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NUR 212 EXAM 2

QuestionAnswer
Occurs in 20% of trauma incidents chest trauma-90% of that 20% die after reaching hospital
occurs when body is struck by blunt object blunt trauma-forces=deceleration, acceleration, shearing compression
type of blunt trauma caused by impact of body parts against another object contrecoup trauma-hit on one side of the body and trauma is on the opposite
most common related injury rib fx
massive force of injury can involve fx of... scapula, sternum, first rib
gunshot or stab wound to chest penetrating injury
related injury to penetrating injuries hemothorax, pneumothorax (open,tension), cardiac tamponade, esphageal injury tracheal tear, great vessel tear
assessment findings for respiratory with chest trauma dyspnea, cough w/w0 hemoptysis, cyanosis(mouth, mucous membranes, nail beds), dec BS on side of injury, audible air escaping from wound, frothy secretions, tracheal deviation, dec O2 sat
cardiovascular s/s with chest trauma thready pulse, dec BP, narrowed pulse pressure, distended neck veins, chest pain, arrythymias
narrowing pulse pressure means... shock
what you will see on chest surface after trauma bruising, abrasions, open chest wound, asymmetrical chest movmt, subQ emphysema (crepitus)
air under tissue. feels like rice crispies crepitus
general tx of chest trauma ensure airway, high flow O2 then dec, IV access, remove clothing, semi-fowlers, monitor VS, high fluids (18g needles)
may be closed or open, disrupts parietal or visceral pleura, air accumulation in pleural cavity pneumothorax-dec mvnt/breathing on affected side, resonant to percussion, confirm w CXR then chest drain
no external wound, air in pleural space closed pneumothorax. pneumo=air
causes of closed pneumothorax mechanical ventilation, insertion of CVC, perforation of esophagus, broken ribs
s/s of closed pneumothorax sharp pain w inspiration, no breath sounds over affected area
sucking chest wound, air enters pleural space through opening in chest wall open pneumothorax
rx for pneumothorax cover w non-porous dressing taped on 3 sides (dec possibility of tension), do not remove object stabilize it
accumulation of blood in pleural space hemothorax
causes of hemothorax blunt or penetrating trauma, usually w open pneumothorax,
rx of hemothorax rapid decompression and fluid resuscitation, chest tube, adm packed red blood cells (PRBC), fluids, sx intervention
s/s of hemothorax dyspnea, SOB, dec BS, dullness to precussion, hypovolemia, shock
rapid accumulation of air in pleural space tension pneumothorax
tension pneumothorax causes inc pressure on hear/great vessels, dec venous return and cardiac output
s/s tension pneumothorax cyanosis, air hunger, violent agitation, tracheal deviation, subQ emphysema, neck vein distention, hyperresonance to percussion.
rx for tension pneumothorax sx, insert large bore needle (14g) to release air in 2nd ICS MCL, chest tube, CXR to confirm placement
purpose of chest tubes remove air/fluid from pleural space, restore normal intrapleural pressure,
insertion of chest tube for air removal 2-3 ICS MCL
insertion of chest tube for fluid removal 8-9 ICS MCL
ns interventions for chest tubes keep system below ins site, no milking/clamping, keep 2 clamps at HOB, tape connections, if CT dislodged place in sterile H2O until hooked back up, I/Os
aie/fluid chest tubes can be drained into same receptical
complications of chest tubes CT malposition, re-expansion pulmonary edema from removing fluid too fast, vasovagal response, hypotension, inf, pneumonia, dec shoulder mobility
chest tube removal once lung re-expands and fluid no longer drains, dc suction prior to removal, cover site w air tight dressing
2 types of drainage units dry, water
continuous bubbling in H20 chamber... air leak in pt, loose connection
only use sterile water in units, NS corrodes equipment
portable suction for little drainage Heimlich valve-one way valve, reacts to pressure diff.
most common thoracic injury ribs 5-10, not protected by chest muscles
suspect vascular injuries w.. upper rib, clavicular and scapular fx
with fax of 7-12 ribs suspect... liver (R) or spleen (L)
s/s of rib fx lots of pain, crepitus and shallow resp
rx of rib fx analgesia/intercostal nerve block, avoid taping, CXR
multiple rib fx produce a mobile fragment, with moves paradoxically w respiration flail chest
s/s of flail chest paradoxil chest movt, resp destress, associated hemothorax, pneumothorax, pulmonary contusion
rx for flail chest stablize flail segment, possible intubation/ventalation, O2, PEEP, aggressive analgesia
PEEP Positive End Expiritory Pressure. doesnt let aveoli collapse totally
blood rapidly collects in pericardial sac cardiac tamponade-compresses heart, medical emergency
s/s of cardiac tamponade distended neck veins, muffled heart sounds, hypostention (Becks triad)
rx for cardiac temponade pericardiocentesis, possible surgical repair, volume resuscitation
reasons for intubation upper airway obstruction, apnea, inc risk for aspiration, ineffective clearance of secretions, resp distress
oral tubing is preferred r/t... larger tube can be used decrease the work of breathing
endotracheal tube make sure... breath sounds are in both lungs. tube can be placed to low and only inflate right lung
the time span endotraceal tubes can be in place 2 wks
NS care of endtracheal tubes maintain correct placement, maintain proper cuff inflation, monitor O2, ventilation, tube patency, oral care, skin integrity, comfort and communication
resp failure is.. symptom of underlying pathology affecting one of the following, lung tissue func, O2 delivery, cardiac output, baseline metabolic state
interference of O2 transfer hypoxemia-the amount of O2 in the arterial blood is less than normal (PaO2 80-100) can lead to hypoxia
insufficient O2 removal hypercapnia-
deficiency in O2 delivery, dec utilization of O2 at cellular level hypoxia-affects brain and tissues
causes of hypoxia dec hemoglobin level (lowered O2 carrying capacity of the blood), diminished concentration of inspired O2 (high altitude), the inability of the tissue to extract O2 from the blood (cyanide poisoning)
causes of hypoxia cont... dec diffusion of O2 from the alveoli to the blood (pneumonia), poor tissue perfusion with oxygenated blood (shock), impaired ventilation (fx ribs, chest trauma)
s/s of hypoxia apprehension, restlessness, inability to concentrate, declining LOC, dizziness, behavioral changes, unable to lay down, appears fatigued, agitated, cyanosis (late sign)
how many mins of hypoxia causes brain death 6
how many mins of hypoxia causes impaired brain 4`
hypoxemia resp failure PaO2 is < 60 when pt is receiving inspirate O2 at 60%
four physiologic mechanisms for hypoxemia ventilation-perfusion mismatch, shunt, diffusion limitation, hypoventilation
1. ventilation-perfusion mismatch the volume of blood perfusing should equal the amount of gas that reaches the aveoli each min. pts less hypoxemic then pts w shunt
causes of ventilation-perfusion mismatch diseases and conditions that alter V/Q mismatching (COPD, secretions), pneumonia, asthma (bronchiospasm), alveolar collapse (atelectasis), pain, pulmonary embolis
occurs when blood exits the heart without gas exchange 2. shunt-O2 therapy doesnt help
blood passes through an anatomic channel in the heart and bypasses the lungs an-atomic shunt-ventricular septal defect
blood flows through the pulmonary capillaries without exchanging gases intrapulmonary shunt-alveoli are filled w fluid, such as ARDS, pneumonia, pulmonary edema
rx for hypoxemic resp failure mechanical ventilation and high fraction of FIO2 to improve gas exchange
3. diffusion limitation gas exchange across the alveolar-capillary membrane is compromised by the process that thickens, damages, or destroys the membrane
diseases that cause the alveolar-capillary membrane to thicken pulmonary fibrosis, interstitial lung disease, ARDS, shunting,
classic sign of diffusion limitation hypoxemia present during exercise, but not at rest
during exercise blood moves thru longs rapidly leaving less time for diffusion of O2 over the alveolar capillary membrane
4. alveolar hypoventilation dec in ventilation resulting in inc PaCO2 and dec PaO2
causes of alveolar hypoventilation restrictive lung disease,CNS disease, chest wall dysfunction, acute asthma, neuromuscular diseases
common causes of hypoxemic resp failure=RESP ARDS, pneumonia, toxic inhalation, hepatopulmonary syndrome (V/Q mismatch), massive pulmonary embolism, pulmonary artery laceration/hemorrhage, inflamatory state and aveolar injury
common causes of hypoxemic resp failure=CARDIAC anotomic shunt (ventral septum defect), cardiogenic pulmonary edema, shock (dec BF to pulmonary vessels),high cardiac output states
results from imbalance of ventilatory supply and demand hypercapnic respiratory failure=ventilatory demand exceeds supply and PaCO2 wont be WNL
four categories of causes of disease that can cause limitation of ventilation abnormal airways/aveoli, CNS suppression, damage chest wall,neuromuscular
ex of abnormal airways/aveoli asthma, COPD, cystic fibrosis
ex of CNS suppression dec resp drive, drug OD, depressant, brainstem injury, severe head injury
ex of chest wall flail chest, rib fx, mechanical restriction, muscle spasms, obesity, kyphoscoliosis
ex of neuromuscular gulliam barrem muscular dystrophy, myasthenia gravis, MS
early s/s of hypercapnic resp failure tachycardia, tachypnea, mild hypertension, severe morning HA. late s/s progressive somolance, tremors, siezures, purse lipped breathing, tripod positioning
positive pressure ventilation is used for managing chronic resp failure, chest wall and neuromuscular disease.
not used for absent resp, excessive secretions, decreased LOC, high O2 requirements, facial trauma, hemodynamic insability
bipap bilevel positive airway pressure. higher inspiration, lower expiration, pt must be cooperative, very high risk for aspiration. try before intubation
bipap used for COPD, acute resp failure, HF, sleep apnea, post extubation. not used for shock, altered mental status, inc airway secretion
CPAP constant pressure airway pressure. pt breaths on own, inc work of breathing, must forcibly exhale,
CPAP is used for weaning, obstructive sleep apnea, can b used mask, ET, or trach. caution w myocardial compromised pts
drugs used to relieve bronchiospasms. to inc aveolar ventilation short acting bronchodialators=metaproterenol, albuterol. neb metered dose
drugs used to reduce airway inflammation and pulmonary congestion corttcosteroids (methylprednisolone), diuretics (Laxis, morphine, nitro), calcium channel blockers (diltiazem), B-adregenic blockers (metoprolol) dec HR to inc cardiac output
rx of pulmonary inf IV antiB (vanco/ceftriaxone), CXR, sputum cultures
goals of drug therapy during ventilation sedation and analgesia. reduction of severe anxiety and restlessness.
drugs used for acute resp failure Diprivan (change tubing q 12hr, high lipid prone to bacteria), benzo=ativan (calming), Versed (amnesia), opiods (morphine, fentenyl)
reason for nueromuscular blockade asynchronouse ventilation despite sedation, paralyzes pt to dec O2 consumption, doesnt stop pain or rx anxiety
drugs for neuromuscular blockade Vecuronium, Nimbex
Train of four peripheral nerve stimulator. shows level of paralytic. thumb moves to indicate level of paralysis
goals in monitoring during resp medical supportive therapy ABGs, adequate cardiac output and hemoglobin concentration
what to monitor for during resp medical supportive therapy BP(S>90), MAP>60(mean arterial pressure), IV fluids/meds for dec CO. hgb.9, blood loss, blood trans to maintain good hgb levels
nutritional rx during resp medical support therapy maintain protein/energy stores, enternal/perenteral, malnurished pts start wi 24hr, well nurished pts start wi 3 days, nocarbs, free H20(FT doesnt have enough H2O
Pulmocare nutrition supp has low carbs. Carbs metabolize and give off CO2 inc CO2 levels.
sudden and progressive progression from acute resp failure ARDS=acute resp distress syndrome. aveolar capillary becomes damaged and fills w fluid. (hypoxemic resp failure)
ARDS 50% die, 90% w gram gram neg septic shock die,
s/s of ARDS severe dyspnea (gasping), restlessness (inc anxiety), hypoxia w O2 supp, reduced lung compliance, crackles
what are common causes of direct lung injury? ARDS aspiration, viral/bacteria pneumonia, sepsis
what are less common causes of direct lung injury chest trauma, embolism, inhalation of toxic substances, near drowning, O2 toxicity, radiation pneumonia
what are common causes of indirect lung injury sepsis(especially gram neg), severe massive trauma
what are some less common causes of indirect lung injury acute pancreatitis, anaphylaxis, cardiopulmonary intravascular coagulation, opioid drug OD(heroin), severe head injury,shock, TRALI
phase one of ARDS interstitial/aveolar edema and atelectasis, injury to aveolar membrane has occured
effects of phase one (1-7 days)dec in gas exchange and lung compliance, initial engourgement of interstitial space, then fluid to aveolar space, R to L intrapulmonary shunt developes, blood returns to L side of heart unoxygenated
phase two of ARDS (1-2wks)inflammatory response. influx of neutrophils, monocytes, lymphocytes and fobroblast proliferation, lung dense fiberous now, pulmonary HTN/vascular resistance, hypoxia worsens
phase three of ARDS (2-3wks)diffuse scaring and fibrosis w dec lung compliance causing pulmonary HTN
clinical mans of ARDS nothing during 1-2days, then dyspnea, tachypnea, cough, restlessness, crackles, ABGs mild hypoxia, resp alkolosis from hyperventilation,CXR minimal infiltrates, diaphoresis, cyanosis, pallor
hallmark sign of ARDS hypoxia despite FIO2 delivery by mask, cannula or ET.
can develop from ARDS or rx of MODS(multiple organ dysfunction syndrome)homeostasis cant b maintained wo intervention. mostly kidneys, liver, heart, CNS, hematoligic, GI
ventilator assisted pneumonia prevention (VAP) strict inf control measures, handwashing, sterile trach care, oral hygiene, ventilation bundle protocols
ventilator bundle protocols HOB 30*, daily sedation vaca to assess extubation readiness, peptic ulcer prevention, DVT prevention
rupture of over extended aveoli from vent settings barotrauma
barotrauma can lead to pneumothorax, crepitus, polmonary interstitial edema
prevention of barotrauma smaller tidal volumes, PEEP, gradual raise of CO2, pH maintained at >7.2
alveolar fx and movt of fluid into alveoli volutrauma
prevention of volutrauma smaller tidal volumes and pressure control ventilation
Complications of ARDS stress ulcers-histamine receptor antagonist(Zantac), PPI(Protonix), mucosal protecting agents(carafate), early nutrition
with ARDS hypotension, hypoxemia, hypercapnia, nephrotic toxic drugs used to rx ARDS(vanco) leads to renal failure
O2 therapy to mange ARDS lowest concentratin to get PaO2>60, intubation w vent
PEEP(positive end expiration pressure) used to keep aveoli open to inc gas exchange
purpose of PEEP keep gas in lungs at end of expiration, dec shunting of blood to lungs, improve gas exchange, dec use of O2 adm
ECMO(extracorporeal CO2 removal) blood passed thru a membrane outside body and returns oxygenated blood to body. used to heal lungs
positioning strategies for ECMO prone-allows airfilled aveoli to become dependent, supine will atelectisis, risk of pressure ulcers, cant do CPR, special rotating bed
management of Ards i/oS, WT, VASOCONSTRICTORS, DIURETICS, low carb diet,
indications for endotracheal intubations upper airway obstruction, apnea, risk of asppiration, ineffective secretion clearance, resp distress
oral intubation thru mouth to vocal cords, larger the tube ease work ob reathing, use of endoscopes and removal of secretions
riskes w intubation chipping of teeth, biting ET TUBE, salavation, sedation and bite block used, oral care more difficult due to space in mouth,
nasotracheal intubation thru nose to vocal cords, blind, smaller tube, inc work of breathing, pressure on septum, secretions diffficult to remove, tube kinks, inc sinus inf and VAP.
endotraceal intubation procedure oxygenate, attempts at 30sec, vent between attempts, inflate cuff, listen to lung sounds, use CO2 indicator(no color change in esophagus, reinsert)
post endotracheal intubation procedure check for chest rise, no L chest rise remove 1-2cm, mark tube at teeth, cut excess tube, connect O2, bite block, wrist restraints, CXR placement, document, ABGs after 25mins
what to assess for intubation for O2 ABGs, PO, change in mental status, anxiety, dusky skin, dysrythmias,
what to assess for intubation for proper ventialation PaCO2 is best for aveolar hyperventilation, RR and rythm, use of accessory muscles
reasons to suction inc HR, RR, dec PO, secretions
to prevent skin breakdoown move tube from one side of mouth to other q 24hr, 2 person job,
communication with intubation white boards, music for comfort
two major complications of intubation unexpected extubation, aspiration,
settings for vents rate, depth depending on ABGs, wt, LOC and muscle strength, set alarms
volume ventilation mode:assist-control mechanical ventialtion pt can breath faster than vent, used for neuromuscular disorders, pulmonary edema, acute resp failure, assess ABGs, PO, fight the vent
synchronized intermittent mandatory ventilation mode synched w pt spontaneous breathing. self regulates the volume of pt breaths
uses of SIMV weaning, continuous ventilation. may inc muscle fatigue
intermittent mandatory ventilation set rate, Vr, insp time and PEEP. pt can breath inbetween mandatory breaths on their own
uses of IMV continuous ventilation, weaning, dec WOB, exercising resp muscles, can cause hypoventilation
PEEP positive end expiratory pressure (5-20)
auto PEEP additional PEEP not cuased by settings results in enadequate exhalation time. may cause inc WOB, barotrauma, hemodynamic instability
prevention of auto-PEEP sedation, analgesia, large diameter ET tube, bronchodilators, short inspiration times, dec resp rates, reducing H2O accumulation in vent circuit
complications of mechanical ventilation=presents of pheumothorax and subq emphysema barotrauma
alveolar hypoventilation vent complications caused by system leaks, inc secretions
alveolar hypertention leads to resp alkalosis
VAP ventilator associated pneumonia
NS implications for complications of mechanical ventilation monitor for crepitus, lung sounds, equal chest expansion, alert for high inspiratory pressure, keep tidal volume low, aseptic technique w suctioning
prevent upper airway damage w ventilation gentle insertion of tube, firm stabilization of tube, freq monitoring of cuff pressures, humidification to prevent drying
prevent oxygen toxicity w ventilation monitor O2 sat, dec O2 need, pt fever free, block care, sedating pt, hemoglobin, add/;inc PEEP
hemodynamic alterations PEEP intrathoracic pressure compromises thoracic vessels
hemodynamic alterations can cause restriction of ventricular filling, restricted BF thru lungs, dec venous return, dysrhythmias r/t less O2
NS interventions for hemodynamic alterations r/t ventilation monitor VS, EKG, elevate feet to promote venous return, SIMV (synchronized intermittent mechanical ventilation) "preserves intrathoracic pump"
sodium and water imbalance w ventilation progressive fluid retention often occurs after 48-72hr of PPV especially w PEEP. associated w dec urinary output and Na retention
what causes sodium and water imbalance w ventilation renin-angiotensin system activated w dec CO2, intrathoracic pressure changes lead to Na retention, inc ADH w stress response, dec insensible fluid loss via airway
NS interventions for sodium/water imbalance w ventilation I/o, daily wt, maintain IV therapy, monitor electrolytes
complications of mechanical ventilation GI bleeding, inf, musculoskeletal,psychosocial trauma
meds for GI bleed histamine H2-receptor blockers (Zantac), proton pump inhibitors "PPI" (Prilosec)
SE of GI meds constipation/ileus-monitor bowel sounds, TF residuals
causes of inf in ventilation suctioning, ET, tubs are entrances for bacteria, oral secretions
NS interventions for inf w ventilation humidified air, consistent hand washing, sterile technique, change tubing per protocol, use in-line suctioning
goals for musculosketal system w ventilation maintain muscle strength, prevent problems associated w immobility
NS intervention for musculoskeletal system w ventilation ROM, up in chair when possible, proper positioning (prevents contractures, pressure ulcers, foot drop(tennis shoes, pillow between footboard and feet), external rotation of hips
causes of psychosocial trauma w ventilation pt unable to speak, eat, move or breath normal. Pt needs knowledge, control, hope and trust
NS interventions w psychosocial trauma w ventilation explain all procedures, use alternate communication methods, allow frequent family interaction, accept pts feeling and frustrations
ventilator alarms "disconnect/malfunction" check machine for setting correct, intact lines, air leak around tube, condensation of water in tube, alarms on. check pt chest expansion, lung sounds
"high pressure alarm" may need suctioning, kink in tube, biting tube, pt coughing as breath delivered, bronchospasm or other inc airway resistance, herniated cuff over ET, ET misplaced, water in tube, dec pulmonary compliance, pneumothorax
"low pressure alarm" tube loose, air leak, disconnected from vent
ventilator settings resp rate.. 6-20/min, if CO2 low dec rate/tidal volume, if CO2 high inc rate/tidal volume
tidal volume volume of gas delivered to pt during each ventilator breath. 6-10
ventilator settings oxygen concentration (FIO2) fraction of inspired O2 delivered to pt. between 21-100%. adjusted to keep PaO2 level >60 or Spo2 level >90%
additional setting for ventilator sigh=deep breath, prevents micro-atelectasis and dec lung compliance
ventilator weaning "preweaning" of sedation, lung sounds, ABGs, breathing trials, CXR, neuros, hemodynamics, fluid/electrolytes, acid-base balance, nutrition, hemoglobin, pt alert, pain managed
"weaning process" spontaneous breathing trial of 30-120min, tolerance,
"outcome phase" period when weaning stops and pt is extubated or weaning stops because no further progress is made.
extubation procedure oxygenated pt, suction, deep breath, deflate cuff, remove tube w suction, deep breath and cough, suction, supp O2, monitor VS, resp status, stridor (laryngospasm), may require reintubation
manifestations of laryngospasm inspiratory stridor, sternal retractions, acute resp distress
NS interventions for laryngospasm call for help, O2, PPV, IV muscle relaxant, lidocaine, corticosteroids
fluid shift from plasma(IV) to interstitial fluid after trauma/injury on 1st/2nd day. Poss shock=hypovolemia
labs for fluid shift inc H&H, BUN, RBC (dry)
Rx for plasma to ISF dilute IV will bring labs down, assess for overload on 3-5 day, I/O, BP, JVD, lung sounds, HR, RR. hypertonic solutions
intracellular fluid volume excess (ICFVE) s/s water intoxication, dec Na, cells swell, confusion, seizures, coma, hyperventilation, wt gain, NV, >SB/P, <DB/P, slow pulse, edema
ICFVE interventions LOC, neuros q 20min c 3% saline
causes of ICFVE >H2O intake, salt wasting kidney disease, too many tap H2O enemas, hypotonic solutions, SIADH
rx for ICFVE restrict fluids, I/Os monitor labs, VS, neuro checks, hypertonic (3-5% NS if Na+ low), Lasix (gets rid of H2O not Na+)
Extracellular fluid excess (ECFVE) s/s vascular and interstitial space overload. JVD, 3rd spacing, edema, rales, S3, wt gain, >BP, cough, <BUN(hemodilution)
causes of ECFVE hypervolemia r/t too much NS IV, CHF, renal failure, liver disease, steroids, fluid shifts 2-3 days post stress.
mechanism of edema fluid overload, dec plasma protein/serum albumin, venous end of capillary cant work, dec absortion of interstitial fluid (lyymphatic obstruction), inc cap permeability (tissue injury), leak of plasma protein into interstitial space.
causes of edema NS IV excesss, heart/renal failure, shifts post trauma/burns, liver disease, steriods, malnutrition, ETOH, hypoalbuminemia, major surgery, acid-base imbalance
aterial end of capillary fluid moves out of capillary here becasue of inc hydrostatic pressures
venous end of capillary fluid move back into capillary here because of inc oncotic pressures
with ECF excess, fluid moves out but not back in
NS interventions of ECF (edema) diuretics, monitor K+, Na+/water restriction, lung sounds, I/Os, wt, careful adm of fluids/IV, inc protein in the diet if possible
intracellular fluid volume deficit (ICFVD) water out of cells, rare except in the elderly
s/s of ICFVD thirst, flushed skin, wt loss, tenting skin, dry coated tongue, in H&H, restlessness, circ collapse
causes of ICFVD dec fluid intake, inc fluid loss, fever, cant concentrate urine, TPN/TF,
Rx of ICFVD fluids slowly (avoid IICP), contolled BS, free H2O, oral care, wt, VS
extracellular fluid volume deficit (ECFVD) dehydration or hypovolemia, shock
s/s of ECFVD postural hypotension, wt loss, dry skin/mucoos membranes, oliguria, N, weakness, >SG urine, tenting
causes of ECFVD dehydration r/t fluid losses, intial fluid losses, intial fluid losses r/t burns trauma.
rx of ECFVD NS and inc PO fluids, blood replacement if hemorrhage
causes of hyperosmolar hyperglycemic syndrom (HHS) elderly type 2, impaired thirst, some insulin so no lipolysis, osmosis of fluid to intravascular space from overload of sugar and subsequent diuresis
causes of diabetic keto acidosis (DKA) type 1, resp/urinary inf, jajor stressors, DM out of control w inc insulin needs, lipolysis leads to acidosis
s/s of HHS r/t dehydration: BG:600-2000, minimal/no ketosis, hyperosmolality of plasma and inc BUN, dry mm
s/s of DKA r/t acidosis (pH<7.3): BG:200-1500, urinary ketosis
tx for HHA correct underlying prob, IV fluids, rapid rate NS followed by Hypotonic (0.45NS), IV insulin=add D5 when BG 250 to prevent hypoglycemia
tx for DKA IV NS or rapid rate 0.45 NS, IV insulin, add D5 when BG 250 or no more ketosis, monitor K+ (dec quickly, K follow sugar into cells), monitor phosphate levels alternate KCL & K phos in IV
NS interventions for both HHS and DKA MONITOR i/oS, LOC freq, wt, skin turgor, BSGM q 1hr on IV insulin, check ketones if ordered
ADH without ADH water not reabsorbed in kidney tubules and lrg amts of dilute urine are formed (fluid volume deficit). Too much ADH water reabsorbed in kidney tubules (fluid volume excess)
Diabetes insipidus (DI) polydipsia(excessive thirst), polyuria, DI=ADH deficit=fluid volume deficit
syndrome of inappropriate ADH (SIASH) water intozication r/t water retention, hyponatremia, hypoosmolality. SIADH=ADH excess=fluid volume excess
causes of DI primary=hypothalmus and/or posterior pituitary defictive. 2ndary=gland tumor, inf, head trauma, surgical removal, lithium and dilantin
causes of SIADH disease lung or pancreas, skull fx or barin lesion, surgery, PEEP, drugs: MS, thiazides, diabenase
s/s of DI NO inc BG or ketosis, polyuria, polydipsia, dehydration, can be slow/fast, conrfusion, dry skin/mm, inc serum osmo, inc serum Na+, urine dec, call DR now, Inc BUN
s/s of SIADH r/t cilutional hyponatremia, weakness, lethargy, confusion, convulsions, wt gain, edema, dec serum Na+, Inc urine Na+, BUN, dec serum osmo, inc urine osmo
tx of DI replace fluids 5-40L/day, Petressin(basopressin: IV, SQ ADH, intranasal DDAVP or desmopressin
tx of SIADH fluid restriction 500-1000ml/day, hypertonic IV (3-5%NS), NaCl, diuretics (exchange K+ for Na+), tx cause, Declomycin:tetracycline antibiotic (blocks ADH secretion)
NS interventions for DI monitor fluids/outputs, VS, assess labs, adm meds, pt/fam education
NS interventions for SIADH I/Os, wt, freq neuro checks,
thyroid storm/crisis in graves disease hyperthryroidism-untreated can cause death
myxedema coma hypothyroidism=do they take their meds
s/s of thyroid storm/crisis hyperthermia(T=106), HTN, tachycardia, hyperventilation, flushed, hot skin, inc CNS irritability, delirium, NO ASPRIN
s/s of myxedema coma hypothermia(severe), hypotension, bradycardia, hypventilation, pallor, cool skin, dec CNS, hard to awaken, paranoid delusional, BG hypo
tx for thyroid storm/crisis antithyroid meds, PTU or Tapazole, cardiac glycosides, beta-blockers, hypothermia blanket, steroids, blucose, fluids
tx for myxedema coma thyroid replacement:Synthroid, ventilator for hypovent, inc vascular vol. warm blankets, steroids, glucose, monitor
progressive disease characterized by destruction of liver cells and tissue caused by fibrosis and disorganized nodular regeneration Cirrhosis=9th leading cause of death in US
Laennac (cirrhosis) ETOH, most common, 30-50% of pts (90% ETOH), portal/nutritional prob, lack of protein causes scar tissue around portal area
Post necrotic cirrhosis(post hepatic) most common worldwide d/t viral hepatitis, massive necrosis from hepatotoxins
biliary cirrhosis 15-20% of pts, bile duct diseases which obstruct liver and bile duct flow
cardiac cirrhosis rare, r/t severe CHF, right heart failure causes a backup into the liver causing damage
assessing cirrhosis jaundice, abrasions on skin from itching (dry skin), spider angiomas on face (will blanch), palmar erytherma, geynecomastia (dec testosterone),
dx tests for cirrhosis dec in serum albumin, anemia, inc PT, NH3, AST, ALT, conjugated/unconjugated bilirubin, urine urobilinogen, alk phos,
other tests for cirrhosis liver biopsy, abd films for hepatic/splenic enlargement, UGI for esophageal/gastric varices, ultrasound w doppler evaluates patency of splenic, portal and hepatic veins, CT organomegaly
more tests for cirrhosis esphagogastroscopy reveals varices and bleeding points, splenoportography radiopaque dye w XR of spleen and portal veins- reveals enlargement of both from back pressure in portal vein
liver biopsy high risk hemorrhage, hold breath during needle expiration (keeps diaphragm elevated to prevent lung puncture/pneumothorax), consent
more liver biopsy CBC & coagulation profiles, vit K given for high PT, bedrest x8-12 hr post procedure, 2+hr on right side to tamponade, post op VS, biopsy site check, inc P, dec BP, cool clammy skin, abd pain, fever (peritonitis)
abnormal accumulation of fluid in peritoneal cavity ascites
liver produces albumin. albumin maintains colloid osmotic pressure dec albumin, osmotic pressure is dec and fluid escapes and stays in interstitial spaces causing edema
scar tissue can block liver microvasculature causing inc portal hydrostatic pressure, ascites, inc plasma/lymphatic pressures causing lymphatic congestion leading to leakage of fluid to peritoneal cavity
assess for ascites daily wt (1L fluid=1kg), BP, electrolytes, mental status, abd girth daily, I/O
dietary mods w ascites Na+/fluid restriction, vit B,A,D,E,K (cant take w liver disease), high CHO, high cal, mod-low fat,
drug tx of ascites Lasix w spironolactone(Na+ &H2O excretion w retention of K+, monitor K+ & Mg, adm salt poor albumin w severe hypoalbuminemia, check lung sounds for pulmonary edema
last resort for severe dyspnea and anorexia from ascites paracentesis. >100cc removal too much, complication of rapid decompensation causes fluid shifts and protein loss=shock
splenomegaly destroys blood cells and plateletes. dec vit K+(less fat absorption & storage in liver), less manufacture of prothrombin & other clotting factors (less vit K+), bleeding depletes cells and clotting facots, GI bleeding from esphageal varices & GI ulcers, dec RBC manufacture d/t folic acid def and lack of protein
esophageal varices r/t blockage of portal vein and microcirculation. back pressure dilates esophageal veins and causes collateral circulation to form esophageal and gastric varices
dilated umbilical veins (Caput Medusa)
rectal varices (hemorrhoids) portal circuation is connected to inferior mesenteric vein the body attempts to develp collateral circulation and rectal veins dilate = hemorrhoids
Sengstaken-Blackmore Tube is used for varices, gastric aspirating tube, esophageal balloon, gastric balloon, tamponade the varices
meds for varices octreotide (Sandostatin) inhibits hormones tha cause vasodilation.
AE of octreotides dizziness, orthostatic hypotension, palpitations, N, <BG
Vasopressin (Pitressin) splanchinic visceral vasoconstriction. causes dec bleeding
meds for ETOH Baclofen(suppress symptoms of wdrawal, benzpdiazapines (ativan, Librium), Thiamine (give before D5 IV, 100mg/day)
what score determines how much Ativan you get for ETOH CIWA (clinical institute withdrawal assessment) of ETOH scale
disorder of protein metabolism and excretion of hepatic encephalopathy
hepatic encephalopathy bacteria and enzymes work on AA in the intestines >amonia, ammonia to liver via portal circ to converted to urea and excreted, damanged liver cant do it, ammonia accumulates, crosses BBB, ammonia is toxic to brain (CNS depressant)
causes of hepatic encephalopathy high protein diet, constipation, dehydration, inf
prevention of hepatic encephalopathy dec protein, dec exercise
s/s of hepatic encephalopathy confused, restlessness, coma
drugs used in liver failure lactulose-takes ammonia from blood to stool.
drugs not used in liver failure tranquilizers, narcs, sedatives
asterixis "liver flap" dorsiflexion of the wrist while holding arms straight out causes abnormal jerking of the hand due to toxins in the brain.
sweet fetid breath order fetor hepaticus
asterixis and fetor hepaticus combined with dec LOC = progressing encephalopathy
dilated branches of capillaries on the skin resembling a spider associated w cirrhosis of the liver spider angioma
rign of varicosities around the umbilicus caput medusa
thermal burns (most common) flame, contact, scald, flash
chemical burns acids, alkalis, organic compounds
electrical burns intense heat from electrical current
radiation burns sun, tanning beds, radiation exposure
cold thermal burns frost bite (localized), hypothermia (systemic)
tx of thermal burns flush w cool water
tx for chemical burns can destruct tissue upto 72hr, neutralize/dilute chemical w water, NS for open skin and eyes, remove clothing, consult poison control
results of electical burns bones and tissues are more resistant, nerves and BV are least resistant, direct damage to nerves and vessels, causing tissue anoxia
interventions for electrical burns assess entry/exit, iceberg effect, all pts considered C-spine injury
risks to consider w electrical burns dysrhymias, cardiac arrest wi 24hr, metabolic acidosis, myoblobinurea (blocks renal tubes=renal failure, thermal burns, immobilize c-spine
frostbite tissue freeze, peripheral vasoconstriction, dec BF, vascular stasis, cell membrane destroyed=edema
interventions for frostbite no squeezing, immerse in warm H2O, avoid heavy blankets(slough tissue), elevate, analgesia, antibiotics, no IMs
partial thickness (first degree) sunburn, heat flash, open flame, steam, hot food. heals in 3-7 days
assessment for first degree redness, blanching, tactile sensation intact, pain, mild edema, no blisters, may blister in 24hr
partial thickness w distruction (2nd degree) flame contact, flash/scald, chemical, tar, electric current. heals in 7-21 days
assessment for 2nd degree blisters, mottled white, pink to read, hypersensitive to touch/air, mod/severe pain, blanching, mild/mod edema, pigment change
full thickness destruction (3rd degree) flame/scald, chemical, tar, electrical. heals in 21 days or no healing, scarring severe
assessment for 3rd degree dry, leathery, waxy white, strong burn oder, no pain (nerve damage), severe pain in surrounding tissue, no blanching, muscles, tendons, bones mayb involved
rule of nines 1st * not included, used for over 10% burn,
burns can cause resp difficulties due to edema, inhaled=resp mucosal damage, circumficial chest burn,
burned hands/feet can dec ADLs
burns susceptible to inf ears/nose (poor blood supply), buttocks/perinium (exposure to feces/moisture
burns with compromise to extremities compartment syndrome from edema
3types of smoke inhalation injury CO poisoning and asphyxiation, thermal burn above glottis, and below glottis
CO poisoning and asphyxiation CO displaces O2 on hemoglobin causing hypoxia and death. CO>20%, skin cherry red
s/s of above glottis burn facial burns, singed nasal hair, hoarseness, painful swallowing, darkened mm, carbonaceous sputum, worse if standing in fire, clothing burned around chest/neck, obstruction comes quickly
s/s of below glottis burn pulmary edema wi 12-24hr, ARDS
tx on site cool burns wi 1 min reduces death. no ice! ABCs
Airway patency, soot, signed nasal hair, dark mm
Breathing adequacy of ventilation
Circulation presence and regularity of pulses, elevate burned limbs above heart to dec pain and swelling
pt w electrical burns tx as c-spine injury
the period of time to resolve life threatening probs from burn emergent resuscitative lasts up to 72 hours
with in th e72 hours what occurs hypovolemic shock, capillary permeability that causes fluid shift to interstitium. ends w beginning of diuresis
chemical burns decontaminate w water or NS
inhalation provide 100% humidified O2, may intubate,
monitor burns for VS, cardiac rhythm, LOC, resp status, O2 sat. check pulses distal from burns w electric
process of hypovolemic/burn shock capillaries more permiable, albumin moves to inerstitial (2nd spacing), hematocrit rises blood more viscus (dec blood volume inc viscosity),fluid moves to unburned areas in form of blisters, exudate, edema (3rd spacing),
shock is defined as dec tissue perfusion dec intravascular volume, dec venous return, dec ventricular filling, dec stroke volume, dec cardiac output, inadequate tissue perfusion.
parkland formulas amount of fluids(lacate ringers) given in the first 24hr. 1/2 in 8*, 1/4 in next 8*, 1/4 in the next 8*. 4mLx70kgx50%TBSA= 875/hr in 1st 8, 438/hr 2nd 8, 438/hr in 3rd 8.
solutions given after 12-24hr colloids(albumin). capillary permeability returning to normal
best assessment for adequate fluid resuscitation urine output. 0.5mL-1.0mL/kg/hr of urine output. ex:70kg pt=70x0.5mL=35mL; 70x1.0mL=70mL. ans=35-70mL/hr of urine.
arterial line preferred d/t vasoconstriction. SBP>90, HR<120, MAP>65
emergent burn care interventions cath if >15%TBSA, ABGs, CO levels, CXR if inhale injury, elevate burned limbs dec edema, IV analegesic (3rd* need less d/t nerve damage.)
assess for sulfa allergy burn ointments contain sulfa, start daily shower and tetanus shot if not done in last 10yrs
ongoing monitoring of burns airway, VS, LOC resp status, O2 sat, cardiac rythm, UA
ongoing monitoring of electrical burns neurovascular of brned limbs, urine for myoglobinuria and hemoglobinuria, NaHCO3 to alkalinize and serum the urine at pH of>6.0
acute phase of healing urine outp0ut inc, edema dec. takes wks to months.
clinical mans of acute healing phase of burns bowel sounds return, phychosocial support, WBC surround burns and phagotize,necrosis tissue sloughs off, fibroblasts lay down collegen and granulation occurs,
rehabilitation phase of burns resumeing func role, heal from functional or cosmetic surgery, most common prob is skin/jt contractures, hypertrophic scaring,
following a traumatic skeletal injury releasing fat globulins into tissues and organs Fat embolism syndrome (FES)
fx that most common cause FES long bones, ribs, tibia, pelvis,
tissues affected by FES lungs, heart, brain, kidneys, skin
s/s of FES chest pain, cyanosis, tachycardia, apprehension, dec PaO2, memory loss, inc temp, petechia axilla, feelings of impending doom, pallor to cyanosis, comotose
dx results of FES fat cells in blood, urine, sputum, dec PaO2<60, ST seg changes, prolonged PT, dec platelet/hematocrit levels, CXR white out
ABCDE of triage airway, breathing, circulation, disability, exposure
airway emergency assessment obstructions. s/s=dyspnea, cant talk, face/neck trauma
tx for airway head tilt, jaw trust, suction, nasal/oropharagel airway, trach, ventilate 100% prior to insertion, seizure precautions
emergency assessment for breathing fx, ribs, anaphylasix, penetrating injury, asthma
s/s of breathing emergency dyspnea, flail chest, dec/absent breath sounds, penetrating injury, cyanosis(asthma), tachycardia, hypotension.
tx for breathing emergency injured/critically ill pts have inc O2 demands, 100% O2 nonrebreather,
emergency assessment of circulation check carotids for rate/quality, skin temp, color, moisture, LOC, delayed CRT
emergency circulation tx insert 2 large bore (16g) needles, LR/NS, pressure to wound, type and cross for blood, check pulse distal to fx.
emergency disability neuro check
emergency exposure tx prevent hypothermia,
secondary survey Full VS,Give comfort, meds, History,Inspect
biologic terrorism. Anthrax inc 1-2 days-6wks. causes lung hemorage.
s/s of anthrax dyspnea, diaphoresis, fever, cough,chest pain. tx: cipro
small pox inc 7-17 days. air droplets,
s/s of small pox fever, HA, maylasia, pustules. tx no cure. 1980 global eradication
botulism 1nc 12-36hrs. death in 24. trans air/food.
s/s of botulism skeletal muscle paralysis, abd cramps, diarhea/NV, cranial nerve palsy. tx toxin inactivated by heating food to 212* or 10min.
plague (bubonic) inc 2-4 days person to person.
s/s of bubonic plaque hemoptysis, cough, fever, resp failure, lymph node swelling. tx streptomycin, gentamicin
tularemia bacterial inf. inc 3-10 days. aersol/intradermal.
s/s of tularemia fever, swollen lymph nodes, pnemonia, plueral effusions, sore throat, tx antibiotics gentamicin
hemolrrhage fever viral inf, person-person, body fluid, aerosl.
s/s of hemorrhage fever conjunctivitis, HA, hemorrhage of tissues/organs, organ failure. tx no cure, supportive measures
advantages of central venous cath (CVC) assess blood samples, dec risk of intravascular injury, immediate assess to central venous system, long term cath use
dis advantages of CVC inc systemic inf, invasive procedure
complications of CVC occlusion, inf, embolism, pneumothorax, cath migration
care for site of CVC sterile technique, transparent dressing, use chlorohexidine, dry x2 min, date/time new dressing, inj caps changed at reg inervals, flush w 10 ml NS.
removal of CVC remove sutures, pt perform Valsalva manuver, hold pressure w ointment dressing. inspect cath tip, document
Created by: vstein