Sep 26, 2014
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Hi everyone, I am a dental student in Australia and I am studying for my exams.

I am stuck on a physiology question from a past paper and I am wondering if anyone can help me.

The question is:

An anxious 22 year old patient enters your consulting room for a dental examination and treatment. Her face is pale, there are beads of sweat on her forehead and upper lip and she has cold clammy hands. You attempt to calm her when she is seated in the dental chair, but she continues to show signs of anxiety and is not hyperventilating. Subsequently her breathing slows and becomes shallow; her lips turn blue.

a) What is the explanation for the pallor, the sweating and the cold clammy hands? Your explanation should contain appropriate detail of the physiological mechanisms involved.

b) What is the explanation for the respiratory changes subsequent to hyperventilation, and why are her lips blue? Your explanation should contain appropriate detail of the physiological mechanisms involved.

c) How would you manage her condition before proceeding with her dental examination.

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For a), I know the symptoms are due to the effects of adrenaline. And c), I would assume the standard treatment for acute asthma.

I am assuming that the condition is anxiety-induced asthma attack, resulting in hyperventilation and hypoxic hypoxia.

However, I don't really understand why her breathing would slow and become shallow after hyperventilation. Is it because she has fainted and thus her breathing reflexes kicks in or something? Please help!
 

sgv

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Sep 5, 2013
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Here's my take and my enforcement of Cunninghams's law: Anxiety -> increased [epi] -> peripheral vasoconstriction and sympathetic activation of sweat glands. High dose epi has preference for alpha receptors. Reflex arc to shift equilibrium back down to basal levels is to increase beta activity which includes beta 1 and beta 2 receptors responsible to bronchodilation, peripheral vasodilation and increased cardiac activity. more likely, the body wouldn't act on the sympathetic and instead act on parasymp via vagus nerve, acetylcholine and muscarinic receptors

if you're at rest (not anxious), parasymp is dominant and you get normal breath and normal levels of co2. when you're anxious, your sympathetic kicks in via epi and you start hyperventilating (short and shallow) breathing. When you're hyperventilating, your lungs expel co2 excessively and your blood co2 levels drop with greater relative [o2] resulting in peripheral vasoconstriction even in the blood supply to brain so patient could faint. this kicks in the parasympathetic reflex to reverse the effects of sympath

i guess i would just watch the patient, keep her seated in case she faints and keep an o2 tank handy just in case

why would you treat this patient with beta agonists as if she had an asthma attack? a beta agonist would cause bronchiodilation but wouldn't affect the somatic muscles responsible for hyperventilation

psssbbbttt... idk
 
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flegg

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So was she originally hyperventilating or not?
 
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