CCAL Exam 2 Review PDF

AIRWAY MANAGEMENT ! maintain a patent airway, maintain adequate ventilation, and maintain adequate perfusion ! Oxygen Administration Artificial Airways - oropharyngeal airway...

AIRWAY MANAGEMENT ! maintain a patent airway, maintain adequate ventilation, and maintain adequate perfusion ! Oxygen Administration Artificial Airways - oropharyngeal airway (OPA) - nasopharyngeal airway (NPA) - endotracheal airway with intubation (ETA) *OPA/NPA emergency use; switch to ETA when possible* Airway Obstruction S/S: STRIDOR, choking, wheezing, nasal flaring, restlessness, LOC Interventions: OPEN AIRWAY! - Heimlich - reposition head - intubation - tracheostomy - cricothyroidotomy Tracheostomy Tube long-term airway assistance Parts Cuff - completely seals airway - works with Pilot Balloon to keep trach secure - cause of pts becoming non-verbal FULL INFLATION PREVENTS ASPIRATION Pilot Balloon - keeps cuff inflated - BIG = INFLATED ; FLAT = NO AIR TRACH CAN DISLODGE IF CUFF IS FLAT Obturator - used if trach dislodges - round tip guides the tube back to its place ALWAYS HAVE AT BEDSIDE Trach Care Insertion: Include RT, Record VS and SpO2, Ensure existing IV is patent, administer sedation, position pt supine, assess bedside suction, emergency equipment at bedside Post-Op Care: Confirm placement (XR #1!), End tidal CO2 (not definitive) Remove obturator, ensure balloon and cuff are inflated, trach sutured in place, monitor VS, SpO2, and vent settings ** GI placement will show no CO2 on monitor ! (white line) —------------------> Trach Management - monitor for complications (bleeding, airway obstruction, and infection) - assess for patency every shift - monitor cuff pressure: 20-25 cm H2O (prevents dislodgement) - PRN suction, hydration, humidified air, and turning (reduces risk for mucus plug => blocks airway) - Clean around insertion site, inner cannula, and change soiled strings when needed (2 nurses; MD order) Suctioning Steps: a STERILE procedure; Semi-Fowler’s (conscious) lateral (unconscious), and ASSESS ASSESS ASSESS !!! #1 HYPEROXYGENATE for 2-3 MINUTES prior to suctioning. #2 Connect the catheter to suction machine. DO NOT touch the end of catheter that will be inserted. #3 Remove oxygen device and insert catheter. DO NOT suction. #4 Pull out and SUCTION INTERMITTENTLY in a CIRCULAR motion; roll the catheter between your thumb and forefinger #5 Give pt time to take a break and oxygenate in between breaks Chronic Trach Care Teach signs of infection and educate on proper trach care: - monthly tube changing then every 1-3 months after - clean tube with soap and water at home (non-sterile; clean technique) - if trach pt is hospitalized, provide them with a new cannula Trach Complications - swallowing dysfunction => thickened liquid diet - lack of speech (unless using a speaking valve; deflation of cuff also allows the pt to talk) Trach Decannulation Removal of trach Criteria Removal Care - hemodynamically stable - apply a sterile occlusive dressing (prevents air - INDEPENDENTLY EXPECTORATES; coughs exchange in neck) successfully independently - apply alternate O2 device (start with a high flow - stable and intact respiratory drive rate at 8-10 L and titrate down) - adequate air exchange - splint stoma (apply pressure when coughing, swallowing, and speaking) Fenestrated Tracheostomy Tube Contains a hole that allows air passage over the vocal cords => allows the pt to speak. The cuff DOES NOT have to be inflated. ONLY FOR PTS NOT AT RISK FOR ASPIRATION Review 1. If the patient needs to be bagged what do you do? Connect the bag over the trach tube by removing the mask attachment 2. True or False: Trach insertion is done at bedside? True 3. A client just arrived from the PACU following a successful tracheostomy procedure. Which nursing action must be taken first? a. Suction PRN b. Clean the inner cannula and stoma c. listen to lung sounds d. Change trach dressing ARDS (ACUTE RESPIRATORY DISTRESS SYNDROME) A serious lung condition where alveoli damage occurs causing decreased oxygenated blood and increase in fluid (noncardiogenic pulmonary edema) => decreased perfusion => OXYGEN deprivation => increased WOB and SOB. EARLY SIGNS LATE SIGNS - Dyspnea - Severe dyspnea - Increased RR - Tachycardia and Increased RR - crackles - Hypoxemia = increased workload of breathing - hyperventilation (respiratory alkalosis) - Central cyanosis - restlessness - Pulmonary edema - decreased LOC - Decreased lung compliance (stiff) - hypoventilation (Respiratory acidosis) DOES NOT RESPOND TO SUPPLEMENTAL O2 - increased Lactate (Metabolic acidosis) CHEST X-RAY NORMAL - Increased peak inspiratory pressures X-RAY SHOWS BILATERAL PATCHY INFILTRATES (GROUND GLASS APPEARANCE) PROGRESSES TO MODS Diagnostics CXR - bilateral opacities = pulmonary edema. Usually occurs within 1 week of known clinical situation or worsening resp symptoms Treatment Treat the underlying cause O2 admin with peep - Vent set to APRV - TPN/enteral feed - Dobutamine/Milrinone increases the heart contractility - Vasopressors (norepi and vasopressin) increase the PT’s BP - Sedation/analgesics/paralytics (increased RR or anxious behavior) * Pronation position (promotes lung expansion, however this is a last ditch effort) Complications MODS (Multi Organ Dysfunction Syndrome) - requires support for each organ - turn frequently (low O2 causes skin breakdown) and place on pronation position Dysrhythmias (acid-base imbalance) Evaluation ASSESS! - ABGs - CXR - VS - CO - Response to interventions PULMONARY EMBOLISM A clot occlusion in vessel within pulmonary circulation Pathophysiology Foreign substance in the lungs resulting in a trigger of the inflammatory response. This then causes the RV to work harder in pumping sufficient blood to the lungs. However, clot may be too large, leading to occlusion. May result in Pulmonary HTN. Risks Factors - Immobility (MOST COMMON) - Surgery < 3 months - Hx of DVT - Malignancy - Obesity - Oral contraceptives/hormone therapy - Cig smoking - Prolonged air/car travel - HF - Pregnancy - Clotting Disorders S/S - CHEST PAIN => HEMOPTYSIS - Hypoxia, tachypnea, use of accessory muscles - respiratory alkalosis - anxiety - TACHYcardia and HYPOtension - cough - Wheezing, crackles, fever, syncope, AMS, hypotension, accentuation of the pulmonic heart sounds Cardiac CODE (due to obstructive shock) Diagnostics Labs: BNP (>400), elevated PT/INR and aPTT; ABGs Imaging: - Spiral CT and Pulmonary angio (MOST DEFINITIVE) - Echo, D-dimer, troponin (rules out cardiac condition/MI) - XR, ECG, V/Q scan Treatment - O2 - Balance rest/activity (reduces stress to lungs) - Inferior vena cava filter = catches clots in blood - Pulmonary embolectomy = surgery to remove clot - Fibrinolytic therapy, heparin, enoxaparin - Opioids CONCERNS: risk for bleeding and Obstructive shock Nursing Considerations: Monitor for hypotension and tachycardia VENTILATION ET tube inserted by CRNA/anesthesia, NP/PA/Physician into trachea & lungs to breathe Indications: hypoxia, hypercapnia, trauma, edema → unable to independently breathe Nursing Considerations: positioning, pre-oxygenation with ambu bag, sedation/paralytic ET verification: X-RAY!!! CO2 detection, bilateral chest rise, lung & abdominal auscultation, improvement in O2 stats INTUBATION ATTEMPT IS NO LONGER THAN 30 SECONDS ONGOING VERIFICATION BY MARKING ET TUBE TO TEETH/LIPS MODES OF VENTILATION AC (Assist Control) - total control of oxygenation (tidal volume, FiO2%, RR, Peep) - RR set by MD - most common vent setting Function: Inflates lungs on inspiration w/ the ordered tidal volume. Pt exhales once tidal volume is reached Complications: - barotrauma/pneumothorax (popped lung) - respiratory alkalosis (hyperventilation, decreased CO2) Nursing Interventions: Respiratory Alkalosis = increase sedation. May add a paralytic. Barotrauma = ensure peak pressure alarm is on Example: The ordered RR is 12 bpm. On assessment, pt is found to have a RR of 28 bpm. This indicates Respiratory Alkalosis. PC (Pressure ventilation) - inflates (inspiration) the lungs with the ordered pressure. Once the pressure is reached the client will then exhale - complication: respiratory acidosis; hypoventilation - patients are heavily sedated and may be on a paralytic APRV (Airway Pressure Release Ventilation) - Main goal is to improve oxygenation - Generally used to open alveoli (ARDS pts) - Combines the principles of AC & PC ventilation - Helps to increase tidal volume - Can spontaneously breath - May or may not require sedation - Inverse ratio: inspiration is extended and expiration is shortened, inverse way of breathing - Bilevel ventilation: 2 different pressure: 1 at inspiration and a lower pressure at exhalation - Complications: hypercapnia (respiratory acidosis too?) SIMV (Synchronized intermittent mandatory ventilation) - Delivers preset tidal volume with preset number of breaths, patient can breath in between breaths - Patient determines the volume with spontaneous breaths - Encourages independent breathing without assistance - Used for weaning - Fights muscle atrophy because patient can initiate breathing What differs this from AC? SIMV takes over when pt is unable to complete their breath. In AC, the vent will continue to deliver the preset settings. BiPAP - Positive airway pressure during inspiration AND expiration - Aids in gas exchange with spontaneous breathing - Assist in achieving full tidal volume CPAP - Provides constant end-expiratory pressure to keep airway open (used for sleep apnea) Risks of Ventilation Barotrauma Pressures Ulcers from ET Tube - Nursing Interventions: Reposition the tube every shift/BID - Nursing Considerations: ET tube should only be used 14-21d -> consider trach after day 14 VAP (Ventilator Associated Pneumonia) pooling of secretions around ET tube cuff which then slide into the lungs S/S: Increased WBC, decreased O2, new infiltrate XR, new onset fever, change in sputum color Nursing Interventions: - drain pooled water back into the vent, not the pt - HOB > 30 degrees (if stable) - CHG Oral care and suctioning - Suction while providing PO care (prevents aspiration) - Stomach ulcer/DVT prevention - Sedation vacation Type of alarms: High Pressure, Low Pressure, and Apnea ACID/BASE BALANCE (TIC-TAC-TOE METHOD) Acidic normal Alkaline pH 7.35 - 7.45 PaCO2 Respiratory acidosis 45 - 35 Respiratory alkalosis HCO3- Metabolic acidosis 22- 26 Metabolic alkalosis PaO2 = 80 -100 Compensation - Uncompensated: one is normal, one is abnormal (PaCO2 or HCO3). PH IS ABNORMAL. - Example: - pH: 7.50 (A) PaCO2: 29 (A) HCO3: 24 (N) - Partially compensated: pH, HCO3, and PaCO2 are ALL ABNORMAL - Example: - pH: 7.48 (A) PaCO2: 53 (A) HCO3: 31 (A) - Fully compensated: PH IS NORMAL - Example - pH: 7.40 (N) PaCO2: 47 (A) HCO3: 29 (A) - Respiratory compensation: tries to correct metabolic disorder → takes 5-15 minutes (QUICK) - Renal compensation: tries to correct respiratory disorder → takes up to 24 hrs Respiratory Acidosis Causes: inadequate breathing (hypoventilation → hypoxia) S/S: dyspnea, rapid shallow respirations, hyperkalemia, dysrhythmias (due to increased K+), decreased BP, disorientation Treatment: treat the cause (hyperkalemia → sodium polystyrene, insulin & dextrose, calcium gluconate; hypercalcemia → furosemide, calcitonin, increased fluid intake) and increase RR/improve ventilation Interventions: elevate HOB, breathing exercises, incentive spirometry, O2 therapy, monitor metabolic panel  Respiratory Alkalosis Causes: ineffective breathing (hyperventilation) S/S: ↑ RR and depth, ↑ HR, ↓ or normal BP, hypokalemia, numbness/tingling of extremities, seizures, hyper reflexes and muscle cramps Treatment: treat cause (hypocalcemia → calcium gluconate IV or PO calcium carbonate; hypokalemia → IV or PO KCL) and decrease RR Interventions: brown paper bag to rebreathe CO2, IV fluids, breathing exercises, pain and anxiety management (lorazepam, morphine, meperidine), sedation, monitor metabolic panel Metabolic acidosis Causes: too much hydrogen ions, DKA, renal failure, dehydration, diarrhea Manifestations: ↓ BP, hyperkalemia, muscle twitching, warm, flushed skin (vasodilation), N/V, ↓ muscle tone and reflexes, Kussmaul respirations (really fast and shallow breaths) Treatment: treat causes (hyperkalemia → sodium polystyrene, insulin & dextrose, calcium gluconate; hypercalcemia → furosemide, calcitonin, increased fluid intake), increase RR Interventions: DKA → IV fluids and sodium bicarbonate, Renal failure → dialysis, Diarrhea → diphenoxylate/atropine (lomotil), Vomiting → antiemetics Metabolic alkalosis Causes: loss of hydrogen ions (body fluids); vomiting, excessive gastric suction, diuretics S/S: restlessness followed by lethargy, dysrhythmias (tachycardia), compensatory hypoventilation, confusion, N/V/D, tremors, hypokalemia Treatment/interventions: - antiemetics (zofran or phenergan) - Diuretics: IV fluids and electrolyte replacements - Dialysis if severe - Treat hypocalcemia (calcium gluconate IV or PO calcium carbonate) and hypokalemia (IV or PO KCL) ***ACIDOSIS → HYPERKALEMIA*** ***ALKALOSIS → HYPOKALEMIA*** ENDOCRINE DM I - Autoimmune disease; will be on insulin forever - S/S: 3 Ps → polyuria, polydipsia, polyphagia; wt loss, weakness, fatigue DM II - Beta cells make less insulin and body cells become insulin resistant - Curable w/ proper diet, lifestyle, and wt loss - Risk factors: fam hx, overweight, advanced age - S/S: prolonged wound healing, visual problems, fatigue, recurrent infections (vaginal yeast or candida) Complications of diabetes Hypoglycemia - Blood sugar is less than 70 mg/dL (may look different depending on patient) - S/S: anxiety, sweaty, hungry, confused, blurred or doubled vision, shaky, irritable, cool, clammy skin - Treatment: give 15g of simple carb (fruit juice or regular soft drink 4-6 oz), recheck in 15 min, give 50% dextrose 20-50 mL IV push for IMMEDIATE resolution Diabetic Ketoacidosis (DKA)  - Blood glucose levels >300 to 600 mg/dL - Check for ketone bodies in the blood and urine - Monitor Cr, BUN, Hct, and BMP - Think metabolic acidosis, Kussmaul respirations and fruity breath - Manifestations: - Polyuria, polydipsia - Blurred vision, weakness, and headache - Hypotension and weak, rapid pulse - Hyperkalemia Hyperosmolar Hyperglycemic State - Blood glucose levels >600 - Alterations in mental status (usually unresponsive) - Related to an acute illness: - Pneumonia - Comorbidities - Uncontrolled Diabetes - Glucocorticoids - Manifestations: - Osmolality > 320 - Hypotensions, Tachycardia - Variable neurological signs - BS 600-1200 - Management: - fluids - Correction of electrolytes - Insulin DKA VS HHS Main Difference - DKA is more rapid - pH DKA is acidic and HHS pH is normal - DKA ketones are present and HHS ketones are absent or minimal Adrenal Insufficiency Treat Addison's with Steroid therapy Treat Cushing's with surgical removal - The patient is on lifelong steroid therapy because they no longer have adrenals to produce steroids (cortisol) Pituitary Disorders Diabetes Insipidus Caused by the hyposecretion of Antidiuretic Hormone Manifestations: - Polydipsia - Polyuria - Think dehydration Treatment: - Fluid replacement and Desmopressin - Monitor VS, Neuro, and Cardiovascular status - Potential for altered LOC - Electrolyte values - I/O - Weight - Urine specific gravity Syndrome of Inadequate Antidiuretic Hormone Secretion (SIADH) Caused by the hypersecretion of Antidiuretic Hormone Manifestations: - Fluid retention - Edema - Serum hypoosmolality - Concentrated urine with normal or increased intravascular volume - DIAGNOSE by measuring serum and urine osmolarity simultaneously Treatment: - Treat underlying cause - Fluid restriction if pt is NOT THIRD SPACING - If PT is third spacing they are dehydrated intravascularly - Furosemide (Lasix) - Initiate seizure and fall precautions - Increased ICP can occur due to fluid retention - Monitor labs - Kidney FNC - I/O - Weight - Low Na+ SHOCK Stages of Shock - Initial, compensatory, progressive, and refractory 1. Hypovolemic shock 2. Cardiogenic shock 3. Distributive shock 4. Obstructive shock Hypovolemic Shock This is a low amount of circulating blood due to trauma (loss of blood) Management:  - Labs (THIS LABS SHOW HOW SEVERE BLOOD LOSS IS) - ABGs - H and H - Metabolic Profile - Lactate - Apply 100% O2 via non-breather - Loss of blood -> low O2 supply - Intubation may occur because the tissues and organs need more O2 than what supplemental O2 is giving - Due to the loss of blood - Large Bore IVs (18 gauge) - Eventually given a Central Line - Fluid rehydration is important - Hypovolemic shock is due to blood loss a lot but can be due to fluid loss Cardiogenic Shock The heart is not able to pump correctly - MI - Severe valvular dysfunction - Severe HF Manifestations: - Decreased Cardiac Output - Decreased BP and Narrow Pulse Pressure (difference between systolic and diastolic pressures) - Pulmonary Congestion - If the heart can't pump blood the blood will go into the lungs - Crackles - Low O2 - SOB - Dyspnea - Coughing up blood or fluid Treatment: - Labs - Give O2 PRN→ Keep O2 sats ideally above 95 but at least 90 - Give fluids and meds to help the heart pump - Vasoactive -> raise BP - Inotropic -> heart pumps harder, contractility - Diuretics -> fluid overload - Morphine -> angina - Don't keep pt bed bound but limit activity due to the limited O2 to the tissues - Don't want them to pass out - Treat the cause HF-> inotropic MI -> PCI Valvular dysfunction-> replacement Distributive Shock Sepsis, Anaphylaxis, and Neurogenic - Severe vasodilation occurs lowering the Pt’s BP, and not allowing proper blood flow and oxygenation Anaphylactic Shock Most common - Characterized by an allergic response - Need of EPI pen Management: - Remove the trigger immediately - Apply 100% O2 because the airway swells - IV fluids immediately - Meds - EPI is very important because it increases the HR and BP - Counteracts symptoms of shock - Corticosteroids and bronchodilators - Supports airway - Antihistamines (Benadryl) Neurogenic Shock Spinal cord injuries above T5 - Vehicular accident - Fall incident - Recreational drug use SEVERE HYPOTENSION and BRADYCARDIA - Major vasodilation - Decreased vascular tone - Inadequate CO -> inadequate tissue perfusion -> organ failure Management - IV fluids to increase BP - Meds - Vasoactive Drips - Increase blood pressure through vasoconstriction - Atropine - Increase HR - Heparin/Lovenox - Increased risk for DVT due to slowed blood flow - Transcutaneous/Transvenous pacing if HR is super low and atropine doesn’t help - Raise HOB to increase BP Obstructive Shock An obstruction occurs not allowing proper mov’t of blood - Tension pneumothorax - Cardiac Tamponade - Blood fills the in the sac of the heart not allowing it to contract - Severe valvular disease Management: - Neuro check is important - Without proper blood flow the brain won't get proper O2 - Intubation and Vent if needed - If other O2 interventions aren't enough - ABGs  - Meds - Vasoactive meds - Anticoagulants - Thrombolytics for PE Tension pneumothorax - Chest tube is inserted to pull out chest air Pericardiocentesis - Fluid drained from pericardial sac - Fixes cardiac tamponade Suction thrombectomy - Massive embolus/clot is removed Severe valvular disease - Replacement Vasoactive Medications (KNOW THESE MEDS FOREVER) Dobutamine: helps the heart pump, used for heart failure, not titratable Dopamine: helps HR and BP increase - THE FIRST LINE FOR THESE SYMPTOMS Epinephrine: helps HR and BP increase just like dopamine - Continuous infusion is the last option because of how vasoconstrictive it is - Can cause damage to peripheral nerves leaving fingers/limbs black and deoxygenated - Only use alongside dopamine (if dopamine isn’t enough) Norepinephrine: increases BP only - Also known as Levophed Phenylephrine: increases BP only - Same as Norepi but it is short term - Also called “Neo” or Neo-Synephrine SEPSIS Sepsis 6: O2, blood cultures, antibiotics, fluids, lactate, urine output Complications of Sepsis - DIC (Disseminated Intravascular Coagulation) - MODS (Multiple Organ Dysfunction Syndrome) An infection or SIRS (systemic inflammatory response syndrome) can cause sepsis to occur. - SIRS - Pancreatitis - Burns - Trauma MODS - Insidious - Tissue is hypoperfused, usually starts in lungs - Lack of fluid, blood flow, oxygen - More than 1 organ system requires interventional homeostasis - Begins with ARDS -> intubation -> initially stable then increasing fluids & pressors -> hypermetabolic state -> hepatic & renal dysfunction after 7-10 days - Hypermetabolic state: increased BP & HR, peripheral insulin resistance, increased protein & lipid catabolism → increased resting energy expenditure, increased temp., total body protein loss, muscle wasting, stimulated synthesis - Cardiovascular: reduced cardiac function, poor oxygen delivery, edema, right ventricle affected more -> pulmonary HTN and acute lung injury - GI: risk for stress gastritis and ulcers (will be on PPIs), tube feeding (monitor bowel movements, residuals) - Renal: acute renal failure (renal hypoperfusion), measuring I/O extremely important, dialysis may be needed (CRRT) - Hematology: thrombocytopenia → poor outcomes, DIC (clotting and bleeding out), if hemoglobin less than 7 then PRBCs, if platelets less than 10-20,000 then give platelets, if fibrinogen greater than 80-100 then give cryo, if PT and aPTT less than 1.5 times normal range then FFP - Endocrine: insulin deficiency -> hyperglycemia (impacts immunity and wound healing), maintain tight glycemic control, check glucose often, adrenal deficiency (steroid therapy to counteract), vasopressin deficiency (give IV vasopressin to improve BP) DIC - Minimal to profuse bleeding from all orifices - Causes: blood transfusion reaction, cancer (certain types of leukemia), pancreatitis, infection in the blood, liver disease, pregnancy complications, recent surgery/anesthesia