Med Surg 2 FINAL EXAM Notes PDF

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Jennifer Remick and Wendy Zeiher...

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Adult perfusion  7-9 questions (heart failure, arrhythmias, medications, ACS, PAD) Perfusion  Reduced CO results in a reduction of oxygenated blood reaching the body tissues (systemic effect) o If untreated can lead to ischemia, cell injury, and cell death o Tachycardia = decreased preload o Increased aortic pressure (increased afterload) = decreased stroke volume  increased preload  Venous system  low pressure, high volume o Preload = volume  Volume of blood in the ventricles at the end of diastole, before the next contraction  Fluid volume in body is a direct correlation to preload  Arterial system  high pressure, low volume o Afterload = pressure  The resistance/force against which the left ventricle must overcome to pump blood out of the ventricle  Edema results from an increase in hydrostatic pressure  Systole  contraction of the myocardium that results in ejection of blood from the ventricles  Diastole  relaxation of the myocardium that allows the ventricles to fill  CO  the amount of blood pumped by each ventricle in one minute  SV  from the left ventricle per beat  See med grid for all these meds o Beta blockers o CCB o Alpha/beta blockers o ACE-I o ARBS o Diuretics  Who’s at risk for impaired perfusion? o Middle-aged and older adults o Men – they don’t have the estrogen protection factor o African Americans  Primary prevention o Smoking cessation – before they start o Diet, exercise, weight control  Secondary prevention o BP and lipid screenings  Treatment strategies depend on underlying condition; often used: o Diet and smoking cessation o Increased activity o Pharmacotherapy

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Cardiac output assessments o Pain, dyspnea, edema, dizziness, fainting  What could cause these o Tissue perfusion  Sparse hair on lower extremities and cool to the touch  Diminishes pulses  Decreased UO o Consequences from impaired perfusion r/t conduction disorders are:  Dysrhythmias and decreased CO o Parasympathetic NS decreases rate of SA node and slows impulse conduction of AV node o Sympathetic NS increases rate of SA node and increases impulse conduction of AV node and contractility  Causes diaphoresis Intrinsic rates: o SA node  60-100 bpm  Primary pacemaker o AV node  40-60 bpm o HIS-purkinje system  20-40 bpm ECG monitoring o P wave  firing of the SA node and represents depolarization of the aorta  0.12 second o PR interval  beginning of P wave until the beginning of QRS complex (not the end of it!)  0.12 - 0.20 second o QRS complex ventricle depolarization  0.04 - 45 (high CO2) & pH < 7.35 (low pH) Causes of respiratory acidosis:  COPD  Retaining/build-up of CO2  Reduced function/suppression of Respiratory Center  Hypoventilation o Leads to a build-up of CO2  Over sedation  Drug OD  Neurological disorders o Not telling you to breathe  Inadequate mechanical ventilation o Treatment is to improve alveolar ventilation  Correct the cause, ↑ ventilation & gas exchange

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 Respiratory Alkalosis

PaCO2 < 35 (low CO2) & pH > 7.45 (high pH) Causes of respiratory alkalosis:  Hyperventilation  Hypoxemia from acute pulmonary disorders  Anxiety  Pain  Respiratory rate setting on vent too high  CNS disorders  Fever  Respiratory stimulant drugs o Symptoms: neuromuscular irritability, vertigo, dizziness o Treatment  Treating the underlying cause  Rebreathing into bag, decreasing anxiety, turn down respiratory vent o o

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Step Three: Analyze the HCO3 o Concentration of bicarbonate in the blood  Metabolic component of ABG o Normal HCO3: 22-26  Increased: > 26 is alkalosis/base  Decreased: < 22 is acidosis

 Metabolic Acidosis o o

HCO3 < 22 (low HCO3) & pH < 7.35 (low pH) Causes:  GI Loss of bicarbonate from intestine  Diarrhea (getting rid of base in intestine), intestinal fistula o Poop out base o Vomit acid  DKA  Starvation, Malnutrition  Renal Failure

Shock – anaerobic metabolism which creates lactic acid and it builds up which causes metabolic acidosis  Lactic acidosis due to anaerobic metabolism from shock o Treatment of symptoms  Give sodium bicarbonate PO or IV  The body tries to compensate by initiating Kussmaul Respirations to get rid of more CO2 

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Anion Gap - measurement of excessive unmeasurable anions (-)  Normal: 8-16 mEq/L  Helpful in classification of metabolic acidosis o High anion-gap metabolic acidosis - increase in minor plasma ions ; increase of nonvolatile acids - seen with DKA, lactic acidosis, renal failure, toxins as salicylates o Non-anion-gap metabolic acidosis - loss of bicarbonate and retention of chloride ion (normal anion-gap) - diarrhea, renal failure

 Metabolic Alkalosis o o

HCO3 > 26 (high HCO3) & pH > 7.45 (high pH) Causes:  Excess bicarbonate, and loss of acid  Vomiting or NGT suctioning (removing acid from stomach)  Diuretic therapy  Diuretics excrete hydrogen ions  In an alkalotic state, the body will retain hydrogen ions and excrete bicarb ions (compensatory)  If acidotic it will be the opposite^ o Lots of hydrogen ions  acidic o High bicarb/low hydrogen  basic  Loss of Hydrogen, potassium, chloride  Antacid administration  Excessive ingestion of licorice

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Treat symptoms and correct cause

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Change diuretic to acetazolamide (diamox)- kidneys excreted more HCO3, for example o Administer chloride (isotonic saline or KCl) Oxygenation Status – PaO2 o Partial pressure of oxygen in arterial blood (3% od O2sat) o Oxygen dissolved in the blood plasma o Normal PaO2: 80-100 mmHg o Increased: administration of high amount of oxygen o Decreased: hypoxia / not well oxygenated o

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Evaluation of ABG Results o Look at pH - normal, acidosis, or alkalosis o Look at PCO2 - normal, acidosis, or alkalosis o Look at the HCO3 (Bicarb) - normal, acidosis, or alkalosis o Look at PaO2 – hypoxemia? o What is the cause (respiratory or metabolic)? o Determine interventions needed

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Compensation o Compensates by trying to return the ratio to 20:1 o Respiratory problem: the compensating system is metabolic  Meaning, if both pH and PCO2 are acidic then this respiratory acidosis  The A’s match and the HCO3 is B o Metabolic problem: the compensating system is respiratory o Respiratory compensation occurs in hours o Kidney compensation takes 2-3 days Compensation – pH returns to Normal o Complete compensation  pH is normal  PaCO2 & HCO3 are abnormal o Partially compensated ABG  pH, PaCO2, & HCO3 are all abnormal (all 3) o Uncompensated ABG  pH is abnormal and only one other component (PaCO2 or HCO3) is abnormal - one direct cause for the abnormal pH

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Respiratory Acidosis o Uncompensated  pH < 7.35  PCO2 > 45  Bicarb 22-26 o Partially Compensated  pH < 7.35  PCO2 > 45  Bicarb >26 o Complete compensation  pH becomes normal (7.35-7.45)  PCO2 > 45  Bicarb >26  May be associated with hypoxia Respiratory Alkalosis o Uncompensated  pH > 7.45  PaCO2 < 35  HCO3 Normal o Partially compensated  pH > 7.45  PaCO2 < 35  HCO3 < 22 o Compensated  PH Normal  PaCO2 < 35  HCO3 < 22 Metabolic Acidosis o Uncompensated  pH < 7.35  PaCO2 Normal  HCO3 < 22 o Partially compensated  pH < 7.35  PaCO2 < 35  HCO3 7.45  PaCO2 Normal  HCO3 >26 o Partially Compensated  pH > 7.45  PaCO2 > 45  HCO3 > 26 o Compensated  pH Normal  PaCO2 > 45

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HCO3 > 26

Assessment for ABG – subjective data o Past health history  Involving kidneys, heart, GI system, or lungs  Specific diseases such as  Diabetes, COPD, renal failure, ulcerative colitis, and Crohn’s disease o Medications  Many prescription drugs, including diuretics, corticosteroids, and electrolyte supplements can cause imbalances o Surgery or other treatments  Ask about past or present renal dialysis, kidney surgery, or bowel surgery resulting in a colostomy o Health perception/health management plan  If the patient is experiencing a problem related to imbalances, obtain a careful description of the illness  Including onset, course, and treatment  Ask about any recent changes in weight o Nutrition-metabolic plan  Ask about current diet and any special dietary guidelines they’re following  Assess for eating disorders  Assess ability to adhere to the dietary prescription o Elimination pattern  Assess normal bowel and bladder habits  Note any diarrhea, oliguria, nocturia, polyuria, or incontinence o Activity/exercise pattern  Ask about activity pattern and any complaints of excessive perspiration  And assess activity level problems that could lead to lack of ability to obtain food or fluids  Determine if pt has been exposed to any extremely high temperatures as a result of work or leisure activity  Ask what the pt does to replace F&E lost through excessive perspiration o Cognitive-perceptual pattern  Ask about any changes in sensations; such as numbness, tingling, twitching, or muscle weakness  Ask both the patient and the caregiver if there has been any changes in the pt’s mentation or alertness  Such as confusion, memory impairment, or lethargy Assessment of ABG – objective data o Physical examination  Complete physical exam is needed because F&E balance affects all body systems o Laboratory values  Assessment of serum electrolyte values is a good starting point

However, they reflect the concentration in the ECF and not the ICF o Potassium is mostly in the ICF, so changes in K+ may be the result of a true imbalance  Abnormal serum sodium may reflect a water problem Lab tests that help find a risk for imbalances:  Serum and urine osmolality, serum glucose, blood urea nitrogen, serum creatinine, venous blood gas sampling, urine specific gravity, and urine electrolytes 

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COPD 

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Defining features o Irreversible airflow limitations  Mucus hyper secretion  Mucosal edema (inflammation, which is the primary process)  Of airways, parenchyma (bronchioles and alveoli), and pulmonary blood vessels o May lead to pulmonary HTN  The end result is structural changes in the lungs  Bronchospasm o Airflow obstruction  Inability to expire are  Volume of residual air is increased b/c protease is breaking the alveolar attachments to small airways  This causes the chest wall to hyper-expand  barrel chest  Pulmonary HTN may occur late in the course of COPD o Smaller pulmonary arteries constrict due to hypoxia o The patient has inhalation of air, but there’s destruction of the sacs so the exchange of gases here is not efficient  They lose the elastic recoil which leads to air trapping and retaining CO2 o Anti-protease  prevents breakdown of normal tissue  Exposure to noxious gases makes the body release oxidants  This produces protease which breaks down the connective tissues in the lungs Signs and symptoms: o Dyspnea o Productive cough o Presence of sputum o Nonspecific complaints of malaise, insomnia, fatigue, depression, confusion, decreased exercise tolerance, increased wheezing, fever without other cause Occurrence is higher in men than women o Fewer men die from COPD than women o Women have more exacerbations Causes of COPD:

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o Smoking (#1)  The smoke causes hyperplasia of the goblet cells and produces more mucus  Hyperplasia reduces airways diameter and increases the difficulty in clearing secretions  Cilia lining the airway dies – this is why the COPD has a terrible productive in the morning because all the gunk is sitting in the lungs o Pollution / gases from job sites o Repeated respiratory infections o Pts with asthma may develop COPD o Older age – loss of elastic recoil, stiffening of chest wall, decrease in exercise tolerance, gas exchange alteration  Number of functional alveoli decreases as the peripheral airways lose supporting tissues  Surface area for gas exchange decreases and the PaO2 decreases o Alpha one antitrypsin deficiency – genetic link/risk factor for COPD  So someone can have no risk factors but still develop COPD because of this genetic link Asthma and COPD are both caused by obstruction (and/or inflammation), but the obstruction with asthma is reversible, and COPD is not o Asthma is from inflammation  Once the irritant is removed, the lungs return to normal o COPD is from obstruction  Breakdown of normal tissue and causes permanent damage  If the pt removes the irritant early in the diagnosis, Common characteristics of COPD o Chronic bronchitis  If pt has a productive cough at least 3-month period in two consecutive years (diagnostic)  Increased mucus and chronic inflammation with destruction and enlargement of air sacs o Emphysema  Barrel chest  Hyperinflation/hypertrophy o Most patients with COPD have some form of both of the above  Some will have one or the other but all cases are treated as if the COPD patient has both chronic bronchitis and emphysema Patient presentation o Cough – usually productive  Chronic intermittent cough – often the first symptom to develop o Sputum production  Discolored (yellow) or clear

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o Weight loss/anorexia/cachectic (muscle wasting, low BMI) o Progressive dyspnea  Early – SOB fatigue and dyspnea  In late stages, there will be dyspnea at rest’ more alveoli become overdistened, increasing amounts of air being trapped  Causing a flattened diaphragm  Person becomes more of a chest breather relying on the intercostal muscles and accessory muscles – which is not effecient o Wheezing or decreased breath sounds / rhonchi  Inflammation of lungs, trapping of air – wheezing, musical sounds  Rhonchi – snoring sound because you have irritants trying to move through secretions o Tripod positional, pursed-lip breathing  Sitting forward and holding themselves up on arms while breathing  PLB – prolonged expiration and prevent lung collapse and air trapping  It will slow RR  Do not puff out cheeks  Patient with COPD has dyspnea with an increased RR with excessive accessory muscle use o Hypoxemia  Polycythemia  Body’s concentration of hemoglobin etc is low because of inadequate oxygen exchange, so the body compensated by producing more – which really isn’t all that good…  High hematocrit hemoglobin and RBC  blood is more viscous and increases risk for clots and stroke o May be pinkish in color o Must address these problems they’re what our nursing care is centered around Classification and diagnosis for COPD:  Level of severity - (corresponding with the FEV1 below) o Mild o Moderate o Severe o Very severe  FEV1 results (post bronchodilator) o FEV1 ≥ 80% Predicted o FEV1 50%-80% Predicted o FEV1 30%-50% Predicted o FEV1 < 30% Predicted o < 70% diagnosis of COPD

FEV1 is to measure airway obstruction o Forced expiratory volume in 1 second o “predicted” is what we expect in a person with a certain size and certain age  People with COPD have air trapping so the worse their COPD is, the worse the air trapping, and the lower their FEV1 percentage is o Spirometry (the golden test to diagnose COPD) looks at FEV1  “pulmonary function test”  Need to be without a bronchodilator for 6-8 hours before taking the test for baseline  Then they will be given a bronchodilator. Once it takes effect, they will repeat the test  Even with the bronchodilator, the results will hardly change (because the obstruction is irreversible/permanent)  (in asthma, the FEV1 will increase because the obstruction is reversible)  Avoid scheduling right after meal times  Assess for pulmonary distress before and after  Chest x-ray o See over-inflation of lungs and flattening of diaphragm o Implications of flattened diaphragm  effects stomach (pushing on it) and makes stomach a little smaller (less room for food which contributes to their weight loss)  GERD may manifest  Will also have less room for inhalation of air  CT scan – used to diagnose a pulmonary embolism o Push fluids before and after procedure  Ventilation/perfusion (V/Q scan) o Used to assess ventilation and perfusion of lungs o IV radioisotope given to assess the perfusion aspect of it o Inhale radioactive gas (xenon or krypton) to assess the ventilation portion o Ventilation without perfusion suggests a pulmonary embolism  COPD assessment test (CAT) o Impact of COPD has on ADL  Modified Medical Research Council (mMRC) Dyspnea Scale o Measuring pt’s level of dyspnea Gas exchange – complications o Acute respiratory failure  Chronic tx with beta blockers may improve survival and reduce risk of future exacerbations o COPD exacerbations  Important to identify when a patient may be at risk for developing exacerbations 

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Increase in sputum production or increase in SOB or increase in symptoms of URI – need to see doctor  These are symptoms of a respiratory infection/failure  Exacerbation, a lot of the time, is caused by infection  May end up with pulmonary HTN  And Cor Pumonale (r/t right-sided HF) o Right ventricle will hypertrophy because of increased afterload (pulmonary HTN) o Shows as  dyspnea, edema in feet/ankles, jugular vein distention, hepatomeagaly, etc o Treatment of cor pumonale is initially focused on treating COPD (maybe a bronchodilator)  Continuous low-flow oxygen improves survival  Diuretics may be used  So, its important to look for S&S ^^ of right-sided HF (especially later stages of COPD) o Conceptual care for gas exchange:  Goals:  O2 sat > 90%  PaPO2 >60 

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Oxygen toxicity – high amounts for a long time causes inflammation and obstruct airway Absorption atelectasis – don’t want to give high levels of oxygen because there’s nitrogen in lungs and high amounts will blow out the nitrogen and cause airways collapse CO2 Narcosis – May not feel the need to breathe due to extra oxygen  COPD patients develop a tolerance to higher CO2 levels High levels of oxygen is not always contraindicated though  If patient is intubated  End-stage COPD

Fatigue, sleep disturbances, and dyspnea are common complaints of pts with COPD  Dyspnea is the only one that causes interference with ADL  So focus interventions on improving dyspnea

Drug therapy o Commonly used bronchodilators  Beta 2 Adrenergic agonists (short-acting inhalers)  albuterol – PRN  Mild to moderate COPD  Can help with exercise  Take 30 minutes prior to eating o Won’t help a whole lot though otherwise, because COPD is irreversible damage, unlike asthma when it reverses the obstruction right away

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Anticholinergic (short-acting for acute)  Not asthma. Just COPD  Relax and enlarge (dilate) the airways in the lungs, making breathing easier (bronchodilators). o They may protect the airways from spasms that can suddenly cause the airway to become narrower (bronchospasm) and may reduce the amount of mucus produced by the airways.  Ipratropium (Atrovent)  Albuterol or ipratropium either separately or nebulized together Long-acting anticholinergic  Tiotropium (Spiriva) given to COPD patients as a bronchodilator one a day (long-acting) Inhaled corticosteroid therapy (ICS)  Used for moderate to severe cases  To help with inflammation  ICS are not used alone for COPD – will add with LABA  “-one” drugs LABA  Used in moderate stage (< 60% FEV1)  Salmeterol  Formoterol  Indacaterol  The addition of ICS (inhaled corticosteroid therapy) to LABA therapy is often prescribed to COPD pt’s with FEV1 < 60% (moderate)  Fluticasone/salmeterol (Advair)  Budesonide/formoterol (symbicort) Oral corticosteroids should only be for short-term use to treat exacerbations Roflumilast (daliresp) is an oral Phosphodiesterase inhibitor which suppresses the release of inflammatory cytokines  It reduces the frequency of exacerbations  Beta blockers help with this too

Upper airway drugs: o Decongestan...