L3+4 Shock etc Flashcards

(70 cards)

1
Q

What is shock?

A

Inadequate oxygen delivery and/or consumption at a cellular level.

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2
Q

What is metabolism?

A

The set of chemical processes that maintain life; includes anabolic (building) and catabolic (breaking down) processes.

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3
Q

What is perfusion?

A

The passage of fluid through the circulatory system or lymphatic system to an organ or tissue.

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4
Q

What is ventilation?

A

The mechanics of air moving in and out of the lungs.

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5
Q

What is oxygenation?

A

The process of oxygen diffusing passively from alveoli to pulmonary capillaries.

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6
Q

What is dead space?

A

The volume of air that is inhaled but does not take part in gas exchange.

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7
Q

What is preload?

A

The stretch of ventricles before contraction; blood volume in ventricles prior to contraction.

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8
Q

What is afterload?

A

The pressure heart must work against to eject blood.

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9
Q

What is third spacing?

A

Shift of fluid from vascular to interstitial space.

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10
Q

What is acidosis?

A

Condition of excess acid in body fluids.

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11
Q

What is the Trauma Triad of Death?

A

Metabolic acidosis, hypothermia, and coagulopathy that reinforce each other in a lethal cycle.

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12
Q

What is oliguria?

A

Decreased urine output.

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13
Q

What is the formula for cardiac output?

A

CO = SV × HR (Stroke Volume × Heart Rate)

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14
Q

What is the formula for blood pressure?

A

BP = CO × PVR (Cardiac Output × Peripheral Vascular Resistance)

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15
Q

How do you calculate approximate blood volume?

A

70ml/kg body weight.

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16
Q

What is hypovolaemic shock?

A

Shock due to decreased blood volume (from haemorrhage, dehydration, burns, etc.).

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17
Q

What is cardiogenic shock?

A

Shock due to heart pump failure, causing decreased stroke volume and cardiac output.

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18
Q

What is obstructive shock?

A

Shock due to mechanical obstruction of blood flow through central circulation.

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19
Q

What is distributive shock?

A

Shock due to loss of blood vessel tone (vasodilation) or inappropriate redistribution of blood volume.

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20
Q

Name three types of distributive shock.

A

Septic shock, anaphylactic shock, and neurogenic shock.

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21
Q

What is aerobic metabolism?

A

Breaking down substrates into ATP with oxygen; occurs in mitochondria.

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22
Q

What is anaerobic metabolism?

A

Breaking down carbohydrates into ATP without oxygen; occurs in cytoplasm.

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23
Q

How much ATP is produced per glucose molecule in aerobic metabolism?

A

~36 ATP.

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24
Q

How much ATP is produced per glucose molecule in anaerobic metabolism?

A

2 ATP.

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25
What is the end product of anaerobic metabolism?
Lactic acid.
26
What are the consequences of lactic acidosis in shock?
Reduced cardiac contractility, vascular hyporesponsiveness to vasopressors, impaired enzyme function, reduced oxygen-carrying capacity.
27
How does the body detect low blood pressure?
Via baroreceptors (in carotid arteries and aortic arch) and chemoreceptors (monitoring O₂, CO₂, and H⁺).
28
What is the 'fight or flight' response?
The sympathetic nervous system's response to stress, including increased heart rate, vasoconstriction, and redirection of blood flow.
29
What are adrenergic receptors?
Cell membrane receptors that respond to catecholamines (epinephrine and norepinephrine).
30
What effect do alpha receptors have?
Cause vasoconstriction of small arterioles and arteries, increasing peripheral vascular resistance.
31
What is the inotropic effect?
Increased force of heart contraction.
32
What is the chronotropic effect?
Increased heart rate.
33
What is the dromotropic effect?
Accelerated electrical conduction through the heart.
34
What hormones are released during sympathetic activation?
Epinephrine (adrenaline) and norepinephrine (noradrenaline).
35
What is the effect of beta-1 receptors?
Increase heart rate and force of contraction.
36
What is the effect of beta-2 receptors?
Cause bronchodilation and vasodilation in skeletal muscle.
37
What are the metabolic effects of alpha receptor activation?
Glycogenolysis and gluconeogenesis, increasing blood glucose.
38
What does RAAS stand for?
Renin-Angiotensin-Aldosterone System.
39
What triggers renin release?
Decreased renal blood flow, decreased filtrate in nephron, and decreased blood pressure.
40
Where is renin produced?
In the juxtaglomerular cells of the kidneys.
41
What does renin convert?
Converts angiotensinogen to angiotensin I.
42
Where is angiotensinogen produced?
In the liver.
43
What is ACE?
Angiotensin-Converting Enzyme, which converts angiotensin I to angiotensin II.
44
Where is ACE primarily found?
In the vascular endothelium of lungs.
45
What are the four major effects of angiotensin II?
1) Direct vasoconstriction of arterioles, 2) Stimulation of aldosterone release, 3) Enhancement of ADH release and action, 4) Stimulation of thirst center.
46
What is the function of aldosterone?
Increases sodium and water reabsorption in kidneys, increasing blood volume.
47
Where is aldosterone produced?
In the adrenal cortex.
48
What does ADH stand for?
Antidiuretic Hormone (also called vasopressin).
49
What are the two primary stimuli for ADH release?
Increased plasma osmolality and decreased blood pressure.
50
Where is ADH synthesized?
In the supraoptic and paraventricular nuclei of the hypothalamus.
51
Where is ADH released from?
The posterior pituitary gland.
52
What receptors does ADH bind to in the kidneys?
V₂ receptors.
53
What is the primary action of ADH in the kidneys?
Increases water permeability of collecting ducts, enhancing water reabsorption.
54
What happens to water following ADH action?
More water is reabsorbed from urine back into circulation, increasing blood volume.
55
What vascular effect does ADH have at higher concentrations?
Causes vasoconstriction by binding to V₁ receptors on vascular smooth muscle.
56
What are the three stages of shock?
Early/Compensatory Phase, Progressive Phase, and Irreversible Phase.
57
What are typical signs of compensatory shock?
Anxiety, tachycardia, cool/pale skin, decreased urine output, increased thirst, rapid respirations.
58
What occurs in the progressive stage of shock?
Lethargy, metabolic acidosis, enzyme leakage, vascular hyporesponsiveness, increased capillary permeability, activation of clotting cascade.
59
What defines irreversible shock?
Circulatory and respiratory failure as compensatory mechanisms fail, leading to death.
60
What percentage of blood loss typically causes hypovolaemic shock?
15-20% acute loss.
61
What happens with 10% blood loss?
No effect on cardiac output or arterial pressure.
62
What happens with 10-25% blood loss?
Cardiac output falls but arterial pressure is maintained via increased PVR.
63
What happens with 30-40% blood loss?
Cardiac output and arterial pressure decrease to zero.
64
How much blood loss occurs with a fractured femur?
1000-2000ml.
65
How much blood loss occurs with a fractured pelvis?
1000ml+.
66
What is the immediate response to hypotension (seconds)?
Sympathetic nervous system activation.
67
What is the short-term response to hypotension (minutes)?
ADH vascular effects.
68
What is the intermediate response to hypotension (minutes to hours)?
RAAS vasoconstriction and ADH renal effects.
69
What is the long-term response to hypotension (hours to days)?
Aldosterone, ADH, and thirst mechanisms.
70
How do RAAS and ADH systems interact?
Synergistically - angiotensin II stimulates ADH release, and both hormones increase water retention and can increase peripheral vascular resistance.