Test 3 AD PDF Past Paper

Exam 3 Study Guide ACNP 805 Questions: 50 | Modules Tested: 4, 5, 6, 8, 9, 10, 11 | Test Time: 1.5 hours Blueprint Information that can be obtained from an ultrasound in critical care. Intraosseous catheter. (Placement/indications/contraindications/medication administration) Arterial lines. (Proce...

Exam 3 Study Guide ACNP 805 Questions: 50 | Modules Tested: 4, 5, 6, 8, 9, 10, 11 | Test Time: 1.5 hours Blueprint Information that can be obtained from an ultrasound in critical care. Intraosseous catheter. (Placement/indications/contraindications/medication administration) Arterial lines. (Procedure/indications/contraindications/normal and abnormal tracings) Central lines. (Procedures/indications/contraindications/management of central lines) Swan Ganz. (Indications/contraindication/normal readings/waveform) Shock. (All shocks states/pathology/parameters/diagnostics/management) Sepsis. Oxygenation and tissue perfusion. (Normal and abnormal oxygenation values) Central venous pressure and relationship to EKG events. Preload and afterload. (Measuring/normal values) Hyperthyroidism and hypothyroidism. (Labs/diagnostics/management) Diabetes Mellitus Type I and II. (Labs/diagnostics/management) Lightening and electrical injury types. (Labs/diagnostics/management) Hyperthermia and hypothermia. (Labs/diagnostics/management) Nurse Practitioner staffing models. Define standard of care. AACN standards for healthy workplace. Communication and “Are You Listening?” concepts. Ultrasounds History of Ultrasounds -In 1991, American College of Emergency Physicians (ACEP) Board of Directors adopted a policy recognizing the need for emergency ultrasound imaging on a 24-hour basis and the policy was endorsed by the Society for Academic Emergency Medicine -POCUS = point-of-care ultrasound; purposed to improve: 1. Patient outcomes 2. Focus and goal oriented 3. Easily recognizable findings 4. Easily learned 5. Quickly performed at bedside Ultrasound Overview -An ultrasound is a technique that uses sound waves to study and treat hard to reach body areas -High frequency sound waves are transmitted to the area of interest and the returning echoes are recorded -Goal: to answer a focused clinical question in a timely manner Reflected Echoes • • • Hyperechoic – diaphragm, tendons, bone o Strong reflections = white dots Isoechoic – solid organs, thick fluid o Weaker reflections = grey dots Hypoechoic (Echofree) – fluid within a cyst, urine, blood o No reflections = black dots Indications for Ultrasound • Basic Critical Care Applications: o Cardiac: cardiac motion, pericardial effusion o Lung: pneumothorax, pleural effusion o Biliary: gall bladder wall thickness, gall stones, cholecystitis, common bile duct dilation o Renal: hydronephrosis o Abdominal aorta: abdominal aorta enlargement o Trauma: hemopericardium, hemoperitoneum, intra-uterine pregnancy • Advanced Critical Care Applications: o Cardiac: acute ischemic heart disease o Trauma: hemothorax, pneumothorax o Gynecologic: ovarian torsion, ovarian mass o Thoracic: DVT o Testicular: testicular torsion, epididymitis, hydrocele o Musculoskeletal: fractures, soft tissue pathology, joint effusions o Orbital: retinal detachment, elevated ICP Ultrasound Findings Information Cardiac Ultrasound • • • • • • Pulseless electrical activity Effusions Left ventricular systolic function Left atrium or aortic root dilation Right ventricular function Intravascular volume • • • • • Preload assessment Mitral valve function Pericardial effusion Pericarditis Cardiac tamponade • • • • Uterine fibroid Ovarian cyst Ovary torsion Hydatidiform mole OBGYN Ultrasound • • • • Suspected ectopic pregnancy Threatened abortion Evaluation of fetal viability Misplaced intrauterine device 1 Exam 3 Study Guide ACNP 805 Abdominal Ultrasound • • • • • • Cholecystitis Gall stones Common bile duct Liver assessment (includes abnormalities) Hepatic tumors or cysts Pancreas assessment (includes abnormalities) • • • • • Splenic contusion Ascites Renal abscess Kidney stone Hemorrhage • Bladder evaluation (includes abnormalities) o Hydronephrosis Testicular mass or possible torsion o Varicoceles, hydroceles, spermatoceles Urinary Tract Ultrasound • • • • Obstructive uropathy Renal colic Hematuria Renal abscess • Bladder Ultrasound • • Bladder volume Bladder trauma Aortic Ultrasound • • Aortic aneurysms (includes AAA) Intraperitoneal fluid Thoracic Ultrasound • • • Pneumothorax Thoracic trauma Airway confirmation of ET tube placement • • • Hemothorax Pericardial tamponade Suspected DVT • • • Thyroid mass Breast mass Pericardiocentesis Musculoskeletal/Soft Tissue Ultrasound • • Subcutaneous foreign bodies Fractures Procedural Ultrasound • • • Insertion of central line Arterial puncture and cannulation Lumbar puncture FAST Exam -Bedside ultrasonographic protocol designed to detect peritoneal fluid, pericardial fluids, pneumothorax, and/or hemothorax in a trauma patient -Visualizes 4 areas: (1) pericardial (2) perihepatic (3) perisplenic (4) pelvic Indications for FAST Exam -Evaluation of injury, hypotension, and/or shock of unknown etiology in a trauma patient to determine need for interventions -Evaluation of unexplained hypotension or shock in the non-trauma patient -Identification of ruptured ectopic pregnancy The BLUE Protocol 2 Exam 3 Study Guide ACNP 805 Intraosseous Catheter Indications for IO Access • • • • Unable to obtain venous or delayed venous access Immediate vascular access during circulatory collapse Blood for laboratory analysis or point of care testing Access for contrast injection for radiologic evaluation Contraindications of IO Catheters • • • • Proximal ipsilateral fracture Ipsilateral vascular injury Severe osteoporosis Osteogenesis imperfecta Complications of IO Catheters • • • • • Cellulitis Osteomyelitis Iatrogenic fracture Physeal plate injury Fat embolism Placement for IO Access • Supplies: o Aspiration needle o Specialized IO infusion needle o IO drill device • Placement: o Children: 2 finger-widths (2cm) below the tibial tuberosity on the medial, flat surface of the proximal tibia o Adults: medial malleolus, distal femur, sternum, humerus, ileum -Avoid the tibia in adults because it is thick and difficult to penetrate • Technique: 1. Prepare site using sterile fashion 2. Infiltrate procedure area with 1%-2% lidocaine to anesthetize the skin and periosteum if the patient is conscious 3. Support and stabilize procedural area with the nondominant hand 4. Grasp the needle in the palm on the dominant hand 5. Direct the needle perpendicular to the bone and away from the joint space 6. Twist and apply constant pressure until resistance if abruptly decreased and the marrow cavity is breached 7. Remove the stylet 8. Confirm placement by either aspiration or continuous infusion 9. Observe for signs of extravasation 10. Secure the IO needle with gauze and a bulky dressing 11. Confirm placement and exclude iatrogenic fracture with a radiograph after stabilizing the patient Pharmacokinetics After IO Access -Each drug administration should be flush with 10mL of fluid to rule out drug persistence in the medullar cavity • Key Drugs Usable with IO Access: Adenosine Amiodarone Atropine Cisatracurium Dobutamine Dopamine Epinephrine Etomidate Heparin Insulin Lidocaine Morphine Norepinephrine Propofol Blood products (i.e., RBC, platelets, FFP) Resuscitation fluids (i.e., crystalloids, colloids) Techniques for IO Access -Bone marrow samples can be obtained from an IO -When administering IO adenosine, ideal placement is as close to the heart as possible -An IO site that is in place for more than 24 hours is at an increased risk for osteomyelitis and another route should be used -Do not ever let go of the guidewire during insertion (increases risk for infection) Arterial Lines Indication for Arterial Lines • • Difficulty obtaining or risk of inaccurate blood pressure cuff in critically ill patients Need for continuous monitoring of arterial blood pressure (i.e., shock, increased SVR, hemodynamically unstable, major surgery, vasopressor/vasodilator medications) 3 Exam 3 Study Guide • • • • ACNP 805 Labile or accelerated hypertension and evidence of progressive vascular damage Confirm acid-base balance, hypoxia, or hypercapnia MAP maintenance at a specific level Continuous access to arterial blood Contraindications for Arterial Lines • Absolute: o Inadequate collateral blood flow distal to where the arterial line will be placed o Significant injury to the same extremity (especially if distal perfusion is compromised) o Hypercoagulable states • Relative: o o o o Severe atherosclerotic or vasospastic arterial disease Local skin compromise (i.e., trauma, infection, burn, severe dermatitis) Anticoagulation from bleeding disorders, anticoagulation therapy, or thrombolytic therapy Synthetic vascular graft Procedures for Placing an Arterial Line • Placement Sites: o Radial – nondominant side is preferred because of proximity to skin surface o Femoral – best for hypotension or ongoing CPR o Brachial – reserved for use if radial artery insertion is contraindicated o Dorsalis pedis o Superficial temporal arteries • Procedural Positioning: o Radial: dorsiflex supine wrist (30 degrees) and externally rotate nondominant hand, with insertion site .5-1in proximal to wrist crease o Femoral: legs straight, externally rotated, with insertion site 1-1.5in distal to inguinal ligament at inguinal crease o Brachial: hyperextend and supinate the arm with the elbow on a rolled towel, with insertion above the elbow crease and proximal to the AC • Modified Allen Test 1. Hold the patient’s hand at the level of the heart and have them open and close the hand multiple times 2. Have the patient make a fist and the clinician will compress the radial and ulnar arteries 3. After 1 minute, lower the hand below the level of the heart and have the patient unclench the fist 4. A positive test indicates color that rapidly returns to the hand Techniques for Atrial Line Placement -Dorsalis pedis must be occluded with compression of the great toenail for several minutes, and observe for flushing upon release of pressure -Location in the artery is confirmed with a blood flash in the needle -If unable to cannulate after blood flash, remove the needle completely and slowly -After 3 unsuccessful cannulation attempts in an artery, discontinue attempts at current site and select a new site Normal and Abnormal Tracings -A 5-20mmHg discrepancy between the cuff and intra-arterial pressure is normal and expected -Improper cuff size, calibration, or transducer zeroing can result in intra-arterial pressure that is higher than the cuff pressure -Dampening of arterial waveform suggests issue with intra-arterial measurement (i.e., air bubbles or blood in transducer line, clot, mechanical occlusion, loose/open connections) • Pressure Discrepancies: o 20-30mmHg: severe vasoconstriction (i.e., shock, hypothermia) cause auscultated pressure to be lower o > 30mmHg: resonance in the system o Directly measured pressure: can be significantly higher than cuff pressure when a single-end-hole catheter is used in a narrow artery with high flow -If hole faces towards the flow, direct BP may be falsely elevated • Wave Form: o Normal peripheral artery waveform will display peak systolic pressure after the QRS complex o Dicrotic notch = closure of the aortic valve -Patients with arteriosclerotic diseases will have a waveform that is steeper in ascend and descend, displaying a shorter duration and less defined notch 4 Exam 3 Study Guide ACNP 805 Central Lines Indications for Central Lines • • • • • • • • • • • • Venous access in patients who are so obese or debilitated that their peripheral veins are not accessible for IV cannulation Emergency venous access after cardiac arrest Administration of cardiac medications during CPR Large-volume parenteral fluid administration when peripheral IV cannulation is not readily obtainable CVP monitoring Administration of certain chemotherapeutic agents Administration of vasopressors Administration of hyperosmolar or other irritating solutions that have the potential to cause thrombophlebitis or soft tissue necrosis Patients with significant burns on peripheral areas that may prevent placement of a peripheral catheter Placement of a Swan-Ganz catheter Placement of a temporary transvenous pacemaker wire Performance of hemodialysis or plasmapheresis Contraindications for Central Lines • • Absolute: o Dependent on the patient’s overall condition, urgency of need, and alternatives available o Patient refusal o Combative or agitated patient o Distortion of local anatomy or landmarks unless ultrasound guidance is available o Superior vena cava syndrome o Cellulitis over the proposed insertion site o Pneumothorax or hemothorax on the contralateral side or inability to tolerate a pneumothorax on the ipsilateral side o Trauma to the proposed insertion site Relative: o o o o o o o o o Suspected injury to proposed vein Morbid obesity Marked cachexia Full-thickness burn Vasculitis that predisposes to sclerosis or thrombosis of veins Prior injection of a sclerosing agent into the proposed vein Previous long-term central catheterization or recently discontinued central catheter in proposed vein Proposed mastectomy on same side of subclavian vein access Patients receiving ventilatory support with high end-expiratory pressure o o o o o o o o o o o o o o o o Venous thrombosis of the proposed vein Avoid internal jugular location if cervical spine fracture, penetrating neck injury, or C-collar in place Avoid femoral vein if known or suspected intraabdominal hemorrhage Allergy to any component of the catheter such as latex or medication impregnated catheters Cardiac-paced patient Highly unstable arrhythmias Right-sided endocarditis or mural thrombus Patients undergoing CPR Children younger than 2 y/o Severe hypovolemia Bleeding diathesis or excessive anticoagulation and a noncompressible vessels Prosthetic right heart valve Avoid internal jugular or subclavian vein locations if patient is unable to lie in Trendelenburg position Left bundle branch block Avoid internal jugular location if known severe carotid artery stenosis or atherosclerosis on the desired side Personnel capable of handling complications not immediately available Procedures for Central Line Placement Subclavian (Left or Right) • • Position: flat or with head slightly town (Trendelenburg) in the center or turned to the opposite side -A towel roll along the patient’s spine can help maintain position Insertion: 1cm lateral to the clavicular head or sternocleidomastoid muscle and 1cm above the superior border of the clavicle o Aim slightly underneath the clavicle in the direction of the contralateral nipple Right Internal Jugular Vein • • Position: Trendelenburg Insertion: percutaneous entry at the apex of the triangle formed by the 2 heads of the sternocleidomastoid muscle and the clavicle o Aim slightly lateral toward the ipsilateral nipple at a 45-degree angle Left Internal Jugular Vein -Not commonly used due to the excessive complications that can occur -Complications include: inadvertent left brachiocephalic vein and superior vena cava puncture with intravascular wires, catheters, and sheaths, or laceration of the thoracic duct with chylothorax External Jugular Vein • • Position: Trendelenburg with the head turned away from the side of insertion -Must have patient perform Valsalva maneuver or gently occlude the vein near its insertion into the subclavian vein to help engorge the vein Insertion: midpoint of the subclavian vein Femoral Vein • • Position: supine Insertion: below the femoral crease Techniques for Central Line Placement -The preferred veins are on the right side of the patient because right-sided veins have a more direct course to the right atrium and can be utilized for placement of a pacemaker wire of Swan-Ganz catheter -Performing the Valsalva maneuver or having the patient hum while attempting IJ cannulation will increase the vessel by 30-40%, and thereby increases the likelihood of success -Subclavian access is preferred for patients with blood dyscrasias or coagulopathy issues -The rate of complications during CVC insertion or maintenance is greater than 15% because at least one complication (i.e., hematoma, thrombosis, CLABSI) typically occurs 5 Exam 3 Study Guide ACNP 805 Management of Central Lines Five Components of Care 1. 2. 3. 4. 5. Hand hygiene Maximal barrier precautions Chlorhexidine skin antiseptic Optimal catheter site selection with avoidance of using the femoral vein for central venous access in adult patients Daily review of central line necessity with prompt removal of unnecessary lines Hand Hygiene -Before and after palpating catheter insertion sites -Before and after inserting, replacing, accessing, repairing, or dressing -When hands are visibly soiled or contaminated -Before and after invasive procedures, and before donning and after removing gloves -Between patients -After using the bathroom Maximum Barrier Precautions -Strict compliance with hand hygiene, wearing a cap, mask, and a sterile gown and gloves -Cover the patient from head to toe with a sterile drape and a small opening for the procedural site Chlorhexidine Skin Antiseptic -Prepare skin with chlorhexidine 2% in 70% isopropyl alcohol -Scrub back and forth for at least 30 seconds and do not wipe or blow -Allow time (2 minutes) for antiseptic solution to completely dry before entering the procedural site Optimal Catheter Site Selection -Subclavian: lowest risk for infection -Femoral: highest risk for infection Daily Review of Central Line Necessity -Include daily review as a part of interdisciplinary rounds and state the line day to remind how long the line has been in place -Define appropriate time frame for regular, weekly reviews when central lines will be used long-term Swan Ganz Swan Ganz Catheters -Generates data on CO, PAWP, SVR, stroke work index, and mixed venous oxygenation Indications for Swan Ganz Catheter • • • • • • • • • • Refractory acute respiratory distress syndrome or pulmonary edema (especially in patients with renal failure) Severe hypoxemia requiring high levels of PEEP (> 10) Presence of hemodynamic deterioration due to mechanical complications ECHO evaluation of left ventricular function is not available Diagnose or manage cardiac tamponade Oxygen delivery and consumption assessment Evaluation of drug titration for severe pulmonary hypertension Unable to transport the patient for further diagnostic testing Sensitive monitoring (i.e., refractory heart failure, refractory sepsis, fluid management, right sided heart failure from ARDS or PE) Therapeutic monitoring (i.e., pacing, aspiration of air emboli during sedated neurosurgery) Contraindications for Swan Ganz Catheter • • • • • • Diagnostic information can be provided by a less invasive technique Prosthetic right heart valve Cardiac-paced patient Severe hypotension or known pulmonary hypertension Highly unstable arrhythmias Lack of nursing staff or clinicians trained in use, and compatible monitoring devices Normal Readings and Waveform • Swan Ganz Catheter Readings and Respective Clinical Relevance: Parameter Normal Values Central Venous Pressure (CVP) 0-6mmHg Right Ventricular Pressure (RVP) 20-30mmHg or 0-6mmHg Pulmonary Artery Pressure (PAP) 20-30mmHg or 6-10mmHg Pulmonary Artery Wedge Pressure (PAWP) 4-12mmHg Stroke Volume (SV) 60-80mL/beat Cardiac Output (CO) Stroke Volume Index (SVI) Cardiac Index (CI) Pulmonary Vascular Resistance (PVR) Systemic Vascular Resistance (SVR) Right Ventricular Stroke Work (RVSW) Left Ventricular Stroke Work (LVSW) 4-8L/min 33-47mL/beat/m2 2.5-4L/min/m2 20-120dynes/sec/cm5 770-1,500dynes/sec/cm5 10-15g-m/beat 60-80g-m/beat Clinical Relevance Determines volume status and RV function; correlates with RVEDP Determines RV function and volume Determines state of resistance in pulmonary vasculature and RV function Determines LV function; correlates with LVEDP Amount of blood ejected during systole; decreased SV indicated ventricular dysfunction Described blood flow through tissues; reflects adequacy of overall cardiac function SV adjusted for patient’s BSA CO adjusted for patient’s BSA Describes state of resistance in pulmonary vasculature Describes state of resistance in systemic vasculature Defines how hard right ventricle is working to pump blood Defines how hard left ventricle is working to pump blood 6 Exam 3 Study Guide Mixed Venous Oxygenation (SVO2) • ACNP 805 60-80% Index of oxygenation status that measures the relationship between O2 delivery and O2 demand; reflects cardiovascular tissue perfusion Waveform: Shock and Sepsis Overview of Shock -Defined as an acute syndrome of organ and system dysfunction precipitated by failure of circulation to meet metabolic needs; inadequate distributed tissue perfusion that results in generalized hypoxia -Can develop within minutes or hours and rapidly progress to organ failure and death General Etiology • • Primary physiologic disturbances that impair cellular function and cause tissue hypoxemia due to decreased oxygen delivery and/or increased consumption and/or inadequate oxygen utilization In shock states, oxygen consumption is greater than oxygen delivery, resulting in cellular hypoxia, dysfunction, and death if not reversed in a timely manner o Reduced oxygen and nutrient supply à anaerobic metabolism à production of acid (lactic, pyruvic) à decreased ATP and energy o Activation of inflammatory response à release of proinflammatory cytokines (TNF, interleukin-1, 06), and endothelial vasodilating oxygen free radicals, protease, nitric oxide, and other inflammatory mediators Classifications of Shock 1. 2. 3. 4. Hypovolemic Cardiogenic Obstructive (extracardiac) Distributive a. Septic b. Neurogenic c. Anaphylactic Stages of Shock • • • Stage I = non-progressive stage; compensatory mechanisms sustain hemodynamics; no obvious signs or symptoms Stage II = progressive stage; compensatory mechanisms that maintain perfusion begin to fail and circulatory and metabolic derangements become more pronounced Stage III = irreversible stage; cardiac failure, presence of acidosis, inadequate cerebral flow, increase in blood clotting Laboratory Findings Associated with Shock Hyperglycemia • Early: increased BG • Late: decreased BG ABGs – hypoxemia, metabolic acidosis, worsening base deficits Total protein and albumin – decreased BUN and creatinine – increased Sodium • Early: increased • Late: increased or decreased Potassium • Early: decreased • Late: increased Chloride • Early: decreased • Late: increased Liver enzymes and bilirubin – initially increased and then decreases with cell death CPK – increased Amylase and lipase – increased Blood cultures – may be + in septic shock Hgb and Hct • Early: increased • Late: decreased WBC – increased Platelets – decreased PT/PTT – prolonged Urine osmolality and specific gravity – increased and then decreased due to inability to concentrate urine 7 Exam 3 Study Guide ACNP 805 Compensatory Mechanisms Associated with Shock • • • • CNS defects – SNS stimulation, increased HR and RR, and vasodilation Renal alterations – activation of RAAS Hormonal – ACTH release, enhanced glycogenesis, increased glucose, increased sodium and water reabsorption Chemical – decreased pulmonary blood flow, respiratory alkalosis, cerebral hypoxia and ischemia Universal Management of Shock 1. 2. 3. 4. 5. 6. 7. 8. Maintain airway and ventilation Hemodynamic monitoring Circulation goals Fluid therapy – crystalloid fluids (i.e., lactate, acetate, gluconate); use the least amount of fluid and lowest CVP to achieve end-organ perfusion (Goal CVP: 8-12mmHg) Correct acid-base imbalance Nutritional support Pharmacological treatment Surgical treatment (if necessary) Types of Shock Hypovolemic Shock -Defined as blood volume that is inadequate to maintain adequate perfusion; associated with a blood volume deficit of at least 15-20% (Normal total blood volume: 5L) • Etiology: o Hemorrhagic: § Traumatic: long bone fractures, solid organ injury (i.e., ruptured liver or spleen), lacerations (i.e., scalp, great vessels, peripheral arteries) § Non-traumatic: GI bleed, surgical site, hemorrhagic pancreatitis, vaginal o Non-hemorrhagic: § Impaired venous return caused by obstruction of the vena cava § GI losses (i.e., vomiting, diarrhea, poor oral intake, large NG tube aspirate, fistulas) § Renal losses (i.e., excessive diuresis) § Exudative lesions or burns § Excessive diaphoresis • Signs/Symptoms: increased HR, decreased BP/CVP/CO/CI/PAP/PAOP, postural or orthostatic hypotension, flat neck veins • Treatment: 1. Restore circulating volume 2. Fluid challenges – 500ml-1L bolus of crystalloids 3. Fluid replacement – blood products (consider coagulation factors) 4. Reversal of anticoagulants 5. Antifibrinolytic agents – crystalloids and colloids 6. Vasopressors 7. Military antishock trousers (MAST) – external counterpressure device that assists with major organ perfusion and splits fractures of the pelvis/long bones, and can tamponade a bleed 8. Tourniquets Cardiogenic Shock -Defined as impaired ability of the heart to pump effectively, resulting in decreased SV/CO and inadequate tissue perfusion • Etiology: AMI Arrhythmias CHF Myocardial contusion or any myocardial damage Dissecting aortic aneurysm Spontaneous damage to heart valves or valvular heart disease (i.e., acute mitral regurgitation, interventricular septum rupture, free wall rupture) Myocarditis End-stage cardiomyopathy Septic shock with severe myocardial depression • Risk Factors: elderly, female, acute or prior ischemic event associated with impaired EF, extensive infarct, proximal LAD coronary artery occlusion, anterior MI, and multivessel coronary artery disease • Signs/Symptoms: increased PAP/PAOP/SVR/CVP, decreased SV/CO/CI/PaO2, < 30% left EF, S3/S4, substernal chest pain, distended neck veins, peripheral edema, oliguria, cool or mottled skin • Diagnostic Testing: ECG ECHO CXR ABG Electrolytes, CBC Cardiac enzymes BNP • Treatment: 1. Fluid resuscitation – 250mL increments 2. Correct electrolyte imbalances 3. Pharmacologic treatment a. Inotropic agents – dobutamine, milrinone, epinephrine, dopamine 8 Exam 3 Study Guide 4. ACNP 805 b. Vasoactive agents – nitroprusside (afterload), nitroglycerin (preload) c. Vasopressors – vasopressin (first line), norepinephrine, dopamine, epinephrine, phenylephrine d. Diuretics Counter-pulsation – IABP Obstructive Shock -Defined as the obstruction of the flow in the cardiovascular circuit and is characterized by impairment of diastolic filling or excessive afterload • Etiology: o Direct venous obstruction: intrathoracic obstructive tumors, massive pulmonary embolism o Increased intrathoracic pressure: tension pneumothorax, high PEEP on ventilator o Decreased cardiac compliance: constrictive pericarditis, cardiac tamponade o Increased ventricle afterload: aortic dissection, pulmonary embolism, abdominal distention, constrictive pericarditis, acute pulmonary hypertension Distributive Shock -Defined as vasodilation and loss of vasomotor tone resulting in venous pooling of blood and decreased venous return -Includes septic, neurogenic, and anaphylactic shock • Septic Shock -Life threatening organ dysfunction cause by dysregulated host responses to infection o Risk Factors: malnutrition, instrumentation with catheters or invasive procedures, trauma, surgical wounds, advancing age, immunosuppressive therapy, neoplastic diseases, chronic diseases (i.e., DM, renal failure), extended hospital stays o Common Infection Sites: GU (most common cause of septic shock in elderly), respiratory tract, wounds, meninges, GI tract, invasive catheters § Gram (-) Causes: E. coli Klebsiella Enterobacter Proteus Pseudomonas § • Gram (+) Causes: Staphylococcus Streptococcus Clostridia Bacteroides o Diagnostic Testing: Leukocytosis Thrombocytopenia Procalcitonin C-reactive protein Lactic acid Blood cultures CXR Sputum gram stains with culture and sensitivity Urinalysis Wound cultures o Treatment: § Initial Resuscitation – 1 hour bundle: 1. Measure lactate level (remeasure if initial lactate > 2mmol/L) (Normal lactate level: 0.5-2.0mmol/L) 2. Blood cultures before starting antibiotics 3. Initiate broad spectrum antibiotics 4. Rapid infusion of 30ml/kg crystalloid for hypotension or lactate > 4mmol/L (typically more than 2L is needed) a. Caution must be used in large volume resuscitation with unwarmed fluids because of the risk for hypothermia and can lead to hypothermia-induced coagulopathy à warm fluids before administration to avoid this complication 5. Vasopressors for MAP < 65mmHg after fluid resuscitation o Pharmacological Treatment: § Antimicrobial – 1 hour bundle: 1. Give antibiotics within 1 hour of initial shock recognition 2. Maintain antibiotic therapy for 7-10 days 3. Hemodynamic support – norepinephrine (first line) Neurogenic Shock -Produced by a disturbance in the nervous system that causes massive vasodilation due to interruption in or loss of sympathetic innervation o Etiology: Injury or disease of the spinal cord or brain stem High levels of spinal anesthesia Vasomotor center depression Drugs that block sympathetic activity o Signs/Symptoms: hypotension, hypothermia, hyporeflexia, bradycardia, warm and dry skin, decreased SVR/SV/CVP o Treatment: 9 Exam 3 Study Guide ACNP 805 1. 2. 3. • Treat or remove cause Careful fluid administration Vasopressors – norepinephrine (first line), epinephrine (first line for ACLS) Anaphylactic Shock -Immediate hypersensitivity reaction with severe antibody or antigen response o Etiology: Foods – nuts, shellfish, fish Food additives Vaccines Diagnostic agents – contrast, iodine Blood products Environmental agents – pollen, latex Drugs – aspirin, barbiturates, muscle relaxants, sulfa Venom o Signs/Symptoms: hypotension, tachycardia, arrhythmias, bronchospasm, laryngeal edema, stridor, hypoxia, hoarseness, “lump in throat”, pruritis, erythema, urticaria, angioedema, restlessness, anxiety, decreased LOC, nausea, vomiting, diarrhea, decreased CO/CI/CVP/PAOP/SVR o Treatment: -Key to management is early recognition and quick treatment 1. Immediate IV, IM, or subQ epinephrine, 0.5-1mg (do not wait to establish IV access prior to administration) 2. Maintain airway 3. Antihistamine – diphenhydramine, 50mg, IV or PO 4. Consider H2 blockers – ranitidine, 50mg, IV 5. Albuterol for bronchospasm 6. Lactated ringers (to expand vascular volume) 7. Corticosteroids – Methylprednisone, 125-250mg, IV or hydrocortisone, 200mg, slow IV 8. Inotropic agents – dobutamine 9. Vasoconstrictor – norepinephrine (first line), epinephrine (first line for ACLS) Shock Tables Shock States Normal Values Cardiac Output (4-8L/min) Cardiac Index (2.5-4.5L/min/m2) Right Atrial Pressure (0-8mmHg) Pulmonary Artery Diastolic Pressure (6-12mmHg) Pulmonary Capillary Wedge Pressure (6-12mmHg) Systemic Vascular Resistance (800-1200dynes/sec/cm5) Mixed Venous Oxygenation (60-80%) Hypovolemic Low Cardiogenic Low Obstructive Low Septic High then low Distributive Neurogenic Low Anaphylactic Low Low Low Low High then low Low Low Low High High Low then high Low Low Low High High Low then high Low Low Low High Normal/reduced Low then high Low Low High High Low SVR, high PVR Low Low Low Low Low High High then low Low Low Causes of Shock States Hypovolemic Results from a loss of > 20% circulating blood volume related to internal or external bleeding, burns, DKA, HHSS, and severe dehydration Cardiogenic Results from pump failure (ineffective contractile function of the heart) related to an acute MI, ventricular aneurysm, dysrhythmia, pericardial tamponade, hypoxemia, pulmonary edema, acute valvular regurgitation, and acute ventricular septal defect Obstructive Inadequate cardiac output because of impaired ventricular filling related to a massive pulmonary embolism, tension pneumothorax, acute cardiac tamponade, obstructive valvular disease, and pulmonary vasculature disease Distributive 3 forms of shock characterized by vasodilation, decreased intravascular tone, reduced peripheral vascular resistance, and loss of capillary integrity Septic Neurogenic Anaphylactic Caused by infective Loss of peripheral IgE mediated response organisms in the blood vasculature motor tone that occurs shortly after an stream that alters related to spinal cord exposure vasculature tone à injuries and regional hypovolemia will develop anesthesia as a result of blood pooling in microcirculation 10 Exam 3 Study Guide ACNP 805 Management of Shock States Hypovolemic • Fluid resuscitation • PRBCs for low Hgb/Hct Cardiogenic • Careful fluid administration • Vasopressors • NTG Obstructive • Blood pressure treatment • Crystalloid fluid resuscitation • Vasopressors Septic • Source control • Crystalloid fluid resuscitation • Vasopressors Distributive Neurogenic • Maintain airway • Crystalloid fluid resuscitation • Vasopressors Anaphylactic • Maintain airway • Diphenhydramine • Epinephrine • Crystalloid fluid resuscitation • Glucocorticoids • Beta agonists Oxygenation and Tissue Perfusion Pulmonary Oxygenation Pulmonary Perfusion -Movement of mixed venous blood through the pulmonary capillary bed for gas exchange between the blood and alveolar air -Pulmonary Vascular System is high volume with low capillary resistance • Factors Affecting Distribution of Pulmonary Blood Flow: Gravity – patient blood flow is against gravity to the apices when the patient is in an upright position Hydrostatic pressure – positive pressure ventilation, decreased right ventricular preload, dehydration, hemorrhage, air trapping in COPD • Decreased PaO2 – local reflex causes vasoconstriction of pulmonary arterioles supplying hypoxic alveoli Ventilation -Mechanical movement of air into and out of the alveoli for gas exchange -Gas flows from high atmospheric to low intrapulmonary pressure during inhalation • Regulation of Ventilation: o CNS § Brainstem, Medulla, Pons – fire automatically to trigger and halt inhalation resulting in passive exhalation § Cerebral cortex – voluntary control to override brain stem centers in response to chemical stimuli and lung inflation changes o Chemical § Central chemoreceptors – respond to increased PaCO2 and decrease pH through medullary stimuli by increased ventilatory depth and rate -Hypercapnia is major stimuli that alters ventilation § Peripheral chemoreceptors – responds to decreased PaO2 (hypoxemia) by stimulating medullary center to enhance ventilation • Ventilation Processes: o Work of breathing: amount of effort required to overcome the elastic and resistive properties of the lung and chest wall o Elasticity: tendency of lungs to return to their original shape o Compliance: measure of distensibility (how easily lungs and thorax can be stretched) o Alveolar diffusion: exchange of O2 and CO2 across the alveolocapillary membrane -CO2 diffuses at a rate of 20x greater than O2 from capillaries to alveoli o Oxyhemoglobin curve – demonstrates affinity for hemoglobin for oxygen § Left shift – greater affinity: caused by alkalosis and hypothermia; binds easily to the lungs, less unloading to tissues § Right shift – decreased affinity: caused by acidosis, increased tissue metabolism, hyperthermia; hemoglobin unloads more oxygen to tissues • Manifestations of Difficult Ventilation: -Increased peak inspiratory pressure Bronchospasm Secretions in airway PE Pneumothorax Mucus plug Intubation in right mainstem Worsening airspace disease Agitated patient with vent desynchronization • Work of Breathing: -Affected by elasticity, compliance, and resistance o High compliance = easily expandible lung tissue (i.e., COPD) o Low compliance = stiff lungs (i.e., ARDS, pneumonia) o Increased resistance = increased effort for ventilation and increased work of breathing Oxygenation -Movement of O2 into the blood, and transport and delivery of O2 to body tissues • Clinical Measurements: Exercise tolerance Dyspnea or air hunger Cyanosis – not a sensitive or specific indicator of hypoxemia ABGs • Pulse oximetry – noninvasive, continuous method for transcutaneous measurement of the degree to which hemoglobin in arterial blood is saturated with O2 • Hypoxemia/Hypoxia: -Results from insufficient delivery of O2 to tissues in states of low CO, low hemoglobin, or low SaO2 -Hypoxemia is the most common cause of hypoxia o Etiology: Hypoventilation – increased CO2; normal A-a gradient 11 Exam 3 Study Guide ACNP 805 Right-to-left shunt – hallmark is failure of arterial oxygen levels to rise in response to supplemental oxygen Ventilation-perfusion mismatch – PE, pneumonia, asthma, COPD, extrinsic vascular compression; increased A-a gradient Diffusion impairment – increased A-a gradient Low inspired oxygen – high altitude or obstructive asphyxia; normal A-a gradient o • Compensatory Mechanisms: -Activated at PaO2 levels < 60mmHg and fail with PaO2 levels < 20mmHg 1. Increased minute ventilation 2. Decreased perfusion to hypoxic alveoli from pulmonary artery vasoconstriction 3. Improved oxygen delivery by increasing CO and HR via sympathetic tone Hypercapnia: -Results exclusively by alveolar hypoventilation (i.e., rapid or shallow breathing, increased dead space, small tidal volumes, reduced respirator drive) -Never results solely from increased CO2 production -HCO3 will increased 3.5mEq/L for each increase of 10mmHg in CO2 -Treatment includes increased minute ventilation (respiratory rate and tidal volume) -Do not withhold oxygen required to maintain minimum saturation levels in any patient with chronic lung disease in an effort to stimulate ventilation Clinical Perfusion -Technique of using blood flow to direct a balloon-tipped catheter from central venous circulation through the right side of the heart in the PA for hemodynamic monitoring -Includes 3 lumens: 1. Distal – opens at tip of catheter 2. Proximal – opens 30cm from the distal tip 3. Intermediate – opens balloon immediately proximal to distal tip Measurement of Clinical Perfusion • • SVO2: supplies information on respiratory and circulatory systems, measures systemic oxygenation CVP: reflects right ventricle end-diastolic filling pressure; good indicator of systemic volume status; used when calculating SVR Oxygenation and Perfusion Trends SVO2 Trends • 60% and tending down – patient has trapped the venous reserve of O2; greater risk for anerobic metabolism o Causes: decreased O2 supply and increased O2 demand • < 40% - anerobic metabolism leading to organ dysfunction • > 80% - decreased tissue extraction of O2; high return of O2 is indicator of change in hemodynamic parameters o Causes: increased O2 supply, decreased O2 demand, decreased effective cellular O2 delivery and uptake CO2 Trends • Respiratory Acidosis (CO2 > 45mmHg) o Goal: decreased CO2 o Hypoventilation • Respiratory Alkalosis (CO2 < 35mmHg) o Goal: increase CO2 o Hyperventilation SpO2 Trends -Methylene blue can falsely lower SpO2 readings • SpO2 90% = PaO2 60% • SpO2 75% = PaO2 40% • SpO2 50% = PaO2 27% Normal Values • • • • • • • • • • Pulmonary blood flow: 6L/min Pulmonary MAP: 15mmHg SVO2: 60-80% pH: 7.35-7.45 CO2: 35-45mmHg HCO3: 22-26mEq/L PaO2: 60-100mmHg SaO2: > 98% Base excess: -3 - +3mEq/L Pulmonary gas exchange: 300-500mmHg Central Venous Pressure (CVP) Central Venous Pressure -Indicator of central blood volume; monitored by a central catheter tip sitting in the superior vena cava -Used intravenously for infusion of fluids, vasoactive drugs, blood sampling, and assessing intravascular volume -Not a measure of central blood volume and cannot be used to determine volume responsiveness -CVP represents back pressure to systemic venous return • CVP Alterations: o Decreased CVP – a decrease > 2mmHg indicates volume response o Increased CVP – indicated larger than normal mean systemic pressure allowing for adequate perfusion CVP Waveform and EKG Relationships 12 Exam 3 Study Guide • • • • • ACNP 805 A = A-wave – due to atrial contraction during diastole (absent in atrial fibrillation) C = C-wave – due to bulging of the tricuspid valve back into the right atrium at the onset of systole V = V-wave – due to the rise in atrial pressure from venous return through the vena cava during systole before the tricuspid valve opens at the onset of diastole X = X-descent – due to atrial relaxation Y = Y-descent – due to atrial emptying into the ventricle during diastole Preload and Afterload Preload -The amount of myocardial fiber stretch at the end of diastole (end-diastolic ventricular volume) -“Stretch” of the heart -Preload is a volume • Dependent Variables: circulating volume, venous time, atrial contraction, intrathoracic pressure • Monitoring Use: CVP, pulmonary capillary wedge pressure • Assessment: o Left ventricular preload: assessed with left atrial filling pressure or pulmonary artery wedge pressure o Right ventricular preload: assess with right atrial pressure, volumetric parameters Preload Treatment Parameters • • Low preload: administer fluids or blood High preload: administer diuretics Afterload -The tension by the myocardium during ventricular systolic ejection; described as resistance/pressure ventricles must overcome with each contraction to eject blood volume -“Squeeze” of the heart -Afterload is a pressure • Dependent Variables: volume and mass of blood ejected, size and wall thickness of ventricles, impedance of vasculature • Assessment: o Left ventricle: SVR (gold standard – highly sensitive) o Right ventricle: PVR Afterload Treatment Parameters • • Low afterload: vasopressors High afterload: vasodilators Hyperthyroidism Hyperthyroidism -Condition of excess secretion of T3 and T$ resulting from clinical disorders -2 types of hyperthyroidism: 1. Primary hyperthyroidism – elevated TSH with low T3 and T4 2. Secondary hyperthyroidism – low TSH with low T3 and T4 • Laboratory/Diagnostic Tests: TSH assay – most sensitive Serum T3, T4, thyroid resin – elevated Erythrocyte sedimentation rate – elevated Serum antinuclear antibody – elevated CBC – hypercalcemia, anemia, decreased granulocytes Iodine uptake – high = Graves’; low = subacute thyroiditis Ultrasound – thyroid nodules 13 Exam 3 Study Guide • • ACNP 805 Thyroid Hormone Values: o Thyroid stimulating hormone – produced in anterior pituitary § Normal Range: 0.3-5.0mIU/L o T4 (total or free) – produced in thyroid gland § Normal Range – Total: 5-12mcg/dl § Normal Range – Free: 0.8-1.8ng/dl o T3 (total or free) – produced in thyroid gland § Normal Range – Total: 60-180ng/dl § Normal Range – Free: 0.9-2.8nmol/L Treatment: 1. Consult endocrinologist 2. Symptomatic relief with resting HR > 90bpm a. Propranolol: 10-40mg, PO, 3-4 times daily (best for subacute thyroiditis) b. Metoprolol: 25mg, PO, every 6-8 hours 3. Antithyroid medications a. Methimazole i. Initial dose: 30-60mg, daily in 3 divided doses ii. Maintenance dose: 5-15mg, PO, daily b. Propylthiouracil i. Initial dose: 300-600mg, daily in 4 divided doses ii. Maintenance dose: 100-150mg, daily in 3 divided doses 4. Radioactive iodine – shrink goiters 5. Thyroid surgery Thyroid Storm -Deadly, hypermetabolic state caused by inadequately controlled hyperthyroidism • Signs/Symptoms: fever (100-105.8°F), dilated vessels, flushing, profuse diaphoresis (fluid loss = 4L/24 hours), marked tachycardia, mental status change (i.e., extreme agitation, delirium, psychosis, stupor, coma), GI disturbances, hyperglycemia • Laboratory/Diagnostic Tests: o Burch-Wartofsky Point Scale § > 45: thyroid storm § 25-44: impending storm § < 25: unlikely storm • Treatment: 1. Basic measures – supportive care (i.e., oxygen, cardiac monitoring, IV fluids, decreasing stimuli), hypothermic measures -Avoid aspirin and NSAIDs because they interfere with the binding of T4 and thyroid-binding globulin and can exacerbate hypermetabolism 2. Pharmacologic therapy a. Antithyroid i. Propylthiouracil: 500-1000mg loading dose, PO, followed by 250mg, PO, every 4 hours ii. Methimazole: 60-80mg, PO, daily b. Iodine preparations i. Lugol’s solution: 8-10 drops, PO, 3-4 times daily ii. Potassium iodide: 5 drops every 6 hours c. Thyroid Hormone Antagonists i. Beta blockers 1. Esmolol: 500mcg IV bolus, followed by 50-250mcg/kg/min maintenance infusion 2. Propranolol: 1-2mg IV bolus; may repeat every 10-15 minutes ii. Calcium channel blockers – reserved for those contraindicated with beta blockers 1. Verapamil or diltiazem iii. Reserpine: 2.5-5.0mg, IM, every 4 -6 hours; reserved for those contraindicated with beta blockers d. T3 and T4 conversion antagonists i. Hydrocortisone: 300mg IV, followed by 100mg every 8 hours until stable ii. Dexamethasone: 2-5mg, IV, every 6 hours 14 Exam 3 Study Guide ACNP 805 Hypothyroidism Hypothyroidism -Rare condition of greatly decreased metabolism resulting from a deficient amount of circulating thyroid hormone -2 types of hypothyroidism: 1. Primary hypothyroidism – low TSH with elevated T4 2. Secondary hypothyroidism – elevated TSH and T4 • Laboratory/Diagnostic Tests: TSH – elevated T3, T4 – low (T3 is not reliable for hypothyroidism CMP – hypoglycemia, hyponatremia, HLD CBC – anemia, elevated transaminases Thyroid-peroxidase – to rule out Hashimoto’s thyroiditis • Thyroid Hormone Values o Thyroid stimulating hormone – produced in anterior pituitary § Normal Range: 0.3-5.0mIU/L o T4 (total or free) – produced in thyroid gland § Normal Range – Total: 5-12mcg/dl § Normal Range – Free: 0.8-1.8ng/dl o T3 (total or free) – produced in thyroid gland § Normal Range – Total: 60-180ng/dl § Normal Range – Free: 0.9-2.8nmol/L • Hypothyroidism Treatment: 1. Levothyroxine (Synthroid) (T4) -Instruct patient to take 30-60 minutes prior to breakfast or at bedtime; wait 4 hours after eating last meal before dosage administration a. < 60 y/o without CAD: 50-100mcg, daily, with 25mcg increase every 1-2 weeks until symptoms stabilize or euthyroid balance -TSH is rechecked 8 weeks after dose adjustment b. > 60 y/o with CAD: 25-50mcg, daily, with 25mcg increased every 1-2 weeks until symptoms stabilize or euthyroid balance • Myxedema Coma Treatment: 1. Oxygen supplementation or mechanical ventilation – for hypercapnia 2. Fluid restriction + 3% normal saline – for severe hyponatremia 3. D50W – for severe hypoglycemia 4. IV thyroid replacement a. Levothyroxine (T4): 200-400mcg, IV, followed by 50-100mcg, daily -Educate patient of need for lifelong therapy b. Liothyronine sodium (T3): 5-20mcg, IV, followed by 2.5-10mcg, every 8 hours for maintenance i. Alternate T3 and T3 scheme: 1. 200-300mcg T4 + 10-25ug T3, followed by 2.5-10mcg T3 every 8 hours (depends on age and cardiovascular risk factors) -Upon clinical improvement, T3 is discontinued, and a daily oral T4 replacement dose is maintained 5. Adrenal insufficiency (suspected) -Draw serum cortisol prior to administration a. Hydrocortisone: 100mg, IV bolus, followed by 25-50mg every 8 hours to avoid excessive hyperadrenalism-like effects associated with rapid thyroid replacement 6. Slow rewarming with blankets -Hyperthermia blankets are contraindicated because rapid vasodilation may further hypotension and lead to circulatory collapse Diabetes Mellitus Diabetes Mellitus (DM) -A group of metabolic diseases resulting from a breakdown in the body’s ability to produce and/or use insulin • Laboratory/Diagnostic Tests: -Must have 2 of the following on different days to be considered positive 15 Exam 3 Study Guide ACNP 805 Obvious symptoms – polyuria, polydipsia, unexplained weight loss Plasma glucose > 200mg/dL – random or casual; any time of the day without regard to time since last meal Plasma glucose > 200mg/dL 2 hours post oral glucose tolerance test with 75g glucose A1c > 6.5% Fasting plasma glucose > 126mg/dL on two separate occasions Urinalysis – can monitor for glycosuria and ketonuria BUN and creatinine • Complications of DM: o Diabetes related retinopathy o Cardiovascular disease o Cataracts or glaucoma o Neuropathy and nephropathy o Infections o Gangrene of the feet o Venous or arterial ulcers o DKA or HHNS • Insulin Management: o Types of Insulin: Onset, Peak, and Duration Rapid Onset: 15 minutes Peak: 1 hour Duration: 3 hours Short Onset: 30 minutes Peak: 2 hours Duration: 8 hours Intermediate Onset: 2 hours Peak; 8 hours Duration: 16 hours Long Onset: 2 hours Peak: none Duration: 24 hours Lispro (Humalog) Aspart (Novolog) Regular (Humulin R) Novolin NPH (Humulin N) Insulin Glargine (Lantus) Insulin Detemir (Levemir) Insulin Degludec (Tresiba) “15 minutes feels like an hour during 3 rapid responses” “Short staffed nurses could have 30 patients for up 2 (to) 8 hours” “Nurses play hero 2 (to) 8, 16 year olds” “The 2 long nursing shifts never peaked but lasted 24 hours” Type 1 Diabetes Mellitus (DM1) -Autoimmune, cell-mediated destruction of pancreatic beta cells -Insulin-dependent; pancreas fails to manufacture insulin -Juvenile-onset • Signs/Symptoms: polyuria, polydipsia, blurred vision, weight lost, paresthesias, altered level of consciousness o Somogyi Effect: nocturnal hyperglycemia that leads to an influx of counterregulatory hormones resulting in the production of high blood glucose by 7am § Treatment: lower the basal dose of insulin at bedtime or have the patient eat a bedtime snack; alternate management is to eliminate the bedtime dose of insulin, instead of lowering it, and administering a long-acting insulin in the morning • Essentials of Diagnosis: Polyuria, polydipsia Weight loss associated with random plasma glucose of 200mg/dL or more Plasma glucose of 126mg/dL or more after an overnight fast on more than one occasion Ketonemia, ketonuria, or both Presence of islet autoantibodies • Nonpharmacological Treatment: 1. Total calories a. Carbohydrates: 55-65% b. Fiber: 25g or 1,000 calories c. Fats: 25-35% d. Protein: 15-20% 2. Meal schedules 3. Supportive therapy – reduce alcohol intake, exercise (30 min/day), examine feet daily a. ADA recommends > 150 min/week of moderate intensity physical activity spread over 3 days/week with no more than 2 consecutive days without exercise b. Wash feet daily in lukewarm water with mild soap and pat dry 4. Smoking cessation • Pharmacological Treatment: 1. Physiologic regimen a. Long-acting – lantus, detemir: once daily, given at same time b. Rapid-acting – lispro, aspart, glulisine: before meals 2. Nonphysiologic regimen a. Morning dose: 2/3 NPH and 1/3 regular b. Evening dose: 1/2 NPH and 1/2 regular 3. Intensive therapy – for poorly controlled DM1 with conventional therapy a. Reduce/omit evening insulin dose and add dose at bedtime i. 10 units of regular + 15 units of NPH every morning ii. 5 units of regular before evening meals iii. 5 units of NPH at bedtime 4. Sliding insulin scale – reserved for when ATC therapy is insufficient Diabetic Ketoacidosis (DKA) -A state of intracellular dehydration that results from elevated blood glucose levels; occurs in type 1 DM 16 Exam 3 Study Guide ACNP 805 • Signs/Symptoms: polyuria, nocturia, polydipsia, nausea, vomiting, weight loss, sunken eyes, poor turgor, diminished vision, headache, weakness, fatigue, abdominal pain, altered level of consciousness, flushed and dry skin, Kussmaul respirations, tachycardia with weak and rapid pulse, acetone (fruity) breath odor, hyperkalemia, hypotension • Laboratory/Diagnostic Tests: Serum glucose > 250mg/dL (frequently > 300mg/dL) Arterial pH < 7.3mol/L CO2 < 40mmHg HCO3 < 15mEq/L Ketones – present in urine and serum Hyperkalemia BUN – increased Glycosuria Hematocrit – increased related to dehydration Leukocytosis – WBC 25,00/mcl Serum hyperosmolality - > 280 mOsm/L (> 320-330 mOsm/L results in coma) Anion gap – increased HLD • Treatment: -Goals: (1) volume repletion (2) reversal of metabolic complications (3) electrolyte and acid-base correction (4) treatment of causes (5) avoidance of complications 1. Fluid replacement, electrolyte correction, hyperglycemia correction 2. Parenteral fluid replacement – 0.9% normal saline at 1000mL/hr for 1-2 hours, followed by 300-500mL/hr for 4hrs to correct fluid deficit of 4-8L -250mL/hr is recommended once dehydration improves -Expect to order 4-8L of fluid to be administered during the first 24 hours of treatment 3. Potassium correction – monitor closely during fluid resuscitation a. Potassium chloride: 20-30mEq/L, IV, added to IV fluids within first 2-3 hours of therapy unless K+ level exceeds 5.0mEq/L 4. Hypotonic solutions – 0.45% NaCl is use once hemodynamic stability is reached to promote intracellular hydration 5. D5W/0.45% NaCl – reserved for when glucose falls to 250mg/dL to prevent hypoglycemia and cerebral edema cause by lowering glucose too fast 6. Regular insulin: 0.1-0.15 units/kg IV, followed by continuous drip at 0.1 units/kg/hr -If plasma glucose does not fall by 10% within the first hour, a second loading dose is indicated 7. Long acting insulin – administered when anion gap has closed, and glucose decreases to 250mg/dL; begin weaning insulin infusion 8. Subcutaneous insulin – administered when metabolic acidosis and anion gap have been corrected and the patient can tolerate oral intake a. Rapid acting: subQ, every 1-2 hours i. Dose: 0.2 unit/kg bolus, followed by 0.1-0.3 units/kg every 1 hour, followed by 0.2unit/kg every 2 hours until glucose < 250mg/dL 9. Sodium bicarbonate: 50-100mEq/L of hypotonic saline – administered if pH < 7.0mol/L or HCO3 < 9 mEq/L Type 2 Diabetes Mellitus (DM2) -Non-autoimmune, chronic metabolic disorder resulting in tissue insensitivity to insulin -Noninsulin-dependent; cells are resistant to the effects of insulin -Adult-onset -Associated with metabolic syndrome (previously referred to as syndrome X) – characterized by 3 or more of the following: 1. Obesity – waist circumference a. Men: > 40 inches b. Women: > 35 inches 2. Hypertension – BP > 130/85mmHg 3. Abnormal HDL a. Men: < 40mg/dL b. Women: < 50mg/dL 4. Abnormal triglycerides - > 150mg/dL 5. Fasting blood glucose - > 100mg/dL • Signs/Symptoms: skin manifestations (i.e., pruritus, vaginitis), body habitus (i.e., overweight, obese), obstetrical complications • Essentials of Diagnosis: > 40 y/o Obese Polyuria, polydipsia Plasma glucose of 126mg/dL or more after an overnight fast on more than one occasion Diagnostic values > 200mg/dL 2 hours after 75g oral glucose A1c > 6.5% Hypertension, dyslipidemia, and atherosclerosis • Treatment: 1. Metformin: 500mg, PO, daily – if serum creatinine < 1.4mg/dL 2. Volume repletion 3. IV insulin – regular 4. Correction of electrolyte imbalances • Pharmacological Treatment: -5 classes (insulin + 4 classes of oral agents) 1. Carbohydrate absorption agonists (decrease/delay carbohydrate absorption) a. Biguanides – Metformin b. Alpha-glucosidase inhibitors – Acarbose 2. Insulin secretagogues (increase insulin secretion a. Sulfonylureas – glipizide, glyburide, glimepiride b. Meglitinides – repaglinide, nateglinide c. Incretin mimetics – stimulate decrease in blood glucose levels d. DPP-4 inhibitors – breaks down incretins and indirectly increases insulin secretion 17 Exam 3 Study Guide ACNP 805 Hyperosmolar Hyperglycemia Nonketosis (HHNS) -A state of greatly elevated serum glucose, hyperosmolality, and severe dehydration without ketone production; occurs in type 2 DM • Signs/Symptoms: weakness, disorientation, lethargy, seizures, stupid, coma, flushed and dry skin, dry mucous membranes, poor turgor, polyuria, hypotension, tachycardia, shallow breathing • Laboratory/Diagnostic Tests: Serum glucose > 600mg/dL (frequently > 1000mg/dL) Serum osmolarity > 310 mOsm/L BUN, creatinine – elevated Sodium – elevated pH - > 7.3mol/L Anion gap – normal Presence of C-peptides • Treatment: 1. Aggressive fluid resuscitation 2. Hypotonic saline – administered if patient is not hypotensive and once serum sodium reaches 145mEq/L -Overall fluid volume deficit 6-10L -Expect to order 4-6L in first 8-10 hours of therapy 3. IV insulin (same protocol as DKA) 4. Continuous electrolyte monitoring and replacement 5. Cardiac monitoring 6. Frequent serum glucose monitoring American Diabetes Association Diabetes Target Recommendations Parameter Recommended Target Pre-meal Plasma Glucose 80-130mg/dL Post-prandial Plasma Glucose < 180mg/dL Hemoglobin A1c < 7.0% Normal Values • • Anion Gap: 7-17mEq/L Serum osmolarity: 275-295 mOsm/L Lightening and Electrical Injuries Lightening Injuries -Lightening causes internal injury through blunt mechanical force current flow through the body -Currents in the body flow through structures that pose the lease resistance (i.e., tissues with high fluid, electrolyte contents, nerves, vessels, muscle, connective tissues) • Resistance to Electricity: (greatest to least) 1. Bone 2. Fat 3. Tendons 4. Skin 5. Muscles 6. Vessels 7. Nerves • Flashover: how lightening travels over the body’s surface -Less likely to cause internal cardiac injury or muscle necrosis than human-generated electrical activity -Wet skin helps the current travel on the outside of the body and decreases the risk of internal injury Electrical Injuries -High voltage (> 1000 volts) (> 600 volts is associated with serious and fatal injuries) -Temperatures as high as 20,000°C AC vs. DC Current • Alternating Current (AC): -Regularly reverses direction -Provides brief moments of muscle relaxation -Can produce tetanic muscle contractions, ventricular fibrillation, respiratory failure, and seizures -Repetition increases the chance of the current to enter the myocardium during the vulnerable period of the cardiac cycle resulting in ventricular fibrillation -Low-voltage can produce ventricular fibrillation -High-voltage can produce ventricular asystole • Direct Current (DC): -Flows in only one direction -Contact will propagate a single muscle spasm and may throw the victim from the source -Short duration of exposure leads to an increased change of traumatic injury -Can produce lethal cardiac arrhythmias -High-voltage can produce ventricular asystole Types of Lightening Injuries • • Direct: victim struck directly by lightening Side Flash: the nearby object is struck and the current transverses through the air to strike the victim (may injure multiple victims at once) 18 Exam 3 Study Guide • • ACNP 805 Contact Strike: lightening strikes the object that the victim is holding Ground Current: lightening hits the ground and the current is transferred through the ground to the victim Types of Electrical Injuries • • • • • Blast Inhalation Ocular Auditory GI Laboratory and Diagnostic Tests for Lightening/Electrical Injuries CBC CMP BUN and creatinine Blood glucose CK Urinalysis ECG – ST-elevation, QT prolongation, T-wave inversion CT, x-ray Complications/Conditions from Lightening Strike and Electrical Injuries • Cardiac Arrest – from depolarization of the myocardium and sustained asystole • Respiratory Arrest – from depolarization and paralysis of the medullary respiratory center o Cardiac vs. Respiratory Arrest