Neuro-intensive care Flashcards

1
Q

What is CPP dependent on?

A
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2
Q

What is CMRO2 dependent on?

A
  • Temperature (7% drop per degree C)
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3
Q

What rises IC blood flow?

A
  • Lowering of patients head. (but also higher ICP due to less venous outflow)
  • Higher Co2
    *
    *
    *
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4
Q

Why is hyperglycemia a bad thing?

A

It exacerbates ischemic deficits

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5
Q

What can be done to protect against ischemic injuries?

A
  • Lower CMRO2
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6
Q

What is neurogenic stress cardiomyopathy?

A

Impaired cardiac function not related to underlying coronary artery disease or myocardial abnormalities. May be reversible

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7
Q

What is the putative mechanism of Neurogenic stress cardiomyopathy?

A

Cathecholamine surge. Possibly in myocardial sympathethic nerves. As a result from hypothalamic stimulation or injury from SAH.

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8
Q

When is the peak incidence of neurogenic stress cardiomyopathy after aSAH?

A

2 days-2weeks after SAH.

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9
Q

What treatment does greenberg suggest for neurogenic stress cardiomyopathy?

A

Dobutamine
Milrinone.

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10
Q

What is the normally used name for Neurogenic stress cardiomyopathy and what nickname is it often given?

A

Takotsubo cardiomyopathy.
The nickname is “broken heart syndrome”.

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11
Q

When can neurogenic pulmonary edema occur?

A
  • SAH
  • generalized seizures
  • head injury.
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12
Q

What are the two possibly synergisic explanations to neurogenic pulmonary edema?

A
  1. sudden ICP raise or hypothalamic injury with sympathetic discharge cause redistribution of blood to the pulmonary circulation. An eleveation of pulmonary capillary wedge pressure occur and increased permeability of the capillaries too.
  2. Cathecholamines disrupt the capillary enothelium which increases alveolar permeability.
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13
Q

What is the treatment of pulmonary edema?

A
  • Low levels of PEEP
  • NOrmalization of ICP
    A PA catheter is useful
    *SOmetimes Dobutamine and Furosemide might help.
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14
Q

What is the advantage of dobutamine to previously attempted alpha and beta blockers?

A

Dobutamine does not reduce cerebral perfusion.

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15
Q

what is critical illness polyneuropathy?

A
  • Affects primarily distal muscles
  • precense of sepsis, multiorgan failure, respiratory failure or septic inflammatory response syndrome - SIRS.
  • Difficulty weaning from ventilator or extremity weakness.
  • EMG show low amplitudes of compound muscle action potentials and SNAP.
  • widespread muscle denervation potentials
  • normal or only mild increase in serum CPK levels.

—–Recovery occurs in weeks to months—-faster than Guillian Barre, –treatment is supportive. Complete recovery 50%

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16
Q
A