NURS 3740 Study Guide PDF

NURS 3740 - Study Guide Week 2-3: Venous access devices =============================== Learning objectives: - Be able to identify types of devices - Be able to identify potential complications and identify appropriate nursing interventions for each complication - Describe and demonst...

NURS 3740 - Study Guide Week 2-3: Venous access devices =============================== Learning objectives: - Be able to identify types of devices - Be able to identify potential complications and identify appropriate nursing interventions for each complication - Describe and demonstrate a complete dressing change for a PICC - Identify, describe, and demonstrate the correct steps for removal of a PICC/CVAD - Identify and list complications associated with removal of CVADS **Vascular access devices (VADS)** - Are catheters for repeated access into the vascular system - PVAD short short term use (72-96 hours) - PVAD midline long term use (7-30 days) - CVADS/PICCs long term use (months-years) **Vad assessment includes:** - Assess patency always use a minimum of a 10ml syringe - Site assessment - Dressing assessment - CVAD/PICC = external length. \*\*need confirmation of placement if 2cm change of length\*\* **Flush IV tubing:** - Before and after all medications, PNs, and transfusions - With IV tube and end cap changes - If occlusion is suspected - If retrograde blood is seen - With continuous and intermittent infusion once per shift **Flush volumes (0.9% NS)** - Flush volume before after med administration - PVAD short = 3mL 10mL - PVAD midline = 10ml 20ml - CVAD PICC/percutaneous = 10ml 20ml - CVAD tunnelled = 10ml 20ml - IVAD = 10ml 20ml **Locking valved + non valved CVADS** - Valved CVADS have no stopper guard on the IV tubing. Flush and lock as normal - Non-valved CVAD have a stopper guard on the IV tubing. After NS flush, lock with 3ml of 100 units/ml of heparin. - IVAD After NS flush, lock with 5ml of 100 units/ml of heparin **Blood sample collection** - PVAD short = yes pre collection discard 3ml - PVAD midline = no - CVAD PICC, percutaneous, tunnelled, IVAD = yes pre collection discard 6ml - \*\* NOTE: no discard if collecting blood cultures. All infusions should be stopped for 2 min pror to all blood collection. Change end caps after all blood collections.\*\* **Dressing changes** - Every 7 days or PRN if soiled/ falling off - If gauze is used under the dressing, every 48 hours **Needleless end cap changes** - Q7 days **IV tubing changes** - Intermittent/secondary Q24h - Continuous primary Q96h **IV fluid bag changes** - Intermittent/secondary Q24h - Continuous primary Q96h **Use for VADs:** - Accessing blood vessels - Med administration - Nutrition - Fluids - Hemodialysis **Types of PVAD lumen sizes:** - 14G Orange - 16G Gray - 18G Green - 20G Pink - 22G Blue - 24G Yellow **Removing a percutaneous CVAD/PICC** - Position patient in 10 degrees Trendelenburg - Remove dressing and clean with 2% chlorhexidine - Maintain principles of asepsis - Ask patient to perform Valsalva maneuver, if they cannot, pull during patients exhalation - Hold cotton ball until bleeding stops, apply a sterile occlusive dressing - Patient must remain supine for 30 minutes Caused by Symptoms treatment **Complications of VADs** - Phlebitis - Cannula rubbing inside of vein - High or low pH of meds - Redness - Pain - Heat - Swelling - Do not use the line, remove IV - Choose smallest gauge necessary - Apply warm compress - Infection - Bacteria/microorganism getting into line due to no use of sterile technique - Redness - Pain, tender - Swelling - Purulent drainage - Malaise - Fever - Do not use the line, remove IV - Get bloodwork tested - Always clean the hub before access, sterile technique, change dressing when saturated - Occlusions - Clot/blockage from inadequate flushing - Sluggish flow rate - Downstream occlusion - Inability to flush - Do not use the line, remove IV - Infiltration - When non vesicant solution is administered into surrounding tissue - Pain - Swelling - Redness - Skin is cool to the touch - Tight skin - Do not use the line, remove IV - Extravasation - When vesicant solution is administered into surrounding tissue - Pain - Swelling - Redness - Skin is cool to touch - Stinging - Blistering - Necrosis - Do not use the line, remove IV - Hemorrhage - Bleeding at the insertion site - Pain - Edema - Swelling - Do not use the line, remove IV - Controlled with manufactured hemostatic product IV Complications - Signs & Symptoms \...  Extravasation injury of the dorsum of right foot following 10% dextrose\... \| Download Scientific Diagram phlebitis intravasation extravasation **Complications only associated with CVADs** Pneumothorax - Can occur during insertion in subclavian placed lines, where accidental puncture of lungs causes air to get into the pleural space - Decreased breath sounds in one lung - Dyspnea - Decreased SPO2 - Sharp pain in chest or shoulder - Subcutaneous emphysema - Elevate HOB - O2 - Vitals, resp assessment - Anticipate chest XRAY and chest tube Cardiac dysrhythmias - Occurs due to catheter malposition or migration from coughing, change in body position, or physical movement - Irregular HR - Change in external length of catheter - Always use securement devices - Anticipate XRAY confirmation Hemothorax - Blood in the pleural space from damage during insertion in subclavian placed lines - Decreased SPO2 - Increased RR - Dyspnea - Hypotension - Decreased or absent air entry into one lung - Elevate HOB - O2 - Vitals, resp assessment - Anticipate chest XRAY and chest tube **Systemic complications of IV therapy** Pulmonary edema - Fluid circulatory overload caused by excess fluid accumulation. - Increased risk if patient has cardiac or renal health challenges, or are pediatrics or elderly - Decreased SPO2 - Crackles in lungs - Increased RR\ dyspnea - Coughing up pink frothy sputum - Increase HOB - Vitals - Administer O2 - Notify prescriber, anticipate diuretics Clots/air embolism - Sudden SOB - Coughing - Breathlessness - Shoulder or neck pain - Agitation - Feeling of impending doom - Hypotension - Wheezing - Tachycardia - Cardiac arrest - Occlude source of air entry - Place patient in Trendelenburg on left side - Administer O2 Catheter related blood stream infection (CRBSI) - Caused by microorganisms that are introduced into the body during insertion - Elevated temperature - Flushed - Headache - Malaise - Tachycardia - Hypotension - Sepsis - Anticipate blood cultures - Anticipate IV antibiotic therapy - Consider IV removal **Hemodialysis lines** - Hemodialysis is a method of removing waste products and excess fluids from the blood using a machine to pump blood through a semi-permeable membrane - Two types of hemodialysis sites: - Arteriovenous fistulas (AVFs) + arteriovenous grafts (AVGs) - Tunneled and non tunneled central venous catheters (CVGs) - AVFs - Preferred hemodialysis access - Created by connecting an artery and a vein together in the forearm to make arterial blood flow through a vein harden the vein to become tough and can withstand repeated venipuncture - AVGs - A synthetic artery attached to both an artery and a vein - Non tunnelled CVGs - Used when immediate access is required. CVC placed in internal jugular with two lumens, one for blood removal and blood return - Tunneled CVGs - Used as an option for patients who have tried all other options Week 4: Blood transfusions ========================== What to know - Identify and describe basics of blood groups and their compatibility with one another - Describe the different components of blood products - Describe indications for transfusions and potential adverse reactions - Describe and be aware of where to find the protocols for preparing and administering blood products - Describe adverse reactions to transfusions and be able to describe the nursing interventions required to manage the event **Blood** - Type A produce anti-B antibodies can accept A + O - Type B produce anti-A antibodies can accept B + O - Type AB no antibodies universal receiver - Type O Produce A + B antibodies can accept O + universal donor - Rh positive contains proteins can accept positive or negative - Rh negative has no proteins can only accept negative **Patient blood typing and grouping** - Tests to determine patients' blood type - Valid for 96 hours **Types of blood components and their use** - PRBCs (carries only RBCs) - Anemia Low RBC, Hgb, Hct - Acute blood loss or hemorrhage drop in RBC - FRBC (can be stored for 10 years, removes the WBCs) - Autotransfusion/autologous transfusion when a pts blood is collected, processed, and retuned to them after surgery - Stockpiling storing a reserve of blood products to ensure an adequate supply - People with alloantibodies the production of antibodies for blood or an organ that is donated to the patient, even if the blood/organ is a match - FFP (plasma, rich in clotting factors, proteins, and electrolytes) - Bleeding caused by deficiency in clotting factors provides rich source of clotting factors - Liver disease prevents the liver, the organ that produces clotting factors - Vitamin K deficiency needed for the synthesis of clotting factors - Excess warfarin inhibits vitamin K, which is needed for clotting factors - Platelets (contains just platelets) - Bleeding caused by thrombocytopenia low platelet levels - Heparin induced thrombocytopenia low platelet levels - Albumin - Hypovolemic shock need albumin to maintain oncotic pressure to help pull fluid into the bloodstream - Hypoalbuminaemia low level of albumin, can contribute to hypovolemic shock - Large volume paracentesis the process of removal of excess fluid into the abdominal cavity with a needle. Causes loss of serum proteins - IVIG (contains antibodies from plasma) - Primary immunodeficiency disorders disorders that result in the ability to produce antibodies - Autoimmune diseases prevents the immune response from responding properly - Infectious diseases helps build antibodies to fight off diseases if the patient is compromised or the infection is severe Autologous transfusion - Donating your own blood for a surgical procedure in the future Autotransfusion - The collection of blood that is loss during surgery, aseptically collecting and filtering it, and returning it back during the procedure **In preparation for blood transfusion** - Verify prescribers orders. Only a prescriber can order for blood - Give pre transfusion medication if needed 30 min prior - Obtain transfusion history, check TMS (transfusion medical services) band - Check IV site for patency and correct size. use a minimum of 22G, 20G, or 18G. blood cannot be given with other medicine running at the same time in the same line - **TUBING** - Blood components, platelets, plasma need 70-260 micron filter tubing - Glass bottles with albumin and IVIG need vented tubing - Prime a separate NS bag, 500-1000ml - Obtain vitals - Have emergency equipment at the bedside (oxygen, suction) **Doing the blood transfusion** - Obtain blood from TMS, you only have 30 minutes to transfuse once taken out - Assess blood bag for leaks, clots, contamination, discolouration - Complete bedside checks with two healthcare providers: - Transfusionist: leads and verbalizes all of the necessary elements - 2^nd^ person verifier: verbally confirms after each element is checked - Invert blood product 5-10 times, then spike and fill the top drip chamber ½ full - **STARTING RATE** - Start RBC at 50mls/hr for 15 minutes - Start plasma 50-100 mls/hr for 15 minutes - Stay with the patient for 5 minutes, recheck vitals at 5 minutes, then 15 minutes, then every hour during and post transfusion - **TRANSFUSION REACTION** - Stop immediately - Flush line with new IV line with NS - Notify MRP for orders - Stabilize patient, check vitals Q15m - Return blood to blood bank or continue with orders - Document incident - Flush line when completed. **Blood and blood tubing changing** - Blood tubing is changed every 4 hours, or 4 units have been administered - Blood tubing must be changed if there is filter debris restricting flow - Blood tubing must be changed if there is a change in the type of blood product being infused (switching from platelets to RBCs) - Blood tubing does not need to be changed within the same product unless 4 hours or 4 units have passed/been given - Blood must be administered within 30 minutes from the lab, and infused within 4 hours - Administer 1 unit of blood over 2-4 hours **Acute transfusion reactions** - Occurs during the transfusion **Delayed transfusion reactions** - Can occur up to 24-48 hours after the transfusion Caused by Symptoms treatment **Acute transfusion reaction** - Acute hemolytic reaction - Infusion of ABO incompatible blood, where antibodies in patients plasma attach to transfused blood and cause RBC destruction - Occurs within first 15 min - Fever + chills - Low back, abdominal, or chest pain - Flushing - Tachycardia, hypotension - Dyspnea, tachypnea - Hemoglobinuria + dark urine - Jaundice - Acute kidney injury - Shock, cardiac arrest, death - STOP transfusion - Treat shock, maintain BP with IV fluids - Get labs + urine sample - Insert foley to monitor urine output, give diuretics as prescribed - Dialysis required if renal failure occurs - Do not transfuse additional RBCs - Febrile, non-hemolytic reaction (most common) - Sensitization to the donors blood - Sudden chills and fever (rise in temperature \>1 degree) - Headache - Flushing - Anxiety - Vomiting - STOP transfusion - Give antipyretic as prescribed - Do not restart until orders are given to restart - Determine if patient has history of transfusion reactions. Consider giving PRN 30 min prior - Mild allergic reaction - Mild sensitivity to foreign plasma proteins. More common in those with allergies - Flushing - Itching - Pruritis - Urticaria (hives) - STOP transfusion - PRN antihistamine, corticosteroid, epinephrine as directed - If symptoms are mild, transfusion may be restarted slowly with order - Do not restart if fever or pulmonary symptoms develop - Anaphylactic, severe reaction - Large sensitivity to foreign plasma proteins - Dyspnea, wheezing, progression to cyanosis - Hypotension - Shock - Anxiety - Urticaria - Cardiac arrest - STOP transfusion - Call a code - Start CPR, apply O2 - Have epinephrine ready with prescriber order - PRN antihistamine or corticosteroid - Do not restart transfusion - Circulatory overload - Fluid administered faster than the circulation can accommodate. Higher risk in those with cardiac or renal disease - Cough - Dyspnea - Pulmonary congestion, crackles - Hypertension - Tachycardia - Distended neck veins - STOP transfusion - Obtain chest xray STAT - Have patient sit upright in high fowlers - PRN diuretics, O2, morphine (vasodilation) - Sepsis - Transfusion of bacterially infected blood components - Rapid onset chills, high fever - Vomiting - Diarrhea - Shock - Hypotension - STOP transfusion - Obtain culture of blood - Send blood and blood tubing to bank - PRN antibiotics, IV fluids, vasopressors - Transfusion related acute lung injury (TRALI) - A reaction between transfused anti-leukocyte antibodies and the patients leukocytes, causing pulmonary inflammation and capillary leak - Arises within 1-6 hours of transfusion - Fever, chills - Hypotension - Tachypnea, dyspnea - Frothy sputum - Hypoxia - Respiratory failure - Pulmonary edema - STOP transfusion - Draw blood for analysis of ABGs, cultures - Chest XRAY STAT - O2 administration - CPR if needed - Mark as unable to donate blood in the future **Delayed transfusion reaction** - Delayed hemolytic reaction - Occurs as early as 3 days or as late as several months. - Result of the destruction of transfused RBCs by alloantibodies not detected during cross matching (alloantibodies = the production of antibodies for blood or an organ that is donated to the patient, even if the blood/organ is a match) - Fever - Mild jaundice - Decreased Hbg - No acute treatment is required - Hepatitis B - Elevated liver enzymes (AST, ALT) - Anorexia - Malaise - N/V - Fever - Dark urine - Jaundice - Usually resolves spontaneously within 4-6 weeks. - Treat symptomatically - Hepatitis C - Similar to hepatitis B but symptoms are less severe - Chronic liver disease and cirrhosis may develop - Treat symptomatically - Iron overload - Excess iron is deposited into the heart, liver, pancreas, and joints, causing dysfunction - Heart failure - Dysrhythmias - Impaired thyroid - Impaired gonadal function - Diabetes - Arthritis - Cirrhosis - Treat symptomatically - Deferoxamine removes accumulated iron via the kidneys **Main signs and symptoms of a transfusion reaction** - Fever (change in degree by 1) - Acute hemolytic transfusion - Febrile, non-hemolytic transfusion - Sepsis - Allergic reaction - Mild allergic reaction - Anaphylaxis, major reaction - Dyspnea - Transfusion related acute lung injury (TRALI) - Circulatory overload - Hypotension - Acute hemolytic transfusion - Sepsis - Transfusion related acute lung injury (TRALI) - Hemolysis - Acute hemolytic transfusion - Cytopenia (low level of RBCs, WBCs, or platelets) - Acute hemolytic transfusion - Infection - Sepsis Week 5: Acute respiratory care with tracheostomies ================================================== **Learning objectives:** - Identify indications and rationale for a tracheostomy and tracheostomy types - List and correctly recognize signs of potential complications and nursing actions - Explore nursing care guidelines for a client with a tracheostomy - Demonstrate evidence based nursing care of tracheostomy clients in the lab - Identify client care considerations including communication and psychosocial support **Tracheostomy** - A surgical incision into the trachea for the purpose of establishing an airway. Inserted into the 2^nd^ and 3^rd^ rings of the trachea. About 16-20 rings in the trachea. **Indications for a trach** - Bypass an upper airway obstruction - Help facilitate the removal of secretions if the patient is unable to do so, or has impaired secretion removal - For long term ventilation **Parts of a tracheostomy** A close-up of a medical device Description automatically generated **Trach strings:** holds the trach in place. Are not changed for at least 24 hours after insertion **Flange / faceplate:** rests against the patient neck, prevents the trach tube from migrating into the trach **Outer cannula:** sits in the trachea **Inner cannula:** Fits inside the outer cannula. Is a safety feature and can be removed and replaced if obstructed. **Obturator:** fits inside the trach tube to provide a smooth surface that guides the trach tube as it is being inserted. Kept at the bedside to reduce the risk of unexpected decannulation th guide or quickly change the trach tube in the airway **Cuff:** when inflated, provides protection from aspiration and prevents the escape of air between the tube and the tracheal wall. When the cuff is deflated, there is increased risk of aspiration, and allows the patient to speak. Cuff should not exceed 20 mmHg of pressure. Deflate the cuff during exhalation. Inflate the cuff during inhalation **Inflation tube:** tube where the air enters into the cuff **Pilot balloon:** controls inflation and deflation of the cuff **Types of tracheostomies** - Non-fenestrated cuffed tube - Used to obtain a closed circuit for ventilation. - Cuffed tubes should be used when patient has risk for aspiration - Cuffs should be inflated when using with a ventilator - Cannot speak. Need a speaking valve and deflated cuff to speak - Non fenestrated cuffless tube - Used for patients with tracheal problems but do not have risk for aspiration - Used for patients who are ready for decannulation (removal of trach) - Patient may be able to eat and speak (without speaking valve) - Fenestrated cuffed tube - Used for patients who are on a ventilator but are not able to tolerate a speaking valve - High risk for granuloma formation at the site of the fenestration - High risk for aspiration - May be difficult to ventilate the patient adequately - Fenestrated cuffless tube - Used for patients who have difficulty using a speaking valve - High risk for granuloma formation at the site of the fenestration  **How often to do trach care** - Q8h + PRN - Do not change trach ties 24 hours after insertion of the trach **What's included in trach care** - Suctioning - Dressing changes - Changing trach ties - Cleaning/ changing the inner cannula - Respiratory assessment **Considerations for tracheostomies** - Patients must lie at 30 degrees or greater to facilitate breathing - Emergency supplies at bedside - NPO when cuff inflated - Can't talk when cuff inflated - Require humidity due to lack of moisture that would normally be added when air passes through the mouth **Tracheostomy emergency supplies to keep by the bed** - Two replacement trach tubes (one same size, one slightly smaller) - Obturator - Spare inner cannula - 10cc syringe - Tracheal dilators - Sterile gloves - Water soluble lubricant - Scissors - Cotton tip applicators - Trach ties - Sterile gauze - Resuscitation bag and mask Interventions Prevention **Complication of tracheostomies** - Hemorrhage - inflate cuff, apply suction, and provide O2 - apply pressure to bleeding if possible - vitals - call CODE BLUE if pulsating frank blood - assess stoma for bleeding often, provide trach care carefully - report neck swelling - report pulsation around the trachea - Stoma/pulmonary infection - Warch for signs of infection. Prevention is best practice - Perform dressing changes q8h and PRN + use sterile technique - Used humidified O2 - Encourage DB&C every 2-4 hours - Tube occlusion - Inner cannula is a safety feature, and can be removed if occlusion occurs. - Place patient supine to expose neck and chest for tube dislodgement. Use ambu-bag for ventilation. If unable to ventilate, try suction - Remove inner cannula if suction catheter does not pass. Check patency and replace with new inner cannula - If still unable to ventilate, deflate cuff and notify respiratory therapist - If still unable to ventilate, call CODE BLUE, remove trach and insert dilators, hold stoma open until new trach is placed. - Perform trach care every 8 hours. - Maintain humidification and hydration - Do DB7C every 2-4 hours - Suction as needed. - Aspiration - Put patient in high fowlers position to promote lung expansion - Report signs of aspiration: excessive coughing, increased secretions, drop in O2 sats - If patient vomits: inflate cuff, suction immediately, raise head of bed - All people with trachs require a swallow assessment prior to oral feeding - NPO when cuff inflated - HOB must always remain \>30 degrees - Accidental decannulation - Partial decannulation: deflate cuff, remove inner cannula, insert obturator, gently reinsert trach tube, remove obturator and replace inner cannula, check placement (feel for air movement from tube, check O2 sats, ensure RR returns to baseline) - Complete decannulation: call for trained provider to reinsert. Maintain tracheal airway and ventilation with bag trach mask, protect airway from aspiration, if stoma less than 7 days old use trach dilators to hold open. - Ensure trach ties are secure - Secure new trach ties before removing old ties - Assess patient for restlessness or confusion **Tracheal suctioning (open suction)** - Purpose is to maintain a patent airway, remove secretions, and stimulate the cough reflex **Indications for suctioning:** - Noisy, moist respirations - Anxiousness, restlessness - Increased RR or WOB - Signs of hypoxia - Excess secretions - Alterations in O2 levels **Suction parameters** - Suction settings: Adult (80-100). Child (60-80). Never go above 150 - Sterile gloves needed - Patient may need hyperoxygenation prior to suctioning to maintain O2 - Do not suction for more than 15 sections at a time - Can only pass through with the suction catheter 3 times until it must be changed for a new one. **Closed suction** - Used when suctioning may be needed more frequently or on an emergency basis - Allows for continuous suctioning - Should be changed every 24-48 hours. - 80-120mmHg Week 6: Spinal cord injuries ============================ **What's included in a neurological assessment** Objective - General appearance - Hygiene - LOC - Eyes, nose, mouth, tongue, teeth - Aids (glasses, hearing aids, mobility aids) - Facial symmetry/asymmetry - Nasal trauma - Neck ROM - Ability to communicate - Neck strength Subjective - Pain scale - Mental status exam (MSE) - Examination of appearance, motor, speech, thought content + process, perception, intellect, and insight - Used to obtain information about someone's mental status - Mini-mental state exam (MMSE) - Used to measure cognitive impairment in the context of someone with dementia - GCS - Used to assess patients with head injuries, suspected brain bleeds, strokes, and cranial surgeries - Measures best eye opening response, motor response, and verbal response - Arm drift - PERRLA - Assessment of pupils after a head injury - Pupils are equal, round, reactive to light and accommodation - Dermatome assessment - Used with patients that have an epidural or block - Ice is best to use because it is the first sense affected - Sedation score assessment - National institute of health stroke scale (NIHSS) - Used when a stroke is suspected. Part of code stroke. Use FASTVAN - Facial drooping - Arm weakness - Speech - Time of onset - Vision - Aphasia - Neglect Spinal segments overview - **Cervical vertebrae** - Controls head, neck, arms, and diaphragm - C1-C7 - **Thoracic vertebrae** - Controls upper back, chest, and abdominal muscles - T1-T12 - **Lumbar vertebrae** - Controls lower back and lower limb movement - L1-L5 - The spinal cord ends at L1-L2. Below this is the vertebral canal that contains the cauda equina, a bundle of nerve roots. - **Sacrum** - Controls pelvis, bladder, bowels - 5 segments that are fused - **Coccyx** - Controls region around the tailbone - 4 segments that are fused Dermatomes - Dermatomes are areas of the skin served by a single spinal nerve - Dermatome T5 is level of the nipple - Dermatome T10 is level of the umbilicus - A diagram of a person\'s body Description automatically generated Cranial nerves 1. Olfactory -- sensory - Smell - Assessment: identify smells with eyes closed 2. Optical -- sensory - Visual acuity - Assessment: visual field test (Snellen eye exam) 3. Oculomotor -- motor - Eye and eyelid movement + pupil size and reactivity - Assessment: use penlight to assess PERRLA 4. Trochlear -- motor - Eye movement -- down and lateral. Serves superior oblique muscle - Assessment: follow finger movement with eyes up, down, and side to side 5. Trigeminal -- both - Chewing and facial sensation - Assessment: see if patient can feel touch to all parts of their face 6. Abducens -- motor - Eye movement -- lateral. Serves lateral rectus eye muscle - Assessment: follow finger movement side to side 7. Facial -- both - Facial expressions - Assessment: get patient to smile, frown, raise eyebrows 8. Vestibulocochlear -- sensory - Hearing and balance - Assessment: can patient hear you 9. Glossopharyngeal -- both - Gagging and swallowing - Assessment: assess swallow 10. Vagus -- both - Gag sensation, pharynx + larynx sensation - Assessment: touch posterior pharynx and watch for gag reflex 11. Accessory -- motor - Head and shoulder movement - Assessment: shrug shoulders, turn head 12. Hypoglossal -- motor - Tongue movement - Assessment: stick out tongue and move it from side to side Spinal cord injuries **Main causes of SCI** - Trauma from motor vehicle accident, falls - Blunt trauma: causes cracked bone, herniated discs, hyperextension/flexion, rotational, or axial loading damage - Fights, shooting, stabbings - Penetrating trauma: directly pierce or sever the spinal cord - Certain movements - Hyperextension: backwards thrust of the head beyond anatomic capacity - Hyperflexion: forceful forward flexion of the cervical spine with the head striking an immovable object - Rotational injury: combination of forward flexion and rotation of the cervicle spine - Axial loading: direct force along the length of the vertebral column - Compression Complete spinal cord injury - Motor and sensory function cease below the level of the injury - Incomplete spinal cord injury - Does not result in a complete loss of movement and sensation below the injury site. Some signals can still get through, causing sensation and motor movements in certain areas below the injury - **Anterior cord syndrome** - Most common form of injury. Caused by high velocity impact trauma - Poor prognosis. 10-20% chance of recovery - Damage to the front of the spinal cord - Bilateral loss of motor function, pain, temperature sensation - **Posterior cord syndrome** - Caused by posterior impact injury or hyperextension of the neck - Results in loss of proprioception (position), vibration, and touch sense - **Central cord syndrome** - Caused by hyperextension injury - Moderate but incomplete recovery - Some signals from the brain are not received, resulting in sensory and motor deficit in the upper and lower extremities. Most signals are able to be sent and received from parts of the body below the injury - **Lateral cord syndrome** - **Brown sequard syndrome** - Caused by penetrating trauma. Injury to lateral half of the spinal cord usually caused by knife or gunshot wounds - Excellent prognosis, 99% recovery rate - Ipsilateral loss of motor function, vibratory sensation, and proprioception. Contralateral loss of pain and temperature sensation Diagnosis of SCI - XRAY - CT scan - MRI if further work is required Function of each spinal cord segment damage to individual segments of the spinal cord will result in certain impacts to function the higher the level of injury, the more serious the damage is due to proximity to the medulla and brainstem - C1-C4 - Breathing + head and neck movement - Damage = paralysis in arms, hands, trunk, and legs. Cannot breathe on own. Ability to speak impaired. Needs full assistance with daily activities. Will need torso support in wheelchair. Loss of innervation to diaphragm - C4-C6 - Heart rate + shoulder movement - Damage to C5: decreased respiratory reserve, inability to use hands. Partial shoulder movement - C6-C8 - Finger, wrist, and elbow movement - Damage = able to move shoulders, but paralysis in hands, trunk, and legs. Possibility can grab and release objects. - Damage to C6: able to flex wrist, elbow movement, weak thumb grasp, wrist extension - Damage to C7: finger extension and flexors. Good grasp with decreased strength - T1-T12 - Sympathetic tone, temperature regulation, trunk stability - Damage to T1-T5 = little to no abdominal muscle function, torso support may be needed. Paralysis in trunk and legs. Normal arm, hand, and upper body movement. - Damage to T6-T10 = all upper extremity functions present. Normal stability in wheelchair. Paralysis in trunk and legs. Functional respiratory muscles and therefore increased respiratory reserve - Damage to T11-T12 = good abdominal and spinal extensor function. Some hip flexion functions. Good stability in wheelchair. Paralysis in trunk and legs. - L1-L2 - Hip motion - L3 - Knee extension - Damage to L3: absence of hamstring flexion - L4-5 - Foot motion, knee flexion - Damage to L1-5: injuries result in some loss of function in the hips and legs. The injured person may need a wheelchair or may walk with braces - S1-S5 - Penile erection + bowel and bladder activity - Damage: some loss of function to the hips and legs. Most likely will be able to walk  **Respiratory system** - Cervical injury between C1-C4 - total loss of respiratory muscle function - Cervical injury between C4-C8 - Hypoventilation + diaphragmatic breathing if phrenic nerve is functioning - Paralysis of abdominal and intercostal muscles leading to poor cough reflex. Unable to remove secretions - Management: - Mechanical ventilation - Incentive spirometry - DB&C - Suctioning - Tracheostomy **Cardiovascular system** - Thoracic injury above T6 - Decreases influences of SNS causes arrythmias and bradycardia - Peripheral vasodilation hypotension - Hypovolemia - Management - Medications: - Atropine increase HR - Vasopressors maintain MAP greater than 85 for perfusion to the spinal cord - IV fluids - Cardiac monitoring **Urinary system** - Urinary retention atonic bladder + distension - Management - In dwelling, foley, or in and out catheter insert ASAP - Important not to keep indwelling in for too long to make the bladder dependent **Gastrointestinal system** - Thoracic injury above T5 - Hypomotility, paralytic ileus gastric distension - Increased HCL acid ulcer formation - Neurogenic bladder - Management - NG tube to decompress the stomach and prevent impinging on the diaphragm - Medications - Metoclopramide treatment for delayed gastric emptying - H2 receptor blockers (ranitidine, famotidine) prevent acid build up - Good bowel care vital to prevent constipation due to paralytic ileus **Integumentary system** - Skin breakdown, pressure injuries due to lack of feeling - Loss of temperature control - Management - Frequent turning - Frequent assessments of skin - Maintain appropriate environmental temperature Shock phase After a SCI, shock will set in: - Spinal shock - Occurs after injury to any part of the spinal cord - A neurological problem that causes loss to spinal cord reflexes, sensation, and motor responses (paralysis) below the level of the injury - **Symptoms**: - Hypotension due to loss of vascular tone - Bradycardia if the injury affects the upper spine - Urinary retention and bowel dysfunction - Flaccid paralysis loss of voluntary movement and reflexes - Lack of sweating (anhidrosis) below level of injury - Hyperreflexia reflexes may gradually return later and become hyperactive. - **Treatment** - ABCs mechanical ventilation if needed - Establish 2 large bore IVs fluid resuscitation to treat hypotension - Atropine for significant bradycardia increases HR - Monitor temperature + vitals - Hyper-oxygenate before suctioning or other procedures that stimulate the vagus nerve - Catheter insertion - Bowel protocol - Continuous turning to prevent bed sores - - - Neurogenic shock - Occurs with SCIs above T6 - The loss of sympathetic nervous system tone following a SCI above the level of T6 that occurs below the level of the injury - **Symptoms** - Hypotension due to loss of sympathetic tone = causes vasodilation - Bradycardia loss of sympathetic stimulation - Warm dry skin from vasodilation - Hypothermia loss of temperature regulation with vasoconstriction/dilation. Patient may feel warm but cannot control temperature within body - Reduced urine output hypoperfusion to kidneys from decreased cardiac output - Shut down of organs from reduced blood perfusion - Treatment - ABCs assess airways and ensure adequate ventilation - IV access for 2 large bore IVs administer fluids to prevent hypotension - Vasopressin constrict vasodilated vessels - Temperature regulation monitor temp, give blankets - Catheter insertion - Continuous monitoring of O2 sats to determine organ perfusion -  - Autonomic dysreflexia - Occurs in those with SCI above the T6 level, but can also occur in people without SCI. - Caused by intense vasoconstriction of the blood vessels in the area supplied by nerves from part of the spinal cord, in other words, an exaggerated autonomic response to a painful stimulus below the level of the SCI. - Common causes include: distended bladder, distended bowel, ingrown toenail, pressure sore, UTI, renal calculi, visceral pain, pregnancy, DVT, severe anxiety - Occurs because a stimulus sends a signal up the spinal cord, which are unable to ascend past the SCI which results in a massive sympathetic reflex - **Symptoms** - Widespread vasoconstriction below the level of the SCI - Hypertension resulting from vasoconstriction. If not resolved leads to cerebral hemorrhage - Bradycardia compensatory response from hypertension - Severe diaphoresis ABOVE the level of the SCI compensatory response from hypertension - Pale and cool skin BELOW the level of the SCI - The body is unable to restore autonomic equilibrium when presented with painful stimuli below the level of the injury, so BP will keep rising until the stimulus is removed - **Treatment** - Sit patient upright helps lower blood pressure - Loosen tight clothing or devices - Check and relieve bladder distension/bowel impaction a common trigger for AD - Administer antihypertensives + monitor BP - Look for additional triggers that may cause AD Immobilization of patients with SCI - **Cervical collar** - Cervical collars are applied right away in the suspect of a SCI or C spine injury. They are for temporary immobilization and stabilization. There are 2 kinds - **C spine collar** - Soft collar for limited support and stabilization - **Hard collar** - Rigid harder collar for greater immobilization - **Aspen collar** - A type of hard collar that is adjustable to the patients neck. - Used for a confirmed C spine injury that needs stabilization of the neck. Aspen collars will replace cervical collars - **Halo device** - A surgically implanted collar fixed to the skull that provides full immobilization of the C spine - Used when a high degree of stabilization of the spine is needed for severe SCI Log rolling - Used to prevent further SCI or ascension of the injury - Needs 3-5 people. One staff member must be designated as the lead and will facilitate the movement of the patient - Log Roll Technique: What It Is, Uses, and More \| Osmosis Week 6: Strokes and seizures ============================ Strokes - **Hemorrhagic stroke** - Caused by bleeding in the brain from a ruptured vessel - **Ischemic stroke** - Caused by a blockage in the brain that stops blood flow from a clot - Caused by a thrombus or embolus - **Transient ischemic attack:** small clot that briefly blocks the artery, with short lived symptoms. Is a warning sign for potential future strokes **Stroke assessment** - FASTVAN - Face - drooping - Arms -- one drooping when raised - Speech -- slurred - Time -- if above present, call 911 - Vision -- sudden loss - Aphasia -- difficulty speaking or understanding - Neglect -- person is ignoring one side of their body - NIHSS -- national institute of health stroke scale - To evaluate the severity of stroke and the impact on neurological function - Brain angiogram - To visualize blood vessels in the brain - Uses a 20G large bore IV in the Rt ACF **Stroke therapies** - Thrombolytics - Endovascular thrombectomy removal of a blot clot from a vessel through a minimally invasive technique - Carotid endarterectomy removal of plaque build-up from the carotid arteries in the neck through open surgery **Nursing care after a stroke** - BP management - Hemorrhagic systolic between 100-140 - Ischemic systolic between 110-180 - Glucose management - Many people experience elevated BGMs after a stroke, which lead to poorer outcomes. Important to monitor - Important to give glucose as it is a primary energy substrate for brain cells, adequate amounts must be given to sustain brain function - Normal saline - For fluid loss from a hemorrhagic stroke - To prevent dehydration - Post void residual - To determine if there is retention of fluids due to affected bladder - Use in and out - Swallow assessment Seizures - A burst of uncontrollable electrical activity between the brain cells that causes temporary abnormalities in muscle tone, movements, behaviours, sensations, or level of consciousness **Causes of seizures** - Medical conditions - Epilepsy - Stroke - Brain tumors - Infections - External triggers - Stress - Sleep deprivation - Substance abuse - Flashing lights **Nursing care for a seizure** - Protect head and airway - monitor vital signs - Turn patient on side to prevent aspiration - Ensure safety equipment is ready - Medication management - Benzodiazepines, barbiturates, phenytoin, propofol Week 7+8: Cardiac + ECG ======================= **Cardiac anatomy**  **Diastole** - Ventricular filling - Begins with closing of the aortic and pulmonary valves, ends with closing of the mitral and tricuspid valves - Ventricles fill with blood as blood returns to the heart **Systole** - Ventricular contraction - Begins with closing of the mitral and tricuspid valves, ends with closing of the aortic and pulmonary valves **Cardiac output = stroke volume x heart rate** - Cardiac output amount of blood pumped by the left ventricle in one minute - Stroke volume amount of blood pumped by the ventricle in one stroke - Preload + afterload + contractility - Heart rate number of beats by the heart in 1 minute - Positive + negative inotropes - Preload the stretching of the ventricles prior to contraction. The end diastolic volume - Blood volume - End systolic volume - Venous return - Atrial kick/contraction - Afterload the force that the ventricles must overcome in order to eject blood out of the heart - Hypertension - Atherosclerosis - Vasoconstriction - Contractility the strength of contraction of the heart - Positive inotropes - Calcium - Cardiac health **Properties of cardiac cells** Automaticity -- able to initiate an impulse spontaneously and continuously Contractility -- able to response mechanically to an impulse Conductivity -- able to transmit an impulse along a membrane Excitability -- able to be electrically stimulated Electrocardiographic monitoring - Measurement of electrical impulses produced in the heart by monitoring the movement of charged ions across the membranes - Lead placement looks at the heart at specific angles **12 lead ECG** - Views the surface of the ventricle from 12 different ankles - Leads I, II, III, aVR, aVL, aVF measure electrical forces in the frontal plane - Leads V1, V2, V3, V4, V5, V6 measure electrical forces in the horizontal plane - Shows changes indicative of structural changes, electrolyte imbalances, drug toxicity, or damage, such as ischemia, infarction, enlarged cardiac chambers - Lateral leads = I, aVL, V5, V6 - Anterior leads = V3, V4 - Inferior leads = II, III, aVF - Septal leads = V1, V2 - 22 **Telemetry monitoring** - Observation of the patients HR and rhythm to rapidly diagnose dysrhythmias, ischemia, or infarction **Holter monitor** - Records ECG while patient is ambulatory and performing daily activities **4 limb leads provides a vertical view of the heart.** - 4 electrodes that are placed on the limbs. Are white, green, black, and red - To remember: white on the right, clouds above grass, smoke over fire. -  **6 precordial leads measures horizontal plane** - 6 electrodes that are placed on the chest. Range from V1-V6 - V1 4^th^ ICS, right to sternum - V2 4^th^ ICS, left to sternum - V3 between V2 and V4 - V4 5^th^ ICS, midclavicular - V5 5^th^ ICS, anterior axillary - V6 5^th^ ICS, mid axillary line - A person with different colored circles on his chest Description automatically generated +-----------------+-----------------+-----------------+-----------------+ | Wave type | Normal duration | Normal | Causes of | | | | | possible | | | | | variation | +=================+=================+=================+=================+ | P wave | 0.06-0.12 | Positive in | | | | | leads I, II, | | | - Atrial | 1.5-3 boxes | aVF, and V2-6 | | | depolarizat | | | | | ion | | | | | and the | | | | | time it | | | | | takes to | | | | | pass | | | | | through the | | | | | entire | | | | | atrium | | | | +-----------------+-----------------+-----------------+-----------------+ | PR interval | 0.12-0.20 | Shorter in | | | | | children | | | - From | 3-5 boxes | | | | beginning | | Longer in | | | of P wave | | adults | | | to | | | | | beginning | | May shorten as | | | of QRS | | HR increases | | | | | | | | - The time it | | | | | takes for | | | | | an | | | | | electrical | | | | | signal to | | | | | spread | | | | | through the | | | | | atria, AV | | | | | nodes, | | | | | bundle of | | | | | his, and | | | | | purkinje | | | | | fibers | | | | | before | | | | | ventricular | | | | | depolarizat | | | | | ion. | | | | +-----------------+-----------------+-----------------+-----------------+ | QRS interval | 0.6-0.10 | | | | | | | | | - Measured | 1.5-2.5 boxes | | | | from | | | | | beginning | | | | | to end of | | | | | QRS | | | | | | | | | | - Time it | | | | | takes for | | | | | both | | | | | ventricles | | | | | to | | | | | depolarize | | | | +-----------------+-----------------+-----------------+-----------------+ | T wave | N/A | Upright in | | | | | leads I, II, | | | - Time it | | V3-6 | | | takes for | | | | | ventricular | | Negative in | | | repolarizat | | leads aVR | | | ion | | | | +-----------------+-----------------+-----------------+-----------------+ | QT interval | 0.34-0.44 | Length can | | | | | vary. | | | - Measured | 8.5-11 boxes | | | | from | | Men usually | | | beginning | | shorter | | | of QRS to | | | | | end of T | | Woman usually | | | wave | | longer | | | | | | | | - Time it | | | | | takes for | | | | | entire | | | | | ventricular | | | | | depolarizat | | | | | ion | | | | | and | | | | | repolarizat | | | | | ion | | | | +-----------------+-----------------+-----------------+-----------------+ | ST interval | Should be | | | | | isoelectric | | | | - Represents | | | | | time | | | | | between | | | | | depolarizat | | | | | ion | | | | | and start | | | | | of | | | | | repolarizat | | | | | ion | | | | +-----------------+-----------------+-----------------+-----------------+ ECG boxes - Small box = 0.04 seconds - Large box = 0.2 seconds **Step 1. Calculate the ventricular and atrial rates** - Calculating the ventricular rate = count each R in a QRS - Calculating the atrial rate = count each P in a QRS - **Method 1**(best for irregular waves): count the number of P/R waves in a 6 second ECG strip (30 boxes) and multiply by 10 - **Method 2** (most accurate): count the number of small boxes between two P/R waves, divide by 1500 to give you the beats **Step 2. Determine the regularity of the rhythm** - Measure the rhythm by determining if there is equal length between each R wave - **Regular rhythm:** R to R is always equal distance - **Irregular rhythm:** the R to R distances are never equal - **Regularly irregular**: the R to R distances are unequal, but there is a repetitive pattern to the unequal distances - **Occasionally irregular:** the R to R distances are equal except for an occasional out of place R, usually seen in premature contractions. **Step 3. Assess P waves** - P waves are the origin of a heartbeat that begins from the SA node. - Can be measured on leads I, II, aVF, and V2-6 - Are the P waves present. If not, the heartbeat is not from the SA node - Do all P waves begin the same. If not, the heartbeat originates somewhere other than the SA node - Do the P waves occur at regular rates - Is there one P wave with every QRS complex. If not, there is a heart block and the signal is not reaching the ventricles **Step 4. Assess the PR interval** - Measure the distance from the beginning of the P wave to the beginning of the QRS complex - Normal = 0.12-0.20 seconds (3-5 small boxes) - Represents = beginning of atrial depolarization to the start of ventricular depolarization. Includes delay at the AV node - Too long delay in an SA to AV node conduction - Too short accelerated AV conduction **Step 5. Assess the QRS duration** - Measure the distance from the beginning to the end of the QRS complex - Normal = 0.04-0.12 seconds (1-3 boxes) - Represents = ventricular depolarization - Too wide heartbeat did not originate in the atria, hyperkalemia, or bundle branch block Step 6. Assess the QT interval - Measures from the Q wave to the end of the T wave - Normal = less than 0.4-0.46 seconds (10-11.5 boxes) - Represents = the start of depolarization to the end of repolarization of the ventricles - Less than 0.36 seconds hypercalcemia, acidosis, hyperkalemia, hyperthermia, arrythmias - QT prolongation side effect of medications, hypocalcaemia, hypomagnesemia **Step 7. Assess the T waves** - T waves show ventricular repolarization - Assess if the T waves are present and the same size. **Step 8. Assess the ST segment** - ST segment represents the end of ventricular depolarization and the beginning of ventricular repolarization - A normal ST segment falls along the isoelectric line and lies at the same level as the PR interval - ST elevation = MI, complete blockage of a coronary artery - ST depression = myocardial ischemia, angina, digoxin toxicity **CODE BLUE** If a patient is unresponsive, pulseless: - Call the code yell for help, push code blue button, pull out cord - ABCs assessment - Start CPR - Switch out with next provider to provide story **Code blue roles:** Resuscitation triangle. compressor, defibrillator, airway control Leadership roles team leader, medication manager, time recorder - Compressor - Gives CPR, switches out every 2 minutes - Airway manager - Places patient in proper position, initiates tight seal, and ventilates 30:2 - Defibrillator - Gets the AED out and places pads, manages shocks - Team leader - Coordinates with all members, conducts what to do next, calls out what medications are needed - Medication manager - Prepares and gives medication - Code blue medications include: - Epinephrine vasopressor + positive inotrope. Increase blood flow to vital organs and improves chance of ROSC (return of spontaneous circulation) - Amiodarone antiarrhythmics. Stabilize heart rhythm - Lidocaine antiarrhythmics. Stabilize heart rhythm - Bicarbonate alkalinizing agent. Corrects metabolic acidosis that can occur from prolonged cardiac arrest - Electrolytes corrects life threatening electrolyte imbalances. - Time recorder - Documents when things occur, what has been given, what is currently happening, tells when CPR has to switch out, announces time of death Unit 7+8: ECG and Rhythm Interpretation ======================================= **Sinus rhythms** - Normal sinus rhythm - Sinus tachycardia - Sinus bradycardia - Sinus arrythmia - Sinus pause/arrest **Atrial rhythms** - Premature atrial contraction (PAC) - Atrial flutter - Atrial fibrillation **Atrioventricular blocks** - First degree AV block - Second degree AV block type 1 (Mobitz 1/ Wenckebach) - Second degree AV block type 2 Mobitz 2) - Third degree AV block **Ventricular rhythms** - Premature ventricular contractions - Ventricular tachycardia - Ventricular fibrillation - Polymorphic ventricular tachycardia - Asystole - Pulseless electrical activity Sinus tachycardia - HR above 100bpm - Originates in the SA node - Regular rhythm - P wave normal, sometimes partially hidden - PR normal - QRS normal - Cause: fever, stress, exercise - Symptoms: dizziness, dyspnea, hypotension - Treatment: underlying cause, this HR cannot be sustained for long, especially in older folks -  Sinus bradycardia - HR below 60bpm - Originates in the SA node - Regular rhythm - P wave normal - PR normal - QRS normal - Cause: athletic, hypothyroidism, drugs - Symptoms: hypotension, weakness, angina, dizziness - Treatment: not usually treated unless symptomatic. Atropine (increase HR), pacemaker - A graph with a red line Description automatically generated Premature atrial contraction - HR may vary - Electrical signal coming from somewhere within the atria, along with a normal rhythm from the SA node - P wave normal. In order to be called a PAC, P wave must be upright - PR wave normal - QRS normal, sometimes narrowed - Cause: stress, caffeine, hypokalemia (increase excitability) - Symptoms: often asymptomatic - Treatment: not significant in those with healthy hearts. Usually just reduce stimulant use -  Sinus arrythmia - The change in heart rate when you breath in and out. Heart rate changes depending on whether you're breathing in or out. HR increases when breathing in, HR decreases when breathing out. - HR 60-100 - Irregular rhythm - P wave normal - PR normal - QRS normal - Cause: respirations in pediatrics - Symptoms: usually none - Treatments: no treatment needed - ECG Educator Blog : Sinus Arrhythmia Sinus pause/arrest - Heart stops beating for 1-2 beats. - No signal coming from the SA node - Irregular rhythm - P wave normal, absent during arrest - PR normal, absent during arrest - QRS normal, absent during arrest - Cause: SA node dysfunction, MI, ischemia - Symptoms: fatigue, dizziness - Treatment: pacemaker -  Atrial flutter - Rapid Identical waves, sawtooth pattern - HR 250-350bpm - Regular rhythm - P wave none, has sawtooth shape - PR varied - QRS normal - Cause: associated with CAD, hypertension, embolus - Symptoms: palpitations, fatigue, low cardiac output, heart failure, thrombi formation - Treatment: anticoagulants (to prevent clot), cardioversion (to restore rhythm), beta blockers/CCB (to slow HR and control rate) - Atrial Flutter: An In-Depth Exploration of a Heart Rhythm Disorder Atrial fibrillation - Total disorganization of atrial electrical activity. Controlled Afib is HR under 100. Uncontrolled is HR above 100 - From multiple sources of electrical signals in the atria - HR 350-600bpm - Irregular rhythm - P wave chaotic fibrillation - PR not present - QRS normal - Cause: CAD, hypertension, heart failure - Symptoms: palpitations, fatigue, thrombi formation - Treatment: anticoagulants (to prevent clot), cardioversion (to restore rhythm), beta blockers/CCB (to slow HR and control rate) -  Junctional rhythms - Arrythmias that originate in the AV node. Can produce a backwards P wave due to moving up the heart, and then down the ventricles. - HR 40-140bpm - Regular - P waves inverted or hidden - PR variable - QRS normal - Cause: AV node dysfunction, digoxin toxicity - Symptoms: dizziness, hypotension, decreased cardiac output - Treatment: rate control, pacemaker, check digoxin toxicity - Clinical significance: AV node kicks in when the SA node cannot fire which must be investigated. Slow rates can cause cardiac output - Treatment: Beta blockers/CCB (rate control), check digoxin toxicity - A graph with a red line Description automatically generated First degree AV heart block - The duration of conduction represented by PR is prolonged by more than 0.2 seconds. - If R is far from P, then you have a first degree. - HR normal - Regular rhythm - P wave normal - PR must be greater than 0.2 seconds to be first degree. - QRS normal - Cause: MI, CAD, digoxin - Symptoms: often asymptomatic - Treatment: no treatment usually needed  Second degree AV heart block - Type 1 (Mobitz 1, Wenckebach) - Includes a gradual lengthening of the PR interval due to prolonged AV conduction until an atrial impulse is not conducted and a QRS complex is blocked - Longer, longer, longer, QRS dropped, then you have a Wenckebach - Atrial regular rhythm, ventricular irregular rhythm - P wave normal - PR long - QRS normal, until 1 is dropped and completely missed. - Cause: CAD, digoxin, ischemia, MI - Symptoms: fatigue, dizziness - Treatment: usually no treatment needed - A graph showing a heart beat Description automatically generated Second degree AV heart block - Type 2 (Mobitz 2) - Occurs when there are 2 or 3 P waves to a QRS in a consistent pattern with missing QRS. Occurs at a rate of 1:2 or 1:3. PR intervals DO NOT lengthen like type 1 - If some Rs don\'t go through, then you have a Mobitz 2 - Atrial rhythm regular, ventricle rhythm irregular - P wave more than QRS - PR normal - QRS widened, some missed in a pattern - Cause: MI, CAD - Symptoms: fatigue, hypotension, decreased cardiac output - Treatment: permanent pacemaker -  Third degree AV heart block - Occurs when no conduction of the atria make it to the ventricles, the atria beat with the SA node and the ventricles beat with the AV node. - If P and QRS don\'t agree, then you have a third degree. - Ventricular rate 20-40, atrial rate 60-100 - Regular rhythm, but out of sync - P wave normal but not connected to QRS - PR absent - QRS normal but not connected to P waves - Cause: severe heart disease, MI, infarction - Symptoms: syncope, shock, heart failure, decreased cardiac output - Treatment: permanent pacemaker - A graph with a line on it Description automatically generated Premature ventricular contraction - Contraction occurring from the ventricles. One PVC is a PVC. If every second beat is a PVC then it is bigeminy. If every third beat is a PVC it is trigeminy. If there are 3 PVCs consecutively in a row, it is ventricular tachycardia. - Electrical signal comes from the ventricle - Irregular rhythm - P wave sometimes not present - PR wave sometimes not present - QRS normal, wide and distorted when PVC occurs - Cause: stress, caffeine, hypokalemia (increased excitability), hyperkalemia (abnormal conduction), hypomagnesemia (abnormal ventricular depolarization). - Symptoms: palpitations - Treatment: usually no treatment needed -  Ventricular tachycardia - When a run of 3 or more PVCs occurs, from multiple electrical stimuluses in the ventricles - LETHAL RHYTHM - HR greater than 100 - Regular or irregular rhythm - P wave not present - PR not present - QRS wide, distorted, and bizarre - Cause: MI, CAD, digoxin toxicity, hypokalemia (increased excitability), hyperkalemia (impaired conduction), hypomagnesemia (abnormal ventricular depolarization). - Symptoms: syncope, hypotension, decreased cardiac output - Treatment: cardioversion if with pulse, defibrillation if pulseless. Ablation used after to correct - A graph with a red line Description automatically generated Ventricular fibrillation - Severe derangement of the heart rhythm from multiple firing of ventricular signals at the same time. - LETHAL RHYTHM - Irregular rhythm - P waves not present - PR not present - QRS not measurable - Cause: MI, CAD, cardiac catheterization, hypokalemia (increased excitability), hyperkalemia (impaired conduction), hypomagnesemia (abnormal ventricular depolarization). - Symptoms: pulseless, unresponsive - Treatment: CPR, defibrillation -  Polymorphic ventricular tachycardia -- torsade's des points - Multiple different electrical signals coming from multiple spots in the ventricles - LETHAL RHYTHM - Irregular rhythm - Unable to measure - Cause: prolonged QT interval, hypomagnesemia (causes prolonged QT) - Symptoms: decreased cardiac output, seizure, aspiration, syncope, code - Treatment: magnesium sulfate, cardioversion, defibrillation - ECG strip Torsades de pointes TDP -  Asystole - No rhythm, no pulse, no electrical activity - LETHAL RHYTHM - Cause: cardiac arrest - Symptoms: no pulse, no rhythm - Treatment: CPR, epinephrine. No electrical activity and cannot be shocked - Figure, Asystole on Electrocardiography. This rhythm\...\] - StatPearls - NCBI Bookshelf Pulseless electrical activity (PEA) - Heart is pumping, there is electrical activity, but blood is not moving and there is no pulse. - LETHAL RHYTHM - Cause: hypoxia, hypovolemia, acidosis, hyperkalemia (disrupts normal electrical activity), hypokalemia (impairs muscle contractions) - Symptoms: no pulse, electrical activity is present, no cardiac output - Treatment: PEA = push epinephrine always. CPR. Continue until a pulse is back -  **Defibrillation** - Amount used to deliver a shock is very high = 360 joules - Asynchronous delivery, not coordinated with the ECG - Treatment for ventricular rhythms: - Ventricular fibrillation - Pulseless ventricular tachycardia **Synchronized cardioversion** - Amount used to deliver an electrical shock is very low = 50-100 joules - Synched delivery with the ECG to deliver electricity during a sensitive phase of electrical excitation of the main chamber - Treatment for atrial rhythms: - Atrial fibrillation - Atrial flutter **Treatment for ventricular rhythms** - Defibrillation (electricity) delivers an electrical shock to the heart to restore normal rhythm - CPR manually maintain circulation and oxygen during cardiac arrest - Medications - Epinephrine vasopressor that increases blood pressure and coronary perfusion by constricting blood vessels. Increases HR - Amiodarone antiarrhythmic that helps to stabilize the hearts electrical activity, used in V tach or V fib to help with arrythmias and restore a normal rhythm - IV beta blockers reduce HR, decrease myocardial oxygen demand, and stabilize abnormal rhythms - Ablation use of heat to destroy abnormal heart tissue in the heart causing arrythmias - Implantable cardioverter defibrillator (ICD) small device implanted under the skin that monitors heart rhythms and delivers shocks when detected - Correct H's and T's identifying and treating reversible causes of cardiac arrest **H's + T's, causes of cardiac arrest. These are reversible causes** - Hypovolemia give IV fluids - Hypoglycemia glucose administration - Hypothermia rewarm patient - Hypoxia oxygenation - Hydrogen ion excess (acidosis) ventilation and sodium bicarbonate - Hypo + hyperkalemia potassium or insulin + glucose - Toxins antidotes - Tension pneumothorax needle decompression - Tamponade pericardiocentesis - Thrombosis (pulmonary or myocardial) thrombolytics, PCIs Alterations in heart rhythms causes: - Stress - Sinus tachycardia - Premature atrial contraction - Premature ventricular contraction - Hypothyroidism - Sinus bradycardia - Hypokalemia (increases excitability) - Premature atrial contraction - Ventricular tachycardia - Ventricular fibrillation - Asystole - Hyperkalemia (abnormal conduction) - Premature ventricular contraction - Ventricular tachycardia - Ventricular fibrillation - Asystole - Hypomagnesemia (abnormal ventricular depolarization) - Premature ventricular contraction - Ventricular tachycardia - Ventricular fibrillation - Polymorphic ventricular tachycardia - MI - Sinus pause/arrest - First degree AV heart block - Second degree type 1 AV heart block - Second degree type 2 AV heart block - Third degree AV heart block - Ventricular tachycardia - Ventricular fibrillation - CAD - Atrial flutter - Atrial fibrillation - First degree AV heart block - Second degree type 1 AV heart block - Second degree type 2 AV heart block - Ventricular tachycardia - Ventricular fibrillation - Ischemia - Sinus pause/arrest - Second degree type 1 AV heart block - Third degree AV heart block - - Hypertension - Atrial flutter - Atrial fibrillation - Heart failure/disease - Atrial fibrillation - Third degree AV heart block - Digoxin - Junctional rhythm - First degree AV heart block - Ventricular tachycardia Week 9: Care of deteriorating patient + shock ============================================= Learning objectives: - Review the causes of deterioration and arrest - Describe the other causes of cardiac arrest and identify prevention strategies for each - Define the different types of shock and identify their etiologies - Understand the common physiological signs for detecting deterioration - Interpret vital signs and other abnormal physiological parameters **Deteriorating patient** - The earlier we can detect changes in the status of the patient, the better the outcome - There are almost always changes that the patient shows before they go downhill - We may miss these signs because of: - Head to toe assessment is not being completed properly - Poor communication over report - Not prioritizing patients appropriately with a large assignment - Time constraints - Afraid to ask for help - Unsure what to do with new information - Not knowing what the patients normal is - Things that will cause patient deterioration - Failure to assess data was not collected - Failure to recognize data was found but don\'t know what it means - Failure to act knew what was going on, but didn't do anything - Failure to communicate found the data, knows what it means, but didn't share it with anyone - Failure to escalate found the data, knew what it means, shared it with someone, but they didn't do anything about it and you didn't escalate it further **Concerning assessment findings that must be investigated further** - Neurological - Change in LOC, GCS - GSC less than 10 - Stroke symptoms (FAST VAN) - Pupils different sizes - Strength has changed - Change in behaviour - Tired, flat affect - Anxious, unsettled - Caregiver expressing patient not acting like self - Respiratory - Increased WOB, SOB, RR - SPO2 less than 90% with supplemental O2 - Accessory muscle usage (normal in babies using their stomach to breath) - Cardiac - Change in capillary refill - Change in colour, pallor - Unrelenting chest pain - Tachycardic or bradycardic. Greater than 120 or less than 50 - MAP below 60 - SBP less than 90, or a decrease of 30 - GI/GU - New onset nausea, vomiting, diarrhea - Abdominal tenderness/distension - Decreased bowel sounds - Decreased or no output. - Lab results - Electrolyte imbalances - Shock (types) - Cardiogenic - Hypovolemic - Absolute hypovolemia - Relative hypovolemia - Distributive - Neurogenic - Septic - Anaphylactic - Obstructive **Modified early warning score** - Used to determine the severity of sick individuals - A score of 5 or higher represents a potentially or definitely critically sick individual - A yellow and green table with numbers and a black text Description automatically generated **Sepsis** - Life threatening reaction to an infection. The infection is transferrable, but sepsis is not. If a sick patient shared a room with another, they may get the infection, but they won't get sepsis. - If left untreated, sepsis can evolve into septic shock - Common infections that lead to sepsis - Bacterial infection of the lungs \#1 - UTI - GI infection - Skin infection - Signs and symptoms of SEPSIS: - Shivering - Elevated heart rate - Pain - Sleepy - "I feel worse than ever" - Short of breath - Medications + treatments - PO/IV fluids - Antibacterials for the infection - Antipyretics for fever - Analgesia for pain - Antinausea for nausea **Stages of sepsis** - SIRS -- criteria - Temperature is greater than 38 or less than 36 - HR greater than 90 - RR greater than 20 - PaCO2 less than 4.3 - WBC elevated - Sepsis - 2 pieces of SIRS criteria + a confirmed/suspected infection - Severe sepsis - Confirmed sepsis + signs of end organ dysfunction - Septic shock - Severe sepsis + persistent end organ dysfunction despite fluid administration **Shock** - A huge critical condition that results in a disturbance in the imbalance between the supply and demand for oxygen and nutrients, leading to hypoperfusion - Shock is characterized by poor tissue perfusion and impaired cellular metabolism. - Types of shock: - Cardiogenic broken pump - Hypovolemic empty tank - Absolute hypovolemia - Relative hypovolemia - Distributive shock leaky pipes - Neurogenic shock - Anaphylactic shock - Septic shock - Obstructive shock blocked pipes **Cardiogenic shock** - The heart is failing to perform, a pump problem - Causes - Severe MI - Diastolic dysfunction (cardiac tamponade, cardiomyopathy) - Systolic dysfunctions (blunt cardiac injury, systemic or pulmonary hypertension - Dysrhythmias - CHF - Drug toxicity - What is happening - Blood is not getting to vital organs - Primary cardiac dysfunction decreases cardiac output decreased organ perfusion ischemia and inflammation in the heart + decreased blood pressure multiorgan dysfunction - Signs and symptoms - SOB - Tachycardia - Weak pulse - Hypotension - Decreased urinary output - Cool extremities - Diagnostic/treatments - ECG - Labs - Medications - IV fluids - PRN oxygen - Vasopressors **Hypovolemic shock** - There is inadequate fluid volume to support perfusion, empty tank - Types: - Absolute hypovolemia loss of fluids that cannot be retuned back to the body, loss through hemorrhage, GI losses, vomiting - Relative hypovolemia loss of fluids within the body, through edema and third spacing from burns, CHF - What happens - Hypovolemia decreased venous return decrease preload decreased CO hypotension perfusion failure and tissue hypoxia organ dysfunction - Causes - Burns - Hemorrhage - Vomiting and diarrhea - Excessive diuresis - Diabetes insipidus - Signs and symptoms - Hypotension - Edema - Decreased cardiac output - Tachycardia - Little to no urinary output - Decreased LOC\ cold extremities - Pale - Diagnostics/treatments - Labs - ECG - Echo - IV fluids - Vasopressors - Warming patient - NPO **Distributive shock** - Systemic vasodilation that results in poor tissue perfusion to vital organs, even with normal blood volume, leaky pipes - Types - Neurogenic shock spinal cord injury above T6 disruption of sympathetic tone vasodilation decrease HR, preload, and stroke volume decrease CO hypotension - Anaphylactic shock exposure to allergen production of IgE activation of mast cell and release of mediators immediate hypersensitivity reaction vasodilation - Septic shock invading microorganisms release of inflammatory cytokines increase capillary permeability and peripheral vasodilation + selective vasoconstriction maldistribution of circulating blood volume decrease in circulating blood volume decrease in cellular oxygen supply decreased tissue perfusion and impaired cellular metabolism - Causes - Allergies - Illness and infection - Spinal cord injury above T6 - Vaccinations - Signs and symptoms - Neurogenic shock - Anaphylactic shock itchy skin, rash, swollen lips, swollen neck - Septic shock chills OR fever, confusion, delirium, mottled skin - Diagnostic treatment - Neurogenic shock labs, ECG, MRI/XRAY for SCI - Anaphylactic shock epinephrine (do not give one from the crash cart, that is 10mls of epinephrine. You only need around 1ml) - Septic shock blood cultures, labs **Obstructive shock** - A blockage that is obstructing blood flow, blockage in the pipes - What happens - Structural compression decrease venous return decrease stroke volume decrease CO decrease cellular oxygen supply decrease tissue perfusion impaired cellular metabolism - Causes - Cardiac tamponade - Tenson pneumothorax - Restrictive cardiomyopathy - Aortic dissection - Signs and symptoms - Respiratory distress - Chest pain - Hypotension - Tachycardia - Altered LOC - Decreased urinary output - Cool and clammy skin - Distended neck veins - Diagnostics and treatment - CT scan - ECHO - ECG - Labs - CPR - Oxygen **The stages of shock** 1. **Initial stage** - Metabolism changes at the cellular level - From aerobic to anerobic, causing lactic acid build up - Early signs = low blood pressure compensated by increased HR 2. **Compensatory stage** - Body activates neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis - Compensatory signs include increased ADH, vasoconstriction, increased HR 3. **Progressive stage** - Begins as compensatory mechanisms fail - Altered capillary permeability due to decreased cellular perfusion, which causes fluid and protein leak out of the vascular space into interstitial space. - Causes changes to mental status, interstitial edema, bronchoconstriction, decrease in functional residual capacity, impaired gas exchange, tachypnea, crackles in lungs, increased WOB. CO begins to fall, hypotension, dysrhythmias, myocardial ischemia, MI - Prolonged hypoperfusion to the kidneys results in tubular ischemia and AKI. Decreased urine output, increased BUN - Loss of functional ability of the liver, failing to metabolize medications and waste products. Jaundice 4. **Refractory stage** - Decreased perfusion and decreased cardiac output exacerbate anaerobic metabolism. Increase in lactic acid leads to increased capillary permeability, which allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in capillaries. Loss of intravenous volume. Leas to worsening myocardial depression and further decline in CO. cerebral blood flow cannot be maintained. - Refractory signs include multi organ failure, low pH, death - Recovery is unlikely at this stage  **MODS = multi organ dysfunction syndrome** - More than 2 organs failing from an infection or issue in the body - Medical emergency - Most common causes sepsis, trauma, and poisoning - Treatment - IV fluids, transfusions - PRN oxygen or ventilation - ECHO - Parenteral nutrition - Dialysis Week 10: Parenteral Nutrition ============================= Learning objectives: - Understand circumstances that lead to the use of parenteral nutrition - Be familiar with the composition of standard commercially prepared PN solutions - Identify steps of PN administration - Know potential metabolic complications associated with PN use and refeeding syndrome **What is parenteral nutrition** - Nutritional support delivered intravenously - Includes proteins, carbohydrates, fats, vitamins, and minerals - Can be for short term and long term nutritional therapy - Can be given at the hospital or at home - Can be given through PVAD or CVAD. CVAD must be used if the solution has greater than 10% dextrose **What is parenteral nutrition for** - Prevent and restore nutritional deficits - Bowel rest - Supplying adequate caloric intake and essential nutrients - Removing antigenic mucosal stimuli **Candidates for PN** - Paralyzed or non-functional GI tract: paralytic ileus, obstruction, trauma, fistula - Bowel rest for pancreatitis or IBD - NPO for 7 days or longer - Critically ill patients - Babies with an immature GI tract or congenital malformations - Chronic or extreme malnutrition - Chronic diarrhea or vomiting needing surgery or chemotherapy - Hyperbolic states: burns, sepsis, trauma **Components of a PN** Depends on metabolic needs, clinical history, and blood work - Amio acids + dextrose solution - Lipid emulsion solution (provides supplemental kilocalories) - Medications - Heparin - Insulin **Formulas** - 1 system (SmofKabiven bag) - - 1 bag with amino acids, electrolytes, lipids, and dextrose in the same bag, but separated - Given peripherally - Contraindicated for patients with soy, egg, peanut, olive, or fish allergies - Use non DEHP filter with 1.2 micron in line filer - 2 + 1 system -  - One bag contains dextrose and amino acids. The other bag contains lipids - 2:1 needs 0.22 micron filter for AA and dextrose. Has DEHP - Fat emulsion bag has a 1.2 filter = fat gets flat filter (its blue and flat)). Has no ports, has no DEHP - Connect the fat emulsion line to the lowest port to the patient - 3 in 1 system - Text, letter Description automatically generated - 1 bag with all units mixed together - 3:1 needs 1.2 micron filter **Peripheral + Central PN administration** - Can only give a peripheral PN if the solution has an osmolality less than 900 mOsm/L and/or is less than D10W in the bag (10% dextrose) - There is less risk of thrombophlebitis and vessel damage if admitted in central IV line - PN is not compatible with any other solutions or medications - Filter tubing: - 2:1 needs 0.22 micron filter (AA + dextrose) - 3:1 needs 1.2 micron filter (fat emulsion, SmofKabiven bag) - Amino acid tubing changed every 24 hours - Lipid solution tubing changed every 8-12 hours - Patients must be on a total fluid intake while on PN to prevent fluid overload - Use NON-DEHP administration sets as DEHP is a toxin that can leak out of tubing's when exposed to highly lipophilic solutions. **Specific to peripheral PN** - Short term only, 5-7 days - Has no additives or multivitamins, do not need to protect it from light - Once activated, is stable for 36 hours at room temperature, and 24 hours once spiked **Plan of care for a PN** **Assessment** **Additional info** ------------------------------- ------------------------------------------------------------------------------------------------------------------------------------ **IV line** Remain patent, free of infection **Daily/biweekly weights** Monitor for evidence of edema or fluid overload. Measurements will reflect weight loss/gain from caloric intake or fluid retention **BGMs** QID to monitor glycemic control **Monitor intake and output** Q8H to watch for S/S of fluid overload by completing a cardiovascular and resp assessment **Daily/weekly blood woek** Review all lab word to detect values out of range **Mouth care** Most patients will be NPO. Proper oral care is required **Vital signs** Monitor vitals more frequently in those with PNs **Lab work** - Pre PN and weekly: - CBC, INR, PTT, electrolytes. Magnesium, calcium, phosphorus, urea, creatinine, GFR, triglycerides, pre albumin, albumin, glucose, ALT, AST, alkaline phosphatase, GGT, bilirubin panel - Day 1, 2, and 3 of starting PN - Glucose, electrolytes, magnesium, phosphorus, urea, creatinine, GFR **Client precautions** - Continuous monitoring: - done when a pt is started on a PN. Frequent monitoring and assessments. PN is usually running 24 h/day - cyclic monitoring - periodic assessments that line up with PN regimen, where PN Is given for a set number of hours per day, not 24h/day. For more stable patients. - Abrupt interruption - If there is an interruption in PN administration, or the solution runs out, it could cause the patient to go into a hypoglycemic state. Run D5W at the same rate of infusion while waiting for the new PN bag - Blood sampling - Do not draw blood on the same line that PN is running - Medication administration - Do not administer meds in the same IV tubing as PN is not compatible with many of them - Increase/decrease rate slowly - Prevent hypoglycemia, as well as refeeding syndrome **Complications of PN** +-----------------+-----------------+-----------------+-----------------+ | **complication* | **Why** | **Symptoms** | **Interventions | | * | | | ** | +=================+=================+=================+=================+ | **Sepsis/cathet | Due to high | Hypotension, | Aseptic | | er | dextrose | elevated/decrea | technique with | | related | concentration | sed | insertion, | | bloodstream | of PN | temp, | care, and | | infection** | | tachycardia, | maintenance | | | | increased RR, | | | | | decreased urine | Avoid | | | | output | hyperglycemia | | | | | | | | | | IV antibiotic | | | | | therapy | | | | | | | | | | 70% alcohol on | | | | | every port | +-----------------+-----------------+-----------------+-----------------+ | **Hyperglycemia | Sudden increase | Osmotic | Monitor BGMS | | ** | in glucose | diuresis, | frequently QID | | | after recent | dehydration, | | | | malnourished | metabolic | | | | state | acidosis, | | | | | ketoacidosis | | +-----------------+-----------------+-----------------+-----------------+ | **Refeeding | Rapid refeeding | Metabolic + | PN initiated | | syndrome** | after a period | hormonal | slowly in high | | | of | changes, | risk patients | | | malnutrition. | electrolyte | | | | Results in | shifts: | Close | | | potentially | hypophosphatemi | monitoring of | | | fatal shift in | a, | electrolytes | | | fluids and | hypomagnesemia, | | | | electrolytes. | hypokalemia, | | | | High risk for | hyperglycemia. | | | | those with | | | | | little intake | Leads to | | | | for more than | cellular | | | | 10 days or are | dysfunction | | | | chronically | | | | | undernourished | Occurs 24-48 | | | | | hours after | | | | | refeeding has | | | | | started | | +-----------------+-----------------+-----------------+-----------------+ **Other complications** - Decreased phagocytosis and glycosylation of immune globulins - Poor wound healing and altered collagen syntheses - Fluid and electrolyte abnormalities - Decreased lipoprotein lipase activity - Gastroparesis - PN induced hepatic changes - Irritation to peripheral veins, monitor peripheral site Q1h, and apply cool compress if complications are noted  See the source image  **Refeeding syndrome** - Starvation prior to feeding causes: - Intracellular electrolytes move to ECF - Decrease in glycogen stores - Decrease in insulin release - When we start to re-feed - Sudden increase in carbohydrates triggers insulin release - Shifts extracellular ions to the inside of the cell - Muscle weakness, resp failure, paralysis, coma, cranial nerve palsies, rebound hypoglycemia. **\ ** Week 11: care of ill child ========================== Learning objectives: - Understand differences of anatomical and physiological presentations of children and adults. - Define the components of a complete pediatric physical assessment, including pediatric assessment triangle - Identify the normal fluid requirements of pediatric patients - Identify normal and abnormal vital signs ranges in infants, children, and adolescents - Identify potential deterioration in a child, recognize risk mitigation strategies and identify care escalation strategies - Demonstrate use of PEWS system to recognize early deterioration risk and initiate early response **Pediatrics** Most common reason pediatrics come into emergency: - Fever - Respiratory issues - Gastrointestinal issues **Differences between pediatrics and adults** +-----------------------------------+-----------------------------------+ | **Difference** | **Consequences** | +===================================+===================================+ | Larger head and trunk compared to | More susceptible to heat and | | the rest of the body | fluid loss | +-----------------------------------+-----------------------------------+ | Small and narrow airways, larger | Increased risk of airway | | tongue, shorter trachea, more | obstruction | | elastic cartilage | | +-----------------------------------+-----------------------------------+ | Nose breathers for the first 2-4 | Ineffective oxygenation in th