MED SURG FINAL EXAM Guide
MED SURG FINAL EXAM Guide
Neuro:
Constricted pupils= miosis dilated pupils= mydriasis
Patient has unequal pupils
... [Show More] first ask for baseline.
Always assume neuro problem until proven otherwise.
Assess patients spo2 and glucose levels if patients appears altered. Hypoxia and hypercapnia will affect mental status.
Medical management for pt with altered LOC→
● Airway! -Intubation may be required
● Circulation-Maintaining BP (MAP >60), HR, Perfusion of brain, IV access – IVF, meds
● Nutrition- OGT (oral gastric tube), PEG
● With inc ICP do not want to give hypotonic solutions /D5W only hypertonic such as Mannitol to draw fluid out of cells
● Potential complications of altered LOC→
○ Pneumonia (aspiration PNA), Aspiration, Pressure ulcer, DVT, Contractures (not using muscles so muscles can shorten) need to do passive ROM to help preserve joint mobility
ICP→
● Monro-kellie hypothesis: Bleeding or swelling within the skull INC the volume of contents within the skull and therefore causes increased ICP. CAN LEAD TO IRREVERSIBLE BRAIN DAMAGE
○ ICP is pressure from the CSF and blood volume and cranial contents (dynamic equilibrium) normal ICP is 5-15mmHg
○ Inc ICP from head trauma (>15mmHg)
○ Whenever there is a shift, it can cause inc ICP
○ Our body compensates by pouring out CSF
○ When body cannot compensate, pressures are elevated above 15
○ Patient will be in cheyne stokes breathing: very irregular breathing
● Complications→
○ Compensation to maintain normal ICP is normally accomplished by shifting or displacing CSF
○ With disease or injury ICP may increase
○ Increased ICP
■ decreases cerebral perfusion ischemia, cell death, and (further) edema
○ Brain tissues may shift through the dura (outermost layer of brain and spinal cord) and result in herniation
○ Autoregulation: refers to the brain’s ability to change the diameter of blood vessels to maintain cerebral blood flow (via vasomotor center)
○ CO2 plays a role:
■ decreased CO2 results in vasoconstriction
■ increased CO2 results in vasodilation
○ Chemoreceptors sense CO2, blood acidity, to try to maintain normal cerebral perfusion
● Vasomotor center:
○ ANS that regulates SNS and PNS
○ Inc ICP can be injury to vasomotor center that can cause high BP, low HR
○ Baroreceptors are pressure centers that monitor BP
○ If pt is retaining CO2, (COPD, not breathing bc of opioid overdose) causes vessels in brain to dilate, if vessels are dilated it causes more blood flow and volume into cranial vault that only has so much room to take in volume
○ When you blow off CO2 it causes vessels to constrict
● Cerebral edema →
○ Inc ICP= dec perfusion which leads to tissue hypoxia In brain which leads to cerebral edema which worsens ICP
○ One way that brain tries to compensate is the body inc BP to get blood flow to the ischemic brain tissue to try to maintain cerebral perfusion
● ICP and CPP→
○ CPP (cerebral perfusion pressure) is closely linked to ICP
○ CPP = MAP (mean arterial pressure) – ICP
○ Normal MAP is 70 – 110 mmHg (average pressure within arteries during one cardiac cycle)
○ MAP MAP = SBP + (DBP X 2)/3
○ Normal ICP is 5 – 15 mmHg
○ Normal CPP is 70 to 100mmHg
○ Heart dysrhythmias can lower CPP.
○ A CPP of less than 50 can result in permanent neurologic damage
■ Dec blood flow to brain tissue
○ Need a CPP > 70 to maintain adequate tissue perfusion
● Increased ICP→
○ Early signs→
■ EARLIEST SIGN – CHANGE IN LOC
■ Restlessness, agitation, sudden quietness, disorientation, mental fog (confusion, forgetfulness, repetitive questioning, slowing of speech,)
■ increased resp. effort, purposeless movements, Pupillary changes, impaired EOM (effects of pressure on midbrain/brainstem (CN II, III, IV, VI)
■ Weakness in one extremity or on one side of the body
■ Headache that is constant, increasing in intensity and aggravated by movement or straining
○ Late signs=vasomotor problems→
○
■ Continued deterioration of LOC, Erratic pulse and RR (or may decrease), BP & temp increase, Widening pulse pressure, Altered breathing patterns, Projectile vomiting, Hemiplegia, Abnormal posturing, Bilateral flaccidity before death, Loss of brain stem reflexes: pupillary, corneal, gag, swallowing (their loss is an ominous sign of approaching death)
○ The RAS system is what gives us our alertness and wakeful state
○ Monitor for cushing’s triad = LATE SIGN OF INC ICP→ Dec resp, low HR, systolic hypertension (widening pulse pressure)
■ Monitor CLOSELY for complications: brain stem herniation, DI, SIADH, cerebral edema, hypoxia, hypercapnia, impaired venous return, increases in intrathoracic pressures or abdominal pressures
■ Occurs due to so much pressure building up within cranium that blood and brain tissue needs to go somewhere so it starts to herniate
■ High pressure→ low pressure
■ HR dec bc of reflex bradycardia due to baroreceptors
■ Has widening pulse pressure
■ May have issues with regulating temp bc of hypothalamus
■ If this does not get fixed they can go into autonomic dysreflexia – autonomic dysfunction
● Management for ICP→
○ Decreasing cerebral edema
■ IV mannitol – osmotic diuretic to dehydrate brain tissue; monitor I&O & serum osmolality to assess hydration
■ Decadron (steroid) - if edema caused by brain tumor
■ Fluid restriction
○ Maintaining CPP
■ manipulating CO with fluidS
■ Inotropics (Dobutamine, Levophed) to maintain CPP >60/ 70 mmHg
○ Reduce CSF & Intracranial Blood Volume
■ CSF drainage via ventriculostomy
■ Keep pCO2 35 – 38 (low pCO2 produces cerebral vasoconstriction (induce hyperventilation)
○ Maintain Oxygenation & Reduce Metabolic Demands [Show Less]