Louis Streb Exam 2

Louis Streb Exam 2 Unit 4 Chapter 29 Where does gas exchange happen? Alveoli in lungs Bad gas exchange = perfusion issue, or clotting issues PE:  clot in lung.  perfusion  Most common cause of preventable death in patients. Symptoms get misdiagnosed.  Thrombus is carried in blood stream & lodges to another area  (Fat emboli, fatty deposit)  DVT/VTE moves/breaks off & travels to r. side of heart.  Causes hypoxemia Risk factors:  immobility, central caths, surgery, pregnancy, obesity, age, genetics, hx of thromboembolism.  Smoking and birth control BIG RISK!!  Estrogen therapy, HF, stroke, cancer, or traumas  Foreign objects (broken IV cath)  Fat emboli from fx of femur; oil emboli from diagnostic procedures Prevention:  ambulating, scds, prophylactic anticaogs, no pressure under popliteal space  Don’t place SCDs if you forgot 4 hours ago- ask dr  Drink plenty of water, position change often, no crossing legs, get up q5 mins  (pts at known risk for PE)Small doses of heparin or LMWH or indirect thrombin inhibitor  Ongoing risk for VTE/PE may need preop placement of retrievable IVC filter  Tell patients to stop smoking esp on hormone contraceptives  Reduce weight, more physical activity S/S:  Resp - dyspnea, pleuritic CP, sudden onset, impending doom, hemoptysis, dry or productive cough, pleural friction rub, crackles/wheezing  Cardiac – tachycardia, JVD, syncope, cyanosis, hypotension  Abnormal heart sounds, s3/s4; EKG change w/ ST segment/ T wave changes  WATCH FOR CARDIAC ARREST/FRANK SHOCK  Apprehension, restlessness, impending doom, diaphoresis, low grade fever, petechiae over chest & axillae,  Sao2. RRT – patient with hypotension, SOB, CP!! Lab:  hyperventilation triggered by hypoxia & pain & causes resp. alkalosis (Low PaCO2) on an ABG.  PaO2-FiO2 falls r/t “shunting” of blood from right side of heart to left w/o picking up oxygen from the lungs. This causes PaCO2 level to  resulting in resp. acidosis.  Later metabolic acidosis happens from buildup of lactic acid caused by tissue hypoxia.  Labs for if a PE is suspected: BMP, Troponin, BNP, D-Dimer.  D-Dimer  w/ PE (if normal or low = NO PE) Genetics: Factor V Leiden Imaging diagnostics:

 Pulm. Angiography is th “gold standard” diagnostic.  Or a CT. (V/Q scans not used as much – but could be considered in certain situation – if patient is allergic to contrast dye)  CXR  Doppler Care of patient w/ PE:  02 – NC/Mask  Reassure patient; high-fowlers; tele monitor; IV access  Continuous pulse ox  Respiratory assessment q30mins – listen to lung sounds, measure rate, rhythm, work of breathing  Checking skin color, cap refill, trachea position  Cardiac status – compare BP in both arms!; check pulses for quality; tele monitor; check JVD  f/u w/ imaging/labs  examine thorax for petechiae, administer anticoags, assess bleeding, handle patient gently, initiate bleeding precautions Massive PE:  clot buster (TPA) right away.  Severe hypotension, cardiac arrest, severe bradycardia, shock, resp. distress  Embolectomy Low risk: fibrinolytics not warranted b/c of risk for bleeding Galen lab values : PT – 11-12.5 seconds; pregnancy  (1.5-2.5 x norm on warfarin ) INR – 0.9-1.2 seconds. Desirable therapeutic range 2-3 x normal level (on warfarin ) PTT – 20-30 seconds. Pregnancy  (1.5-2.5 x normal on heparin ) aPTT – 30-40 seconds (1.5-2.5 x normal on heparin )  Look @ pts PTT/aPTT b4 therapy.  tPa/Activase/Alteplase  INR should be 2-3 w/ heparin/warfarin  Antidote for heparin is protamine sulfate  Antidote for warfarin is Vit K (injectable phytonadione ) Iv crystalloid solutions  restore plasma/prevent shock  Monitor ekg & pulm artery and central venous/right atrial pressure.   fluids can worsen pulm. HTN and lead to r. sided HF Drug therapy  vasopressors for hypotension  Norepinephrine (levophed), epinephrine (adrenalin) dopamine (intropin)  Drugs that increase myocardial contractility (positive inotropic agents) milrinone (primacor) dobutamine (dobutrex)  Vasodilators nitroprusside (nipride, nitropress) Respiratory failure  PaO2 under 60 failure  PaO2 70-80 resp distress

Displaced tube, obstructed tube(secretions/mucous plug), pneumothorax, equipment problems Maintain a patent airway by suctioning if these conditions are present:  Secretions,  peak airway (inspiratory) pressure (PIP)  Rhonchi   breath sounds How to prevent VAP  HOB above 30  Perform oral secretion suctioning  Ulcer prophylaxis  Aspiration precautions  Pulm. Hygiene Chest trauma: Flail chest –  broken ribs. Paradoxical motion. Seesaw breathing  2 or more ribs broken in 3 or more places or 3 or more ribs broken in 2 places.  Monitor for pneumothorax for broken ribs Causes: traumas, falls, maybe a large heavy dressing. Hemothorax: blood in thoracic cavity Chest tube. Pneumothorax: air in thoracic cavity Chest tube. Tension pneumothorax: worse of the thoraxes; when you have a pneumothorax without relieve. For example you get a open chest wound and put a occlusive dressing & tape all 4 sides. Air can’t get out. Causes a worsening pneumo. If you have a chest tube that is occluded. Lung is unable to re-expand, worsens the pneumothorax or hemothorax. Can reduce cardiac output and cause cardiac tamponade. Needle aspiration first then chest tube . Chapter 27 Pg 559-563 Chest tubes : used for lung reexpanision 3 chambers – Chamber 1 – close to patient; drainage from patient Collected in the first 24 hrs. Mark it at the start of your shift. Check it sporadically during your shift. Chamber 2 – 2cm of water – water seal chamber. Check at beginning of shift. Add sterile water to chamber If lower than 2 cm. this prevents backflow. Chamber 3 – suction control (dr will decide if they want suction ordered or not/how much) If chest tube doesn’t seem to be working notify dr that they may want to order suction. If suction is needed it’s normally (-20mmHg) When to notify the physician:  Drainage of fluid should never fill so much that it goes back into the tubing. It will occlude that pathway and cause obstruction.  (If you can’t get more drainage/air out of pleural space r/t blockage it will cause a tension pneumothorax!)  Excessive bubbling = air leak. Notify! (start at pt & work way down to look for leaks)  No drainage w/in 24 hrs. Notify!

 Drainage of > 70 mL/hr. Notify!  Seeing eyelets. Notify!  Tracheal deviation  Sudden onset/  intensity of dyspnea  Oxygen sat < 90%  Chest tube falls out of patients chest (first cover w/ dry sterile gauze)  Chest tube disconnects from chamber? Put in sterile water and keep below level of patient) Patient chest tube comes out? Assess respiratory status first before deciding if you need to call RR. If patient is tolerating the tube out & respiration assessment looks good, you do not need to call rapid. But let physician know patient’s status & that tube came out. What to assess if issue w/ chest tube:   drainage/no drainage – Tracheal deviation, listen to lung sounds, check 02 sats, work of breathing, look at rise/fall of chest.  Assess chest tube hourly for the first 24 hrs. assess type of drainage in collection chamber.  After 24 hours start checking q8hr.  Tidaling/gentle bubbling is normal. Causes: know natural causes/unnatural causes Placement: hemo - 5 th interior costal space/mid axillary Air drainage – typically higher about 3 rd inter costal space mid axillary Do not “strip” chest tube! Use hand over hand “milking” motion!! Once chest tube is out: Monitor 02 sat/rr/work of breathing. Monitor 2qhr. Semi fowler position or chair ASAP. IS. **Empyema – complication of pneumonectomy – purulent material in pleural space. Develops a bronchopleural fistula. Chapter 24 Pleural effusion  Fremitus- vibration felt through chest wall when patient speaks  Fluid in pleural space.  Restricts lung. Perfusion problem. Chapter 37 HIT heparin induced thrombocytopenia  Serious immunity mediated clotting disorder. Unexplained drop In plts.  Occurrence  b/c of  use of heparin.  More common after exposure to unfractionated heparin.  Antibodies are directed against the heparin rather than patients own cells. Incidence higher in females who are treated w/ unfractionated heparin longer than 1 week. Thrombocytopenia  first seen in skin/mucous membranes resulted from excessive bleeding in tissues.  Ecchymoses  Purpura  Mucous membranes bleed easily  Can result in anemia  Small micro clots can block capillaries in major organs causing tissue ischemia

** extra dose can be taken if develop  thirst or urine. **severe dehydration** Desmopressin IV/IM If patient ends up with ulcers of the mucous membrane, allergy, sensation of chest tightness, lung inhalation, upper resp lung infx then switch to Oral or SubC Vasopressin. DW. Measuring intake/output, check urine specific gravity. Teach patient to take in what they put out!! Polyuria & polydipsia indicate need for another dose. Drug therapy for DI can cause fluid overload. Weigh self daily. Weight gain of 2.2lb , along w/ s/s of water toxicity, persistent h/a, acute confusion, N/V, instruct pt to go to ED immediately. Syndrome of Inappropriate Antidiuretic Hormone: SIADH or Schwartz-barter syndrome is a problem in which antidiuretic hormone (ADH, vasopressin) is secreted when plasma osmolarity is low/normal. Resulting in water retention & fluid overload.  in plasma osmolarity normally inhibits ADH production & secretion. Dilutional hyponatremia (  in serum Na) & fluid overload. (Na didn’t actually decrease – it’s just diluted)  in blood bL.  kidney filtration & inhibits releases of renin & aldosterone which  urine Na loss & causes greater hyponatremia. Conditions that cause SIADH: recent head trauma, cerebrovascular disease, TB or other pulm disease, Cancer, past/current drug use) s/s –  fluid vL overload signs/sx (crackles, SOB, edema, JVD)  patients can experience serum Na < 110. May be lethargic, h/a, hostile, disoriented, change in LOC. Can cause szs & coma.  H20 retention causes urine vL. To  & urine osmolarity to  . Nursing interventions for SIADH:  restrict fluid intake, promote excretion of h20, replace Na. Interfere w/ action of ADH. Monitor response, prevent complication. Teach pt about fluid restriction.  Fluid restrictions can be from 500-1000 mL/day.  Use saline instead of h20 to dilute tube feedings, irrigate GI tubes & when giving drugs by GI tube.  Weight gain of 2.2 lb or more per day/gradual  over several days is a major concern.  1 KG = 1 L of fluid.  Use frequent oral rinses but teach patient to not swallow the rinse. v/s changes include full bounding pulse to hypothermia Drug therapy: vasopressin receptor antagonist ( vaptans ) tolvaptan or conivaptan . Treats SIADH when hyponatremia is present in hospitalized patients. These drugs promote h2o excretion w/o loss of Na. Tolvaptan is PO. (black box warning that rapidly  in serum Na levels (those greater than 12 mEq/L increase in 24 hrs) causes CNS demyelination that can lead to complications including death. When this drug is used at higher doses/longer than 30 days, r/f liver failure & death. Conivaptan is IV. Tolvaptan & Conivaptan can only be administered in the HOSPITAL SETTING. Need to monitor serum Na closely for development of hypernatremia!! Water retention causes:  Urine vL.   Urine osmolarity   Plasma vL. 

 Plasma osmolarity    urine Na   urine specific gravity   urine concentration   serum Na Adrenal Gland Hypofunction  Salt, sugar, sex, steroids   in adrenocorticotropic hormone (ACTH)  Symptoms develop gradually or occur quickly w/ stress.  Acute adrenocortical insufficiency (adrenal crisis) life threatening sx may appear w/o warning  Insufficiency of adrenocortical steroids causes problems through the loss of aldosterone & cortisol action   cortisol = hypoglycemia  Gastric acid production & glomerular filtration    of GF leads to excessive BUN which causes anorexia & weight loss  K+ excretion is  causing hyperkalemia.  Na & H20  causing hyponatremia & hypovolemia.  K+ retention promotes reabsorption of hydrogen ions which leads to acidosis. Acute adrenal insufficiency (Addisonian crisis)  Think of Addison’s as add, add salt, add sugar, add steroids  Life threatening event in which the need for cortisol & aldosterone is greater than the body’s supply. Often occurs in response to stressful event.  w/ intervention initiation promptly, na  and k+  rapidly (hyperkalemia = dysrhythmias, death from MI)  severe hypotension results from blood vL. Depletion that occurs from loss of aldosterone. Hormone replacement! Start rapid infusion of NS or dextrose 5% in NS.  Initial dose of hydrocortisone sodium (solu-coref ) or dexamethasone is admin. as IV bolus  Additional hydrocortisone sodium by continuous IV infusion over the next 8 hours.  Give additional dose of h ydrocortisone IM concomitantly w/ hydration q 12 hrs  Initiate an H2 histamine blocker ( cimetidine ) IV for ulcer prevention Hyperkalemia management  Admin insulin in units = to same # of mg of extra dextrose in NS IV to shift K+ into cells.  Give k+ binding & excreting resin  Loop/thiazide diuretics  Avoid k-sparring diuretics  Initiation k+ restriction  Monitor i/o, heart rate, rhythm, ekg, s/s of hyperkalemia & hypokalemia (slow HR, heart block, tall/peaked T waves, fibrillation, asystole) Hypoglycemia management  Admin IV glucose; prepare to admin glucagon prn  IV access  Monitor BGL hourly  Expect prednisone to be ordered Adrenal insufficiency  Muscle weakness; Joint/muscle pain  Salt craving  Vitiligo  Hyperpigmentation

Cushing’s is caused by excess of cortisol.  Anterior pituitary gland over secretes adrenocorticotropic hormone (ACTH) this hormone causes hyperplasia of the adrenal cortex in both adrenal glands & excess of glucocorticoid production.   in androgen production occurs.  acne,  body hair growth (hirsutism) & clitoral hypertrophy.   in progesterone & estrogen.  Oligomenorrhea. Priority problems:  Fluid overload r/t hormone induced h20 & na retention  Injury r/t thinning of skin, poor wound healing, and bone density loss  Protentional for infx r/t hormone induced reduced immunity  Protentional for acute adrenal insufficiency Cushing syndrome ( exogenous administration) excessive glucocorticosteroids excreted from adrenal cortex. Most common cause is adrenocortical hyperplasia or adrenocortical adenoma (tumor) Causes – therapeutic use of ACTH or glucocorticoids – most commonly for tx of: Asthma Autoimmune DO Organ transplantation Cancer chemo Allergic response CF Cushing disease ( endogenous secretion)  Bilateral adrenal hyperplasia  Pituitary adenium  production of ACTH  Malignancies carcinomas of lung, GI, pancreas  Adrenal adenomas or carcinomas  Ask patient about other health problems, & if glucocorticoid drug therapy is common.  General appearance: moon face, buffalo hump, truncal obesity, weight gain, HTN, frequent dependent edema, bruising,  immunity,  r/f infx, muscle atrophy, osteoporosis,  facial/body hair, thin skin  Changes in fat distribution: neck, back, shoulder, enlarged trunk, thin arm/legs, moon face. Weakness  Na and h20 reabsorbed & retained leading to hypervolemia and edema. BP is elevated, P is bounding.  Monitor for pulm edema, HF, JVD, crackles,  peripheral edema,  UOP  **pulm edema occurs QUICKLY  Monitor skin  Restrict sodium & fluid  Teach family how to check for sodium. 2-4 g/daily  High calorie, high protein before surgery.  High cal diet includes  amt of calcium & vit. D  Milk, cheese, yogurt, green leafy & root vegs add ca to promote bone density.  No caffeine, alcohol ( increases r/f for GI ulcers & reduced bone density.)  GI bleeds common w/ hypercortisolism.

 Cortisol inhibits production of thick, gel like mucus that protects stomach lining which  blood flow to the area & triggers release of excess hydrochloric avid.  Interventions focus on drug therapy to  irritation, protect GI mucosa &  secretion of hydrochloric acid.  PPO, H2 receptor sites – cimetidine, famotidine, nizatidine, omeprazole, esomeprazole. No NSAIDS /drugs that contain aspirin/other salicylates. Hypothyroidism Chapter 59 DKA  type 1 DM  K+ is moved out of circulation into cells along w/ glucose  thanks to insulin  Remember type 1 DM don’t produce insulin/little to none  Sudden Uncontrolled hyperglycemia, metabolic acidosis w/  production of ketones  Results from insulin deficiency & an  in hormone released that leads to  liver & kidney glucose production  Most common precipitating factors of DKA is infx  Hyperglycemia leads to osmotic diuresis w/ dehydration & electrolyte loss  3 P’s, rotting citrus fruit odor, vomit, abd pain, kussmaul respiration  Ketones rise = blood pH  & causes acidosis.  Kussmaul respirations cause respiratory alkalosis in an attempt to correct met. Acidosis. By breathing off c02.  First assess airway, loc, hydration status, electrolytes, BGL  Check pts bp, P & RR q15mins  BGL > 300 mg/dL  Ph <7.35  Ketones + at 1:2 dilutions  Closely monitor & assess for acute weight loss,  skin turgor, dry mucous membranes, oliguria. Weak/rapid pulse, flat neck veins,  temp,  CVP, muscle weakness, postural hypotension, cool, clammy, pale skin.  Maintain perfusion to vital organs.  Initial infusion rates are 15-20 mL/kg/hr during first hour.  Assess status of fluid replacement by monitoring BP, I&O, changes in daily weight.  Only  BGL hourly by 50-75.  Bicarb is only used for severe acidosis.  Sodium bicarb give slowly IV over several hours. Indicated when arterial pH is <7.0 or serum bicarb is < 5mEq/L  Keto acidosis occurs because the body starts to break down fat tissue in order to get that glucose for energy.  DKA considered resolved when BGL reaches 200.  Hyperkalemia is common w/ hyperglycemia  But monitor for HYPOKALEMIA. Hypokalemia is most common death w/ DKA  s/s hypokalemia 0 muscle weakness, malaise, confusion, fatigue, shallow respirations, abd distention  before giving IV K+ make sure patient is peeing at least 30 mL/hr!!!