Critical Care Exam One Review.pdf

Critical Care Exam One Review Respiratory Assessment Analyze health history and assessment while considering lab and diagnostic results Make sure ventilator are set as prescribed and alarms are on Assess for patient-ventilator synchrony and fo...

Critical Care Exam One Review Respiratory Assessment Analyze health history and assessment while considering lab and diagnostic results Make sure ventilator are set as prescribed and alarms are on Assess for patient-ventilator synchrony and for agitation, restlessness, and other signs of respiratory distress (nasal flaring, excessive use of intercostal and accessory muscles, uncoordinated movement of the chest and abdomen, and SOB). Chest auscultation, percussion and palpation are essential Lethargy and somnolence are signs of increasing CO2 levels Report evidence of hemodynamic instability to provider Acute Respiratory Failure/ ARDS Respiratory Failure: ○ Gas exchange is not adequate to maintain adequate ABG’s. PaO2 < 50 with or without PaCO2 > 50 Types of Acute Respiratory Failure: ○ Hypercapnic Hypoxemic = Low O2 and Elevated PCO2 ○ Hypoxemic = O2 < 50 despite supplemental O2 Compliance = Stretch ability of lungs ○ Very compliant lungs are easy to ventilate and take only a small amount of pressure to deliver volume. An example is Emphysema. ○ Lungs that are not compliant are“stiff” and hard to ventilate. They take an increased amount of pressure to deliver a volume of gas. Examples are ARDS and Pneumonia. Pts on ventilator with acute respiratory failure ○ Ventilator Bundle Head of bed 30-45 degrees Oral care every 4 hrs Pepcid for peptic ulcer DVT prophylaxis Sedation vacation - breaks off sedation to see how they breathe on their own ONLY if NO paralytics being administered Adult Respiratory Distress Syndrome ○ AKA DaNang lung, Wet lung, Black lung, Non Cardiac Pulmonary Edema. ○ It is a rapidly occurring progressive form of hypoxemic respiratory failure which occurs in those who have sustained a severe physiological insult. Pulmonary or non pulmonary in origin. ○ Most ARDS patients die from MODS ( Multiple Organ Dysfunction Syndromes) and Sepsis.  Those who survive need extensive rehab therapy 2ndary to prolonged bed rest. Despite our best efforts ARDS continues to have a high mortality rate ○ Non pulmonary insults could include: Burns, Sepsis, Drug overdose, Trauma, Pancreatitis, Eclampsia, Hypo or Hyperthermia, Blood Transfusion ( >3 units), DIC, CABG Sx, Shock (any type) ○ Pulmonary insults include Pneumonia : Bacterial ,Viral, Fungal Inhalation Injuries:Smoke, Chemical Aspiration : gastric content, Near drowning Pneumonitis ○ ARDS ‘s pathophysiological consequence a massive inflammatory response causing the increase of permeability of pulmonary alveolar capillary membranes. This results in fluid moving into the interstitial and alveolar space causing a non-cardiac pulmonary edema. This causes a decrease in lung compliance and difficulty in oxygen transport! The fluid consists of fibrin, protein exudate, & blood which increases the distance gas has to cross the capillary membrane. Surfactant production is decreased - alveolar collapse & atelectasis occurs Micro emboli also form and increase pulmonary pressures. ○ Phase Acute Exudative Phase This can last up to a week Injury occurs (damage to alveoli capillary endothelial + epithelial cells) This causes proteinaceous flooding and decreases gas exchange. Concurrently the fluid inactivates surfactant production. ○ Proliferative Phase: Lasts up to 3 weeks Resolution of acute phase and initial repair of lung. The patient may recover or move to next phase ○ Fibrotic Phase This is where normal lung tissue is replaced by fibrotic tissue Leads to vascular occlusion and Pulmonary HTN Patients become vent dependent, and death is very common ○ Severity of ARDS: P/F Ratio “P” represents PaO2 (arterial pO2) from the ABG. “F” represents the FIO2 – the fraction (percent) of inspired oxygen that the patient is receiving expressed as a decimal (40% oxygen = FIO2 of 0.40). P divided by F = P/F ratio. mild (PaO2/FiO2 200 to 300 mmHg),  AKA Acute lung injury moderate (PaO2/FiO2 100 to 200 mmHg), severe (PaO2/FiO2 less than 100 mmHg) Example: PaO2 = 90 on 40% oxygen (FIO2 = 0.40): 90 / 0.40 = P/F ratio = 225. A P/F ratio of 225 is equivalent to a pO2 of 45 mmHg, which is significantly < 60 mmHg on room air. ○ Risk factors of ARDS Aspiration (gastric secretions, drowning, hydrocarbons) Covid 19 pneumonia Drug ingestion and overdose Fat or air embolism Hematologic disorders Localized infection Major surgery Metabolic disorders Prolonged inhalation of high conc of oxygen, smoke or corrosive substances Sepsis Shock Trauma (pulmonary contusion, multiple fractures, head injury) ○ Symptoms of ARDS : typically not seen till 4 – 48 hrs after insult. ARDS classified according to the severity of hypoxemia experienced by the patient Dyspnea and tachypnea are 1st S&S Acute phase of ARDS marked by severe dyspnea that occurs less than 72 hours after precipitating event Increasing respiratory distress Intercostal / suprasternal retractions Use of accessory muscles Pt. Breaths faster to compensate BUT O2 can’t cross the membrane. O2 levels in blood drops later CO2 drops as well Change on LOC (agitation, lethargy, confusion etc.) Diaphoresis Cyanosis Systemic hypotension due to hypovolemia ○ Symptoms of Shock Initially NO lung congestion, Then Pulmonary edema occurs which leads to -> Atelectasis, decrease in compliance, and alveolar collapse. ○ Assessment of ARDS Physical exam  Intercostal retractions and crackles Pulse oximetry Pulmonary function testing ○ ARDS Lungs on X Ray Normal lung on X Ray the black spaces can be seen ARDS lungs are infiltrated and have a lot of gray, cant see intercostal spaces. White out of ARDS ○ Diagnosis of ARDS Hx. of S/S CXR- interstitial & alveolar infiltrates (often not apparent till after 24 hrs.) BNP Echocardiography Pulmonary artery catheterization ABG’s- early in the disease PO2 < 50 mmHg PCO2- low due to fast RR Respiratory Alkalosis as above ABG’s - later in disease PO2 continues to drop despite supplemental O2 – (at 100%) PCO2 is now increasing due to fluid accumulation Refractory Hypoxemia- hypoxemia that does not improve with O2 therapy. Heart normal size R/O cardiogenic Pulmonary Edema ○ Management of ARDS Primary focus is identification and treatment of the underlying condition ICU Supplemental O2 very early on -> ET Intubation & Mechanical Ventilation Attempt to keep PAO2>60mmHg or O2 sat at 90% at the lowest possible FiO2 PEEP – Positive End Expiratory pressure. A setting on the vent to keep alveoli from collapsing at the end of exhalation. High levels may cause depressed cardiac output Increasing O2 will not help as it is a diffusion problem and need to watch out for O2 toxicity Circulatory support Adequate fluid volume Nutritional support 35 to 45 kcal/kg/day requirement Medical Management  Heparin: prevent DVT and PE Surfactant Therapy Vasopressors for Hypotension Glucocorticoids reduce edema Neuromuscular blocking agents or sedative to improve patient ventilator synchronization and decrease hypoxemia Antibiotics if indicated Proning ○ Treatment Options; Mechanical Ventilation with Peep Nutrition Nebulizer CPT Suctioning Bronchoscopy Frequent positioning Monitor deterioration in oxygenation Reduce anxiety Rest Pressure Ventilation with inverse i/e ratio HFV- High Frequency Ventilation- low tidal volume with rapid rate. Artificial surfactant Prone Positioning: Total aeration of Lung Fields for a minimum of 12 hours/day Oxygen mixture with Helium Feasibility depends on hemodynamic status, use of Vasopressors, and environment and size of institution’s respiratory capabilities Roto Bed for Proning Pulmonary Embolism 3rd Leading cause of Death in the US !!! 70–80 % Found on Autopsy 10 % Mortality Rate in First Few Hours Definition: ○ Sudden Occlusion of a Pulmonary Artery or one of its branches by a thrombus. There may be other types of emboli such as air or fat. Most PE’s originate from the pelvic area or below and travels with the blood through the right side of the heart to the lung The pathogenesis of PE and Deep Vein Thrombosis can be explained by Virchow’s Triad  ○ Hypercoagulability ○ Venous stasis ○ Endothelial injury Risk Factors ○ Bedrest, Recent Surgery, Orthopedic surgery, Obesity, Trauma, Age, Oral contraception, MI, COPD, Smoking, Dehydration, Burns, Atrial Fibrillation, Atrial Flutter, Sedentary Lifestyle/Job, Joint replacement Signs and Symptoms: ○ Dyspnea and Tachypnea: most common symptom, intensity depends on size of emboli ○ Chest pain: only about 17 % c/o c/p however it can mimic an MI ○ Other symptoms include anxiety, apprehension, tachycardia, diaphoresis, PVC’S, diminished lung sound in area, hemoptysis (coughing up blood) and can appear to be other issues. Diagnosis ○ Wells Criteria: ○ Chest X ray: Helps to R/O other causes\ ○ ABG: Resp Alkalosis, and 02 Sats ○ Pulmonary Angiogram Gold Standard : invasive, dye, ○ D Dimer Test:  ○ V/Q Ventilation Perfusion Scan Management  ○ Hemodynamically Stable: anticoagulation with Heparin or LMWH, for 6 months, If recurring IVC filter ○ If Hemodynamically Unstable: Embolectomy, thrombolytics Patient Education: ○ Hydrate ○ No sitting /standing for prolonged periods ○ Do not cross legs while sitting ○ No Restrictive/tight clothing ○ Stretching time out on long rides ○ Anticoagulation Tx. 3 –6 months ○ INR testing Protocol 2.5 – 3./ PT PTT value 1.5 – 2.5 x’n ○ Diet: No increase in green leafy veggies ○ Antidote for heparin: protamine sulfate ○ Antidote for coumadin: Vitamin K Chest Trauma Two Types: Blunt vs. penetrating trauma Chest traumas are life threatening injuries Can lead to ○ Hypoxemia(low levels of oxygen in blood): due to disruption of airway, injury to the lung, parenchyma, rib cage, and respiratory musculature, massive hemorrhage, collapsed lung, pneumothorax ○ Hypovolemia (excessive loss of fluids): from massive fluid loss from the great vessels, cardiac rupture, or hemothorax ○ Cardiac failure: from cardiac tamponade, cardiac contusion, or increased intrathoracic pressure Blunt trauma ○ Sternal/Rib fractures Sternal fractures have anterior chest pain, overlying tenderness, ecchymosis, crepitus, swelling, and possible chest wall deformity Rib fractures have severe pain, point tenderness, and muscle spasms over the area of the fracture aggravated by coughing, deep breathing and movement Results in diminished ventilation, pneumonitis and hypoxemia Management ○ Control pain (sedation, intercostal nerve block, ice over fracture site) , avoid excessive activity, and treat any associated injuries, chest binder for stability ○ Flail chest ○ Pulmonary contusion  Blunt trauma can cause flail chest ○ Flail chest — defined as two or more contiguous rib fractures with two or more breaks per rib One of the most serious of these injuries and is often associated with considerable morbidity and mortality. Occurs when a portion of the chest wall is destabilized, usually from severe blunt force trauma. Look out for Paradoxical breathing Complication: pulmonary contusion ○ Symptoms of Flail Chest? Bruising, discoloration, or swelling in the area of the broken bones. Marks from being thrown against a seat belt (after a car accident) Sharp, severe chest pain. Difficulty inhaling or getting a full breath. ○ Treatment of Flail chest Flail chest is usually diagnosed by medical evaluation and a chest CT scan. Treatment options typically involve splinting, or direct pressure to the chest; supplemental oxygen; IV fluids; pulmonary hygiene and physiotherapy; and pain management. All patients will be monitored via chest xrays, ABG, Pulse ox, bedside pulmonary function monitoring Only a small segment of chest involved: clear airway through positioning, coughing, deep breathing and suctioning, relieve pain with intercostal nerve blocks, high thoracic epidural blocks or IV Opioids Mild to moderate flail chest: underlying pulmonary contusion treated via monitor, I&O, fluid replacement, pulmonary physiotherapy Severe flail chest: ET intubation and mechanical ventilation Intubation and ventilator support are often required for all patients with large flail segments and for any patient with underlying acute or chronic lung disease. Penetrating trauma ○ Gunshot/stab wounds ○ Pneumothorax ○ Cardiac tamponade can result from penetrating trauma (fluid or blood in cardiac space) ○ Subcutaneous emphysema  ○ Medical Management Goal: to restore and maintain cardiopulmonary function DX: chest XR, chemistry profile, ABG analysis, pulse ox, and ECG Adequate airway ensured and ventilation is established, examination for shock and intrathoracic and intra abdominal injuries Chest tube inserted in most patients Assessment ○ Time is critical/ time of injury ○ Mechanism of injury ○ Responsiveness ○ Specific injuries ○ Estimated blood loss ○ Recent alcohol use ○ Pre-hospital treatment ○ Diagnostics: chest XR, CT scan, CBC, clot studies, type and crossmatch, electrolytes, o2 sat, ABG, ECG. Management ○ Goal: To initiate aggressive resuscitation ○ Airway ○ Need for O2, some cases ET intubation and vent support ○ Reestablish fluid volume ○ Reestablish negative intrapleural pressure ○ Drainage of intrapleural fluid/blood Mechanical Ventilation, Intubation, & Tracheostomy Tubes Mechanical Ventilators ○ Positive or negative pressure breathing device that can maintain ventilation and oxygen delivery for a prolonged period ○ Generate, deliver, regulate the flow of gas (O2) that the patient receives into their lungs. Other reasons include control respirations during surgery, oxygenate blood when ventilatory efforts are inadequate and rest the respiratory muscles. ○ Will not CURE they can only support ventilation until the issue is resolved. An exception to this would be if one became dependent on a ventilator as in the case of a quadriplegic Terminology ○ Tidal volume; volume of gas delivered with each breath (this is weight based) ○ Minute volume; total amt. Of gas delivered in one minute (RR X TV= MV) ○ Indications Evidence of resp. Failure or compromised airway Continuous decrease in PaO2  Increase in PaCO2 Persistent acidosis Thoracic or abdominal surgery, drug overdose, neuromuscular disorders, inhalation injury, COPD, multiple trauma, shock, multisystem failure, coma. ○ The flow of gas continues for a preset time, preset pressure, or preset volume. At that point the gas flow will stop allowing for exhalation to occur. ○ The prescription includes: Mode of ventilator (the way the gas is delivered) , Fi02 concentration , the TV( tidal volume) , and the Respiratory rate.. ○ Complications of mechanical ventilation Pneumothorax Atelectasis TE Fistulas Vocal cord Injury Sub Cut Emphysema F & E Imbalances Ph Imbalances Decreased Venous Return Hydration Issues Tracheal Damage (excessive cuff pressures) Ulcers: Gastric & Local 02 Toxicity IICP VAP Types of Ventilation ○ Negative Pressure: “ old iron lung”, chest cuirass, rarely used ○ Positive Pressure Ventilation: Ventilator inflates the lung by exerting positive pressure on the airway, pushing air in and forcing alveoli to expand during inspiration. Exhalation occurs passively.. These can be classified by the method used to end the respirations: Volume-cycled, pressure-cycled and high-frequency oscillatory support. Volume-Cycled Ventilators Delivers a preset volume of air with each inspiration. Once preset volume is delivered the ventilator cycles off and exhalation occurs passively. Disadvantage is that patients may have barotrauma (trauma to trachea or alveoli) Pressure-Cycled Vent Delivers a flow of air until it reaches a preset pressure and then cycles off and expiration occurs  Major limitation is the volume can vary as the Pts airway resistance or compliance changes. TV may be inconsistent High Frequency Oscillatory Support Vent Delivers high RR that are accompanied by low TV and high airway pressures Modes of Ventilation ○ Control ventilation: Vent does all, it delivers a pre-set rate (BPM), pre-set 02 concentration (%), pre-set tidal volume (TV) with each breath and locks out the patient’s efforts. ○ Assist-control/ continuous mandatory volume (CMV) Vent delivers a pre-set rate, pre-set 02 %, pre-set TV with each breath. If a patient initiates (tries to breathe spontaneously) , the vent will take over the breath and give the pre-set TV. Allows patient to start to start the breath ○ Intermittent Mandatory Ventilation: IMV Vent delivers a pre-set RR, pre-set 02 %, pre-set TV BUTTTTTTTTT, When the patient attempts to take a breath the vent allows the patient to take a totally independent breath, at their own TV. It is used in weaning the patient off the vent. ○ Synchronized intermittent mandatory ventilation SIMV Most frequently used is Synchronized IMV. It does not compete with spontaneous breaths. Preset TV and RR. Between vent delivered breaths a Pt can breathe with no assistance from the vent As patient breathes spontaneously, the preset RR is decreased ○ Pressure Support Ventilation PSV Flow of pressure applied at the beginning of a spontaneous breath, which reduces the work of breathing. ○ Airway pressure release ventilation APRV Time triggered, pressure-limited, time-cycled mode Allows spontaneous breath with a long inflation period Breaths can also be initiated by the ventilator ○ Proportional Assist Ventilation PAV Partial ventilatory support, ventilator generates pressure in proportion to the patient’s inspiratory efforts Ventilator synchronizes with patients efforts No targeted pressure or volume. As inspiration pressure is generated by patient the more pressure ventilator generates  Adjunct Modes ○ Positive End Expiratory Pressure: PEEP Pressure is applied at the end of exhalation which prevents the alveolar sacs from completely closing down with each exhalation; this increases functional residual capacity and makes it easier to open again with the next inspiration. Use of it may help reduce high levels of 02. ○ Continuous Positive Airway Pressure CPAP: Positive pressure is continuous through the inspiratory and expiratory phase of breathing. Patients initiate breaths with little help from the vent. Patients can receive the same therapy when not intubated, via mask. To use patient must be breathing independently ○ Bilevel Positive Airway Pressure (BiPAP) Independent control of inspiration and expiration while providing pressure support ventilation (PSV). Two levels of positive airway pressure Either patient or machine can initiate the breath Back up rate ensures a set number of breaths per min Successful with motivated patients ○ Rarely used modes: Inverse ratio Inspiration longer than Exhalation High Frequency Jet Ventilation Ventilator Alarms ○ High Pressure : Ventilator senses more than expected resistance in delivering a breath. Secretions, Kinked tube, Condensation in tube ○ Low Pressure: Ventilator senses no resistance at all when delivering a breath. Disconnected, Deflated inner cuff/balloon, Accidental extubation, Blown inner cuff!! Nursing care for Mechanical vents ○ Assess patient coping with mechanical vent, RR, VS, breath sounds, breathing efforts and potential hypoxia ○ Semi fowlers position ○ Note controlling mode (ex. CMV or SIMV), TV and rate settings, FiO2, PIP, Sensitivity, Inspiratory to expiratory ratio, minute volume, sigh setting, humidification, alarms Successful weaning/ able to start weaning ○ Disease/injury: cured/controlled ○ Fi02: less than 40%, C02 less than 60  ○ Peep: less than 5 Cm ○ Adequate :RR, TV, VC(vital capacity), IP < -20 (inspiratory pressure/ PIP), Sa02 ○ Afebrile: Well Hydrated ○ + Nutrition: Protein 1.2–1.5 g/kg/day ○ Ability to maintain a patent airway ○ Prepare: coached Process of Weaning ○ Individualized by MD usual course ○ A/C decreasing rate and if possible Fi02. ○ Patient should be attempting to take spontaneous breaths. > ○ SIMV gradually decreasing rate with addition of CPAP or PS perhaps > ○ Trial on humidified 02 (tube still in) ○ Extubate provide face mask/tent 50% 02 Artificial Airways ○ These are various types of tubes placed either through the nares or oral cavity down through the vocal cords and sit just above the bifurcation of the bronchus. In that position it can provide gas to both L & R lung fields. ○ Cuff is inflated to prevent air from leaking out of the tube and minimize possible aspiration. Also secures the tube ○ Check positioning of tube by checking end-tidal CO2 levels and CXR ○ Tubes come in all sizes ○ Endotracheal Tube Place with aid of laryngoscope Only used for 14 to 21 days then trach tube ○ Oral Intubation: The tongue is pressed down by the laryngoscope , tube enters through vocal cords and down into mainstem bronchus. It’s placed above the carina where the mainstem divides into L & R. Oral Intubation- Advantages Most common easier, quicker Allows for larger tube to be used (7-10 id) Less likely to kink Less trauma and infections Oral Intubation Tube Disadvantages Limited oral hygiene Difficulty communication and comfort Dry mucous membranes –lip ulcers-infections ○ Naso-Tracheal Intubation Advantages Less discomfort Access to mouth is better - oral care, lip reading  More stable, less chance of ulcer developing ○ Naso-Tracheal Intubation Disadvantages Greater risk of bleeding when placing Limited tube size Greater risk for Sinusitis ○ Nursing Care Check symmetry of chest expansion Auscultate breath sounds Obtain end tidal CO2 Check cuff pressure every 6 to 8 hrs Monitor for signs of aspiration Suctioning Reposition patient every 2 hrs Position and placement: via CXR: Patency Security: tape on face, mark the end for position maintenance Documentation Humidification: visible mist in tubing Communication and support : yes or no questions→ life one finger, blink your eyes, communication board Tracheostomy Tubes: ○ Opening in the trachea ○ Used for longer term ventilator support (vent dependant) or, if intubation is prolonged 2 wks ○ Most comfortable: best for oral care & communication, looks better for family. ○ Better tolerated, less risk of accidental extubation. ○ More effective suctioning. ○ No damage to vocal chords. ○ Complications of Trach tube Dislodgement Accidental decannulation Bleeding Pneumothorax Air embolism Aspiration Subcutaneous or mediastinal emphysema Recurrent laryngeal nerve damage Posterior tracheal wall penetrations Long term  Airway obstruction, infection, rupture of innominate artery, dysphagia, tracheoesophageal fistula, tracheal dilation, tracheal ischemia and necrosis ○ Disadvantages of Tracheostomy Tubes Risk of surgical procedure, anesthesia Increased chance of infection Risk for TE fistula development Neck scar Difficult to replace if accidental extubation occurs within the first week or so. ○ Nursing Care: HOB elevated Oral care q 4 hr VAP Prevention Chlorhexadine Document:Tube size, Lip Line, Mode ,Rate, TV, OETT→ Vent-A/c or mode, 12(respiration), TV- 400, O2 45%, 23 @LL *cc’s in the cuff Security and patency Suction and Chest PT PRN Monitor VS, RR, Sa02, Pain and Sedation possible paralytics and restraints: mildly sedated to prevent uncomfortable, ease the muscle→sedative-propofol (drip form), surgical with pain → pan medication (fentanyl)start off, then increase if pain is increased, antianxiety agent (ativan) Saline soaked in their eyes to prevent ulceration→ if patient is on paralytic medication ○ If pt. Is on ativan and its not working→ we paralyzed them Stimulus applied- 4 twitches=no blockade then increased the paralytic 2 twitch is good 0 twitches= 100 % blocked Meds are listed on medication list!!!! Complications Post Extubation ○ Laryngeal Spasm ○ Laryngeal Edema ○ Hoarseness ○ Sore throat ○ Aspiration ○ Check gag before liquids, No hot beverage or cold beverage. Nursing Care for all  ○ Security ○ Patency of airway ○ HOB elevated/ semi- fowlers ○ Alarms on at all times ○ Document: Tube size, Lip Line Settings ○ Check cuff pressure every 8 hrs ○ Oral care: q 4 h. VAP prevention: Chlorhexidine ○ Monitor Vitals, RR, Sa02, ABG’s ○ Suctioning PRN, Chest PT ○ Pain, Sedation needs. possible paralytics ○ Support/coaching to patient and Family ○ Provide a means of communication WHAT IF??????????? ○ My patient’s alarm sounds? Kink, high pressure, condensation, secretions, bite plucked ○ My patient C/O SOB? Notify pulmonologist to increased their breath ○ My patient pulls out his ETT or Trach tube? Take trach insert and give couple of breaths ○ What if I cannot pass the suction catheter down? Check if its in the lipline, pull suction and suction and go put back the cathether down ○ My patient who is intubated starts to talk to me?check the cuff ○ My patient is fighting during intubation? Ativan and propofol ○ My patient is in distress and is bucking the vent? Suction and increased sedation ○ My patient CAC’s and is on a vent?take them off vent and give ambu bag ○ My patient has told me they do not want to be intubated? You gotta find out ○