Neuro Flashcards
Name 4 types of glial cells:
Astrocytes
Ependymal cells
Oligodendrocytes
Microglia
What is the function of Astrocytes?
- Most abundant type of glial cell.
- Regulation of metabolic environment.
- Repair neuron after neuronal injury
What is the function of ependymal cells?
- Form the choroid plexus, which produces CSF.
- Concentrated in the roof of the 3rd and 4th ventricles and spinal canal.
What is the function of the Oligodendrocytes?
- Form the myelin sheath in the CNS.
- “Schwann cells form the myelin sheath in the PNS.
What is the function of Microglia?
-Act as macrophages and phagocytize neuronal debris.
List the name and function of the 4 lobes of the cerebral cortex:
- Fontal: contains motor cortex
- Parietal: contains somatic sensory cortex
- Occipital: contains vision cortex
- Temporal: contains auditory cortex and speech centers
- Wernicke’s area= understanding speech
- Broca’s area= motor control of speech
Name the 12 cranial nerves:
Mnemonic: oh oh oh to touch and feel virgin girls vagaina ah heaven
- Olfactory
- Optic
- Oculomotor
- Trochlear
- Trigeminal
- Abducens
- Facial
- Vestibulocochlear
- Glossopharyngeal
- Vagus
- Spinal accessory
- Hypoglossal
Cranial nerves: motor, sensory, or both?
Mnemonic: Some say marry money but my brother says big boobs matter more.
- Olfactory (SENSORY)
- Optic (SENSORY)
- Oculomotor (MOTOR)
- Trochlear (MOTOR)
- Trigeminal (BOTH)
- Abducens (MOTOR)
- Facial (BOTH)
- Vestibulocochlear (SENSORY)
- Glossopharyngeal (BOTH)
- Vagus (BOTH)
- Spinal accessory (MOTOR)
- Hypoglossal (MOTOR)
What cranial nerves provide motor control of the eyes?
How does each nerve contribute to the eye’s movement? (see photo in Neuro: CNS brain)
CN3 Oculomotor: all directions except lateral and down medial
CN4 Trochlear: eyes move down medial (cross eyed)
CN 6 Abducens: eyes move laterally
How do you test the Olfactory nerve (CN1)?
Smell
How do you test the optic nerve (CN2)?
Vision
How do you test the oculomotor nerve (CN3)?
Eye movement
pupil construction
How do you test the trochlear nerve (CN4)?
Eye movement
How do you test the trigeminal nerve (CN5)?
3 branches:
V1= ophthalmic
V2= maxillary
V3= mandibular
facial sensation
anterior 2/3 tongue sensation
chewing movement
How do you test the abducens nerve (CN6)?
eye movement
How do you test the facial nerve (CN7)?
5 branches: Temporal Zygomatic Buccal Mandibular Cervical
- Facial movement except chewing
- eyelid closing
- Anterior 2/3 taste
How do you test the vestibulocochlear nerve (CN8)?
hearing and balance
How do you test the glossopharyngeal nerve (CN9)?
Posterior 1/3 of tongue sensation
How do you test the vagus (CN10)?
swallowing
How do you test the spinal accessory nerve (CN11)?
shoulder shrug
How do you test the hypoglossal nerve (CN 12)?
tongue movement
Which cranial nerve resides in the central nervous system?
What is the implication of this?
All CN are part of the Peripheral NS except for the OPTIC nerve (CN2).
Only CN surrounded by dura and CSF.
If you inject LA into the optic nerve during regional anesthesia of the eye, you will have a big problem.
What is tic douloureux?
What CN contributes to this problem?
aka trigeminal neuralgia (CN5) causes excruciating neuropathic pain in the face.
What is Bell’s palsy?
What cranial nerve contributes to this problem?
results from injury to the facial n. (CN 7).
Causes ipsilateral facial paralysis.
What is the function of the CSF, and where is it located?
- cushions the brain
- provides buoyancy
- delivers optimal conditions for neurologic function
Location:
- Ventricles (left and right lateral, 3rd, and 4th)
- Cisterns around the brain
- Subarachnoid space in brain and spinal cord
What regions of the brain are NOT protected by the BBB?
The BBB separates CSF from plasma.
Contains tight junctions that restrict pass of large molecules and ions.
BBB is NOT present at:
- chemoreceptor trigger zone
- posterior pituitary glad
- Choroid plexus
- parts of hypothalamus
What is the normal volume of CSF?
150mL
What is the normal specific gravity of CSF?
1.002-1.009
CSF production:
Ependymal cells of the choroid plexus produce CSF at a rate of 30ml/hr.
CSF circulation:
see photo in Neuro: CNS brain
“Love My 3 Silly 4 Lorn Magpies
Left/Right lateral ventricles–> Foramen of Monro–> 3rd ventricle–> Aqueduct of Sylvius–> 4th ventricle–> Foramen of Luschka (paired) AND foramen of Magendie–> subarachnoid space (brain/spinal cord) and central canal of spinal cord–>superior sagittal sinus
*all ventricles are sights of production
CSF reabsorption:
Venous circulation via the arachnoid villi in the superior sagittal sinus.
What is the formula for cerebral blood flow?
CBF= cerebral perfusion pressure/ cerebral vascular resistance
What are the normal values for global, cortical, and subcortical flow?
Global: 45-55mL/100g tissue/min OR 15% of CO
Cortical: 75-80mL/100g tissue/min
Subcortical: 20mL/100g tissue/min
What are the 5 determinants of cerebral blood flow?
- Cerebral metabolic rate for O2 (CMRO2)
- Cerebral perfusion pressure
- Venous pressure
- PaCO2
- PaO2
What is CMRO2 and what are the normal value?
CMRO2 describes how much O2 the brain consumes per minute.
3.0-3.8mL/O2/100g brain tissue/min
What factors increase and decrease CMRO2?
Decreased:
- hypothermia (7% per 1degree decrease)
- halogenated anesthetics
- propofol
- etomidate
- barbiturates
Increased:
- hyperthermia
- seizures
- ketamine
- nitrous oxide
What is the formula for cerebral perfusion pressure?
What is normal?
(see chart in neuro: CNS brain)
CPP = MAP - ICP (or CVP whichever is higher)
Cerebral vasculature autoregulates its resistance (vessel diameter) to provide a constant CPP of 50-150mmHg.
This ensures relatively stable blood flow and protects against swings in BP.
*50-150 is CPP, not MAP.
To ensure CPP of 50, MAP must be 60-65 if ICP is normal 10-15. If ICP is elevated, CPP requires a higher MAP.
What influences cerebral autoregulation?
- products of local metabolism
- myogenic mechanisms
- autonomic innervation
What are the consequences of a CPP that exceeds the limits of autoregulation? (too high and too low)
Too low: < 50mmHg
- Vessels are maximally dilated
- CBF becomes pressure dependent
- Risk of cerebral hypoperfusion
Normal: 50-150mmHg
- Range of autoregulaiton
- CBF is constant over a range of pressure
Too high: >150mmHg
- Vessels are maximally constricted
- CBF becomes pressure dependent
- Risk of cerebral edema and hemorrhage
List 4 conditions that reduce CPP as a function of increased venous pressure:
High venous pressure decreases cerebral venous drainage and increases cerebral volume. This creates back pressure to brain reducing the arterial/venous pressure gradient (MAP-CVP).
Conditions that impair venous drainage:
- Jugular compression secondary to improper head positioning.
- Increased intrathoracic pressure secondary to coughing or PEEP.
- Vena cava thrombosis
- Vena cava syndrome
What is the relationship between PaCO2 and CBF? What physiologic mechanism is responsible for this?
There is a linear relationship btwn PaCO2 and CBF.
- The pH of the CSF around the arterioles controls cerebral vascular resistance.
- At a PaCO2 of 40mmHg, CBF is 50mL/100g brain tissue/min.
At what PaCO2 does maximal cerebral vasodilation and vasoconstriction occur?
Maximal vasodilation at PaCO2 of 80-100mmHg.
Maximal vasoconstriction at PaCO2 of 25mmHg
For every 1mmHg increase (or decrease) in PaCO2, CBF will…
Increase (or decrease) by 1-2mL/100g brain tissue/min
What is the relationship between CMRO2 and CBF?
What is an exception?
Things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF). EX: hyperthermia or ketamine.
Things that decrease CMRO2 tend to cause vasoconstriction (decreased CBF). EX: hypothermia, propofol, and thiopental.
*Halogenated agents are exception. they decouple the relationship btwn CMRO2 and CBF (they reduce CMRO2 but cause vasodilation). This explains why pts with intracranial hypertension should have TIVA.
How does Acidosis affect CBF?
Respiratory acidosis increases CBF.
*metabolic acidosis/alkalosis does NOT directly affect CBF. This is b/c H+ does NOT pass through the BBB. A compensatory change in minute ventilation can affect CBF.
How does alkalosis affect CBF?
Respiratory alkalosis decreases CBF.
*metabolic acidosis/alkalosis does NOT directly affect CBF. This is b/c H+ does NOT pass through the BBB. A compensatory change in minute ventilation can affect CBF.
How does PaO2 affect CBF?
PaO2 below 50-60mmHg causes cerebral vasodilation and increases CBF.
When PaO2 is above 60mmHg, it does not affect CBF.
What is normal ICP?
What is abnormal?
ICP is the supratentorial CSF pressure.
Normal ICP is 5-15mmHg.
Cerebral HTN occurs if ICP>20mmHg.
When is ICP measurement indicated?
What is the gold standard for measurement?
when GCS score < or = 7
Intraventricular catheter is the gold standard for ICP measurement. ICP can also be measured with subdural bolt or catheter placed over convexity of the cerebral cortex.
List the s/s of intracranial HTN:
Headache N/V Papilledema (swelling of optic nerve) Focal neurologic deficit Decreased LOC Seizures Coma
Discuss the Monroe-Kellie hypothesis:
see photo in Neuro: CNS Brain
The brain lives in a rigid bony box with 3 components: Brain, Blood, CSF.
MK hypothesis describes the pressure-volume equilibrium btwn the brain, blood, and CSF w/I the confines of cranium.
Its says an increase in one component must be countered with a decrease in one of both to the others or pressure in the cranium will rise.
Causes of increased volume in the cranium:
Brain: swelling or tumor
Blood: increased CBF or bleeding
CSF:
- Increased CSF production by choroid plexus.
- Reduced CSF removal by arachnoid villi
- Obstruction to reabsorption (bleed, infection, tumor)
- Passage of fluid across the BBB
What is Cushing’s triad?
What is the clinical relevance of this reflex?
Indicates intracranial HTN.
- HTN
- Bradycardia
- Irregular respirations
Increased ICP reduces CPP. In an effort to preserve CP, blood pressure increases. HTN activates the baroreceptor reflex, leading to bradycardia. Compression of medulla causes irregular respirations.
Name 4 areas where brain herniation can occur:
- Herniation of the cingulate gyrus under the falx.
- Herniation of the contents over the tentorium cerebelli (transtentorial herniation)
- Herniation of the cerebellar tonsils through the foramen magnum.
- Herniation of contents through a site of surgery or trauma.
How does HTN affect CBF?
What is the ideal PaCO2 to achieve this effect?
CO2 dilates the cerebral vessels–> decreased cerebral vascular resistance–> increased CBF–> increased ICP
Hyperventilation (PaCO2 30-35mmHg) constricts the cerebral vessels–> increased cerebral vascular resistance–> decreased CBF–> decreased ICP
Lowering PaCO2 < 30mmHg increases the risk of cerebral ischemia d/t vasoconstriction and shifting the oxyhemoglobin dissociation curve to left (this reduces O2 offloading)
How do nitroglycerine and nitroprusside affect ICP?
Cause cerebral vasodilation–>increases CBF–>increased ICP.
How does head position affect ICP?
Head elevation >30 degrees facilitates venous drainage away from brain.
Neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP.
Head down position increases CBV and ICP.
How does mannitol reduce ICP?
What problems can arise when mannitol is used in this way?
Osmotic diuretic (mannitol 0.25-1.0g/kg) increases serum osmolarity and “pulls” H2O across the BBB towards the bloodstream.
- If BBB is disrupted, mannitol enters the brain and promotes cerebral edema.
- Mannitol transiently increases blood volume, which can increase ICP and stress the failing heart.
Describe the Anterior circulation of the brain:
Internal carotid arteries supply the anterior circulation. They enter the skull through the foramen lacer.
Aorta –> Carotid a. –> Internal carotid a.–> Circle of Willis–> cerebral hemispheres
Describe the Posterior circulation of the brain:
Vertebral arteries supply the posterior circulation. They enter the skull through the foramen magnum.
Aorta–> subclavian a. –> vertebral a. –> basilar a. –> Posterior fossa structures and cervical spinal cord
Describe the anatomy of the circle of willis:
see photo in Neuro: cos brain
the anterior and posterior circulations converge at the circle of willis.
Its primary function is to provide redundancy of blood flow in the brain. If one side occludes, the other side should theoretically be able to perfuse the affected areas of the brain.
Which population of stoke pts should receive a thrombotic agent?
Type of CVA must be determined prior to treatment. Thrombolytic should NOT be given to pt with hemorrhagic stroke. Patient should receive emergent non-contrast CT to determine type.
If treatment can begin <3 hrs after onset of s/s, pt with ischemic CVA should receive IV thrombolytic such as recombinant tissue plasminogen activator (tPA).
ASA is an acceptable alternative if tPA cannot be administered.
What is relationship btwn hyperglycemia and cerebral hypoxia?
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue and is associated with worse outcomes. Monitor serum glucose and treat hyperglycemia with insulin.
Think about this when administering IV fluids that contain dextrose.
In the context of cerebral aneurysm, how is transmural pressure calculated?
TP = MAP - ICP
MAP is the pressure pushing outward against aneurysmal sac. ICP is counter pressure. In essence, ICP creates a tamponade effect. Risk of rupture is increased by hypertension and/or acute reduction in ICP (opening of dural)
What is the problem with high transmural pressures?
An increased transmural pressure predisposed the aneurysm to rupture. As vessel bursts, blood flows into the subarachnoid space.
What is the most common clinical finding in a patient with subarachnoid hemorrhage (SAH)? What are the other s/s?
“worst headache of my life”
- Consciousness is lost 50% of the time.
- focal neurologic deficits
- N/V
- photophobia
- fever
- Meningismus occurs as blood spreads throughout and irritates the subarachnoid space.
- Blood can block CSF flow, causing obstructive hydrocephalus and increased ICP.
What is the most significant source of morbidity and mortality in the pt with SAH?
Cerebral vasospasm is delayed contraction of cerebral arteries. Can lead to cerebral infarction.
Free hemoglobin that is in contact with outer surface of cerebral arteries increases the risk of vasospasm.
There is a positive correlation btwn the amount of blood observed on CT and incidence of vasospasm.
What is the incidence of cerebral vasospasm?
When is it most likely to occur?
It occurs in about 25% of pts following SAH and is most likely 4-9 days following SAH.
Tx for cerebral vasospasm?
Standard of care is “Triple H therapy”: Hypervolemia, Hypertension, Hemodilution to Hct 27-32%
Liberal hydration supports BP and CPP. It also hemodilutes which reduces blood viscosity and CVR. Together these improve cerebral BF.
Nimodipine is only CCB shown to reduce morbidity/mortality. It does not actually relieve the spasm, but instead increases collateral BP.
During end-vascular coil placement for cerebral aneurysms, the aneurysm ruptures. What is the best tx at this time?
Give protamine 1mg per 100U of heparin (coil placement procedures require heparinized pt).
MAP should be lowered into low/normal range.
*Adenosine can be given to temporarily arrest the heart, so interventional radiologist can control bleeding.
Be able to calculate GCS:
What score is consistent with traumatic brain injury?
GCS < 8 = TBI
Eye opening: 4-spontaneous 3-to speech 2-to pain 1-none
Motor response: 6-Obeys commands 5-Localizes 4-Withdraws (flexion) 3-Abnormal flexion 2-Extensor response 1-None
Verbal response: 5-Oriented 4-Confused conversation 3-Inappropriate words 2-Incomprehensible sounds 1-None
How do you treat patients with intracerebral bleed who is on warfarin?
Warferin can be reversed with FFP, Prothrombin complex concentrate, and/or recombinant factor VIIa.
Vitamin K is not the best option for acute warfarin reversal.
How do you treat the patient with intracerebral bleed who is on Clopidogrel?
Clopidogrel, ASA, or both can be reversed with platelet transfusion.
Also evidence of reversal with recombinant factor VIIa.
2 common ways to reduce ICP that should specifically be avoided in pts with traumatic brain injury?
Hyperventilation can worsen cerebral ischemia in TBI. It is only indicated as temporary measure to acutely reduce ICP.
Steroids worsen neurologic outcome.
Is N2O safe in pt with traumatic brain injury?
Other injuries (such as pneumothorax) may only become evident after anesthetic induction and PPV. N2O can rapidly expand pneumothorax or cause pneumocephalus. DO NOT use in pt with TBI.
5 types of seizures:
- Grand mal
- Focal cortical
- Absence (petit mal)
- Akinetic
- Status epilepticus
Describe a grand mal seizure:
how do you treat it?
Generalized tonic-clinic activity:
Tonic phase= whole body rigidity
Clonic phase= repetitive jerking motions
Respiratory arrest–>hypoxia
-Increased O2 consumption d/t increased brain activity and muscle contraction
Acute tx: propofol, diazepam, thiopental
Surgical tx: vagal nerve stimulator or resection of foci
Describe a focal cortical seizure:
Localized to particular cortical region
- Can be motor or sensory
- Usually no LOC
Describe an absence (petit mal)
Temporary loss of awareness
More common in children
Describe an akinetic seizure:
Temporary LOC and postural tone:
-can result in fall–>head injury
More common in children
Describe status epilepticus:
Seizure activity that lasts >30min OR 2 grand mal seizures w/o regaining consciousness in-between.
Respiratory arrest–>hypoxia
-increased O2 consumption d/t increased brain activity and muscle contraction
Acute treatment:
- Phenobarbital
- Thiopental
- Phenytoin
- Benzos
- Propofol
- even GA
What is the relationship between etomidate and seizures?
Etomidate commonly causes myoclonus. This is not associated with increased EEG activity in patients that do NOT have epilepsy.
In patients with seizures disorders, etomidate (or methohexital or alfentanil) increases EEG activity and can be used to help determine the location of seizure foci during cortical mapping.
Describe the pathophysiology of Alzheimer’s disease:
Development of diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain.
Consequences of plaque formation include:
- Dysfunctional synaptic transmission (most noticeable in nicotinic Ach neurons)
- Apoptosis (programmed cell death)
What class of drugs is used to treat Alzheimer's disease? How do they interact with succinylcholine?
Tx for Alzheimer’s is palliative and aims to restore the concentration of Ach. This is accomplished with cholinesterase inhibitors.
EX: tacrine, donepezil, rivastigmine, and galantamine.
Cholinesterase inhibitors increase the duration of action of succinylcholine (clinical significance of this is debatable)
Describe the pathophysiology of Parkinson’s disease:
Dopaminergic neurons in the basal ganglia are destroyed.
Decreased dopamine + normal acetylcholine = relative acetylcholine increase –> suppression of corticospinal motor system + overactivity of extrapyramidal motor system
What drugs increase the risk of extrapyramidal s/s in the patient with Parkinson’s disease?
Drugs that antagonize dopamine should be avoided.
EX: Metoclopramide
Butyrophenones (haloperidol and droperidol)
phenothiazines (promethazine)
What is the most common eye complication in the perioperative period?
Corneal abrasion
What is the most common cause of vision loss?
Ischemic optic neuropathy
Describe the pathophysiology of ischemic optic neuropathy (ION):
Most likely explanation is venous congestion in optic canal reduces perfusion pressure. Increased intraabdominal and/or intrathoracic pressure can also increase intraocular pressure.
Ocular Perfusion Pressure = MAP - Intraocular Pressure
Central retinal and posterior ciliary arteries are at highest risk because they “watershed” areas- they lack anastomoses with other arteries. A rise in IOP can compress these vessels, which reduce O2 delivery to retina.
What surgical procedures present the most significant risk of ION?
ION is most common after spinal surgery in prone position.
- Prone position
- Use of Wilson frame
- Long duration of anesthesia
- Large blood loss
- Low ratio of colloid to crystalloid resuscitation
- Hypotension
What are patient risk factors for ION?
- Male
- Obesity
- DM
- HTN
- Smoking
- Old age
- Atherosclerosis
How is the spinal cord perfused?
see photo in Neuro: CNS spinal cord
1 anterior spinal artery (anterior 2/3 of spinal cord)
2 posterior spinal arteries (posterior 1/3 of spinal cord)
6-8 radicular arteries
What is the most important radicular artery? Which spinal segment does it typically enter the spinal cord?
The artery of Adamkiewicz.
It supplies the anterior cord in the thoracolumbar region.
Its most commonly originates between T11-T12.
Anatomy of the spinal cord and spinal nerve in cross section: (must see photo in Neuro: CNS spinal cord)
Sensory neurons from the periphery via the dorsal nerve root.
Motor and autonomic neurons exit via the ventral nerve root.
Describe the organization of the 3 neuron pathways common to the spinal tracts:
- First order neuron links the peripheral nerve to the spinal cord or brainstem.
- Second order neuron links the spinal cord or brainstem to a subcortical structure.
- third order neuron links the subcortical structure to the cerebral cortex.
Structure and function of the dorsal column:
Dorsal column- Medial lemniscal system:
- Transmits mechanoreceptive sensations (fine touch, proprioception, vibration, pressure)
- Capable of 2 point discrimination- a high degree of localizing the stimulus.
- Consists of large, myelinated, rapidly conducting fibers.
- Transmits sensory information faster than the anterolateral system.
- Think of this as a more evolved system.
Structure and function of the spinothalamic tract:
Anterolateral system- spinothalamic tract:
- Transmits: pain, temp, crude touch, tickle, itch, sexual sensation.
- 2 point discrimination not present.
- consists of smaller, myelinated, slower conducting fibers.
- Think of this as a more primitive system
What bedside exam can assess the integrity of the corticospinal tract?
How do you interpret it?
Corticospinal tract is most important motor pathway. It’s often referred to as pyramidal tract. All other motor pathways outside of the corticospinal (pyramidal) tract are known collectively as the extrapyramidal tract.
The babinski test is a method that tests the integrity of the corticospinal tract. A firm stimulus is applied to the underside of the foot yields the following response:
- Normal: Downward motion of all toes
- Upper motor neuron injury: upward extension of the big toe with fanning of other toes.
- Lower motor neuron injury: No response.
Contrast the presentation of upper- vs lower-motor neuron injury:
Upper motor neurons begin in the cerebral cortex and end in ventral horn of spinal cord.
Lower motor neurons begin in the ventral horn and end at the neuromuscular junction.
- Upper motor neuron injury presents with hyperreflexia and spastic paralysis.
- Lower motor neuron injury presents with impaired reflexes and flaccid paralysis.
Discuss pathophysiology of neurogenic shock:
- Impairment of cardioaccelerator fibers (T1-4)–>unopposed cardiac vagal tone–> bradycardia and reduced inotropy.
- Decreased SNS tone–> vasodilation–> venous pooling–> decreased CO and BP
- Impairment of sympathetic pathways from hypothalamus to blood vessels–>inability to vasoconstriction or shiver–>hypothermia.
- Hypothermia is result of inability of cutaneous vasculature to vasoconstriction, causing a redistribution of blood flow towards the periphery and allowing more heat to escape from body.
How can you differentiate neurogenic shock from hypovolemic shock?
Neurogenic:
- bradycardia
- hypotension
- hypothermia with pink warm extremities (cutaneous vasodilation)
Hypovolemic:
- Tachycardia
- hypotension
- cool, clammy extremities
Discuss the use of succinylcholine in the patient with spinal cord injury:
Succinylcholine should be avoided 24 hours after injury and should not be used for at least 6 months thereafter (some books say 1 year)
When does a patient with a spinal cord injury become at risk for autonomic hyperreflexia (AH)? what factor (other than time) contributes to this risk?
After neurogenic shock phase ends (1-3wks), body begins to mend in pathologic and disorganized way. There is return of spinal sympathetic reflexes below the level of injury, however w/o inhibitory influences that would normally come from above the level of injury, the sympathetic reflexes below injury exist in overactive state. This places pt at risk for AH (mass reflex).
While up to 85% of pts with injury above T6 will develop AH, it’s very unlikely to occur in pt with injury below T10. (higher the level of injury, the more intense the response)
6 situations that can precipitate AH:
- Stimulation of the hollow organs (bladder, bowel, uterus)
- Bladder catheterization
- surgery- especially cystoscopy or colonoscopy
- bowel movement
- cutaneous stimulation
- child birth
Discuss the presentation and pathophysiology of AH:
Classic presentation is HTN and bradycardia.
Stimulation below level of SCI triggers sympathetic reflex arc which creates profound degree of vasoconstriction below level of SCI. This activates baroreceptor reflex in carotid bodies, which slows HR. Body attempts to reduce after load with vasodilation above level of injury.
Other s/s:
- Reflex vasodilation above level of SCI–> nasal stuffiness.
- HTN–> headache and blurred vision
- Malignant hypertension–> stroke, seizure, LV failure, dysrhythmias, pulm edema, and/or MI
Detail the anesthetic management of patient with AH:
Even though pt doesn’t have sensation below SCI, stimulation below can elicit autonomic hyperreflexia- prevention is paramount!
- General or spinal are best options.
- Epidural maybe used for laboring mom (but compared to spinal, epidural does not inhibit sacral nerve root to same degree).
- HTN best treated with removal of stimulus, deepening anesthetic, and rapid acting vasodilator (like nitroprusside).
- Bradycardia can be treated with atropine or glycopyrrolate.
- Positive chronotrope w/ vasoconstrictive properties will worsen HTN
- Lidocaine jelly to cystoscope or foley doesn’t help prevent AH.
- Succ should be avoided for at least 6 months following SCI.
- AH may present in the postoperative period as effects of anesthesia wear off; close postop monitoring is warranted.
Discuss the pathophysiology of amyotrophic lateral sclerosis (ALS):
ALS causes progressive degeneration of motor neurons in corticospinal tract. Astrocytic gliosis replaces the affected motor neurons. Both upper and lower neurons are affected.
Anesthetic management of ALS:
- No evidence of clear benefit of any particular anesthetic technique.
- Succ can cause lethal hyperkalemia. Lower motor neurons dysfunction is associated with proliferation of post junctional nicotinic receptors.
- There is increased sensitivity to non-depolarizing neuromuscular blockers.
- Bulbar muscle dysfunction increases the risk of pulmonary aspiration.
- Chest weakness reduces vital capacity and maximal minute ventilation.
- Consider postop mechanical ventilaiton.
Describe the pathophysiology of myasthenia gravis (MG)?
an autoimmune disease that manifests as skeletal muscle weakness that becomes worse later in the day or develops with exercise. Periods of rest allow for recovery of muscle function.
IgG antibodies destroy post-junctional, nicotinic, acetylcholine receptors at the neuromuscular junction. Although Ach is present in sufficient quantity, there aren’t enough receptors to translate the extracellular signal into an intracellular response.
What surgical procedure can reduce symptoms in the pt with MG?
The thymus gland plays key role in MG, thymectomy can bring symptom relief.
- Thymectomy reduces circulating Ant-AchR IgG in most pts
- Surgical approach may be via median sternotomy or transcervical approach.
How does MG affect the pregnant mother and fetus?
1/3 of women, pregnancy intensifies the symptoms of MG.
Anit-AchR IgG antibodies cross the placenta and cause weakness in 15-20% of neonates. This can persist up to 2-4 weeks, which is consistent with the half-life of the Anti-AchR IgG antibodies in the neonate’s circulation. These neonates may require airway management.
How can you tell the difference between cholinergic crisis and myasthenic crisis?
Pryidostigmine (an anticholinesterase) is the first line treatment for myasthenia gravis. Overdosed can cause cholinergic crisis, which can include skeletal muscle weakness. Myaesthetic crisis also presents with skeletal muscle weakness.
The diagnosis is made by administering 1-2 mg IV edrophonium, otherwise known as “Tensilon test.”
- if muscle weakness is made worse, patient has cholinergic crisis (tx = anti-cholinergic).
- if there is an improvement in muscle strength, the patient had an exacerbation of myasthenic symptoms (tx = anticholinesterase, immunosuppression, plasmapheresis).
How do patients with MG respond to neuromuscular blockade?
There is a reduction in the number of nicotinic receptors (type M) at the neuromuscular junction, therefore they have an increased sensitivity to NDMR and resistance to Succ.
VA causes skeletal muscle relaxation by acting in the ventral horn of the spinal cord therefore in many cases this illuminates the need for NMBs.
Why are patients with MG prone to aspiration?
Bulbar muscle weakness (mouth and throat) manifest as difficulty handling oral secretions. This increases the risk of pulmonary aspiration.
Describe the pathophysiology of Eaton–Lambert syndrome:
Caused by IgG mediated destruction of the presynaptic voltage-gated Ca++ channels at the presynaptic nerve terminal.
When the action potential D polarizes the nerve terminal, Ca++ entry into the presynaptic neuron is limited thereby reducing the amount of Ach that is rebased into the synaptic cleft.
Postsynaptic nicotinic receptors present in normal quantity and functions normally.
Compare/contrast Eaton-Lambert and MG:
- Region Affected
- Defect
- Region of NMJ Affected
- Common comorbidities
- Response to Succ
- Response to NDMR
- Effectiveness of AchE-I
EL syndrome:
- Voltage-gated Ca++ channel
- Decreases Ach release
- Presynaptic neuron
- Small-cell lung carcinoma (oat-cell carcinoma)
- Sensitive
- Sensitive
- Poor
MG:
- NM receptor (postsynaptic
- Decreased response to Ach
- Postsynaptic at motor endplate
- Thymoma
- Resistant
- Sensitive
- Adequate
Describe the pathophysiology of Guillian-Barre syndrome:
GB (acute idiopathic polyneuritis) characterized by an immunologic assault on myelin in the peripheral nerves. The action potential can’t be conducted, so motor endplate never receives the incoming signal.
Usually persists for ~2weeks and ends with full recovery in ~4weeks.
Discuss the presentation of GB syndrome:
A flu-like illness usually precedes paralysis by 1-3 weeks.
S/S:
-Flaccid paralysis begins in distal extremities and ascends bilaterally towards the proximal extremities, trunk, and face.
-Intercostal muscle weakness impairs ventilation.
-Facial and pharyngeal weakness causes difficulty swallowing
-Sensory deficits include: paresthesias, numbness, and/or pain.
-Autonomic dysfunction is common: tachycardia or Bradycardia, HTN or hypotension, diaphoresis or anhidrosis, and orthostatic hypotension.
What is familial periodic paralysis?
FPP are two distinct diseases processes that are characterized by acute episodes of skeletal muscle weakness that is accompanied by either hypo- or hyperkalemia.
How can 2 variants of familial periodic paralysis be distinguished from each other?
Hypokalemic periodic paralysis:
diagnosed if skeletal muscle weakness follows a glucose-insulin infusion. The patient becomes weak after the serum K+ is reduced.
Hperkalemic periodic paralysis:
-diagnosed if skeletal muscle weakness follows oral potassium administration. patient becomes weak after the serum K+ increased.
What drugs should be avoided in the patient with HYPOkalemic periodic paralysis? How about temperature?
Do NOT administer:
- Glucose containing solutions
- K+ wasting diuretics
- Beta-2 agonists
Safe to administer:
- Succ
- NDMR
- Acetazolamide*
- Acetazolamide is tx for both forms of FPP. It creates a non-anion gap acidosis, which protects against hypokalemia. It also facilitates renal K+ excretion, which guards against hyperkalemia.
- *Avoid hypothermia for both types
What drugs should be avoided in the patient with HYPERkalemic periodic paralysis?
Do NOT administer:
- Succ
- K+ containing solutions
Safe to administer:
- Glucose containing solutions
- K+ wasting diuretics
- Beta-2 agonists
- NDMRs
- Acetazolamide*
- Acetazolamide is tx for both forms of FPP. It creates a non-anion gap acidosis, which protects against hypokalemia. It also facilitates renal K+ excretion, which guards against hyperkalemia.
- *Avoid hypothermia for both types
Detail the functions of the following receptors in skeletal muscle:
-Nicotinic
-Dihydropyridine (DHP)
-Ryanodine (RyR1)
-SERCA2
Which is dysfunctional in MH pt?
(see photo in Neuro: musculoskeletal disease)
When T-tubule is depolarized (Ach binds to nicotinic-R at NMJ), extracellular Ca++ enters myocyte via dihydropyridine-R (DHP) at T-tubule.
This activates defective ryanodine-R (RyR1)–> instructs sarcoplasmic reticulum to release way too much Ca++ into cell. (think of RyR1 as Ca++ faucet that can’t be turned off). Not only is there more Ca++ to engage with contractile elements, but cell attempts to return excess Ca++ to SR via SERCA2.
Both processes consume substantial amount of ATP, increase O2consumption, and increase CO2 production.
When skeletal myocyte consumes all ATP, there isn’t enough to maintain the integrity of cell membrane. It breaks down and intracellular components (myoglobin and K+) are released into systemic circulation.
List 8 consequences of too much calcium inside the skeletal myocyte:
- sustained muscle contraction
- accelerated metabolic rate in rapid depletion of ATP
- increased oxygen consumption
- increased CO2 and heat production
- mixed respiratory and lactic acidosis
- Sarcolemma breaks down
- K+ and myoglobin leak into systemic circulation
- rigidity from sustained contraction
Identify 3 conditions that are definitely linked to MH:
- King-Denborough syndrome
- Central core disease
- Multiminicore disease
MH is NOT linked to these conditions:
- Duchenne muscular dystrophy*
- Becker muscular dystrophy
- Neuroleptic malignant syndrome
- Myotonia congenita
- Myotonic dystrophy
- Osteogenesis imperfecta
*Duchenne muscular dystrophy is associated with MH-like condition characterized by rhabdomyolysis. It’s possible that halogenated agents and succ can initiate this MH-like syndrome in patient with DM, so it is prudent to avoid these agents. Dantrolene does not treat this condition.
What is the most sensitive indicator of MH?
EtCO2 that rises out of proportion to minute ventilation. MH can occur as late as 6 hours after exposure to a triggering agent.
Early signs of MH:
Tachycardia Tachypena Masseter spasm Warm soda lime Irregular heart rhythm
Intermediate signs of MH:
Cyanosis
Patient warm to touch
Irregular heart rhythm
Late signs of MH:
Muscle rigidity
Cola-colored urine
Coagulopathy
Irregular heart rhythm
What is the difference between trismus and masseter muscle rigidity d/t MH?
Trismus and masseter muscle rigidity are 2 entities that exist on a continuum.
- Trismus describes a tight jaw that can still be opened.
- Masseter muscle rigidity describes a jaw that can’t be opened.
How should you proceed if the patient present with either trismus or masseter muscle rigidity d/t MH?
Trismus is normal response to succinylcholine, so its ok to proceed with surgery if trismus occurs in isolation. But wise to convert to non-triggering agent.
Masseter complicates airway management. Spasm is d/t increased Ca++ in myoplasm. Since this site of action is distal to NMJ, a neuromuscular blocker will not relax the jaw. If the patient experiences masseter muscle rigidity, assume MH until proven otherwise.
What is the definitive test for susceptibility to MH?
Anyone who has experienced MH or masseter spasm should be referred to a halothane contracture test for diagnosis. Although this is the definitive test for dx, it only has 80% specificity, so there is a risk of false-negative.
How does dantrolene treat MH?
What are the most common side effects?
Dantrolene is classified as a muscle relaxant.
- It halts Ca++ release from the RyR1 receptor
- It prevents Ca++ entry into the myocyte, which reduces the stimulus for calcium-induced calcium release.
*Most common side effects are muscle weakness and venous irritation.
How is dantrolene formulated?
How is it prepared?
Each vial contains 20mg of dantrolene + 3g of mannitol. The vials must be reconstituted with preservative free water.
NaCl introduces additional solute, which prolongs the time required for dantrolene to dissolve into the diluent. Mixing dantrolene is a chore so enlist help early. Warming the diluent will make the process much faster.
Treatment for MH:
- d/c triggering agent
- 100% O2 at >10L
- Dantrolene (or Ryanodex) 2.5mg/kg IV and repeat q5-10min
- Hyperventilate
- Correct lactic acidosis with Bicarb
- Treat hyperkalemia (CaCl 5-10mg IV and insulin 0.15u/kg + D50 1mL/kg)
- Protect against dysthymia (class 1 agent lidocaine 2mg/kg or procainamide 15mg/kg)
- Maintain urine output (IV hydration, mannitol 0.25g/kg, furosemide 1mg/kg)
- Cool patient until temp drops below 38C (cold IVF, cold fluid lavage, Ice packs)
- Monitoring coagulation (DIC is late complication and signals impending demise)
*Calcium channel blockers should not be given with dantrolene, b/c dangerous hyperkalemia will result.
Describe the pathophysiology of Duchenne muscular dystrophy:
Dystrophin is critical structural component of the cytoskeleton of skeletal and cardiac muscle cells. It helps anchor actin/myosin to cell membrane. The absence of dystrophin destabilizes the sarcolemma during muscle contraction and increases membrane permeability.
Absence of dystrophin allows exntrajunctional receptors to populate the sarcolemma. This predisposes pt to hyperkalemia following succ administration. Succ has a black box warning that details the risk of cardiac arrest and sudden death secondary to hyperkalemia in children with undiagnosed skeletal muscle myopathy. Classic teaching suggests that DM increases the risk of MH. however a more recent meta-analysis refutes this claim.
How does Duchenne muscular dystrophy affect pulmonary function?
Kyphoscoliosis (restrictive lung disease)–>decreased pulmonary reserve–>increased secretions and risk of pneumonia
Respiratory muscle weakness
How does Duchenne muscular dystrophy affect cardiac function?
- Degeneration of cardiac muscle –> reduced contractility, papillary muscle dysfunction, mitral regurgitation, cardiomyopathy, and CHF.
- S/S of cardiomyopathy: resting tachycardia, jugular venous distension, S3/S4 gallop, and displacement of point of maximal impulse.
- The gold standard of cardiac evaluation is echocardiogram.
What EKG findings might you expect for a patient with Duchenne muscular dystrophy?
Impaired cardiac conduction–> sinus tachycardia and short PR interval.
Scarring of the posterobasal aspect (back/bottom) of the lot ventricle manifests as increased R-wave amplitude in lead 1, and deep Q waves in the limb leads.
What is the Cobb angle?
What is its significance?
(see photo in Neuro: musculoskeleta disease)
Describes the magnitude of the spinal curvature.
40-50 degrees: indication for surgery
60 degrees: Decreased pulmonary reserve
70 degrees: pulmonary symtoms present
100 degrees: Gas exchange significantly impaired; Higher risk post-op pulmonary complications
Scoliosis alters thoracic geometry, which…
compresses the lungs and creates a restrictive ventilatory defect. One side of the thorax becomes smaller than the other.
Early respiratory complications of scoliosis:
Restrictive ventilatory defect:
- FEV1 and FRC are decreased
- FEV1/FVC ratio is normal
Decreased lung volumes:
- VC
- TLC
- RV
- FRC
Decreased chest wall compliance
Late respiratory complications of scoliosis:
- V/Q mismatching
- Hypoxemia
- Hypercarbia (sign of impending failure)
- Pulmonary HTN
- Reduced response to hypercapnia
- Cor pulmonale
- Cardiorespiratory failure
3 ways rheumatoid arthritis (RA) affects the airway:
- Temporomandibular joint: Limited mouth opening
- Cricoarytenoid joints: decreased diameter of glottic opening
- Cervical spine: Atlanto-occipital subluxation with flexion; limited extension
What is the most common airway complication of RA?
What is its clinical significance?
Atlantoaxial subluxation d/t weakening of transverse axial ligament, which allows the odontoid to directly compress the spinal cord at the level of the foramen magnum.
Patient is at risk for quadriparxsis or paralysis.
*Patients with Down syndrome are also at risk for AO subluxation.
Discuss the pathophysiology of RA:
Autoimmune diseases that targets synovial joints.
Widespread systemic involvement d/t infiltration of immune complexes into the small and medium arteries leading to vasculitis. Cytokines (TNF and interleukin-1) play a central role in the pathogenesis or RA.
*2-3x more common in women.
s/s of RA:
- morning stiffness that generally improves with activity.
- Joints are painful, swollen, and warm.
- weakness
- fatigue
- anorexia
- Lymph node enlargement in the cervical, axillary, and epitrochlear regions.
Airway complications of RA:
TMJ synovitis- limited mouth opening
cricoarytenoid arthritis- narrow glottic opening
AO instability- risk of spinal cord and vertebral a. compression
Pulmonary complications of RA:
Pleural effusion
Restrictive ventilatory pattern:
-diffuse interstitial fibrosis
-Costochondral involvement limits chest wall expansion
Cardiac complications of RA:
- Pericardial effusion or tamponade
- Restrictive pericarditis
- Aortic regurgitation
- Valvular fibrosis
- Coronary artery arteritis
Hematologic complications of RA:
Anemia
Platelet dysfunction secondary to NSAIDs
Renal complications of RA:
Renal insufficiency d/t:
- vasculitis
- NSAIDs
Endocrine complications of RA:
Adrenal insufficiency and infections d/t steroids
GI complications of RA:
Gastric ulceration d/t NSAIDs and steroids
Eyes complications of RA:
Sjogren’s syndrome- risk of corneal abrasion
nervous system complications of RA:
peripheral neuropathy d/t nerve entrapment
Describe the pathophysiology of systemic lupus erythematosus (SLE):
Autoimmune disease characterized by proliferation of antinuclear antibodies.
It affects nearly every organ system, and most of the consequences are a direct result of antibody induced vasculitis and tissue destruction.
SLE targets who?
most common problems with SLE?
Targets young women (~1:1000)
Most common problems are polyarthritis and dermatitis.
Arthritis can affect any joint, but generally not spine.
Only 33-50% of patients develop the malar “butterfly” rash.
Airway complications of SLE:
Cricoarytenoiditis–> hoarseness, stridor, and airway obstruction.
Recurrent laryngeal nerve palsy.
Pulmonary complications of SLE:
- Restrictive ventilatory defect
- Pulmonary HTN
- Interstitial lung disease w/ impaired diffusion capacity
- Pleural effusion
- Recurrent pulmonary emboli
Cardiovascular complications of SLE:
- Pericarditis (tamponade is uncommon)
- Raynaud’s phenomenon
- HTN
- Conduction defects
- Endocarditis
Hematologic complications of SLE:
- Antiphospholipid antibodies
- hypercoagulability
- Anemia
- Thrombocytopenia
- Leukopenia
Renal complications of SLE:
Nephritis w/ proteinuria
Nervous system complications of SLE:
Stroke
What can exacerbate SLE?
Drug induced lupus generally persists for several weeks to months and presents with mild symptoms of arthralgia, anemia, leukopenia, and fever.
"PISSED CHIMP" Pregnancy Infection Surgery Stress Enalapril D-penicillamine
Captopril Hydralazine Isoniazid Methyldopa Procainamide
What is the relationship between SLE and antiphospholipid syndrome?
Patients with SLE are prone to developing antiphospholipid antibodys. Although the aPTT is prolonged, these patients are prone to a state of hypercoagulability and thrombosis.
At risk for stroke, DVT, and pulmonary embolism.
- pregnant patients with SLE are at higher risk.
Discuss the pathophysiology of myotonic dystrophy.
Characterized by a prolonged contracture after a voluntary contraction. This is the result of dysfunctional Ca++ sequestration by the sarcoplasmic reticulum.
Contractions can be so severe that they interfere with ventilation and intubation.
What 3 things can increase the risk of contractures in patients with myotonic dystrophy?
- Succ
- Reversal of NMB with anticholinesterase (theoretical)
- Hypothermia (shivering–> sustained contractions)
Discuss the pathophysiology of Marfan syndrome:
Autosomal dominant trait (not acquired).
Connective tissue disorder that’s associated with an elevated risk of aortic dissection, mitral valve prolapse, mitral regurgitation, and aortic insufficiency.
Dissection of the ascending aorta can extend into the pericardium, and this increases the risk of cardiac tamponade. (BECK’s triad: JVD, hypotension, and muffled heart tones)
Spontaneous pneumothorax is very common complication.
Discuss the pathophysiology of Ehlers-Danlos syndrome:
Inherited disorder of procollagen and collagen. Several types but only type 4 is associated with blood vessel rupture (think AAA).
Most important thing to remember is there is an increased bleeding tendency. This is the result of a lack of blood vessel integrity and NOT coagulopathy.
Avoid regional anesthesia and IM injections since hematoma is common complication.
Invasive line placement or trauma during intubation management poses a threat as well.
Pneumothorax is common so be careful with PIP.
