Shock Flashcards

(53 cards)

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
clinical signs and symptoms of the later stage of shock?
pale skin and mucous membranes drop in body temp cold extremities slow resp rate dull and depressed appearance unconsciousness weak or absent pulse
26
compensatory responses in shock for the CV system?
increased heart rate (tachycardia) vasoconstriction increased myocardial contraction - redistribution of blood flow
27
compensatory responses in shock for the resp system?
increased resp rate (tachypnea) hyperventilation bronchodilation
28
compensatory responses in shock for the endocrine system?
activation of the sympathetic nervous system - release of epinephrine + norepinephrine renin-angiotensin-aldosterone system (RAAS) activation cortisol release antidiuretic hormone (ADH) secretion
29
what are the 4 cv responses in shock?
baroreceptor-mediated reflex peripheral vasoconstriction auto-transfusion of interstitial fluid long-term volume restoration
30
what does baroreceptor-mediated reflex result in?
increased heart rate (tachycardia) enhanced myocardial contractility
31
what is the baroreceptor-mediated reflex?
decreased arterial blood pressure --> decreased stimulation of baroreceptors in carotid sinuses + aortic arch triggers decreased vagal tone and increased sympathetic outflow
32
what is peripheral vasoconstriction?
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
what is auto-transfusion of interstitial fluid?
arterial hypotension, arteriolar constriction and reduced venous pressure and lower capillary hydrostatic pressure
34
what does auto-transfusion of interstitial fluid promote?
promotes reabsorption of interstitial fluid into capillaries
35
what does auto-transfusion of interstitial fluid help with?
helps to temporarily restore circulating volume dilates plasma proteins and decreases colloid osmotic pressure
36
what does long term volume restoration require?
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
goal of cv response to shock?
maintain perfusion of vital organs (brain and heart) while restoring intravascular volume and pressure
38
what are the 3 respiratory response in shock?
chemoreceptor activation respiratory compensation cardiovascular impact
39
what does chemoreceptor activation lead to?
stimulation of peripheral chemoreceptors carotid bodies, aortic bodies and cardiac chemoreceptors sensitive to decrease in pO2, increase in pCO2 and decrease in pH
40
MABP?
mean arterial blood pressure
41
what is chemoreceptor activation?
mean arterial blood pressure does not directly activate baroreceptor reflex for resp control instead low BP --> decreased tissue perfusion --> hypoxia & lactacidosis
42
what does resp compensation help with?
helps improve oxygen uptake and reduce CO2 (corrects acidosis)
43
what is resp compensation?
chemoreceptor activation --> resp stimulation increased resp rate (tachypnea) resp alkalosis may result transiently from hyperventilation
44
what is the cardiovascular impact for resp response in shock?
enhanced resp activity supports venous return via thoracic pump mechanism sympathetic vasoconstriction
45
what is sympathetic vasoconstriction?
it amplifies vasoconstriction initiated by baroreceptors and maintains blood pressure and organ perfusion
46
what is the integrated goal of the resp response in shock?
maintain oxygenation, support circulation and mitigate acidosis during shock
47
what are the 4 endocrine compensatory response in shock?
sympatho-adrenal axis activation vasopressin (ADH) secretion renin-angiotensin-aldosterone system (RAAS) erythropoietin (EPO) release
48
effects of sympatho-adrenal axis activation?
increased heart rate + myocardial contractility arteriolar vasoconstriction --> maintains blood pressure mobilisation of glucose + fatty acids for energy
49
what is sympatho-adrenal axis activation?
decreased blood pressure + tissue perfusion --> triggers sympathetic nervous system (SNS) Catecholamine release from adrenal medulla
50
catecholamine release from adrenal medulla includes?
adrenaline (epinephrine) - exclusively from adrenal medulla noradrenaline (norepinephrine) - from adrenal medulla + sympathetic nerve endings
51
what are the functions vasopressin?
potent vasoconstrictor enhances renal water reabsorption --> conserves circulating volume mediated via the hypothalamic -pituitary-adrenal (HPA) axis
52
describe vasopressin (ADH) secretion:
secreted by the posterior pituitary in response to a decrease in blood volume/pressure and increased plasma osmolarity
53