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Study Notes: NURS 370 Student Preparation Health Literacy Impacts of Inadequate Health Literacy Increased healthcare costs Less knowledge of diseases and treatments Fewer self-management skills Poor compliance and more medical errors Limited ability to navigate the healthcare system Less access to...

Study Notes: NURS 370 Student Preparation Health Literacy Impacts of Inadequate Health Literacy Increased healthcare costs Less knowledge of diseases and treatments Fewer self-management skills Poor compliance and more medical errors Limited ability to navigate the healthcare system Less access to healthcare services Consequences Greater risk for hospitalization Higher utilization of expensive services (emergency care, in-patient admissions) Negative Effects on: Prevention and screening Health-promoting behaviors Proper history taking Explanation of diagnosis and treatment plans Strategies Implement health literacy as a social policy in school-aged kids Screening for health literacy in a clinical setting Personalized health decisions, well-being, motivation, critical/analytical skills Reduction in morbidity and mortality Mental Health Literacy Combatting mental health crises, addictions, and risky behaviors Definition Skills enabling access, understanding, and use of health information Competence Categories Autonomous Competence Personal empowerment Ability to judge and use information Interactive Competence Collaboration with others Self-management, problem-solving, and decision-making Cultural Competence Interpretation of social practices Recognition of social influences on health information Informational Competence Authority and currency of information Need, strategy, retrieval, analysis, understanding, and utilization Operational Competence Utilization of tools, procedures, and techniques Mastery of environment and understanding of personal context Contextual Competence Mastery of environment with an understanding of personal context Learning and interaction affected by the environment Acid-Base Imbalances and Pneumonia Respiratory Basics Respiratory rate: number of breaths Ventilation: gas exchange on a molecular level Perfusion: oxygenation of tissues Pneumonia Inflammatory process triggered by pathogens Alveoli fill with pus, reducing ventilation Types: Bacterial, Viral, Fungal Common pathogens: Streptococcus pneumoniae, COVID-19 Risk Factors Immunocompromised, elderly, post-op, children Unsanitary or crowded living conditions Pre-existing ventilation issues Exposure to smoke or pollution PNEUMONIA Acronym Productive cough Neuro changes Elevated WBC, Bands, CO2 retention Unusual breath sounds, fever, decreased O2 sat Nausea, vomiting, increased HR, RR, aching Assessment and Treatment Skin assessment: cyanosis, diaphoresis, temperature Respiratory assessment: muscles used, trach tug, posture, sound, SOB, tactile fremitus Education Prevention: vaccines, avoiding sick individuals, social distancing, handwashing, diet, and exercise ABGs – Arterial Blood Gases Regulators of Acid-Base Balance Respiratory system (O2/CO2), renal system (bicarbonate), chemical buffers Normal Ranges pH: 7.35-7.45 (Low = acidic) HCO3: 22-26 (Low = acidic) PaCO2: 35-45 (Low = basic) Acid-Base Balance Assessment Identify respiratory or metabolic problem Determine acidosis or alkalosis Evaluate compensation (partial, full, or uncompensated) ROME Acronym Respiratory acidosis: high CO2, low pH Respiratory alkalosis: low CO2, high pH Metabolic acidosis: low HCO3, low pH Metabolic alkalosis: high HCO3, high pH Example pH: 7.33, PaCO2: 52mmHg, HCO3: 26mEq/L Uncompensated Respiratory Acidosis with hypoxemia Chest Tubes – LAB Purpose Respiratory problems affecting the pleural space Components Suction set to 80mm on the wall Atrium controls suction Compartments A, B, C, D control drainage, water seal, and suction Tidaling indicates proper ventilation Assessment of fluid color and consistency Chest tube insertion site: 2nd intercostal space Respiratory Changes Pulmonary Embolism Definition Obstruction of a pulmonary artery branch 1/1000 affected in hospitals, 10-20% mortality within 48h Causes Trauma, surgery, pregnancy, HF, age over 50 Prolonged immobility, hypercoagulable states, smoking, obesity DVT, air bubbles, fat, tumor material Virchow Triad Blood stasis, endothelial injury, hypercoagulative state Signs/Symptoms Hemodynamic instability Anxiety, fear, diaphoresis, tachycardia, cough Diagnosis: Spiral CT, Chest X-ray, ECG, Pulmonary Angiogram, D-Dimer, VQ Scan Treatment Oxygen, hemodynamic support, inotropes Foley catheter for monitoring fluid output to watch for fluid retention Thrombolytic therapy, venous filter Pleural Effusion Definition Abnormal fluid collection in pleural space Disruption of hydrostatic/osmotic balance Diagnosis X-ray, CT scan Treatment Address underlying cause Oxygen, analgesics, antipyretics, antibiotics Thoracentesis for fluid removal (1-1.5L max) Hemothorax Definition Blood in pleural space, rapid accumulation Causes: trauma, clotting issues, infection, adhesions, TB Signs/Symptoms Dyspnea, chest pain, hypovolemic shock signs Dullness on percussion Treatment Larger chest tube, oxygen, PRBCs, thoracotomy, autotransfusion Pneumothorax Definition Air in pleural space Types: Open, Simple, Tension Symptoms Chest pain, dyspnea, tachypnea, anxiety Signs of tension pneumothorax: tracheal shift, hypoxia, shock Treatment High-flow oxygen, chest tube, needle decompression for tension pneumothorax Monitoring and imaging (Chest X-ray, Pleur-evac) Oxygen Therapy Acute Hypoxia Signs and Symptoms: Heated High Flow Nasal Cannula (new method) 21-100% concentration for rates up to 60L/min at 37 degrees, seen in ICU. Treatment for respiratory failure with hypoxemia and hypercapnia. Decreases need for intubation. Delivery Methods: Nasal Cannula – (1-6L/min @ 24-44%) Oxygen Conserving Cannula - (Home; 8L/min 30-60%) Simple Mask – (6-12L/min, 35-50%) Partial non-rebreather (10-15L/min, 60-90%) Venturi mask (Humidity added; low constant O2, 24-50%) High flow nasal cannula (Up to 60L/min, wide range of O2) Pediatric Respiratory Distress Anatomy Considerations: Small and shorter trachea. Breath through the nose primarily for the first 6 months. Larger tongue can obstruct airway. Ribs are soft, trauma to organs occurs more easily. Weakened immune systems. Common Acute Conditions: Foreign body aspiration. Croup: barking cough, swollen airway, partially obstructed airway. Viral and bacterial infections: RSV, pneumonia. Severity Levels: Mild: colds and flus. Acute: Bronchiolitis (RSV). Chronic: Asthma, cystic fibrosis. Life-threatening: epiglottitis, obstruction. Pediatric Assessment Triangle: Appearance: Abnormal tone, interaction, consolability, look/gaze, speech/cry. Work of Breathing: Abnormal sound, position, retractions (intercostal, subcostal, collarbone, trach tug, head-bobbing), nasal flaring, apnea/gasping. Circulation: Pallor, mottling. Assessment Guidelines: Position of comfort. Vital signs and blood gas. Respiratory effort and cough. Color. Behavior change. Hydration status. History. Normal Respiratory Rate: Infant: 30-60. Toddler: 24-40. Preschool: 20-30. School-aged: 12-25. Adolescent: 12-16. Mild Respiratory Distress: Symptoms: Restless, Tachypnea, tachycardia, diaphoretic. Teaching: Teach parents how to use bulbs if frequent secretion blockages. Change position of baby – lying down will make it more difficult to breathe Bronchodilators, antihistamines, antibiotics. Moderate Distress (Early Decompensation): Symptoms: Nasal flaring, retractions, grunting, wheezing, anxiety, and irritability. Interventions: Chest x-ray, O2 therapy, call rapid response team, obtain blood gas ABG’s Severe Respiratory Distress (Resp Failure/Imminent Arrest): Symptoms: Dyspnea, Bradycardia, Cyanosis. Stupor/coma, GCS change due to hypoxia. Nursing Interventions: Start IV, Oxygen is set, code cart in the room. Call rapid response team. Full arrest = call a code (do not have to wait for cardiac arrest). Adverse Outcomes: Frequently preventable. Must identify deteriorating child, use a bedside score. MET Team (Rapid Response Team): Early Identification of at-risk patients. Important initiative for safety and quality improvement. Bronchiolitis (RSV): Inflamed airways with hypersecretions due to a viral infection Children have few alveoli for gas exchange, only 10% of adults. Early signs: runny nose, fatigue. Few days later, come into emerge with mild, moderate, and severe symptoms. Central Venous Access Lines (CVADs) Types of CVADs: Non-Tunneled CVAD: Used for 5-10 days, 3-5 lumens, varying length and size. Sub-clavian, Jugular, or femoral. Possible to obtain hemodynamic and venous pressure recordings. Skin-Tunneled CVAD: Sub-Clavian, or jugular. In-situ for many months for long periods or chemo, nutrition, or antibiotics. Implanted Subcutaneous Ports: Prolonged IV therapy. Easier to hide if they want to be active and less noticeable. PICCs (Peripherally Inserted Central Catheters): Basilic, Median cubital, or cephalic veins inserted. 1-3 lumens. Prolonged periods of antibiotic or chemotherapy. Implantable Port: Long term, change the needle access every 7 days. Huber needle used (non-coring). Primary Complications: Pneumothorax. Cardiac Tamponade. Arterial Puncture. Hemorrhage. Hemothorax. Hydrothorax. Air Embolism. Occlusions. Thrombosis. Infiltration. Extravasation. Phlebitis. Dress Change: Clear dressing every 5-7 days. Gauze dressing every 48h. Head Injuries Assessing Level of Consciousness: The most important neurological assessment in high acuity patients. Altered Level of Consciousness: Alert: Are they awake and interacting with their environment. Aware: Orientation to person, place, time. Level of Consciousness (GCS): Changes in a person’s LOC is the earliest and most sensitive indicator of a neurological change. Can use GCS on intubated, use hand signals or head nodding. For pediatrics, utilize parents to rate on GCS. Impairments to LOC: Meds (seizure meds, pain meds, medical marijuana), general anesthesia, procedural sedation (epidural, nerve block). Opioids, Barbiturates, marijuana, Alcohol. AEIOU – Alcohol, Epilepsy, Insulin, Opiates, Urates. TIPPS – Trauma, Infection, Psychological, Poisons, Shock. Traumatic Brain Injury: Scalp, Skull, or brain injury from a sudden external physical assault. Example: Concussion, Hypoxia, Lacerations, or infection. Risk factors: Falls, Car accidents, advanced age + polypharmacy, Alzheimer’s, muscle weakness, young kids (no coordination) + teens (risky behaviors), military service, domestic abuse. Primary vs. Secondary Injury: The source of injury Is primary traumatic events, infection. The secondary injury is the subsequent reaction/Inflammatory response that may cause more injury. Prevention of further injury from the secondary source is what interventions are targeted towards. Most common secondary injuries: Infection, hypoxia or ischemia, building up of CO2, from occluded vessels, ICP, hemorrhaging. Clinical Manifestations: Laceration will bleed a lot (infants can become hypovolemic from scalp wounds). Altered Level of consciousness. Pupillary abnormalities. If pupils are uneven, unreactive, may mean damage is unrepairable. Blown pupil = cannot repair Basal skull fracture. May see bleeding and bruising around eyes and ears (battle sign). Halo Sign: Blood and CSF leaking from ear or nose, the two fluids will separate make sure to test that it is not snot from nose. Sudden neurological deficits or changes. Headache. Seizures Penetrating trauma more at risk for seizure disorder developing. Changes in vital signs. Lowered and sporadic resp rate. Temperature may be unregulated depending on where injury is. Pulse will begin to drop. BP will begin to widen. Concussions: Temporary, functional neurological impairment resulting from a direct or indirect hit to the head. Orientation questions, scales are used to rate concussion and develop baseline. Common Signs: Loss of consciousness. Retrograde amnesia (can’t remember events leading up to injury). Light sensitivity, headache, fatigue. Sensitivity to noise. Concerning Finding: Changes in vitals. Unnatural sleeping (rest is okay, but if sleep reduces alertness or orientation, bad sign). Patient teachings: No activity for 24h or more. No videogames (no light or stimulation), introduce slowly. No alcohol. Gradually return to work or school. Hydration, eating well. Intracranial Pressure (ICP): The pressure inside the cranium can increase due to a TBI. Signs: MINDCRUSHED. M – mental status change (GCS). I – irregular breathing. N – Nerve changes (optic nerve change). D – Decerebrate or decorticate posture. C – Cushing’s triad bradycardia, bradypnea, widening pulse pressure. R – Reflex (positive Babinski reflex). U – Unconsciousness. S – Seizures. H – Headache. E – Emesis. D – Deterioration of motor function. Interventions: Keep them slightly alkalotic. DO NOT SUCTION PRESSURE: P – Position. R – Respiratory (prevent hypoxia or hypercapnia). E – Elevated temp – prevent this. S – Systems to monitor (neuro, CV). S – Straining activities avoid (coughing, sneezing, bowel movement, vomiting). U – Unconscious care (mouth care, repositioning, elimination, eyecare, range of motion, DVT prevention). R – RX, meds to keep stable. E – Edema management (mannitol, fluid restrictions, other diuretics). Stages: 1 and 2 are stages of compensation. 1 – Awake, normal vitals. 2 – Restless, confused, normal vitals. Stage 3: Changes in vitals, beginning to decompensate. Resps irritate, widening BP, pulse decrease. Small, reactive pupils. Stage 4: Cheyenne stokes breathing. Uneven, blow pupils either bilateral or ipsilateral. Progress into a coma. Management of increased ICP Maintain CPP Decrease cerebral volume Decease CSF volume Decrease cerebral pressure Decrease metabolic rate Normal ICP is 5-15mmHg, children are 10mmHg. Can be controlled/measured with a drain inserted into the lumbar space of skull. Cerebral perfusion pressure: Impacted by BP and the amount of space available in the brain for perfusion. Ideally between 60-100mmHg. CPP = MAP – ICP. MAP = mean arterial pressure After ICP is stable, manage cerebral perfusion. How well is the heart pumping, what is blood volume, viscosity. If blood is not circulating, cellular death occurs in 5min. If ICP is not treated, herniation of brain matter occurs. Cardiac Rhythms Cardiac Output Formula: Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV) Stroke Volume Influenced by: Contractility: Shouldn't be excessively contractable. Preload (End Diastolic Volume): the force that stretches the ventricles prior to contraction/the amount of blood sitting in the heart before it contracts which depends on the venous return and/or valve function. Afterload (Mean Arterial Pressure): Inversely proportional to CO. The pressure the heart contracts at to move blood out of the heart. Can depend on resistance (stenosis) or no resistance. Diastolic Time: Ventricular fill time, crucial for optimal function. If it is too fast, the heart will not fill up properly/entirely. Conduction System Components: SA Node: (Pacemaker) in the top of the right atrium, 60-100 bpm. Bachmann’s Bundle: In the left atrium. AV Node: In the bottom of the right atrium. Bundle of His: Conducts impulses from the AV node to the ventricles. Perkinje Fibres: Can fire at rates as low as 20 bpm. ECG Monitoring Cardiac Monitor (Telemetry): 5 leads, continuous transmission to nursing station computers. Allows mobility (seen in coronary care units). Stable patients are using this monitor 12-Lead ECG: Captures a 12-second strip during acute events to identify damaged heart areas. Can also determine if they are having angina or tissue necrosis Continual monitoring Snapshot of what is happening, not long term. Holter Monitor: 24-hour investigatory monitoring, records daily activities, including exercise. Does not record in real time. Need to go back and look at it to determine problem. Event Recorder: Longer-term monitoring, activated by the patient during potential events. ECG Interpretation P-Wave: Atrial contraction (depolarization). P-R Interval: 0.12-0.2 seconds. Prolonged P-R Interval may indicate SA-AV node block. Absent or sporadic P waves suggest Atrial Fibrillation. QRS Complex: R is left ventricle depolarization; S is right ventricle depolarization. Fires quickly, 0.04s-0.12s. Prolonged QRS suggests slow ventricular conduction. Each Small Box in Strip: Represents a measurement of 0.04s. A strip is always printed in 6 second intervals. Normal Criteria: 1:1 Conduction (P wave followed by QRS and T). Correct rate (60-100 bpm). Right time intervals (P-R: 0.12s-0.2s, QRS: 0.04s-0.12s). Regularity of each QRS Complex and P wave. Cardiac Rhythms Normal Sinus Rhythm: Sinus node firing properly, all parameters within normal range. Atrial Fibrillation (A-Fib): Irregular rhythm with a regular semi-sustainable pattern. Atrium is not contracting – just quivering. AV node is not able to keep up. Causes decreased Cardiac Output. Thrombin can be a result of blood stasis in atria Embolus may develop and travel to brain causing a stroke Risk factors: Hyperlipidemia, electrolyte imbalance, alcohol, caffeine, smoking, stress, underlying heart disease (angina, MI). Treatment: Rate and rhythm control via calcium channel blockers, anticoagulants (to prevent stroke), cardioversion (synchronized, pharmacological), catheter ablation, MAZE procedure. Symptoms: Easily fatigued, feeling of abnormality, lowered BP and profusion, anxiety, irregular pulse, high headed Can be asymptomatic if they have a HR between 60-100bpm. Sinus Bradycardia: Sinus node firing at less than 60 bpm. Everything is “normal” just rhythm is slower than normal Normal in trained athletes or during sleep. Treatment: Atropine (increases HR), pacemaker. Symptoms: Hypotension, pale, cool skin, weakness, angina (not getting enough O2 to the heart, dizziness/syncope, confusion, SOB Ventricular Tachycardia: Emergency, collapse rhythm if pulseless. Monomorphic or polymorphic. Associated with myocardial infarction, electrolyte imbalance (especially potassium & magnesium), coronary artery disease, toxicity. Ventricular Fibrillation: Emergency, may deteriorate into asystole. CPR sustains VF; defibrillation needed. Risk factors: Electrical shock, hyperkalemia, acidosis, hypervolemia. ICD (Implantable Cardioverter-Defibrillator) used for high-risk patients. Heart Medications for A-Fib: HR controlling Medications: Beta blockers end in “lol” Calcium channel blockers Digoxin Hear Rhythm controlling medications: Sodium channel blockers Potassium channel blockers Pacemakers: Can be temporary or permanent Can be atrial (fires before p-wave – SA node isn’t working), ventricle (fires after p-wave ventricles aren’t contracting after p-wave), or dual (fires before and after p-wave) Can be on demand when the HR goes below the set pace Complications: Failure to capture: when the heart fails to respond to the impulse sent by the pacemaker. Failure to sense: when the pacemaker doesn’t sense that the heart rhythm is off so it doesn’t fire. Acute Stroke Management (CVA) Types of Strokes Ischemic Stroke: Sudden blockage caused by clot, atherosclerosis, A-fib, DVT, dehydration (lock is thicker) limiting blood delivery to the brain cells. Embolism type: Clot from another body part lodges in cranial vessel. Thrombosis: Clot forms within the artery wall in the brain. Symptoms: weakness and paralysis on 1 side, speech problems, severe headache, vision problems/loss Management: Stroke team, acute BP management (low BP= decrease in brain perfusion but don’t want it too high = rupture of vessels), blood glucose control, aspirin therapy (anticoagulant prevents clots for getting bigger/forming) Acute thrombolytic therapy (breaks down existing clot) IV administration of tPA (Alteplase) need to be 18yrs+ and needs to be administered within 4.5hours of stroke Reperfusion injury if you give tPA after the 4.5 hours, the blood enters back into tissues, however, tissue is already dead = increase in pressure which will cause another head injury Hemorrhagic Stroke: Break in vessel leads to reduced perfusion, swelling, and increased ICP. Caused by brain aneurysm, uncontrolled hypertension, or aging (less resilient vessels). Longer recovery time than ischemic stroke Risk factors = HTN, age, smoking Symptoms = high BP, nausea, vomiting, headache Management: microsurgical clipping or endovascular coiling (coil fills up space to stop blood from pounding into one area to prevent it from exploding Transient Ischemic Attack (TIA): (type of ischemic stroke) Mini stroke - resolves within minutes to hours. Warning sign for an imminent full stroke. Symptoms: Same as ischemic but temporary Brain Function and Anatomy Blood Supply: From carotid and vertebral arteries. Stroke impacts cells within 5 minutes. Areas of the Brain: Right Side: Creativity, emotions, critical thinking. Left Side: Logic, reading, writing, speaking. Various lobes with specific functions: Frontal, Parietal, Temporal, Occipital, Cerebellum, Brain Stem. Risk Factors for Stroke Modifiable: Smoking, hypertension, diabetes, hyperlipidemia, atrial fibrillation, physical inactivity, obesity, alcohol, drug abuse. Non-Modifiable: Age, gender, race, family history, previous stroke, or TIA. Signs and Symptoms Sudden onset, 911 or rapid response needed. Use FAST: F for Face A for Arms S for Speech T for Time Additional symptoms include aphasia, dysarthria, apraxia, agraphia, alexia, agnosia, dysphagia, hemianopia. Care Priorities Post Stroke Monitor for and prevent further complications such as: Vasospasm – acts like a stroke Increased ICP – keep bed at 45-degree angle, quiet, no stimulation, monitor blood glucose Hemorrhagic transformation – blood brain barrier may be irritated control BP & HTN by being hydrated to dilute blood Seizures Diagnosis and Potential Orders Diagnostic Procedures: CT Scan of head to rule out hemorrhagic stroke. MRI to determine affected lobes. tPA administration for ischemic stroke within 3 hours (strict criteria). TPA Administration tPA (tissue plasminogen activator): Dissolves clot in ischemic stroke (fibrinolysis). Given within 3 hours (up to 4.5 hours in strict criteria). Post-tPA interventions: Neuro assessments, BP management, fall prevention, monitoring vitals, labs, and glucose. Diet Evaluated SLP Thickened liquids, crushed meds, mechanical soft foods Watch for pouched food in cheek Aspiration risk Tuck in chin to chest while swallowing to close airway Assessment Tools: NIH Stroke Scale (0-42 score). Monitoring VS, airway, cranial nerves, bladder and bowel function, skin and limb integrity, hemianopia, diet. Communication: Adjust communication for aphasia, using gestures, communication boards, and providing a supportive environment. Cardiac Alterations Acute Coronary Syndrome (ACS): Imbalance in oxygen supply and demand to the heart muscle. Causes: HR, O2 content, perfusion, contractility, afterload, preload, often due to atherosclerosis. Types: Reversible Angina (increased demand). Progressive Angina (associated with a heart attack). Coronary Blood Supply: LAD (Left Anterior Descending) Artery: Large artery, critical; called "widow-maker" if blocked. Right Coronary Artery. Assessment: PQRSTU: P: Precipitating factors. Q: Quality of pain. R: Radiation of pain. S: Severity of pain. T: Timing of pain. U: Understanding. Men and women may present differently; women may dismiss symptoms. ECG Changes: STEMI: ST elevation in at least 2 leads damage is damage of full thickness of heart. ST Depression: Indicates injury/ischemia, angina. NSTEMI (partial thickness tissue damage). Cardiac Biomarkers: Troponin: Gold standard = indicates heart muscle damage. Troponin is exclusive to heart muscle any elevation of troponin in labs means there has been damage to heart Going to order troponin labs multiple times to see if levels are decreasing or not. If they continue to go up, that means there is damage still being done to the heart. If they are decreasing, then no more damage is happening. Myocardial Infarction Symptoms: Chest pain & discomfort Shortness of breath Pain in jaw, neck, back, arm, or shoulder Feeling nauseous, lightheaded, or unusually tired (women only) Nursing Interventions: OIL: Oxygen, IV, leads (12) leads are to see if we have a problem at that specific moment in time. Medications for Myocardial Infarction: Aspirin: Chew 2 tablets, anticoagulant will stop future clots from forming and from current clots to stop growing. Heparin: Anticoagulant. Beta-Blockers: Reduce blood pressure. Make sure BP is good before administering nitrates as they will lower BP drastically. Also make sure HR is within normal range as beta blockers can cause a dangerous drop in HR quickly Nitrates: Vasodilator (check BP first) opens vessels up in body. Statins: Long-term lipid-lowering. ACE Inhibitor: Helps with HR remodeling. Treatment for ACS: Angiogram for diagnostic test Angioplasty: Balloon opens the artery; mesh keeps it open. Can also be done without mesh. PCI (Percutaneous Coronary Intervention). Cardiac Catheterization: Explain the procedure and post-procedure steps. Consent, risks, any education, labs (troponin), infections, dental work, VS, height, weight, cardiac and respiratory assessment, allergies, GOC. Assessments, vital signs, allergies, history. Complications: Bleeding, thrombus, pseudoaneurysm, retroperitoneal bleed. Post-procedure care and teaching. No bending/lifting, cleanliness (especially if done femoral), post procedural medication. CABG (Coronary Artery Bypass Graft): Good for STEMI within 12h or NSTEMI within 24h. Can be single, double, triple, or quadruple CABG. Never do CABG on peds, do heart transplant Open Heart Surgery: Valve replacement/repair. Repair of abnormal or damaged areas. Medical device implantation not for implantation of pacemaker. Pumps or mechanical valves for adults Berlin heart for pediatric patients – pumps outside of the body Transplant. Heart Surgery/CABG Nursing Priorities: Assessment and pain management. Dressing care. Drain care drain fluid from surgery. Pacemaker monitoring. Medication administration. Hygiene cannot shower with dressing on. Heart Surgery/CABG Complications: Infection Pneumonia DVT need to wear squeezy boots. Heart muscle dysfunction Arrythmias higher or lower HR Kidney failure Stroke from clots, equipment, stimulating plaque. MI Decreased cardiac output. Cardiac Rehabilitation: Focus on improving quality of life and reducing future risks. Includes education, exercise, nutritional support, social support. Ensuring insurance coverage for necessary treatments. Acute Heart Failure: Increased contractility compensates, but walls may thicken or thin inefficiently. LSHF = pulmonary problems Left-sided symptoms: Pink frothy sputum, SOB, exercise intolerance, fluid in lungs = crackles, O2 sats drop. RSHF is often caused by LSHF Right-sided symptoms: Edema, hepatic hypertension, possible ascites/varices. Medications administered before ventricle dies: ACE inhibitors, ARBs, diuretics (helps to decrease preload), beta-blockers, anticoagulants, vasodilators (nitroglycerin), digoxin (helps heart pump stronger). Management includes oxygen, pacemaker/ICD, ECMO, VAD, heart transplant. Peripheral Vascular Disease: Problems with arteries & veins in arms and legs Risk = poor diet, diabetes, sedentary lifestyle, smokers Arterial (problem in artery): Intermittent claudication, cool, pale skin, weak pulse, lack of hair. Diagnosed by assessment and ultrasound. Treatments: Risk factor reduction, compression socks, statins. Venous (problem with veins) Edema in legs/arms Atherosclerosis: Usually widespread (through whole body). Pathological hypertension can lead to ruptures and clots. Treatment: Femoral-popliteal bypass (pass by the plaque) to maintain circulation. Aneurysm: Abdominal Aortic Aneurysm: Stretching of aorta Listen for a bruit around abdomen area. DO NOT push on it as it may rupture = dead patient. Aneurysm is usually in the back area and can sometimes be asymptomatic. Major risk factor is having HTN. Leaking or ruptured = Hypovolemic shock. Treatment: Endovascular repair with a stent-graft similar to angioplasty (go home 2 days after surgery) Complications: bleeding, infection (fever, redness), bruising, kidney failure due to not enough blood to kidneys Types: Fusiform, Pseudoaneurysm, Saccular, Dissecting, Rupture. Shock & Sepsis Shock: Definition: Inadequate tissue perfusion leading to lactate production and metabolic acidosis. Anerobic production. Consequences: Leads to multisystem failure, kidney failure, Classifications: Hypovolemia (bleeding, dehydration, burns, third-spacing). Cardiogenic (MI). Obstructive (Pulmonary Embolism). Distributive (extreme vasodilation - anaphylactic, septic, neurogenic). Shock is the result of Compensatory Mechanisms: Sympathetic nervous system activation (epinephrine release) increase in BP & HR Endocrine response (anti-diuretic hormone) decrease in blood flow to kidneys so they stop secreting. Renin-aldosterone – angiotensin system. Stages: Initial Compensatory: Tachycardia. Hyperventilation/tachypnea. Decreased urine output. Decreased pulse Lactate increase (1 to 4), acidosis. Shunting blood to vital organs brain, heart, lungs. Confusion, anxiety, decreased peripheral pulses. Decreased urine output Pale + cool hypovolemic shock Increased temperature septic No bowel movements or sounds can lead to paralytic illuis Progressive: Hypoxic injury to organs. Signs of myocardial ischemia chest pain, v-tach Vasodilation, blood pressure dropping. Cyanosis Tachypnea crackles in lungs due to fluid overload Confusion Slowed speech Edema due to inflammatory response (vasodilation), decreased blood volume. Cerebral perfusion pressure changes, V-fib or V-tach. DIC, ulcerations, little to no urine or bowel movement. Irreversible (refractory): Worsening of all systems with organ failure. Cardiac death. General Management of Shock: ABCs: Airway: Loss of consciousness may require ventilation; tongue may get in way. Breathing: Tachypnea, oxygen mask. Circulation: Increase fluid volume cautiously (do not administer with obstructive shock), vasoconstriction meds (dopamine/epi). 1-2L of IV fluid in the first hour, monitor closely. Use colloids if necessary. Administer albumin (blood product) is needed Continuously monitor BP with an arterial line. Disability: Monitor blood glucose (going to increase) and potassium shifts. Nutritional Support: Ensure adequate nutrition within 8 hours. Going to be on TPN or tube feed to maintain glucose levels Types of Shock: Hypovolemic Shock: Fluid volume depletion (bleeding, vomiting, diarrhea). Start with NS, LR 1-2L every 10 to 15 minutes. Blood work immediately Move to blood products if bleeding is an issue. Monitor pulmonary congestion closely. Distributive Shock: Anaphylactic, neurogenic, septic. Loss of blood pressure due to vasodilation. Vascular resistance decreases, capillary leak = more damage. Anaphylactic Shock: Extreme airway restriction. Epinephrine, prednisone (helps with allergic reaction after epi stabilizes), H1, and H2 blockers. Septic Shock: High temperature as a distinguishing factor. Early warning signs: Altered mental status, high resp rate, low blood pressure. Clinical Manifestations that differ from other shocks: Compensatory: Skin hot & flushed, pulses are bounding Causes: Pneumonia Abdominal infections appendicitis UTI Soft tissue/bone infection Indwelling vascular catheters Sepsis Resuscitation bundle Measure serum lactate – confirms septic shock Obtain blood cultures prior to antibiotic administration Prompt administration of broad-spectrum antibiotics Administer crystalloid for hypotension 1-2L in first 15 minutes if no response, admin vasoconstriction meds Administer vasopressors for hypotension to maintain MAP >65mmHg Symptoms for infants: Poor feeding, irritability, lethargy, vomiting, poor colour, high temperature Any suspicious of sepsis in infants require full blood workup CBC, UA, cultures of blood/urine/USF cell count/protein/glucose qSOFA criteria for sepsis 2 or more needed = greater risk for poor outcome Altered mental status, fast resp (>22breaths/min), low BP (systolic <100mmHg) Complications: Multi-organ dysfunction, DIC (disseminated intravascular coagulation = no clotting factors = bleed out). Gastrointestinal Upper gastro = esophagus, stomach, duodenum Blood coffee grounds = bleed past the duodenum Ulceration (perforation) Lower gastro = colon, rectum Frank blood = bleed close to the end of the gastrointestinal system Diverticulosis – bleed in sigmoid colon Hemorrhoids may rupture = bleed We cannot put pressure on a GI bleed. Crohn’s Disease Entire GI covered in ulcers Right lower quadrant pain (ilium) Bleeding Can jump from different places and has multiple phases Ulcerative Colitis Large colon disorder starting at the rectum Passing of blood Left lower quadrant pain Mucus Esophageal Varices Dilated, tortuous veins located in the submucosa of the lower esophagus Life threatening emergency Liver has hardened, vessels around esophagus become irritated and rupture into esophagus causing large amounts of blood being vomited. Risk Factors: Alcohol (irritating to stomach, vomiting) NSAIDS Age thinning mucus membrane, polypharmacy, stress, history of ulcers Aspirin Hepatitis (damage to liver, hepatic hypotension Symptoms: Hematemesis Melena Altered LOC, restlessness, anxiety Cool, clammy skin Weak peripheral pulses Tachycardia & hypotension hypovolemic shock, anemic Decreased urine output preserve fluids Shock in severe cases Diagnosis: Endoscopy gold standard, can see ulcerations, GI bleed Can clamp vessels or cauterize Barium swallow gives picture CT & MRI looking at cause such as cancer, liver problems Labs platelet counts, clotting factors, liver enzymes (ALT, AST, ALP, bilirubin, albumin) hemoglobin (need to be 70 before giving blood), electrolytes Nursing interventions: O2 admin IV insertion IV fluids, electrolyte replacement, volume expanders (bolus) Blood transfusion Parenteral nutrition TPN via CVAD Oral hygiene clean/rinse mouth Foley catheter monitor in & outs Reassurance & support blood may be everywhere, provide support Medication somatostatins octreotide (decreases blood flow, decreases portal HTN), beta-blockers Meds can only be used for upper GI bleeds Surgical Interventions Esophageal banding therapy identify where varicose are and put band around them to prevent rupture Transjugular Intrahepatic Portosystematic Shunting Liver transplant Pancreatitis Pancreas/body attacking itself Can be caused by: alcohol abuse Obstruction of the common bile duct Symptoms: Severe sharp pain in back No toleration for eating Interventions: IV fluids NG to empty stomach Pain management Diagnosis: Blood amylase (increase 3-6hr), lipase (24-48hr after), glucose (best determinator, insulin production is affected) Ultrasound, CT (most often used), MRI ERCP – endoscopic retrograde cholangiopancreatography scope to look at problem but can trigger an attack Hepatic Cirrhosis Replacement of normal liver tissue with diffuse scaring that interrupts functioning Permanent Hep C = main cause of liver disease Fluid going into lungs = SOB, respiratory issues Ascites fluid pushed into abdomen has to be drained Classifications: Hepatocellular Hepatitis, cells of liver causing problem Metabolic Metabolic problem, high levels of iron in blood Cholestatic High levels of bilirubin = clogged ducts Symptoms: Compensated – still functioning/ managing Decompensated – not functioning Diagnosis Serum (albumin, serum globulin, alkaline phosphatase, AST, ALT, GGT, bilirubin, PTT) CT or MRI Biopsy – can cause bleeding Complications: Bleeding/coagulations Fluid volume excess Ascites Hepatic encephalopathy Portal hypertension proximity to esophagus Renal Alterations: Lab Indicators: Creatinine, BUN, C-reactive protein, ESR. Urea: Waste product from protein breakdown. Increased in injury, plateau, then returns to normal. Kidney Function: Toxins build up without proper function. Electrolyte and fluid imbalances. Controls BP by excreting or holding on to fluid Activates vitamin D Ultrasound: Investigates kidney stones or masses. Labs: Urea will be elevated first, then creatinine Creatinine comes from and is broken down by muscles and excreted via kidneys Elevated Potassium: Life-threatening; dialysis may be necessary. Elevated Potassium and Heart: T-wave changes may lead to asystole. Hypovolemia and Kidneys: Administer fluids to prevent kidney injury. Types of Renal Injury: Pre-renal (hypovolemic shock, dehydration) no blood to kidney intra-renal (problem within kidney, infection, medication – NSAIDS, chemo, antibiotics) post-renal (obstructions, kidney stones). GFR Rate: Determines severity and effectiveness of treatment. Stages of Kidney Injury: Oliguric, Diuretic, Recovery. Post-Surgery Renal Failure: Oliguria, flank pain may indicate bleeding. Kidney Transplants: Increased cancer risk (immunosuppressants).