Shock Flashcards

1
Q

what is tissue hypoperfusion?

A

oxygen supply does not meet metabolic demands

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2
Q

what is cellular dysfunction?

A

often leads to multiple organ failure if prolonged

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3
Q

what is cardiac output loss?

A

fundamental cause of shock

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4
Q

what is shock?

A

a life-threatening condition characterised by inadequate tissue perfusion, leading to cellular hypoxia and metabolic dysfunction

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5
Q

what does shock include?

A

tissue hypoperfusion
cellular dysfunction
cardiac output loss
multiple factors involved (especially in late-stage shock)
severity and rate determine progression

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6
Q

causes of impaired oxygen delivery:

A

decreased cardiac output
decreased haemoglobin saturation or conc
increased afterload (elevated diastolic pressure limiting ejection)

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7
Q

causes of decreased cardiac output?

A

decreased stroke volume, heart rate, preload or contractility

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8
Q

key determinants of oxygen delivery?

A
  • DO₂ = CO × CaO₂ (Cardiac Output × Oxygen Content)
  • CO = SV × HR (Stroke Volume × Heart Rate)
  • CaO₂ = (Hb × 1.39) × SaO₂ (Hemoglobin Concentration × Oxygen
    Saturation)
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9
Q

describe oxygen utilisation and energy production when in shock?

A

decreased oxygen –> anaerobic metabolism –> (2 ATP/glucose) lactic acidosis & ATP depletion

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10
Q

what does a reperfusion injury include?

A

oxygen reintroduction –> reactive oxygen species –> DNA and protein damage

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11
Q

what does cellular dysfunction and death include?

A

Na+ & Ca+ accumulation –> cellular swelling and ischemia
inflammation: capillary permeability increases, leukocyte activation, mitochondrial dysfunction

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12
Q

what is hypovolemic shock?

A

inadequate circulating volume

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13
Q

cause of hypovolemic shock?

A

fluid loss (trauma, internal bleeding, burns) –> decreased preload –> decreased cardiac output –> shock

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14
Q

what is cardiogenic shock?

A

heart pump failure

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15
Q

what is the cause of cardiogenic shock?

A

arrhythmia, myocardial infarction (MI), congestive heart failure (CHF)

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16
Q

what is distributive shock?

A

relative hypovolemia (vasodilation & TPR)

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17
Q

three types of distributive shock?

A

septic shock
anaphylactic shock
neurogenic shock

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18
Q

what is septic shock?

A

where bacterial toxins –> systemic vasodilation –> total peripheral resistance (TPR)

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19
Q

what is anaphylactic shock?

A

histamine release –> vasodilation –> decreased total peripheral resistance

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20
Q

what is neurogenic shock?

A

loss of autonomic nervous control –> vasodilation –> decreased TPR

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21
Q

what is obstructive shock?

A

blood flow obstruction

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22
Q

what is the cause of obstructive shock?

A

physical obstruction –> decreased cardiac output –> circulatory arrest

23
Q

examples of obstructive shock?

A

constrictive pericarditis, pneumthorax

24
Q

clinical signs and symptoms of the early stage of shock?

A

panting
rapid heart rate
bounding pulses
bright red mucous membranes (lips, gums, tongue)

25
Q

clinical signs and symptoms of the later stage of shock?

A

pale skin and mucous membranes
drop in body temp
cold extremities
slow resp rate
dull and depressed appearance
unconsciousness
weak or absent pulse

26
Q

compensatory responses in shock for the CV system?

A

increased heart rate (tachycardia)
vasoconstriction
increased myocardial contraction - redistribution of blood flow

27
Q

compensatory responses in shock for the resp system?

A

increased resp rate (tachypnea)
hyperventilation
bronchodilation

28
Q

compensatory responses in shock for the endocrine system?

A

activation of the sympathetic nervous system - release of epinephrine + norepinephrine
renin-angiotensin-aldosterone system (RAAS) activation
cortisol release
antidiuretic hormone (ADH) secretion

29
Q

what are the 4 cv responses in shock?

A

baroreceptor-mediated reflex
peripheral vasoconstriction
auto-transfusion of interstitial fluid
long-term volume restoration

30
Q

what does baroreceptor-mediated reflex result in?

A

increased heart rate (tachycardia)
enhanced myocardial contractility

31
Q

what is the baroreceptor-mediated reflex?

A

decreased arterial blood pressure –> decreased stimulation of baroreceptors in carotid sinuses + aortic arch
triggers decreased vagal tone and increased sympathetic outflow

32
Q

what is peripheral vasoconstriction?

A

generalised arteriolar and venoconstriction via sympathetic activation
most pronounced in cutaneous, skeletal muscle and splanchnic vascular beds
renal vasoconstriction in prolonged/severe hemorrhage –> decreased renal perfusion
cerebral + coronary circulations spared (minimal vasoconstriction)
preserves perfusion to the brain and heart at the expense of other organs

33
Q

what is auto-transfusion of interstitial fluid?

A

arterial hypotension, arteriolar constriction and reduced venous pressure and lower capillary hydrostatic pressure

34
Q

what does auto-transfusion of interstitial fluid promote?

A

promotes reabsorption of interstitial fluid into capillaries

35
Q

what does auto-transfusion of interstitial fluid help with?

A

helps to temporarily restore circulating volume
dilates plasma proteins and decreases colloid osmotic pressure

36
Q

what does long term volume restoration require?

A

water and electrolyte retention (via ADH & RAAS)
synthesis of albumin and plasma proteins (by liver)
stimulation of erythropoiesis (in bone marrow) to restore RBC mass

37
Q

goal of cv response to shock?

A

maintain perfusion of vital organs (brain and heart) while restoring intravascular volume and pressure

38
Q

what are the 3 respiratory response in shock?

A

chemoreceptor activation
respiratory compensation
cardiovascular impact

39
Q

what does chemoreceptor activation lead to?

A

stimulation of peripheral chemoreceptors
carotid bodies, aortic bodies and cardiac chemoreceptors
sensitive to decrease in pO2, increase in pCO2 and decrease in pH

40
Q

MABP?

A

mean arterial blood pressure

41
Q

what is chemoreceptor activation?

A

mean arterial blood pressure does not directly activate baroreceptor reflex for resp control
instead low BP –> decreased tissue perfusion –> hypoxia & lactacidosis

42
Q

what does resp compensation help with?

A

helps improve oxygen uptake and reduce CO2 (corrects acidosis)

43
Q

what is resp compensation?

A

chemoreceptor activation –> resp stimulation
increased resp rate (tachypnea)
resp alkalosis may result transiently from hyperventilation

44
Q

what is the cardiovascular impact for resp response in shock?

A

enhanced resp activity supports
venous return via thoracic pump mechanism
sympathetic vasoconstriction

45
Q

what is sympathetic vasoconstriction?

A

it amplifies vasoconstriction initiated by baroreceptors and maintains blood pressure and organ perfusion

46
Q

what is the integrated goal of the resp response in shock?

A

maintain oxygenation, support circulation and mitigate acidosis during shock

47
Q

what are the 4 endocrine compensatory response in shock?

A

sympatho-adrenal axis activation
vasopressin (ADH) secretion
renin-angiotensin-aldosterone system (RAAS)
erythropoietin (EPO) release

48
Q

effects of sympatho-adrenal axis activation?

A

increased heart rate + myocardial contractility
arteriolar vasoconstriction –> maintains blood pressure
mobilisation of glucose + fatty acids for energy

49
Q

what is sympatho-adrenal axis activation?

A

decreased blood pressure + tissue perfusion –> triggers sympathetic nervous system (SNS)
Catecholamine release from adrenal medulla

50
Q

catecholamine release from adrenal medulla includes?

A

adrenaline (epinephrine) - exclusively from adrenal medulla
noradrenaline (norepinephrine) - from adrenal medulla + sympathetic nerve endings

51
Q

what are the functions vasopressin?

A

potent vasoconstrictor
enhances renal water reabsorption –> conserves circulating volume
mediated via the hypothalamic -pituitary-adrenal (HPA) axis

52
Q

describe vasopressin (ADH) secretion:

A

secreted by the posterior pituitary in response to a decrease in blood volume/pressure and increased plasma osmolarity