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SURGERY (2nd Year) > SHOCK > Flashcards

SHOCK Flashcards

1
Q

Most common type of shock in surgical patients

A

[HaNSCOT]

Hypovolemic
Neurogenic
SEPTIC
Cardiogenic
Obstructive
Traumatic

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2
Q

Cause of hypovolemic shock from loss of interstitial fluid

A

BOWEL OBSTRUCTION

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3
Q

Shock caused by decreased resistance within capacitance vessels

A

VASOGENIC SHOCK

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4
Q

Shock from vasodilation due to acute loss of sympathetic tone

A

Neurogenic shock

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5
Q

Shock resulting from failure of the heart as a pump

A

Cardiogenic shock

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6
Q

Cardiogenic shock from mechanical impediment to circulation leads to depressed cardiac output rather than primary cardiac failure

A

Obstructive shock

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7
Q

Shock from inflammation triggered by soft tissue and bone injury

A

Traumatic shock

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8
Q

What type of shock happens during pulmonary embolism

A

Obstructive shock

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9
Q

Core principles in the management of critically ill or injured patient

A

a. definitive control of airway
b. control of active hemorrhage
c. volume resuscitation
d. recognition and adequate correction of hypoperfusion
e. excessive fluid resuscitation may exacerbate bleeding

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10
Q

What is the main goal of the neuroendocrine response to hemorrhage?

A

maintain perfusion to the heart and brain

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11
Q

What is the initial stimulus for the neuroendocrine response during hemorrhagic shock?

A

loss of circulating blood volume

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12
Q

Afferent pain signals transmit via the ______ resulting in activation of the hypothalamic-pituitary-adrenal axis as well as activation of ANS to induce direct sympathetic stimulation of the adrenal medulla to release _______

A

spinothalamic tract, catecholamines

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13
Q

Baroreceptors are found in _____, ______ and _____

A

atria, aortic bodies, carotid bodies

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14
Q

T/F Normally the baroreceptors inhibit the ANS (sympathetic tone). When activated, they disinhibit ANS, causing vasoconstriction

A

T. baroreceptor activation -> diminished baroreceptor output -> disinhibition of ANS -> increased peripheral vasoconstriction

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15
Q

T/F arotic and carotid bodies do not have chemoreceptors

A

F. They have chemoreceptors that detect O2 concentrations

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16
Q

Give 3 cardiovascular responses to diminished venous return and decreased CO due to hemorrhage

A

increased cardiac heart rate (1) and contractility (2), venous and arterial vasoconstriction (3)

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17
Q

Heart rate and contractility are increased by which adrenergic receptors?

A

beta-1

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18
Q

arteriolar vasoconstriction is brought about by activation of which adrenergic receptors?

A

alpha-1

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19
Q

What is the effect of sympathetic output on the adrenal medulla?

A

release of catecholamines

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20
Q

What is the effect of cortisol on gluconeogenesis and insulin

A

stimulatory to gluconeogenesis, inhibitory to insulin (insulin resistance)

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21
Q

What hormones are released by the ff. organs during shock?
Hypothalamus -
Kidney -
Pituitary -

A

H: ACTH
K: Renin
P: ADH

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22
Q

adverse effect of ADH on the intestine

A

intestinal ischemia

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23
Q

The primary determinant of preload

A

venous return

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24
Q

The law states that the force of ventricular contraction is a function of its preload

A

Frank-Starling Law

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25
Q

The force that resists myocardial work during contraction

A

AFTERLOAD

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26
Q

In neurogenic shock and sepsis, the microvessels

a. vasodilate
b. vasoconstrict

A

A. VASODILATE

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27
Q

In hemorrhagic shock and sepsis, the microvessels

a. vasodilate
b. vasoconstrict

A

B. VASOCONSTRICT

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28
Q

T/F
In hemorrhagic shock, correction of hemodynamic parameters and restoration of O2 delivery does not lead to restoration of tissue O2.

A

TRUE

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29
Q

Most common type of shock in surgical or trauma patient

A

hemorrhagic/hypovolemic

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30
Q

Result of acute blood loss EXCEPT
a. reflexive decreased baroreceptor stimulation
b. sympathetic stimulation
c. increased output from atrial stretch receptors
d. release of epinephrine and norepinephrine

A

c. increased output from atrial stretch receptors

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31
Q

T/F

Shock in trauma patient should be presumed to be due to hemorrhage until proven otherwise

A

T

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32
Q

Patient A with hemorrhagic shock, stable vital signs, no CNS symptoms has a percentage blood loss of _____ and estimated volume of blood loss of _____

A

<15%, 750mL

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33
Q

Patient B with tachycardia (>120 bpm) and hypotension has approximated % blood loss of _____ and estimated volume of blood loss of _____.

A

30-40%, 1,500-2000mL

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34
Q

Patient C with tachycardia (>100bpm) and orthostatic hypotension has an approximated % blood loss of _____ and an estimated volume of blood loss of _____.

A

15-30%, 750-1,500mL

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35
Q

What is the CNS symptom of C? (tachycardia and orthostatic hypotension)

A

Anxiety

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36
Q

What is the CNS symptom of patient B? (tachycardia and hypotension )

A

Confusion

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37
Q

What is the CNS symptom of patient A ? (stable vitals)

A

none

38
Q

Patient D Obtunded with HR >140bpm, and severe hypotension has an approximated % blood loss of _____ with an estimated volume of _____?

A

> 2,000

39
Q

In the non-trauma patient, ______ must always be considered as a site for blood loss

A

GI tract

40
Q

The pleural cavity can hold how many L of fluid?

A

2-3L

41
Q

Retroperitoneal hemorrhage typically occurs in association with _______

A

pelvic fractures

42
Q

In the resuscitation bay, what confirms retroperitoneal hemorrhage secondary to pelvic fractures?

A

pelvic radiography

43
Q

In damage control resuscitation, initial resuscitation is limited to keep SBP around __ to __ mmHg

A

80 to 90

44
Q

Following hemorrhage, large arterioles vasoconstrict;

A

Microcirculation

45
Q

In Microcirculation
these 3 Reserve perfusion of the myocardium and CNS to
limit organ perfusion to organs such as skin, skeletal
muscle, kidneys, and the GI tract

A

Vasopressin
angiotensin II
endothelin-1
(vasoconstriction)

46
Q

Tissue perfusion (Adequate O2 support), need :

A
  1. Efficient pump (Heart)
  2. Good pipes (Blood vessels)
  3. Well-distributed flow
47
Q

PHYSIOLOGICAL RESPONSE
Predominant form of response:

A

Increased sympathetic activity
Increased catecholamine levels

48
Q

These effector responses are designed to

A

expand plasma volume
maintain peripheral perfusion
maintain tissue O2 delivery
restore homeostasis

49
Q

Vasodilation of the coronary arteries
slowing of the heart rate
vasoconstriction of the splanchnic and skeletal circulation.
- Its purpose is to maintain perfusion
of the vital organs first usually the heart and the brain.

A

Chemoreceptors

50
Q

Renin angiotensin system and antidiuretic hormone is stimulated in response to stress particularly in

A

hemorrhagic and iatrogenic shock

51
Q

ACTH&raquo_space; Cortisol – induce catabolic rate

A

o Stimulates gluconeogenesis and insulin resistance resulting in hyperglycemia as well as muscle cell protein breakdown and lipolysis to provide substrates for hepatic gluconeogenesis

o Retention of sodium and water by the nephrons of the kidney and even aldosterone also

52
Q

SEPTIC SHOCK
NEUROGENIC SHOCK

A

VASODILATION
-others vasoconstriction

53
Q

METABOLLIC EFFECTS
Impaired oxidative phosphorylation
– DYSOXIA or lack of
oxygen

A

2 moles of ATP from 1 mole of glucose

  • Complete oxidation of 1 mole of glucose – 38 molesof ATP
54
Q

have a profound impact on cellular metabolism.

A

Epinephrine and norepinephrine

55
Q

the deficit in tissue oxygenation overtime that occurs during shock

A

CELLULAR HYPOPERFUSION
− O2 DEBT

56
Q

Release of intracellular products from damaged and injured cells can have paracrine and endocrine-like effects on distant tissues to activate the inflammatory and immune responses, is known as

A

DANGER SIGNALING

57
Q

Endogenous molecules are capable of signaling the presence of danger to surrounding cells and tissues. These molecules that are released from cells are known
-recognized by cell surface receptors to effect intracellular signaling those primes and amplifies the immune response.

A

damage associated molecular patterns (DAMPs)

58
Q

Recognized effectors

A

PRRs
TLRs
LPS (PAMPs)
↓
Amplification of immune response (Cytokines)

59
Q

Insults: Bacteria or endotoxin, hemorrhage, ischemia

produce peripheral vasodilation

A

TNF-a

60
Q
  • Febrile response to injury; anorexia
  • More common
  • Augments the secretion of ACTH, glucocorticoids,
    and β- endorphin
A

IL-1

61
Q

ANTI-INFLAMMATORY

A

Interleukin – 4
Interleukin – 10
Interleukin – 13
Prostaglandin E2
TGFβ

62
Q

Activation of the complement cascade → organ dysfunction

A

Activated C3a, C4a, and C5a

  • It acts synergistically with endotoxin – TNF-a and IL- 1
  • ARDS and MODS
63
Q

Neuroendocrine and Organ-Specific Responses

Regulated at multiple levels of responses particularly the
sympathetic system

A

a. Stretch receptors and baroreceptors in the heart and vasculature (Carotid sinus and aortic arch)
b. Chemoreceptors,
c. Cerebral ischemia responses
d. Release of endogenous vasoconstrictors particularly
the hormonal
e. Shifting of fluid into the intravascular space
f. Renal reabsorption and conservation of salt and
water

64
Q

The imbalance between cellular supply and demand leads to

A

neuroendocrine and inflammatory responses

65
Q

direct effect to shock

A

HEMORRHAGIC
NEUROGENIC
CARDIOGENIC

66
Q

release 1st endogenous molecules
cellular activation
tissue perfusion
ischemia
schock

A

TRAUMA SHOCK
SEPTIC SHOCK
- No direct effect

67
Q

• Persistent hypoperfusion: Hemodynamic derangements
and cardiovascular collapse
• Extensive enough parenchymal and microvascular injury:
DEATH

A

IRREVERSIBLE
PHASE OF SHOCK

68
Q

In hemorrhagic shock, the body can compensate for the initial loss of blood volume primarily through the neuroendocrine response to maintain hemodynamics. This represents the In hemorrhagic shock, the body can compensate for the initial loss of blood volume primarily through the neuroendocrine response to maintain hemodynamics. This represents the

A

COMPENSATED PHASE OF SHOCK.

69
Q

With continued hypoperfusion, which may be unrecognized, cellular death and injury are ongoing, and the___ ensues.

A

DECOMPENSATION PHASE OF SHOCK

70
Q

Most common cause of shock

A

Hypovolemia

71
Q

Most common cause of hypovolemic shock

A

HEMORRHAGE

72
Q

Physical findings of shock by class of hemorrhage

A

• Class I: Minimal change in vital signs
• Class II: Tachycardia, a decreased pulse pressure, and
delayed capillary refill mildly anxious, oliguria
• Class III: Hypotension, tachycardia, tachypnea, and mental confusion progressing to lethargy
• Class IV: Obtundation, profound hypotension, and anuria

73
Q

Hypotension, tachycardia, tachypnea, and mental confusion progressing to lethargy

A

CLASS 3

74
Q

Obtundation, profound hypotension, and anuria

A

CLASS 4

75
Q

Minimal change in vital signs

A

CLASS 1

76
Q

Tachycardia, a decreased pulse pressure, and
delayed capillary refill mildly anxious, oliguria

A

CLASS 2

77
Q

NON-HEMORRHAGIC hypovolemic shock
− GI losses or Urinary tract
Obstruction; Kidney dses

A

Extravascular fluid sequestration or “Third space” fluid loss

• Peritonitis can cause a lot of fluids; (Septic shock)
• Tx: Adequate fluid resuscitation, source control plus supportive measures

78
Q

More than 30-40% of burn to the body surface area requires the patient to have a massive resuscitation protocol. But later on, when infected, it becomes toxic. That’s why it is considered a high index suspension.

A

BURNS +/- wound infections

79
Q

INCREASE MYOCARDIAL CONTRACTILITY
DECREASE MOVEMENT OF PLASMA INTO THE INSTERSTITIUM
(change formation of albumin molecules)

A

MODEST HYPERCHLOREMIC ACIDEMIA

80
Q

An indirect marker of tissue hypoperfusion, cellular O2 debt and the severity of hemorrhagic shock

A

Serum lactate and base deficit

81
Q

− Minimize crystalloid solution – NSS can cause metabolic acidosis later on for massive infusion
− Doctors prefer whole blood nowadays

− In a patient with ongoing hemorrhage, the risk of death
increases 1% for every 3 minutes in the ER

A

DAMAGE CONTROL

82
Q

Components of Damage control or hemostatic resuscitation:

A

• Permissive hypotension until definitive surgical control
• Minimize crystalloid use
• Initial use of 5% hypertonic saline
• Early use of blood products (PRBCs, FFP, platelets, cryoprecipitate)
• Consider drugs to treat coagulopathy (rFVIIa, Prothrombin concentrate, TXA)

83
Q

in septic schock

Vasodilatory effects:

A

isoform of nitric oxide synthase
(iNO)

84
Q

IMMEDIATELY LIFE-THREATENING CAUSES OF SHOCK

A

• Tension pneumothorax
• Massive hemothorax
• Cardiac tamponade

85
Q
  • there is decreased breath sounds, tracheal shift to the left, and hyper resonant sound
    − There will be a mediastinal shift, decreased venous return,
    end-diastolic volume, stroke volume, and cardiac output
    resulting in hypotension later on.

which has tympanitic (hypertympany) percussion

A

TENSION PNEUMOTHORAX

86
Q

we have blood accumulating in the thorax. This blood can also cause problems: decreased cardiac output leading to hypotension. There is also decreased breath sounds and tracheal shift.

percussion would be dull since there is fluid.

A

MASSIVE HEMOTHORAX

87
Q

BECK’S TRIAD (CARDIAC TAMPONADE)

• Distended neck veins
• Muffled heart sounds
• Hypotension (Most consistent)

A
88
Q

NEUROGENIC SHOCK
“Classic signs and symptoms”

A

-Decrease blood pressure associated with bradycardia
-warm extremeties
-motor and sensory, deficits
-radiographic evidence

89
Q

RESUSCITATION
Initial approach to treatment

A

• A – Airway
• B – Breathing, adequate ventilation
• C – Circulation
- Volume status – IV fluids
- Pump status – Inotropic
- Flow status – Vasopressors
• D – Determine and treat the cause of the shock - Operating room resuscitation

90
Q

CRITERIA ADEQUAE PERFUSION

A

− Complete when O2 debt is repaid, tissue acidosis is corrected, and aerobic metabolism is restored.

SURGERY (2nd Year) (2 decks)

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