Shock Flashcards

1
Q

Define shock

A
  • Inadequate tissue perfusion
  • Switch from aerobic to anaerobic metabolism
  • Oxygen delivery is not equal to oxygen consumption
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2
Q

What is the equation for oxygen consumption(VO2)?

A
VO2= Q x 13.4 x Hb x (Sao2-Svo2)
Q= flow
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3
Q

What is the equation for oxygen delivery (DO2)

A

DO2= Q x 13.4 x Hb x Sao2

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4
Q

List the different types of shock

A

-Hypovolemic (bleeding profound dehydration from vomiting, diarrhoea,sweating)
-Cardiogenic shock ( MI, end-stage cardiomyopathy, arrhythmias)
-Obstructive shock (PE,tension pneumothorax,cardiac tamponade,atrial myxoma)
-Distributive shock (severe sepsis,anaphylaxis, neurogenic)
All types can co-exist)

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5
Q

State the signs a patient with shock may present with

A
  • Anxiety, confusion,aggression, restlessness, lethargy,coma
  • rapid shallow breathing
  • intense thirst
  • nausea
  • rapid( weak) pulse
  • BP generally low
  • pulse pressure always low
  • pale, grey or cyanotic, with clammy skin
  • reduced urine output
  • acidosis
  • decreased coagulation time and increased neutrophils (after 2-5hours)
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6
Q

What is the relationship between oxygen consumption and metabolic rate of oxygen in the case of shock?

A

VO2< MRO2= SHOCK

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7
Q

What issues may a patient involved in a car crash, hit on the right be involved in?

A
  • Liver laceration
  • Problem with your renal pelvis
  • Sheering of mesentary
  • Renal laceration
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8
Q

Describe the immediate compensatory mechanisms for shock.

A

These mechanisms help to maintain BP& CO despite the fall in blood volume

  1. ) Reverse stress relaxation:
    - veins shrink around reduced blood volume
    - Helps maintain venous pressure & therefore venous return (starts after about 10mins, takes an hour or so to develop fully)
  2. ) Reflex responses:
    - Increase in HR& force
    - peripheral vasoconstriction, particularly of skin (pallor,cold), gut, kidney & muscle( weakness)
    - Increased sweating (cold clammy skin)
  3. ) CNS responses(BP<50mmHg)
    - powerful peripheral vasoconstriction
    - Gut & renal perfusion severely reduced,dangerous if sustained
  4. ) Activation of RAAS
    - allows for electrolyte & water retention; vasoconstriction; thirst; increased ADH
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9
Q

Outline the baroreceptor reflex

A
  • Decreased BP is detected by baroreceptors & chemoreceptors
  • signals are sent to the brain stem
  • This decreases parasympathetic drive and increases sympathetic drive
  • This results in venoconstiction ( so increased CVP); vasoconstriction of splanchnic, skin, renal and skeletal muscle leading to increased TPR
  • This also results in an increased HR, force & CO
  • Blood pressure is therefore restored
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10
Q

Outline the acute response involving cardio-pulmonary stretch receptors during more severe blood loss

A
  • Decreased blood vol results in detected due to decreased stretch in the atria and by the cardio-pulmonary receptors
  • This info is sent to the hypothalamus brain stem
  • ADH is increased leading to vasoconstriction, increased thirst and water reabsorption, therefore restoring blood vol
  • Adrenaline( adrenals) is increased leading to vasoconstriction
  • The vasoconstriction results in increased CVP& TPR and therefore increased BP& CO
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11
Q

What are cardio-pulmonary stretch receptors?

A

Mechanoreceptors in the heart and large pulmonary vessels which respond to changes in blood volume. They activate reflexes which act to reverse the change in volume and support BP and CO

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12
Q

Outline the renal mechanisms used to restore blood volume

A
  • Decreased BP is detected by baroreceptors in the carotid sinus
  • Decreased blood vol results in decreased atria stretch and therefore decreased ANP which leads to increased Na and water retention allowing for restoration
  • The hypothalamus brain stem picks up info from the decreased atria stretch and baroreceptors
  • This results in thirst; increased ADH release and increased sympathetic renal nerve activity
  • All these responses caused by the info received by the hypothalamus brain stem result in reduced diuresis; increased renin –> increased Ang2—> increased aldosterone
  • the end result also causes increased sodium and water reabsorption
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13
Q

Outline what happens in progressive& refractory shock

A
  • Sustained circulatory failure causes a viscious cycle and can lead to multi-organ failure
  • The gut and renal circulations and specifically deprived in shock, so there’s a risk of acute renal failure & intestinal mucosal damage
  • Transfusions less effective at volume repletion due to increased vascular permeability and loss of transfused fluids to tissues
  • ischemia
  • decreased BP
  • decreased vascular tone & increased vascular permeability leading to fluid loss to tissues and therefore loss of protein to interstitium and loss of oncotic pressure gradient
  • decreased cardiac function and CO
  • hypoxia, increased acidosis & toxins,
  • Disseminated intravascular coagulation
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14
Q

Outline what may occur in multi-organ failure

A
  • Renal failure
  • Damage to intestinal mucosa
  • Sepsis
  • Cardiac failure
  • ARDS
  • Hepatic failure
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15
Q

When might an injury result in vagal inhibition of HR being unopposed

A

-If the injury is above T4
(This will result in bradycardia)
-This only occurs in neurogenic shock and with injury to C or Upper T-spine

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