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Cardiorespiratory CC > Shock > Flashcards

Shock Flashcards

1
Q

Clinical Shock

A

Acute circulatory failure with inadequate or inappropriately distributed perfusion resulting in cellular hypoxia

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2
Q

Cellular hypoxia effect

A 
Cells switch from aerobic to anaerobic
Lactic acid production
Cell function ceases + swells
Membrane more permeable
Electrolytes + fluids seep in + out of cell
Na+/K+ pump impaired
Cells swell
Mitochondrial damage
Cell death
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3
Q

Normal CO

A

5l/min

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4
Q

Normal Systolic BP

A

120mmHg

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5
Q

Mean Arterial Pressure

A

100mmHg

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6
Q

Shock diagnosis

A

Likely if MAP<60mmHg

Clinical signs of hypo-perfusion of vital organs (tachycardia, tachypnoea, mental confusion, pallor)

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7
Q

BP equation

A

BP = Co x systemic vascular resistance

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8
Q

Low CO

A

Either HR low or Stroke Vol low

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9
Q

HR controlling factors

A

Feedback signals from baroreceptors in carotid sinus –> activate or inhibit medullary vasomotor centres –> activate or inhibit autonomic NS
Conscious perception of arousing stimuli activates or inhibits ANS

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10
Q

Stroke Volume controlling factors

A

Amount of blood in heart before start to contract- “preload”

Myocardial contractility

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11
Q

Stroke volume

A

Volume of blood pumped from left ventricle per beat

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12
Q

Preload on SV

A

Greater the preload –> greater the force of contraction –> greater the stroke volume

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13
Q

Starling’s Law

A

The force of contraction increases as the end diastolic volume increases

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14
Q

Decrease in Myocardial Contractility

A 
Cardiac disease
Hypoxia/hypercapnia
pH or electrolyte distribution
Drugs
Shock
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15
Q

Systemic vascular resistance

A

Maintained by balance between vasoconstrictors and vasodilators

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16
Q

Vasoconstrictors place of action

A

Mainly arterioles in end organs

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17
Q

Vasoconstrictor mechanism

A

1) Sympathetic NS- Release noradrenaline locally on alpha receptors on outside of arterioles
2) Angiotensin II in plasma acts on angiotensin AT1 receptor on endothelium lining arterioles –> contraction of underlying smooth muscle

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18
Q

Local vasoconstrictors

A

Released locally from endothelium

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19
Q

Endothelin

A

Local Vasoconstrictor

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20
Q

Prostacyclin

A

Vasodilator
Produced in endothelial cells from arachidonic acid
PGI2

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21
Q

Prostacyclin MOA

A

Reduces Ca entry into smooth muscle cells surrounding the endothelium
–> Reduces contractility of smooth muscle

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22
Q

Nitric Acid

A

Vasodilator
Gas
Produces in endothelial cells from arginine
Continually produced in healthy arterioles by action of moving blood on glycoproteins on the endothelial membrane

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23
Q

Nitric Acid MOA

A

Diffuses into underlying smooth muscle where it stimulates cyclic AMP formation –> decreases Ca entry and relaxes muscle

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24
Q

Adenosine

A

Released from endothelial cells + smooth muscle during activity

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25
Vasoconstrictors
Noradrenaline Angiotensin 2 Endothelin 5HT
26
Vasodilator
Prostacyclin Nitric Oxide Adenosine
27
Tissue Perfusion
Requires good CO and appropriate BP
28
Cardiac Output regulation
Preload | Heart Rate
29
BP regulation
CO | Systemic vascular resistance
30
Shock
Systemic vascular resistance not maintained OR | Preload decreases
31
Obstructive shock
Physical obstruction to vessels entering or leaving heart | e.g. pulmonary embolism
32
Distributive shock
Loss of vasoconstriction in one or more end organs | Produce excess blood flow in system + poor perfusion of organs
33
Hypovolaemic shock (Haemorrhagic shock)
Normally due to haemorrhage
34
Cardiogenic shock
Due to failure of heart to pump efficiently and supply blood to the body
35
Cardiopulmonary obstructive shock
Cardiogenic and obstructive shock grouped together
36
Septic shock
In US | Distributive shock due to sepsis
37
Obstructive shock example
Pulmonary embolism Pneumothorax Cardiac tamponade
38
Distributive shock example
Sepsis Anaphylaxis Neurogenic
39
Hypovolaemic shock example
Haemorrhage Burns Surgery or trauma Loss of fluid + electrolytes from gut
40
Cardiogenic shock examples
MI Heart failure Arrhythmias Ventricular septal rupture
41
Hypovolaemic shock signs explanation
Indicate that SNS attempting to maintain O2 supply to heart + brain despite decreased preload - -> if succeeding, compensating shock - -> if failing, decompensating shock
42
Hypovolaemic shock signs
``` Confusion/anxiety Cold Clammy skin Low BP High HR Slow capillary refill Greyish pallor Oliguria- low output of urine ```
43
Suspected GI bleeding
``` Hematemesis Melena Alcohol drinking history Excessive NSAID use Coagulopathies ```
44
Cardiogenic shock Signs
Most have AMI- chest pain, shortness of breath, diaphoresis, nausea, vomiting Pulmonary oedema Acute circulatory collapse Presyncopal or syncopal symptoms
45
Septic (distributive) Shock signs
Low BP Tachycardia Non-specific symptoms- fever, chill, rigor, fatigue, malaise Fever common in sepsis
46
Septic shock fatality
Up to 50% patients will die/have permanent organ damage despite treatment
47
Obstructive shock main cause
Tension pneumothorax
48
Obstructive shock signs
``` Tachycardia Anxiety Chest pain Affected breath sounds Tracheal deviation if pneumothorax ```
49
Pulmonary embolism presentation
Abrupt onset of pleuritic chest pain Shortness of breath Hypoxia
50
Hypovolaemic shock- haematological system
Activation of coagulation cascade Contraction of bleeding vessels- local thromboxane A2 release Activation of platelets- thromboxane A2 Immature clot formation
51
Hypovolaemic shock- CV system
Sympathetic NS activation Help redistribute blood to brain, heart and kidneys Increased HR Increased myocardial contractility Constriction of peripheral blood vessels in skin, muscle + GI tract
52
Hypovolaemic shock- Renal system
Increases renin secretion- Angiotensin II increase as a result
53
Angiotensin II effect
Vasoconstriction of arteriolar smooth muscle in skin, muscle + GI tract Stimulation of aldosterone secretion --> increases sodium reabsorption + water reabsorption
54
Hypovolaemic shock- neuroendocrine system
Releases ADH from posterior pituitary in response to decreased BP + decreased Na plasma conc.
55
ADH effect
Increased reabsorption of water + salt by distal tubule, collecting ducts + loop of Henle
56
Total body water
45 litres
57
Intracellular water
27 litres
58
Extracellular water
18 litres
59
Blood volume
4.5-5 litres
60
Life threatening blood loss
Acute loss >40% (>2 litres)
61
Venous Bleed compensatory response- haemorrhage | Immediate- seconds to mins
Drop in venous return reduces SV + CO --> decreased BP Baroreceptors increase sympathetic outflow --> increase in HR + contractility Sympathetic NS constricts large veins to move blood out from venous reservoir + restore preload
62
Arterial bleed compensatory response- haemorrhage | Immediate- seconds to mins
BP drops Baroreceptors detect --> increase sympathetic outflow Vasomotor centre in medulla signals to hypothalamus to release vasopressin (ADH) Reduced preload --> reduced ANP --> urine flow + Na excretion decreased
63
Haemorrhage Long term compensation
Increased renin release --> angiotensin II release Aldosterone release by Angiotensin II- long lasting effect in increased Na retention Thirst stimulated by Angiotensin II receptors in brain (subfornical organ above hypothalamus) --> increased water intake
64
Haemorrhage long term compensation pt 2
Albumin + other protein synthesis in liver | Fibroblasts sensitive to hypoxia- release EPO to stimulate RBC production --> haematocrit back to normal
65
Hypovolaemic shock CLASS 1
``` Loss <15% BV Blood donation/minor injury Fully compensated normally Normal/slightly fatigued Don't drive for a few hours ```
66
Hypovolaemic shock CLASS 2
``` Loss 15-30% BV Tachycardia Tachypnoea Decrease pulse pressure Cool clammy skin Delayed capillary refill Slight anxiety --> rest + food + water patients will recover ```
67
Hypovolaemic shock CLASS 3
``` Loss >30% BV Persistent BP drop Anxious/Confused Most require plasma vol. expanders/blood transfusion End-organ damage, especially kidneys ```
68
Hypovolaemic shock CLASS 4
``` >40% loss BV V confused/unconscious Tachycardia No urine Severely decreased systolic BP Life threatening Blood transfusion ```
69
Sepsis
Systemic response to presence of pathogens in blood or other organs Bacterial toxins and/or host response leads to microvascular damage in one or more organs
70
Sepsis Manifestations
``` equal or more than 2 of: Temp >38 or <36 HR > 90bpm RR > 20bpm WBC > 12x109/L ```
71
Septic shock
Sepsis without hypotension
72
Sepsis damage
Lipolysaccharide (LPS) in Gram -ve bacterial cell walls stimulate neutrophils + monocytes to release cytokines - -> damage endothelium + prevent normal vasoconstriction - -> decreased vascular resistance in organs
73
Management hypovolaemic shock
``` Restore BV with IV colloids (gelatins, dextrans, 4% or 20% albumin) or crystalloids (isotonic or hypertonic saline, ringer lactate) Vasopressor drugs (dopamine, noradrenaline etc.) to restore BP ```
74
Sepsis shock management
Appropriate antimicrobials
75
Therapeutic Goals shock
Central venous pressure 8-12mmHg MAP >65mmHg Urine output 0.5ml/kg/h Central venous oxygenation saturation >70%

Cardiorespiratory CC (34 decks)

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