NURS 3020 Respiratory System PDF

Respiratory System PATHOPHARMACOLOGY NURS 3020  Objectives 1. Recognize the pathophysiological concepts related to patients presenting with an acute respiratory condition. 2. Discuss the mechanisms of actions, indications, contraindications, cautions, drug interactions, adverse effect...

Respiratory System PATHOPHARMACOLOGY NURS 3020  Objectives 1. Recognize the pathophysiological concepts related to patients presenting with an acute respiratory condition. 2. Discuss the mechanisms of actions, indications, contraindications, cautions, drug interactions, adverse effects, dosages, and route of administration for acute respiratory conditions. 3. Describe the role of the nurse in collaborating with the health care team, patients, and families in safely administering drugs used for acute respiratory conditions. Quick Overview-physiology When we think of complications: Inspiration: ◦ Movement of the diaphragm is needed ◦ During moments of increased demand of oxygen , more muscles engage: external intercostals, sternocleodomasteoid, serratus anterior, and scalene muscles. (these lift the rib cage) ◦ Combining the use of assessory muscles and contraction of diaphragm can help with inspiration but could be a sign of a complication Expiration is a passive process when the diaphragm relaxes Respiration ◦ Exchange of oxygen and carbon dioxide at the alveolar level ◦ Conc of O2 is higher within the alveoli therefore it goes through the respiratory membrane into the RBC ◦ Conc of CO2 is higher in the RBC causing it to diffuse into the alveoli ◦ When there is a complication, there are differences in concentrations Reminders: Perfusion-movement of oxygenated blood into the tissues Acid-base balance-exchange of carbon dioxide for oxygen in the lungs and the renal secretion of bicarbonate maintain the body’s pH between 7.35-7.45 ◦ CO2 rises-leads to a decrease pH-acidosis ◦ CO2 decrease-leads to an increase pH- alkalosis Alveoli secrete a substance called surfactant that prevents collapse or atelectasis from occurring. Visceral pleura-thin membrane lining lung surface, then parietal pleura and space between pleural space Obstructive Sleep Apnea OSA-Patho common disorder characterized by repetitive narrowing or collapse of the pharyngeal airway during sleep 2 results: substantially reduced airflow despite ongoing breathing efforts complete cessation (apnea) of airflow despite ongoing breathing efforts These disruptions to breathing lead to intermittent blood gas disturbances (hypercapnia(excessive CO2) and hypoxemia(low oxygen) and surges of sympathetic activation OSA Patho Causes: vary considerably between individuals: upper airway anatomy the ability of the upper airway dilator muscles to respond to respiratory challenge during sleep, the propensity to wake from increased respiratory drive during sleep (arousal threshold), the stability of the respiratory control system (loop gain) the potential for state-related changes in lung volume to influence these factors. There are periods of apnea-therefore no gas exchange occurs at the alveoli Patho and Presentation***** Hypertension and dysrhythmias-due to hypoxia and release of inflammatory mediators, can also show A-Fib bc of hypoxia ◦ This leads to adherence of WBC to endothelium- leading to endothelial damage and atherosclerosis. Because of hypoxia-the body releases endothelin (proteins that cause vasoconstriction). nocturnal hypoxemia= MI, Sudden Cardiac death, heart failure OSA and CPAP constant and continuous positive pressure into the patient's airway The continuous flow of air gently keeps the tongue, uvula and soft palate from shifting too far into your airway. Pleural Effusion  Pleural Effusions What is it? Accumulation of fluid between the layers of the pleura of the lungs More often in left lung should be 50-100 mL of fluid surrounding the lugs Pleural Effusion Pleural Effusions-Patho Fluid Accumulates within the pleural space (thin cavity between the pleural layers surrounding in the lungs) Etiology: Heart failures Pneumonia Lung cancer Inflammatory disorders 2 types of fluid—transudative(comes from cirrhosis it’s more watery, it’s due to more of a pressure buildup) and exudative( more of a protein based fluid comes from cancer and infection) Lymphatic effusion Prevention of empyema Empyema COLLECTION OF PUS IN THE PLEURAL CAVITY Medication-Pleural Effusions Medications truly depend on the cause! Diuretics Antibiotocs Vasodialators Loop Diuretics Antibiotics Ampicillin and Sulbactam Nitroglycerin (Nitrostat, Furosemide (Lasix) Chemotherapy (Unasyn) Nitro-Dur, Nitrolingual) Sclerosing agents Imipenem and cilastatin (Primaxin) Piperacillin and tazobactam sodium (zosyn) Clindamycin (cleoncin) gentamicin Lets look at some antibiotics more closely Piperacillin and tazobactam sodium (zosyn) Gentamicin -broad spectrum penicillin antibiotic -aminoglucosides (very potent antibiotic) - usual daily dosage of ZOSYN for adults is -serum levels monitored due to nephrotoxicity 3.375 g every six hours and ototoxicity -The usual duration of ZOSYN treatment is Peak-highest drug level from 7 to 10 days. Trough-lowest drug level -Administer ZOSYN by intravenous infusion over 30 minutes (diluted in 50mL diluent) - trough concentration is measured within (less than) 30 minutes before the next dose, and -can cause diarrhea. Use with caution in renal peak concentration after 30 minutes of the patients end of intravenous infusion -trough levels should be below 2mcg/mL Let’s look at furosemide (Lasix) Loop diuretic-Loop diuretics INHIBIT the sodium-potassium-chloride (NKCC2) cotransporter in the thick ascending limb of the loop of Henle. This inhibits the amount of sodium that is reabsorbed by the kidneys, which will cause the nephron to decrease the amount of water it reabsorbs…hence leading to more water leaving the kidneys via the urine (leading to its diuretics affects). IV onset is 5min, peak 30min, duration 2hrs IV (Adults): 20–40 mg; may repeat in 1–2 hr and ↑ by 20 mg every 1–2 hr until response is obtained; maintenance dose may be given every 6–12 hr; Continuous infusion: Bolus 0.1 mg/kg followed by 0.1 mg/kg/hr; double every 2 hr to a maximum of 0.4 mg/kg/hr. IV Push: Dilution: Administer undiluted (larger doses may be diluted and administered as intermittent infusion [see below]). Concentration: 10 mg/mL. Rate: Administer at 20 mg/min. (preventing otoxicity) Pulmonary embolism/DVT Pulmonary Embolism (PE) What is It? When a substance (solid, gas, or liquid) enters the venous circulation and forms a blockage in the pulmonary vasculature Emboli originating from venous thromboembolism (VTE) are the most common cause What does it do: ◦ Increases hypoxia to pulmonary tissue ◦ Impairs blood flow PE and Labs Normal lab values: PaO2, 80-95mmHg PaCO2, 35-45mmHg pH, 7.35 to 7.45 HCO3- , 22 to 26 mEq/L Due to initial hyperventilation, PaCO2 levels low (respiratory alkalosis). But as hypoxemia progresses, respiratory acidosis occurs Even further progression of the condition leads to metabolic acidosis due to buildup of lactic acid from tissue hypoxia PE Labs D-Dimer: Protein fragment found in blood after a blood clot breaks down. D-Dimer test measure the amount of D-dimer in a blood sample. Positive when higher than 0.5. Expect patient to have a positive D-dimer with a pulmonary embolism Medications Anticoagulants-used to decrease the formation of new clots and prevent the existing clot from increasing in size while the body is naturally dissolving it ◦ i.e. inhibit the action or formation of clotting factors and therefore prevent clots from forming ◦ Aka antithrombic All anticoagulants work in the clotting cascade, but they do so at different points Anticoagulant drug interactions: With NSAIDS and herbal therapies such as garlic, ginkgo, kava: increased bleeding  Example of labs from a hospital labs Monitoring bleeding times For warfarin: Prothrombin Time (PT) 10-13seconds International normalized ratio (INR) 0.9-1.1 For Heparin Partial thromboplastin time (aPTT) 25-35 seconds Anti Xa 0.1-0.4U/mL Heparin (table 27.4) Usually refers to unfractionated heparin Primarily binds to activated factors II, X, IX Requires more frequent laboratory monitoring of blooding times as activated partial thromboplastin time (aPTT) – usually every 6 hours until therapeutic effects seen Or they will draw and anti-Xa assay every 6 hours Weight based protocol (wt in kg)—ensure a proper weight on patients Available only in injectable formats in strengths ranging from 10 to 40,000 units/mL Protamine sulfate-heparin antidote In general, 1mg of protamine sulfate can reverse the effects of 100 units of heparin LMWH enoxaparin (Lovenox) dalteparin (Fragmin) Much more specific for activated factor X (Xa) therefore gives a more predictable anticoagulant response No monitoring needed Make sure to check to see if heparin is used in combination with LMWH ( potential deadly medication error) SubQ injection. Prefilled syringes. Protamine sulfate-reverse the effects of LMWH. 1mg protamine for 1mg enoxaparin Coumadin Warfarin (coumadin) inhibiting vitamin K synthesis by bacteria in the GI tract. ◦ This in turn inhibits the production of clotting factors II, VII, IX, and X ◦ These 4 are usually synthesized in the liver and are known as vitamin k-dependent clotting factors ◦ Oral ◦ Significant interactions with other medications ◦ Nutrition considerations ◦ Elimination half life is 0.5-3 days ◦ Often started during the heparin infusion and when warfarin therapeutic ranges is met, heparin is D/C ◦ Warfarin toxicity- Vitamin K ◦ High doses of vitamin K can be given IV Laboratory test:PT/ INR therapeutic range INR for warfarin is 2-3.5 Additional anticoagulants Inhibiting thrombosis by specific action against factor Xa alone: fondaparinux (Arixta) ◦ Treatment of PE of DVT ◦ Cannot be given in patients with a creatine clearance less than 30mL/min ◦ There is no antidote and effect is not measured by standard anticoagulant tests ◦ SubQ Take Aways MIGHT FIX THE EMBOLISM BUT PLACE THE PATIENT AT RISK FOR BLEEDING Medications Thrombolytic Therapy- given to dissolve the clot Essentially, thrombolytic drugs work by mimicking the body’s own process of clot destruction Thrombolytics activate the conversion of plasminogen to plasmin which breaks down (lyses) the thrombus. Plasmin is a proteolytic enzyme (breaks down proteins) These medications utilized if the patient is hemodynamically compromised alteplase- (Activase) IV. Short half life. tPa- tissue plasminogen activator No antidote COPD Exacerbation COPD Exacerbation (reread patho pg 533) Airway resistance is abruptly increased This worsens expiratory flow limitation The time constant for lung emptying in prolonged Expiratory lung volume is increased Furthermore: Rapid, shallow breathing limits time available for lung emptying and promotes dynamic hyperinflation COPD Exacerbation Pharmacology Decreasing the exacerbation rate by prevention—vaccines ◦ Influenza and pneumococcal vaccinations Short-acting beta-2 agonists (SABAs)- initially albuterol (nebulizer) Maintenance LABA (long-acting beta-2 agonist) Salmeterol For nebulizers----delivers fine liquid mist of medication through a tube or a mask that fits over the nose and mouth or with a mouthpiece, using air or oxygen under pressure Systemic Corticosteroids( decrease inflammation) Antibiotics (oral preferred over IV) Oxygen Asthma exacerbation/status asthmaticus Asthma (reread patho pg 524) Status asthmaticus –acute exacerbation of asthma that is unresponsive to repeated doses or treatment with bronchodilators Bronchospasm, airway inflammation, and mucus plus that can cause difficulty breathing, carbon dioxide retention, hypoxemia, and respiratory failure Remember there are absent or diminished breath sounds because there is a decrease in the movement of air due to increased obstruction or respiratory exhaustion---wheezing =lack of air movement Increase PaCO2 levels signify a worsening condition Early stages lead to respiratory alkalosis Status Asthmaticus -pharmacology Bronchodilators-β2-agonists ◦ Initial treatment consists of 2.5 mg of albuterol (0.5 mL of a 0.5% solution in 2.5 mL normal saline) by nebulization every 20 minutes for 3 doses, followed by hourly treatments during the first several hours of therapy. Corticosteroids Methylpredisolone (Solu-Medrol) IV Anticholinergics Usually administered as a 0.5mg dose of ipratropium combined with albuterol administered by nebulization Oxygen Let’s look closer-Nebulizer -used to aerosolize liquid medications to be inhaled for delivery directly to the lungs -Another benefit of nebulizer treatment is that the pressurized oxygen powering the nebulizer will raise the patient’s oxygen levels. Common meds: Albuterol, the most frequently used, stimulates receptors (called β2 receptors) on the outside of muscles that surround the bronchi, causing them to relax. Albuterol is often mixed with ipratropium, which works in a different manner by antagonizing a transmitter substance called acetylcholine, which causes bronchoconstriction. Let’s look closer- methylprednisolone (Solu-Medrol) Steroid Powder medication diluted in: 5% dextrose in water, isotonic saline solution, or 5% dextrose in isotonic saline solution Usually given in 10-40mg per dose Usually given Q6hours Monitor the patient’s blood sugar level (esp if they have diabetes as this will raise blood sugar) Tracheostomy Opening in the anterior trachea to facilitate respirations.—often indicated for upper airway obstructions ◦ Elective tracheostomies often due to prolonged vent dependence, OSA, cancer etc Breathing take place through the trach tube instead of through the nose or mouth. Therefore, very little air passes through the nose, mouth, or larynx. Remember, the nose and mouth warm and clean air during breathing. Air that passes through the larynx forms sound. What now Go to Modules on Canvas and look at the readings Read and add to your notes Also, review the medications from last semester as some of the respiratory medications are the same, we are just giving as a nebulized form!