NURS 422 Exam 1 Study Guide PDF

NURS 422 Exam 1 Study Guide Exam one will consist of 50 multiple choice questions, including select all that apply, fill in the blank as well as two case study questions that are 6 points each for a total of 60 points. *know nursing diagnoses for each con...

NURS 422 Exam 1 Study Guide Exam one will consist of 50 multiple choice questions, including select all that apply, fill in the blank as well as two case study questions that are 6 points each for a total of 60 points. *know nursing diagnoses for each condition. PE ​ Risk factors ○​ Presence of DVT ​ Risk factors for DVT ​ Obesity ​ Smoking ​ Chronic heart disease ​ A-fib ​ Fracture ​ Hip or knee replacement ​ Major surgery ​ Major trauma ​ Spinal cord injury ​ History of previous VTE ​ Malignancy ​ Estrogen use ​ Age > 50 ​ Pregnancy ​ MAjor DVT risk factor: Virchow’s triad ​ Venous stasis ○​ PVD, immobility ​ Vessel wall damage ○​ Diabetes, HTN, high cholesterol ​ Hypercoagulability ○​ Blood disorder ​ Causes/Patho ○​ Blood clot lodge in pulmonary artery- PE ​ Can also be air, tumor, amniotic fluid, fat ○​ V/Q mismatch ​ Ventilation is good but gas exchange isn’t occurring → no perfusion ​ Heart works extra hard → R sided HF ​ As R side expands → pushes on L side → can’t fill → L sided HF ​ Clinical Manifestations ○​ Dyspnea ○​ Pleuritic chest pain ○​ Tachypnea  ○​Tachycardia ○​Hemoptysis ○​Cough ○​Accessory muscle use ○​Anxiety/restlessness, feelings of doom ​ d/t not enough perfusion to brain ​ Diagnostics ○​ Imaging studies ​ ECG to r/o MI ​ CXR to r/o other causes of respiratory distress ​ CT scan with contrast to identify PE ​ Hold metformin with contrast ​ VQ scan to visualize PE if CT not available ​ > 0.8 ​ Pulmonary angiography most definitive test ​ Cath lab ​ LE doppler to id DVTs ○​ Laboratory studies ​ D-dimer ​ Tells you if fibrin is elevated in blood d/t body trying to break down a clot ​ ABGS ​ Start with respiratory alkalosis and eventually progresses to metabolic acidosis ​ Treatment-pharmacologic and nonpharmacological (ex. IVC filter). ○​ Know side effects and teaching for pharmacological treatment ​ Pharmacologic ​ Anticoagulants ○​ Don’t dissolve clot → prevents growth of clot and new ones from forming ○​ Heparin drip ○​ Warfarin ​ aPTT ​ 40-90 seconds or 1.5-2.5 x normal range ​ INR ​ 2.0-3.0 with heart valve = 2.5-3.5 ○​ Why use two meds at the start? ​ Warfarin takes a few days to reach therapeutic dose so give heparin in the meantime ​ Thrombolytics ○​ tPA ○​ Alteplase ○​ Streptokinase  ○​ Catheter directed thrombolysis (CDT) used for large PE or submassive ​ Surgical management ​ Embolectomy ○​ Catheter ○​ Surgical- most common if thrombolytics are contraindicated ​ Inferior vena cava filter ○​ Catches clots from lower extremities while still allowing blood flow to prevent clot from traveling up ​ Nursing management/interventions ○​ Assessment ​ Airway ​ Oxygenation ​ Frequent vital signs ​ BP might be elevated but if it starts to drop → worried about heart failure ​ Chest pain ​ Lab values ​ ABGS, lactic acid, aPTT, PT/INR ​ Urine output ​ < 0.5 ml/kg/hr sign of shock ​ < 30 ml/hr never a good sign ○​ Kidneys not being perfused ○​ Actions ​ Elevate head of bed ​ Administer IV fluids ​ Thins blood a little but monitor for HF ​ Administer medications ​ Thrombolytics ​ Anticoagulants ○​ Maybe also digoxin or pressors ​ Institute bleeding precautions ​ Be prepared for intubation and resuscitation ​ Have intubation tray and crash cart ready ​ How to prevent complications ○​ Disease process/lifestyle modifications ○​ Medications ​ Avoid vitamin K ​ Bleeding precautions ○​ Bleeding precautions ○​ Diet ​ Cardiac diet ​ Avoid vitamin K ​ Be familiar with therapeutic range of PTT if on heparin drip and goal INR for Warfarin ○​ aPTT  ​ 40-90 seconds or 1.5-2.5 x normal range ○​ INR ​ 2.0-3.0 ​ With heart valve = 2.5-3.5 Chest Trauma ​ What is the purpose of a chest tube. Review nursing care for chest tubes ○​ To remove fluid from the pleural space ○​ If chest tube comes out ​ Petroleum gauze → then sterile gauze → then tegaderm (leave one side open) ​ Signs and symptoms of tension pneumothorax and cardiac tamponade, treatment for each condition. ○​ Tension pneumothorax ​ Signs and symptoms ​ Air or blood collection in pleural space ​ Tracheal deviation = cardinal sign ○​ Medical emergency → organs pushing on heart ​ Can lead to pressure on heart and PEA arrest ​ Treatment ​ Chest tube ○​ Cardiac tamponade ​ Signs and symptoms ​ Heart cannot adequately fill or contract because of the compression of the ventricles ​ Hypotension, muffled heart sounds, and distended neck veins → collectively known as beck’s triad ​ Cause of PEA arrest ​ Treatment ​ Pericardiocentesis ​ Signs and symptoms of chest wall contusion ○​ Tachypnea ○​ Tachycardia ○​ Shortness of breath ○​ Decreased oxygenation ○​ Decreased level of consciousness ○​ Decreased or absent lung sounds ○​ Asymmetrical chest excursion (in the case of a flail chest) Respiratory Failure/ARDS ​ The signs/symptoms of respiratory failure ○​ Hypercapnia ​ Headache, confusion, decreased LOC ​ Can appear to be pink ○​ Hypoxemia  ​ Changes in respiratory rate, heart rate, blood pressure ​ Appear blue ○​ Symptoms tend to worsen as there is less cerebral perfusion ​ Anxiety, restlessness, confusion ​ Signs/symptoms of ARDS ○​ Tachypnea ○​ Tachycardia ○​ Refractory hypoxemia ​ Low O2 despite oxygen delivery ○​ Sudden SOB ​ Within 12-48 hours of lung injury ○​ Labored and fast breathing ○​ Coughing ○​ Tiredness ○​ Dizziness ○​ Headaches ○​ Cyanosis ​ Management/Treatment/Complications of ARDS ○​ Mechanical ventilation ​ Low tidal volume ​ d/t scarring of lungs ​ High PEEP ​ Positive end expiratory pressure ○​ High-flow nasal cannula ○​ ECMO ​ Takes blood out, oxygenates blood, puts it back in ○​ Prone positioning ​ 16 hours prone, 8 hours supine ​ Recruit alveoli ○​ Medications ​ Antibiotics ​ After culture is done ​ Neuromuscular blockade ​ Train of 4, paralyzing medications, analgesia, anesthesia ​ Promote vent synchrony ​ Hydration ​ Thin secretions ​ Nutrition ​ Tube feedings Ventilator Therapy ​ Have a general understanding of: ○​ FiO2 ​ Fraction of inspired O2  ​ Normally we breathe 21% FiO2 on room air ○​ Peep ​ Positive pressure applied at the end of expiration of ventilator breaths ​ Usual setting 5 cm H2O ​ Usually, the higher the PEEP → the sicker the patient ○​ Tidal Volume ​ Volume of gas delivered with each ventilator breath ​ Usually 6-8ml/kg or 500 ml ○​ Pressure Support ​ Positive pressure used to augment patient’s inspiratory pressure ​ Usual setting 5-10 cm H2O ​ The goal of medications for patient on ventilator therapy ○​ Sedation ​ Drips: propofol, precedex, versed ​ IVP: fentanyl, versed, dilaudid ​ You need to have orders for these to titrate based on RASS score (Richmond Agitation Sedation Score) ○​ VAP prevention: Famotidine, CHG PO ​ Ventilator associated pneumonia prevention ​ Famotidine to prevent stress induced stomach ulcers Sepsis/MODS ​ Pathophysiology ○​ Deregulated host response to infection ○​ Excessive release of proinflammatory cytokines ​ Vasodilation ​ Decreased vasomotor tone ​ Increased capillary permeability ​ → lack of return of blood flow to the heart ​ Clinical manifestations ○​ Early stage / “warm” phase ​ Tachycardia ​ Bounding pulses ​ Fever ○​ Late stage / “cold” phase ​ Cool, pale skin ​ Weak, thready pulses ​ Tachycardia ​ Hypotension ​ Labs to monitor ○​ ABGS ​ Usually respiratory alkalosis with progression to metabolic acidosis as sepsis gets worse ○​ Venous oxygen saturation  ○​ Metabolic profile ○​ Lactate ○​ Clotting studies ​ Treatment options-review Bundle of care ○​ Hour 1 ​ Activities that need to be completed within 1 hour after identifying sepsis ​ Treatment may not be completed in 1 hour ​ Treatment should begin immediately ○​ Antibiotics ​ Administered within 1 hour upon arrival ​ Cultures should be done before antibiotics are administered ○​ Labs: CBC, coagulation factors, CMP, ABGS ○​ Fluid resuscitation → priority!! ○​ Vasopressors ○​ Corticosteroid therapy ​ Conflicting evidence for this because it’s an immunosuppressant, some hospitals use it and some don’t ○​ Ongoing monitoring ​ Complications of septic shock ○​ DIC ​ Disseminated intravascular coagulation ​ Rare but life threatening condition ​ Accelerated clotting within blood vessels → elevated consumption of platelets and clotting factors → uncontrollable bleeding ​ Treated by correcting the cause and blood transfusions ○​ MODS ​ Multiple Organ Dysfunction Syndrome ○​ Stress ulcers ​ Nursing management/interventions ○​ Assessments ​ Neurological status ​ Vital signs ​ Fevers → then progression to hypothermia ​ Tachycardia ​ Hemodynamic readings ​ Urine output ​ Skin color and temperature ​ Bleeding ​ ​ Stool, urine, gums → signs of DIC ○​ Lab tests ​ ABGs ​ Usually respiratory alkalosis with progression to metabolic acidosis ​ Venous O2 saturation ​ Metabolic profile  ​ Lactate ​ Clotting studies ○​ Actions ​ Meticulous hand washing, aseptic technique ​ Oxygenation ​ Prepare for intubation ​ Lactate level ​ Blood cultures ​ Administer antibiotics ​ Start with broad spectrum and then switch to more specific when cultures come back ​ Fluid replacement ​ Vasoactive support ​ Mouth care ○​ Teaching ​ Cause of sepsis ​ Teach women how to wipe properly ​ Handwashing ​ Allow family visitation ○​ Evaluating care outcomes ​ Satisfactory BP ​ Satisfactory cardiac output ​ Tissue perfusion ​ S/S of MODS ○​ Respiratory failure/distress → ARDS ○​ → then renal failure → then liver dysfunction → then GI dysfunction ○​ Three or more systems are associated with an 80% to 90% mortality rate ○​ There can be a 100% mortality rate if the cardiovascular and neurological systems are involved Shock ​ Review stages of shock and symptoms ○​ Initial ​ Hypoxia due to decreased oxygen delivery (DO2) to cells d/t decreased perfusion ​ Clinical manifestations are subtle but cellular damage is occuring ​ Subtle heart rate changes ​ Decreased cardiac output ○​ Compensatory ​ Neural compensation ​ Endocrine compensation ​ Chemical compensation ​ Manifestations ​ Tachycardia ​ Tachypnea ​ Low but normal BP with narrow pulse pressure (normal is 40)  ​ Decreased urine output ○​ Progressive ​ Failure of compensatory mechanisms to maintain adequate blood pressure and fluid volume ​ Extensive shunting of blood to vital organs ​ Manifestations ​ Profound hypotension ​ Worsening metabolic acidosis (lactic acidosis) ​ Respiratory acidosis ​ Electrolyte imbalance ○​ Refractory ​ Prolonged inadequate blood supply to cells ​ Cell death ​ Multisystem organ failure ​ Irreversible! ​ Review the different types of shock, know the differences (such as patho, symptoms) between them/Causes of each type of shock/Treatment options for each type of shock/Nursing management for each type of shock/Labs to monitor/Review hemodynamic findings for each type of shock ○​ Hypovolemic shock ​ Patho ​ Acute loss of volume ○​ Blood or fluid ​ Decreased venous return ​ Decreased stroke volume and cardiac output ​ Decreased tissue perfusion ○​ Kidneys → RAAS ​ Symptoms ​ Restlessness or confusion dt/ decreased O2 ​ Decreased urine output d/t decreased perfusion to kidneys ​ Pale, cool, clammy skin ​ Weak pulses ​ Delayed cap refill ​ Hyperventilation → respiratory alkalosis ○​ Trying to retain O2 and blow out CO2 ​ Hypoactive bowel sounds ○​ Shunting blood away to vital organs ​ Hyperglycemia d/t increased cortisol/stress ​ Causes ​ Acute blood loss ○​ Trauma, GI bleed ​ Rapid fluid loss ○​ Vomiting, diarrhea, burns ​ Treatment options  ​ Optimize oxygenation ​ Fluid resuscitation (NS or LR) ​ Identify and treat underlying cause ○​ Fluid ○​ Blood products ​ Nursing management ​ Assessment and analysis ○​ Varies depending on stage of shock ​ Progressive ​ Hypotension ​ Tachycardia ​ Weak pulses ​ Tachypnea ○​ Neurological status ○​ Vital signs ○​ Hemodynamic readings ○​ Urine output ○​ Skin color and temp ​ Actions ○​ Optimize oxygenation ○​ Prepare for intubation ○​ IV access ○​ Fluid replacement ​ LR not good for people with liver conditions ​ Teaching ○​ Cause of hypovolemia ○​ Allow visitation ​ Evaluating care outcome ○​ BP ○​ Filling pressures ○​ Venous O2 saturation ○​ LOC ○​ Urine output increased ○​ Lactate decreased ​ Labs to monitor ​ ABGs ​ Venous oxygen saturation ​ Hemoglobin and hematocrit ​ Metabolic profile ​ Lactate ​ Hemodynamic findings?? ○​ Cardiogenic shock ​ Patho ​ → myocardial injury→ decreased myocardial contractility  ​ → decreased cardiac output → hypotension → increased filling volumes ​ → compensatory mechanisms increasing vasoconstriction and fluid retention increasing myocardial workload → increased myocardial oxygen demand → decreased myocardial oxygen supply → ​ Symptoms ​ Chest pain ​ Diaphoresis ​ Nausea/vomiting ​ Decreased cardiac output ○​ Hypotension ○​ Decreased LOC ○​ Decreased urine output ​ KIDNEYS go first ​ Creatinine is the most accurate for kidney dysfunction ○​ Weak pulses ○​ Cool skin ○​ Hypoactive bowel sounds ​ Metabolic acidosis ​ Elevated CVP d/t blood going backward toward right d/t weak forward flow ​ VO2 sat will be down ​ Pulmonary pressure down ​ Causes ​ ​ End stage HF ​ Cardiomyopathy ​ Hypertension ​ Diabetes ​ Multivessel disease ​ Acute vascular disease ​ AKA myocardial injury and decreased myocardial contractility ​ Treatment options ​ ECG, cardiac enzymes, chest X-ray ​ Airway/oxygenation ​ Emergency revascularization, mechanical circulatory support ​ Vasopressors, inotropes ○​ Levophed, norepi, dobutamine ​ → monitor pulse with these ​ Nursing management ​ Assessment and analysis ○​ Decreased cardiac output ○​ Impaired tissue perfusion ​ Normal skin = pink and warm ○​ Neurological status  ○​ Vital signs ○​ Hemodynamic parameters ○​ Breath sounds ○​ Urine output ○​ Skin color and temp ​ Actions ○​ Oxygenation ​ Non-rebreather ○​ Prepare for intubation ○​ Administer medications as ordered ○​ Administer fluids ​ But be cautious of fluid overload / assess lung sounds ○​ Restrict activity ​ Don’t want to overwork heart ​ Teaching ○​ Rest periods ○​ Causes of cardiogenic shock and MI ​ Evaluating care outcomes ○​ Adequate cardiac output ○​ Adequate BP ○​ Adequate tissue perfusion ​ Labs to monitor ​ ABGs ​ Venous O2 saturation ​ Metabolic profile ​ Lactate ​ Hemodynamic findings? ○​ Obstructive shock ​ Patho ​ Mechanical barrier to ventricular filling or emptying ○​ Pulmonary embolism, tension pneumothorax, pericardial tamponade ​ Decreased cardiac output ​ Impaired tissue perfusion ​ Symptoms ​ Decreased LOC ​ Decreased urine output ​ Poor pulses ​ Pale, cool skin ​ Decreased bowel sounds ​ Chest pain ​ Nausea vomiting ​ Shortness of breath ​ CVP isn’t a good indicator here because it depends on the cause  ​ Causes ​ Extracardiac disorders that impair ventricular filling ○​ Acute PE ​ Impaired cardiac emptying ○​ Cardiac tamponade ○​ Tension pneumothorax ​ Heart itself is fine but there’s something else going on that’s preventing it from filling and/or pumping correctly ​ Treatment options ​ Treat cause ○​ Diminished lung sounds → pneumothorax ○​ Muffled heart sounds → cardiac tamponade ​ Supplemental oxygen ​ Vasoactive infusion ​ Nursing management ​ Assessment and analysis ○​ Decrease in cardiac output ○​ Impaired tissue perfusion ○​ Neurological status ○​ Vital signs ​ Usually hypotension and tachycardia ○​ Hemodynamic parameters ○​ Urine output ○​ Skin color and temp ​ Actions ○​ Supplemental oxygen ○​ Prepare for intubation ○​ Administer medications as ordered ○​ Prepare for definitive treatment of cause ​ Teaching ○​ Causes of PE/DVT ○​ Anticoagulation teaching ​ Evaluating care outcomes ○​ Adequate blood pressure ○​ Adequate cardiac output ○​ Adequate tissue perfusion ​ Labs to monitor ​ ABGs ​ Venous oxygen ​ Hemodynamic findings ○​ Distributive shock – neurogenic shock ​ Patho ​ Sympathetic nervous system disruption ○​ Decreased vascular tone  ○​ Increased peripheral vascular volume ○​ Decreased venous return ○​ Decreased cardiac output → relative hypovolemia ○​ Unopposed parasympathetic activity → profound bradycardia!!! ​ Neurogenic = bradycardia ○​ Systemic hypoperfusion ​ Symptoms ​ Warm, dry skin ​ Flushed appearance ​ Decreased cardiac output ​ Decreased systemic vascular resistance ​ CVP is low ​ Causes ​ Cervical spine injury ​ Any factor that stimulates parasympathetic activity or inhibits sympathetic activity of vascular smooth muscles can cause neurogenic shock, which results in widespread and massive vasodilation ​ Spinal cord injury above T5 ​ Spinal anesthesia ​ Vasomotor center depression (e.g. severe pain, drugs, hypoglycemia) ​ Treatment options ​ Treat cause ​ Fluid resuscitation ​ Vasoactive medications ○​ Epi/norepi ○​ Levophed ○​ Dobutamine ○​ Atropine ​ Atropine ​ Transcutaneous or transvenous pacing ​ Ventilatory support ​ Nursing management ​ Assessment and analysis ○​ Decreased cardiac output ○​ Bradycardia ○​ Vital signs ​ Hypotension and bradycardia ○​ Hemodynamic parameters ○​ Respiratory rate and SpO2 ​ Actions ○​ Administer IV fluids as ordered ○​ Administer IV meds as ordered ○​ Prepare for pacing  ○​ Raise head of bed slowly d/t risk of orthostatic hypotension ○​ Apply venous thromboembolism prophylaxis ​ Teaching ○​ Anticipated impact of spinal cord injury ○​ Multi-disciplinary psychosocial support ​ Evaluating care outcomes ○​ Normal heart rate ○​ Stable blood pressure ○​ Adequate cardiac output ​ Labs to monitor ​ ?? ​ Hemodynamic findings ​ Decreased systemic vascular resistance ​ Preload = low ​ CVP is low ○​ Distributive shock – anaphylaxis ​ Patho ​ Hypersensitivity reaction ​ Histamine release ​ Widespread venous dilation ​ Increased capillary permeability ​ Smooth muscle contraction ​ Symptoms ​ Shortness of breath → airway closes ​ Tachypnea ​ Wheezing ​ Stridor ​ Cyanosis ​ Confusion ​ Urticaria (hives) ​ Hemodynamic changes ○​ Low CVP ​ Causes ​ Hypersensitivity/allergic reaction ​ Treatment options ​ Removal of trigger ​ Intramuscular epinephrine ​ Maintain patent airway ○​ O2, non rebreather ○​ Albuterol ​ Circulatory support ○​ Antihistamines ○​ Steroids ​ Nursing management  ​ Assessment and analysis ○​ Respiratory distress ○​ Circulatory collapse ○​ Skin reactions ○​ Vital signs ​ Hypotensive, tachycardia, increased RR ○​ Hemodynamic parameters ○​ Respiratory ​ Stridor, SOB, decreased O2 ○​ Skin/peripheral perfusion ​ Actions ○​ Remove trigger immediately ○​ Administer IM epi ○​ Maintain oxygenation ○​ Establish IV access ○​ Administer meds as ordered ​ Teaching ○​ Avoidance of triggers ○​ EpiPen administration ​ Evaluating care outcomes ○​ Resolution of wheezing and shortness of breath ○​ Resolution of skin reactions ​ Labs to monitor ​ ?? ​ Hemodynamic findings ​ Low CVP ○​ Septic shock ​ See above ​ Causes ​ Bacterial infection enters bloodstream ○​ UTI, pneumonia, wound, etc Hemodynamics ​ Understand what information can be gathered from the various central lines ○​ Pulmonary catheter ​ Pulmonary artery pressures ​ Normal parameters are pulmonary artery (PA) ​ Systolic 15-30 ​ Diastolic 4-12 ​ Pulmonary artery occlusion pressure or pulmonary artery wedge pressure (PAOP/PAWP) ​ To get read on the left side of the heart  ​ Obtained by inflating the balloon with a syringe included in the PA catheter kit and specifically designed for use with the balloon (1.5 mL of air) ​ Normal = 4-12 ​ Cardiac output can be measured ​ Thermodilution ○​ Central line ​ CVP = RA pressure ​ Measure of RV filling pressures and blood return from systemic circulation ​ Normal = 2-6 ​ Low CVP = low volume ​ Trauma, blood loss, etc ​ High CVP ​ Forward flow issues ○​ Ex: CHF ​ High intrathoracic pressure ○​ Tension pneumothorax, pulmonary hypertension, pericardial tamponade ​ Can use for infusions, blood draws, transvenous pacemaker insertion ○​ Arterial line ​ Continuous blood pressure monitoring ​ Real time data for patient on vasopressors ​ ABG samples ​ ZERO INFUSIONS THROUGH THIS LINE ​ General causes for when CVP, PA, PAOP are abnormally high/low (look at the chart) ○​ Central venous pressure (CVP) ​ Abnormal low ​ Hypovolemia or peripheral vasodilation ​ Abnormal high ​ Right HF, tension pneumothorax, pulmonary hypertension, or pericardial tamponade ○​ Pulmonary artery (PA) ​ Abnormal low ​ May be normal state or signs of hypovolemia and vasodilation ​ Abnormal high ​ Pulmonary hypertension, right HF ○​ Pulmonary artery occlusion pressure (PAOP) ​ Abnormal low ​ May be normal state or signs of hypovolemia and vasodilation ​ Pulmonary hypertension, cardiogenic shock, hypoxia, and acute respiratory distress syndrome ​ Nurse management/considerations of the central lines ○​ Central line  ​ Placed in internal jugular (IJ), subclavian (SC), or femoral vein ​ Tip at junction of SVC and RA ​ Removal ​ Place patient in Trendelenburg position or supine ○​ Avoid air embolism ​ Remove dressing, sutures ​ Ask patient to take a deep breath and hold their breath ​ Remove catheter ​ Apply sterile gauze and hold pressure ​ Observe for bleeding, air embolism, infection ○​ Pulmonary catheter ​ Can be inserted through subclavian, internal, or external jugular, or femoral vein ​ How much do we fill the syringe to? ​ 1.5 ml of air ○​ Arterial line ​ Insertion ​ Can be placed on radial, ulnar, axillary, brachial, femoral, dorsalis pedis artery ​ Allen test needs to be performed ​ Gather materials ○​ A line kit ○​ Pressure bag with 500 ml NS ○​ Sterile gloves and gown ​ Removal ​ Suture removal kit, gauze, pressure tape ​ Pressure bag and transducer set up ​ Need to zero A line with every shift ​ Major changes in position Myocardial infarction ​ Pathophysiology ○​ Destruction of heart muscle from lack of oxygenated blood supply ○​ Most common cause = atherosclerosis ○​ Plaque in artery → rupture of plaque → thrombus formation → obstruction of blood flow ○​ Progression ​ Coronary artery disease (CAD) ​ Acute coronary syndrome ​ Angina– stable – relieved with rest ​ Angina– unstable – unrelieved ​ MI ​ Diagnostic tests: imaging, labs ○​ Lab tests ​ Troponin ​ Best blood test!!!  ​ CK ​ Tells us if there’s muscle damage in body but could be anywhere ​ CK-MB ​ Specific to heart ​ Elevated within 3 hours and stays elevated for ~36 hours ○​ Diagnostic testing ​ EKG ​ Gold standard! ​ Look for ST elevation or other abnormalities ​ 12 lead → can tell us where ​ Stress test ​ ECHO (ultrasound) ​ Coronary angiography (cath lab) ​ Treatment options: pharmacological, reperfusion therapy, CABG (Know the differences between each treatment and the nursing management for each treatment) ○​ Priority = remove the clot ○​ Medical management– treatment ​ Increase blood flow to cardiac tissue, or reperfusion therapy ​ Maximize oxygenation ​ Control pain ​ Dilate coronary arteries ​ Prevent clots ​ Decrease myocardial workload ○​ Medical management– medications ​ Oxygen ​ Nitroglycerin ​ Aspirin ​ Pain medication ​ Antiplatelets and antithrombolytics are the main focus ​ ASA, Heparin, LMHW, Plavix ○​ Reperfusion therapy ​ Percutaneous coronary intervention ​ Fibrinolytics ○​ Surgical management ​ Coronary artery bypass graft (CABG) ​ Revascularization intervention that bypasses blockages in the coronary arteries causing the myocardial muscle damage ○​ Not the first line since in acute phase ○​ May be needed for complications of MI ​ ICU after ​ Nursing management post CABG– assessment ​ HR and BP ​ Hemodynamic monitoring ​ Continuous cardiac monitoring  ​ Heart tones ○​ Muffled = cardiac tamponade ○​ S3 or crackles = HF ​ Breath sounds and O2 sat ​ Core temperature ​ LOC, pupils, responsiveness ​ I&Os ​ Skin color and temp, pulses, edema, and cap refill ​ Chest tube output, color, and volume ​ Labs ○​ Troponin, H&H, electrolytes, kidney function ​ Incisions and signs of infection ​ Nursing management post CABG– actions ​ BP ○​ ICU with A-line ​ Administer fluids and medications as ordered ​ Rewarm patient slowly ○​ Too fast can cause arrhythmias ​ Administer pain meds and continuous sedation meds ​ Pulmonary hygiene ○​ Wash their mouths ​ Early mobility and ambulation ​ Wound care ​ Nursing interventions– teaching post CABG ​ Signs of infection ○​ Red, warm, drainage ​ Sternal precautions ​ Cardiac rehabilitation ​ No heavy lifting → lie flat ​ No baths ○​ Shower ok (don’t soak) ​ Teaching post MI ○​ Report s/s of MI ○​ Medication education ○​ American Heart association “life’s simple 7” ○​ DRESS ​ Diet ​ Low sodium and fluids (2g/2L per day) ​ Report new rapid weight gain ​ Reduce stress, alcohol, caffeine, cholesterol ​ Exercise (30 min x 5 days/week) ​ Smoking cessation ​ Sex (2 flights of stairs with no SOB) ○​ Teaching post CABG  ​ Signs of infection ​ Sternal precautions ​ Cardiac rehabilitation Cardiomyopathy ​ Review the various types of cardiomyopathy and clinical manifestations ○​ Something wrong with structure of heart ​ Dilated ​ S3 murmur ​ Cardiomegaly ​ Hypertrophic ​ Typically asymptomatic (no s/s) until heavy exercise and then child dies ​ Restrictive ​ Same general low O2 and HF ○​ Patho ​ Structural changes to heart ​ Weak ​ Enlarged ​ Thick or rigid ​ Decreased function in heart muscle ○​ Clinical manifestations ​ Combo of angina and HF symptoms ​ Chest pain ​ Dizziness ​ Indigestion ​ Nausea ​ Vomiting ​ Sweating ​ Palpitations ​ SOB ​ Fatigue ​ Edema ​ Be familiar with medications and their indications for cardiomyopathy ○​ GOAL: ​ Treat clinical manifestations ​ Prevent worsening of function ​ Reduce complications ○​ ACE inhibitors → RAAS system ○​ ARBS → RAAS system ○​ Beta blockers ​ Reduce workload of heart ○​ Calcium channel blockers ​ Reduce afterload ○​ Sodium-glucose cotransporter-2 inhibitors (SGLT2Is) ​ Excretion of sugar through urine  ○​ Mineralocorticoid receptor antagonists ○​ Diuretics ​ Monitor potassium ○​ Digoxin ○​ ABCDD ​ Ace inhibitors ​ Beta blockers ​ Calcium channel blockers ​ Digoxin ​ Diuretics EKGs ​ Be able to interpret rhythm strips ○​ One small box = 0.04 seconds ○​ One large box = 0.2 seconds ○​ ​ Be familiar with interval ranges ○​ PR interval ​ Normal = 0.12-0.20 seconds (3-5 small boxes) ​ You can count the number of small boxes between P wave and QRS then multiply this number by 0.04 seconds ○​ QRS interval ​ ​ Normal = 0.06-0.12 seconds (1.5-3 small boxes) ​ You can count the number of small boxes between the start and end of the QRS complex then multiply this number by 0.04 seconds ○​ QT interval ​ Normal QT interval is 0.36-0.44 seconds (9-11 small boxes) ​ You can count the number of small boxes between the QRS complex and end of the T wave and multiply this number by 0.04 seconds ○​ Look at the ST segments to evaluate for an elevation or depression ○​ If the ST segment is displaced from the isoelectric line → note the number of mm the deviation is from this line