Exam 2 PDF

Nervous System Intracranial dynamic: Intracranial circulation, CSF, brain parenchyma ○ Monro-kellie doctrine: increase in 1 volume = decrease in 1 volume to compensate/maintain ICP Volume/pressure ○ Limit to intracranial compliance -> decompensation with increa...

Nervous System Intracranial dynamic: Intracranial circulation, CSF, brain parenchyma ○ Monro-kellie doctrine: increase in 1 volume = decrease in 1 volume to compensate/maintain ICP Volume/pressure ○ Limit to intracranial compliance -> decompensation with increased ICP ○ Volume increase -> major ICP increase Cerebral perfusion pressure ○ 60-100 mmHg (normal), 100: hyperfusion, increased ICP ○ less volume -> less pressure Cerebral vasodilation: increase intracranial blood volume -> more volume -> more pressure ○ Normal CO2 Low CO2: cerebral vasoconstriction High CO2: cerebral vasodilation High ICP ○ Cerebral vasodilation (no autoregulation) Hypoxia, hypercapnia, brain trauma ○ Hydrocephalus (high CSF) Overproduction of CSF, blocked CSF circulation, inadequate CSF reabsorption ○ Masses ○ Cerebral edema Compensation mechanisms ○ Working Shunt CSF into spinal subarachnoid space Increase CSF absorption Decrease CSF production Shunt blood out of skull ○ Not working Brain tissue shift toward open space in skull Uncal/central herniation ICP ○ 0-15 mmHg ○ s/s: change in LOC (confused, restless, lethargy, combative, coma) Pupils sluggish/fixed, unequal size Motor function decline (posturing, no motor activity)  ○ Cushing triad: increased ICP -> neuro decompensation Increased pulse pressure Decreased heart rate Change in respiratory pattern ICP monitoring ○ Indications Comatose patient: manage care Abnormal CT finding: hematoma, confusion Poor neuro status: posturing Severe TBI NOT FOR: mild-moderate brain injury (meningitis risk) ○ Ventriculostomy (intraventricular): Monitor/treat high ICP (drain CSF), INFECTION RISK ICP management ○ Position: neutral head, avoid hip flexion (blood flow ot brain), elevate HOB 15-30º ○ Hyperventilation: decrease ICP to decrease CO2 ○ Temperature: keep cool -> metabolism slow -> decrease tissue demands ○ Respiratory: mechanical ventilation, RR, assess CO2, PEEP, limit suctioning (cough) ○ Blood pressure: adequate MAP, prevent hypotension, treat hypertension (meds) ○ Environment: decrease cerebral metabolic rate/blood flow ○ Seizure prophylaxis: keppra, phenytoin; increase metabolic rate/CBF ICP management administration ○ Hypertonic solution: osmotic gradient -> draw water away from brain into vessels Fluid overload ○ Mannitol: decrease cerebral edema -> water cross brain tissue into vascular space -> lower CBF/ICP Diuresis -> hypovolemia ○ Hypertonic saline 2-23%: concentration gradient -> fluid pull out of cerebral into vascular -> decrease CBF/ICP Hypernatremia Sedation ○ Severe brain injury (GCS brain room to swell ○ Hypothermia: reduce brain metabolic demand  Shivering -> increase ICP Neuro Disorders Brain tumors ○ s/s: headache, seizure, mental status change, nausea, vomit ○ Treatment: Corticosteroid: dexamethasone (decrease edema) Antiepileptic: seizure prophylaxic Surgery: stereotactic biopsy, craniotomy Radiaton Chemo Aneurysm: weak arterial wall -> balloon ○ Genetic vs acquired (HTN, smoking, atherosclerosis via drugs, AVM) ○ Patho: intimal layer of vessel weak -> blood flow stretch wall -> wall rupture -> subarachnoid hemorrhage -> fatal Rebleed happen in 24-48h ○ s/s: silent unless ruptured, worst headache of my life, change in LOC (lethargy to coma), seizure, n/v, neck pain, CN dysfunction ○ Diagnosis: CT skin, cerebral angiography ○ Treatment Preop: minimize stimulation, BP management, sedation Postop: vasospasm (3-12 days postop) prophylaxis nimodipine. TCD, hypervolume, hemodilution ○ Medical management Prevent rebleed: quiet environment, bowel regimen, limit visitor Antihypertensive: labetalol, nitropusside Stool softener Pain management Antipyretic Manage ICP ○ Complications Vasospasm Vasospasm: 3-12 days post subarachnoid hemorrhage (7-12 days) ○ Cause cerebral ischemia ○ Diagnose TCD ○ Treatment: reduce spasm, maximize perfusion Hypervolemia: volume expanders -> increase volume -> improve CPP > 10 Hypertension: vasopressor/art line -> increase perfusion -> decrease neuro deficit Hemodilution: decrease blood viscosity -> increase CBF -> increase O2  Nimodipine Balloon angioplasty Intra-arterial vasodilator (verapamil) ○ Complication Hydrocephalus: imbalance between CSF production/absorption -> RBC clot -> occlude transport channel -> shunt Seizures: subarachnoid space blood -> irritant Rebleed Arteriovenous malformation ○ s/s: headache, increase ICP, neuro deficit, bruits, visual symptom, asymptomatic (hemorrhage) ○ Diagnosis: CT, MRI, angiogram ○ Treatment Envovasculer embolization: small AVMS -> minimally invasive Stereotactic radiosurgery: gamma knife Surgery Stereotactic biopsy: diagnose pathology Craniotomy Transphenoidal surgery: pituitary problem; monitor nose CSF leak Transnasal surgery Stroke: sudden impairment of cerebral circulation 1+ blood vessel ○ Causes Thrombosis of cerebral artery Embolism from thrombus (heart, aorta, carotid artery) Hemorrhage (HTN, rupture, aneursym, AVM, trauma, hemorrhagic disorder) ○ Types Ischemic: lack of O2 to neurons -> trigger inflammatory process -> edema -> increase ICP -> cell injury Hemorrhagic: lack of O2 to neuron -> blood exert pressure on brain tissue -> autoregulation to maintain CPP ○ s/s: neuro deficit with sudden onset (blood flow disurpted to brain -> ischemia/necrosis -> permanent damage) L = R, R = L Weakness in arm/leg (1 side) Numbness (face, arm, leg) Visual change (decreased/blurry) Dysarthria (facial droop Aphasia/dysphagia ○ Risk factors: HTN, family hx, cardiac disease (a-fib), hyperlipidemia, smoke, cancer, BCP, obesity, anticoag)  ○ Diagnosis history/physical assessment (last normal) NIH stroke scale (0-42, >22 bad) CT scan MRI Cerebral angiography ○ Treatment IV tPA: fracture/dislocation ○ Fracture: simple vs compression vs wedge compression vs teardrop ○ Dislocation: subluxation, fracture-dislocation ○ Complete: total loss of sensory/motor function below level ○ Incomplete: area damaged Level of injury ○ C1-C2: mechanical ventilation forever (monitor airway) ○ C3-C8: respiratory complication (atelectasis) ○ T1-T12 T6-T12: paraplegia, motor loss below waist ○ L1-L5 ○ S1-S5: rectal tone for sensation Spinal cord syndromes ○ Central cord syndrome: cervical tract -> paralyzed arms, no leg/bladder deficit ○ Brown-sequard Motor paralysis on same side below level of lesion Opposite side below lesion: loss of pain, temp, touch Autonomic dysfunction ○ Spinal shock: flaccid paralysis below level of injury Hypotension, bradycardia, loss of temp control ○ Neurogenic shock: loss of sympathetic heart/vessel control Hypotension, bradycardia ○ Orthostatic hypotension: cannot compensate for changes in position ○ Autonomic dysreflexia: below level of injury -> sympathetic discharge HTN, throbbing headache Autonomic dysreflexia: after acute phase in spinal cord lesion T7 above ○ Medical emergency: death ○ s/s: bladder/intestine distention, spasticity, pressure ulcer, skin stimulation below level of injury Sympathetic response: reflex vasoconstriction, extreme HTN, bradycardia, throbbing headache, flushing, blurry vision, congestion ○ Treatment Elevate HOB Check catheter for kinks, bowel impaction Admin sublingual nifedipine Management ○ Cervical spine stabilized  ○ Airway: resp assessment (RR, pulse ox, hypoventilation), ventilatory support, tension pneumo? ○ Circulatory: VS, I&O, cardiac monitor ○ Neuro: LOC, level of function, cranial nerve testing, digital rectal exam (tone) ○ bowel/bladder: indwelling catheter Diagnose ○ CT, MRI, spine x-ray Treatment ○ Cervical traction, rods, laminectomy, fusion Neuro Assessment Basics ○ Chief complaint ○ History present illness ○ Past medical hx ○ Family hx ○ personal/social hx ○ Review systems (TKN timing admin) Early ID -> early treatment Report changes fast (confusion, gait, face droop) Neuro history ○ Dizziness, syncope, seizure ○ Frequent headache ○ vision/audio changes (tinnitus, light sensitivity) ○ Difficulty swallowing ○ Slurring word, finding words ○ Confusion, memory loss, concentration changes ○ Gait disturbances ○ Motor: weakness, paresthesia, paralysis, decreased ROM, tremor Responsiveness ○ awake/alert: normal ○ Awake: sleep more than usual, confused to awake, fully oriented when aroused ○ Lethargic: drowsy, follow simple command when stimulated ○ Obtunded: aroused with stimulation, response with 1-2 words, follow simple commands ○ Stuporous: hard to arouse, inconsistent follow commands, limited spontaneous movement ○ Semicomatose: move away from pinch, do not follow commands, incoherent ○ Comatose: reflexive posturing, no response to stimulus Speech deficit ○ Receptive dysphagia: can’t understand words ○ Expressive dysphagia: understand words, cannot initiate sounds ○ Global dysphagia: cannot understand words ○ Dysarhria: cannot move mouth  Motor function ○ Stimuli Level of awareness, follow commands, move against gravity ○ Noxious stimuli Sternal rub, trap pinch, supraorbital ridge pressure Localization decorticate/decerebrate Motor strength ○ with/without resistance ○ Size, muscle tone ○ 0-5 scale ○ Hemiparesis: weakness ○ Hemiplegia: paralysis Cerebellum: synchronization, balance ○ Romberg ○ Finger to nose ○ Rapid alternating movement ○ Heel to shin Pupil changes ○ Size, shape, equality (swell on 1 side) ○ Direct response: brisk pupil constriction ○ Consensual response: both constrict at same time ○ Accommodation: constrict when object gets close ○ Pinpoint pupil: drugs, drops, damage in pons ○ Dilated pupil: fear, seizure, coke, crack Pupil function ○ CN III, CN IV, CN VI ○ Aniscoria: unequal pupil ○ Change in size/shape Vital signs ○ RR: increased ICP, spinal cord lesion, cerebral trauma ○ Temperature: CNS fever -> metabolism increase; low -> pituitary damage or spinal cord injury ○ Pulse: increased ICP, bradycardia (herniation) ○ BP: medulla/cerebral edema damage Cranial nerves ○ I olfactory: aromatic substance ○ II optic: visual acuity ○ III oculomotor, IV trochelar, VI abducens: eye movements ○ V trigeminal: corneal reflex, face sensation, clench jaw ○ VII facial: raise eyebrows ○ VIII acoustic: weber/rinne ○ IX glossopharyngeal, X vagus: gag ○ XI spinal accessory: shrug shoulders  ○ XII: stick out tongue Reflexes ○ Normal abnormal absent ○ Superficial: light stroke to elicit muscle contraction ○ DTR ○ Plantar reflex: stroke outer edge Babinskis: toes flare Changes ○ Reflexes ○ 4+: very brisk response ○ 3+: brisk ○ 2+; normal ○ 1+: low-normal ○ 0: no response Sensation ○ Normal Intact spinal cord Sensory pathway PNS ○ Proprioception: direction of movement eyes closed ○ Vibration: tuning fork over bony prominence ○ Perception of touch: light touch, eyes closed ○ Pain Signs of trauma ○ Battle’s sign: bruising over mastoid areas (basilar skull fracture) ○ Raccoon eyes: periorbital edema/bruise (frontobasilar fracture) ○ Rhinorrhea: drain CSF from nose (fracture of cribiform plate) ○ Otorrhea: drain CSF from ear (fracture of temporal bone)  ○ Meningeal irritation: nuchal rigidity, fever, headache, photophobia ICP ○ Increase Decrease LOC, restless, confusion, combative, coma Sluggish pupils to fixed/dilated, unequal Change motor function Change VS (late) Cushings triad (increase systolic, bradycardia, decreased irregular respirations) Diagnostic ○ CT: seizure, headache, LOC, hemorrhage, tumor, lesion, skull fracture, hematoma, abscess Check renal function (contrast dye), hold metformin (contrast) ○ MRI: small lesion, tumor, hemorrhage No metal ○ Angiography: aneurysm, AVM, cerebral vasculature assessment Check coag studies (contrast) ○ Cerebral blood flow study: cerebral blood flow, vasospasms ○ Lumbar puncture: measure CSF, pressure, instill meds High ICP -> brain herniation Pulmonary assessment Acid base compensation ○ Metabolic acidosis: low pH Increase RR ○ Metabolic alkalosis: high pH Decrease RR ○ Respiratory acidosis: low pH Increase H+ secretion, bicarb reabsorption ○ Respiratory alkalosis: high pH Decrease H+ secretion (retain in blood), decrease bicarb reabsorption (pee out) Respiratory acidosis causes ○ COPD ○ Emphysema ○ Severe asthma ○ PNA ○ Pulm edema ○ guillain-barre ○ Opioid OD Metabolic acidosis causes ○ DKA ○ Lactic acidosis ○ Aspirin OD  ○ Thyroid storm ○ Oliguria ○ Diarrhea ○ Intestinal drain Respiratory alkalosis causes ○ Acute hypoxia ○ Acute pain ○ Acute anxiety/distress ○ Central stimulation of brain (head injury, meningitis) Metabolic alkalosis causes ○ Massive blood transfusion ○ Diuretic therapy ○ Excess bicarb admin Pulmonary Disorders Acute resp failure: inadequate gas exchange -> hypoxemia ○ Alveolar hypoventilation, V/Q mismatch O2 50, pH tired Wheeze, rhales, diminished, absent ○ Management O2, ventilation (positioning, suction) Meds: steroid, bronchodilator, antibiotic Bicarb meds: micarb, Ca Nutrition: TPS ○ Complication Encephalopathy, dysrhythmia, thromboembolism, GI bleed Hypoxemia ○ s/s: Restless, tachycardia Tachypnea, extra breath sound, accessory muscle Tachyarrhythmia-early, bradyarrhythmia-late hyper/hypotension Cyanosis Hypercapnia  ○ s/s Decreased LOC (lethargic, obtunded, stuporous, unresponsive) Shallow breathing, bradypnea Acute respiratory distress syndrome: lung response to multi-organ failure (sepsis) ○ Cause Direct vs indirect injuries Sepsis, aspiration gastric content, diffuse pneumonia, trauma ○ Patho Stimulate inflammatory-immune system (enter/irritate lung) -> exudative face (mucus -> no gas exchange) -> fibroproliferateive phase (form mass) -> resolution (stiff lung -> no expansion) ○ s/s Refractory hypoxemia ○ Diagnose ABG (refractory hypoxemia( CXR: whiteout ○ Management Ventilation, O2 therapy (PEEP), tissue perfusion Positioning, suction Pneumonia: acute inflammation of lung (infectious agent) ○ Cause Severe community-acquired, hospital acquired, health-care associated ○ Patho Aspirate organism inhale infectious particle organisms migrate into lung vaccine adjacent structures latent infection ○ s/s Fever, cough, SOB Tired, pale Diminished lower lobe, crackles ○ Diagnose CXR, sputum culture, bronchoscopy, ABG ○ Management Antibiotics (broad -> narrow) O2, ventilation (independent) Fluid, nutrition Positioning, suction, cough/deep breathe Aspiration pneumonitis: injury due to aspiration (chemical, mechanical, bacteria) ○ Patho Acid liquid -> hole in lung Acid food particle -> fall apart in lung, hard to retrieve  Nonacid liquid -> worse bacteria nonacid food particle -> block airflow ○ s/s Temperature, fatigue, confusion, tachycardia, BP, Crackle, rale, wheeze, tachypnea, cough ○ Diagnose Gastric content in oropharynx High WBC ABG CXR- infiltrate ○ Management Suction, support O2 Prevent aspiration Acute pulmonary embolism: thrombotic embolus vs nonthrombotic embolus (fat, tumor, amniotic fluid, air, foreign body) ○ Cause Hypercoagubility, injury to endothelium ○ Patho Increase dead space, bronchoconstrict, compensatory shunt, pulm HTN, increase PVR, RV fail ○ s/s anxious , dyspneic, tachypnea, impending doom, tachycardia, restless, positioning, red/hot legs ○ Diagnose ABG- hypoxemia with respiratory alkalosis high D-dimer- clotting factors ECG- tachycardia Abnormal pulm angiogram Abnormal spiral CT- angio-clot in lung Medications- thinners ○ Management Prevention: VTE prophylaxis Clot dissolution (heparin, TNK, fibrinolytics), reverse pulm HTN Monitor bleed, prevent DVT Status asthmaticus: severe asthma unresponsive to bronchodilator ○ Cause Upper resp infection, allergy, decrease anti-inflam meds ○ Patho Increase airway resistance, HR increase ○ s/s Emergent Cough, wheeze, dyspnea Cyanotic, dyspneiz, accessory muscle, nasal flare, wheeze ○ Diagnose  Deteriorate pulm function test (inhale/exhale change) ○ Management Bronchodilator, corticosteroid (IV push), nebulizer O2, intubation, mechanical vent Air leak disorder: extra-alveolar air accumulation ○ Cause Disrupt parietal/visceral pleura, alveoli rupture ○ Patho Pneumothorax, barotrauma ○ Diagnose Chest radiography Subcutaneous emphysema (crepitus) ○ Management Tension pneumo -> rapid Maintain chest tube COPD: chronic bronchitis, emphysema ○ Cause Permanent damage to alveoli (air escape) Increase secretions/thickness/inflammation ○ s/s Barrel chest, rales, diminished ○ Management Suction, cough, increase fluid Maintain O2 with some hypoxia Medications: bronchodilator, steroid No smoking Pleurisy: inflammation of lung lining ○ Cause Infection ○ s/s Increased chest pain with inspiration ○ Management NSAID, pain met, antibiotics Renal Anatomy Renal tubules ○ Glomerulus: filter fluid/solute from blood ○ Proximal tubule: reabsorb Na, K, Cl, HCO, urea, glucose, amino acid ○ Loop of henle: reabsorb Na, K, Cl, block H2O absorption ○ Distal tubule: Na, K, Ca, PO absorb, H2O absorb with ADH, Na absorb with aldosterone ○ Collecting duct: H2O absorb with ADH, HCO/H reasborb for urine Hormones ○ ADH: increase water reabsorption  ○ Renin: convert angiotensin into angiotensin I ○ Angiotensin II: vasoconstrict smooth muscle (increase BP), trigger aldosterone ○ Aldosterone: increase Na/water absorption Kidney function ○ Urea: protein end product ○ Creatinine: indicate kidney function ○ Erythrocyte production: erythropoietin control RBC production in bone marrow ○ Vit D: absorb Ca, blood clotting Acute kidney injury ADH ○ Pituitary gland ○ Reabsorb water in tubules, concentrated/small amount urine Aldosterone ○ Adrenal cortex ○ Increase Na/H2O reabsorption, decrease Na/H2O excretion in urine, excrete K Blood pressure ○ Kidney -> renin -> angiotensin I -> angiotensin II ○ Angiotensin II: increase peripheral vasoconstriction, stimulate aldosterone secretion Reabsorb H2O/Na to correct fluid deficit, blood flow to kidney GFR: 120 mL/min; filter blood ○ Cause Capillary permeability, vascular pressure, filtration pressure ○ Creatinine Glomeruli remove creatinine, not reabsorbed by tubules Renal assessment ○ BUN: differentiate kidney injury Intrarenal: BUN, creatinine high; 10:1 ratio Prerenal: BUN, creatinine normal; 20:1 ratio Dehydrated, no blood Postrenal: 10:1 to 15:1 Kidney stone, hold on to urea Creatinine excreted by functioning tubule, urea nitrogen retained (poor GFR, hemoconcentration) ○ AKI: rapid loss renal function Abnormal fluid, electrolyte, acid-base balance s/s Decreased GFR, azotemia (urea/creatinine high) ○ Specific gravity: hydration status Prerenal: >1.020 (concentrated) High: fluid volume deficit Low: fluid volume excess Prerenal AKI: hypoperfusion  ○ Compensation: RAAS BP increase, blood shunt to heart/brain, angiotensin II maintain GFR ○ Autoregulation Renal Change urinary composition/volume Drug interfere: NSAID, ACE inhib, ARB Severe compromise renal perfusion: not maintain kidney perfusion, GFR decrease BUN increase (azotemia), creatinine increase, oliguria, kidney damage ○ Causes Decreased volume Dehydration Hemorrhage Hypovolemia: GI loss, diuretic, DI hypovolemic shock third spacing: burn, peritonitis Cardiovascular failure HF MI Cardiogenic shock Valve heart disease Renal perfusion decrease Sepsis Cirrhosis Renal artery stenosis Neurogenic shock Low CO LV dysfunction Fluid volume excess Edema, crackle, pulm edema, high BP ○ Management Replace volume/electrolytes (fluids, positive inotrope, vasopressor/dilator) Maintain MAP >65 (renal perfusion) Postrenal AKI: obstruction in flow of urine from collecting duct to urethral opening ○ Causes Ureteral obstruction: stones, stricture, blood clot; cancer, lymphoma Bladder problem: tumor, stone Urethral block: stricture, BPH, obstructed catheter Intrarenal AKI ○ Interstitial (structure damage) Causes Infections (pyelonephritis) Inflammatory (sepsis, glomerulonephritis)  ○ Acute tubular necrosis Ischemic injury causes: prolonged prerenal injury Nephrotoxic injury causes: contrast dye, drugs, rhabdomyolysis, eclampsia Phases Onset: hours-days from injury oliguric/nonoliguric: ≤400 mL output (worse) vs >400 mL output ○ Support renal function until injury heal (increase BP) Diuretic: increase in urine output ○ Monitor hydration, electrolyte depletion Recovery: renal function return to normal ○ Prevent recurrence ○ Patho Epithelial cells destroyed (proximal, distal tubes) -> slough build up -> form casts -> lumen obstruct -> cellular debris ○ Nephrotoxin: chemical/metal toxic to kidney Meds, antibiotics, chemo, contrast, insecticide, heavy metal Conditions ○ Diabetes: glucose -> buildup -> damage capillaries ○ HTN: increase pressure -> glomeruli damaged ○ Sepsis: decrease BP -> no perfusion ○ Dehydration: can’t filter blood ○ Hypoxemia: can’t perfuse kidney ○ Lisinopril: RAAS ○ Vancomycin: nephrotoxic Diuretics ○ Loop diuretics: block Na reabsorption (furosemide, torsemide, bumetanide) ○ Thiazide diuretic: work on different part of nephron, admin with loop diuretics (chlorothiazide, metolazone) ○ Osmotic: increase urine output, proximal tubule (mannitol -> no Na effect -> head injury p/t) Renal diagnostic ○ Ultrasound: size, shape, contour (cyst, mass, stenosis, stone, infection) ○ Xray: dize/position (calculi, masses) ○ CT/MRI: masses, vascular disorder ○ Angiogram: stenosis, thromboembolism Chronic kidney disease: irreversible deterioration in renal function Kidney can’t eliminate waste, maintain fluid balance ○ Cause Diabetes, HTN ○ Patho Abnormal glomerular hemodynamic: compensation -> nephron loss Hypoxia: reduced capillary perfusion -> fibrosis/injury Proteinuria: accumulate -> inflammation/fibrosis  ○ Stages: 1-3: >90, 60-89, 30-59 4, 5: 15-29, more removal Solution dwell 30-45 minute Dialysate drain by gravity ○ Management I&O, daily weight (fluid volume status) Maintain sterility (infection) Mechanical issue Slow drainage dialysate: turn patient, elevate HOB, abdominal massage Incomplete recovery of dialysate: determine cause (block, where going), monitor fluid overload ○ Complications Hypotension: too much fluid removed (s/s FVD) HTN: not enough fluid removed (s/s FVE)  Abdominal discomfort: distension, chemical irritant of peritoneum Peritonitis: peritoneal lining infection s/s: fever, abdominal pain, clody effluent Management: broad spectrum antibiotics