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CR2 > Shcok > Flashcards

Shcok Flashcards

1
Q

CO = [] X []?

BP = [] x []?

A

CO = HR X SV

BP = CO x Systemic vascular resistance

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2
Q

What are the overall physiological consequences of shock ? [3]

A
  • Increased afterload
  • Reduced systemic vascular resistance (Failure to maintain peripheral vasoconstriction)
  • Decreased CO
    i) reduced preload
    ii) reduced contactility
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3
Q

Vasoconstriction is predominately activated by which molecule on which receptors? [2]

Name two alternative compounds that can cause vasoconstriction [2]

A

Vasoconstriction is predominately activated by which molecule on which receptors? [2]
Noradrenaline on alpha 2 recptors

Name two alternative compounds that can cause vasoconstriction [2]
Angiotensin
Vasopressin

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4
Q

Vasodilation is mediated by the activation of which two compounds? [1]

Explain their basic mechanism [1]

A

Nitric oxide and prostacyclin [1]

MoA: Through cGMP and cAMP respectively, secondary messengers cause decrease in calcium and smooth muscle relaxation

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5
Q

How does obstructive shock ?

A
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6
Q

What are the 4 classifications of shock? [4]

A

Obstructive shock
Distributive shock
Cardiogenic shock
Hypovolaemic shock

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7
Q

Name and describe the 4 stages of shock

A
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8
Q

Describe how shock is a positive feedback cycle

A
  1. Increased circ. shock with worsening perfusion
  2. Causes inadequate blood flow to tissues: deterioation of end organ tissue function
  3. Causes heart and circ system failure to start
  4. Further reduction in CO
  5. Repeat 1 f
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9
Q

Explain three examples that could cause obstructive shock xx [2]

A

PE
Tension pneuomothorax air gets trapped in pleural space: compresses against vena cava and heart: stops blood flow into right side of heart: reduced preload: reduced CO
Cardiac tamponade :accumulation of pericardial fluid: causes increas in intrapericardial pressure which reduceds cardiac filling

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10
Q

Describe the effects to cells of hypoxia and hypoperfusion

A
  • Cells switch from aerobic to anaerobic metabolism
  • Lactic acid production
  • Cell function ceases & swells
  • Membrane becomes more permeable
  • Electrolytes & fluids seep in and out of cell
  • Na+/K+ pump impaired
  • Cells swell causing mitochondria damage
  • Cell death
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11
Q

What are the signs of shock?

A
  • Pulse is weak and rapid
  • Pulse pressure reduced - mean arterial pressure (MAP) may be maintained - NOTE; ARTERIAL BP is NOT A GOOD INDICATOR OF SHOCK since it will be maintained until a very large amount of blood loss
  • Reduced urine output
  • Reduced pH
  • Confusion, weakness, collapse and coma
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12
Q

Describe how disitributive shock works xx

A

Results from excessive vasodilation and the impaired distribution of blood flow

Characterized by a significant drop in peripheral vascular resistance and, as a result, hypotension

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13
Q

Explain 3 examples of distributive shock x

A

Sepsis: dysregulated host response to infection where bacteria in blood release chemicals causing uncontrolled hypotension

Anaphylactic shock: allergic response to antigen: IgE mediated mass degranulation releasing histamines: vasodilation and capillary leaking

Neurogenic shock: Sudden loss of vasomotor tone throughout the body. Occurs due to loss of sympathetic input due to spinal injury above T6 / Spinal anaesthesia with high block / brain damage in brainstem

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14
Q

Explain the mechanism of septic shock xx

A

Pathogens have unique cell wall molecules called pathogen associated molecular patterns (PAMPS) that bind to pattern recognition receptors (TLRs) on immune cells

Causes pro-inflam cytokines: activates the adaptive immune, which causes direct and indirect host injury

Causes release of NO: vasodilation and drop in BP

Cytokine release causes the endothelial lining of blood vessels to become more permeable. This causes fluid to leak out of the blood and in to the extracellular space leading to oedem, a reduction in intravascular volume, and therefore amount of oxygen reaching tissues

Activation of the coagulation system leads to deposition of fibrin throughout the circulation further compromising organ and tissue perfusion. It also leads to consumption of platelets and clotting factorsas they are being used up to form the clots within the circulatory system.

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15
Q

What is cardiogenic shock?

Name 4 causes of cardiogenic shock xx [4]

A

Failure of the heart to pump blood
Occurs as a result of ventricular dysfunction (esp. LV)

Causes:
* Acute myocardial infarction leading to ventricular dysfunction
* Arrhythmias
* Valvular rupture
* Decompensated heart failure

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16
Q

What is hypovolaemic shock?

A

Reduced circulating volume leads to reduced venous return and therefore preload

17
Q

Explain 4 causes of hypovolaemic shock xx

A
  • Haemorrhage
  • GI losses: severe diarrhoea and vomiting
  • Surgery: exposure of internal structures to heat
  • Burns: fluid shift into extravasuclar space due to inflam response
18
Q

Explain the compensatory mechanisms for haemorrhagic shock [3]

A

Baroreceptors detect drop in arterial pressure

Activates sympathetic stimulation:
- Constriction of small arterioles increasing total peripheral resistance thereby maintaining BP
- Veins and venous reservoirs constrict, maintaining venous return
- Increased heart rate and contractility to maintain cardiac output

CNS ischaemia results in increased noradrenaline and adrenaline secretion from adrenal medulla

19
Q

How does RAAS system work to compensate shock? [3]

A
  • Water retention and salt reabsorption
  • Vasomotor centre in the medulla signals to the hypothalamus to release vasopressin (ADH)
  • Urine flow and sodium excretion decrease
20
Q

Describe the 4 classes of haemorrhagic stroke

A
21
Q

Name 3 long term compensatory mechanisms of shock [3]

A
  • There is (by an unknown mechanism) stimulation of albumin and other plasma protein synthesis in the liver.
  • Increased fluid absorption from GI tract
  • Fibroblasts surrounding the kidney tubules are sensitive to hypoxia and release increased amounts of erythropoietin: Red cell production
22
Q

Anaphylactiv shock is which type of hypersensitivity? [1]

A

Type 1

23
Q

Explain the MoA of anaphylactic shock

A

pathological allergic response:

  • an antigen (usually inhaled or swallowed) reacts with IgE on mast cells & basophils; This is called Type 1 hypersensitivity.
  • The cells degranulate and release inflammatory mediators including histamine.
  • Histamine reacts on capillaries and arterioles to cause endothelial cells to lose their tight junctions and separate. This allows water to leak out into tissues.
  • Causing swelling and vasodilation leading to uncontrolled hypotension and anaphylactic shock
24
Q

MI would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

A

MI would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

25
Q

MI would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

A

MI would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

26
Q

PE would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

A

PE would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

27
Q

Neurogenic shock would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

A

Neurogenic shock would cause which of the following type of shock?

Hypovolaemic shock
Obstructive shock
Distributive shock
Cardiogenic shock

28
Q

Which immunoglobin is associated with anaphylactic shock?

IgD
IgM
IgE
IgG
IgA

A

Which immunoglobin is associated with anaphylactic shock?

IgD
IgM
IgE
IgG
IgA

29
Q

Explain which of HR or BP falls first in major haemorrhage stroke :)

A

Cardiac output can accommodate c. 10% blood loss before change in CO
Between 10-20% fall in blood loss, arterial pressure compensates by vasoconstriction

SO you see a raise in HR to compensate fall in SV BEFORE you see a fall in BP

30
Q

Whats the A-E of shock management?

A

Airway: probs ok unless they have analphylaxis
Breathing: usually ok, may have compensatory increase in RR to compensate hypoxia in tissues. OR might have tension pneumothorax. Later stages: hypoxic
Circulation: give IV access: increase fluids to increase BP
Disability: Low: cant respond bc of lack of 02
Exposure: look at skin – rash / burns / pale

CR2 (59 decks)

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