Neuro ICP & Pharmacology Flashcards

1
Q

What is ICP a measure of?

A

Intracranial pressure refers to the supratentorial CSF pressure.
-Measured in the lateral ventricles or in subarachnoid space over cerebral cortex.
-ICP is measuring the compliance within the cranium

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2
Q

What is contained in the Cranial Vault?

A

-Brain-80-90%, Blood-12%, CSF-8%, Intracellular H2O
-Small increases in volume are tolerated well.

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3
Q

What is the Monro-Kelly Doctrine?

A

-The brain is enclosed and non-compressible.
-Any increases in total intracranial volume = increased ICP.
-Because the skull is rigid, any expansion of one of these compartments must be compensated by a reduction in size of the others if ICP is to remain constant.

Nagelhout:
The brain is enclosed within the cranium, and because the brain is not compressible any increase in total intracranial volume produces an accompanying increase in ICP.

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4
Q

What are Compensatory Mechanisms for increased ICP?

A

Initially, displacement of CSF from cranial to spinal compartment.
-Increase in CSF absorption
-Decrease in CSF production
-Decrease in total blood volume (mainly venous drainage)

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5
Q

What is normal ICP in adults?

A

5-15 mmHg

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6
Q

What ICP is Intracranial HTN?

A

> 15 mmHg
-Treatment is needed if >20 mmHg

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7
Q

What does increased ICP due to CPP & CBF?

A

Marked increases in ICP can decrease CPP & CBF and cause regional or general ischemia. (!!)

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8
Q

What is Cushing’s Triad?

A

A sign of severely increased ICP indicating impending brain herniation.
-Widening Pulse pressure (↑systolic ↓diastolic)
-↓HR
-irregular RR

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9
Q

What are the S/Sx of increased ICP?

A

-Headache
-n/v
-Papilledema
-focal neurologic deficits
-altered ventilatory function
-decreased consciousness (LOC)
-seizures
-coma

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10
Q

What are causes of increased ICP?

A

-Trauma
-Hemorrhage
-Infection (encephalitis)
-Edema (3 different kinds)
-Increased CBF or decreased venous outflow (thrombosis)
-Systemic hypertension
-Inadequate CSF absorption
-Post traumatic seizure
-Mass effect from tumors, abscesses, bleeds

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11
Q

What are the kinds of edema associated with increased ICP?

A

1) Cytotoxic
2) Vasogenic
3) Interstitial

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12
Q

What is Cytotoxic Edema?

A

Increased intracellular water.
-Cells lose their ability to regulate what comes in and out.
-Traumatic brain injury and stroke.

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13
Q

What is Vasogenic Edema?

A

A loss of BBB integrity; proteins flow out and causes an osmotic gradient with more fluid following.
-Tumors
-Steroids are good here to get rid of edema around the tumor

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14
Q

What is Interstitial Edema?

A

hydrocephalus, extracellular water

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15
Q

What is the gold standard for ICP Monitoring?

A

Intraventricular catheter
-Requires skill to place
-Low cost, accurate, reliable

Nagelhout:
-Very precise
-Highly invasive
-Can drain CSF to lower ICP
-Infection risk

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16
Q

What are other methods of ICP monitoring?

A

-Intraparenchymal: small hole, can’t recalibrate.
-Subarachnoid, subdural, and epidural aren’t used much.

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17
Q

What increases the risk of infection with a Ventricular Drain?

A

-Drain in place > 5 days
-Other infection in body
-Previous Craniotomy
-Hemorrhage
-CSF leaks

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18
Q

What is important to know regarding Intraparenchymal Probes?

A

-Popular method of measuring ICP
-Low risk of infection
-Inserted through burr hole and tunneled subcutaneously
-ICP may be localized and not equal ventricular CSF pressure
-Only measures local pressure. Not equal to ventricular pressure. Trend it.

19
Q

What is a Transcranial Doppler?

A

-Non-invasive blood flow velocity measurement
-Most often measures Middle Cerebral Artery (MCA) flow velocity, also used for PCA, ACA and the basilar artery
-Flow velocity that is greater than expected = stenosis, emboli, or vasospasm
-Cannot determine actual CBF

20
Q

What are strategies to maintain brain protection?

A

-Perfusion: optimization of MAP (80-90 mmHg) & CPP (60-70 mmHg)
-Avoid hypo/hyperglycemia
-PaCO2 levels should be normal or slightly decreased to 30-35
-Hyperventilation can work for short-term brain relaxation and decreases CBF (6 hours)
-Temperature: Normal or hypothermic
-Prevent seizures (increases CMRO2)

Goal is to maintain physiologic homeostasis!

21
Q

How can we improve ICP via the blood compartment?

A

Flow related:
↓Venous congestion
↑HOB
Head neutral
↓Airway pressure or peep
↓Inhalation
↓CO2
↓CMRO2 (↑sedation, avoid histamine releasing NMB, Succ, vasodilators, prevent seizures)

22
Q

How can we improve ICP via the CSF?

A

-Administer meds that decrease production
-Drain (no more than 20mL/hour)

23
Q

How can we improve ICP via the Interstitial Compartment?

A

-Diuretics (Mannitol can decrease the size of brain during surgery)
-Steroids

24
Q

How can we improve ICP via the cellular compartment?

A

-Remove tumors via surgery

25
Q

What is the treatment for increased ICP?

A

-HOB elevated 30 degrees
-Make sure neck is straight (promotes drainage)
-Hyperventilate to PaCO2 of 30-25 mmHg
-No PEEP, remove airway obstructions
-Reduce brain water with diuretics, Hypertonic Saline (Lasix, Mannitol)
-Metabolic suppression (barbs, propofol = uncoupling)
-Corticosteroids: Decadron (NO steroids if TBI, check BS)
-Ventricular Drain (no more than 15-20 mL/hr)
-Emergency craniectomy to prevent herniation
-Control seizures
-Hypothermia

26
Q

PaCO2 is ___ mmHg higher than EtCO2.

A

The PaCO2 is approximately 2 to 5 mm Hg higher than end tidal carbon dioxide (ETCO2) (!!!)

27
Q

Why should you avoid rapid administration of Mannitol?

A

May produce vasodilation, increases in CBF, a transient rise in ICP, and a transient increase in circulating blood volume.
-Push slowly over 20-30 minutes, especially in patients with underlying cardiac dysfunction (risk of pulmonary edema)

27
Q

What is Mannitol?

A

An Osmotic Diuretic.
-Decreases ICP within 15 minutes by increasing plasma osmotic pressure and drawing fluid into the circulation.
-It also causes vascular smooth muscle relaxation.
-0.25 - 1 gm/kg.
-Lasts about 2 hours
-1-2 L of urine/hour
-May cause hypovolemia, plasma hyperosmolarity, hypokalemia hypochloremic alkalosis

28
Q

What is the dose of 3% Normal Saline?

A

-Therapeutic dose: 1.4 ml – 2.5 ml/kg of 3% NaCl
-Check Serum Na before starting gtt or giving bolus

Nagelhout:
-Like mannitol, hypertonic saline produces an osmolar gradient causing shrinkage of brain tissue and reduction in ICP.

29
Q

Why do you want to avoid rapid increases in Serum Na Concentration when administering 3% NS?

A

A rise in serum sodium concentration >9 mEq/L in 24 hours can lead to an osmotic demyelination syndrome, also known as central pontine myelinolysis.
-Side effects: secondary bleeding due to platelet aggregation and delayed coagulation time, hypokalemia, hyperchloremic acidosis

30
Q

What are the effects of Volatile agents on ICP?

A

-Dose dependent increase in CBF
-Decrease in CMRO2 and decrease in Luxury Perfusion or Cerebral steal

Nagelhout:
-Inhalation agents decrease mean arterial pressure (MAP) and increase ICP, reducing cerebral perfusion pressure (CPP). Isoflurane produces the greatest increases in CBF and ICP, followed by sevoflurane and desflurane.
-All inhalational agents are known to increase CBF, CBV, and ICP.

31
Q

What is the effect of Isoflurane on CBF?

A

Isoflurane at 0.6 to 1.1 MAC no increase in CBF. However, at 1.6 MAC, CBF doubles.

32
Q

What are the effects of Nitrous Oxide on CBF?

A

N20 increases CBF and CMRO2

Nagelhout:
-N2O can produce increases in CBF, CMRO2, and ICP.
-N2O is more soluble than nitrogen and expands closed-gas spaces. Its use should be avoided in patients with an intracranial or intravascular air compartment such as pneumocephalus.

33
Q

What are the effects of Propofol on CBF?

A

-↓ CBF, CMRO2
-CPP may drop if BP drops

Nagelhout:
-The cerebral effects are a dose-dependent reduction in CBF and CMRO2.
-PP may decrease because of reductions in blood pressure after bolus induction doses; however, the reduction in CBF appears to be independent of systemic hemodynamic changes. They are most likely due to the metabolic depressant effect and cerebral vasoconstriction. Reductions in systemic blood pressure produce corresponding reductions in CPP.

34
Q

What are the effects of Etomidate on CBF?

A

Causes Cerebral Vasoconstriction
-Dec CMRO2
-But, causes myoclonus, adrenal suppression, Nausea and vomiting.
-Not recommended for ICP issues

Nagelhout:
-Etomidate, like other CNS depressants, reduces CMRO2 and CBF. Benefits associated with etomidate use include cerebral vasoconstriction, which results in the reduction of ICP without reducing CPP.
-Major disadvantages include a high incidence of myoclonia, thrombophlebitis, nausea, vomiting, and suppression of the adrenocortical response to stress. Many clinicians feel that etomidate should be avoided in brain-injured patients.

35
Q

What are the effects of Ketamine on CBF?

A

↑ CMRO2, CBF by 60-80%, Not used in neurosurgery.

Nagelhout:
-The primary advantage associated with ketamine is the stable hemodynamic course in the presence of hypovolemia that may occur in patients with traumatic head injury and multisystem trauma. Ketamine is known to produce untoward alterations in cerebral physiology, increasing CBF by 60% to 80% and potentially elevating ICP.

36
Q

What are the effects of Dexmedetomidine on CBF?

A

-Dose dependent sleep, anxiolysis, no respiratory depression
-Easy to do wake up tests
-Electrophysiological mapping stays intact and SSEP are maintained when added to desflurane and remifentanil.
-Does not change CMRO2
-Cerebral blood flow is decreased because of “uncoupling” (Cerebral vasoconstriction)
-Central sympatholytic action decreases catecholamines so neuroendocrine responses to surgery are attenuated
-Decreased shivering and emergence delirium

37
Q

What are the effects of opioids on CBF?

A

No effect on CBF (unless you drop MAP and decrease CPP or over sedate and they become hypercarbic)

Nagelhout:
-The synthetic opioids produce dose-related reductions in CBF (decrease to 25 mL/100 g/min) and CMRO 2 (40%–50%). Later investigations in patients after acute head injury or in those undergoing supratentorial craniotomy noted increases in ICP and decreases in CPP after administration of induction doses of fentanyl, sufentanil, and alfentanil. These opioid-induced changes in ICP have been suggested to occur secondarily to an autoregulatory response to decreases in MAP.

38
Q

What are the effects of Benzos on CBF?

A

CBF-minimal change unless you over-sedate and increase CO2

Nagelhout:
-Benzodiazepines produce a dose-dependent decrease in CMRO2 and reductions in CBF; however, their effects on ICP are minimal.

39
Q

What are the effects of Succinylcholine on CBF?

A

-Transient 10-15 mmhg increase in ICP that can last 5-8 min.
-Rise in CBF and fasciculations in the neck causing Jugular Vein stasis may be an issue.
-Defasiculating dose first!

Nagelhout:
-Succinylcholine-induced fasciculations can cause transient increases in ICP (transient rise of 10 to 15 mm Hg for 5 to 8 minutes after administration)
-The effects on ICP may be inhibited by pretreatment with a small dose of nondepolarizing relaxant.
-Furthermore, the administration of an anesthetic induction agent prior to succinylcholine may reduce the potential for ICP increases.
-As mentioned previously, succinylcholine is contraindicated in patients with neurologic or denervated muscle because of the potential for life-threatening hyperkalemia.
-Succinylcholine should be avoided in patients with cerebrovascular accident, upper and lower motor neuron lesions, coma, encephalitis, closed head injury, and after severe burns and prolonged bed rest.

40
Q

What should be used for intubation in neuro patients?

A

Roc + Sugammadex for reversal if needed.
-Avoid Histamine releasing MRs!

Nagelhout:
A nondepolarizing alternative, such as rocuronium (at 1.2 mg/kg intubating dose), also facilitates endotracheal intubation within 60 to 90 seconds and avoids the known complications of succinylcholine. Rocuronium is being used with more frequency for rapid sequence induction since the availability of sugammadex, which provides rapid reversal if necessary.

41
Q

What are Beta Blockers used for in neurosurgery?

A

Beta blockers have great use in control of inotropic & chronotropic effects by sympathetic stimulation (DL, intubation, extubation, pin placements, etc.)
-Esmolol – rapid acting, effects on ICP are negligible, forgiving quick on and off
-Labetalol – longer lasting

42
Q

Can you use Sodium Nitroprusside or Nitroglycerin in Neuro patients?

A

No. These increase CBV & ICP, can lead to herniation.

43
Q

Which drugs can help with the prevention of vasospasm?

A

Calcium Channel Blockers.
-Nimodipine (decreases mortality)
-Nicardipine