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56 Cards in this Set
- Front
- Back
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A&P
CNS |
-comprises the brain and spinal cord
-is covered by 3 layers of tissue, called meninges -pia, arachnoid layer, and dura mater -subarachnoid space, lies between the pia mater and arachnoid layer, contains CSF -the CNS is supplies with blood and vessels that bring oxygen and nutrients to the cells there -many substances cannot easily be exchanged between blood and brain because the endothelial cells of the vessels and astrocytes of the CNS form extremely tight junctions collectively referred to as the blood brain barrier -polar molecules and large molecules such as proteins do not cross, but lipid soluble molecules cross with ease |
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A&P
Brain |
-cerebral hemisphere (the cerebrum), divided into left and right hemispheres, consists of frontal, parietal, temporal, and occipital
Cortex: -also known as the gray matter, composed of neuronal cells -is the most superficial layer of the cerebrum, -responsible for all higher mental function, judgement, language, memory, creativity, and abstract thinking -it also function in the perception, localization, and interpretation of all sensations and governs all voluntary motor activities Diencephalon: -lies below the cerebral hemispheres directly above the brainstem -most important areas are the thalamus and hypothalamus Brainstem: -consists of the midbrain, pons, and medulla and contains resp and autonomic control centers Midbrain: -lies between the diencephalon and the pons Pons: -lies between the midbrain and the medulla, serves as a relay station for information, contains pneumotaxic center Medulla: -lies between the pons and merges with spinal cord -contains centers that regulate vital functions such as breathing, cardiac rate, and vasomotor tome -as well as centers for vomiting, gagging, coughing, and sneezing reflex behaviors Cerebellum: -is located just superior and posterior to the medulla |
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A&P
Nervous System |
-consists of 12 pairs of cranial nerves and 31 pairs of spinal nerves
-the Peripheral Nervous System is separated into sensory and motor divisions -motor division inclludes motor neurons that innervate skeletal muscles and the autonomic nervous system -Autonomic Nervous System innervates smooth and cardiac muscle and the glands |
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A&P
Cranial nerves |
-supply motor and sensory fibers to structures of the head and neck and upper back
-most originate in the brainstem -classified as sensory, motor, or mixed -they bring input from special senses, vision, hearing, smell, and somatic sensory input from the face and head into the brain -the also send motor commands out to the muscles and glands of the head and neck to control facial, eye, movements of the mouth, throat, head and neck, and autonomic function |
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A&P
Cranial nerves cont |
-I olfactory, sensory, sense of smell, origin in diencephalon
-II optic, sensory, vision, origin diencephalon -III oclulomotor, parasympathetic motor, pupillary constriction, origin midbrain -IV trochlear, motor, downward inward movement of eye, origin midbrain -V trigeminal, motor sensory, muscles of jaw and sensation of cornea, nasal, and facial skin, originates in pons -VI abducens, motor, lateral deviation of eye, origins in pons -VII facial, parasympathetic, salivation and tears, movement of facial expression, origin in pons -VIII vestibulocochlear, sensory, equilibrium and hearing, origins in pons -IX glossopharyngeal, parasympathetic, swallowing, sensation of pharynx and tongue, gag reflex, origins in medulla -X vagus, parasympathetic, autonomic activity of viscera of thorax and abd, involuntary activity of muscles of heart, lungs, and GI tract, origins in medulla -XI spinal accessory, motor, sternocleidomastoid muscles, origins in medulla -XII hypoglassal, motor, tongue movement, origins in medulla |
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A&P
Autonomic Nervous System |
-contains sympathetic and parasympathetic
-sympathetic nervous system receptors are known as adrenergic receptors -the vagus nerve alone is responsible for a tremendous amount of the parasympathetic control over the body -acetylcholine is the neurotransmitter synthesized by all autonomic neurons both SNS and PNS -when an action potential is conducted down the axon, acetylcholine is released into the synapse between the axon terminals -alpha receptors have alpha1 or alpha 2 receptors -beta receptors have beta1 or beta2 -heart has mostly beta1 (beta1 - 1 heart) -smooth muscles of the arteries and veins have mostly alpha1 and alpha2 receptors (A for Arteries & A for Alpha) -the SNS innervates organs with alpha1, alpha2, and beta1 receptors and norepi activates these receptors to changes - |
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A&P
Autonomic Nervous System cont |
-activation of beta1 receptors in the SA node by norepi results in depolarization of the SA node and inc HR
-activation of alpha1 and alpha2 receptors in the arteries results in inc contraction by arteriolar smooth muscle and an inc BP -beta2 (beta2 - 2 lungs) receptors are not innervated by SNS and norepi does not bind or activate beta2 receptors -epinephrine is powerful stimulator of beta2 receptors, which it reaches through the blood stream after being secreted by the adrenal medulla -dilation of bronchiolar smooth muscle or dilation of blood vessels in skeletal muscles are important effects of beta2 receptors that are mediated by circulating epinephrine rather than norepi. (beta2 - 2 lungs) -the SNS and PNS are antagonistic -the SNS inc the rate of firing of the SA node and inc the speed of conduction in the AV node of the heart, the PNS does the opposite -blood vessels are not innervated by the PNS |
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Level of Consciousness
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-Full consciousness: is a state of awareness and ability to respond optimally to one's environment
-Coma: is the opposite, A state of total absence of awareness and ability to respond even when stimulated -arousal is a function of the brain brain stem pathways that govern wakefulness, particularly RAS -two general categories for causes of altered LOC are structured and metabolic -a persistent vegetative state is a condition that can develop after a severe brain injury, they exhibit no cognitive function -locked in syndrome, the motor pathways in the brain stem are destroyed but the RAS and higher cognitive functions remain intact, patients are unable to move or speak what they are capable of interacting with their environment -brain death is the third unique alteration in LOC, criteria are, a known cause of of coma so that reversible causes can be ruled out, unresponsive to external stimuli, absent brainstem reflexes, absent respiratory effort |
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Intracranial dynamics
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-The skull is rigid box, a nonexpansile and noncontractile space
Its contents are divided into three intracranial sections: -Blood that is maintained in the blood vessels -CSF -brain parenchyma The brains ability to self regulate is based on the Monroe doctrine: -The volume of the intracranium is equal to the volume of the cerebral blood, 3-10% -Plus the volume of the CSF, 8-12% -Plus the volume of the brain tissue, more than 80% -To maintain this equilibrium, there cannot be any increase in volume of one of these components without a compensatory decrease in the other two -Normal ICP is 0-15 mmHg |
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Cerebral blood flow
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-Autoregulation is the ability of an organ to maintain consistent blood flow despite marked changes in arterial circulatory and perfusion pressures
-When autoregulation is impaired, the CBF is dictated by and fluctuates in correlation with the systemic BP -Autoregulation is the brains protective device against constant BP changes -The first of three components that my undergo changes as the body attempts to maintain a consistent intracranial volume is the CBF -Normal CBF is provided by a CPP in the range of 60-100 mmHg For autoregulation to be functional, C02 levels must be in an acceptable range and hemodynamic pressures must be within the following ranges: -CPP over 60 -MAP under 160 -systolic pressure between 60-140 -ICP under 30 -CARBON DIOXIDE, or hypercapnia (inc C02 levels) is the MOST POTENT VASODILATOR of CEREBRAL VESSELS, causing increased CBF and increased volume, leading to increased ICP -Hypocarbia (low C02 levels) is an effective way to reduce CBF because of its strong vasoconstrictive effect on the cerebral arteries |
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Cerebral fluid circulation
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-CSF also contributes to fluctuations in intracranial hemodynamics
-Disturbances in production, circulation, and absorption can contribute to changes in ICP |
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Parenchyma
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-Third most difficult component to manipulate
-The brain tissue does respond to increased ICP and changes within the other two intracranial components Summary of compensatory mechanisms to maintain normal ICP: -Shunting of CSF into the spinal subarachnoid space -Increased CSF absorption -Decreased CSF production -Shunting of venous blood out of the skull -When these compensatory mechanisms have been exhausted pressure increases rapidly until shifting of the brain occurs and blood supply to the medulla is cut off |
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Cerebral perfusion pressure
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-The blood pressure gradient across the brain
-CPP=MAP-ICP -When the CPP is greater than 100mmHg there is a potential for hyperperfusion and increased ICP -When the CPP is less than 60mmHg, blood supply to the brain is inadequate, and neuronal hypoxia and cell death may occur -If MAP and ICP are equal, CPP is zero indicating no CBF -The autoregulation system for maintenance of constant blood flow does not function at pressures less than 40mmHg -When CPP decreases the cardiovascular response is a rise in systemic pressure -CPP- Net pressure of blood flow to the brain -Normal 70-90mm Hg -Target a CPP greater than 60mm Hg for head injuries -Normal ICP is 0-10 mmHg -CPP is regulated by 2 opposing forces: -Map- force that pushes blood into the brain -ICP- force that keeps blood out -Raising MAP raises CPP -Raising ICP lowers CPP -Increasing ICP in TBI is potentially deadly |
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Cushing’s syndrome
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-Classic syndrome of increased ICP and includes increased BP, decreased pulse, and decreased respiration with papillary changes
-It is a sign of increased ICP -Possible impending herniation of the brain |
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Cerebral edema
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-Leads to secondary complication related to the expansion of brain tissue within the closed space of the cranium
-Treatment includes the use of corticosteroids as well as osmotic diuresis -These agents work by increasing plasma osmolarity, which draws fluid out of the brain tissue and into the bloodstream -Goal is to maintain plasma osmolarity up to 320mOsm/L |
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Vasogenic edema
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-Characterized by a disruption in the blood brain barrier and the inability of the cell walls to control movement of water in and out of the cells
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Cytotoxic edema
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-Cytotoxic edema occurs as the intracellular Na-K pump fails, allowing an influx of Na and water into the cell and an efflux of k
-Characterized by swelling of the individual neurons and endothelial cells, which increases fluid in the intracellular space and reduces available extracellular space affecting the gray matter |
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Management of increased ICP
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-Management techniques for increased ICP are oriented toward control of CBF and CSF circulation
-Measures to reduce ICP are usually initiated when the patients ICP increases to 15mmHg -Osmosis- diffusion of water across a membrane from a high to low area of water -Osmotic pressure- is the press that must be applies to a solution to prevent the inward flow of water across a membrane |
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Osmotic diuretic:
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-inc urination caused by certain substances in the small tubules of the kidneys
-These substances cause an inc in osmotic pressure within the tubule, causing retention of water and reducing the reabsorption of water, thus inc urination (diuresis) -Substances in the circulation can also inc the amount of circulating fluid by increasing the osmolarity of the blood -This has the effect of pulling water from the interstitial space, making more water available in the blood and causing the kidneys to compensate by removing it as urine |
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Mannitol administration
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-Mannitol is an osmotic diuretic, it elevates blood plasma osmolality, and results in enhanced flow of water from tissues to plasma, as a result of osmosis (water flow from high to low concentration)
-causes water extraction from intracellular compartments and expanding extracellular fluid volume -A hypertonic crystalloid solution that decreases cerebral edema -diuresis occurs in 15-30min -contraindicated in renal failure, pulmonary edema, CHF, shock -Plasma osmolality- a measure of the concentration of substances, Na, Cl, K, urea, glucose in the blood -Osmolality of blood inc with dehydration -Osmolality of blood dec with overhydration -Administered as a bolus infusion over 10-30min in doses from 0.25-2g/kg body weight -Air Care protocol- 1gm/kg over 5-10min -Use is secondary to use of controlled ventilation to control elevated ICP -If it is administered in large doses there is a significant risk for development of ATN -When mannitol is used during the early resuscitation phase of hypovolemic head injured patients, crystalloid solutions are infused simultaneously to correct Hypovolemia -Crystalloid fluid administration facilitates rapid renal excretion of mannitol, preventing renal failure |
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Respiratory support
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-Mean airway pressure is the leading factor affecting ICP in the patient who is ventilated
-Positive airway pressure is transmitted to the intracranial cavity through the midiastinum -Hypocapnia is an effective way to reduce CBF because of its strong vasoconstrictive effect on the cerebral arteries -Extreme hyperventilation which causes hypocapnia, is believed to cause secondary ischemia by constricting cerebral vasculature -Hyperventilation may become necessary for brief periods when there is acute neurological deterioration, or if increased ICP is refractory to sedation, paralysis, CSF drainage, and osmotic diuresis |
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Analgesia and sedation
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In patients with a severe head injury, pain meds and sedatives are used to:
-Reduce agitation, discomfort, and pain -Facilitate mechanical ventilation by suppressing coughing -Limit responses to stimuli such as suctioning, which my increase ICP |
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Anesthetic
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-Propofol is administered to decrease agitation, may decrease CBF, ICP, CPP, can be discontinued for frequent neurological exams, side effects include hypotension
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ANEURYSMS = ARACHNOID
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ANEURYSMS = ARACHNOID
-A round saccular dilation of the arterial wall that develops as a result of weakness of the wall |
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Aneurysm Pathophysiology
Pathophysiology |
-A defect in the smooth muscle layer, or tunica media, allows the endothelial lining to bulge through, creating an aneurysm
-Hemorrhage from an aneurysm usually occurs in the subarachnoid space because aneurysm forming vessels usually lie in the space between the arachnoid layer of the meninges and the brain -The force of the rupturing vessel can be so great that it can push blood through the pia mater and into the brain substance, causing an intracerebral hemorrhage -It can also push through the arachnoid into the subdural space causing a subdural hemorrhage |
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Aneurysm Clinical manifestations
Aneurysm |
-Some patients have some warning signs before an aneurysm ruptures
-Headaches, lethargy, neck pain, noise in the head -After an aneurysm has bled or ruptured the patient usually complains of a horrific headache -May be a decrease in LOC, visual disturbances, hemiparesis, hemiplagia, and vomiting -With an SAH, there are signs of meningeal irritation, stiff and painful neck, photophobia, blurred vision, irritability, fever, positive kernigs sign and positive brudzinskis sign -Bleeding stops because ICP in the subarachnoid space reaches MAP quickly, stopping the bleeding long enough for the rupture to seal -When there is blood in the subarachnoid space, it irritates the brainstem, causing abnormal activity in the autonomic nervous system, often with cardiac arrhythmias and HTN -aneurysmal rupture can cause indirect damage to the myocardium, results from the sudden rush of catecholamines that accompanies aneurysmal ruptures -pt are at further risk for development of vasospasm -vasospasm occurs when blood comes into contact with the outside walls of the brains arterial blood supply |
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-Some patients have some warning signs before an aneurysm ruptures
-Headaches, lethargy, neck pain, noise in the head -After an aneurysm has bled or ruptured the patient usually complains of a horrific headache -May be a decrease in LOC, visual disturbances, hemiparesis, hemiplagia, and vomiting -With an SAH, there are signs of meningeal irritation, stiff and painful neck, photophobia, blurred vision, irritability, fever, positive kernigs sign and positive brudzinskis sign -Bleeding stops because ICP in the subarachnoid space reaches MAP quickly, stopping the bleeding long enough for the rupture to seal -When there is blood in the subarachnoid space, it irritates the brainstem, causing abnormal activity in the autonomic nervous system, often with cardiac arrhythmias and HTN -aneurysmal rupture can cause indirect damage to the myocardium, results from the sudden rush of catecholamines that accompanies aneurysmal ruptures -pt are at further risk for development of vasospasm -vasospasm occurs when blood comes into contact with the outside walls of the brains arterial blood supply |
-the blood acts as an irritant, which causes a reflexive spasm of the smooth muscle in the vessel wall, causing marked decrease in the diameter of the vessel lumen
-lysed RBCs release Ca ions which are believed to be mediators for spasm -vasospasm can cause severe hypoperfusion to all distal tissue fed by the affected arterial structures -vasospasm do not occur in all cases of SAH -vasospasm do not occur in cases of traumatic SAH -CCB are being utilized in an effort to decrease the incidence and severity of vasospasm in pt with SAH -arterial vasospasm results primarily from prolonged smooth muscle contraction -CCB blockers may alleviate the abnormal contraction of vascular smooth muscle that may contribute to vasospasm -Calcium ions regulate contraction in smooth and cardiac muscle -CCB inhibit the movement of Ca ions across myocardial and vascular smooth muscle -this leads to decreased myocardial contractility and decreased myocardial oxygen demand |
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Aneurysm management
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-CCB are being utilized in an effort to decrease the incidence and severity of vasospasm in pt with SAH
-arterial vasospasm results primarily from prolonged smooth muscle contraction -Calcium ions regulate contraction in smooth and cardiac muscle -CCB inhibit the movement of Ca ions across myocardial and vascular smooth muscle -this leads to decreased myocardial contractility and decreased myocardial oxygen demand -CCB also improve coronary blood flow via direct smooth muscle relaxation -they also cause peripheral vasodilation from direct smooth muscle relaxation -Diltiazem administered at initial bolus of 0.25mg/kg IV over 2min -followed by infusion of 10mg/hr -vasospasm are heralded by deterioration of the pt neuro exam -often present as increasingly erratic or impulsive behavior in the otherwise cognitively intact pt -treatment of vasospasm is primarily intended to ensure adequate perfusion -triple H therapy helps force blood into areas that are being hypoperfused -aneurysmal rupture can cause indirect damage to the myocardium -caused by the sudden rush of catecholamines that accompanies aneurysmal rupture |
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Aneurysm management cont
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-Triple H therapy is the standard
-Consists of hypervolemic expansion, hemodilution, and induced hypertension: -Hypervolemia is accomplished by volume expansion, given to increase intravascular volume and decrease blood viscosity, cerebral vessels dilate and the MAP increases, thereby improving CPP -Hemodilution through the administration of IV fluid decreases blood viscosity, increases regional CBF, and may decrease infarction size and increase oxygen transport -Vasopressors are used to induce HTN, the objective is to maintain SPB at greater than 20mmHg over normal -Blood viscosity- is a measure of the resistance of blood to flow thru -Viscosity of blood depends on the viscosity of the plasma, in combination with the hematocrit -Viscosity is thickness, water is thin having a low viscosity, while honey is thick having a higher viscosity -Hematocrit- is the proportion of blood volume that is occupied by RBCs -Plasma viscosity- is determined by water content a large molecule components -When hematocrit rises its flow through blood viscosity vessels is greatly retarded because of inc resistance to flow -Plasma- liquid component of blood, mostly water about 90%, and contains proteins , glucose, clotting factors, hormones, C02 |
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STROKE
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-Ischemic brain injury occurs when arterial occlusion lasts longer than 2-3hrs
-A stroke occurs when there is a disruption of blood flow to a region of the brain -Ischemic can be thromobolic or embolic -Hemorrhagic can be intracerebral or subarachnoid |
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Circle of willis
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-majority of the population is the region of the brain perfused by the left middle cerebral artery (left MCA)
-the MCA's on both sides of the circle of willis are responsible for perfusing the majority of the lateral aspects of the frontal, temporal, and parietal lobes -the speech centers of the brain are contained in the left MCA distribution of the temporal lobe in all patients who are left hemisphere dominant -damage to the speech centers of the brain may result in the inability to express or understand speech. -the majority of the population has left hemisphere dominance -all persons with right handed dominance and roughly 75%-85% of people with left handed dominance are left cerebral hemisphere dominant |
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Circle of willis
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-middle cerebral artery MCA: perfuses frontal lobe, lateral aspects of the temporal and parietal lobes, proximal or total MCA occlusion will cause contralateral hemiplegia, global aphasia, facial weakness, ipsilateral gaze toward the lesion
-anterior cerebra artery ACA: perfuses the medial aspects of the temporal and parietal lobes and frontal lobes, occlusion causes contralateral lower extremity weakness, as well as intellectual and behavioral changes -posterior cerebral artery PCA: involvement of the occipital lobe can contribute to visual or visual accessory loss, including the loss of ability to see in all quadrants of the visual field -vertebral and basilar arteries: varying degrees of motor and sensory loss can occur, infarction of the entire pons can result in a phenomenon know as locked in syndrome -cerebellar arteries: causes both contralateral and ipsilateral patterns of ataxia, motor weakness, sensory deficits, an vertigo |
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Hemisphere involvement
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left hemisphere
-the speech centers of the brain are contained in the left MCA distribution of the temporal lobe in all patients who are left hemisphere dominant -damage to the speech centers of the brain may result in the inability to express or understand speech. -motor deficits on the right side -language deficits, right visual deficits -slow cautious behavior -severe anxiety, intellectual impairment, of frustration and depression Right hemisphere -motor deficits on the side -left visual field deficits -spatial deficits -denial, poor judgment, distractibility, unconcerned over losses |
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Stroke pathophysiology
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-on a cellular level, ischemia causes a transition to anaerobic metabolism, which produces damaging by products such as lactate
-anaerobic glycolysis does not generate sufficient ATP to provide energy for the active transport of the Na-K pump across the cell membrane, and hence intracellular accumulation of Na occurs. -extracellular water moves into the cell to maintain the osmotic gradient, and cellular edema and death occur -Cerebral ischemia is a complex process that depends on the severity and duration of the decline in CBF -The goal of acute stroke management is to salvage the ischemic penumbra or the territory at risk -penumbra, is a region of tissue that will become necrotic after an infarct occurs if perfusion is not restored -A stroke caused by an embolus may be a result of blood clots, fragments of atheromatous plaques, lipids, or air, most often have a cardiac source -If hemorrhage is the etiology of a stroke, HTN often is a precipitating factor -Thrombotic strokes often are caused by atherosclerosis, there is risk of a future stroke in a pt who already has had one |
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Stroke management
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-Management of an ischemic stroke comprises four primary goals:
1. Restoration of CBF 2. prevention of recurrent thrombosis 3. neuroprotection 4. supportive care |
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Pharmacological management for strokes
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-primary purpose of fibrinolytic therapy is the dissolution of thromboembolic clots that have caused infarction of tissue perfused by the vessel that hey have occluded
-Tissue plasminogen activator- is a protein involved in the breakdown of blod clots, as an enzyme it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown -t-PA may be manufactured using recombinant technology, and referred to recombinant tissue plasminogen activator (r-tPA) -recombinant tissue plasminogen activator (r-tPA)- includes activase (alteplase), retavase (retaplase), TNKase (tenecteplase) -A major risk of this therapy is intracerebral hemorrhage -Thrombolytic agents are exogenous drugs that dissolve clots -IV thrombolytic therapy should be initiated within 3hrs or less of the onset of neurological symptoms -The clock begins for the pt from the time he or she was last seen well -A dose of Activase, (t-PA) at 0.9mg/kg is administered as 10% of the total dose as a bolus over 1-2 minutes, with the remainder infused over 60min -Dose of retavase, 10units IV x 2, 2nd dose given 30min after 1st |
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PRIMARY HEAD INJURIES
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-Primary injury is the result of the initial injury
-Causes disruption of the electrical, chemical, and physical integrity of the cells in the area, leading to cell death -Secondary injury encompasses the physiological response to brain injury, including cerebral edema, cerebral ischemia, biochemical changes, and changes in cerebral hemodynamics |
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Skull fractures
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-Depressed skull fractures are fractures in which bone is pressed into the dura
-Injury to the dura places the pt at risk for meningitis -Basilar skull fracture occur at the base, or floor, of the skull -Assessment of extraocular movements is important in detecting the impingement or damage of cranial nerves that can become entrapped in a basilar skull fracture -Drainage of CSF from the ear or nose indicates injury to the dura -Ecchymosis (bruising) behind the ear (battles sign) is a delayed sign of a basilar skull fracture |
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Epidural hematoma
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-A collection of blood located between the dura and the inner table of the skull
-Usually caused by laceration of an extradural artery -Accumulate rapidly because of arterial bleeding -May initially lose consciousness, regain consciousness, and then rapidly deteriorate to unconsciousness -Posturing and unilateral dilation of the pupil represent late signs of cerebral herniation |
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Subdural hematoma
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-An accumulation of blood below the dura and above the arachnoid covering of the brain
-Tearing of the surface veins or disruption of venous sinuses can causes a subdural hematoma -Acute subdural hematoma manifest symptoms within 24-48hrs after injury -Symptoms include worsening headache, focal neurological deficit, unilateral papillary abnormalities, and a decreased LOC -Subacute subdural hematoma are associated with an onset of symptoms 2 days to 2 weeks -Chronic subdural hematoma may experience an initial small bleed that does not cause symptoms -Over time slow capillary leaking causes expansion of the mass and produces symptoms of increased ICP |
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Intracerebral hematoma
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-A collection of blood within the brain tissue
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Traumatic subarachnoid hemorrhage
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-Occurs with tearing or shearing of microvessels in the arachnoid layer where CSF flows around the brain
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Diffuse axonal injury
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-Occurs with tearing or shearing of microvessels in the arachnoid layer where CSF flows around the brain
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SECONDARY BRAIN INJURY
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-Encompasses all events leading to further brain damage that occur after the initiating trauma
-The mechanisms by which functional neurons are endangered include inflammation, ischemia, and CBF disturbances -Prevention of hypotension, hypercarbia, hypoxemia, and seizures is extremely important -Cerebral autoregulation is a protective mechanism that enables the brain to achieve a constant blood flow over a range of fluctuating systemic blood pressures |
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Cerebral edema
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-Commonly occurs in patients with head injuries 24-48hrs after the primary insult and typically peaks at 72hrs
-Cytotoxic edema occurs as the intracellular Na-K pump fails, allowing an influx of Na and water into the cell and an efflux of k -Vasogenic edema occurs with a disruption of the blood brain barrier, can occur as a result of injury or a surgical procedure |
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Ischemia
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-Occurs whenever blood flow is either diminished or inadequate to meet metabolic demands
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Herniation syndrome
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-A state in which cerebral structures shift inside the cranium under high pressure
-Cushing’s triad describes the three late signs of herniation: -Increased BP, decreased HR, and an irregular respiratory pattern -Herniation of the medial temporal lobe through the tentorium is termed uncal herniation -Uncal herniation often produces unilateral pupillary dilation from compression of the third cranial nerve, with contralateral hemiplegia or posturing -Changes in vital signs are often a late sign -Tonsillar herniation describes the downward displacement of the cerebelar tonsils through the foramen magnum -Clinical signs include LOC early, respiratory changes and arrest, flaccid paralysis, neck pain head tilt |
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Comatose state
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-Divided into three levels of reflex motor activity:
-Decorticate state the pt is unconscious and gives no evidence of awareness, flexion of the arms occurs, this posturing may occur spontaneously or by painful stimuli, can indicate damage to the midbrain -Decerebrate posturing shows extensor rigidity on all four extremities, indicates brain stem damage, and lesion in the lower brain -Progression from decorticate to decerebrate is often indicative of uncal herniation -Flaccid patients have no motor response to painful stimuli |
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Head injury management
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-Airway management is a crucial initial step in providing care to the head injured patient because hypoventilation is common with a decreased LOC, and hypoxia and hypercarbia are extremely detrimental
-Initial mechanical ventilation strategies aim to maintain normal ventilation or a PaC02 within normal limits 35-45 -Further evaluation of neurological status may reveal the need for hyperventilation therapy if signs of cerebral herniation are present -Management of circulation in patients with head injuries aims to promote adequate cerebral perfusion through fluid resuscitation and the use of vasopressors if necessary -Hypertension in head injuries is compensatory and required for survival -Uncontrolled hyperventilation promotes vasoconstriction, and the entire brain becomes vasoconstricted, preventing adequate blood delivery to uninjured parts of the cerebrum, resulting in secondary brain injuries |
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Head injury management cont
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-Only controlled hyperventilation is allowed with use of anesthesia
-Should be used to alter acid-base status to alkolotic end of normal pH -Controlled hyperventilate the CO2 to get the pH around 7.45 and C02 32-35 -Head injury pt’s should remain properly hydrated and adequately perfused -TBI management includes hyperventilating to alkolotic state, BP supported with pressors to support perfusion needs -Triple – H involve hypertension, hypervolemia, hemodilution -Coordinate with pilot in reference to climb rate, cabin pressurization and takeoff/landing procedures to limit ICP spikes -Provide neutral alignment with 15-30 degree reverse trendelenburg positioning (inclined) -Provide protection from noxious stimuli |
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Maintaining cerebral perfusion
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-CPP can be managed either by decreasing ICP or increasing MAP
-Aggressive management of increased ICP is attempted with the overall goal of maintaining the CPP |
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Protocol: Acute ischemic stroke
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-consider reducing BP for MAP >130
-do not reduce more than 10-20% |
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Protocol: Intracranial bleeding traumatic in nature
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-treatment of BP should be with a physician order
-obtain parameters -treatment considered until MAP is consistently over 130 -nipride is not an appropriate medication |
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Protocol: Spontaneous bleeds or space occupying lesions
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-maintain in range of 70-130
-for SAH bleeds first treat with pain and or sedation -then reduce BP if MAP >130 consistently over 10min |
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Protocol: Nicardipine
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-medication blocks the movement of calcium into the smooth muscle cells surrounding the arteries of the body and the heart
-Since calcium promotes contraction of muscle, blocking calcium entry into the muscle cells relaxes the arterial muscles and causes the arteries to become larger. -This lowers blood pressure, which reduces the work that the heart must do to pump blood to the body. Reducing the work of the heart -also it leads to decreased myocardial contractility and decreased myocardial oxygen demand -contraindicated with sensitivity, and advanced aortic stenosis -onset is several minutes -mix 25mg/250ml D5W -initiate 5mg/hr -titrate q 10min -increments of 2.5mg/hr to desired MAP -max dose 15mg/hr |
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Protocol: Mannitol
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-see mannitol section above
-use is secondary to use of controlled ventilation to control elevated ICP -1gm/kg over 5-10min |
