGF-Beta.

61
Q

Minimum rate of resuscitation during first 4-6 hours of septic shock should be

A. 40 mL/kg
B. 30 mL/kg
C. 20 mL/kg
D. 10 mL/kg

A

ans B -

Because vasodilation and decrease in total peripheral resistance may produce hypotension, fluid resuscitation and restoration of circulatory volume with balanced salt solutions is essential. This resuscitation should be at least 30 mL/kg within the first 4-6 hours.

NOTE - use of starch based colloid solutions should be avoided in case of septic shock.

62
Q

which of the following is the first line vasopressor used in sepsis

A. Vasopressin
B. Norepinephrine
C. Epinephrine
D. Dobutamine

A

Ans B -

Catecholamines are the vasopressors used most often, with norepinephrine being the first line agent following by epinephrine. Occasionally patients with septic shock develop resistance to the effects of catecholamines. Vasopressin is often efficacious in this setting and if often added to norepinephrine.

Majority of septic patient have hyperdynamic physiology with supranormal cardiac output and low systemic vascular resistance.
On occasion, septic patients may have low CO despite volume resuscitation and even vasopressor support. Dobutamine therapy is recommended for patients with cardiac dysfunction as evidenced by high filling pressures and low cardiac output or clinical signs of hypoperfusion after achievement of restoration of blood pressure following fluid resuscitation.

63
Q

As per 2012 guidelines by surviving sepsis campaign, all of the following should be completed within 3 hours of patient presenting with sepsis

A. Lactate levels
B. Obtain blood culture prior to administration of antibiotics
C. Administer broad spectrum antibiotics
D. Administer 30 mL/kg crystalloid for hypotension or lactate =or>4mmol/L
E. Measure Central venous pressure

A

Ans E -

Completed within 3 hours

A. Measure lactate levels
B. Obtain blood cultures prior to administration of antibiotics
C. Administer broad spectrum antibiotics
D. Administer 30mL/kg crystalloid for hypotension or lactate =or> 4mmol/L

Completed within 6 hours
E. apply vasopressors (For hypotension that does ot respond to initial fluid resuscitation to maintain MAP more than or equal to 65mmHg
F. In the event of persistent arterial hypotension despite volume resuscitation
- measure CVP
- Measure Central venous O2 sat.
G. Remeasure lactate levels if initial lactate elevated.

Targets for qualitative resuscitation included -

  1. CVP 8mmHg or greater
  2. central venous Saturation of 70% or greater.
  3. normalisation of lactate.

Goal directed therapy of septic shock initiated during first 6 hours significantly improved outcomes.

  • higher mean Oxygen venous sat.
  • lower lactate levels
  • lower base deficit
  • higher pH
  • lower 28 day mortality
  • lower frequency of sudden cardiovascular events

Patients on goal directed therapy recieved more fluids during the first 6 hours, but they recieved less fluids compared to standard therapy over 72 hours.

64
Q

All of the strategies are recommended in ARDS and ALI except -

A. Prone position
B. Alveolar recruitment maneuvres
C. High tidal volumes
D. high PEEP

A

ans C-

Patients with ARDS and ALI, mechanical ventilation with lower tidal volumes than is traditionally used results in decreased mortality and increases the number of days without ventilator use.

additional strategies -

  • higher levels of PEEP
  • Alveolar recruitment maneuvres
  • prone positioning.
65
Q

True of false -

Hydrocortisone at 200 mg/d for 7 days in four divided doses is recommended in patients of septic shock.

A

Ans False

Steroids cannot be recommended as routine adjuvant therapy for septic shock.

However, if SBP remains below 90 mmHg despite appropriate fluid and vasopressor therapy, hydrocortisone at 200mg/d for 7 days in four divided doses or by continuous infusion should be considered.

66
Q

Hemodynamic criteria for cardiogenic shock include all except

A. SBP <90 mmHg for atleast 30 min
B. Reduced cardiac index (<2.2L/min/sq.m)
C. elevated pulmonary artery wedge pressure (>15mmHg)
D. Lactate >4mmol/L

A

ans D -

Cardiogenic shock is circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume. Hemodynamic criteria include sustained hypotension (i.e. SBP <90 mmHg for atleast 30 min), reduced cardiac index (<2.2L/min/sq.m) and elevated pulmonary artery wedge pressure (>15mmHg)

67
Q

Mortality rates for cardiogenic shock are -

A. 20-40%
B. 30-50%
C. 50-80%
D. 30-80%

A

ans C.

68
Q

Most common cause of Cardiogenic shock is -

A. Myocarditis
B. Atrial fibrillation
C. Acute MI
D. Drug reactions

A

Ans C -

Acute extensive MI is the most common cause.

Other causes

  • Arrthymias
  • End stage cardiomyopathy
  • Myocarditis
  • Severe myocardial contusion
  • Left ventricular outflow obstruction - Aortic stenosis, HOCM
  • Obstruction to left ventricular filling - Mitral stenosis, Left Atrial myxoma
  • Acute Mitral Regurgitation
  • Acute aortic insufficiency
  • Metabolic
  • Drug reactions
69
Q

what percentage of patients with acute MI develop cardiogenic shock

A. 5-10%
B. 10-15%
C. 15-25%
D. 30-40%

A

ans A -

Cardiogenic shock is also the most common cause of death in patients hospitalized with acute MI.

70
Q

All of the following are true regarding cardiogenic shock in acute MI except -

A. Cardiogenic shock is the most common cause of death in patients hospitalised with acute MI

B. Typically shock is present on admission

C. 75% of those who develop shock, do so within 24 hours of onset of infarction

D. Average duration for developing signs of cardiogenic shock is 7 hours from onset of infarction

A

Ans B -

Typically shock is not present on admission, eventhough patients who eventually have cardiogenic shock 75% develop it within first 24%, average 7 hours from onset of infarction.

71
Q

Mortality rate after achieving complete re-perfusion after Transluminal coronary angioplasty is

A. 15%
B. 33%
C. 50%
D. 83%

A

ans B -

Expeditious restoration of cardiac output is mandatory to minimise mortality; the extent of myocardial salvage possible decreases exponentially with increased time to restoration of coronary blood flow.

The degree coronary flow after percutaneous transluminal coronary angioplasty correlates with in-hospital mortality - 33% mortality with complete reperfusion; 50% mortality with incomplete reperfusion and 85% mortality with absent reperfusion.

72
Q

all of the following are effects of dobutamine except

A. Increased cardiac contractility
B. Decreased systemic blood pressure
C. Increased total peripheral vascular resistance
D. Acts of Beta-1 receptors in the heart.

A

Ans C

Dobutamine primarily stimulates cardiac Beta-1 receptors to increase cardiac output but may also vasodilate peripheral vascular beds, lower total peripheral resistance, and lower systemic blood pressure through Beta-2 receptors.

73
Q

Amrinone all are true except -

A. routinely used in patients with cardiogenic shock

B. long half life

C. Thrombocytopenia

D. Hypotension

A

Ans A -

Amrinone and Milrinone may be required in patients with resistant cardiogenic shock. These agents have long half lives and induce thrombocytopenia and hypotension. Their use is reserved for patients unresponsive to other treatment.

74
Q

All of the following are true regarding pericardial tamponade except

A. Small volumes can cause pericardial tamponade in acute settings

B. Upto 2000mL of the fluid may accumulate in the pericardium before tamponade occurs in setting in uremia and heart failure

C. Major determinant of the degree of hypotension is the pericardial pressure

D. None of the above

A

Ans D

Hemodynamic abnormalities of pericardial tamponade are due to elevation of intra-cardiac pressures with limitation of ventricular filling in diastole with resultant decrease in cardiac output.
Acutely the pericardium does not distend, thus small volumes of blood may produce cardiac tamponade. If the effusion accumulates slowly (eg. in setting of uremia, heart failure, malignant effusion) the quantity of fluid producing cardiac tamponade may reach 2000mL.
The major determinant of degree of hypotension is the pericardial pressure.

75
Q

most common cause of obstructive shock in trauma patients

A. Tension pneumothorax
B. Open pneumothorax
C. Hemopericardium
D. Massive hemothorax

A

Ans A -

Causes of obstructive shock -

  • pericardial tamponade
  • pulmonary embolism
  • tension pneumothorax
  • IVC obstruction - DVT, Gravid uterus, Neoplasm
  • Increased intrathoracic pressure - Excessive PEEP, neoplasm
76
Q

Site for placement of ICD -

A. Fourth ICS Anterior axillary line
B. Fifth ICS anterior axillary line
C. 4th ICS, mid axillary line
D. 5th ICS, Mid axillary line

A

Ans A -

Most recommend placement in the 4th ICS nipple level at the anterior axillary line - Schwartz.

77
Q

Beck’s triad consists of all of the following except -

A. Distended Neck veins
B. muffled heart sounds
C. Hypotension
D. Dyspnea

A

Ans D-

Beck's triad is seen in pericardial tamponade. 
consists of - 
 - Low BP
 - Muffled heart sounds
 - distended neck veins

Other features of pericardial tamponade are -

  • dyspnea
  • orthopnea
  • cough
  • peripheral edema
  • chest pain
  • tachycardia
78
Q

Pulsus paradoxus is a feature of which of the following

A. Cardiogenic shock
B. Neurogenic shock
C. Obstructive shock
D. Endocrine shock

A

Ans C -

Pulsus paradoxus is decreased systemic arterial pressure with inspiration. It can be present in cardiac tamponade.

79
Q

Investigation of choice for the diagnosis of pericardial tamponade -

A. ECG
B. ECHO
C. CT
D. Doppler USG

A

Ans B - Echocardiography

Good results depend on -

  • experience
  • body habitus
  • absence of wounds that preclude visualisation

Standard 2D ECHO as well as TEE can be used.

Characteristics are -

  • Large volume of fluid
  • Right atrial collapse
  • Poor distensibility of right ventricle.
80
Q

Which of the following is the most direct method to determine the presence of blood within peri-cardium -

A. Needle Pericardiocentesis
B. USG guided Pericardiocentesis
C. Diagnostic Pericardial window
D. ECHO

A

Ans C -

Diagnostic pericardial window it the most direct method to determine the presence of blood in the pericadium. The procedure is best performed in the operating room, under GA.
It can be performed through subxiphoid or transdiaphragmatic approach. Once the tamponade is relieved, hemodynamics improve dramatically and formal pericardial exploration can ensue. Exposure of the heart can be achieved via -
- Left anterior thoracotomy
- Extending incision to median sternotomy
- Bilateral anterior thoracotomy or clamshell.

81
Q

All of the following are cardinal features of neurogenic shock except -

A. Increased vascular capacitance
B. Decreased Cardiac output
C. Increased venous return
D. Decreased mixed venous saturation

A

Ans C -

Loss of vasoconstrictor impulses results in -

  • increased vascular capacitance
  • decreased venous return
  • decreased cardiac output.
82
Q

Warm extremities with hypotension can be seen in -

A. neurogenic shock
B. Obstructive shock
C. Cardiogenic shock
D. Hemolytic shock

A

Ans A -

Warm exteremities with hypotension are typically seen in septic shock, however they can also be seen in neurogenic shock.

83
Q

Which of the following is false regarding neurogenic shock -

A. Patients with complete motor injuries are over five times more likely to require vasopressors than incomplete lesions

B. Hypotension with bradycardia and warm extremities is commonly seen.

C. severeity of spinal cord injury correlates with teh magnitude of cardiovascular dysfunction

D. In penetrating injuries to the spina cord, neurogenic shock is the most common etiology of hypotension

A

Ans D -

In penetrating spinal cord injuries, most of the patients with hypotension had blood loss as the etiology rather than neurogenic causes.
Only 7% had classic findings of neurogenic shock.

84
Q

All of the following are true regarding neurogenic shock

A. Most patients respond to resuscitation of intravascular volume alone

B. Dopamine is the agent of choice in patients refractory to volume resuscitation

C. Phenyephrine is used in patients refractory to dopamine

D. Treatment with vasoconstrictors usually needed for 7-10 days

A

Ans D -

Secure airway.
Fluid resuscitation and restoration of intravascular volume.

Most patients with neurogenic shock will respond to restoration of intravascular volume alone, with satisfactory improvement in perfusion.

Administration of vasoconstrictors should only be considered once hypovolemia has been ruled out as the cause of hypotension.

Dopamine may be used first. A pure alpha agonist such as phenylephrine used primarily in patients unresponsive to dopamine.

Specific treatment for hypotension is often brief duration as the need to administer vasoconstrictors usually for 24-48h.

Some cases life threatening arrhythmias and hypotension may last upto 14 days.

85
Q

An actively bleeding patients should be resuscitated in -

A. Emergency room
B. Operating room
C. Trauma bay
D. ICU

A

Ans B

Attempts to stabilise an actively bleeding patient anywhere but in the operating room are inappropriate.

Any intervention that delays the patient’s arrival into the operating room for control of hemorrhage increases mortality.

86
Q

All of the following are systemic end-points of resuscitation -

A. Lactate
B. Base-deficit
C. Mixed venous oxygen saturation
D. Pulmonary artery wedge pressure
E. Membrane potential
A

Ans E -

Global -

  • Vital signs
  • Cardiac output
  • Pulmonary artery wedge pressure
  • Lactate, base deficit
  • Oxygen delivery and consumption (Mixed venous oxygen saturation)

Tissue specific -

  • Gastric tonometry
  • Tissue pH, Oxygen, carbon dioxide
  • Near infra-red spectroscopy

Cellular -

  • membrane potential
  • Adenosine triphosphate.
87
Q

All of the following are true regarding occult hypoperfusion except -

A. Even after normalisation of blood pressure, heart rate and urine output, nearly 80-85% of trauma patients have inadequate tissue perfusion

B. failure of reverse the lactate acidosis within 12 hours is an independent predictor of mortality

C. Failure to correct lactic acidosis and ISS are independent predictors of infection

D. none of the above

A

Ans D -

100% survival was noted among the patients with normalisation of lactate within 24 hours, 78% survival when lactate was normalised between 24-48 hours, and only 14% survival if normalisation of lactate took more than 48 hours.

The admission lactate, the highest lactate levels, and time interval to normalise the serum lactate are important prognostic indicators for survival.

Base deficit and volume of blood tranfusion required in first 24 hours - may be better predictors of mortality than plasma lactate alone.

88
Q

Maximum uptake of lactate is done in -

A. Kidneys
B. Lungs
C. GIT
D. Skeletal muscle

A

Ans A -

The liver accounts for approximately 50% of lactate uptake, and kidneys account for 30%.

89
Q

Severe base deficit is defined as -

A. -15 mmol/L or less.
B. -6 to -14 mmol/L
C. -1 to -5 mmol/L

A

Ans A -

Patients with base deficit worse than -15mmol/L have a mortality of 70%.

Base deficit worse than 6 mmol/L is associated with increased mortality (Bailey)

Mild Base deficit 3-5 mmol/L
Moderate base deficit 6-14 mmol/L
Severe base deficit 15 mmol/L or less.

90
Q

Severe base deficit is defined as -

A. -15 mmol/L or less.
B. -6 to -14 mmol/L
C. -1 to -5 mmol/L

A

Ans A -

Patients with base deficit worse than -15mmol/L have a mortality of 70%.

Base deficit worse than 6 mmol/L is associated with increased mortality (Bailey)

Mild Base deficit 3-5 mmol/L
Moderate base deficit 6-14 mmol/L
Severe base deficit 15 mmol/L or less.

91
Q

Increased base deficit is associated with all except-

A. Increased length of ICU stay

B. Increased tranfusion requirements

C. Increased frequency of organ failure

D. None of the above

A

Ans D-

Indeed when elevated base deficit persists or lactic acidosis persists in trauma patients, ongoing bleeding is often the etiology.

Trauma pts admitted with base deficit greater than 15 mmol/L required twice the volume of fluid infusion and six times more blood tranfusion in the first 24 hours compared to patients with mild acidosis.

Transfusion requirements increase
ICU stay increased
Hospital Stay increased
Mortality increased. 
Frequency of organ failure increased
ARDS increased.
92
Q

Factors that may compromise the utility of Base deficit in estimating Oxygen Debt include all except -

A. Bicarbonate
B. Hypothermia
C. Hypocapnia
D. Hypoglycemia

A

Ans D -

Factors that may compromise the utility of base deficit in estimating Oxygen debt are -

  • Administration of bicarbonate
  • Hypothermia
  • Hypocapnia (hyperventilation)
  • Heparin
  • Ethanol
  • Ketoacidosis.
93
Q

All of the following are true regarding gastric tonometry except -

A. Used as a tissue specific endpoint of resuscitation to assess GI tract perfusion.

B. Concentration of carbon dioxide accumulating in GI mucosa is measured.

C. Henderson-Hesselbach equation is used to calculate Gastric intramucosal pH

D. pHi increase is a poor prognostic indicator

A

Ans D -

With the assumption that the gastric bicarbonate is equal to serum levels, gastric intramucosal pH (pHi) is calculated by applying the Henderson-Hasselbalch equation.

pHi should be greater than 7.3.
pHi will be lower in decreased oxygen delivery to the tissues.
pHi is a good prognostic indicator.
Patients with normal pHi have better outcomes than those patients with pHi less than 7.3.

Use of pHi as a singular endpoint in the resuscitation of critically ill patients remains controversial.

94
Q

Which of the following is not true regarding Near IR spectroscopy

A. Uses IR spectrum of 650-1100 nm

B. Based on the redox state of cytochroma a-a1

C. Flow independent mitochondrial oxidative dysfunction suggestive of need for further resuscitation can be detected.

D. Can simultaneously measure tissue oxyhemoglobin levels

A

Ans B -

Near IR spectroscopy can measure tissue oxygenation and redox state of cytochrome a-a3 on a continuous non-invasive basis.

NIR spectrum of 650-1100nm is used.

Reduction of cytochrome a-a3 correlated with tissue lactate elevation.

NIR spectroscopy can be used to compare tissue oxyhemoglobin levels to cytochrome a-a3 with mitochondrial O2 consumption, thus demonstrating flow independent mitochondrial oxidative dysfunction and the need for further resuscitation.

Trauma patients with decoupled oxyhemoglobin and cytochrome a-a3 have redox dysfunction and have been shown to have a higher incidence of organ failure.

95
Q

Left ventricular power output threshold used as endpoint of resuscitation is -

A. >200 mmHg/L/min/sqm
B. >250 mmHg/L/min/Sq.m
C. >300 mmHg/L/min/Sq.m
D. >320 mmHg/L/min/sq.m

A

ans D -

Right ventricular End Diastolic Volume index and Left ventricular power output have described as end points of resuscitation by Chang et al.

50% of trauma patients had persistent splanchnic ischemia that was reversed by increasing the RVEDVI
It is found to more accurately predict preload for cardiac index than does PCWP.

Left ventricular Power output as an endpoint is associated with improved clearance of base deficit and a lower rate of organ dysfunction following injury.