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NUR 212 EXAM 1

QuestionAnswer
assess the heart IPPA=Inspection, palpation, percussion, auscultation
right atrium receives blood from vena cava, sends to right ventricle via tricuspid valve
right ventricle receives blood from right atrium, sends to pulmonary artery via pulmonic valve
left atrium receives blood from pulmonary vein, sends to left ventricle via mitral valve
left ventricle receives blood from left atrium, sends to the body via aortic valve
landmarks of the heart Mid clavicular line, Mid axillary line, Midsternal line, Vertebral line, Scapular line,
Auscultation - Stethoscope Bell“light low”; Diaphragm “high heavy" heart sounds
S1 sounds Lubb-closure of mitral/tricuspid valves, loudest over apex, synched with carotid pulse (systole)
S2 sounds Dubb-closure of aortic/pulmonic valves, loudest over base (dystole)
S3 sounds heart-fail-ure; heard in children and young adults (normal)early diastolic sound heard loudest over the apex of the heart just after S2
S4 sounds hy-per-ten-sion; hard wall, late diastolic sound heard loudest over the apex of the heart just before S1
Heard with problems related to flow across valves Murmur. Sound may radiate to axilla, neck, Heard in diastole and systole
murmur causes blood has touble going thru mitral valve. "woosh" backs up to lungs-cracles on left side
asses for JVD edema lung sounds, HR/sound, O2, pulse, place in supine position
JVD causes R sided hear failure-COPDers
tactile fremis vibration in apicies and dec. no vibration=blockage
bronchial lung sounds inspiration < expiration heard over the trachea, loud high pitched. heard elsewhere ABNORMAL
bronchovesicular lung sounds expiration = inspiration heard over the bronchioles, med pitched. heard elsewhere ABNORMAL
vesicular lung sounds inspiration > expiration heard over alveoli, soft, breezy
Abnormal Lung sounds Adventitious sounds-crackles “rales” not continuous rhonchi: continuous sound pleural friction rub, stridor
What if wheezing suddenly stops? bad. airways have closed
When is assessment of lung sounds necessary q 4* prn, assess skin color, I/Os, chest pain? SOB?
What if you do not hear any lung sounds check stethoscope
interview phase orientation Introduction / Purpose of interview
working phase Nurse gathers information r/t client’s health status
termination phase Summarize important points, validate this with client, indicate when you’ll be back
Clinical judgment r/t individual, family, or community responses to actual or potential health problems / life processes. Ns dx
Nursing Diagnosis Require nursing intervention, Within scope of nursing practice, Multiple diagnoses, Change frequently, Focus on human response, Provide “care”
Medical Diagnosis Requires medical intervention, Within scope of medical practice, Single diagnosis, Stay the same, Focus on disease, Provide “cure”
def of ns dx clinical judgement r/t individual , family, or community responses to actual or potential health problems
Nursing Diagnosis – (PES) P (problem), E (etiology), S (signs & symptoms)
actual ns dx 3 parts-: Impaired skin integrity r/t prolonged immobility secondary to fractured pelvis, as evidenced by (aeb) a 2 cm lesion on back
ns dx risk or high risk 2 part-Ex: Risk for injury r/t lack of awareness of hazards
ns dx for possible 2 part-Ex: Possible disturbed body image r/t isolating behaviors post surgery
ns dx wellnes 1 part-Ex: Readiness for enhanced nutrition
ns dx xyndrome Cluster of predicted actual or high-risk nursing diagnoses r/t a certain event or situation. 1 part statement.
ns dx for collaborative problems Actual or potential physiological complications that can result from disease, trauma, treatment, or diagnostic studies for which nurses intervene in collaboration with personnel of other health care disciplines. written as "risk for complication" w/o "r/t
ns goals Specific and measurable behavior or response that reflects a client’s highest possible level of wellness and independence in function Ex: “Will achieve pain control within 48 hours.”
ns expected outcomes Specific measurable change in a client’s status that is expected to occur in response to nursing care Objective criterion for measuring goal achievement Ex: “Will report pain severity below 4 on a scale of 0-10 by 24 hours.”
NOC - Nursing Outcomes Classification standardized language for nursing outcomes to evaluate effectiveness of nursing interventions. 5 point measurement scale for each outcome. Ex: Will have activity tolerance at a level of 3 (moderately compromised) on all selected indicators in 2 days.
NIC - Nursing Intervention Classification Standardized classification of treatments that nurses perform. 500 + interventions grouped into 30 classes
evaluation-NS dx 1. Assess client’s status 2. Compare response to the outcome criteria (goals) 3. Conclude whether the client is progressing toward outcome achievement 4. Continue / Revise / Discontinue problem
evaluation-collaborative problems 1. Assess the client’s status 2. Compare data to established norms 3 Judge whether data falls within acceptable ranges 4. Conclude if the client’s condition is stable, improved, unimproved or worse
Cardiac Blood Flow Oxygen-poor blood flows from the body into the RA. Through the RA into RV. RV pumps the blood to the lungs, where the blood releases waste gases and picks up O2. Newly oxygen-rich blood returns to the heart and enters the LA. Flows through the LA into the
Sympathetic NS of heart All areas of heart. HR,contractility, conduction AV node, vasoconstriction
Parasympathetic NS of heart SA, AV, some ventricular. HR, contractility, slow thru AV node
Properties of the Cardiac Cell-Automaticity Initiate an electrical impulse
Excitability Ability to be electrically stimulated
Conductivity Transmits an impulse along a membrane
Contractility Respond mechanically to an impulse
SA node: Fastest rate of automaticity *Primary pacemaker*of the heart Rate 60-100 bpm-Electrical Conduction System
AV node: Has a delay which allows for atrial contraction and filling of the ventricles. Rate 40-60 bpm-Electrical Conduction System
Bundle of His Has the ability to set initiate electrical activity. Rate: 40-60 bpm-Conduction System
Purkinje Fibers : Network of fibers that carry an electrical impulses directly to the ventricular muscle cells. Rate: 20-40 bpm-Conduction System
Heart Rate Count the QRS complexes in a 6 second strip and multiply X 10 8 X 10 =80 bpm
Heart Rate-Rule of 300. R-R interval R-R interval is 1 large boxes, rate = 300 beats/minute (300 ÷ 1) 2 large boxes, rate = 150 beats/minute (300 ÷ 2) R-R interval is 3 large boxes, rate = 100 beats/minute (300 ÷ 3) R-R interval is 4 large boxes, rate = 75 beats/minute  (300 ÷ 4)
Heart Rate-Rule of 1500 R-R interval is 11 small boxes, rate = 1500 ÷ 11=136 bpm
Sinus Bradycardia SA node fires at a rate < 60 bpm. May be normal rate for athletes
Symptomatic bradycardia HR < 60 bpm and is inadequate for the pt’s condition, causing symptoms, ex. chest pain, syncope.
s/s of sinus bradycardia Pale, cool skin, hypotension, weakness, angina, dizziness, confusion or disorientation, shortness of breath.
causes of bradycardia Valsalva maneuver, hypothermia, increased intraocular pressure, vagal stimulation Medications (B-adrenergic blockers, calcium channel blockers) Disease states: Hypothyroidism, increased intracranial pressure, hypoglycemia, Inferior MI
tx of bradycardia Atropine to increase HR Pacemaker (temporary initially) and Medication induced: hold, d/c, reduce dose
Transcutaneous pacemaker (External pacer) Used in emergency situations to provide adequate heart rate and rhythm. uncomfortable muscle contactions
electrical capture Rhythm strip
mechanical capture Check pulse, BP, on-going assessment.
Transvenous pacemaker Leads threaded transvenously to the right atrium or right ventricle and attached to external power source. emergent.temporary until permanent pacemaker in place
Epicardial pacing Atrial and ventricular pacing leads to epicardium during heart surgery.
Permanent Pacemaker Power source implanted, Overnight stay to monitor function Reprogrammed before discharge Monitor wound Arm sling No vigorous activity with affected arm, shoulder for 6 weeks Phone check
Premature Ventricular Contractions (PVCs) in the ventricles.QRS is wide and distorted.Normal heart: Usually benign.Heart disease: May reduce CO, precipitate angina, HF,depending on frequency. Ventricular irritability in CAD/acute MI.Monitor pts response to PVCs.Assess pts apical-radial pulse ra
associated w PVCs Stimulants; caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol. Digoxin. Electrolyte imbalances Hypoxia Fever Exercise Emotional stress. Disease states: MI, mitral valve prolapse, HF, CAD
tx for PVCs Oxygen therapy for hypoxia Electrolyte replacement Medications: B-adrenergic blockers, amiodarone, lidocaine.
Ventricular Tachycardia occurs with 3 or more consecutive PVCs, LIFE Threatening, dec cardiac output, risk for V-fib,
ventricular tachycardia is associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome, drug toxicity, central nervous system disorders. May have no evidence of cardiac disease.
significance of V-tach Stable: Pt can have pulse/BP wnl. Unstable: NO PULSE or become unstable with sustained VT. Sustained VT causes a severe decrease in cardiac output due to decreased ventricular diastolic filling times and loss of atrial contraction. Results in hypotensi
tx for V-tach with pulse Medications: IV amiodarone, lidocaine, sotalol, procainamide. Synchronized cardioversion
tx for V-tack with no pulse Call Code CPR Defibrillation Vasopressors: Epinephrine/Vasopressin Antidysrhythmics: Amiodarone/Lidocaine
Ventricular Fibrillation LIFE Threatening. Death without rapid interventions. sudden cardiac death. Associated with: Acute MI Myocardial ischemia Heart failure Cardiomyopathy
V-fib tx NO PULSE: No cardiac output Call Code- unless DNR status CPR and ACLS measures. Defibrillation Vasopressors: Epinephrine/Vasopressin Antidysrhythmics: Amiodarone/Lidocaine
CPR 30:2, breath enough to make chest rise, rotate rescuers q 5 cycles,
AED (defibrillator) Defib X 1 then CPR with rhythm checks every 2 minutes First shock eliminates VF 85% of the time
use of Defibrillation Emergent VF & pulseless VT Conductive pads/paddles w/gel Not synchronized No sedation Energy level
use of Cardioversion Elective or emergent Afib, Aflutter, SVT, V.tach w/pulse Conductive pads/paddles w/gel Synchronized Sedation preferred Energy level
Implantable Cardioverter-Defibrillator (ICD) functions Monitors HR and rhythm Identifies VT or VF,paces and fibrillates
ICD for Survivors of sudden cardiac death Have spontaneous sustained VT Have syncope with inducible VT/fib High risk for future VT/V fib (cardiomyopathy)
Pulseless Electrical Activity Electrical activity, but no mechanical activity. NO PULSE, no cardiac output Prognosis is poor. can be any rhythm, but no pulse
Most common causes of pulseless electrical activity Hypovolemia, hypoxia, metabolic acidosis, hyperkalemia, hypokalemia, hypothermia, drug overdose, cardiac tamponade, MI, pneumothorax, trauma, pulmonary embolus.
tx for pulseless electrical activity CPR Epinephrine Correct underlying cause
Asystole Total absence of ventricular electrical activity. pt is Unresponsive, pulseless, apneic
tx for asystole CPR and ACLS measures, if not DNR status Medications-epinephrine- (Atropine is no longer recommended for routine use in the management of asystole). (AHA 2011 guidelines) Family presence/engagement.
wandering base line on EKG.. pt moving around
Hyperkalemia serum K concentration > 5.5 mEq/L, Neuromuscular, resulting in muscle weakness and cardiac toxicity When severe, can degenerate to ventricular fibrillation or asystole.
causes of hyperkalemia The most common cause is pseudohyperkalemia caused by hemolysis of RBCs in the blood sample. Increased K intake Drugs that impair renal K excretion Acute or chronic kidney disease Metabolic acidosis as in diabetic ketoacidosis.
signs of hyperkalemia 1st sign: peaked T waves K+ level >6 meq/L. 2nd sign: prolonged PR interval K+ >7 meq/L. 3rd sign: absent P wave with widen QRS complex > K+ 8-9 meq/L. Atrial activity is lost and stage is set for VT/VF. 4th sign: VT/VF leading to SCD. Price paid for ign
tx for hyperkalemia from fastest to slowest IV Calcium Gluconate (antagonizes adverse cardiac conduction abnormalities – only lasts a few minutes) IV Glucose-Insulin-bicarb (shifts K+ into cells) Albuterol Kayexalate Hemodialysis
Hypokalemia < 3.5 mEq/L, Deficit in total body K stores The most common causes are excess losses from the kidneys or GI tract. s/s=muscle weakness and polyuria; cardiac hyperexcitability may occur with severe hypokalemia. sinus bradycardia
causes of digoxin toxicity Increased doses Reduced kidney function Including dehydration
s/s of digoxin toxicity Confusion Irregular pulse Loss of appetite Nausea, vomiting, diarrhea Palpitations Visual changes
do not remove telemetry for showers
Parenteral Solutions Crystalloids (solutions with small molecules that flow easily from vascular into cells and tissues)
Isotonic same osmo as body fluid No fluid shifts
Hypertonic >serum osmo Fluid shifts from intracellular to extracellular fluid
Hypotonic <serum osmo Fluid shifts from extracellular to intracellular and interstitial
Parenteral Solutions Colloids plasma expanders, stay in vascular space
Hypertonic Colloids Albumin, dextran, hetastarch. Other=Whole blood, TPN, tube feedings
Isotonic concentration of dissolved particles similar to plasma solutions remain in EC space and increase IV. 0.9% NS, LR, 5% DW, ringers solution
hypotonic lower solute concentration fluid shifts from IV space to IC & IS. 0.45% NS, 0.33% NS, 0.2% NS, 2.5%DW
hypertonic higher solute concentration fluid shifts from IC space to EC. 3 & 5% NS, 5%D&0.45%NS, 5%D&0.9%NS, D5LR, D
s/s of fluid excess inc BP, edema, JVD, crackles
first use isotonic to fill the tank, then hypotonic to fill the cells, hypertonic pulls out of cells
renal pts shouldnt have NSAIDS
name electrolytes K, Na, Cl, Ca, Phos, Mg
functions of electrolytes muscle contractions, neural function, hormone, release, enzyme reactions, acid/base balance
causes of hypokalemia (kidney) burns, trauma, diuretics,GI losses, cushings, stess, dec K intake, alkalosis
effects o hypokalemia (kidney) impairs neuromuscular trans, dec resp muscles, inc exretion of urine, dec GI func, impairs electrical conduction of the heart
s/s of hypokalemia (kidney) dec/absent deep tendon flexes, hypoventilation, polyuria, inverted t wave, dysrhythmias, prolonged QT inters
tx for hypokalemia (kidney) enc inc intake of K, parenteral replace of K, monitor postural BP, I/Os, iv site infiltration, check dig level (dec K protentiates Dig tox)
causes of hyperkalemia (kidney) dec excretion of K, excess K intake, acidosis (inc release of K from cells)
Effects of hyperkalemia (kidney) dysrhythmias, dec GI func,
s/s of hyperkalemia (kidney) weakness/flaccidity, muscle irritability (twitching), paresthesias, N, cramps, diarrhea, oliguria, tented T waves, prolonged PR inters, widened QRS, bradycardia, V-fib, asystole
tx for hyperkalemia (kidney) restrict K, ROM, telemtry
meds for hyperkalemia (kidney) IV Ca=dec effects on heart, NaHCO3, Glucose, Insulin=drives K back into cells, Cation-exchange resins=inc excretion of K, dialysis=inc excretion of K
causes of hyponatremia (brain) escessive H2O intake, V, diarrhea, diuretic, 3rd spacing (Na trapped), ascites, Edema, Burns, SOB, dec Na intake, too many tap H2o enemas(3 max)
effects of hyponatremia (brain) cellular edema leads to crebral edema, weakness, muscle cramps
s/s of hyponatremia (brain) lethargy, coma, HA, weakness, abd pain, muscle twitching, convulsions,, apprehension, dec volume may lead to shock
tx for hyponatremia (brain) IV NS, DC diuretics, monitor postural VS, I/O, daily wt, inc Na intake, always irrigate w NS, 3 enemas max
causes of hypernatremia (brain) dec H20 intake, excess Na intake, inc aldosterone output, dec renal excretion, IV overload
effects of hypernatremia (brain) thirst
s/s of hypernatremia (brain) Hypertonic=dry, sticky muscus membranes, tenting turgor, mental changes, flushing, dec urine output, thirst, inc serum osmolality. Isotonic=wt. gain, edema, inc BP, tachycardia
causes of hypocalcemia (check albumin) dec absorption r/t kidneys, retention of phosphorus, dec ionized Ca r/t alkalosis, inc loss (draining fistulas), dec intake
effects of hypocalcemia (check albumin) muscle spasms, hyperactive cardia muscle
s/s of hypocalcemia (check albumin) alt mental status, siezure, numb/tingling in fingers/toes, bleeding, prolonged QT/ST, chvostecks, trousseaus sign
Chvostecks tap below temple on facial nerve twitching
Trousseaus sign contrect circulation w BP cuff for 2 min-palmer flexion.
tx for hypocalcemia (check albumin) EKG, VS, bleeding, safety, trach tray for glottis spasm, teach effect of antacids on absorption
causes for hypercalcemia (check albumin) immobility, metastasis, multiple myeloma, inc intake, acidosis, inc PTH
effects of hypercalcemia (check albumin) dec muscle tone, numbness, anorexia, mental lethargy
s/s of hypercalcemia (check albumin) lethargy-coma, bone pain, muscle cramps, hypotonicity, numbness/tingling infingers and toes, anorexia, N/V, constipation
tx for hypercalcemia (check albumin) NS IV (dilutes Ca serum), loop diuretics (enhances Ca excretion), no thiazides (inhibits Ca excretion), phosphorus preps/mithramycin (inc bone deposition of Ca), assess for renal caluli
causes of hypophosphatemia (r/t nutrition/diuretics) dec intake, chronic antacid ingestion, hyperparathyroidism, hypercalcemia, vit D def, alkalosis, ETOH abuse
effects of hypophosphatemia (r/t nutrition/diuretics) impaired cellular energy and O2 delivery to cells, dec platelet aggregation
s/s of hypophosphatemia (r/t nutrition/diuretics) muscle weakness/ pain, bleeding, depressed WBC func, confusion, anorexia
tx for hypophosphatemia (r/t nutrition/diuretics) phosphorus supps, DC phosphate binders, DC antacids
causes of hyperphosphatemia (r/t nutrition/diuretics) dec excretion of P, inc intake, hypoparathyroidism, hypocalcemia, acidosis, bone metastasis, liver disease
effects of hyperphosphatemia (R/T NUTRITION/DIURETICS) tetany (short term), soft tissue calcification (long term)
s/s of hyperphosphatemia (r/t nutrition/diuretics) tetany, numbness/tingling fingers/toes, soft tissue calcification, chvostecks/trousseaus sign, coarse, dry skin
tx for hyperphosphatemia (r/t nutrition/diuretics) phosphate binding antacids, Ca supps, vit D, ,restrict P
Ca and Mg act as.. sedatives to muscles
sodium think... brain
K=potassium is.. kidney. when inc kidney can get rid of K
Ca and Phos is always... inverse of each other
Ca, Mg and K go... together
electrolyte issues pt must be put on... monitor
causes of metabolic acidosis
what are the minimal observations that must be made during a blood administration VS before, 15 minutes after starting and after completion
when is a transfusion reaction most likely to occur within 15 minutes after begining the transfusion
what is the most common transfusion reaction fever
whole blood is rarely given unless... 25% of total volume is lost
whole blood is... hypertonic, has everything in it.
need transfusion when hemoglobin is at 7
packed red blood cells 90% of plasma is removed, 70% of leukocytes are removed. dec reactions to happen (fever)
each unit raises ... hgb=1gm and hct=2-3%
our bodies react to what part of the blood from donar WBC
fresh frozen plasma is used for... rapid reversal of coumadin. inc clotting factors. 1mL of FFP=1iu of each coag factor
pt needs infusion of platlets when count is < 10000
1 dose of platelets = 6 units (60000 platelets) (1u=10000) lifespan is 3-4 days
factor given before procedure if low fibrinogen cryoprecipitate: factor VIII< XIII
protein component of blood albumin. used for volume expansion. osmotically. may cause volume overload
reasons for transfusions increase volume, increase RBC, component replacement.
pt with dec RBC can be due to chemo tx
autologous/autotransfusion self. may donate 1u q 3-4 days up to 3 days before tx if hgb>11.
donor is ... the majority of transfusions, more risk
order of transfusion (first 5 steps) obtain consent, take VS, prime the tubing/filter w NS, inspect the bag for leaks, clots, unusual color, compare the bag label with the pt chart and blood bank forms
order of transfusion (last 4 steps) two nurses compare ID blood band with tag on blood bag, transfuse the first 50ml slowly, monitor, repeat VS after 15 mins and every hour until complete, document outcomes, names of personnel, start and end times
procedure before adm consent, assess the pt, verify IV site (NS only w filter), report T of 100>, preordered meds (tylenol, benadryl 30 min prior), laxis between units, go for the blood
blood must be transfused... within 15 minutes of arrival to room or returned to blood bank
procedure when blood enters room ID in the room 2 licensed nurses, label with slip and armband, name and BD, Mr. #, blood type, Rh, exp date, inspect the unit of blood, teach the pt
begin the transfusion 50ml over first 15-20 min and stay w pt, adjust rate.
preference of time of a normal blood transfusion 2 hours
preference of time of a transfusion on a pt with CHF 4 hours
NO IVPB or other meds in blood
during the transfusion may arm blood per P/P, assess T >1.8F, chills, tachycardia, lung sounds, SOB, wheezing, hives, rashes, cyanosis, hypotension
listen for crackles ... before during after
priority assessment for an inc temp of 1.8 VS, look at bag, stop trans call dr. Dr will order tylenol, blood cult, antibiotic, give washed RBC
systemic response (ABO) incompatibility (hemolytic) immediate reaction, life threating, chills, fever, low back pain, jematuria, renal failure, >HR, >RR, <BP.
intervention of systemic response incompatibility (hemolytic) stop transfusion, call dr, tuging and unit to blood bank, get UA
most common reaction of transfusion febrile r/t sensitization to donor WBCs, platelets or plasma proteins. stop trans, call dr, meds, washed RBC
allergic reaction to transfusion mild to severe, reaction to plasma poteins. itching, hives, chills, chest pain, SOB, coughing, >BP & HR, JVD.
intervention of allergic reaction to transmission raise HOB, O2, slow blood trans, call dr, meds
transfusion reaction-sepsis contaminated product
intervention for sepsis from transfusion stop transfusion, call dr, cultures, send bag with tubing to lab, transfusion wi 4hrs of start.
s/s of sepsis chills, V, fever, diarrhea, shock
TRALI-transfusion related acute lung injury within 30 min-6hrs, hypoxia PO<90 (room air), new bilatreal infiltrates on frontal CXR consistent w edema, self limiting
happens because antibodies to leukocytes, more common in multiparous women
s/s of TRALI fever, SOB, cough, hypoxemia, hypo or hypertension, tachycardia, cyanosis
tx for TRALI stop the trans, may need a ventilator, self limiting improve over 4 days, give leukocyte reduced products
what is blood screened for.. syphilis, HBV, VBC, human t-cell lymphotropic virus, HIV
trans of packed RBC, 90 min in pt c/o SOB...priority assessment... lung sounds, VS, JVD, I/O, hives, chest pain.
what is the Ns next course of action dec trans, call dr
what med will the NS anticipate administering lasix
trans of FFP..PO=89% on RA, T 101.4 take rest of VS. pt has TRALI
Ns responsibility during reaction stop trans, NS KVO, call dr, VS freq, stay w pt, ready for code, meds (antihistimines, steroids, vasopressors, fluids), notify blood bank, UA and lab draw, blood, tubing and records to lab, do paperwork for suspected reaction
the fifth VS pain
pain prevents cough and DB, amb
ability to reduce or increase the decgree of perceived pain through modulation of the impulses at the gate gate control theory
open or close the gate by pharmacological manipulation, transduction, transmission and modulation and psychological intervention
sudden , time limited, normal healing, know cause.. acute pain
gradual or sudden lasting > 3 months, waxes and wanes chronic pain
if we dont tx acute pain it will be chronic
#1 reason for adult disability pain
pain due to damage or dusfunctional nerves neuropathic. assess motor functioning
spinal nerves serve both deep structures and skin so sensations can be mislocated refered pain
3rd leading cause of work absence untreated pain-affects ability to do ADLs, inc morbidity w untreated acute/chronic pain
elderly tend to under report pain
interventions for pain rest, ice, compression, elevation (RICE), reposition, exercise, immobilization, heat, massage, counterstimulation (TENS, acupuncture)
psychological interventions for pain diaphragmatic breathing, relaxation, imagery, hypnosis, reduce anxiety, music, distraction,
analgesic ladder steop 1 (mild 1-3) non-opioid +adjuvant, step 2 (mod 4-6) + opioid (codeine or oxycodone), step 3 (severe 7-10) opioid round clock
Non-opioid- ketorolac (Toradol) loading dose 30mg IV then 15-30 q 6hrs. (15mg if <50Kg and/or elderly). no more than 5 days, GI toxicity, no renal pts (can cause failure)
NS interventions for Toradol VS, I/O, give slow and higher up on tubing
interventions for narcotics monitor resp func, N/V, contipation, urinary retention
adjuvant meds tricyclic antidepressants, anticonvulsants, steroids, muscle relaxants, local anesthetics
fear of pts associated with pain will become addicted to opioids (<1% do), if pain is tx early theyll run out of options in future, unpleasant side effects, inc pain means disease is getting worse, worry about being a good pt
narcotics and the elderly provider fears, changes in LOC, RR, delirium, drug interactions, constipation
dosing the elderly dec normal adult dose by 25-50% and >40 w < renal function
drugs to avoid with the elderly demerol, propoxyphine, pentazocaine,antihistamines, sedatives, benedryl
delivery methods of drugs IM, R, PO, nasal, SC, transdermal, SL, PCA
opiate naive pt unresponsive, RR 6, PO 44% stop the PCA, O2, call Dr, narcan,
priority assess this pt prior to PCA and during pain, resp, PO, VS, lungs, LOC, no family push, if pt has cpap then no PCA
risks for resp depression basal infusion, advanced age, obesity, upper abd surgery, OSA, concurrent use of CNS depressants, renal, cardiopulm or hepatic impairment, pump programing errors, families pushing PCAs, lack of opioid tolerance
PCA meds morphine, Hydromorphone (Dilaudid), demoerol, fentanyl
rules of PCA compentant pt, no family pushing, on demand and/or basal,
interventions for PCA VS, how much, how often, how many attempts, night time awakening
catheter into the potential space between the dura and vertebral canal epidural-for analgesia not anesthesia
epidural for ortho, abd prodecures L4-5 or L3-4
epidural for OB, thoracotomy T5-6
meds for epidural presevative free, MS, Dilaudid, Demerol, Fentanyl, Bupivicaine, Ropivicaine
assessment for Epidural VS (opiate), motor (aneshetic), sensation (anesthetic),
the order in which things leave us pain, temp, touch, proprioception, skeletal muscle tone. goal is to rid pain and leave motor
effects of narcotic resp depression, pruitis
effects of anesthetic systemic, circumoral numbness, tingling, ringing in ears, metallic taste, slow speech, twitching, orthostatic hypotension, motor
assessment for epidural dressing, tubing, pump, no other narcotics, VS (RR <8 stop), narcan available, I/Os, voidingassess protime before DCing
give med to purposefully lower the level of consciousness conscious sedation-need concent
properties of conscious sedation respond purposefully to tactile or verbal commands, maintain reflexes to protect airway, CV function maintained
meds for conscious sedation medazolam(versed), fentanyl(Sublimaze), ketamine(Ketalar), propofol(Diprivan)
assessment for conscious sedation NPO, consent, cardiac monitor continuous
anxiolysis light sedation. respond normally to commands, may be drowsy, but easily awakened, no consent. assess VS, PO
Complete spinal cord injury total loss of motor and sensory below the level of the lesion
incomplete spinal cord injury varying motor and sensory loss
anterior cord syndrome complete motor loss, loss of temp and pain below level. proprioception, vibration, touch, deep pressure intact
brown Sequard syndrome can feel the side they cant move, cant feel the side they can move
central cord syndrome motor loss upper extremities, varying sensory loss
posterior cord syndrome vary rare, good muscle power, pain and temp, difficulty coordinating movement of limbs, loss of proprioception
T11-12 damage to lumbar nerve roots Conus Medullaris-arcflexic bowel and bladder, flaccid lower extremities
injury to lumbrosacral nerve roots below conus medullarus cauda Equina Syndrome-loss of sensation in sacral area, arcflexic bowel and bladder, flaccid extremities
vertebral deslocation, herniated disc, compression Posterior syndrome-weakness in isolated muscle groups, tingling, pain, bowel and bladder dysfunction
assessment and tx immediate at the scene airway, supine, cardiac monitor, stabilize neck, avoid rotating, flexing, extending, immobilization
assess in ED VS, O2, cardiac monitor, IV access NS or LR, Stabilize spine, steroids, NG tube, foley, ted hose, PPI, DVT prophylactics, analgesics, vasopressors, external fixation device
if pt can feel you stroke their inner thigh.. they have bowel and bladder function. if not call dr
high doses of steroids reduce edema to allow flow
immediate resonse that occures with complete transection spinal shock
spinal shock parasympathetic dominates. resp insufficiency in C1-4, Poililothermia, dry skin, loss of skeletal muscle func, bowel and bladder dysfunction, loss of sexual function, autonomic reflexes and venous tone
medulla cant reg temp, no sweat poikilothermia
C1-2 injury fatal at the scene
C3-4 weak diaphragm
D5 shrug shoulder and off vent, use motorized wheelchair
C7 independent feed and transfer
upper motor neuron impulses from cortex to cord-lesion above the sacral segment
upper motor neuron injury reflexes are initially flaccid, then hyper, muscles atrophy later, spastic or reflex bladder, bowel (above S2)
lower motor neuron spinal and motor neurons correspond to vertebral segment.-lesion at or below sacral
lower motor neuron injury flaccid muscles, no tone, no reflex respnse early atrophy, paralysis, flaccid bladder, enema digital removal
after spinal shock is over autonomic dysreflexia-T6 and above, exaggerated response to noxious stimuli, message cannot go thru the cord. HOB at 90% call DR
autonomic dysreflexia constriction of vessels below the level of the lesion and vasodilation above lesion
what happens with autonomic dysreflexia above lesion=flushing, bradycardia, HA, nasal stuffines. below lesion=HTN, pale skin, goose bumps, N, restlessness
autonomic dysreflexia can cause CVA, SAH, seizure and death
patchy sensation in upper extremities, very weak bicep/tricep strength bilaterally, mod strength in LE, no fx, central cord injury. bedrest w hard cervical collar, Methylprednisolone IV per protocol
full active range ROM of the LLE w no sensation. sensation intact to the RLE w no voluntary mvmt browns Sequard
resp depression can occur in pts recieving... opioids
what leads pts to think pain is necessary spiritual beliefs
after an initial dose of opioid analgesic is given subsequent doses should be... adjusted in accordance w the individual pts respnse
vicodin (hydrocodone 5mg+acetaminophen 500mg) is equal to... 5-10mg of morphine
Created by: vstein