CC HOLY GRAIL Nursing Exam Review PDF

autosomal dom marfan Nur 409 Exam #1 Review Sheet 50 questions, some SATA Genetics Review Quickly (One question)! Sachs Tay sickle cell Thalassemia ashJews AA medd recess SSD actora goefebsoenu.rogenes multir ae ipipaiaie neural tax cong pyloricstenosis Nursing Care of the Terminally Ill Patient Psychosocial and Regulatory Issues Education and support Doesn’t matter if you agree with patient’s wishes, must honor and advocate Key role in educating and helping patient and caregivers as they adapt ○ Life review, goes over treatment, decision making, end of life goals As a nurse, you can sign as a witness for health care proxy or witness for telephone consent But you can NEVER put your name on anything of legal nature outside of hospital (NO signing their living will) Cultural awareness Be aware that each culture may have different traditions Sensitivity Every case is different Patient Self Determination Act of 1991 Advanced Directives (health care proxy, DNR/ DNI) Durable power of attorney; power of attorney finances Living will POLST/MOLST to Place Drs orders EOL TX goes from place Communication You need to develop skill and the ability to provide comfort and help guide in patient and family responses ○ Talk at eye level, provide quiet space to speak with family, be sensitive= NO “I know how you feel”- Allow the family to react and respond Individualized/tailored Interdisciplinary approach Effective listening, sensitivity and honesty Culturally sensitive care at the end of life ○ Patient mistrust of providers Will be hard to get too many pain med scripts sometimes from PCP ○ Lack of education ○ Language barriers ○ Socioeconomic disadvantages Goal Setting & Palliative Care The shift from cure to comfort ○ Each and every case is different ○ Conversation is difficult and may need to come in small doses Spiritual care and religiosity ○ Spirituality contains elements of religiosity but differences in the concepts ○ Spirituality includes domains such as how pt derives meaning from life One's' beliefs and faith Attitudes toward death For most people, contemplation of one's' own death raises issues, like meaning of life, purpose of suffering, and an afterlife ○ Study showed peoples’ greatest concern was getting honest answers, understanding treatment options and spiritually themed concerns If people are on the younger side or middle aged, very hard to face Palliative Care: Getting patient to cope with chronic illness, making them as comfortable during this time. Doesn’t necessarily mean they are dying ASAP Hospice: 6 months or less to live Some meds that can be given to alleviate pain/suffering: Fentanyl, morphine, ativan, valium (Benzo) Remember: Opioids (Fentanyl, morphine) can lead to respiratory depression, hypotension, slow GI motility Reversal for opioids: Narcan ○ However, don’t want to give Narcan if in the act of dying ○ Short acting drug/half life→ Can pull someone out of crisis but as time goes on, it gets metabolized out of the body and the opioids are still there and can get to receptor sites. Make sure pt goes to ICU for close monitoring after Narcan Reversal for benzos: Romazicon (Flumazenil) ativan Valium What things can either enhance HOPE or diminish it? Hope can foster or hinder Make sure has family and friends in their corner Don’t want to take away the thought that relative can get better Medication for no distress and pain control Open dialogue and humor Can make decisions for self Bad: Lack of communication, no pain control HOPE Hope Fostering Categories: Love of family & friends, spirituality/faith, setting goals and maintaining independence, positive relationships with clinicians, humor, personal characteristics, and uplifting memories* Hope Hindering Categories: Abandonment and isolation, uncontrolled pain/discomfort, and devaluation of personhood If dying, no need to push them (To walk, etc) Nursing Interventions: Listen attentively, setting realistic goals, provide accurate information Encourage sharing of feelings, facilitate effective communication within families Encourage and support patients control whenever possible Making referrals for psychological and spiritual counseling Develop supports in the home Managing Physiologic Responses to Terminal Illness Terminal patients approaching the end of life have the same symptoms regardless Dyspnea (SOB, difficulty breathing, elevated RR) ○ Some people can be dyspnea with normal pulse ox, RR, breath sounds ○ Can help to put them on low o2 flow (1-2 L) with doc’s order ○ Can be brought on by anxiety ○ Also helps to give ativan, valium, xanax N&V: Can give Zofran Patient goals should guide treatment ○ Thoracentesis: Removal of fluid to help breathe ○ Paracentesis: Attack the abdominal cavity ○ Pharm: Opioids, diuretics ○ Increased saliva production could be a problem: May need meds to stop aspiration risk (Atropine, robinul) A spraiduaction Patient goals >> Clinician goals always Anticipating and planning for interventions ○ Helping the patient and family members cope Pain management Pain comes from diseases as well as the modalities to treat the pain Meds: Fentanyl, Morphine, Ativan Can cause hypoventilation, hypotension, constipation (have bowel regimen***) Reversal drug for benzodiazepines → Romazicon (Flumazenil) Reversal drug for opiates → Naloxone (Narcan) ○ Narcan- Short half life, the opiate overdose can come back Nutrition and Hydration Anorexia A disturbance in carb, fat metabolism, endocrine dysfunction, and anemia Different from starvation ○ Not starvation. UNABLE to eat and don’t want to (nauseous, no appetite) Supplemental tube feedings will not replace lean body mass or muscle loss Cachexia Severe muscle wasting (anabolic and catabolic changes) ○ Albumin (Long term nutritional prob) and prealbumin (Short term) In terminal illness the severity of tissue wasting is greater than normally expected Increase in cytokines Loss of appetite Families mean well but they don’t understand it’s not always best for them to eat Artificial nutrition has risks and may not provide comfort or improve survival rates Give them what they want Delirium: A disturbance in level of consciousness, psychomotor behavior, and or memory, thinking or sleep-wake cycles Comes on rapidly (Example: Post surgery and a few days later, they are pulling out their IV. Older people who are out of their element and sick) ○ NOT dementia (Takes a long time to develop) Sleep deprivation and hallucinations may occur Causes: Underlying treatable conditions, med side effects, pain or discomfort, hypoxia, dyspnea, a full bladder or fecal impaction. Brain metastsis, metabolic changes, infection, and organ failure Treatment: Benzodiazepine meds (Ativan) Neuroleptics Haldol Nursing Interventions Aimed at identification of the underlying causes of delirium ○ Med side effects, pain, full bladder (Someone had a foley and it was removed by urine still in), fever, infection The ICU confusion assessment method *RASS score* is done once a shift! ○ An instrument designed to assess the level of alertness and agitated behavior in critically-ill patients ○ If have a higher level of sedation, at a -3, -4: You will get talked to BASS CAM ICU level of assess confusion delirium sedation ^Just to show what RASS Score consists of- DO NOT memorize chart* The CAM-ICU Assessment *Don’t have to use this assessment on exam but know it is used in the clinical setting* Feature 1: Alteration/ fluctuation in mental status (+ result for either) Is the patient’s mental status different from his/her baseline? Has the patient had any fluctuation in mental status in the past 24 hours? Feature 2: Inattention/fluctuation in mental status (letters attention test) Tell the patient you are going to read them a series of 10 letters. Place your hands in theirs. Whenever they hear the letter “A” they are to squeeze your hand. Spell out: SAVEAHAART. If greater than 2 errors, it’s positive Feature 3: Present if the RASS score is anything other than alert calm and zero Feature 4: Ask the patient to respond to yes/no questions Will a stone float on water? Are there fish in the sea? Does one pound weigh more than two pounds? Can you use a hammer to pound a nail? If features one & two are BOTH present PLUS either 3 OR 4 are present = CAM-ICU is positive, delirium is present! (NEED 1&2 PLUS 3 or 4 to be positive) *Don’t have to use this assessment on exam but know it is used in the clinical setting* Depression: Clinical depression should not be accepted nor considered an inevitable consequence of dying Emotional and spiritual support Pain and suicide risk Allow space for sadness and loss Intervention: SSRI tricyclic antidepressant intervention early Palliative Sedation: Used to relieve suffering, not to hasten death Euthenasia: The painless killing of a patient suffering from an incurable and painful disease or in an irreversible coma. The practice is illegal in most countries. Common Drugs Used: Midazolam, Haloperidol, phenobarbital, Ketamine, Thorazine, Fentanyl, Propofol (Diprivan) PROPOFOL: LET ALTAST Metabolized in the liver - check liver enzymes* Fat emollient, IV tubing needs to be changed every 12 hours. Has the propensity to become contaminated with bacteria ALWAYS paired with ventilator Can cause hypotension and bradycardia I Basic ABG info Normal PaO2: 80-100 → Not involved in Acid/Base Imbalance Carbon Dioxide: An acid that is product of cellular metabolism Bicarbonate: A base chemical, produced by the body Body Regulation of pH Lungs: Work fastest and can correct pH imbalances in minutes Can reverse hypercapnic situation very quickly by intubating people back up to a normal range (faster with ventilator) Kidneys: Work slower and can take several hours to correct pH imbalances Blood has to go through kidneys, be excreted, and reabsorbed- Bicarb Two systems will attempt to compensate for each other ROME Remember: Can be both metabolic and respiratory acidosis at the same time! pH ↑ PaCO2 ↓ = Respiratory Alkalosis pH over 7.45 with PCO2 below 35 Causes: Hyperventilation ○ Breathing too fast: Anxious, need to blow off CO2 (If helping with DKApurposely do this) pH ↓ PaCO2 ↑ = Respiratory Acidosis pH below 7.35 with a PCO2 above 45 Causes: Respiratory failure, hypoventilation syndrome ○ Respiratory Failure: Hypoxia with hypercapnia (Bipap= Balances out both) ○ Hypoventilation Syndrome= Sleep apnea (Often on CPAP= O2 issues) pH ↑ HCO3 ↑ = Metabolic Alkalosis Ph over 7.45 with a bicarbonate over 26 Causes: Vomiting, excessive antacid use, contraction alkalosis ○ Vomiting over & over→ Gets rid of stomach acid→ Depleting H+ ions ○ Contraction Alkalosis: If giving too much lasix or diuretics, the body will get rid of fluid but leaves back higher bicarb ratio in the blood Stop the diuretics pH ↓ HCO3 ↓ = Metabolic Acidosis PH below 7.35 with a HCO3 below 22 Causes: Kidney Dz, DKA, *Sepsis*, lactic acidosis, Aspirin overdose ○ Sepsis: Primary cause in ICU ○ ASA: Metabolized in kidneys, too much can go into acidotic state by damaging the nephrons Complete ABG Practice Problems! 5 on each exam Respiratory 1 Assessment of Respiratory Function (This assessment is a patient on ventilator) Acutely or critically ill patient Respiratory status: Are they struggling to breathe? Breath Sounds: ○ Crackles, rhonchi, wheezing, normal (If you don’t know exactly what you are hearing- Write adventitious lung sounds) ○ Auscultation anterior and POSTERIOR- More accurate but harder to do ○ If on a ventilator make sure to do the 3 point check: Both sides and then abdomen to make sure not in the stomach SpO2 (Pulse Ox) Peak flow meter Capnography test after ○ It goes over the ETT with ambu bag and as they compress it there will be a color change (Yellow to purple- Indicates CO2) ○ If there’s a chance of the intubation going into the right bronchus, you would do this test to be sure When someone is on a respirator, ALWAYS check that the settings on the macchine match the patient's orders! intubation *EMERGENCY: If not hearing breath sounds on the left side, the lung field is not aerating. The ETT should be retracted a little to get bilateral sounds. Then get CXR. *What to Look for during Emergency Intubation*: Improvement in pulse oximetry ○ Pulse ox should improve with the ventilation- Monitor to see if getting better. If someone is 83 when intubating, when ventilation starts, it should go up until the 90s and normal ○ If not in the correct spot, that pulse ox will drop!! *Monitor* Capnography test (+ CO2) Three point check: To ensure bilateral breath sounds and no air in stomach ○ Left lung (Anterior, posterior) ○ Right lung (Anterior, posterior) ○ Stomach Make sure that the tube is in place and then get an CXR right away to confirm! Endotrachial and Nasogastric tubes: ETT has sonometer markings on to determine how deep it is in the body ○ 21 sonometers is a typical measure of an endotracheal tube at the lip line (Have to document this information) ○ Now have holders for ETT and every few hours you can move it around to decrease the risks of sores around the mouth NG tube or OG tube are often times part of being on a ventilator ○ Usually about 50-55 sonometers ○ NG tube goes through nose and will have clamps that must be lubricated or it can breakdown tissue Diagnostic Evaluation: PFT: Don’t see PFT (Peak vital capacity, etc) much in CC Pulse Oximetry: Pulse Ox: 95-100% but in ICU is 93-100% COPD: Can go to 89-90% even esp on a ventilator and be their “normal” (They don’t oxygenate that well) Pulse ox difficulties: ○ Poor circulation (Vasopressor therapy- Clamp down on arterial system to raise the BP, force blood back to the core and away from the extremities) ○ Nail polish ○ Anemia ○ Carbon monoxide poisioning (CM has an affinity to RBCS, shows a normal pulse ox but is actually hypoxic since CM is taking up space on RBC) ○ Shivering, ○ Anything that has to do with blood flow ○ Agitation: Can sedate but then that decreases the resp system CXR: Used often in CC, everyone on a ventilator gets a CXR at least once a day Cat Scan: Good for detecting mass or PE in lungs ABGs: Normal variations Sometimes the doctor will miss the artery and get the VBG. ○ pH may be very similar, may have a little elevation in the PaCO2 ○ O2 may show some hypoxia. They will look at the saturation level If 70% or below- it’s a venous sample and have to do again Can also get a mixture of an arterial and venous sample Bloodwork: Always used to tell what’s going on in the body Biopsy: Assess respiratory status, post bloodwork if abnormal EKG: Helps with COPD people bc will show distress on right side of the heart o Function of Respiratory System Upper Respiratory Tract: Filters impurities and warms the air Lower Respiratory Tract: Lungs Three lobes on the right, two on the left ○ To accommodate the heart on the left side *Right lung is more likely to be intubated by mistake* ○ With the left bronchus up higher and at a more direct angle, if the patient is intubated and it is not inserted properly, more of a chance of it going down the right bronchus anatomically. Left is making room for the heart to lay under it so there’s more of a chance to make that right. At which point, you will have a + caponography test (Still getting CO2) Pleura: Two sheaths that go around the lungs Visceral: Vital (closest to the lungs)- FIRST Parietal: Lines the pleural cavity (goes around visceral) Gas Exchange & Oxygen Transport Cells derive energy from oxidation of carbs, fats and proteins which require O2 By circulation of arterial blood and to the capillary system, O2 is supplied and CO2 is removed After the exchange at the cellular level blood enters the venous system and is delivered to the pulmonary circulation Once at the alveolar level the low O2 and high CO2 cause a gas exchange The whole process of gas exchange between the atmosphere, blood and cellular exchange is called respiration! Respiration: The whole process of gas exchange between the atmosphere and the blood including the cellular exchange of O2 and CO2 Ventilation: Air in and out of lungs. Movement of the walls, thoracic cage, diaphragm Inspiration is active, Expiration is passive One doesn’t guarantee the other: Can have an intact respiratory system capable of performing the exchange of CO2 and O2 but have a problem with ventilation Airway resistance: Sarcoidosis, lung disease, obesity, neuromuscular disease Obstructive disease: Asthma, COPD, bronchiectasis Example: Morbidly obsese pt’s thoracic area couldn’t expand because of his weight so they had to put him on a ventilator. Appeared to be respirating but could not ventilate Deoxygenated blood goes from the heart to the lungs to absorb O2 and release CO2 CO2 moves from the blood in the capillaries to the air in the alveoli Oxygenated blood flows from the lungs back to the heart Inhaled O2 moves from the alveoli to the blood by binding with Hb molecule and then will be released to the body tissue Ventilation: Air coming into the alveoli (Blue) 4 M / min D Blood flow: Venous and Arterial blood 5M / min Normal VQ: 0.8 (4/5) D Shunt: Perfusion without ventilation (Left) VQ mismatch Cause: Mucus plug or tumor growth pressing on alveolis and narrowing it Mucus Plug Treatment: Ambulation, chest percussion, bronchodilator, incentive spirometer Dead Space: Aeration without perfusion, blockage with circulation Could be deadly Cause: PE PE Treatment: TPA, heparin Chest Trauma Chest trauma can be anything that strikes the chest wall or an acceleration accident such as a car accident or fall TRAUMA often includes: Chest wall fractures, dislocations, diaphragmatic injuries, barotrauma, injury to the pleura, lungs, aero digestive tracts (upper airway, beginning digestive tract) Blunt vs penetrating trauma ○ Blunt Trauma is more common than penetrating trauma Life Threatening Injuries: Hypoxemia (Low O2 in blood) Hypovolemia (Low circulating blood volume) Cardiac failure Assessment of Chest Trauma: Time is crucial- From injury to getting to ED Mechanism of injury determines severity (fistfight vs gunshot) Level of Responsiveness Specific injuries Inspection, especially the airway looking for stridor, difficulty breathing, chest wall motion, symmetry, entrance or exit wounds Make sure airway is not compromised and no increased chest work for breathing If chest trauma, want to call for trauma team to come (gunshot or stab wound) Estimated blood loss- Hard to do, pts sitting on white sheets with red blood spreading What can you expect if someone is bleeding from this wound? Shock, hypoxia (want to be intubated), cardiac arrest Monitor VS S&S of shock: Low BP, tachycardia, sweating, cold & clammy skin, decreasing orientation, hypovolemic. Body is trying to clamp and send blood to major organs *Respiratory distress: Looking for stridor, difficulty breathing Recent alcohol use Clouds sensorium and interferes with assessment Pre-hospital treatment- Done in the field Example= Intraosteos is a device that in an emergency situation if you need blood, you can get through the bone and reach blood supply in the middle Diagnostics- CXR, CT scan, CBC, type and screen, ultrasound, VS, measurements, met profile for electrolyte levels Management of Chest Trauma: Close monitoring of vital signs, looking for S&S of shock, *pulse oximetry, EKG Give isotonic solution- Normal saline, RL, PRBCs ○ For low BP, to re-establishing fluid volume Chest tube is to drain and reestablish negative pressure in the chest and allow the lung to expand again *Ensure NO stridor ○ Narrowing of the trachea- VERY specific and dangerous. Can be deadly Bleeding badly, shocky, not oxygenating….Transfusion with packed RBCs! ○ Anticipate giving O-. Unless blood type & screen is known D Blunt Chest Trauma: Symptoms of blunt trauma are more difficult to treat because they are frequently vague Because of this people often delay seeking out treatment since they think they don’t need it Common Causes: MVA’s, falls, bicycle accidents Treatment of Trauma: Ensure airway, monitor ventilation, watch for shock, intra-thorasic, or intra-abdominal injury If they come in for car accident, strip them down and examine whole body O2 support Intravascular support (IV fluids, blood, vasopressor therapy) Chest tube insertion (to re-expand lungs) Decompression of the pericardium (pericardial tamponade) Sternal/Rib Fractures: Ribs 4-10 are often involved Older people with three or more rib fxs are at increased risk for complications: Atelectasis and pneumonia Lung can be lacerated (If near clavicle) Treatment of Sternal/Rib Fractures: Focused on pain relief, sometimes a chest binder is used but with caution Educate patients to be up & about/not to avoid movement but to be mindful of excessive activities Sometimes O2 therapy as well (ventilator if bad enough) Surgical repair is rare Most cases don’t provide a splint ○ Want to cough, deep breathe, incentive spirometer to avoid pneumonia Priorities: Manage pain and ensure oxygenation!! AtFlail Chest: Three or more contiguous rib fxs that are fractured in *two or more spaces per rib Problem with Flail Chest: (Left) Breathing in→ Lungs going out and segment is going in (Right) Breathing out→ Lungs going in and segment going out ○ Paradoxical= Not insync with chest wall ○ Lungs right under rib cage Results in: Floating section, *paradoxical chest movements*, decreased alveolar ventilation, hypoxemia, CO2 retention with acidosis, hypo-perfusion, CO decrease Complications of Flail Chest: P ulmonary contusion, pneumothorax, pulmonary effusion, death Treatment of Flail Chest: *Stabilize chest wall with a pressure dressing, positioning Analgesia Possible intubation *Diuretics *Prevent pneumonia *O2 Complication of flail chest Pulmonary Contusion: Very dangerous! Abruise of the lung as a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia) Also known as lung contusion Loss of continuity with the lung, known to bleed, fluid accumulation = Dangerous Frequent complication of flail chest Complications of Pulmonary Contusion: Older people are predisposed to atelectasis and pneumonia Treatment of Pulmonary Contusion: Usually based on pain relief and O2 therapy If trauma is bad enough they could end up on a ventilator Surgical repair is very rare Stab Puncture f Penetrating Chest Trauma: Gunshot Pericardial Tamponade: Beck's Triad is indicative of a Cardiac Tamponade Beck's Triad: ○ The pericardial sac starts to fill ○ Heart has trouble bleeding ○ When auscultating, you hear muffled heart sounds ○ BP drops ○ Narrowing of pulse pressure (Diastolic- systolic. Norm=30-40) ○ Distended JVDs Other Symptoms of Cardiac Tamponade: Dizziness, chest pain, other signs that the heart is not working properly- hypotension, tachycardia Complications of Cardiac Tamponade: Leads to Pulseless Electrical Activity (PEA) Caused by the: Five H’s and five T’s ○ Hydrogen ions- acid, hypokalemia, hyperkalemia, hypothermia, hypoxia ○ Tension pneumothorax, pulmonary thromboembolism (clot), cardiac tamponade (heart beats off), cardiac thromboembolism= MI, toxins= strokes You’ll see a normal EKG, no BP, no heart sounds, essentially in cardiac arrest= See the electricity but the actual pump/perfusion is not there ○ Will have to resuscitate them→ CPR followed by epi every 3-5 mins Have to figure out WHY in PEA ○ If cardiac tamponade, can put in a drain and decompress the heart Subcutaneous Emphysema: Anytime air gets into layers of the skin. Skin starts to get puffy and when you press on it it sounds like crackling Cause of Subcutaneous Emphysema: Chest trauma, putting in a central line Treatment of Subcutaneous Emphysema: Don’t really treat it, let it get reabsorbed. Only will if it is pressing on the trachea and blocking the airway no Gunshot or Stab Wounds: Call chest trauma team Treatment: Compress bleeding, chest tube insertion, type and screen. RL or NS, infuse O- blood if blood type unknown. Prepare for surgery. Airway protection and oxygen Pneumothorax: Collapsed lung, occurs when air leaks into the space between the lung and chest wall causing pressure on the lung and it collapses. Can be partial or complete Causes of Pneumothorax: Bleb rupture (simple pneumothorax), lung disease (COPD, cystic fibrosis, asthma), blunt or penetrating trauma, central line insertion, mechanical ventilation (Didn’t talk much about) Other Causes of Pneumothorax: COPD (Little bubbles on visceral pleura from disease can rupture and cause this) Trauma Iatrogenically induced (Central line going in) Some people genetically predisposed (Small % of population) Traumatic Pneumothorax: Blunt force, penetrating trauma or gunshot/stab injury, thoracentesis Treatment: Bronchial lung biopsy, line placement (Didn’t talk about this) Pneumothorax don’t always turn into tension pneumothorax can Tension Pneumothorax: Lungs start to collapse and actually starts to compress the great vessels of the heart and the heart itself fo Symptoms: Mediastinal shift, tracheal deviation, absent breath sounds, chest pain, tachycardia, respiratory distress, hypotension *TELL TALE SIGN: Tracheal deviation! o unaffected side tension ○ If my left lung is collapsing, compressing on a great vessel, compressing on my right lung, the trachea will actually deviate to the unaffected sign ○ LIFE THREATENING EMERGENCY.. must be treated RIGHT AWAY. Complication of Tension Pneumothorax: PEA or cardiac arrest (If not treated ASAP) Treatment of Pneumothorax: Put a chest tube in (Air or water) Air: Works on suction only. Put water into a chamber which fills to hold the air seals, hook up to suction ○ Set at: -20 mmHg so it’s always a negative draw ○ Want to make sure the suction on the wall is ON. If it’s high on the wall, it will regulate when it gets down to the macchine to a -20 anyways ○ They RARELY want to add more suction, doesn’t really happen Water: Put sterile water into chambers to put water seal there. Bubble as patient breathes in and out or as suction is applied to it Both Chest Tubes: Always make sure the connection is good and tight Want to xeroform (vaseline in) gauze on where the chest tube goes into the wall Always use cloth tape on it (NOT clear tape bc it separates over time) Never milk the tubings Responsible for recording the drainage (Take pen and mark off- 850 cc, 7pm) If the drainage is almost nothing, they’ll decide to take the chest tube off the wall suction but leave the macchine in. Then they will shoot a CXR the next day and if the lung is inflated, they’ll take it out ○ If going to take it out, advocate for patient if their BP meds are unstable or if they need pain meds bc it can be a painful removal Issue can also be if receptacle is full and you need to change it out, you have to be very careful that you don’t clamp that chest tube with suction on VERY important: In order to clamp the tube, the suction MUST be OFF. Then, the clamp must be OPENED BEFORE the suction is put back on ○ *Can’t clamp with suction on, unclamp before suction goes back on Pulmonary Embolism: Obstruction of the pulmonary artery (DANGER) or one of its branches by a thrombus Originate in the venous system ○ DVT ○ DVT + PE = VTE DVT→ PE: Blood comes out of the right side of the heart and if a person has had a DVT and they had a venous thrombotic event, it can come into the heart and go into the pulmonary artery and lodge itself in the lungs. DVT with PE= Venous thrombotic event Blood clot on the right= PE Blood clot on the left= Stroke Risk factors PE is Associated With: Trauma Surgery Pregnancy Heart failure Age ( > 50) Hypercoagulable states: CA, deficiencies, birth control pills Prolonged immobility: Move patients out of bed in hospital! Atrial fibrillation: Common cause ○ When they come into the hospital with new AFib, have to be put on heparin. When leaving, put on coumadin ○ Never cardiovert AFib without ECG first PE Pathophysiology Blood Clot: Complete of partial obstruction of a PA Gas exchange impairment/absent: Alveolar dead space is increased = No blood flow! Ventilation is continued Can also have obstructive shock (Causing right ventricle to go into failure) Pulmonary vasoconstriction: Increased pulmonary vascular resistance: Increased right ventricular work Size: Degrees of hemodynamic instability Clinical Manifestations of PE Size dependent Dyspnea, tachypnea (*most common side effect) ○ First symptoms ○ Can cause chest pain Chest pain Cough, can lead to hemoptysis (secondary to cell death) ○ Coughing blood is from trauma/no blood supply to alveoli Anxiety, apprehension Fever, tachycardia, diaphoresis ○ Foreign clot in there *Results in refractory hypoxemia (PaO2: Less than 60) Assessment and Diagnosis of PE: CXR, ECG, pulse ox (SpO2), ABG ○ CXR could be normal or show infiltrates ○ ECG could show right ventricular sided heart strain ○ ABGs: Can have low O2 but also blowing off too much CO2 Respiratory Alkalosis with refractory hypoxemia V/Q scan ○ Minimally invasive, use of a contrast agent Pulmonary angiogram * ○ Best test if time/condition allows ○ If hemodynamically unstable, you cannot do this Pulmonary spiral CT scan* D-dimer (blood test): Shows clotting somewhere in the body Medical Management of PE: Emergency management Lyse the existing emboli (TPA) ○ Know TPA criteria: Recent surgery, active bleeds, pregnancy, another clot recently, intracranial AVM Prevent new one from forming* Treatment of PE: Death can occur within 1 hour- Must treat ASAP Improve respiratory and cardiovascular status ○ O2 treatment ○ Intubation if needed ○ IV fluid, sedation, pain control Anticoagulation therapy ○ Heparin in hospital Minimize venipuncture attempts (Do as many sticks at one time) ○ Coumadin when leaving Thrombolytic therapy (TPA) rongiffenaif Could also need vasopressor therapy Surgical intervention ○ Can go in mechanically and get it but it’s risky e leafy diet green embolus Patwchnite V/Q Ventilation Perfusion Scan: If there’s an embolus, it will show up as a patch of white (Won’t be pefusing down that side) Mismatch of inhaled and injected compounds on lung scans= + PE (blood clot in the pulmonary artery) White space When going home: Have to transition them from heparin to coumadin Anti10 AB test for heparin levels If someone is going to be discharged start coumadin and then about 24 hours after, they will slowly take away heparin and they will go just on coumadin PE Prevention: (DVT/VTE) Know signs of DVT: Swelling, redness, heat Avoid venous stasis Activity/ leg exercises Early mobilization ○ Even if on bedrest, encourage leg movement ○ See what happens when they get up, dangle, stand, sit If you move someone around too much that you can release another embolus, be careful ○ See how dependent they are on external oxygen ○ Look for changes in VS, work of breathing, pulse ox, and how they feel If they don’t do too well, give them another day with anticoag treatment and try again Anti-embolic stockings Sequential compression devices Anticoagulant therapy ○ Full dose heparin Hospital setting DVT prophylaxis SQ 2-3x daily, different than treatment dose PTT of 60-90 secs Reversal agent is Protamine Sulfate Be careful with Vit K as well (Be consistent with leafy greens) Do blood work every week when first discharged to monitor levels Acute Respiratory Failure Sudden and life threatening Decline in gas exchange Failure to provide oxygen Presents often in the ICU, can be secondary to trauma to pH LESS THAN 7.35 PaO2 LESS THAN 60 mmHg (Hypoxemia) PaCO2 MORE THAN 50 mmHg (Hypercapnia) ○ Acid-base imbalance: Going to be intubated VERY quickly Chronic Respiratory Failure Deterioration in the gas exchange function Hypoxemia and hypercapnia develops gradually and is harmful Persisted for a long time after an episode of acute respiratory failure Absence of acute symptoms COPD, neuromuscular diseases → Gradually sicker over time Failure to Ventilate: Not enough air or volume Failure to Oxygenate: COPD, PE, CHF Pneumothorax also can result in failure Be ready to intubate!! *Just know it can be caused from many different places* Lung Failure: Hypoxia Pump Failure: Actual breathing mechanism, ventilation problem *Know Type 1 Vs Type 2 Respiratory Failure* TYPE ONE: Failure to oxygenate (Hypoxemia) Pulmonary edema, pneumonia, ARDS I I TYPE TWO: Failure to oxygenate and eliminate CO2 (Hypercapnic) COPD, ALS, Guillean Barre Acute Resiratory Failure Assessment: Early: Restlessness, fatigue, HA, dyspnea (visibly struggling to breathe), tachycardia, hypertension, hypoxemia Progression: Confusion, lethargy, tachycardia, tachypnea, central cyanosis, diaphoresis, respiratory arrest (Shows it is getting worse) o Acute Resiratory Failure Nursing Management: Rapid response if they are struggling to breathe or ventilate ○ Restore gas exchange in the lung THE THREE POINT CHECK ABGs ○ If it shows hypoxemia, hypercapnia, acid/base imbalance - Must intubate them emergently at the bedside right away ○ Tested often on ventilators bc want them off ASAP Correct underlying cause ○ If pneumonia: Abx & in ICU ○ If COPD exacerbation: Steroid & in ICU Assess respiratory status ○ VS, pulse ox, LOC, respiratory system Try bipap but most likely *intubation and *mechanical ventilation ○ Bipap→ O2 and CO2 management 100% oxygen HOB at 30 degrees Care of vented patient ○ Mouth care ○ T&P ○ Prevent complications ○ Means of communication Ig 100 Start FiO2 Until then adequate a Pt Ventilator Guidelines: On ventilator when has 50% FiO2 or lower Anything over 50% is causing barotrauma to the lungs and causing problems ○ GET THEM OFF ASAP This is why keep testing ABGs! LAST lower Nurse’s Job During Ventilation: Making sure the respiratory therapist has what they need to intubate: Emergency box with regular suction, suction tubing, argyle tubing, yankauer catheter, VAP Have sedation (Versed, Fentanyl) on hand incase provider calls to give ○ Assess with RAS Scale if on sedation- Make sure it matches *Watch the vital signs & PULSE OX duringTtMBagMMMMMMM ventilation!!!! INTUBATION ○ Some providers don’t notice the pulse ox decreasing as they are are intubating bc focused on the task ○ If pulse ox goes below 92, start saying the numbers out loud to inform them what is going on ○ If goes below 90, can go into cardiac arrest. They will need to remove the intubation if it gets low. After intubated, SpO2 should immediately improve, so monitor for this Immediate capnography test, three point stethoscope check, CXR ASAP within 10-15 mins of insertion for taking care of pt on a ventilator: ** at Be** Bundle Make sure HOB is at least at 30 degrees q2 4h Oral care with chlorhexidine at least once a shift and frequent oral care ○ Pre-exposed to infections, mucous membrane can crack DVT prophylaxis and GI prophylaxis ○ Tendency to develop DVTs since in bed on ventilator ○ Tendency to develop stress ulcers (Pepcid or protonix) Sedation vacation ○ If on these drugs, make sure at least once a day they can be arousable ○ This is for the purpose to start to wean them Also Important to: Turn and position them Q2H Ensure correct setting Ensure all tubing is good Suction T Strict NPO 1 ice chips Check RASS IX Shift Communication & Education with Ventilated Pt: Tell the patient you can’t speak, eat, drink, open your mouth. I will take care of you but will give you a communication board for you ○ Not even ice chips- Can make its way into lungs as water Educate the family as well 2 Acute Respiratory Distress Syndrome (ARDS) Damage to the alveoli membranes, alveoli fills with fluid, tend to collapse and separate from the vascular bed whcih also gets fluid → STIFF non compliant lung The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream, depriving organs LT Most recognized form of noncardiogenic pulmonary edema (Presents itself white & patchy) Severe form of acute lung injury ○ Severe inflammatory process Sudden and progressive pulmonary edema Hypoxemia unresponsive to oxygen ○ Regardless the amount of PEEP Reduced lung compliance Death from non pulmonary multi-system organ failure, with sepsis Bilateral infiltrates on chest x-ray LT whpiatffynes r BN To differentiate between ARDS and PE: Releases the BNP enzyme so test BNP level! PE ARDS Pathophysiology: Inflammation triggers the release of cellular and chemical mediators Causes injury to the alveolar capillary membrane Severe ventilation-perfusion mismatch occurs Inactivated surfactant levels Alveolar collapse Separate from vascular bed Small airway constriction Lung compliance decreased Shunting IT Causes of ARDS: Usually pneumonia→ Sepsis→ Complication of ARDS Multitrauma→ ARDS Hemorrhage→ Multiple transfusions→ ARDS Secondary complication= Have to PREVENT! VERY serious manifestation with high mortality Many people in ICU get this complication and almost always dangerous Sepsis= Primary in ICU PA Eo2 PAO2 FIO2 Ratio: Take ABG, look at patient’s arterial blood (PAO2) divided by the percentage of oxygen delivered (FIO2)- Set on the macchine G *KNOW THESE VALUES FOR EXAM* 300-500: Normal 300-200: Acute injury with mild ARDS (27% mortality) 200-100: Moderate ARDS (32%) Less than 100: Severe ARDS (45%- Almost half will die from it) ARDS Clinical Manifestations: Resembles severe pulmonary edema Develops over 48-72 hours *Rapid onset, severe dyspnea ○ Less than 72 hours after the precipitating event *Visible bilateral infiltrates (CXR) *Intercoastal retractions, increased work of breathing *Arterial hypoxemia ○ Refractory to O2 therapy Decreased pulmonary compliance: stiff lungs Alveoli: Poor ventilation, poor perfusion Ax *Pulmonary Edema is one of the causative factors tfiodiuadres PEEP A ARDS TREATMENT *Treatment: High level of PEEP, high level of O2, small tidal volumes* At 402 Treat underlying condition *Ventilation (aggressive), hemodynamic support (supportive) *Prone positioning ABGs, pulse ox SaO2, SpO2 *Circulatory and fluid volume support ○ Fluid or vasopressor therapy *Nutrition ○ Body is using calories so need to ↑ to 35-45 kcal/ day via NG tube Pharm ○ Sedatives: D iprovan, propofol, ativan= Keep in mind all can cause respiratory depression or hypotension ○ Analgesics ○ Inhaled nitric oxide: Help with vasodilating the lungs ○ Neuromuscular blockade: Paralytic Therapy I TRAIN OF FOUR *Paralytic Therapy: Neuromuscular Blockade* Allows the body to recover and not fight the ventilator (Sedate and paralyze) Used in ARDS, sepsis, bad pneumonia to need paralyic therapy *HAVE to get their threshold of stimulation ○ Example: Take a device called tranophor (neurostimulator) with two e electrodes on it and place it on the ulnar nerve. Red lead (closer to the heart) and black lead, with a small dial on the side that increases electrical impulse. While you are slowly increasing it, you are pressing a button, and the tranophor gives 4 stimulations. If you see the hand and fingers have a reaction, then you know the person stimulated at a level 5 will get 4 contractions Sedation before paralytic therapy!! So scary for patients if they are not sedated first. Sedation should continue as well after the paralytic is stopped until the paralytic metabolizes out of the patient’s body completelyAte Paralytic therapy is given increasing until it gets to what the provider ordered to the degree of blockade ○ Usually about 2 impulses through tranophor- 2 twiches means the patient is 80% blocked unhfffitparalytic But want them off these ASAP because not good to stay on You will check the tranophor every hour. If you all of a sudden don’t get those 2 metabolised ticks, you have to decrease the paralytic ○ Sticks around in the body for a while- Don’t take it lightly Also do good eye care with this Extracorporeal Membrane Oxygenation ECMO: Actually takes blood out of the body, oxygenate it and returns it Have to be very very sick for this, ARDS is not responding at all NOT something to do unless absolutely need it!!! VERY serious therapy Lots of complications with this: Infection, bleeding, blood clots Respiratory 2 Airway Management & Intervention Overview Emergency Management Devices: ○ Advanced airways: ETT, oral airway, LMA, nasal airway ○ Mechanical ventilation: Several modes “Usual” order if getting worse: Ventimask → Bipap → Intubation (Step up) Monitor ABGs Emergency Management Upper airway obstruction Food Vomitus ○ FIRST turn on side /make sure head is UP ○ If conscious, have them cough/clear their own airway ○ If unconscious → suction back of throat with yankauer ○ Oxygen ○ Alert provider for antiemetics (Zofran, Tigan) Sometimes prolong QT so can be a concern in CC ○ May need to eventually decompress the stomach with NG tube or Salem sump if continuous vomiting occurs Blood clots Epistaysis/serious nosebleed → Use emergency kit with pack, saline/afrin ○ Probably anticoagulation problem like too much coumadin Enlargement of tissue ○ Anaphylaxis (angioedema) Give epi or racemic epi (aerosolized epi dose), steroids, bronchodilator, pepcid (blocks histamines) If blocked airway, may hear stridor= EMERGENCY → Give 100% oxygen and racemic epi stat (could happen during extubation) Pressure on the walls of the airway (from tumor) Altered LOC ○ Stoke, alcoholic, diabetes pts ○ HOB 30 degrees ○ Make sure airway does not become compromised Loss of tone (pharyngeal muscles, tongue) ○ Post stroke patients, dysphagia problems, parkinsons ○ Risk for aspiration Interventions: Inspect, palpate, auscultate What do they look like? Tachypneic Anxious, sitting upright May or may not have retractions in supportive respiratory muscles Abdominal breathing May be able to hear narrowing of airway (stridor) What should you do? Listen & palpate over trachea for swelling Advanced Airway Devices Oral Airway Used for: Unconscious patients who you are worried about patent airway or without gag reflex ○ In surgery with ETT w/ oral airway ○ NEVER awake & oriented= Gag reflex intact so can vomit Pt on ventilator if biting the tube: ○ Use sedation → propofol (used 1st to maintain*), versed (during intubation, fast acting), fentanyl (during intubation) with insertion Also take it out and clean it when sedated to avoid sores Sizing: Measured from tip of mouth to the ear Usually 7-8 in adult ICU How to Insert: Start with oral airway upside down & twist it when halfway into oral area T If propofol is used: Tubing gets changed Q12H due to bacterial growth Watch liver enzymes because they are metabolized there Can cause respiratory depression (Need to be on a ventilator) Can also lower HR- Monitor them Dexmedetomidine: Can be used as well for sedation in ICU patients. MUST be on a ventilator. All these meds: Cause respiratory depression, lower BP, and lower HR Make sure they don’t get too much= Monitor RAS Score! to Intubation for Emergencies: Proprofol (dipavan), ativan, fentanyl, dexmedetomidine (presadex), paralytics Nasal Airway Used for: Need lots of suctioning (COPD) or don't have gag reflex Can be used on unconscious(more) /conscious If can’t take an oral airway Sizing: Measured from tip of earlobe to tip of nose How to Insert: Use water soluble jelly before inserting BEVEL end UP towards septum Take out every 2-3 days to clean Disposable/one time use Laryngeal Mask Airway (LMA) AKA King airway (Used in field, not so much in hospitals) Used for: Emergency situations Allows for ventilation without visualizing vocal cords Sits in oralpharyngeal area, into esophagus Oxygen comes through the hole in the cuff (use as little oxygen as possible) t 2 Want to use least amount of oxygen to get desired results If just emergently intubated, 100% O2= PaO2 is 230, trend that O2 down. Drop to 80% and recheck ABG (Keep dropping it down and look at ABGs as coming off) Want to get a ventilator below 50% or can cause toxicity! Endotracheal Tube (ETT) Used for: To provide a patent airway for mechanical ventilation Removal of secretions When inserting: Inserted with the aid of a glidescope (laryngoscope-Old) Nurse Job: WATCH pulse ox reading carefully!! When they are ambuing and the number gets to 95-96, they will take it away and try to get the tube in. Since the person is in resp failure, it clearly can drop low. ○ Make sure to report if it goes below 92 ○ If it goes below 88-87, they can go into respiratory arrest pretty quick, don’t want to tax them, so they will most likely take it out and put ventimask back on Can possibly get OG or NG tube at same time since already sedated After ETT is Inserted: Capnography test is done (Ambu to look for color change indicating right spot with CO2) Three point check must be done to make sure in trachea ○ Not right* bronchus or stomach ○ If you don’t hear breath sounds, could not be aerating ○ Then go for CXR to confirm placement Purpose & Complications Related to the Tube Cuff: Assessment of pressure, cuff is maintained at 20-25 mmHg Respiratory therapist will monitor small pig-tail like device on end of tube every 8 hours & take measurement/ add air if needs it OK to have air leak when ventilating (as long as oxygen and pressure in range) Patient Assessment: Sonometer markings to see if tube moved ○ If 22 at night, 25 in AM. Have to see if person is aerating, good O2, pulse ox, and get confirmatory CXR Most patients are sedated, so watch RAS ○ If RAS is at a -1 and they are okay, leave it because you don’t want to retard them from getting off the macchine ○ If someone is weanable, provider will want to lighten sedation to see where they are Risk for Injury/Airway Compromise Related to tube removal Patient and Family Teaching: Normal to hear air leaking May need to use an alphabet board for communication NO eating Vent care DA *Five Things You Want for People on The Ventilator:* HOB up 30 degrees DVT prophylaxis GI prophylaxis Sedation vacation Oral care (1x shift or day with chloro and then just a bunch regular cleans) Nursing Care of the Patient with ETT: Check respiratory status Turn and position patient O2H!! Will report where sonometer markings are every shift (22, 23 at lips) If ANY problem with vent & help on the way → FIRST pop of ventilator and use ambu bag to properly ventilate patient Air from ventilator is warmed from HME (heat moisture exchange) Suction set up to suction out back of airway Pg. 505 Disadvantages of Ventilator: Uncomfortable, suppresses natural cough reflex, no communication, no eating *Can only go in for 14-21 days max= After is too many complications ○ Move onto tracheostomy ETT Complications: Vocal cord damage TEF → At risk for reflux, stomach content in lungs Impairment of swallowing reflex Reaction to ETT: Gagging, choking, excess saliva High pressure alarms could be from ○ Secretions ○ Airways issues like biting tube or dyschronous with ventilator → Sedation or paralytic ○ If can’t figure out why beeping: Take off ventilator, ambu mask, turn up O2 to flood bag, ambu, then get help Tracheostomy Long-term mechanical ventilation /respiratory management ○ Replace ETT don’t work in 14-21 days* ○ More stable and comfortable ○ Pressure: 20-25 mmHg (resp therapist) Bypass the upper airway (obstruction) ○ More ventilation, less dead space Allow removal of secretions= prevent aspiration Used for respiratory failure or compromised airway Tracheostomy Advantages: Long term ventilation Can move people back and forth and put them on weaning modalities Cuff provides seal in trachea to be ventilated through ○ If long term: Get to point put in a fenestrated tracheostomy where deflate the cap, you move the inner cannula, move the cap (valve) and allows the pt to breathe in normal fashion (past vocal cords) and can possibly eat normal food and fluids and still maintain the trache ○ When they get tired, develop a little respiratory distress, you will reverse it back. Take the valve off, inflate the balloon, put the inner cannula in, and put them back on macchine. Can go back and forth, unlike the ETT in Tracheostomy Procedure: Surgical procedure ○ Ventilation will be controlled Indwelling tube inserted into the trachea ○ Temporary or permanent Size of catheter matters (Typically shorter like 8 inches as opposed to ETT at 12) Dangers: Can go in false passage and put it in layers of the tissues causing problems maing them take it out and redo it again Tracheostomy Short-term Complications: *Bleeding: Minimal only risk is artery is so close *Pneumothorax *Aspiration: Can occur anytime *Subcutaneous or mediastinal emphysema Laryngeal nerve damage Posterior tracheal wall penetration (Unlikely in real life) Tracheostomy Long-term Complications: Airway obstruction Infection Rupture of innominate artery Dysphagia Fistula formation (TEF) Tracheal dilation Tracheal ischemia & necrosis *Tracheostomy Nursing Management: Requires continuous monitoring & assessment Early interventions ○ Suction with yankauer tubing ○ VS *monitor pulse ox closely* ○ HOB 30 degrees ○ Analgesia/sedatives (ex: Versed IV push) ○ Anxiety, apprehension Humidified in the first couple of days Change gauze bc secretion build up & clean around stoma Change inner cannula once a shift (disposable) Extra trach kit at bedside Make sure strap is 1 finger between or can cause rash Preventing Tracheostomy Complications: Administer oxygen & humidified warm air right away Maintain cuff pressure Suction*** Maintain skin integrity Auscultate lung sounds (POSTERIOR IS BEST) Monitor for infection a technique for trach care/when suctioning* ○ Use sterile Replace tracheostomy every few months if long term Issue: Tracheostomy pops out After a few days= EMERGENCY! After a few weeks, it developed a stoma, put some sterile saline on it and reinsert it! Let the provider know incase they want to provide abx Now, PCP will stitch it in to avoid Advanced Airway Advantages & Disadvantages Advantages: Patent airway ○ If in respiratory distress, give 100% O2, take away work of breathing and improve breathing and oxygenation Mechanical ventilation Suctioning Decrease work of breathing Improve oxygenation Disadvantages: Discomfort Cough reflex/swallowing depressed Increased risk of aspiration ○ Pause feeds when you have to turn and clean them Ventilator associated pneumonia (VAP) ○ Every single day on ventilator is more risk for development Ulceration, stricture Inability to verbally communicate Inadvertent removal ○ Patient can pull out tubing or can become stuckk Use of restraints ○ Avoid, use guidelines Mechanical Ventilation Oxygenate the blood for patient with poor ventilation Control respirations during surgery (sedated, paralyzed) Rest inspiratory muscles*** ○ RASS at -2: Allows lungs to get a break ○ Macchine is doing all breathing work Indications: ○ Decreased PaO2 (Pt’s O2 level) ○ Increased PaCO2 Lungs are quick at normalizing pH (CO2 moves quickly) ○ Persistent acidosis ○ Treat respiratory failure ○ Compromised airway Used in: Respiratory failure, COPD (on for a while), pneumonia (on for a while), ARDS, CHF (if diuresis quickly then they can get off within 24 hours) Classification of Ventilators (Machine) Negative Pressure Ventilators (OLD DAYS) When we breathe in naturally, there is negative pressure ○ When we breathe in, diaphragm up, lungs expand, chest wall out Still out there but not as common Exert negative pressure on the external chest ○ Similar to spontaneous breathing (pulls chest wall out) ○ Used for chronic respiratory failure/neuromuscular disorders DOES NOT require intubation “Iron lung” (old machine not used anymore) Chest cuirass: Used for patients with neuromuscular disorders who need support from the machine o Positive-Pressure Ventilators Most common Exert positive pressure on the airway and force/push air in ○ Counter how we normally breathe Force alveoli to expand during inspiration Expiration occurs passively Advanced airway required (ETT, Trach) Classified by the method of ending the inspiratory phase of respiration ○ Volume cycled, Pressure cycled, Flow cycled, Time cycled **Pt @ risk for dehydration, skin breakdown, aspiration, caustrophobia Non-Invasive Ventilator Can be used as a bridge to try and avoid ventilation CPAP: Used for O2 Airway problem like with sleep apnea BIPAP: Used for O2 and CO2 *Needs to be highly motivated to work or they will pull the mask off* Try this first if someone comes in with CHF because pressure can push fluid back into the system. If it doesn’t work, they get ventilated Volume-Cycled Ventilator (volume controlled) Most common Volume of air is preset Volume is relatively constant Once the volume is delivered, the inspiration stops Example: 450 cc tidal volume of prescribed volume. When they get to this volume, it will kick off. However, not all people get RIGHT on the set volume number (around 440 or 460) Pressure-Cycled Ventilator (pressure controlled) Delivers inspiration until it reaches a preset, prescribed pressure Major Limitation: Volume delivered is varied (tidal volume) ○ Machine gives inspiration until it reaches set pressure and then machine kicks off Volume delivered depends on patient’s airway resistance and compliance Alterations in tidal volume can compromise ventilation Example: May not get tidal volume of 450, may be at 300. But if they hit the pressure, it will stop Used in: ARDS, often times in neonatal ICU no High Frequency Oscillatory Ventilator Very high respiratory rate ○ 180-900 breaths/minute Very low tidal volume High airway pressure Small pulses of oxygen enriched air Open the alveoli ○ Atelectasis, ARDS Lung protective ○ From pressure injury Nursing Care with High Freq Oscillatory Ventilator: *PT MUST BE PARALYZED/SEDATED* ○ Imagine breathing 800-900 little breathes and not being sedated *Do train of four test and document* ○ Sedated first ○ Train of four test to establish their baseline. Red prong closer to heart and black to hand. Line ulnar nerve (Pinky). Gives four impulses, start and lower level until they get 4 impulses and thumb will twitch (hold thumb to notice it better). ○ Once get baseline, doc will prob order 2 impulse per train of 4. ○ Test to see if the neuromuscular blockade is working up to that order every HOUR and document!! ○ 2/4 is like 80% paralyzed ○ SO if 1/4 or 0/4 and they don’t respond after paralytic, you have given too much drug. Have to letten up on it. Remember stuff stays in system and can prevent them getting better and cause a lot of damage ○ Have to be sedated coming off paralytic therapy until 4/4 impulses at baseline Noninvasive Positive–Pressure Ventilation (NIPPV) Use of facemask or other device to maintain a seal and permit ventilation Indications: Acute Respiratory Failure, Acute Pulmonary Edema, COPD, sleep related disorder (sleep apnea) Continuous Positive Airway Pressure (CPAP) Usually O2 problem, can help stop gag if not going into resp failure right away Trying to avoid ventilation (Barotrauma or complications avoided) ○ Pressure Support ○ PEEP Bi-level Positive Airway Pressure (Bi-PAP) Inspiration and exhalation pressure Helps with O2 and helps blow off CO2 Have to be very motivated for this, not easy Ventilator Settings (Prescriber orders) Mode (AC, CPAP) air deliveredbreath mbeyenanical Respiratory Rate (RR) Volume toof lungs w each Tidal Volume (TV or Vt): The volume of air breathed out after the deepest vent inhalation ○ 6- 8 cc per kg of body weight Fractional Inspired Oxygen (FiO2): Concentration of 02 that patient inhales, macchine delivers delivered ○ **Want to keep under 50% or at risk for barotrauma** Positive-End expiratory Pressure (PEEP): Positive pressure maintained by the ventilator at the end of expiration ○ Constantly puts pressure on the chest so it can decrease CO from amount of t pressure to prevent pressure gradient alveoli from closing Oa Ventilator Modes HOW the machine will ventilate and breaths are delivered** Assist Control (AC) Intermittent mandatory ventilation (IMV) Synchronized intermittent mandatory ventilation (SIMV) Constant Positive Airway Pressure (CPAP) Pressure Support (PS) Positive-End expiratory Pressure (PEEP) Assist Control (AC) Controlled Mandatory Ventilation (Can be called CMV) Provides full ventilator support Preset tidal volume, RR If patient initiates a breath before the preset rate, the ventilator will deliver the preset volume and “assist” the breath Every breath (machine or patient) will receive the preset volume What Finnegan said: Full ventilatory support when pt takes a breath Examples setting: Macchine AC set at 16, tidal volume 450, 50% O2 (everyone gets), 5 PEEP *Patient decides they want to breath at 18 or 20, the machine will still give them FULL SUPPORT with PEEP, tidal volume, and oxygen! IBM riantne t Pt Intermittent Mandatory Ventilation (IMV) Allows for a combo of assisted (machine) and spontaneous breaths (patient) Machine breaths are delivered at preset time and with a preset volume Spontaneous breaths are determined by patient and volume is limited to the tidal volume generated by the patient (no machine assist) Allows patient to use own muscles for ventilation Potential increases to “buck” the ventilator What Finnegan said: Prescribed amount of ventilations. If patient breathes over that, they *will NOT get tidal volume or PEEP, Oxygen ONLY (Makes them WORK), weaning Same setting: 16 breaths, 450, 5 PEEP. If the body decides to breathe at 18 or 20, the other 2-4 breaths will be on own, only with O2 *Issues: Mandatory! Gives the breath every x amount of seconds so patients can ”buck the ventilator” is breathing at same time as ventilator (high pressure alarm) → Could sedate or switch to SIMV IT Synchronized Intermittent Mandatory Ventilation (SIMV) Machine delivers a preset tidal volume and rate Spontaneous breaths can occur Between machine breaths the patient can determine own tidal volume, no assist Machine senses the patient breath and will not initiate a machine breath in opposition of the patient's breath (synchronized) “Bucking the vent” is decreased What Finnegan said: Same thing as IMV, except the macchine anticipates person breathing on own *Breathe at 18, gives NO tidal volume, NO peep, Oxygen ONLY (like IMV). *However, SIMV anticipates that the person is trying to breathe on their own and stops the macchine/holds back and minimizes “bucking the ventilator” IffentEELIFrent IT Positive-End Expiratory Pressure (PEEP) Positive pressure maintained by the ventilator at the end of expiration Increase functional residual capacity Opens collapsed alveoli Improves oxygenation and allows for a lower FiO2% Keep alveoli inflated *Complications*: ○ Barotrauma or pneumothorax from the constant pressure (balloon pops) ○ Decreases venous flow to the heart & can cause cardiac issues Typically put PEEP and PS together Ah I won Pressure Support (PS) from tube *WEANING MODALITY *“Breathing through a straw”. Compensation/ helps take away this uncomfortable breathing feeling Machine applies a pressure to the airway throughout the patient triggered breath Decreases resistance in the ETT and machine tubing Decreases work of breathing for the patient PS is reduced as patient’s strength increases thing Constant Positive Airway Pressure (CPAP) *WEANING MODALITY *Oxygen problem ONLY (Airway like sleep apnea) Administered via ETT, trach, mask ○ Wear mask overnight for sleep apnea or on ventilator + pressure applied throughout respiratory cycle to a spontaneously breathing pt ○ PS + PEEP = CPAP ○ PS 10 + PEEP 5 = CPAP Promotes alveolar and airway stability ○ Continuous pressure on alveoli and keeping them inflated Patient must breathe spontaneously Let them breathe on this 20mins- 1 hour to see progress and test **BOTH WEANING MODALITIES: CPAP AND PS! 2 Care of the Patient: Systematic assessment include all body systems In-depth respiratory assessment (All indicators of oxygenation status) ○ Effort of breathing ○ Pulse ox ○ Auscultate BACK ○ Ventilator check ○ Emergency Vent: THREE POINT CHECK! Comfort ○ If pt needs sedation, ask for an order, just make them comfortable!* ○ Just monitor RAS Score Coping, emotional needs ○ Imagine what it is like to have a tube down throat, can be painful Communication ○ Alphabet board or writing *Make sure pt is fed!!! (even if obese), they need the calories for energy Initial Ventilator Settings: Set tidal volume (6-10 mL/kg) Set FiO2 % ○ Initial setting is 100%, quickly reduced as patient oxygenation improves ○ Lowest concentration of oxygen to maintain normal PaO2 (80-100 mmHg) ○ COPD will run 60-80. DON’T try to make run normal PaO2, they will crash Set rate (12-16 bpm) Set mode (AC) Set PEEP (5-10) cm H2O For ARDS (Secondary syndrome due to trauma to the lungs from transfusion or sepsis) → LOW tidal volume & HIGH PEEP A Oxygen Collaborative Problems: Alterations in cardiac function ○ Effects of PEEP on Cardiac Output (Decreased venous pressure) Barotrauma (Traumatize alveoli) ○ Too much O2 or PEEP Increases risk of ventilator acquired pneumonia → Sepsis → ARDS → MODS ○ Risk of pneumonia goes up everyday they are on it Goals: Optimal gas exchange Maintenance of patent airway Attainment of optimal mobility Absence of trauma or infection Adjustment to nonverbal methods communication (use alphabet board) Acquisition of successful coping measures Absence of complications Enhancing Gas Exchange: Monitor ABGs and other indicators of hypoxia ○ How to get them off: Monitor ABGs ○ Signs of hypoxia (confusion, restlessness) Follow trends Auscultate lung sounds frequently Judicious use of analgesics ○ Analgesics slow people from getting off machine→ Be careful Monitor fluid balance ○ *Want 0 or negative fluid balance. Unless sepsis or hypovolemic shock* A complex diagnosis that requires a collaborative approach Promoting Effective Airway Clearance: Assess lung sounds at least every 2-4 hours Measures to clear airway: ○ Suctioning, CPT, position changes, promote early mobility Humidification (HMAs) Medications Optimal Mobility: Physical deconditioning and prolonged motor weakness accompanying critical illness have profound and lasting consequences ○ The closer you get to normal activity, the better but hard to do ○ Bedrest for 1 week can age 10 years *Early mobility is facilitated by change in intensive care unit culture Preventing Trauma: Tube care ○ *Oral care/suction Cuff management ○ Maintain cuff pressure of 20-25 mmHg (Respiratory therapist will do this) Preventing Infection: Hand washing protocol f *Ventilator Associated Pneumonia (VAP)* Daily interruption of sedation (sedation vacation) Daily readiness to extubate prevention DVT and PUD prophylaxis Daily oral care with Chlorhexidine Every 2-4 hours oral care with peroxide Elevation of HOB at least 30 degrees CPAPIPS Weaning: Process of gradual withdrawal from dependence upon the ventilator ○ Some people don’t get this process, just happens right away (if physician decides that’s best) Successful weaning is a collaborative process Criteria for weaning (psychological and physiological prep) ○ Careful assessment ○ VS, ABG stable, signs of improvement Patient preparation Methods of weaning (CPAP trial) TO TELL IF READY FOR EXTUBATION:* At*HOW Weaning trial 1) 2) 3) 4) 5) Wake up from sedation Bring down O2 to 40% FiO2 Go out of sedation Switch to CPAP w/ PS or just PS Monitor and let them work for 20 to 60 minutes If: 1) Rapid Shallow Breathing index is good (LOW) Rapid Shallow Breathing Index= RR (20) / Tidal volume (.45) = 44.4 If 105 or lower = GOOD. Want LOW #! 2) Pulse Oximetry is within range 3) Breathing is good, RR is under 30-32 breaths/min 4) At least 300cc of tidal volume, or greater than 5 mL/kg 5) ABG is good while weaning 6) No vasopressor agents infusion Then: The person is ready to be extubated!! Usually put on 40% aerosol mask for humidification and transfer to nasal cannula Example in Powerpoint: Daily Nurse Screening for Weaning Trial 1) FiO2 under 50% 2) PEEP under 5cm H2O 3) No vasopressor agents infusion 4) No sedative agents infusion 5) Patient is awake and understands simple orders Yes or No? Do they have Clinical Intolerances? 1) Is the Pulse Oximetry above 90%? 2) Is the Respiratory Rate under 32/min? 3) Variation of heart rate or Systolic arterial pressure greater/equal to 20%? (^he didn't explain this one, but I wrote it anyway) 4) Agitation? The patient may not comply and pull out the tube when sedation wears off o Extubation: Extubation is described as the discontinuation of an artificial airway Judgement call by PCP Indications for its original placement no longer exist: ○ Obstruction alleviated ○ Protection of airway ○ Suctioning ○ Ventilatory failure ○ Hypoxemia Will have lots of respiratory secretions post extubation May have to advocate for a patient ○ For example if he can’t protect his airway: If still sedated ○ You’ll go from 40 to 20 proprofol then check on them slowly arising and do ABGs then go to 10 proprofol (turns around fast, doesn’t stick around) Guidelines of adequate pulmonary mechanical function include: Discontinuation of the airway is based on assessment of pulmonary mechanics Respiratory rate less than 25 bpm Spontaneous tidal volume greater than 5 ml/kg Inspiratory force of at least -20cm H20 (be able to suck in air) Vital capacity of at least 20ml/kg ABG: ○ PaO2 greater than 60 mm hG with an FiO2 of less than 0.5 ○ PaCO2 in the “normal” range for the patient ○ pH greater than 7.35 (TEXTBOOK^) *Finnegan Said Focus On These Guidelines of Adequate Pulmonary Function:* Rapid shallow breathing index less than 105 RR less than 32 Tidal volume at least 300 Completely awake, oriented Normal pulse ox Good ABG Not a lot of secretions If have lung disease: PaO2 to be greater than 60 Normal lungs with bad pneumonia: 80-100 FiO2 less than 50% Chronic Ventilation: Mechanical ventilation is required ○ When a patient's spontaneous efforts are unable to sustain adequate ventilation of the lungs Conditions such as stroke and spinal cord injury ○ Damage the nerves that control breathing and make spontaneous breathing impossible or an extended period or for life Chronic stable illnesses, such as neuromuscular disorders and chest wall deformities, and/or advanced age (LG, MS, Scoliosis) ○ May make long-term mechanical ventilation necessary for extended periods or for life Chronic illness that requires recurrent ICU hospitalization ○ May require frequent repeated treatments with mechanical ventilation and repeated attempts to wean from mechanical ventilation Terminal Wean: The removal of ongoing ventilator support is a necessary evil when these devices are hindrances to ending life rather than sustaining a manageable quality of life for the pt (Palliative wean) Indications: Pt is no longer responsive or pt is in agreement KEEP patient & family wishes in mind and support them ○ ADVOCATE Keep patient comfortable, no distress, no pain ○ Ask provider for morphine or fentanyl drip if needed Once extubated pt could die immediately or may survive for a few minutes- hours Check patient’s temperature (Will be febrile when close to death) ○ *Can give tylenol suppository to cool pt off a little* Never let them suffer! Pulmonary Rehabilitation: A broad program that helps improve the well-being of people who have chronic breathing problems. Benefit people who have COPD, sarcoidosis, idiopathic pulmonary fibrosis, or cystic fibrosis PR also can benefit people who need lung surgery, both before and after the surgery. PR doesn't replace medical therapy. Instead, it's used together. May include: ○ Exercise training ○ Nutritional counseling ○ Education on your lung disease or condition and how to manage it ○ Breathing strategies ○ Psychological counseling and/or group support Nur 409 Exam #2 Review Sheet Tuesday March 16th Topics: Cardiovascular 1, 2, 3, 4 Cardiovascular Function 1: Dysrhythmias Management of the Patient with Dysrhythmias and Conduction Problems: Old Material Normal Electrical Conduction: Comes from SA node→ Atria→ AV node→ Bundle of His→ L & R Bundle Branches→ Terminating the Purkinge Fibers and causing a contraction Normal SA Node: 60-100 Normal AV Node: 40-60 Normal Ventricle Pace: 20-40 Every cell in the heart can function as a pacemaker (Beneficial) If the SA node becomes damaged or impaired from illness or injury, there are cells in the atria that can take over the pacing If the AV node or secondary pacemaker becomes damaged, there are cells in the ventricle that can take over for pacing Concept of automaticity is very important NSR: Typically a rate of 60-100. Most of us have a HR between this. Sinus Tachycardia: Rate of 100 or greater Predicted MAX HR= 220-AGE. The heart can take at that age ○ An 80 year old man cannot tolerate a HR as fast as a 20 year old boy ○ 70 year old: 220-70= 150 MAX HR You can also find a predicted max zone they are in. 150 HR x 50% (.50)= 75 pretty tight. t ○ Then take 80% = 128 ○ 75-128 = Zone!!! ○ Just pay attention to this If you have a patient just lying there in bed, it’s important to investigate why If they just had a heart attack and after are tachycardic, what med might you need as an intervention? Core treatment for MI- Nitroglycerin, BB (Try to get HR below 100) Causes: Pain, infection, anxiety, dehydration, recent MI If HR is greater than 100= NOT being controlled Realways check k it Sinus Arrhythmia: Irregular rhythm from sinus node (with P waves), typical in peds. Almost always a benign rhythm. HR will increase when pt breathes in and decrease when pt breathes out (Pattern: 83, 76, 83, 76) PAC: Premature beat. Differentiate from JVC→ If you can see a P wave. If you see a P wave, determine it is coming from atria. Atrial Flutter: Arrhythmias of the atria, more organized rhythm, saw tooth pattern (Saw blade upside down), can be irregular sometimes, also flutter and fib sometimes go back & fourth, upper case F waves. Atrial Fibrillation: Arrhythmias of the atria, completely unorganized, no P waves, fibrilatory waves= lower case “f waves”, can actually count them (3:1 atria to ventricular contractions), typically irregular rhythm What Causes Arrhythmias? Any CV Disease, like hypertension, CAD, valve problems Smoking, Age, Anxiety, too much caffeine Caused by those diseases: HISDEBS Hypoxia = Causes Cardiac Arrthymias (myocardium deprived of O2, MI, blockage, muscular death below the blockage) ○ COPD causes strain on right side of the heart (Bc R ventricle has to pump to pulmonary vasculature, increased pressure in R ventricle) ○ Pulmonary Embolism does the same thing Ischemia= Can cause ischemic heart disease, arrthymias, MI, viral infections of myocardium, angina = Lead to arrhythmias Sympathetic stimulation = Hyperthyroidism, exercise, anything that causes heart to beat faster to meet metabolic disease of the body Drugs = All meds used to treat arrhythmias can also cause it, abx can cause elongation of QT segment as well = Lead to arrhythmias Electrolytes = Lead to arrhythmias (Three electrolytes for cardiac: Calcium, potassium, magnesium) Bradycardia = Slow enough can cause arrhythmias Sympathetic Stretch = Enlargement of the atria or ventricles, pt that hasn’t taken care of hypertension develops an enlarged heart can lead to arrhythmias Diseased heart can do anything!!! Can have a whole bunch of different things like AFib and randomly P Waves show up. When you don’t know what you are looking at, best thing is to go to a 12 lead EKG and go to the provider to reflect what you are seeing together Cardiac Conduction System SA node → Atria → go over to left side by bachman’s bundle → SA node picks up the impulse carries it to the bundle of his to the L & R bundle branches I SA node Atria GO 100 2 AV node ventricle 40 60 20 40 Management of the Patient with Dysrhythmias and Conduction Problems: New material Junctional Dysrhythmias PJC: Premature Junctional Contractions Premature beats Causes: Digoxin toxicity (often! Reversal= Digibind) heart failure, CAD ○ Arrthymias in the junction are probably due to this! Less common than PACs Impulse starts in the AV nodal area before the next sinus impulse reaches the AV node NORMAL P QRS T (repeated), then all of a sudden you see a premature beat come in, looks like other tight QRSs You are looking for a p wave or some kind of morph in the preceding T wave of the complex in front of it (higher, dimpled, weird looking like something is in there electrically) ○ If you don’t see the T wave morphed and don’t see any P waves= PJC P wave may be absent, before, or after the QRS 0 PJC Criteria: Premature Inverted P Wave (Sometimes just a short PRI, no inversion). Usually absent P wave most of the time. sinus rhythm w 2 PICS Junctional Rhythm: Sinus nodes becomes slow, impulse cannot be conducted, the AV takes over Ventricle rate 40-60 (Diagnosed by slow rate!) Regular QRS is normal ○ Nice and tight Different looking P waves→ Very close to the QRS ○ Almost always appears behind it ○ No P waves before the segment ○ Retrograde (backwards) or hidden in here behind it If P wave present, PRI is less than 0.12 seconds (Very short) S&S reduces cardiac output Treatment like bradycardia ○ Emergency atropine IV push if symptomatic and put pacemaker on, dopamine drip (vasopressor, increases BP) 0 invertedp Pacemaker shifted from SA node → AV node (New dominant pacemaker of the heart) Site is now shifted very low in the atria Anytime the heart beats too fast or too slow, have to worry about CO Have to make sure perfusing rest of body and brain May need a transcutaneous or venous pacemaker if not working If too fast, not feeding myocardium→ Chest pain or MI Junctional Escaped Beat/Rhythm: Normal rhythm (PQRST), beat is DELAYED (not premature). Heart is sending out impulse but there’s a delay; heart notices SA node isn’t firing so it goes from the AV node Ventricular Dysrhythmias PVC Premature Ventricular Complex: Impulse starts in the ventricle and is conducted through the ventricles before the next normal sinus impulse (Starts in ventricle and stays in the ventricle for as long as the heart can react) Normal rhythm Premature beat Wide and bizzare QRS (.12 or greater!) Inverted wave following the QRS (conduction abnormality) Couplet= 2 PVCs back to back Three in a row= 3 PVCs back to back 3 or more= VTach ○ Monomorphic/all coming from same folci or can be multifoci from multiple places in the heart Ventricular Tachycardia: V TACH 3 or more PVCs in a row (coming from same ectopic point in ventricle) Rate exceeding 100 bpm (100-200 bpm) Regular Wide bizarre QRS Treatment: Make sure pt is ok and then treat them ○ Some pts just sit there with v tach ○ Ask them about symptoms/how they are feeling ○ Get the person to cough to try to break the rhythm ○ Always check K & Mg!! ○ May try amiodirone (chemical conversion) over 10 mins. Hopefully this will convert them V tach can be stable or CODE situation!!! ○ Can have ppl in cardiac arrest with v tach as well ○ Code board under, get thers in the room to help, CPR, defib, Epi 7no SIDE NOTE: Pt’s K is slightly low 3.5 (norm: 3.7-5.3) and mg is slightly low 1.5 (norm: 1.7-2.2). What do you give first?? Mag FIRST! Stabilizing the heart. If K was SUPER low (2) with VTach and PVCs all over, of course give K first! But if you have a choice, give mag first (stabilizing k in the system) Also, K is 3.3 and you give 40 mEq klor by mouth, what do you expect the K to be? For every 10 mEq of k you give, you can expect their serum to raise by.1 ○ You should see 3.7! Do NG tube or orally ideally. Hospitals usually restrict the amount of K going in at once via IV. Keep in mind most of these ppl are very unstable so extra fluid is not a good idea D Ventricular Fibrillation: Most common dysrhythmia with cardiac arrest Rapid rate (greater than 300 bpm) V FIB Disorganized Quivering of the heart Heart is quivering in the chest= NO CO Treatment: CODE!!! Start CPR, defibrillate ASAP, 2 rounds of Epi, may order vasopressin Idioventricular Rhythm: Ventricular escape rhythm VERY SLOW rate. 20-40 bpm Wide & bizarre QRS Regular rhythm Often occurs before people die, not ok with it. Precode or code situation. About Treatment: Would NOT want to give anyone in this situation lidocaine or amiodirone because they have one little tiny pacemaker in their heart. If the provider wants to treat that, it could be very bad for the patient. Give atropine or epi to speed it up Canaan There are subdivisions: Accelerated Idioventricular Rhythm: 40-100. Same principle (Anything over 100 is Vtach) *Not sure if need to know this* Ventricular Asystole: Flatline, absent QRS (ventricular standstill and atria-top of heart doesn’t contribute much to CO) r.D0 I Treatment: CODE SITUATION!!! Start CPR and administer epi ○ Change out providers Q2M to keep strong compressions going Make sure the board is under them for strong compressions as well Should be differentiated from fine VFib: Can mimmick but diff rhythm Let’s say you are in a code for 20 mins and they are getting ready to call it. After 6-8 mins questionable brain activity, before they say he or she is expired, they should check And 2 leads. Fine ventricular fib: Can defibrillate or do something with *With aystole, you should NOT defibrillate. ○ Every time you shock the chest, you raise the level of transthoracical resistance in the chest so if you shock asystole, you can be doing more harm and blocking later efforts Conduction Abnormalities AV Blocks (1st, 2nd I and II, 3rd degree): Relationship of P wave to QRS would distinguish the diff types of heart block 1st Degree AV Block: delay1pause P wave, prolongation (PRI needs to be measured and is longer than normalGreater than.20)= Delayed and slower than normal More of a pause than a block When naming: SR/SB with first degree AV block Cause: Can happen after an MI ○ If new occurence, bring to the provider’s attention ASAP 2nd Degree AV Block Type 1: Mobits 1, winkybok, type 1 (three names) longer PRI then drop Repeating pattern in which all but one atrial impulses are conducted through the AV node into the ventricles Progressive lengthening of the PR interval, until one QRS is dropped WHY is this happening: QRS not being conducted (Bottom of the heart/ ventricle is not contracting from the electrical impulse), which delays the P even more. Then, extra P waves form because it is taking more and more time to get down to the ventricles ○ ANYTIME MORE Ps THAN QRSs= THINK HEART BLOCK!!! Example: PRI:.16,.28,.32. Then, T wave with a P then nothing=drops. Repeats over again in a cycle More dangerous than 1st degree because randomly droppping the CO Look and measure PRI- Will get progressively longer and then result in dropped QRS (PRI=.20 where QRS follows. PRI=.24 where QRS follows, PRI=.28 where QRS follows, Then just P wave with NO QRS bc it drops off 2nd Degree AV Block Type 2: Called mobits two PB constant then drop 2 P: 1 QRS PRI is consistent P wave, QRST (repeated over & over) then….Randomly NO MORE QRS= SUDDEN drop. Random P waves without QRS. Some of the atrial impulses are conducted through the AV node into the ventricles More dangerous→ Decreased CO ○ ANYTIME MORE Ps THAN QRSs= THINK HEART BLOCK!!! ○ Remember there’s injury/illness in an area of the heart causing issues like heart block 3rd Degree Heart Block: Complete dissociation between atria and ventricle. Atria beating at one rate and ventricle beating at another rate, not working together at all No atrial impulses are conducted through the AV node into the ventricles Two impulses stimulate the heart (two pacemakers) ○ Atria: P waves may be seen ○ Ventricle: QRS complexes Seems to be together, but not connected ○ Caliper will show equally spread out P waves *No coordination between the P waves and QRS!* ○ Top part of heart is beating faster than the bottom part Treatment: Needs a pacemaker Cardiovascular Function 2: Adjunctive Modalities & Management of Dysrhythmias Adjunctive Modalities and Management External Electrical Therapy: Things outside of the body Cardioversion: Done while the patient is awake, amount of electricity used, timed therapy Defibrillation: Board→ CPR→ Defib ASAP. Cardiac arrest, code situation Pacemakers: ○ Transcuteanous- Most common ○ Transvenous- Early 80s-90s until transcutaneous ○ Permanent pacemaker ○ Epicardial pacing- Electrodes go right to the heart, like in open heart surgery ○ monomowoommarmommonmamama Swangas catheter?? Swan ICD 9am Diagnostic Testing Ecocardiogram ○ TTE: Transthoracic echo, using sound waves, noninvasive, easy to do. Spot on site check. Just to give an idea on how the heart is functioning, how valves are working and walls are moving Through chest wall, skin, fat tissues, muscles, bone, more abstract ○ TEE Transesophageal Echocardiogram: More invasive, requires consent, moderate sedation or heavier if on ICU on vent Superior to TTE Tube is inserted into the esophagus like an EGD (endoscopy). Layers of tissue between the heart and esophagus are very thin, so they get a good picture with it. Percutaneous Coronary Intervention (PCI) ○ PTCA ○ Coronary Artery Stent Interventions Angioplasty Stent placement ○ Types of stents: Drug-elluding and non-drug elluding Dysrhytmia Treatments Acute or Chronic Medications Depends on dysrhythmia and duration Presence of heart disease Response to previous treatment Depends on the provider Use treatment guidelines LT Medication Examples: Sodium channel blockers (Lidacaine and norpace) Beta blockers (Metoprolol) Potassium blocking agents (Amiodorone, burtilim) Calcium channel blockers (Cardizem, nifedipine/procardia) ○ Know a little bit about how the docs pick them External Electrical Therapy Cardioversion Defibrillation Pacemakers ICD V TACH if When someone is in ventricular tachycardia, what do you do…… See if person is awake and sitting there, ask them how they are doing and do VS OR opposite- Eyes rolled in back of head, CODE, cardiac arrest If awake, ask them to cough or bare down to break the rhythm ○ If it doesn’t, get provider and stop the arrhythmia ASAP Amiodirone (EMERGENCY, cardiac arrest dosing= 300 mg direct IV push) If in Vtach but NOT out/cardiac arrest, put 150 mg in 100 cc of d5w IV piggyback Also use lidocaine (For numbing and vtach and arrhythmias) ○ But can cause confusion in the elderly I Just admitted to the hospital for a heart attack (naive to BP meds), going on rounds and going to give someone lopressor (Hold for systolic BP less than 100, hold for HR less than 60)- Can be kind of strong for them in the beginning. On a low dose (25mq Q12). Check BP at end of shift and BP is 98 systolic. It is possible their BP is lower just bc they are waking up Because new to this type of therapy, come back in 10-15 mins and check BP If you check again then and it’s still in 90s, hold it If it goes up, give it ○ Essential treatment for CAD, heart disease (VITAL) If there’s a problem with medication, it’s better to find out this in the hospital than at home!! Vfib, Vtach (PVCs particularly): Check mg & K!!!! For every 10 mEq of K given: The serum level should go up by 0.1 Remember if both levels are moderately low: Give mg first bc it will stabilize k Also avoid giving cardiac patients extra NS: Just going to hold onto that extra water!! Give it by mouth (tablet) whenever you can 2 Old Fashion Defibrillator Every shift, a nurse checks the defibrillator in the beginning. Run a strip, set energy level to 30 Jewels, charge it, and press the button to see if it works Write on strip: Date, time, initials Now-a-days they usually use pads with pics on them. Make sure pads aren’t expired because they dry out If using paddles, make sure you use approved defibrillator gel!!* NOTHING ELSE Make sure you put around 20-25 lbs of pressure on the chest= Get a good seal on there!!! Need good defibillation effort to patient Everytime you cardiovert/defibrillate somebody, you raise the amount of transthoracic electrical resistance in their chest. You need more energy to get things done. Don’t want to use too much by accident and then the next time have to increase it even more if you have to rescue them again Shocks are sequential: Increasing levels of energy when you cardiovert/defibrillate Could get paddle burns if defibrillate a lot ○ Could hurt, ask pt if they want tylenol or something for pain Monophasic and Biphasic Defibrillators Mono: Sent energy to only one paddle, other paddle is a ground. That paddle required a lot more energy. 200-360 jewels. Older one Bi: Energy distributed between two pads, use less energy. 100-150. 200 is max. AED Most important thing: #1 TURN IT ON!!! Always know where it is If someone is in cardiac arrest (not breathing, not perfusing, no pulse) send a friend to get AED and call 911. Start CPR, start AED- just follow directions 1: Apply pads and turn on One pad on upper right pectoral region And other is over the heart 2: CPR and macchine will tell you when to stop CPR to analyze rhythm 3: Will say shock is needed and deliver shock. Or say no shock indicated- continue CPR 4: This will continue every 2 mins Correct Pad Placement Preconditioned pad: Saline impregnated. Come in a package, open them up, and they come right out and go on the chest Placement is different depending what using it for: If cardioversion/defibrillation: This placement If in cardiac arrest, may come with the pads on Remove any med patches so don’t get burned Make sure they don’t have any metals or wet clothing (conduct electricity accidentally) If pacing: One over heart and other one on back like a sandwich If person is awake tell them to roll so you can put on Cardioversion & Defibrillation Used to treat tachyarrythimias Electrical current that depolarizes a critical mass of myocardial cells After repolarization occurs the sinus node is able to restart as the heart’s pacemaker IMPORTANT: Difference is the timing of delivery of the electric current D Cardioversion: Synched with the heart’s electrical activity…patient MUST have a pulse MUST click the sync button l Want it on R wave You and provider will say ok, going to cardiovert at 50 jewels. If using paddles, you are holding it to the person’s chest and push the button If cardioverting, can have a delay for macchine to find the right timing to deliver energy Don’t want to have R on T phenomenon = DANGEROUS ○ T Wave: Absolute refractory period of the ventricle of the heart (vulnerable, about to repolarize). ○ If the energy delivers at this moment, can precipitate vtach or vfib ○ VERY dangerous Will try to do a cardioversion on these things IF the person is not hemodynamically compromised and not symptomatic ! ○ When the heart goes too fast The heart can’t feed itself on diastole It cannot fill or perfuse properly Can become hemodynamically unstable and decrease in CO Cardioversion > Defibrillation If new arrhythmia and not sure of the status of it exactly, you don’t want to defibrillate them because there’s a chance the patient can have a clot sitting in their heart Don’t want to do this unless sure this isn’t the case ○ May try to coagulate first before doing so There could be something sitting in the left atrium (Small appendage on the left atria that is like a little half tunnel and can form clots there)= Watchman procedure (Little umbrella they deploy that builds up epithelial cells over time so it becomes smooth and takes this out of the equation) ○ Could easily have a stroke on left!!! ○ On right, could easily have PE Just don’t want to cardiovert pts without knowing status Unless emergent They will usually put a big bolus of heparin beforehand to prevent anything from happening Cardioversion is timed and want to make sure they don’t have a blood clot sitting in the atria, and if the arrhythmia is more than 48 hrs, they will try to sit on the person a little bit and manage them as long as not hemodynamically compromised But if they become compromised, inject with heparin and try to save their life Hold dig with Cardioversion: Want SA node to kick in. Dig blocks AV node from kicking in. Want to make sure dig is on hold.. want impulse to get through F If cardioverted: Fully cared for IV for meds Administer some sedation (A little versed- Fast acting, out of system quick) Lidocaine: Numbs the heart and the brain Make sure respiratory and anesthesia is there incase if planned ○ Advocate!!! ○ It is like getting kicked in the chest: Cruel if you don’t give something!! AFTER: If lucky and get normal sinus rhythm, get EKG done to be sure Might be changes in their meds after this Defibrillation: Immediate, unsynchronized…patient has no pulse, no BP (EMERGENCY) Delivery of Electric Current Paddles: Old fashion Conductor pads, multifunction pads: ○ More common, make sure not expired, come with pictures, multifunctional ○ Can use for cardioversion, defibrillation, or pacing ○ Hands free Automatic External Defibrillator (AED): Uses pads Implanted device Internal Cardiac Defibrillator (ICD): Can come with pacemaker too, not always though Example: Pt of his had a pacemaker with ICD and was going down to comfort care. Had to tell them to turn off the defibrillator portion. When people are starting to die, they can have arrthymias (VTach), you don’t want the defibrillator to randomly fire. NEVER shut off the pacemaker= Still treating them. Don’t want them to be moving toward dying and then the device shoots them back up. KEEP this in mind!! Tell the provider if they transfer care Role is essential: Advocating for patient Placement Standard: Anterior chest Safety Measures Good contact ○ Pads to skin (20-25 lbs against chest with paddles) ○ Conductive median ○ Prevent arching on discharge Leaking of electrical current through air (Don’t want to shock yourself) Clear patient ○ Three clear check: Make sure you yell out I’m clear, your clear, all clear Or someone else can accidentally defibrillate themselves ○ Prevent contact with patient or anything touching the patient when the defibrillator is discharged Use correct conductive gel A female with large chest= Might have to go underneath or on the side IF Cardiac Arrest Occurs: Start CPR immediately Five cycles then do pulse check Rotate out providers Q2M Give Epi Q3-5M IV Push If someone is in VTach/VFib= Defibrillation is PRIMARY treatment ASAP!! Cardioversion: Delivery of a timed electrical current SYNCHs with the EKG (Synch button) ○ Patient needs to be connected to a cardiac monitoring on the defibrillator ○ R wave will be “marked”= Timed! ○ Discharges energy on ventricular depolarization (In the QRS) ○ Prevents discharge during repolarization (T wave)= BAD! Delay in discharge ○ Discharge buttons must be held down until shock is delivered ○ Expect when press shock button or press the tabs on the paddles= there can be a delay as the macchine finds the right time to send the shock Type of Cardioversion: Elective ○ Dysrhythmia has lasted longer than 48 hours Anticoagulation may be indicated ○ Digoxin is held ○ NPO (Incase emergency intubation is needed) ○ Pads placed anteroposteriorly (Back & front) ○ Sedation, analgesic, anesthesia To make the patient more comfortable Advocate for the patient! ○ Voltage varies (50-360 joules) If it goes higher than 90, no longer cardioversion. Now, defib ○ If elected cardioversion or at all possible, do a TEE. Much more accurate than TTE when diagnosing clot in atria Urgent: Emergency! Slap it on the chest ○ Unstable SVT, afib, rapid aflutter, or vtach with pulse Make sure no clot= Heparin IV push If Vtach or have a pulse with SVT: Try to get them to cough, bare down, vagal manuever, carotid massage (ONLY PROVIDER- can break off a piece of plaque in carotid and cause a stroke) f Drugs for SVT: Adenosine (Dose of 6mg IV push, can be repeated twice 12mg 2x) Before you give the drug, warn the patient they may feel a little lightheaded Stopping heart for a few seconds, so kind of scary (Don’t tell patient this) Push this med FAST then follow with 10 cc of normal saline fast A Post Cardioversion Rhythm conversion Peripheral pulses* BP* Airway patency, LOC Monitor ○ VS ○ SpO2 ○ EKG* *EKG, pulses, BP= Watch closely over next several hours and make sure it does not repeat again, make sure electrolytes are good (mg, k), LOC, airway, VS, pulse ox D Treatment: Persistent tachyarrthymia (with a pulse) causing: Hypotension Altered mental status Signs of shock: Hypotension, tachycardia, cold clammy skin Ischemic chest pain: Heart going too fast→ HF Acute heart failure Causes hemodynamic compromise Uncontrolled Afib: HR over 100 (Can go up to 180) Cardizem for afib D SVT: Fast rate, 130 or more, one bump Typically give adenosine Try to slow down to get an idea what’s under there so they can better treat it (Distinguish between SVT and afib) VT: Amiodorine (go to drug), lidocaine (caution with elderly), pronestel/procanamide D Defibrillation Emergency ○ VFib, Pulseless Vtach ○ Early defibrillation=better survival rate!! ○ AEDs Depolarizes a critical mass of myocardial cells all at once Higher voltage than cardioversion ○ 120-360 joules (monophasic defibrillator) ○ 100/150-200 joules (biphasic) ○ Cause more damage the higher you go If unsuccessful ○ CPR and ACLS protocols: Board under them, defibrillated (try to stop vtach, vfib from occurring), epi Q3-5M, rotate out providers with CPR Q2M, make sure CPR is fast and deep (100-120) If within a min, 90% survival rate. If delayed up to 12 mins, 2- 5% survival rate Quicker you shock them, the better you are!! Tyes of Defibrillators Monophasic Deliver current in one direction Requires increased energy selection VERY OLD, not really used anymore Biphasic Delivers energy from positive paddle/pad , then reverse back to the original paddle/pad Allows for lower energy usage, non progressive Communication between two pads (one is +) ○ More efficient and cardioprotective Meds During CPR Epinephrine Full strength Epi IV push Convert to NSR Increase cerebral and coronary artery blood flow Amiodorone, Magnesium If ventricular rhythm persists for Vtach Amiodorone: NOT benign drug Treats atrial and ventricular arrhythmias Usually after 24 hours on drip dose, start to transition them to oral dose Complications: Blue man’s syndrome Bradycardia Interstitial lung disease (major problem→ High degree of pulmonary toxicity) Hypo/hyper-thyroidism Cornea problems (discolored), cutaneous probs (skin rashes) even with oral form IV form: Hepatic problems, hypotension skin rashes Remember: If grandma comes in with recurring VT, should be fine. If mom starts getting this drug at 50, they should think about this again Dangerous drug!! But good drug VFib CODE!, defib, CPR, Epi Q3-5M Vtach If nonperfusing: CODE!, Defibrillation, CPR, Epi Q3-5M Check mg, k, treated with amiodorone, lidocaine If with a pulse, sitting in bed: Will try to cardiovert with drugs. If that doesn’t work, they will try with defibrillator (less energy) IscaE eky Asystole Start CPR, Epi Q3-5M DO NOT defibrillate ○ Can prevent further resusitative efforts with defibrillator Ensure it is NOT fine Afib ○ If it is, then you would shock because could get a rhythm back Check this in how many leads? 2!! ○ EMERGENCY SITUATION T mega D D PEA pouts BP Looks like sinus arrhythmia. What if pt has no BP, no pulse, no HR? PEA!!! Heart has electrical and pump parts- Possible the electrical part is working great but the pump isn’t working Causes: Five H’s Five T’s Hydrogen Ions (Acidosis) Hypo/hyper-kalemia ○ If renal failure pt, could have high K ○ Blood gas will show! May decide to treat with regular insulin IV push followed by D50. Force K into cells. Also give calcium bc renal pts run low Hypothermia ○ If found out in the cold, try to warm them up Hypovolemia ○ Ringer’s lactate, NS, type & screen, try to get O- blood as fast as possible Hypoxia Thrombosis (coronary)- heart Cardiac taponade (Bec’s Triad- lowering systolic BP, narrowing pulse pressure, JVD, muffled heart sounds)- heart Tension pneumothorax- lungs PE- lungs Toxins (Overdose on drugs) ○ If they have done a bunch of cycles and this is the turn out, will look at a bunch of factors to determine if PEA infeagin Dso t ca POINT IS = TREAT UNDERLYING CAUSE!!! renalfailure Sire Profound Bradycardia Slow HR & symptomatic Treatment: Give atropine ○ To raise the HR temporarily ○ SE: Can also dilate the pupils= BEWARE when look at eyes. Not neuro Can also order dopamine on IV drip Put external pacemaker pads on patient as well incase need them D Second Degree Heart Block Type 2 Check relationship by counting PRI to see if they are the same. This one has communication between the two ○ Different from 3rd degree, which has no communication between top & bottom parts of heart HR is also VERY slow (35 bpm) 3:1 conduction deficit Treatment: Need pacemaker Third degree heart block No relationship with P waves and QRS. All different PRIs or can’t calculate Pacemaker Therapy Device that will deliver an electrical stimuli to the heart Permanent or temporary Can be combined with AICDs Indicated for: Slow pulse formation (Bradycardia) ○ NOT all people with bradycardia- not the 20 year old track athlete with HR of 54. People who have bradycardia→ Hemodynamic compromise AV or ventricular conduction disturbance ○ Conduction problem → Inferior wall MI- Right side In about 60% of people, the right coronary artery feeds the SA node In 90% it feeds the AV node? If someone has a right sided infarct, watch for heart block!! Can also be used in bad cases of CHF to resynchronize the left and right ventricles to work together better (resynchronization therapy) Pacemaker Design Two components: Generator Circulatory to detect intracardiac electricity and cause a response (sensitivity), measured in millivolts (mV) ○ Milivolts: Sensitivity, how much does the pacemaker see ○ If the sensitivity is very high, the pacemaker can’t see anything. If it can’t see anything and the heart has an intrinsic native beat, it won’t see it and may try to initiate a complex ○ If the sensitivity is too low, the pacemaker can see everything. Every sort of artifact it will interpret as a heartbeat. Then it doesn’t initiate the shock and stimulate the my

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