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CVS physiology > cardiovascular responses to shock (CVS 12) > Flashcards

cardiovascular responses to shock (CVS 12) Flashcards

1
Q

different types of shock

A
  • hypovolaemic (haemorrhagic, non-haemorrhagic)
  • cardiogenic (eg. acute myocardial infarction)
  • obstructive (eg.cardiac temponade, tension pneumothorax, pulmonary embolism, severe aortic stenosis)
  • distributive (neurogenic eg.spinal cord injury, vasoactive eg.septic shock, anaphylactic shock)
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2
Q

what is shock

A

an abnormality of the cirulatory system resulting in inadequate tissue perfusion and oxygenation

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3
Q

what is the effect of inadequate tissue perfusion and oxygenation during shock

A

inadequate tissue perfusion -> inadequate tissue oxygenation -> anaerobic metabolism -> accumulation of waste products -> cellular failure

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4
Q

MAP

A
  • mean arterial pressure

- MAP = cardiac output (CO) x total peripheral resistance (TPR)

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5
Q

CO

A
  • cadiac output
  • the volume of blood pumped by each ventricle of the heart per minute
  • CO = stroke volume (SV) x heart rate (HR)
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6
Q

stroke volume (SV)

A

= volume of blood pumped by each ventricle of the heart per heart beat

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7
Q

adequate tissue perfusion

A
  • adequate tissue perfusion depends on adequate blood pressure and adequate cardiac output
  • > MAP= CO x TPR
  • > CO = HR x SV
  • > factors that affect stroke volume: preload (affected by venous return), myocardial contractility, afterload
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8
Q

hypovolaemic shock

A
  • > haemorrhagic
  • > non-haemorrhagic
  • loss of blood volume -> decreased bood volume -> decreased venous return -> decreased end diastolic volume -> decreased stroke volume -> decreased cardiac output and blood pressure -> inadequate tissue perfusion
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9
Q

effect of end diastolic volume (EDV) on stroke volume (SV) - frank starling curve

A
  • as end diastolic volume (ml) increases, as does stroke volume (ml)
  • stroke volume = tension
  • EDV = fibre length = preload
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10
Q

cardiogenic shock

A
  • > eg. acute myocardial infarction
  • decreased cardiac contractility -> decreased stroke volume -> decreased cardiac output and blood pressure -> inadequate tissue perfusion
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11
Q

obstructive shock

A
  • can be due to cardiac temponade, tension pneumothorax, pulmonary embolism, severe aortic stenosis
  • > in this case = tension pneumothorax
  • increased intrathoracic pressure -> decreased venous return -> decreased end diastolic volume ->decreased stroke volume ->decreased cardiac output and decreased blood pressure -> inadequate tissue perfusion
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12
Q

neurogenic shock (type of distributive shock)

A
  • type of distributive shock
  • can be due to injury to spinal cord
  • loss of sympathetic tone -> massive venous and arterial vasodilation -> decreased venous return and decreased TPR -> decreased stroke volume (as a result of decreased venous return as it decreases end diastolic volume) -> decreased cadiac output and decreased TPR -> decreased blood pressure -> inadequate tissue perfusion
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13
Q

vasoactive shock (type of distributive shock)

A
  • type of distributive shock
  • eg. septic shock
  • release of vasoactive mediators -> massive venous and arterial vasodilation, and also increased capillary permeability -> decreased venous return and decreased TPR -> decreased cardiac output and decreased blood pressure -> inadequate tissue perfusion
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14
Q

vasoactive

A

affecting the diameter of blood vessels (and hence blood pressure)

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15
Q

outlines of treatment of shock

A
  • ABCDE approach
  • high flow oxygen
  • volume replacement
  • inotropes for cardiogenic shock
  • immediate chest drain for tension pneumothorax
  • adrenaline for anaphylactic shock
  • vasopressors for septic shock
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16
Q

vasopressors

A

a drug or other agent which causes the constriction of blood vessels

17
Q

anaphylactic shock

A
  • an extreme, often life-threatening allergic reaction to an antigen to which the body has become hypersensitive
  • anaphylaxis = an acute allergic reaction to an antigen (e.g. a bee sting) to which the body has become hypersensitive.
18
Q

cardiovascular responses to hypovolaemic shock

A
  • compensatory mechanisms can maintain blood pressure until >30% of blood volume is lost
  • > autoregulation of cerebral blood flow (myogenic response)
  • > baroreceptors reflex (response to decreased blood pressure)
19
Q

hypovolemia

A

hypovolemia (also hypovolaemia, oligemia or shock) is a state of decreased blood volume; more specifically, decrease in volume of blood plasma

20
Q

causes of hypovolaemic shock

A

-haemorrhage (eg. trauma, surgery or GI haemorrhage) -> causes decreased blood volume -> which causes decreased cardiac output -> causing circulatory shock (decreased MABP causing inadequate tissue perfusion)
OR
-vomiting/diarrhea/excessive sweating -> causes decreased ECFV (including plasma) -> causing decreased blood volume -> causing decreased cardiac output -> which causes circulatory shock (decreased MABP causing inadequate tissue perfusion)
->loss of blood volume -> decreased bood volume -> decreased venous return -> decreased end diastolic volume -> decreased stroke volume -> decreased cardiac output and blood pressure -> inadequate tissue perfusion

21
Q

regulation of cerebral blood flow

A
  • autoregulation of cerebral blood flow (myogenic response)
  • By definition, the myogenic response is the contraction of a blood vessel that occurs when intravascular pressure is elevated and, conversely, the vasodilation that follows a reduction in pressure
  • therefore if there is blood loss, cerebral blood flow decreases and therefore the myogenic response causes vasoconstriction following a decrease in blood pressure
22
Q

baroreceptors reflex in response to decreased blood pressure

A
  • decreased ABP -> decreased baroreceptor discharge -> which is detected by the cardiovascular/ CV integrating centre (medulla) ->this does three things in response
    1. decreases vagal activity which -> increases HR
    2. decreases cardiac sympathetic activity which -> increases HR and SV
    3. increases sympathetic constrictor tone which causes -> venoconstriction which also increases SV, and causes vasoconstriction which increases TPR
  • > the increase in HR and SV cause an increase in cardiac output as CO= HR x SV
  • > and as TPR and CO increase, this increases MAP again as MAP = CO x TPR
  • as hemorrhagic shock leads to decreased MAP and CO and therefore inadequate tissue perfusion, this acts as a control mechanism

CVS physiology (11 decks)

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