Final Exam Med-Surg 2 PDF

ICP: 9 Head Injury: 7 Spinal Cord Injury: 8 Seizures: 7 Stroke: 11 Sepsis-Shocks: 12 Acute Coronary Syndromes: 8 Dysrhythmias: 4 Heart Failure: 8 Respiratory/Vents: 6 Intracranial Pressure (ICP) 9 Q - Cerebrospinal fluid (CSF): 10% - Intravascular blood: 12% (arteries, veins and capillaries...

ICP: 9 Head Injury: 7 Spinal Cord Injury: 8 Seizures: 7 Stroke: 11 Sepsis-Shocks: 12 Acute Coronary Syndromes: 8 Dysrhythmias: 4 Heart Failure: 8 Respiratory/Vents: 6 Intracranial Pressure (ICP) 9 Q - Cerebrospinal fluid (CSF): 10% - Intravascular blood: 12% (arteries, veins and capillaries) - Brain tissue: 78% → Any changes in any of these volumes will cause changes in the pressure in the brain 1. ICP: what is it, what are normal ranges ICP (Intracranial Pressure) is the pressure exerted by the contents within the skull: brain tissue, cerebrospinal fluid (CSF), and blood. The balance of these components is critical for maintaining normal ICP. Normal ICP range: 5 to 15 mmHg. - Elevated: 20 mmHg need treatment Q: What is a priory finding with ICP/ Head injury? Change in mentation (LOC) Decorticate: Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities Decerebrate: All four extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet (worst) Cushing’s Triad:( Late) Increase of Systolic blood pressure and Diasyslic is low Decrease heart rate, decrease RR (abnormal) Reflex (postive) Babinski (toes fen out) Unconscious… late Seizures Headache Emesis (vomiting w/out nausea) Deterioration of moter function hemiplegia (weakness of one side of the body) 2. Calculating CPP Cerebral Perfusion Pressure (CPP) is the pressure needed to ensure adequate blood flow to the brain and is calculated using the following formula: CPP=MAP−ICP Where: MAP (Mean Arterial Pressure) =(2×Diastolic BP)+Systolic BP​/3 ICP (Intracranial Pressure) is measured in mmHg. A normal CPP range is typically 60-100 mmHg. Lower CPP values (below 50 mmHg) can lead to ischemia and inadequate brain perfusion. Other words when cpp falls too low the brain is not perfused and brain tissue dies Q: A 70 yr old patient came into the ED after he hit his head from a ladder fall. He is now in the Neuro ICU with altered LOC. His BP is 152/80 mm Hg, HR 82 bpm, RR 14 breaths/minute, and Temp 98.9° F. ICP monitor shows 42mmHg. What is his CCP? BP: 144/54 MAP= SBP + 2 (DBP) 3 Step 1: 144+ 2(54)=252 Step 2: 252 ÷ 3=84 Step 3: CPP=MAP-ICP 84-40= 44 Answer: CPP 44mmHg Other example: Practice: A 70 yr old patient came into the ED from a car accident where he hit his head on the windshield. He is now in the Neuro ICU with altered LOC. His BP is 144/54 mm Hg, HR 76 bpm, RR 12 breaths/minute, and Temp 98.9° F. ICP monitor shows 40mmHg. What is his CCP? 2x54= 108 108+144=252 252/3= 84 mmhg 3. NGT and OGT related to head injuries NGT (Nasogastric Tube) and OGT (Orogastric Tube) are often used in patients with head injuries for feeding, administering medication, and preventing aspiration. They are inserted when the patient is unconscious or unable to swallow safely. Both tubes can increase ICP if improperly inserted or if there is an increased abdominal pressure (e.g., during tube feeding). OGT may be preferred in cases where nasogastric placement is not possible or when there is facial trauma, as it avoids sinus issues. Note that in cases where a basilar skull fracture is suspected, an orogastic tube should be inserted rather than a nasogastic tube 4. Ventriculostomy: purpose and management Ventriculostomy is a procedure where a catheter is inserted into one of the ventricles of the brain to monitor ICP and drain excess CSF in cases of increased ICP. This procedure is used to manage hydrocephalus, severe head injuries, or conditions causing raised ICP. Management involves: Ensuring the catheter is correctly placed and functioning. Monitoring ICP readings regularly. Ensuring the drainage system is set at the correct height (usually at the level of the tragus of the ear). Preventing infection by keeping the system sterile and closed. Carefully regulating drainage to avoid over-draining and causing hypotension. CSF can be drained via a ventriculostomy when ICP exceeds the upper pressure parameter set by the physician. Intermittent drainage involves opening the three-way stopcock to allow CSF to flow into the drainage bag for brief periods (30 to 120 seconds) until the pressure is below the upper pressure parameters. ICP, Intracranial pressure Q: What is ventriculostomy and what is it indicate for? Monitoring ICP, brain perfusion and treatment if drain in is indicated 5. ICP & hyponatremia: effects and treatment Hyponatremia (low sodium levels) is a common complication in patients with increased ICP. It can occur due to SIADH (Syndrome of Inappropriate Antidiuretic Hormone secretion), which leads to excessive water retention, diluting the sodium concentration in the blood. Effects of Hyponatremia: It can exacerbate brain edema and increase ICP, leading to more severe symptoms like confusion, seizures, and coma. Treatment: Management includes: Monitor for DI (decrease in ADH) results increased U/O and delusional hyponatremia → cerebral edema, Sz., change in LOC Monito and minimize increases in ICP Restricting fluids to prevent further dilution of sodium. Administering hypertonic saline (e.g., 3% NaCl) to raise sodium levels gradually. Monitoring sodium levels closely to prevent rapid changes that could cause damage. Q: A patient with ICP has serum sodim level of 120 mEq/L. She is complaining of H/A and is increasingly somnolent. What do you expect to give? —---> IV Hypertonic Saline 6. Nursing interventions to improve cerebral perfusion 1. Maintain head in the midline position, prevent extreme neck flexion 2. HOB elevated appropriately, not greater than > 30 - Promotes drainage from the head and decreases cerebral edema - Raising the head of the bed above 30 degrees may decrease the cpp by lowing systemic BP 3. Turn slowly  4. Avoid coughing, straining, Valsalva →Increases intrathoracic pressure contributes to increases ICP by impeding the venous return. 5. Avoid hip/neck flexion: decrease the risk of raising the intra-abdominal pressure, which increases ICP Psychologic considerations: esp. For family. Provide support education using the simplest explanation (e.g) Ventriculostomy: (“The catheter in his head tell us about his blood flow to brain”) 7. Effects of mannitol Mannitol is an osmotic diuretic used to reduce ICP. It works by drawing fluid out of the brain and into the bloodstream, which is then excreted by the kidneys, thereby decreasing cerebral edema. Effects: plasma expansion omotic effect monitor fluid and electrolyte status Reduces ICP by creating an osmotic gradient that removes excess water from brain tissue. Improves cerebral perfusion by increasing blood volume and reducing brain swelling. Side effects can include dehydration, electrolyte imbalances (especially hypokalemia), and renal dysfunction. It is important to monitor renal function and fluid balance during therapy. Risk for HF and thirst and renal function Interprofessional Care: Drug Therapy to Decrease ICP 1. IV Mannitol (Osmitrol) : Decreases ICP by osmotic gradient (fluid moves from tissues to blood vessels) Plasma expander: reduces the hematocrit and blood viscosityincreasing CBF and cerebral oxygen delivery. Osmotic diuretic Monitor fluid and electrolyte status 2. Hypertonic saline: Moves water out of brain cells and into blood Monitor BP and serum sodium levels just as effective as mannitol, sometimes used concurrently when caring for severely brain-injured patients. 3. Corticosteroids (e.g., dexamethasone [Decadron])  Action: prevents the formation of proinflammatory mediators, improve neuronal function by improving CBF and restoring autoregulation Vasogenic edema surrounding tumors and abscesses, do not use in TBI Complications with use: hyperglycemia, increased incidence of infections, and GI bleeding * * Monitor fluid intake, serum sodium and glucose levels Concurrent antacids, H2 receptor blockers, proton pump inhibitors More info from slides: Cerebral Blood Flow: Stages of increased ICP Stage 1: Total compensation: accommodation and autoregulation intact Stage 2: ↓ Compensation: compliance is beginning to decrease increase in volume places the patient at risk for ↑ICP and secondary injury. Stage 3: compensatory mechanisms fail, loss of autoregulation, patient will exhibit manifestations of increased ICP (e.g., headache, changes in level of consciousness or pupil responsiveness). With a loss of autoregulation, there is an attempt to maintain cerebral perfusion by the body's attempt to increase systolic BP. decompensation is imminent patient’s response is characterized by systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations (Cushing’s triad)and is a neurologic emergency. Stage 4: herniation occurs: brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure, intense pressure is placed on the brainstem if continues brainstem death is imminent. Cerebral Edema Definition: ↑ accumulation of fluid in the extravascular spaces of brain tissue. Variety of causes: the extent & severity of original insult determines degree of cerebral edema Three types of cerebral edema 1. Vasogenic 2. Cytotoxic 3. Interstitial More than one type may occur in the same patient 1. Cerebral Edema: Vasogenic: Leakage of Fluid from intravascular to extravascular space (Most common type) Occurs mainly in white matter Variety of causes (e.g. Brain Tumors, abscesses, ingested toxins)  Be aware in Neuro pts: headache may seem benign, in cases of cerebral edema, it can quickly progress to coma and death. Be vigilant in your assessment skills. 2. Cerebral Edema: Cytotoxic (“Cell-toxic”) Caused by: Disruption of cell membrane integrity Develops from/Secondary to: destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia and syndrome of inappropriate antidiuretic hormone (SIADH) secretion Cerebral edema occurs as a result of a fluid and protein shift from the extracellular space directly into the cells, with subsequent swelling and loss of cellular function 3. Cerebral Edema: Interstitial Cause: Usually result of hydrocephalus Hydrocephalus: build-up of fluid in the brain and is manifested by ventricular enlargement. Excess CSF production, obstruction of flow, or inability to reabsorb Usual treatment: ventriculostomy or shunt Clinical Manifestations: Increased ICP Change in level of consciousness Level of alertness & arousal the most sensitive and reliable indicator of the patient’s neurologic status. Changes in LOC are a result of impaired CBF → oxygen deprivation to the cells of the cerebral cortex and reticular activating system (RAS). Change in consciousness can be dramatic or subtle (ie.Flattening affect) can be associated with coma Change in vital signs: ICP increased/sudden increase Cushing’s triad: systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations Ocular signs Clinical manifestations: increased ICP: Headache Often continuous Nocturnal/worsening in the morning cause for concern and may indicate a tumor or other space occupying lesion that is causing increased ICP.  Straining, agitation, or movement may accentuate the pain. Not always treated with Acetominophen (Tylenol) may be more effective to use IV solutions (Mannitol or Hypertonic Saline) Diagnostic studies CT scan/MRI PET: ID the cause of the increased ICP NO LUMBAR PUNTURE: cerebral herniation could occur from the sudden release of the pressure in the skull from the area above the lumbar puncture. Interprofessional Care: Drug Therapy that decrease metabolic demands of brain 1. Antiseizure medications: prophylactic or treatment if Sz. present 2. Antipyretics: for temps >38, strict maintenance of 36°-37° May need concurrent cooling measures but avoid shivering causes increased metabolic workload 3. Sedatives: to “calm” 4. Analgesics: for pain 5. Barbiturates: High doses (e.g., pentobarbital [Nembutal], thiopental [Pentothal]) for patients with increased ICP refractory to other treatments. Barbiturates decrease cerebral metabolism Non-pharmacological: quiet and calm environment with minimal noise and interruptions. Observe the patient for signs of agitation, irritation, or frustration. Also teach the caregiver and family about decreasing stimulation. Coordinate with the interprofessional team to minimize procedures that may produce agitation. Brain Injury Q7 8. Concussion discharge instructions report: headache that worsens or doesnt go away, nausea, uncontrolled vomiting, increased confusion, change of personality, drowsiness/inability to wake up, slurred speech, weakness, numbness, seizures, loss of consciousness, - ensure rest then gradually return to regular activities - ibuprofen or acetaminophen for headaches Seizure disorders: May/may not develop, if so usually in the 1st week. Mental and emotional difficulties: TBI may accompany personality changes, memory/concentration issuesprovide referrals as needed Progressive recovery - Family participation and education discharge planning: patient, caregiver, and family need specific posthospitalization instructions to avoid family- patient friction. - Special “no” policies appropriate: suggested by: No driving no drinking of alcoholic beverages, no driving, no use of firearms, no working with hazardous implements and machinery, and no unsupervised smoking Seizure Disorders: Possible but rare; may occur within the first week post-injury. Monitor for signs. Mental and Emotional Difficulties: Traumatic brain injury (TBI) can cause personality changes and issues with memory or concentration. Provide referrals to counseling or therapy as needed. Progressive Recovery: Emphasize the gradual return to normal activities, understanding that recovery timelines vary. Family Participation and Education: Discharge planning should include caregivers and families to prevent friction and misunderstandings. Special “No” Policies: Recommendations include avoiding driving, alcohol, firearms, hazardous machinery, and unsupervised smoking​ 9. Signs and symptoms of a subdural hematoma Subdural hematoma: bleeding between dura mater and arachnoid, usually results frominnjury to the brain tissue and its blood vessels. Acute: Develops within 24–48 hours. Symptoms include decreased LOC, headache, and possibly a dilated and fixed ipsilateral pupil if severe. Subacute: Develops over 2–14 days and may expand due to fluid buildup. Chronic: Develops weeks to months later, especially in older adults. Symptoms mimic those of aging: confusion, lethargy, and memory loss​ Diagnostic studies 1. CT scan: Best diagnostic test to determine craniocerebral trauma; rapid allowing for rapid intervention. 2. MRI, PET: MRI scan is more sensitive than the CT scan in detecting small lesions, but study takes time. 3. Transcranial Doppler studies: allow for the measurement of cerebral blood flow (CBF) velocity Cervical spine x-ray 4. Glasgow coma scale (GCS)  5. A cervical spine x-ray series, CT scan, or MRI of the spine may also be indicated since cervical spine trauma often occurs at the same time as a head injury 10. Blood thinners and head injuries Blood thinners (e.g., warfarin) increase the risk of intracranial bleeding. Patients should be monitored closely for delayed signs of hematoma, especially after falls or trauma 11. Battle’s signs and racoon eyes. Battle’s Sign: Ecchymosis→Bruising behind the ears, indicating a basilar skull fracture. Raccoon Eyes: Ecchymosis→Bruising around the eyes, also suggestive of a basilar skull fracture. These signs may accompany CSF leakage (from the nose or ears), increasing the risk of meningitis​ 12. Emergent interventions for epidural hematomas Neurological emergency requiring immediate surgical intervention. Symptoms: Unconsciousness, followed by a lucid interval and then deterioration in LOC, headache, nausea, and vomiting. Prepare for rapid surgical evacuation and monitor for increased ICP 13. CSF: how to verify presence of Glucose Test: Use Dextrostix to check for glucose (positive in CSF). Blood in the fluid may render this test unreliable. Halo Test: Allow fluid to drip onto gauze; a yellow halo around the blood suggests CSF​ 14. Glasgow coma score: know how to score Measures eye-opening (1–4), verbal response (1–5), and motor response (1–6). Total score ranges from 3 (deep coma) to 15 (normal). Example: Eyes open to sound (3), incomprehensible speech (2), withdraws to pain (4) → GCS = 9​ 15. Blood thinners and trauma patients Trauma patients on anticoagulants face higher risks of complications such as hematomas. Early imaging and cautious reversal of anticoagulation are often needed​ Potential for increased hemorrhage if on anticoagulants (think: older population &mFalls) 16. Discharge teaching with concussion victims Reinforce avoiding high-risk activities (e.g., sports, alcohol, or strenuous tasks). Educate on signs of worsening conditions, such as severe headaches, confusion, repeated vomiting, or seizures. Encourage follow-ups for ongoing evaluation of cognitive and emotional symptoms​ 17. Delegation in the neuro ICU VS (routine) setting up room feeding (oral and pt can chew) walk to bathroom (if pt allowed and stable) Side notes: Craniotomy: Temporary removal of bone (skull) w/replacement (Ex. Tumors) Craniectomy: Removal of bone (skull) not immediately replaced (Ex. Emergent TBI) Cranioplasty: Replacement of bone regardless of craniotomy/craniectomy Spinal Cord Injury (SCI) Q:8 18. Neurogenic shock. Signs and symptoms. What unique features does it have that is not typically found in other shocks? Signs/Symptoms: Hypotension (less than 90 mmHg) , bradycardia, and temperature dysregulation (due to loss of sympathetic tone)​. Unique Features: Bradycardia (compared to tachycardia in other types of shock) and warm, flushed skin due to peripheral vasodilation​ Occurs within 30 mins of SCI (T5 or above) Can last 1-3 weeks Affects sympathetic chain of ANS: lead to profound vasodilation and blood pooling in their periphery, profound hypotension and bradycardia, inability to regulate body temp (poikilothermia), hypovolemia, decreased CO 19. Neuro assessment possible findings with cervical spine injuries. Findings can include paralysis/weakness in all four extremities (tetraplegia), respiratory insufficiency (due to C3-C5 involvement), and sensory deficits below the injury Tetraplegia (paralysis of four extremities) Loss of resp muscle function Resp insufficiency: loss of phrenic nerve innervation to the diaphragm, decreased strength in chest and abd wall, require intubation Ineffective cough Ortho hypo: lightheadedness, dizziness, nausea Q: What is the biggest concerns with Cervical injuries above C5? Answer: Respiratory compromise 20. Functional limitation with cervical spine injury Tetraplegia: Dependency on assistive devices, impaired respiratory function (especially above C3), and significant challenges in mobility and self-care​ thoracic injury - risk for paraplegia - advocate for full independence and self care in a wheelchair Q: What are potential Thoracic injury-paraplegia patients able to do? Answer: Full independence in Self care & in wheelchair Q: Drive using hand-controls Independent standing in standing frame 21. Preventing autonomic dysreflexia. Establish and maintain a bladder and bowel training regimen. Avoid tight clothing and monitor for noxious stimuli such as pressure injuries​ massive UNCOMPENSATED cardiovascular reaction mediated by SNS for SCI at or above T6 Return of reflexes after spinal shock resolved No peripheral or visceral vasodialtion: efferent implses cant pass through injured spinal cord Present most often in chronic phase after SCI  Most common precipitating cause is a distended bladder or rectum - Big preventative intervention: starting bladder and bowel training program acutely continuing into rehab (facility/home) Needs immediate resolution: can lead to status epilepticus, stroke, MI, death 22. Recognizing autonomic dysreflexia Sudden hypertension (SBP 20-40 mmHg above baseline), severe headache, bradycardia, diaphoresis, and piloerection above the injury level​ Hypertension (suspect AD with SBP 20 to 40 mmHg above baseline) Throbbing headache (if reported, check BP) Flushing and marked diaphoresis above level of injury Bradycardia (30 to 40 beats/min) Piloerection Blurred vision or spots in visual field Nasal congestion Anxiety Nausea 23. Intervening for autonomic dysreflexia Actions: Elevate the HOB, remove triggering stimuli (e.g., catheterize to relieve a distended bladder), and notify the provider. Treat hypertension if unresolved Elevate HOB 45 degrees or sit upright Remove stool impaction cause d/t Neurogenic bowel Start bladder and bowel training program acutely continuing into rehab (facility/home) Assess for and remove cause: immediate cath, remove stool impaction, remove constricting cloth/right shoes Notify HCP Monitor and tx BP Monitor VS Q: What is Autonomic Dyreflexia? Massive uncompensated cardiovascular reaction mediated by SNS for SCI at or above T6 Q: What is the most cause? distended bladder or rectum Q: What is the biggest preventative treatment? starting bladder and bowel training program acutely continuing into rehab (facility/home) 24. Promoting independence after SCI: rehabilitation phase (e.g., at home) Focus on physical rehabilitation (mobility aids, wheelchair training), caregiver education, home modifications, and psychological support​ Include EVERYONE in planning 25. Therapeutic psychosocial nursing intervention associated with SCI Include counseling for depression and loss adaptation, setting realistic goals, and involving patients in decision-making​ Q; What is most important when developing a rehabilitation plan for a patient & care givers/family with SCI? Answer: Include them in the plan while maintaining patient’s independence More info Causes: Most related to trauma 38% motor vehicle collisions 30.5% falls 13.5% violence 9% sports injuries Types: primary and secondary injury Primary: DIRECT physical trauma from blunt or penetrating trauma. Spinal cord compression by Bone displacement, Interruption of blood supply, Traction from pulling on cord and Penetrating trauma, causing tearing and transection Secondary: Causes further permanent damage and Begins a few minutes after injury and lasts for months. Causes further permanent damage. Begins a few minutes after injury and lasts for months LEVEL OF INJURY Skeletal level: Vertebral level with the most damage to vertebra and related ligaments Neurologic level: Lowest segment of the spinal cord with normal sensory and motor function on both sides of the body Occur at: Cervical, Thoracic, Lumbar, Sacral. Cervical and lumbar are most common due to greatest flexibility and movement at those areas C1-T1 injury tetraplegia (previously quadriplegia). Paralysis of four extremities. Level of cervical injury determines impairment in the arms Below T2 injury, causing paraplegia. Paralysis and loss of sensation in the legs NCLEX QUESTION The nurse is admitting a patient who has a neck fracture at the C6 level to the intensive care unit. Which assessment findings indicate neurogenic shock? A. Involuntary and spastic movement B. Hypotension and warm extremities C. Hyperactive reflexes below the injury D. Lack of sensation or movement below the injury Seizures (SAFETY) (Q:7) Tonic-clonic seizure Body stiffens (tonic) with subsequent jerking of extremities Tx with ativan, dilantin, tegretol Characterized by loss of consciousness and falling to the ground Body stiffens (tonic) with subsequent jerking of extremities (clonic) Cyanosis, excessive salivation, and tongue or cheek biting, incontinence Postictal phase characterized by muscle soreness, fatigue Patient may sleep for several hours May not feel normal for hours or days No memory of seizure Absence seizures Typical: unresponsive, staring spell - Usually occurs only in children and rarely beyond adolescence - May stop as child matures, or may evolve into another type - Characteristic: Brief staring spell, lasts less than 10 seconds; unresponsive during Atypical: staring + jerking-eye/lips - Characteristic: staring spell plus other manifestations - Eye blinking - Jerking movements of the lips - Lasts longer than 10 seconds (as much as 30secs) - Usually continue into adulthood Myoclonic seizure Rhythmic arm abduction (3 movements/sec) followed by arm elevation Tx with zarontin, klonopin - Characterized by rhythmic arm abduction (3 movements per second) leading to - progressive arm elevation - Usually lasts 10 to 60 seconds - Eyelid myoclonia refers to jerking of the eyelids 26. Interventions during a seizure Protect the patient from injury, maintain airway patency, and do not restrain movements. Place the patient on their side if possible​ maintain safety: maintain airway, support head, turn to side, loosen constrictive clothing, ease to floor, do not restrain pt or place any objects in mouth Assess: start time/how long, bitten tongue, soft tissue damage, cyanosis, abnormal resp rate, apnea (ictal) absent or abnormal breath sounds, airway occlusion, HTN, tachy/brady, bowel incontinence, urinary incontinence May need oxygen, suctioning after Assess for any injuries if pt falls as a result of a seizure --> head injuries Q: How do we keep our patients safe? Observe and record time and frequency of seizure Maintaining patient safety during a seizure: 1. Open and maintain patent airway, support head, turn to side, loosen constrictive clothing, ease to floor 2. Do not restrain patient or place any objects in their mouth 3. May require positioning, suctioning, or oxygen after seizure 4. Assess for any injuries if patient falls as a result of a seizure (think: head injury especially) Nursing Management Role of RN Teach patient about risk for seizures, drug plan Assess and record seizure details Assess and position patient and give antiseizure drugs Make appropriate referrals Collaborates with physical, occupational, or respiratory therapist **All other responsibilities can be delegated to LPN/LVN MUST KNOW Pad side rails Suction as needed Assist ventilations if patient does not breathe spontaneously after seizure ( may require oxygen device (e.g. facemask) 27. Dilantin administration Oral antiseizure Maintain good oral hygiene Take with food, no milk, no antacids Don't stop abruptly Sx: diplopia, drowsiness, ataxia, mental slowness 28. Anticipating for a seizure: what do you need? Seizure precautions In hospital VEEG If the patient has had seizures, monitor for aural phase signs 29. Seizure precautions Maintain bed in a low position, pad side rails, and keep airway equipment at the bedside Avoid sharp objects and furniture in the room Cushion head with a pillow Suction and oxygen delivery system PRN meds ready​ 30. Psychosocial nursing dxs related to seizures Risk for social isolation, powerlessness, and low self-esteem Difficulry coping High risk for isolation 31. Status Epilepticus: nursing interventions, & medications State of continuous seizure activity or condition when seizure recur in rapid succession without return to consciousness between seizures Any seizure lasting longer than 5 mins, neuro emergency, can occur with any type of seizure Causes brain to use more energy than supplied: neurons become exhausted and cease to function; permanent brain damage may result Dysrhythmias and muscle fatigue Interventions ABC Give meds Support airway Meds Rapid acting IV lorazepam (ativan) or diazepam (valium) Antiseizure drugs should not be discontinused abruptly as this may cause seizures, including IP’s who are NPO Seizure phases 1. prodromal phase: Can sense when they are gettinga seizure 2. aural phase: They are learning about their seizure each time it happens 3. ictal phase: Time period of first symptom to the end of seizure 4. postictal phase: Recovery period after seizure Complications of seizures Status epilepticus (SE) State of continuous seizure activity or condition when seizures recur in rapid succession without return to consciousness between seizures Any seizure lasting longer than 5 minutes Repeated seizures, brain uses more energy than supplied Neurologic emergency: d/t neurons becoming exhausted & cease to function brain damage Can occur with any type of seizure (e.g tonic-clonic, myoclonic, absences) More info: Medications for: Tonic/Clonic, Status Epilepticus, focal onset Sz. Ativan: 1st line treatment for Tonic-Clonic Sz./Status Epilepticus Dilantin, Tegretol Generalized-onset, Myoclonic Sz.: Zarontin, Klonopin NCLEX Question A 16 yr old who has just been diagnosed with epilepsy tells the nurse, "I don’t want to go out with my friends anymore, I'm afraid I'll have a seizure in public." Which nursing diagnosis is the most appropriate? A. Powerlessness B. Non-compliance C. Alteration in Body Image D. Risk for Isolation Stroke (Q:11) TIA (mini stroke) Transient (brief) episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of brain Hx of TIA is associated with an increased risk of stroke DO NOT GIVE anticoagulant Tx with asprin 81-160 to reduce stroke occurrence CVA/stroke Occurs when there is an interruption, either from ischemia to a part of the brain or hemorrhage into the brain, in the blood supply that results in the death of brain cells. First Line Drug: Antithrombolytic (if ischemic)-tPA Second line drug: ASA* do not use on suspected hemorrhagic stroke patients Q: What’s one of the biggest clinical s/sx difference between ischemic and hemorrhagic strokes?: Intracerebral hemorrhage ◦ Manifestations ◦ Neurologic deficits/Decreased levels of consciousness ◦ Severe Headache (“worst h/a of my life”) ◦ Nausea and/or vomiting ◦ Hypertension 32. Priority diagnostics in CVA Interruption of the blood supply that results in the death of brain cells Ischemia to part of brain Severity of loss of function varies according to location and extent of brain damage: physical, cognitive, and emotional impact on pt and family Non-contrast CT scan or MRI to differentiate ischemic from hemorrhagic stroke 33. Modifiable risk factors CVA Hypertension, heart disease, diabetes, smoking, obesity, and physical inactivity 34. The role of ASA in stroke prevention Antiplatelet to prevent the development of a thrombus or embolus 35. tPA inclusion criteria Must be given within 3-4.5 hours of symptom onset for ischemic strokes. Contraindicated if hemorrhage is present used to reestablish blood flow through a blocked artery to prevent cell death Must be administered within 3-4.5 hrs of onset of clinical signs of ischemic stroke During infusion pt VS and monitor closely to assess improvement or potential deterioration related to intracerebral hemorrhage Pt carefully screened: no GI bleed, any recent bleed (15-20 days ago) 36. Working around hemianopsia Place items on the unaffected side and encourage scanning of the environment Blindness occurs in the same half of the usual field of both eyes Move objects into the visual field that the pt can see During rehab, train pt to adapt to things in the affected side --> stimulates return of normal function 37. Prioritizing care amongst 4 neuro patients. Prioritize based on airway/breathing status, level of consciousness, and potential for worsening neurologic deficits LOC, bleeding risk, resp system 38. Strategies for communication difficulties in CVA Use simple sentences, gestures, and allow time for responses. Use visual aids if needed​ supportive Assess for ability to speak and understand Speak slowly and calmly using simple words or sentences Gestures may be used to support verbal cues Speech therapy Yes and no questions 39. Bladder & Bowel Training post CVA (can apply to SCI as well) Bladder: avoid indwelling catheters, avoid bladder overdistention, adequate fluid intake Bowel: prophylactic stool softeners or fiber, physical activity Toileting schedule: Q1-2hrs have a bathroom break More info Clinical manifestations: communication Aphasia occurs when stroke damages dominant hemisphere of brain (typically left hemisphere) and affects language Receptive – loss of comprehension Expressive – loss of production of language Global – total inability to communicate Spatial-Perceptual Alterations Stroke on right side of brain is more likely to cause problems in spatial-perceptual orientation 4 Categories: Incorrect perception of self and illness (parietal lobe damage) Unilateral neglect of all input from the affected side (erroneous perception of self in space) Homonymous hemianopsia (blindness occurs in the same half of the visual fields of both eyes) Agnosia: inability to recognize an object by sight, touch, or hearing Apraxia: the inability to carry out learned sequential movements on command Interprofessional Care for Ischemic Stroke: Preventive Drug Therapy Measures to prevent development of a thrombus or embolus are used in patients at risk for stroke - Antiplatelet drugs are used in patients who have had a TIA related to atherosclerosis - Aspirin is most frequently used antiplatelet agent (81-325mg) - Ex: ticlopidine (Ticlid), clopidogrel (Plavix), dipyridamole (Persantine), and combined dipyridamole and aspirin (Aggrenox). Oral anticoagulation: Pts w/atrial fibrillation - Ex. warfarin (Coumadin), rivaroxaban (Xarelto), dabigatran (Pradaxa), and apixaban (Eliquis). Statins: who have experienced a TIA in the past - Ex. simvastatin [Zocor], lovastatin [Mevacor] Interprofessional Care: Drug Therapy for Ischemic Stroke Recombinant tissue plasminogen activator (tPA) - Fibrinolytic therapy used to reestablish blood flow through a blocked artery to prevent cell death - Patients are carefully screened - Must be administered within 3 to 4 ½ hours of onset of clinical signs of ischemic stroke - During infusion patient’s VS & neuro status monitored closely to assess for improvement or for potential deterioration related to intracerebral hemorrhage: this patient takes priority! - Must confirm type of stroke from non-contrast CT first: contraindicated for hemorrhagic stroke Q: Pneumonia is the most frequent cause of death after a stroke. Which intervention would be contraindicated in the acute care of a patient with a hemorrhagic CVA? A. Thicken liquids to ease swallowing and prevent aspiration. B Change position every 30 to 60 minutes.... C. Maintain adequate fluid intake, orally or IV.... D. Encourage forceful coughing to stimulate deep breathing. Q: A patient with homonymous hemianopsia is in the rehabilitation phase of a CVA. When arranging this patient’s environment where should the nurse assure persons approaching and important items are visible and available? A. Unaffected side B. Affected side C. Direct front D. Either side - Rationale Making the patient scan the affected side helps stimulate the return of normal function in the rehabilitation phase. Vs. If patient is in a new phase of homonymous hemianopsia, will need to place on the unaffected side Sepsis/Shock (Q:12) 40. Sepsis: main causes, interventions, treatments *know your priorities Systemic infection that triggers a host response: inflammatory response Leads to organ dysfunction and death Interventions Oxygen: titrate O2 to saturations of 94-98% or 88-92% in chronic lung disease Cultures: Take blood cultures before giving antimicrobials (if no significant delay i.e >45 minutes) and consider source control Fluids: start IV fluid resuscitation if evidence of hypovolemia 500mL bolus of isotonic crystalloid over 15 mins and give up 30mL/kg, reassessing for hypovolemia, euvolemia, or fluid overload Antibiotics: give IV antimicrobials according to local antimicrobial guidelines Blood: culture, lactate, CBC, U&E, LFTs, coags Urine output: assess urine output and consider urinary cath for accurate measurement Assessment Lactate levels :Low (0-2.0) Intermediate (2.1-3.9) Severe(>4.0) Blood draw for causative agents Start broad spectrum abx Start fluids Sepsis causes Resp infection: 35-50% Urinary tract (aka Urosepsis): 15-25% Intra-abdominal: 15-25% Skin: 11% Cath related, device related, intra-articular, boney, post-procedural 41. Priority intervention in anaphylactic shock Epinephrine SQ Benadryl IVP to stop allergic process Steroids to decrease swelling Bronchodilators  Monitor: RR and O2 sat Significant Co-morbidities COPD Frailty Age >75yrs DM CKD CLD Cancer Immunosuppressed Anaphylactic shock Hypersensitive allergic reaction Immediate vasodilation due to release of vasodilation due to release of vasoactive mediators Sx: wheezing, stridor, angioedema Closely monitor respiratory status: RR O2 sats 42. Signs and symptoms and interventions for septic shock Aserious condition that occurs when an overwhelming bacterial infection affects the body Systemic inflammatory response Severe sepsis Interventions Vasopressor if fluids do not reestablish BP and perfusion Steroids Oxygen Abx SS Hypotension even with aggressive fluid admin (persistent) Vasodilation Lactate levels +4 Compensatory: tahy, tachypnea, shunting from the GI, skin, and kidneys Worsening: paralytic ileus, oliguria, cold clammy skin 43. Interventions and outcomes of anaphylactic shock Administer IM epinephrine promptly, followed by oxygen therapy and IV fluids to address hypotension and maintain perfusion. Adjunct treatments, including antihistamines, corticosteroids, and bronchodilators, help mitigate symptoms and prevent recurrence. Monitor the patient closely for airway patency, improved oxygenation, and stabilized vital signs while preparing for possible biphasic reactions. Expected outcomes include restored airway function, normalized blood pressure, and symptom resolution, with education on allergen avoidance and epinephrine auto-injector use to prevent future episodes. What is it? Acute, life-threatening hypersensitive allergic reaction What is the priority assessment? respiratory status: RR, O2 sats What is first line drug: Epinephrine 44. Hypovolemic shock: S/sx, interventions Loss of intravascular volume hemorrhage Causes: GI loss, vomiting, diarrhea, wound drainage, hyperglycemia, diuresis Relative fluid loss: extravascular space leakage (third spacing) bowel obstruction, ascites, burns SS Hypotension, tachycardia, decreased urine output, pale, cool, slow cap refill (>2 sec), dry mucosa Worsening: neuro status changes --> not getting volume Decreased stroke volume, CO, renal flow Interventions Monitor BP, pulse, RR, o2 sat and weights daily Place patient's legs elevated Administer fluids (3mL for every 1mL of blood loss) Provide oxygen as needed Monitor patients for signs of Fluid overload such as: Crackles in the lungs, swelling, weight gain Antcipate an order for CBC, Electrolytes, BUN, Creatinine Q: What is it? Loss of intravascular volume hemorrhage Causes: ◦ GI loss, vomiting ◦ diarrhea ◦ wound drainage ◦ hyperglycemia ◦ diuresis Q: What is normal compensatory vs. signs of worsening? Tachycardia, tachypnea, shunting from GI, skin, kidneys Worsening: Neuro status changes 45. Cardiogenic shock: S/sx., main medications Results from systolic and/or diastolic pumpling actions resulting in decreased CO MIs, cardiomyopathies, blunt trauma, severe systemic or pulmonary HTN, cardiac tamponade, metabolic changes Monitor lung sounds for pulmonary congestion with crackles, increased PAWP SS Looks like HF First: tachy, HTN, Worsening: narrow pulse pressure, pulmonary congestion with crackles Skin shows signs of shock: pale, diaphoretic Cardiogenic shock main meds Nitrates to dilate coronary arteries (e.g. Nitroprusside) Diuretics to decrease preload Vasodilator to decreased afterload Q: What is it? Results from systolic and/or diastolic pumping action resulting in decreased cardiac output/low blood flow; resembles heart failure Q: What is normal compensatory vs. signs of worsening? ◦ First manifests as tachycardia, HTN. ◦ Worsening: pulmonary congestion with crackles More info… 4 stages of shock 1.Initial stage - cardiac output (CO) is decreased, and tissue perfusion is threatened. 2. Compensatory - Almost immediately, the compensatory stage begins as the body’s homeostatic mechanisms attempt to maintain CO, blood pressure, and tissue perfusion. 3. Progressive - The compensatory mechanisms begin failing to meet tissue metabolic needs, and the shock cycle is perpetuated. 4. Refractory - Shock becomes unresponsive to therapy and is considered irreversible. Interprofessional Care Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion 1 to 2 large-bore IV catheters , intraosseous access device, or central venous catheter Isotonic crystalloids (e.g., normal saline, lactated Ringers), colloids (e.g., albumin) Interprofessional Care Assessment on tissue perfusion Skin (temp,color, moisture) Urine output Neurogenic Shock Q: What is it? Occurs within 30 minutes of a spinal cord injury (T5 or above) Affects the sympathetic chain of the ANS ◦ Leads to profound vasodilation and blood pooling in the periphery Q: What is normal findings for this shock ◦ Profound hypotension and bradycardia ◦ poikilothermia inability to regulate body temperature (consider keeping pt room warm) Any new onset change in status (e.g. confusion, disorientation) should be considered 1st priority (intervention, MD notification etc.) Q: SVRA new registered nurse (RN) is caring for patients experiencing shock, which action by the new RN indicates a need for more education? A. Placing the pulse oximeter on the ear for a patient with septic shock B. Keeping the head of the bed flat for a patient with hypovolemic shock C. Maintaining a cool room temperature for a patient with neurogenic shock D. Increasing the nitroprusside infusion rate for a patient with a very high ACS/HF/ Dysrhythmia (Q20) 46. Chest pain: chronic angina vs. MI Chronic angina - chest pain when there is an increased demand in vessel with plaque --> vessel cant dialate to allow blood flow to meet the myocardial demand --> O2 demand >O2 supply - artery blocked 70% or more or left main artery blocked 50% or more - intermittent pain with the same onset, duration, and intensity - prinzmetal's angina: hx of headache --> spasm of major coronary - usually goes away with nitroglycerin administration and rest - negative troponin - tx with nitro, ACEs and ARBs, beta blockers, and calcium channel blockers angina assessment - onset: sudden/gradual? - location: precordia, substernal, diffuse ache in arm - characteristics: precipitating, quality, radiation, sensing, timing unstable angina - new in onset - occurs at rest - increase in frequency, duration, or with less effort - pain lasting greater than or equal to 10 min - need immediate tx - sx in women often under-recognized MI - severe chest pain that is not relieved by rest, position change, or nitrate admin, - pain can radiate to neck, lower jaw, arms, and back - release of catecholamines causes increase HR, BP, vasoconstriction --> BP will then decreases after compensation - skin is ashy, clammy, and or cool to touch - dysrhythmias: Vtach/fib- crackles, JVD, S3 S4, new murmur, fever, N/V - thrombolytic therapy: give within 30 mins of arrival to ED, ensure no recent bleed, surgery, 2 IVS 47. Cardiac meds: Nitroglycerine, Digoxin, Amiodarone Nitroglycerin indications: CHEST PAIN from stable angina --> same onset, duration, feeling of pain --> to relieve chest pain  admin: check BP, sublingual or nasal spray --> Sublingual every 5 mins for three times --> if pain does not relieve call 911 side effects: headache, light headed, dizzy, stand up slowly --> FALL RISK contraindications: viagra - action: dialate vessels to allow more blood to flow to heart --> decrease O2 demand/ increase O2 supply digoxin - indications: chronic heart failure, afib - administration: daily, check HR before administering, get labs checked for drug and potassium - side effects: headache, dizziness, N/V, confusion and weakness (bad)- contraindications: MI, hypokalemia, decreased HR - adverse reaction: ventricular dysrhythmias - action: increases heart contractility by increasing the sodium and therefore calcium amiodarone - indications: dysrhythmias --> junctional rhythm, PVC, vtach --> and symptomatic with chest pain - administration: high HR but stable pulse - side effects: hypotension, bradycardia 48. Complications of CABG CABG complications - abrupt closure from coronary artery dissection and vascular injury at the artery access site - bleeding, infection, stroke CABG - tx of STEMI and ACS - requires sternotomy and cardiopulmonary bypass - uses arteries and veins for grafts --> radial graft being used - palliative tx - coronary revascularization CABG assessment - surgical site care, check incision - graft site frequent assessment: pulse, color, temp, cap refill - radial artery harvest site - leg incisions - pain management: NGT , morphine - DVT prevention - pulmonary hygiene - cognitive dysfunction 49. Heart Failure pt. teaching: management, s/sx to call HCP, most common medications (e.g., Digoxin, diuretics, beta blockers, calcium channel blockers) HF - abnormal clinical syndrome that involves failure to pump and/or fill the heart - heart cannot supply enough blood to meet the oxygen needs of the tissue and organs - involves diastolic or systolic dysfunction - ejection fraction: am of blood pumped by LV with each heart beat --> 55-65% HF teaching - monitor: faces (fatigues, limitation of activities, chest congestion, edema, SOB) reappearance of SX, what to report, go to follow ups, join support groups - get vaccines and reduce risk factors - low sodium diet --> DASH diet, individualized recs HF common meds - digoxin - diuretics: furosemide --> check BP and HR, give in AM, increases release of fluid, can cause hypokalemia --> dig toxicity - beta-blockers: relax blood vessel and decreases HR and improve blood flow, decreases workload and O2 demand - calcium channel blockers 50. Nighttime shortness of breath: what is it associated with, s/sx Carvediolol (Coreg) - contraindicated in pulmonary edema - brady, heart block, or sick sinus syndrome (unless a pacemaker is in place) - decompensated HF requiring IV inotropic agents Paroxysmal nocturnal dyspnea - sudden wakening of SOB - pt feels suffocated - sx of Left sided hf --> CHF sx - sit pt up when sleeping - can be a sign of mitral valve regurgitation 51. JVD: how to perform & what does it indicate - position pt supine with head elevated and observe for pulsation that does not match radial pulse rate - sign of: MI, right sided HF, cardiac tamponade, and myocarditis - complication of pulmonary edema 52. MI discharge instructions. - stay on meds - start activity slowly and gradually - relaxation therapy - rehab outside of the hospital - low sodium diet - cant resume intimacy until three flights of stairs without SOB 53. How adenosine works: action & side effects  Action: Adenosine is an antiarrhythmic medication that acts on the heart by slowing conduction through the atrioventricular (AV) node. It interrupts reentrant pathways that cause paroxysmal supraventricular tachycardia (PSVT) and allows the heart to reset to a normal sinus rhythm. It works by activating adenosine receptors, causing hyperpolarization of cardiac cells and reducing electrical impulses in the AV node. Onset and Duration: Its effects are almost immediate (within seconds) after rapid IV administration, with a half-life of less than 10 seconds. Common Side Effects (typically transient): Facial flushing Chest discomfort or pain Dyspnea (shortness of breath) Lightheadedness or dizziness Nausea Palpitations or a brief period of asystole (flatline) Serious Side Effects (rare): Prolonged bradycardia Hypotension Bronchospasm (caution in asthma patients) 54. Vagal response: examples of and effects on heart rate - vagal stimulation: bearing down, massaging chest, mechanically slowing down HR nonmedical response to tx SVT - response: brady and risk for cardiac arrest with stimulation 55. Be able to identify the rhythms that were presented on EKG day. - P wave: upright - PR interval: 0.12-0.20 secs - QRS interval: less than or equal to 10 ses - QT interval - regularity of R-R interval 56. Safe administration of amiodarone - indications: supraventricular tachycardia - administration: on cardiac monitor, stops hr for a sec (like a reboot) change position slowly with pt - side effects: hypotension, SOB 57. Determining NSTEMI, STEMI: Diagnostics NSTEMI - the plaque rupture and thrombus forms causing partial occlusion to the vessel --> injury and infarct --> some O2 still being able to flow - longer duration and more severe than UA - inverted T waves, ST depression - elevated troponin STEMI - complete occlusion of the blood vessel lumen by thrombus --> injury and infarct to the myocardium and irreversible cell death --> no O2 being able to flow, no blood flow - elevated T wave or ST elevation - elevated troponin - cath lab within 90 mins --> CABG if occlusion too severe - longer duration and more severe than UA with irreversible tissue damage if perfusion not restored ISAL (IS anthony lazy) Inferior area of Stemi II, III, aVL Septal area of stemi V1 and V2 Anterior area of STEMI V3 and V4 Lateral area of stemi I, aVL, V5 and V6 Respiratory/Vents (Q6) 58. Interpreting blood gases - pH: 7.35-7.45 - pO2: 80-100 - pCO2: 35-45 - HCO3: 22-26 partial compensation of ABG: acid-base imbalance is dx when the body makes changes that will cause the pH to eventually correct itself, but has not completely accomplished the correction compensation of ABG: occurs when the pH has returned to normal, even though the responsible component remains abnormal 59. Administering oxygen Least to most invasive Start with NC If no noninvasive dont work prepare for intubation 60. Management of ETT Safe sedation Ween off asap Assess lung sounds, chest rise and fall, ABC, comfort Check circuit connection 61. Complications of ETT suctioning Hyperoxygenate before and after 100%, limit each pass to 10 secs or less, monitor ECG and SpO2 before, during and after suctioning Right way to suction: suction coming out for 10 secs after oxygenating the pt at 100% Suction when: coughing, restless, increased VS, decreased O2 sat Monitor ECG and SpO2 before, during, and after suctioning: Stop suctioning if complications seen 62. Preventing VAP Good hand hygiene, Elevate HOB 30-45 degrees Daily oral care w/ CHG Daily assessment for readiness for extubation Stress ulcer prophylaxis Venous thromboembolism prophylaxis, Minimizing sedation --> sedation vacations Early exercise and mobilization (ROM) Subglottic secretion drainage port No routine changes of vent circuit tubing 63. Priority respiratory assessment findings. Do frequently Assessment of ability to breathe and provide assistive measures Breath sounds LOC changes  VS 64. Complications of PEEP Increased WOB Barotrauma: air can escape into pleural space from alveoli or interstitium and become trapped, causing pneumothorax Hemodynamic instability Use with caution with increased ICP, low cardiac output, hypoventilation Increase airway pressure that can decrease preload, CO, and BP 65. ETT placement Allow for pt to breathe when they cannot on their own Indications: upper airway obstruction (ex: tumor), apnea, high risk aspiration, ineffective clearance of secretions, resp distress Safe sedation Ensure placement with chest rise and fall, x ray, markings on tube, and balloon cuff size Check cuff size and length every shift Complications of PPV cardiovascular system Increased mean airway pressure transmitted to structures of thorax; vessels are compressed causing decreased venous return to heart ◦ Decreased preload ◦ Decreased cardiac output ◦ Decreased BP PEEP increases effect peak pressure/high pressure alarm - ET tube displacement - increased bronchial secretions - pneumothorax (barotrauma) - agitation - coughing or gagging reflex - biting ET tube - kinked or pinched circuit low pressure alarm - loose connections (leaking) - leak in cuff ETT/trach - pt disconnected from circuit - high pt inspiratory demand High RR - useful during weaning - pt in resp distress - can indicate increased work of breathing - neuro or metabolic pt low tidal volume - useful during spontaneous breathing trials (CPAP/spontaneous mode) - leak in system - pt coughing, gagging, or biting ETT - pt not able to sustain physiological needs