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NUR 212 EXAM 1
| Question | Answer |
|---|---|
| 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 |
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vstein
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