NURS 480 – CRITICAL CARE FINAL EXAM (use this) STUDY GUIDE | 100% VERIFIED.

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NURS 480 – CRITICAL CARE FINAL EXAM BLUEPRINT MODULE 1 INTRODUCTION TO CRITICAL CARE NURSING 5-6 QUESTIONS o EBP in critical care nursing o Synergy Model o Stress and the critical care ... environment o Teaching and learning o Rapid response teams/code teams o Inter-facility transport/EMTALA MODULE 2 INTRODUCTION TO COMPLEX CARDIAC CARE 8-9 QUESTIONS o Cardiac Monitoring o Terms: ▪ cardiac output ▪ preload & afterload ▪ cardiac contractility o Cardiac Pharmacology o EKG monitoring -interpret basic cardiac rhythm strips and treating abnormal cardiac rhythms. o Cardiac Catheterization MODULE 3 DYSRHYTHMIAS AND MONITORING 8-9 QUESTIONS o Patient Assessment: Cardiovascular system o Hemodynamic monitoring. o Patient Management: Cardiovascular System o intra-aortic balloon pump o cardiac pacing o pacemakers ▪ complications & nursing assess. o implantable cardioverter-defibrillator (ICD) o Shock, SIRS, and MODS o Cardiogenic shock MODULE 4 COMMON CARDIOVASCULAR DISORDERS 9-10 QUESTIONS o Heart Failure o Aortic Aneurysm o Hypertensive Crisis MODULE 5 MYOCARDIAL INFARCTION AND CARDIAC SURGERY 11-12 QUESTIONS o PCI and the CABG procedure o Myocardial Infarction (MI) o Atherosclerosis o Angina o Myocardial infarction MODULE 6 COMPLEX DISORDERS OF THE RENAL SYSTEM 18-19 QUESTIONS o Pathophysiology of the kidney o Physiology of Dialysis o Acute vs Chronic Kidney Disease o Renal Failure MODULE 7 HEMATOLOGIC AND IMMUNOLOGIC DISORDER 11-12 QUESTIONS o Organ and Hematopoietic Stem Cell Transplantation o Review the following disorders under this section: o Engraftment Syndrome o Typhlitis/Necrotizing Entercolitis o Superior Vena Cava Syndrome o Pleural effusion o Tracheobronchial obstruction o Hypercalcemia o Tumor lysis syndrome Module 1 (5-6 QUESTIONS) RESEARCH: o Ultimate purpose of examining research by levels of evidence is to translate best evidence into practice o Lowest level: opinions of authorities or expert committees o Single descriptive, qualitative, or physiologic study o Systematic review of descriptive, qualitative, or physiologic study o Single correlational or observational study o Systematic review of correlational or observational study o Single RCT and nonrandom control trial (quasi-experimental) o Highest level: systematic review of RCTs (meta-analysis) o Barriers to implementation: lack of knowledge of research process, limited access to literature, lack of skill to critique research, limited interest in scientific inquiry, limited power to change practice, time factors, lack or organizational support and commitment, volume of research being published, availability of mentors SYNERGY MODEL: Underlying principles: o Patient characteristics and nurse’s competencies are important to the other o Patients characteristics drive nurses competencies o Outcomes are optimal when patient characteristics match and synergize with nurses competencies Characteristics of patients, clinical units, and systems of concern to nurses: 1. Resiliency 2. Vulnerability 3. Stability 4. Complexity 5. Resource availability 6. Participation in care 7. Participation in decision making 8. Predictability Nursing competencies: 1. Clinical judgement 2. Advocacy and moral agency 3. Caring practices 4. Collaboration 5. Systems thinking: nurse make’s use of limited resources 6. Response to diversity 7. Clinical inquiry NURSING INTERVENTIONS FOR CRITICALLY ILL: Promoting sleep: o Large clocks and calendars o Block sleep times; cluster care o Provide quiet time during day shift o Use earplugs and eye mask o Assess sleep o Provide 5-minute back rub before sleep o Use white noise or ocean sounds o Eliminate pain o Position for comfort o Do not bathe in middle of night o Turn down lights, alarms, and decrease noise o At bedtime, provide information to reduce anxiety: review of day and remind patient of progress made toward recovery o “PM care”: brush teeth, wash face o Relaxation techniques o Patient privacy o Post designated sign “patient sleeping” Overcome barriers to learning: o Verbal sharing of information remains the most trusted form of communicating with patients and families, but many health care professionals rely solely on providing written materials for patient education. Since patients typically remember less than half of what is discussed, limiting the amount of information presented at one time can improve learning recall. o Education may need to be redirected to family members o Teach “need to know” basic information first, repeat essential information o Reduce environmental stress (close door, reduce sounds of alarms, turn of TV) o “Teach back” method RAPID RESPONSE TEAMS: Functions: o Reach hospitalized patients at first sign of hemodynamic instability o Rapidly assess critically ill patient and stabilize patient o Rapidly collect patient data o Facilitate communication to redirect plan of care o Provide education and support to nursing staff initiating RRT call o Assist with triage decisions to appropriate care area and transfer to higher level of care (if needed) Benefits: o Early recognition of deteriorating patient o Prompt notification of clinical staff trained in advanced resuscitation o Critical care expertise to bedside of patients who are clinically deteriorating outside of ICU or ED Triggers to Call RRT: o Staff member with significant concern about patient’s condition o Altered mental status o HR < 40 OR HR > 140 o RR < 8 OR RR >22 o Systolic BP < 90 or > 180 o O2 < 90% despite supplemental oxygen o Urine output < 50 mL over 4 hours o Chest pain unrelieved by nitroglycerin o Threatened loss of an airway o Seizure o Uncontrolled pain SBAR: o Situation, background, assessment, & recommendation o Nurse should provide RRT with template for gathering pertinent information, facilitating communication with physician, and facilitating triage decision making CODE TEAMS: o First step is to determine responsiveness, then observe chest for breathing while palpating carotid pulse at the same time o Call for help & call code blue o CPR always starts with chest compressions – begin cycles of 30 compressions and 2 breaths, use AED as soon as available o Check rhythm – if shockable, give 2 shock and resume CPR for 2 minutes o If not shockable, resume CPR for 2 minutes and re-check o Indications for defibrillation include pulselessness ventricular tachycardia and ventricular fibrillation Roles of Code Team: o Leader (physician, NP): make diagnosis, direct treatment o Primary nurse: provide information, assign roles to staff o Recorder: document people involved, record resuscitation efforts, time keeper for code o Charge nurse: coordinate people performing CPR, coordinate care of other patients o Second nurse: coordinate use of emergency cart, prepare medications, assembles/pass equipment, defibrillates o Medication nurse: administer medications, manage IV therapy & drugs o Nurse supervisor: control crowd, arrange transfer of patient if indicated o Anesthesiologist/CRNA: intubate, manage airway and oxygenation o Respiratory: assist with manual ventilation, draw ABGs, assist with intubation, sets up mechanical ventilator INTERFACILITY TRANSPORT: o Transfers may be done after a risk-benefit analysis reveals benefits exceed risks o American College of Emergency Physicians (ACEP): outlined physician responsibilities for interfacility transfer; guidelines contribute to an algorithm for interfacility transfer of patients (1) sending physician performs patient assessment and determines appropriate level of care during transfer (2) receiving physician ensures facility is capable of providing necessary patient services to care for patient Appropriate Interfacility Transfer: o Optimal health and well-being of patient should be principle goal of transfer o Advanced providers should abide by laws regarding patient transfer; all patients should be given medical screening examination (MSE) and stabilizing treatment within capacity of facility before transfer o Transferring facility is responsible for informing patient about risks and benefits related to transfer o Examining physician at transferring hospital will decide on time of transfer, mode of transportation, level of care needed during transfer, and destination of patient o Options for transport include ambulance, air transport, and private vehicle – IV access can remain o Payment shouldn’t be retrospectively denied by insurance companies o Agreement to accept patient should happen in advance of transfer o Patient should come with all relevant medical records (electronic transfer) o Written transfer protocols and interfacility agreements should be in place Emergency Medical Treatment & Labor Act (EMTALA): o Ensures public access to emergency services regardless of the ability to pay o Also known as “antidumping law” Module 2 • Cardiac output: is the amount of blood, in liters, ejected from the left ventricle each minute. It is a product of HR and stroke volume (SV), which equals the volume of blood that is ejected per ventricular contraction: CO = HR (beats/min) X SV (L/beat) • Preload: the amount of blood in the heart prior to contraction. It is the amount of stretch placed on a cardiac muscle fiber just before systole (Morton & Fontaine, 2018, p. 179). • Afterload: the amount of pressure that the heart exerts to move blood. It is the force or pressure against which a cardiac chamber must eject blood during systole Cardiac contractility: Contractility is the intrinsic strength of the cardiac muscle independent of preload, but a change in preload will affect the force of contraction. a. Cardiac contractility: the force of the heart’s contractions. Contractility refers to the velocity and vigor of contraction during systole. Although vigorous contractility requires more oxygen, it is a benefit to cardiac function because it ensures good, efficient pumping, which increases cardiac output ANATOMY & PHYSIOLOGY: o Resting negative charge (membrane potential) o Negative membrane potential 3 positive = depolarization o Depolarization means muscle cell can squeeze down o Sinoatrial node (SA node) in RA depolarizes itself and takes highway to AV node and to LA o Atrioventricular node (AV node) = connection between atria and ventricles; creates delay between atria and ventricles (don’t contract simultaneously) ELECTROCARDIOGRAM (EKG/ECG): o Test that measures electrical activity of heartbeat o P wave: atria depolarization o PR interval: atrial depolarization 3 onset of ventricular depolarization (0.12 to 0.2 seconds) o QRS complex: ventricular depolarization (0.06 to 0.11 seconds) o Atrial repolarization happens at same time of QRS complex (not visible on strip) o ST segment: end of ventricular depolarization -> start of ventricular repolarization (isoelectric) o Elevated ST 3 acute myocardial injury o Depressed ST 3acute myocardial injury or myocardial ischemia o T wave: represents ventricular repolarization or recovery o U wave: rarely seen; indicates hypokalemia o QT interval: start of ventricular depolarization to end of ventricular repolarization o NSR with one-to-one correspondence between P waves and QRS complex, atrial rate = ventricular rate o Atrial rate: P waves; Ventricular rate: R waves NORMAL SINUS RHYTHM: ASYSTOLE: o Clinical significance: normal finding o Management: nothing o Clinical significance: flatline o Management: check leads; immediate CPR PREMATURE VENTRICUALAR CONTRACTIONS (PVC): Clinical Significance: no P wave, premature QRS that is wide & distorted Management: -Isolated PVC require no treatment -Correct electrolyte imbalance (potassium) -Stop drug causing toxicity -Treat underlying cause -IV antiarrhythmic drug in emergency (lidocaine) VENTIRUCLAR TACHYCARDIA: o Clinical significance: three or more PVC’s in a row; no P wave; wide, bizarre QRS complex o Management: o If stable, give IV lidocaine o If pulseless, immediate CPR and defibrillation o Implantable cardioverter-defibrillator (ICD) if recurrent ventricular tachycardia VENTRICULAR FIBRILLATION: o Clinical significance: most common cause of sudden cardiac death o Management: rapid defibrillation, CPR with drugs if no response to defibrillation, ICD for long-term SUPRAVENTRICULAR TACHYCARDIA: o Management: o If unstable, immediate cardioversion o If stable, vagal stimulation, Valsalva’s maneuver, carotid sinus massage or IV adenosine o After rhythm converts, calcium channel blockers or beta-adrenergic blockers ATRIAL FLUTTER: o Clinical significance: saw-toothed pattern o Management: o Cardioversion and drug therapy (CCB, beta-blockers, amiodarone, digoxin) o Long-term: radiofrequency ablation, pacing, implantable device o Anticoagulation therapy ATRIAL FIBRILLATION: o Clinical significance: No discernable P waves, quivering fibrillatory waves o Management: o Same as atrial flutter o Goal of therapy is to achieve rate control or to convert rhythm to sinus PREMATURE ATRIAL CONTRACTIONS (PAC): o Clinical significance: premature P wave, wide/bizarre QRS complex o Management: no treatment, assess for underlying conditions and treated FIRST DEGREE HEART BLOCK (AV block): o Clinical significance: similar to NSR but long PR interval o Management: o No treatment; correction of underlying cause o Cautious use of drugs (digoxin, beta-blockers, and CCB) COMPLETE HEART BLOCK (3rd degree AV block): o Clinical significance: sinus node continues to fire normally but impulses don’t reach ventricle; no relationship between P waves or QRS complex; inferior or anterior wall MI o Management: o Temporary or permanent pacemaker • Describe the cardiac catheterization procedure; Discuss the teaching points the nurse would include in the teaching plan for patients and families. To best prepare my patient, I would teach them about the catherization procedure and answer questions that they might have. I might provide other resources like pamphlets, videos, or other educational tools to reinforce learning. It will be the cardiologists responsibility to discuss the risks and the benefits of the procedure. I will also be sure that the patient has provided informed consent. As a nurse, one of my many responsibilities will include patient and family education. I would explain that this is a very commonly performed procedure to evaluate the coronary artery lumen. Using fluoroscopy, a catheter is inserted into one or both sides of the heart and CO and pressures are then assessed. Based on the findings during the procedure, interventions are performed to treat the problem. I would then guide the family and patient through what to expect before the procedure, during, and after. I would next explain that the femoral and brachial arteries are the most common catheter insertion sites, although the radial artery is also an option that the cardiologist may choose. I would then assess and mark pulses on the extremity being used, I would have the patient void, and I would administer analgesics and sedatives as ordered. a. Pre-Procedure Guide: • NPO for no less than 6 hours’ prior • If an IV is not already placed, one will be inserted to maintain fluids and medications • There will be preoperative medication prior to transport to the procedure • Only a gown is worn • The Cath lab is typically a cool environment and the procedure table will be firm • Tasks during the procedure may include: turning heading, holding breath, or coughing • Discomfort may be experienced, but local anesthetic is administered • A cardiac monitor will be used during and after the procedure • It will be necessary to lie flat for several hours following the procedure to reduce risks for bleeding • Oral fluids should be consumed as tolerated following the catheterization • Allow for questions ii. During Procedure Guide: • Notify the HCP of any chest pain • Lie still • Provide reassurance and ways to reduce anxiety • Encourage questions iii. Post Procedure Guide: • Lie still and keep extremity used very straight (transfemoral) • Radial band placed to prevent risk of bleeding (transradial) • Verbalize any occurrence of chest pain • Explain when the sheath will be removed • Encourage oral fluids, as ordered • The HCP will review findings • Outline the nursing responsibilities when preparing the patient and family. There are several nursing responsibilities prior to a cardiac catheterization procedure include: • Explain procedure to patient and family • Verify that the patient has taken nothing by mouth for at least 6 hours before the procedure except prescribed medications as advised by the physician • Ensure that ordered preoperative laboratory studies have been completed and results are available • Verify patient, identify allergy information; alert physician if patient is allergic to radiographic dye, medications, or specific foods • Ensure that informed consent has been obtained • Establish IV access per institutional protocol or physician order • Place patient on cardiac monitoring system with blood pressure and pulse oximetry monitoring • Provide supplemental oxygen as ordered/indicated • Premedicate patient per physician order • Obtain vital signs before transfer to catheterization laboratory • Outline and discuss the nursing priorities of patient care after the procedure. Following the procedure, the patient requires meticulous monitoring of VS including BP, HR, and respirations with pulse oximetry. The entry site of the procedure needs close monitoring for signs of bleeding. When a transfemoral approach has been used, any bleeding or hematoma formation must be managed to prevent serious vascular complications, including retroperitoneal bleeding. IV fluids after the procedure promote elimination of the renal-toxic contrast media and protect the patient from hypotension due to dehydration or increased vagal tone during potentially painful portions of the recovery (Morton & Fontaine, 2018, p. 210). Other interventions that should be performed following a cardiac catheterization procedure including: • Ensure that patient vital signs are stable before transfer • Check catheterization site dressing for bleeding and integrity • Check distal pulse below catheterization site; if femoral site was used, check distal pulse, extremity color, capillary refill, and neurosensory status • With transfemoral approach, keep extremity straight and instruct patient not to bend leg or arm • With transradial approach ensure that hemostasis band is properly placed and inflated. Follow manufacturer’s instructions regarding deflation/removal • Maintain IV infusion per physician order or institutional protocol • Maintain supplemental oxygenation support as ordered or indicated • Encourage oral fluids as ordered • Check patient’s coagulation status per institutional protocol before sheath removal; the nurse must carefully watch for signs of bleeding • When femoral artery catheter is removed: a. Apply direct pressure over invasive site for 20 to 30 minutes to prevent bleeding or apply commercial hemostatic compression device per institutional protocol. b. Check distal extremity for pulse, color, capillary refill, and c. sensorium d. Remind patient to lie flat for 4 to 6 hours per institutional protocol e. Check site dressing every 4 to 6 hours for bleeding and integrity MODULE 3: Cardiac Pacemaker: o Indicated if arrhythmia or conduction defects compromise electrical system & hemodynamic response ▪ Heart block Patient assessment: o Assess for dysrhythmia o Assess patient’s medical/social history – subclavian approach avoided in pt. with hx of collapsed lung or previous lobectomy, understand preferred arm dexterity o Must understand pacemaker code to know type of pacer used and programmed mode to anticipate appropriate function o Patients underlying rhythm is assessed so if pacemaker fails, nurse is prepared to treat any life- threatening arrhythmia – chest radiograph can show o Assess pulse rate, underlying cardiac rhythm, BP, activity tolerance, evidence of dizziness, syncope, dyspnea, palpitations, edema Patient & family education: o Teaching starts at time decision for pacemaker insertion is made o Pacemaker takes place of or complements spontaneous rhythm o Initial teaching should be confined to positive aspects of life with pacemaker - knowledge of function and care of pacemaker are of no interest until the patient is able to accept it as part of life Electrocardiogram monitoring: o First step is examining strip for evidence of pacemaker stimulation – evidenced noted by presence of pacing spikes on strip o If pacing lead is in atria, pacing spike is followed by P wave o If pacing lead is in right ventricular, spike is followed by QRS complex o Second step is to examine sensing function o If under-sensing (doesn’t sense intrinsic cardiac activity), inappropriate spikes may show throughout underlying rhythm o If over-sensing, problem detected when pacemaker senses events other than intrinsic rhythm and is inappropriately inhibited in that chamber or causes a triggered response in the other chamber o Third step is to measure Living with a Pacemaker Patient Activity o Passive & active ROM on affected arm 48 hours after implantation to avoid frozen shoulder o Avoid abduction of affected arm above shoulder level for 4-6 weeks to prevent lead dislodgement o Avoid activities that may result in high impact or stress at implantation site o Return to whatever degrees of sexual activity you prefer o Pacemaker will set off alarm on metal-detector devices in airports, so avoid going through detector gates o Show pacemaker identification card o Do not allow wand to linger at pacemaker site because magnet in wand may temporarily put pacemaker into asynchronous mode Signs of Pacemaker Malfunction o Be alert for symptoms of pacemaker malfunction: those associated with decreased perfusion to brain, heart, or skeletal muscles o Be particularly mindful of return of symptoms you experienced before pacemaker implantation o Report any dizziness, fainting, shortness of breath, undue fatigue, or fluid retention (sudden weight gain, puffy ankles, tightness of rings) o Take your pulse once daily after awakening o Report pulse rate over 5 beats/minute slower than that at which pacemaker is set o Be aware that pulse may be somewhat irregular with demand pacemaker and has some spontaneous beats and paced beats – does NOT signify malfunction Signs of Infection o Report any redness, swelling, warmth, drainage, or increase in soreness at implantation site o Report fever of undetermined source o Call doctor if infection in other area of the body does not resolve in a reasonable time period Medications o Antibiotics given within 24 hours of implantation o Medications that were withdrawn before pacemaker implantation may need to be restarted o If warfarin is restarted, check INR Considerations for Home Care o Carry identification card at all times –brand and model of pacemaker, date of insertion, implanting physician, and manufacturer contact info o Wear medical ID bracelet or necklace o Adhere to schedule of follow-up visits o Visits help determine pacemaker and lead performance, battery longevity, frequency of device therapies, and any arrhythmias that may have occurred o “Remote check” can be done over the phone o Pacemaker should be checked at least 1 time per year o Be alert for malfunction: unexplained dizzy spells, fatigue, or slow pulse o Avoid MRI scans, unless you have specific MRI compatible pacing system Pulse Generator Replacement o Follow-up is intensified when pacemaker battery approaches its elective replacement indicator (ERI) o Avoid extended absences or vacations without consulting physician at this time o Generator should be replaced within 6-8 weeks of reaching ERI o Be aware that when batter reaches end of life, it may revert to VVI pacing at 40 bpm o Battery cannot be removed from generator, so entire generator is replaced when battery is low o Generator replacement can be done as a same day surgery, as long as leads are in good condition Considerations for Older Patient o Report any changes in skin condition at pacemaker site; sudden weight loss or poor nutrition may predispose elderly patients to pocket erosion o Report fatigue, neck pulsations, & lack of energy. Patients with CHB or high % of ventricular pacing over time may develop AV dyssynchrony (pacemaker syndrome) o If pacemaker feels like its “flipping” inside the pocket, report to doctor and don’t reposition. When skin is loose or patient twiddles with pacemaker, leads can become tangled or coiled and may fracture Pacemaker functioning: o When heart rate is adequate, pacemaker inhibits pacing stimulus (appears as straight spike line) o When heart rate drops to programmed minimum rate, pacemaker delivers stimulus through the lead – when pacemaker discharges, artifact known as a pacing spike appears on ECG o As a result of the stimulus, the cardiac chamber containing the pacemaker lead is depolarized o Capture = indicates depolarization of atria or ventricle in response to pacing stimulus o Pacing threshold = minimal amount of voltage required from pacemaker to initiate consistent capture Malfunction Problem Causes Intervene Failure to Discharge -No evidence of pacing stimulus -Patient’s HR below programed rate Generator problem, battery depletion Replace battery or generator, check all connections for tightness, *patient may need temporary transvenous pacemaker* Failure to Capture Pacing stimulus not followed by ECG evidence of depolarization Atrial failure: spike appears but not followed by P wave Ventricular failure: spike appears but not followed by QRS complex Lead dislodgement, increase in pacing threshold related to medication or metabolic changes Review chest film and ECG, turn patient to left lateral decubitus position, review lab results for metabolic alterations Oversensing Device detects noncardiac electrical events and interprets them as depolarization Oversensitive settings Reduce sensitivity Under-sensing Device fails to detect intrinsic cardiac activity and fires inappropriately Asynchronous mode Reprogram to synchronous mode, increase sensitivity Pacemaker Complications: o Pneumothorax o Ventricular irritability o Perforation of ventricular wall or septum o Catheter or lead dislodgement o Infection and phlebitis o Hematoma formation o Abdominal twitch or hiccups o Pocket erosion Implantable Cardioverter-Defibrillator (ICD): o Indications include ventricular tachycardia and ventricular fibrillation o Immediate post-implantation: monitor patient for development of ventricular arrhythmias o Patient with ICD & sustained, hemodynamic unstable rhythm should be treated the same way for someone without an ICD and unstable rhythm – CPR and ACLS protocol o Device information should be at patient’s bedside– including both pacing and defibrillation therapies o If device fires in absence of arrhythmia, high probability of oversensing due to dislodged or damaged lead, loose connection at header, or oversensitive pacemaker setting o If inappropriate shock, VT storm, or emergent surgery where electrocautery is used, magnet can be placed over ICD pocket to inhibit defibrillation therapies o Magnet will not affect pacing function of an ICD, nor will it turn the device completely off Teaching points for ICD: o Benefits of support groups o Purpose of ICD and indications o Components of ICD, how it works o How a shock feels o How ICD will be implanted o Expected length of hospitalization o Rate cutoff and therapies programmed in ICD, including pacing parameters o Plans for follow-up care and when to call doctor o Importance of carrying an ICD identification card and/or wearing medical identification devices o Safety precautions: avoid electromagnetic fields, using tools with strong vibrations, no MRI o Keep emergency phone numbers readily available and what to do after a shock o Importance of calling physician immediately if you get more than one shock or several in succession o What the patient and family should do if a shock occurs o Inform family, coworkers, and traveling companions about the ICD; encourage CPR training o Precautions to take when traveling by air and informing security personnel of ICD HEMODYNAMIC MONITORING: o Evaluating intracardiac and intravascular volumes, pressure, and cardiac function o Purpose is to aid in diagnosis of various cardiovascular disorders, guide therapies to optimize cardiac function, and evaluate patient’s response to therapy o Indications include conditions in which CO is insufficient to delivery oxygen to cells due to: o Alterations in intravascular volume (preload) o Alterations in vascular resistance (afterload) o Alterations in myocardial contractility o Specific conditions include cardiogenic shock, severe heart failure, severe sepsis or septic shock, multiple system organ dysfunction, or acute respiratory distress syndrome o Assess balance of oxygen delivery and demand as evaluated by measurement of oxygen consumption or venous oxygen saturation Non-Invasive Monitoring Invasive Monitoring o Indirect blood pressure with cuff o Heart rate, pulses o Mental status o Skin temperature o Capillary refill o Urine output o Central venous pressure (CVP) o Right atrial pressure (RAP) o Right ventricular pressure (RVP) o Pulmonary artery pressure (PAP) o Pulmonary artery occlusion pressure (PAOP) o Pulmonary artery catheter = Swan-Ganz System Components: monitors pressures and oxygenation levels within blood vessels (arterial or venous); 1. Check tubing for patency 2. Check for continuous pressure (300 mmHg) 3. Level transducer to phlebostatic axis 4. Zero the transducer 5. Square wave testing for dynamic accuracy Patient  Transducer  Amplifier  Recorder o Catheter: coming from patient’s vascular system, attached by pressure tubing to transducer o Rigid tubing: connects to transducer, allowing pressure in wave forms to go to transducer o Transducer: connected to amplifier/monitor o Stopcocks: work on various sections of system o Syringe: can draw blood o Flush device: can add extra flush o Pressurized fluid: 300 mmHg o Amplifier/Monitor: visually displays a waveform and systolic, diastolic, and mean pressure values Arterial Waveform: 1. Peak systolic pressure: tallest point of systolic wave 2. Dicrotic notch: closing of aortic valve 3. Diastolic pressure: decline of pressure during rest 4. Anacrotic notch: prefilling increase in pressure Central Venous Pressure Monitoring: o Measures pressures in right atrium o Reflects vascular blood volume, right ventricular end diastolic pressure, and right ventricular function Pulmonary Artery Pressure Monitoring: o Assessment of right ventricular function, pulmonary vascular status, and left ventricular function o Measures RAP, RVP, PAP, & PAOP o PAOP reflects left ventricular end-diastolic pressure (indicator of left ventricular function) Square Wave Testing: o For dynamic accuracy – use flush system to send bolus into system causing spike in wave, looking for oscillations when returning to baseline Problem Cause Prevention Intervention No waveform o Transducer not open to catheter o Settings incorrect or off o Catheter clotted o Faulty cable or transducer o Check stopcocks for proper position o Correct setting on monitor o Maintain continuous flush o Use functioning cables o Check and correct stopcock position o Check scale setting and monitor setup o Aspirate blood clot o Do not fast flush or irrigate with syringe o Check function of cables and transducer Overdamped waveforms *too few oscillations* o Air bubbles o Blood clot o Forward migration of catheter o Catheter tip occluded by balloon or vessel wall o Leak in pressure system; bag not at 300 mmHg o Improper scale selection o Flush system o Remove air bubbles o Use heparinized solution o Tighten all connections o Inflate or apply pressure to device to 300 mmHg o On initial set up, expel all air from flush solution bag o Aspirate clots with syringe o Reposition patient o Check for kinks o Reposition by pulling back catheter while observing waveforms o Tighten all connections and stopcocks o Reinflate bag or activate device o Change to proper scale Underdamped waveforms *too many oscillations* o Excessive movement of catheter o Air bubbles in tubing o Correct catheter placement o Appropriate catheter size for vessel o Eliminate excessive length of tubing o Check for very rigid pressure tubing o Try different catheter tip position o Eliminate excessive tubing o Change tubing o Eliminate excessive stopcocks Complications Atrial Pressure Central Venous Pressure Pulmonary Artery Pressure o Infection o Accidental blood loss o Impaired circulation to extremity o Infection o Thrombosis o Air embolus o Infection o Ventricular dysrhythmia o Pneumothorax o Pulmonary artery rupture or perforation INTRA-AORTIC BALLOON PUMP (IAPB): o Designed to increase coronary artery perfusion pressure and blood flow during diastolic phase of cardiac cycle by inflation of a balloon in the thoracic aorta o Deflation of balloon decreases afterload and thus LV work, with decreased myocardial oxygen consumption o Inflation and deflation counterpulse each heartbeat o Goals are to increase oxygen supply to myocardium, decrease LV work, & improve cardiac output Indications: 1. Treatment of cardiogenic shock after MI 2. Low cardiac output following cardiac surgery 3. Unstable angina during PCI placement MECHANICAL CIRCULATORY SUPPORT: o Replaces left ventricular function o Left ventricular assistive device (LVAD) o Device can support circulation until heart recovers or donor heart is available for transplant o Primary goals of VAD are adequate tissue perfusion and improved end-organ function Indications: 1. Acute LV failure after a MI 2. LV failure after a surgical procedure 3. End-stage heart failure Complications: o Bleeding o Thromboembolic events o Right ventricular failure o Infection o Dysrhythmias o Nutritional Deficits o Psychosocial factors: refer to psychologist Differentiation between Shock, SIRS, MODS SHOCK Although shock states have different causes and different clinical presentations, some features, such as hypoperfusion, hypercoagulability, and activation of the inflammatory response, are common to all shock states. Once a shock state develops, the subsequent course of illness is less dependent on the initial cause and more significantly influenced by the physiologic response to shock, including activation of the sympathetic nervous system, the inflammatory response, and the immune system. Thus, shock can be considered as a derangement of compensatory mechanisms that results in further circulatory and respiratory dysfunction with subsequent multiple organ damage. Shock can be classified as hypovolemic , cardiogenic , or distributive . o Hypovolemic and distributive shock occur because of inadequate venous return to the heart. Inadequate venous return may result from hypovolemia (dehydration, hemorrhage) or widespread vasodilation (sepsis, anaphylaxis, or loss of sympathetic tone with a spinal cord injury), which cause a relative hypovolemia. o Cardiogenic shock is caused by the failure of the heart to pump effectively. Pump failure may result from myocardial infarction, abnormal heart rate or rhythm, or impaired diastolic filling. SYSTEMIC INFLAMMATORY RESOPNSE SYNDROME (SIRS) The progression of shock states involves systemic activation of the inflammatory response. In addition to protective effects, the inflammatory response also has potentially detrimental effects that result in damage to tissues and organs. The term systemic inflammatory response syndrome (SIRS) is used to describe patients in whom the inflammatory response is fully and systemically activated. Efforts have been made to identify patients in whom this systemic reaction is occurring, with the thought that prompt, effective intervention may prevent progression of the shock to an irreversible stage. SIRS is manifested by two following: Figure 54-3 Cellular effects of systemic inflammatory response. Inflammation, coagulation, and impaired fibrinolysis result in MODS. MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS) MODS is defined as a progressive physiologic failure of several organ systems in acutely ill patients. The physiologic threat is so disruptive to systemic homeostasis that homeostasis cannot be maintained without intervention. The inability to maintain end-organ perfusion and oxygenation because of SIRS or any type of shock may result in MODS. o Nurses have a key role in preventing, recognizing, and managing patients with MODS. o Prevention strategies include enforcement of measures to prevent nosocomial infections, such as proper positioning (head of bed elevated during mechanical ventilation), oral care, turning and skin care, invasive catheter care, and wound care. o There is no specific medical treatment for MODS, other than supportive care, is available. o Management focuses on treating hemodynamic and metabolic derangements MODULE 4: HEART FAILURE: CLASSIFICATIONS: o Acute vs. Chronic o Acute: symptoms progressed to point where immediate or emergency intervention is necessary to save the patient’s life o Chronic: baseline conditions and limitations patient lives with on daily basis o Left-Sided vs. Right-Sided o Left sided HF: failure of LV to fill or empty properly leading to increased pressure inside ventricle and congestion in pulmonary vascular system o Right sided HF: failure of RV to pump adequately ▪ Most common cause of right sided HF is left sided HF ▪ Can also occur in presence of perfectly functioning left ventricle ▪ Pulmonary embolus is common cause of acute right-sided HF o Diastolic vs. Systolic (further classification of left sided heart failure) o Systolic dysfunction: ejection fraction less than 40%; caused by decrease in contractility ▪ Ejection fraction: percentage of left ventricular end-diastolic volume (LVEDV) [AKA PRELOAD] that is ejected from the ventricle in one cycle o Diastolic dysfunction: difficult to measure; caused by impaired relaxation and filling New York Heart Association Functional Classification (NYHA): o Measure of how much symptoms of heart failure limit the activities of patients o Class I: No limitation of physical activity o Class II: Slight limitation of physical activity; comfortable at rest, but ordinary physical activity results in fatigue or dyspnea o Class III: Comfortable at rest but minimal activity causes symptoms of HF o Class IV: Unable to carry on any physical activity without symptoms; symptoms present at rest American College of Cardiology/American Heart Association Guidelines (ACC/AHA): o Outlines four stages of heart failure that are useful for organizing the prevention, diagnosis, management, and prognosis for patients with HF o A: Patient at high risk for HF because of presence of conditions that are strongly associated with development of HF. Such patients have no identified structural or functional abnormalities of pericardium, myocardium, or cardiac valves and have never shown S/S of HF. o B: Patients who have structural heart disease that is strongly associated with development of HF but who have never shown S/S of HF. o C: Patients who have current or prior symptoms of HF associated with underlying structural heart disease. o D: Patients with advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions. CARDIAC OUPUT: o CO = stroke volume x heart rate o Any rhythm that doesn’t include rhythmic atrial contraction compromises filling  stroke volume  CO o Too slow of heart rate (i.e. heart block) decreases overall CO directly CARDIAC INDEX: o Relates CO to body size o Need patient’s height and weight HEART FAILURE PATHOPHYSIOLOGY/CAUSES: DECOMPENSATION: o Patients with chronic heart failure may live with no symptoms of HF or well-controlled symptoms o However, chronic heart failure may become acutely worse – resulting in an increase in symptoms and limitations associated with left ventricular dysfunction o Acute decompensated heart failure (ADHF): sudden worsening of S/S of heart failure 1. Any factor that increases oxygen demand, and therefore demands for increased CO beyond the ability of the ventricle to function (HTN, tachycardia, anemia, exercise) causes exacerbation 2. Any factor that depresses the function of the already compromised ventricle (alcohol, drugs that exert a negative inotropic effect such as CCB and beta-blockers) causes exacerbation SYMPTOMATIC PATIENT: o Airway, breathing, circulation o Once these issues are addressed, etiologic factors and long-term strategies can become focus of care ASSESSMENT: o Natriuretic peptides (BNPs) are naturally occurring substances synthesized and released by cardiac myocytes when ventricles are overfilled o Rise in PAOP causes more wall stretch on ventricular wall, and a rise in BNP level occurs o BNP level greater than 80 pg/mL o Show evidence of PAOP, which confirms heart failure decompensation as source of dyspnea OTHER NOTES: o PAOP is reflective of left ventricular end diastolic filling pressure o Increased PAOP represents systolic heart failure o CVP is indicative of right sided pressure as a volume measurement o Increased CVP represents right sided heart failure (diastolic HF) o Goal with elevated pressure is decreasing circulating volume with Lasix o Restrict salt intake; do NOT use salt substitutes o Weigh yourself every day at about the same time o If you are going out for a few hours and will not have easy access to the bathroom when you need it, hold off on your diuretic until you return home; but, don’t skip a day’s dose PHARMACOLOGIC MANAGEMENT: Medication Action Adverse Effect Beta-Blocker Ex. metoprolol Block effects of hormone epinephrine; increase exercise tolerance, decrease hospitalizations and mortality Orthostatic hypotension, dizziness, fatigue Calcium-Channel Blocker Ex. verapamil, amlodipine Inhibits influx of calcium, which produces vasodilation Hypotension, AV block, bradycardia, flushing, peripheral edema ACE Inhibitor Ex. lisinopril Block RAAS system Angioedema, cough that is non- productive and dry, elevated potassium Inotrope Ex. digoxin Increase force of myocardial contraction and cardiac output Digoxin toxicity – anorexia, vomiting, confusion, colored or blurred vision Diuretics Ex. lasix Gets rid of excess fluid volume Electrolyte imbalances, orthostatic hypotension ABDOMINAL ANEURYSM AND DISSECTION: Abdominal Aortic Aneurysm: o Pathophysiology o Aortic aneurysm defined as localized dilation of the aorta o Assessment o Most patients are asymptomatic; typically identified at health screening for another problem o Most common complaint is abdominal or back pain o Worsening of symptoms is related to expansion or rupture of aneurysm o Assess abdomen for presence of bruit or masses, and peripheral pulses o Confirm diagnosis: abdominal ultrasonography o Management o Control of HTN & elimination of risk factors (i.e. smoking) o For stable patient, follow with serial noninvasive tests  ultrasonography o Surgical repair: diameter larger than 5.5 cm o Endovascular repair: treatment of choice for high-risk patients Aortic Dissection: o Pathophysiology o Medial layer of aorta undergoes degeneration -> wall stress and dissection  false channel (lumen) forms o Assessment o Sudden, intense chest pain described as ripping or tearing accompanied with syncope o Murmur of aortic regurgitation or alteration in peripheral pulses with presence of known risk factors (i.e. HTN) o Management o Survival depends on location of dissection, severity of complications, and rapidity of diagnosis o Clinical management focuses on controlling blood pressure and managing pain (nurse role) o Treatment of choice for dissection involving ascending aorta  surgery o Long-term prevention focuses on management of risk factors (BP, smoking cessation, cholesterol management, avoiding intense isometric exercises, avoiding powerful stimulants (illicit substances), and controlling stress) HYPERTENSIVE CRISIS: o Acute elevation of BP (greater than 180/120 mmHg) associated with acute or close target organ damage o Encephalopathy: headache, visual disturbances, confusion, nausea, vomiting o Papilledema  increased intracranial pressure o Eyes: retina wool spots and hemorrhages  damage to retinal nerves & rupture of retinal vessels o Chest pain  acute coronary syndrome or aortic dissection o Kidney damage: decreased urine output (oliguria) or azotemia (excess urea in blood) o Management o Goal is to reduce mean blood pressure within 1 hour of starting treatment and to prevent or reverse target organ damage o Several IV medications are indicated to treat HTN crisis o Constant monitoring is needed to avoid lowering BP too quickly (hypoperfusion) - best done with intra-arterial catheter o Once BP is stabilized, treatment goals depend on etiology of crisis o All patients require careful long-term management to control their BP and prevent future episodes MODULE 5 ACUTE CORONARY SYNDROME: o Patients with clinical symptoms compatible with acute myocardial ischemia or infarction that are due to an abrupt reduction in coronary blood flow o Acute coronary syndrome o Unstable angina: chest pain at rest o Acute myocardial infarction (AMI) ▪ STEMI: ST-segment elevation MI; detectable biomarkers in circulation ▪ NSTEMI: non-ST segment elevation MI; ischemia is severe enough to cause myocardial damage and release biomarker indicating myocardial necrosis (similar to unstable angina) Angina: transient, reversible myocardial ischemia precipitated by an imbalance between myocardial oxygen demand and supply o Common cause of reduced supply of oxygen is atherosclerotic narrowing of coronary arteries o Common causes of increase in oxygen demand: fever, tachycardia, thyrotoxicosis STABLE ANGINA UNSTABLE ANGINA VARIANT ANGINA MICROVASCULAR ANGINA o Paroxysmal substernal pain o Predictable with physical exertion or emotional stress o Relieved with rest or nitroglycerin o Chest pain at rest o Prolonged and severe o Type of ACS o Requires immediate treatment o Increase risk for AMI, dysrhythmias, and cardiac sudden death o Form of unstable angina o Happens at rest, between midnight and 8am o Result of coronary artery spasm o Chest pain with normal epicardial coronary arteries (largest vessels on surface of heart) o Endothelial dysfunction and reduced flow in tiny “resistance” blood vessels of heart ASSESSMENT: o History o 5 important assessment pieces to determine likelihood of ischemia from coronary artery disease: 1. Description of symptoms 2. Prior history of coronary artery disease 3. Sex 4. Age 5. Number of risk factors present o NOPQRST pain assessment: normal, onset, precipitating/palliative factors, quality, region/ radiation, severity, & time o Pain of myocardial infarction (MI) is not relieved by sublingual nitroglycerin o Physical Exam o Tachycardia, hypertension, hypotension, pallor, cold & clammy skin o Take blood pressure on both arms o Pulsus alternans: regular alteration of force of arterial pressure o Xanthomas: yellow nodules or plaques on skin that indicate hypercholesterolemia o Auscultation of carotid or femoral bruit indicates obstructive cardiovascular disease o Paradoxical split of S2 or S3 sound indicates left ventricular failure o S4 sound indicates decreased left ventricular compliance o Diagnostic Tests o 12-lead ECG = standard diagnostic test o Biochemical cardiac markers = troponin o Stress test MANAGEMENT: o Overall goal is to restore balance between oxygen supply and oxygen demand o Pharmacologic therapy o Nitroglycerin: vasodilator that reduces myocardial oxygen demand o Morphine sulfate indicated for pain not relieved by nitroglycerin o Beta-blockers: decreased myocardial oxygen consumption by reducing myocardial contractility o Calcium channel blockers: decreased myocardial oxygen demand by decreasing afterload, contractility, and heart rate o Combination of aspirin, an anticoagulant, and additional antiplatelet drug recommended for patient with unstable angina or NSTEMI o Invasive therapy o Intra-aortic balloon pump (IABP) o Percutaneous transluminal coronary angioplasty (PTCA): infarction-related coronary artery is dilated with balloon catheter o Stent placement o Coronary artery bypass grafting (CABG) o Risk factor modification o Stop smoking, obtain healthy weight, exercise daily o Avoid exposure to cold and windy weather MYOCARDIAL INFARCTION (MI): o Caused by prolonged ischemia related to imbalance of oxygen supply and oxygen demand o Prolonged ischemia causes irreversible cell damage and muscle death o Most MI’s characterized by coronary artery thrombosis ASSESSMENT: o History o Most common complaint is chest discomfort/pain o Unlike angina pain, pain of MI is more prolonged and unrelieved by rest or nitroglycerin o Women & elderly present with complaint of shortness of breath o Nausea/vomiting -> inferior wall MI o Physical Exam o Precordial pulsations in left lateral decubitus position o Diminished S1  decreased contractility o S3  left ventricular systolic dysfunction o S4  decreased left ventricular compliance o After 48-72 hours, patients acquire a pericardial friction rub o Patients with right ventricular infarctions may present with jugular vein distention, peripheral edema, and elevated central venous pressure (CVP) o Diagnostic Tests o Electrocardiogram (ECG): detect patterns of ischemia, injury, and infarction ▪ Ischemia: T-wave inversion or ST-segment depression ▪ Injury: ST-segment elevations ▪ Infarction: change in T wave, ST segment, and Q wave o Labs: troponin, blood chemistry, CBC, coagulation tests, lipid panel o Other: chest radiograph, echocardiogram, MRI, CT, perfusion imaging MANAGEMENT: o Early Management o Chewable aspirin, ECG, supplemental oxygen, nitroglycerin, morphine, B-blocker, ACE inhibitor o Percutaneous coronary intervention (PCI) ▪ Reperfusion therapy that reestablishes blood flow to ischemic myocardium ▪ PTCA is type of PCI used o Fibrinolytic therapy ▪ Lyse coronary thrombi by converting plasminogen to plasmin ▪ Assess for any contraindications (intracranial hemorrhage, vascular lesion, active bleeding, intracranial or intraspinal surgery i.e. any high risk bleed situation) o Intensive Care and Intermediate Management o Maximize cardiac output while minimizing cardiac workload o Pharmacologic Therapy ▪ Daily aspirin ▪ Clopidogrel for patients with STEMI and continued for 14 days ▪ B-blockers and ACE inhibitors started within 24 hours o Hemodynamic Monitoring ▪ Pulmonary artery catheter for MI patient with severe heart failure, pulmonary edema, cardiogenic shock, progressive hypotension, or suspected mechanical complications ▪ Monitor pulmonary artery occlusion pressure (PAOP) for assessment of left ventricular filling pressure ▪ Invasive arterial monitoring indicated for patients with MI who have severe hypotension or are getting vasopressor or vasodilator drugs o Additional Diagnostic Testing ▪ Stress tests, echocardiograms, myocardial perfusion imaging, radionuclide angiocardiography, CT scans, MRI, or positron emission tomography COMPLICATIONS: o Prompt recognition and management is essential in reducing mortality & morbidity HEMODYNAMIC COMPLICATIONS: o Anteroseptal wall MI damages left ventricle, which can lead to serious complications o Cardiogenic shock is most serious myocardial complication of MI o Results from loss of contractile forces of heart, resulting in left ventricular dysfunction o Clinical manifestations of cardiogenic shock: o Rapid, thread pulse o Narrow pulse pressure o Dyspnea o Tachypnea o Inspiratory crackles o Distended neck veins o Chest pain o Cool, moist skin o Oliguria o Decreased mentation o Diagnostic tests of cardiogenic shock: o ABGs: decreased PaO2 and respiratory alkalosis o Systolic BP < 85, MAP < 65, cardiac index < 2.2 o Management of cardiogenic shock would include positive inotropes & vasopressors, with potential need for IABP or left ventricular assist device Hemodynamic o Hypotension: inotropes, vasopressors o Pulmonary congestion o Cardiogenic shock o Right ventricular infarction o Recurrent ischemia or infarction Mechanical o Mitral valve regurgitation from papillary muscle rupture: diuretics, afterload-reducing agents, IABP o Left ventricular free wall rupture o Ventricular septal rupture: fluids, inotropes, vasodilators, IABP o Left ventricular aneurysm Dysrhythmia o Ventricular tachycardia: ICD o Ventricular fibrillation: ICD o Supraventricular tachydysrhythmias: cardioversion o Bradydysrhythmias o Atrioventricular block (1st, 2nd, or 3rd degree): transcutaneous pacing Myocardial o Diastolic dysfunction o Systolic dysfunction o Heart failure Pericardial: aspirin o Pericarditis o Dressler syndrome o Pericardial effusion Thromboembolic o Mural thrombosis o Systemic thromboembolism o Deep vein thrombosis o Pulmonary embolism PERCUTANEOUS CORONARY INTERVENTIONS (PCI): o PCI is term used to describe less invasive procedures to treat coronary artery disease (CAD) o PTCA o Laser angioplasty o Atherectomy o Stenting INDICATIONS FOR PCI: o Purpose is to alleviate angina pectoris unrelieved by medical treatment and to reduce risk for MI in symptomatic and asymptomatic patients with significant stenosis o Coronary arteries that have at least 70% narrowing o Those who underwent CABG whose symptoms recurred because of stenosis and graft closure or progression of coronary disease in native vessels or vein grafts o Those deemed ineligible for traditional medical therapy (cardiogenic shock, high risk for bleeding) PROCEDURE: o Judkins approach (femoral) or brachial or radial artery o Catheter passed through ascending aorta to the left ventricle o Exact placement of dilation balloon and stent facilitated under fluoroscopy o During PTCA, coaxial catheter system introduced into coronary artery tree and advanced into area of coronary artery stenosis; balloon attached to catheter is then inflated, increasing the luminal diameter and improving blood flow through dilated segment ASSESSMENT & MANAGEMENT: Patient Preparation: o Laboratory Tests o Cardiac enzymes, electrolytes, coagulation studies, serum potassium creatinine, BUN ▪ Hypokalemia -> increased sensitivity and excitability of myocardium -> dysrhythmias ▪ Creatinine & BUN -> radiopaque contrast material is hard on kidneys o Preoperative Medications o Aspirin should be given 24 hours before procedure o Clopidogrel before and after PCI procedures decreases adverse events such as acute closure and subacute thrombosis o Withhold metformin before procedure (use of contrast dye) o Withhold warfarin, anticoagulant medications for a number of days before (risk for bleeding) o Informed Consent o Surgical Standby Nursing Management During PCI: o Understand ACLS, emergency medications, defibrillator, IABP, ventilator, temporary pacemaker o Monitor ECG and arterial pressure for changes o S/S of contrast sensitivity: urticaria, blushing, anxiety, nausea, laryngospasm o Anticoagulation status during procedure is of utmost importance o Activated Clotting Time (ACT) ▪ Before PTCA ▪ 5 minutes after heparin bolus ▪ Every 30 minutes thereafter for duration of procedure o Facilitated PCI: platelet GP IIb/IIIA antagonist + aspirin + heparin Precautions for Post-Percutaneous Transluminal Coronary Angioplasty (PTCA) Remain on bed rest for 4 to 6 hours Maintain the involved leg in a straight position (for Judkins technique) Avoid an upright position Avoid vigorous use of the abdominal muscles (coughing, sneezing, or moving bowels) Nursing Management After PCI: o Monitor for S/S of myocardial ischemia o Most overt symptom of possible complication is early recurrence of angina pectoris, which requires immediate attention o Judkins approach requires monitoring for bleeding, may have 5 lb. sandbag over puncture site after sheath removal; keep leg straight and HOB < 45 degrees o Minimum requirements of thrombi prevention following stent replacement: o Clopidogrel (Plavix) 75 mg and Aspirin 325 mg ▪ 1 month after bare-metal stent implantation ▪ 3 months after sirolimus DES implantation ▪ 6 months after paclitaxel DES implementation ▪ 12 months if not high risk for bleeding COMPLICATIONS: o Major complications that can result in ischemia and possible severe LV dysfunction necessitating emergent CABG include angina unrelieved by maximal administration of nitrates and calcium channel blockers, MI, coronary artery spasm, abrupt closure of dilated segment, coronary artery dissection leading to occlusion, and restenosis o Angina, Myocardial Infraction, and Vasospasm o Ischemia requiring immediate intervention: ▪ Persistent chest pain ▪ Changes in HR & BP o Abrupt Closure of Dilated Segment ▪ Elevated ST segments o Caused by coronary artery dissection, coronary artery spasm, and thrombus formation o Treatment options: repeat dilation, emergent CABG surgery, and pharmacologic therapy o Coronary Artery Dissection o Major luminal obstruction associated with coronary artery occlusion -> deterioration in blood flow -> severe ischemia or MI  emergent bypass surgery o Stent Thrombosis, VT, VF, bleeding Complication of PCI Signs & Symptoms Possible Interventions Angina Chest pain CABG or repeat PCI Myocardial Infarction (MI) Dysrhythmias: tachycardia, bradycardia, VT/VF, ST elevation Redo PCI, supplemental oxygen Abrupt Reclosure Dissection/Intimal Tear Marked hypotension Acute ECG changes (ST- segment) Medication: -vasodilators (nitrates), CCB, analgesics, anticoagulants, vasopressors Hypotension Nausea/vomiting Intra-aortic balloon pump (IABP) Coronary Branch Occlusion ST-segment elevation Repeat PCI Restenosis Angina pectoris, positive exercise test Redo PCI, coronary artery bypass graft Marked change in HR (bradycardia, VT, VF) Rate below 60 or above 250 No discernible cardiac rhythm Pallor Loss of consciousness Hypotension Medications -antiarrhythmics -vasopressors Vascular: excessive blood loss Hypotension Decreased urine output Decreased Hgb/Hct Pallor Hematoma at puncture site Possible surgical repair, fluids, transfusion, oxygen, flat in bed Allergy Hypotension Urticaria, hives, erythema Nausea/vomiting Shortness of breath Laryngospasm Medications: -antihistamine, steroids, antiemetics, oxygen Clear liquids/NPO Anaphylaxis: fluids for volume expansion, epinephrine, vasopressor for hypotension Central Nervous System Events Change in LOC; respiratory depression Hemiparesis, hypoventilation Oxygen Withhold sedatives; narcotic antagonist as respiratory stimulant VALVULAR DISEASE: o Valves maintain unidirectional blood flow in forward direction through heart chambers & vessels o Diseases may result in valvular stenosis or insufficiency (regurgitation) o Stenosis: narrowed orifice creating partial obstruction to blood flow ▪ Increase pressure behind valve ▪ Decrease pressure forward blood flow o Insufficiency: incompetent valve ▪ Blood flows backward ▪ Increase pressure and volume behind valve o Characteristic murmur o Diagnosis confirmed by echocardiography & catheterization of both sides of heart, at which time the pressure across the valves or valvular gradients are measured Mitral Stenosis o S/S: fatigue, exertional dyspnea, orthopnea, pulmonary edema o Most frequently result of rheumatic heart disease o Restricts blood flow from LA to LV o Decreased CO and systemic perfusion o Increase left atrial pressure -> pulmonary hypertension -> left and right sided HF Mitral Insufficiency o S/S: fatigue, palpitations, shortness of breath o LV blood flows into LA rather than being ejected through aortic valve o Decreased CO o Results in left ventricular hypertrophy & increased left atrial pressure and dilation o Acute mitral insufficiency may result from MI Aortic Stenosis o S/S: angina, syncope, compromised renal perfusion, fatigue, orthopnea o Decreased CO o Results in left ventricular hypertrophy that decrease ventricular cavity volume and filling and increases myocardial oxygen demand at the same time cardiac output and coronary artery perfusion are decreased Aortic Insufficiency o S/S: fatigue, low diastolic pressure, widened pulse pressure o Blood flow regurgitated backward from aorta into left ventricle during ventricular diastole o Decreased CO o Results in left ventricular hypertrophy o Acute problems result in left-sided HF, pulmonary edema, and increased systemic vascular resistance (SVR) SURGICAL TREATMENT: o Indicated before left ventricular function deteriorates significantly and patient’s activity becomes severely limited or before severe signs and symptoms (i.e. pulmonary HTN from mitral stenosis or angina/syncope from aortic stenosis) o Valve Reconstruction o Considered only for mitral valve problems o Commissurotomy indicated for moderate stenosis with minimal calcification & regurgitation o Valve Replacement - done through median sternotomy incision Biologic Valves Mechanical Valves Indicated for those unable to comply with anticoagulation regimen, for those in which long-term anticoagulation is contraindicated, and for women of child-bearing age who plan to become pregnant Indicated for young patients and those able to comply with anticoagulation therapy. o Limited long-term durability o Better hemodynamics o No hemolysis o Low incidence of thromboembolism o Decreased bleeding events o Good long-term durability o Adequate hemodynamics o High risk for thromboembolism o Need long-term anticoagulation o Increased risk for anticoagulation related bleeding CORONARY ARTERY BYPASS GRAFT SURGERY (CABG): o Native vessels or conduits are “harvested” during initial phase of surgery and used to reroute or bypass blood flow past diseased areas of coronary arteries o Common conduits used include internal mammary artery, saphenous vein, or radial artery o Acceptable treatment for coronary artery disease (CAD) o Relief of angina and improvement in exercise tolerance, and prolongs life in patients with left main CAD, three-vessel disease with poor left ventricular function, and two vessel disease with significant stenosis in the proximal left anterior descending o Indications include those who are older, have more advanced coronary disease, have more impaired left ventricular function, and have had previous CABG before CARDIAC SURGERY Preoperative Phase: o Physiological: history, physical exam, chest radiograph, ECG, labs o Psychological: teach about care in ICU Postoperative Phase: o Immediate postoperative care involves cardiac monitoring and maintenance of oxygenation and hemodynamic stability o Prevent hypothermia, monitor for systemic-inflammatory response syndrome (SIRS), control pain Prevention of Complications Cardiovascular o Volume resuscitation o Monitor for dysrhythmias o Improve cardiac contractility o Control blood pressure Pulmonary o Monitor for effective oxygenation with pulse oximetry with intermittent ABG sampling o Adequate ventilation maintained by selecting tidal volumes appropriate for body size o Wean from mechanical ventilation Neurologic o Standard neurologic exam to assess level of consciousness and motor and sensory ability Gastrointestinal o Ice pops and ginger ale to help with compliance and decrease possibility of nausea, vomiting, and aspiration Renal o Oliguria: loop diuretics o Renal failure: dialysis Endocrine o Monitor blood glucose R/T wound healing o Risk for adrenal insufficiency and hypothyroidism Postoperative Bleeding o Monitor chest tube drainage o Follow-up coagulation studies Infection o Prophylactic and empiric antibiotics MODULE 6 DIALYSIS: o All forms of dialysis make use of the principles of osmosis and diffusion to remove waste products and excess fluid from the blood o Semi-permeable membrane between the blood and the dialysate o Blood = greater concentration o Dialysate  lesser concentration; formulated with varying concentrations of dextrose or sodium to produce osmotic gradient (excess water is pulled from circulatory system) o Dissolved substances (urea and creatinine) diffuse from area of higher to lower concentration o Ultrafiltration: process of fluid moving across a semipermeable membrane in relation to forces created by osmotic and hydrostatic pressures o Net filtration pressure: hydrostatic and osmotic pressure forces EXTRACORPOREAL THERAPY: o "Outside the body” circuit – need access to patient’s circulation and anticoagulation of the circuit o Access to circulation: (1) venous catheter, (2) arteriovenous fistula, (3) synthetic vascular graft o Required for hemodialysis and continuous renal replacement therapy Venous Catheter: o Dual-lumen venous catheters Indicated for patients who are temporarily ill or patients on chronic dialysis who are waiting for more permanent access to mature o Tunneled dual-lumen central venous catheter used as permanent means of access for patients where all other means of entry into circulatory system have been exhausted o Maintain catheter patency with proper and routine flushing to prevent formation of thrombosis (may need to use thrombolytics) Arteriovenous Fistula: o Two venipunctures are made at the same time of dialysis: one for blood outflow and one for blood return o Indicated for long-term access for hemodialysis o Advantages: avoidance of inserting a foreign object into the body & reduced infectious complications o Palpable thrill + bruit (loud, swishing sound) indicates a functioning fistula o Fistulas are developed and ready to use 1 to 3 months after surgery Synthetic Vascular Graft: o Graft is used in same manner as arteriovenous fistula o Used when patient’s own vessels are not adequate for fistula formation or when patch areas of arteriovenous fistula have stenosed or developed areas of aneurysm o Avoid venipuncture in new grafts for 2 to 4 weeks while patient’s tissue grows into the graft HEMODIALYSIS: o Water and excess waste products removed from blood as it is pumped by the dialysis machine through an extracorporeal circuit into a device called a dialyzer (artificial kidney) o The dialyzer acts as the filtration system of the kidney o Semi-permeable membrane = thin, porous sheet made of cellulose or a synthetic material o Membrane allows small weight substances (urea, creatinine, uric acid) but does not allow larger substances (plasma proteins, bacteria, and blood cells) through o Water moves freely through the membrane Removes by-products of protein metabolism Removes excess water Maintains/restores body’s buffer system Maintains/restores electrolyte levels in the body Indications: o Chronic renal failure o Complications of acute kidney injury o Uremia, fluid overload, acidosis, hyperkalemia, and drug overdose Contraindications: o Coagulopathies – extracorporeal circuit must be heparinized o Hypotension, low CO, or sensitivity in abrupt changes of volume status Assessment and Management: o Evaluate fluid balance before dialysis so correct measures may be initiated at the start of the procedure o Start procedure by checking equipment: prime lines and dialyzer, test alarms, inspect connections o Results of dialysis determined by assessing amount of fluid removed (post-dialysis weight) and degree to which electrolyte imbalances have been corrected Complications: o Dialysis disequilibrium o Hypovolemia o Hypotension o Hypertension o Muscle cramps o Dysrhythmias and angina CONTINUOUS RENAL REPLACEMENT THERAPY (CCRT): o Blood circulates outside body through a highly porous filter similar to hemodialysis o CCRY happens continuously for an extended period and is accompanied by a simultaneous reinfusion of a physiologic solution o A pump is used and incorporates a weighing system so that fluids can be balanced hour to hour o Ultrafiltration rate is titrated to reach an hourly goal and is based on patient’s cardiac and pulmonary status, as well as hourly intake and output Indications: o High risk of instability who don’t tolerate rapid fluid shifts occurring w/ intermittent hemodialysis o Large amounts of IV fluids needed or parenteral nutrition o More than usual 3 to 4 hour hemodialysis treatment to correct metabolic imbalances of acute renal failure Contraindications: o Patients who become hemodynamically stable or no longer require continuous therapy – intermittent hemodialysis should be used Assessment and Management: o Fluid is either removed or replaced each hour in varying amounts to achieve the fluid balance goal o Hourly maintenance includes measuring blood and dialysate flows, calculating net ultrafiltration and replacement fluid, titrating anticoagulants, assessing the integrity of the vascular access, and monitoring hemodynamic parameters and blood circuit pressures Technical Complications o Access problems o Clotting o Air in circuit o Blood leaks Physiologic Complications o Hypotension o Hypothermia Psychological Aspects o Anxiety o Depression PERITONEAL DIALYSIS: o Semi-permeable membrane is the peritoneum & osmosis used to remove fluid o Effective alternative method of treating acute renal failure when hemodialysis is not available or when access to the bloodstream is not possible Advantages o Required technical equipment and supplies are less complicated and more readily available o Less training required by personnel o Adverse effects associated with more efficient hemodialysis are minimized o Patients can learn to manage their own peritoneal dialysis at home Disadvantages o Requires more time to remove metabolic wastes adequately and to restore electrolyte and fluid balance o Repeated treatment may lead to peritonitis o Long periods of immobility may result in complications such as pulmonary congestions and venous status Assessment and Management: o Empty bladder before procedure o Maintain accurate intake and output and weights to assess for volume depletion or overload o Monitor for S/S of peritonitis: fever, abdominal pain, cloudy peritoneal fluid are early signs o Sterile when abdominal dressing is being changed and when catheter is being accessed or discontinued Technical Complications: o Incomplete recovery of fluid o Leakage around catheter o Blood-tinged peritoneal fluid Physiologic Complications: o Peritonitis o Catheter infection o Hypotension o HTN and fluid overload o High BUN & creatinine o Hypokalemia o Hyperglycemia o Pain o Immobility o Discomfort ELECTROLYTE IMBALANCES: o Sodium is major predictor of serum osmolarity and controls movement of water o Hyperkalemia is caused by reduced renal excretion (elevated BUN & creatinine) o Dialysis is typically used to manage hyperkalemia in patients with renal disease o Renal failure is often complicated by elevated potassium, phosphate, and magnesium with a decreased sodium and calcium ACUTE KIDNEY INJURY: o Sudden onset of reduced renal function that can result in derangements in fluid and electrolyte balance, acid-base homeostasis, calcium and phosphate metabolism, blood pressure regulation, and erythropoiesis o Azotemia: elevated BUN and serum creatinine (AKA decreased glomerular filtration rate) o RIFLE classification: risk, injury, failure, loss of kidney function, end stage kidney disease o Labs: BUN, creatinine, urine volume (oliguria, anuria, nonoliguria), urine osmolality, SG & sodium o Oliguria = <400 mL/day; nonoliguria = > 400 mL/day; or anuria = < 100 mL/day 1. Prerenal Acute Kidney Injury o Characterized by any physiologic event that results in renal hypoperfusion o Most commonly caused by hypovolemia and cardiovascular failure o Sudden, drop in BP  hypoperfusion  prerenal acute kidney injury o Decrease renal perfusion  increase renin  renin-angiotensin-aldosterone cascade (RAAS) o Activation of RASS leads to angiotensin II & aldosterone, with goals of preserving circulatory volume to maintain adequate blood flow to essential organs o ACE inhibitors, ARBs, and NSAIDs can overwhelm kidney’s ability to regulate (moderate hypovolemia or CHF) o NSAIDs: disrupt prostaglandin-mediated afferent arterial vasodilation o Improved renal function is indicated by increase in urinary volume and urine sodium concentration and a decreased urine specific gravity 2. Intrarenal Acute Kidney Injury o Characterized by actual damage to the renal parenchyma o MANY different causes – glomerular, vascular, interstitial, & tubular o Common cause is acute tubular necrosis (ATN) – ischemia or nephrotoxicity Ischemic Acute Tubular Necrosis Toxic Acute Tubular Necrosis o Results from prolonged hypoperfusion o Prolonged hypoperfusion -> hypoxic tubular cells -> damage where restoration of renal perfusion no longer causes an improvement in glomerular filtration o Starts with concentration of a nephrotoxin in renal tubular cells which causes necrosis o Necrotic cells slough off and may cause obstruction and impairment of glomerular filtration 3. Postrenal Acute Kidney Injury o Any obstruction in flow of urine from the collecting ducts to the external urethral orifice o Commonly results from a blockage o Children at risk secondary to congenital anomalies & elderly men at risk because of high prevalence of benign or malignant prostatic hypertrophy o Obstruction slows the rate of tubular fluid flow and lowers the GFR o Causes increased reabsorption of sodium, water, and urea, leading to lowered urine sodium concentration and increased urine osmolality, BUN & creatinine CHRONIC KIDNEY DISEASE: o Slow, progressive, irreversible deterioration in renal function that results in kidney’s inability to eliminate waste products and maintain fluid and electrolyte balance o Leads to end-stage renal disease (ESRD) and requires RRT or renal transplantation to sustain life o KDOQI defines CKD: o Kidney damage with or without decreased GFR for 3 or more months -OR - o GFR of less than 60 mL/min/1.73 m^2 for greater than 3 months ▪ Represents loss of half or more of adult level of normal kidney function ▪ Prevalence of complications from CKD increases o Most common causes are diabetes mellitus and hypertension o Intact nephron theory: millions of nephrons per kidney, some individual nephrons are diseased and other nephrons compensate by increasing their individual filtration rates (increase rate of blood flow and hydrostatic pressure in their glomerular capillaries) National Kidney Foundation Stages Stage Description GFR 1 Kidney damage with normal or increased GFR >90 2 Kidney damage with mild or decreased GFR 60-89 3 Moderately decreased GFR 30-59 4 Severely decreased GFR 15-29 5 Kidney failure <15 or dialysis G-stages (based on GFR) 1. G1: lack of clear filtration deficit and defined as normal or increased kidney function (GFR >90) 2. G2: mild reduction in kidney function (GFR 60-89) that occurs in association with kidney damage 3. G3a: mildly to moderately decreased kidney function (GFR 45-59) 4. G3b: moderately to severely decreased kidney function (GFR 30-44) 5. G4: severely decreased kidney function (GFR 15-29) 6. G5: GFR less than 15 or need for dialysis; ESRD correlates to G5 CKD and represents those patients getting or eligible for RRT by dialysis or transplantation Albuminuria- A stages 1. A1: ACR < 30 mg/g 2. A2: ACR 30 to 299 mg/g 3. A3: ACR > 300 mg/g Prevention Progression of Chronic Kidney Disease: o Rapidly loss of nephrons from CHF or intravascular volume depletion, administration of nephrotoxic agents, urinary obstruction, and urinary infections o Avoid, monitor, and aggressively treat if they occur o Educate patient and families about continuous progression o Recognize S/S of urinary infection and get quick treatment o Avoid nephrotoxic drugs ▪ NSAIDs: causes rapid deterioration in renal function and should be avoid in CKD patients o Control blood sugar, blood pressure, restrict sodium intake (2 g/d), healthy body weight Management of Renal Failure Fluid Balance: o Monitor fluid status: intake and output, daily weight, urine output trends, vital signs, CVP, and PAOP o Monitor for S/S of hypervolemia: HTN, pulmonary edema, peripheral edema, jugular vein distention, and increased CVP o Administer fluids or diuretics to maintain intravascular volume and renal function o Once CKD is at stage G5, oliguria is shown with S/S of fluid overload (edema, HTN, pulmonary edema, heart failure, and jugular vein distention) Contrast-Induced Nephropathy (CIN): o Sudden decline in renal function following IV injection of contrast media o Only proven way to reduce risk for CIN is by aggressive volume expansion with isotonic crystalloids (normal saline solution) before and after contrast agent administration o Although CIN is believed to involve production of oxygen free radicals (i.e. alkalinization of urine with sodium bicarbonate), evidence-based practice shows no clear benefit to using sodium bicarbonate compared to saline solution Increased Bleeding Tendency: o Related to impaired platelet aggregation and adhesion and altered platelet-vessel wall interaction o Monitor platelet counts, coagulation studies, and assessing for bleeding (especially GI bleeding) o Administer blood products as needed o Protect patient from injury o Avoid medications that alter platelet function (NSAIDs & aspirin) o If heparin (for dialysis) or aspirin (for MI prevention) is prescribed with renal failure, monitor platelet counts closely Anemia: o Erythropoietin (produced by kidneys) stimulates red blood cell production in response to hypoxia o Anemia can result R/T erythropoietin deficiency, decreased red blood cell survival time, & blood loss from increased bleeding tendency o Treating anemia in patients with renal failure is important: o Increase oxygen-carrying capacity of blood o Increase intravascular volume o Increase quality of life (appetite, energy, work capacity) o Prevent negative consequences of anemia on the cardiovascular system ▪ Exacerbates myocardial, cerebral, and peripheral ischemia ▪ Increases risk for development/acceleration of left ventricular hypertrophy o Monitor hemoglobin, hematocrit, red blood cell indices, and reticulocyte counts Module 7 Hematologic and Immunologic Disorders Organ and Hematopoietic Stem Cell Transplantation (p. 919-921) Review the following disorders under this section: o Engraftment Syndrome (p. 965) • A recently identified disorder that occurs infrequently prior to or in association with the return of bone marrow growth after treatment of hematologic malignancies and hematopoietic stem-cell transplantation. • Patients most at risk for engraftment syndrome are women, those with acute leukemia (especially lymphocytic subtype), those who have just had haploidentical or fully myeloablative allogeneic hematopoietic stem cell transplantation (especially with human leukocyte antigen [HLA]-mismatched donors, umbilical cord stem cells), patient who previously received immunomodulatory agents (e.g., bortezomib, lenalidomide) or syngeneic transplant, and those who have had transplantation for autoimmune disorders or solid tumors. • Patients who have had early engraftment after high-dose marrow-ablative treatment are also at risk for engraftment syndrome. • Pathophysiology ▪ Regrowth of bone marrow cells, particularly myelocytes, results in release of inflammatory cytokines that produce vasodilation and capillary leaking similar to sepsis (it is hard to distinguish the two – there is no definitive diagnostic test to differentiate them) ▪ Lymphocytes and myelocytic precursors engraft the bone marrow earliest, and patients often still appear leukopenic at the onset of symptoms. ▪ Patients with engraftment syndrome often present with signs and symptoms similar to infection at a time when their blood counts are still low, and they are equally at risk for engraftment syndrome and severe infection. o Assessment ▪ Fever, total-body erythema or rash, fluid retention, and symptoms of respiratory distress ▪ Many patients exhibit additional signs or symptoms of cytokine effects, such as oliguria or hematuria with elevated creatinine, abdominal discomfort with elevated aminotransferases, and gastrointestinal bleeding. ▪ The Spitzer criteria for diagnosis includes these symptoms and the presence of the inflammatory marker of increased C-reactive protein. ▪ The onset of symptoms is rapid, usually occurring over 24 to 48 hours, and symptoms dissipate after the neutrophils engraft and the WBC count reaches about 2,500 to 3,000/mm. ▪ Even elevations of C-reactive protein are more reflective of inflammation than a true diagnostic test of differentiation. ▪ The cornerstones of diagnosis are the constellation of clinical symptoms, subsequent increase in WBC count in patients with previous leukopenia, and absence of a positive microbial culture. o Management ▪ Engraftment syndrome is managed supportively and conservatively. ▪ Patients are presumed septic and treated with broad-spectrum antimicrobial agents. ▪ Acetaminophen and diphenhydramine are administered as needed for erythema and pruritus. ▪ Hepatic dysfunction requires cautious monitoring and adjustment of fluids & meds ▪ IV fluids are used to prevent vasodilatory hypotension, but, occasionally, vasoconstricting agents such as phenylephrine or norepinephrine are necessary. ▪ Rapid-acting IV corticosteroids have been used effectively when clinical symptoms are strongly suggestive of this disorder, methylprednisolone dosed initially at 1 mg/kg/day is the usual treatment. ▪ Post-transplantation cyclophosphamide has been used with perceived success at Small studies using thrombomodulin to counteract capillary permeability have also shown promise to reduce symptoms in engraftment syndrome. ▪ Mechanical ventilation and renal replacement therapy are initiated as indicated, with the understanding and presumption that the syndrome is usually very short-lived. o Complications ▪ The long-term outcome for most patients with engraftment syndrome is excellent, and there are no significant clinical sequelae. ▪ Patients rarely die or have long-term ischemic organ damage, although the incidence of acute graft-versus-host disease is more prevalent in these patients. o Typhlitis/Necrotizing Entercolitis (p. 967) • Pathophysiology ▪ Patients with severe or prolonged neutropenia are at risk for acute gastrointestinal symptoms related to the presence and activity of microbes within the gastrointestinal tract. ▪ Resident Gram-negative organisms can produce serious clinical disease in patients without granulocytes. ▪ Microbial infiltration of less perfused areas of the bowel, such as the cecum and appendix, produces an acute inflammation of the bowel wall, edema, and paralytic ileus, a condition termed neutropenic enterocolitis (also known as typhlitis and ileocecal syndrome). ▪ Gases produced by these bacteria can also lead to air in the bowel wall, ischemia, and possible infarction, which is termed necrotizing enterocolitis or pneumatosis intestinalis. ▪ While reported more frequently in children, high-dose marrow suppressing therapy in any individual can lead to typhlitis. o Assessment ▪ Patients with prolonged or severe neutropenia are at risk for developing typhlitis, although other specific risks include presence of an appendix, 70 prior bowel surgery, and Clostridium difficile (“C. diff”) infection. ▪ Medications that have been linked to increased incidence of typhlitis (e.g., carboplatin, cyclophosphamide, cytosine arabinoside, daunomycin, docetaxel, doxorubicin, idarubicin, methotrexate, paclitaxel, pegylated asparaginase, pemetrexed, rituximab, topotecan, and vincristine) ▪ Consistent administration of oral antimicrobials to sterilize the gut reduces the risk of bacterial translocation and subsequent sepsis. Nonadherence to this medication regimen has been associated with development of this disorder. ▪ Patients present with diffuse abdominal pain that is semi-localized in the right upper or middle quadrant. ▪ Guarding, abdominal distention, diarrhea, and reduced bowel sounds are common, and rebound tenderness or gastrointestinal bleeding signals a more severe disease that has progressed to bowel ischemia and infarction. ▪ Most patients demonstrate symptoms of acute abdominal sepsis such as fever, fluid shifting with oliguria, weight gain, and hypotension, although in antibiotic-controlled disease, these septic symptoms may be intermittent. ▪ Initial screening tests include an abdominal flat plate x-ray to detect possible air under the diaphragm, and a CT scan with contrast, while also evaluating lactic acid and amylase levels for signs of bowel ischemia. ▪ An enlarged and edematous cecum is considered diagnostic, although other tests are better at predicting the severity of bowel wall injury or ischemia. o Management ▪ First, high-risk patients are administered oral antimicrobial antibiotics (usually in liquid form) that destroy intestinal bacteria, producing sterile conditions within the bowel. ▪ Second, patients with anticipated severe neutropenia are administered prophylactic hematopoietic growth factors, unless acute myeloid leukemia where there is concern the growth factors may enhance tumor growth (these patients may perhaps then have reduced neutropenia) ▪ In patients who develop less severe typhlitis, potent broad-spectrum antimicrobials aimed to destroy a variety of both gram-positive and gram-negative bacteria, gut rest, and observation may be warranted and adequate until the patient’s own WBCs repopulate their bone marrow and can destroy an existing complication, lactic acid levels are followed and IV fluids are administered to maintain gut perfusion. ▪ Vasopressor agents are avoided if at all possible. In more serious cases, granulocyte transfusions have been administered in an attempt to boost the patient’s immune activity. ▪ In severe, sepsis-related disease or pneumatosis, emergent surgical resection may be necessary. o Complications ▪ This continuum of bowel wall abnormalities may lead to acute bowel perforation, bowel infarction or gastrointestinal bleeding. These serious consequence often herald poor outcomes as the patients are also too high of risk to consider surgical resection of the bowel, even though this intervention may be the only potentially effective measure to arrest the sepsis. o Superior Vena Cava Syndrome (p. 971) • Superior vena cava syndrome (SVCS)—obstruction of the superior vena cava—results in venous blockage that produces pleural effusion and facial, chest, arm, and neck edema (it is not considered fatal) • Pathophysiology ▪ The superior vena cava is a thin-walled, low-pressure blood vessel in the mediastinal cavity that collects blood from the venous vessels that drain the head and neck and the upper thoracic cavity. ▪ The mediastinum is a rigid anatomical structure that contains the trachea, the vertebral column, the sternum and ribs, and the lymph nodes. ▪ Most cases of SVCS result from mediastinal malignancies or involved lymph nodes that cause extrinsic compression or invade the vessel and impair return of venous blood. ▪ Other tumors that have been associated with SVCS include metastatic malignant melanoma, renal cell cancer, and thymic cancer. ▪ Obstruction of the vessel lumen by a thrombus may also occur; it is most commonly caused by a central venous catheter or a hypercoagulability syndrome due to cancer. ▪ Nonmalignant causes are less common but may include tuberculosis, syphilis, or granulomatous disease. o Assessment ▪ Signs and symptoms of SVCS depend on the rapidity of compression of the superior vena cava. ▪ If it is compressed gradually and collateral circulation develops, indications of SVCS may be more subtle. ▪ Initial symptoms are most prominent in the early morning and include periorbital and conjunctival edema, facial swelling, and Stokes sign (tightness of the shirt collar). These signs may disappear after the patient has been upright for a few hours. ▪ The patient may also complain of visual disturbances and headache. ▪ Altered consciousness and focal neurologic signs may result from brain edema and impaired cardiac filling. ▪ Late signs and symptoms include distention of the veins of the thorax and upper extremities, dysphagia, dyspnea, cough, hoarseness, and tachypnea. ▪ All patients, including children, most commonly visit health care providers because of dyspnea. ▪ Pleural or pericardial effusions are present in some cases, compounding respiratory symptoms and providing a complex dimension for treatment planning. ▪ Most pleural effusions are transudative and related to obstruction of pleural and lymphatic outflow. ▪ Until recently, diagnostic evaluation of SVCS required multiple tests to validate the location, size, and vena caval involvement of tumors or thrombus. ▪ Conventional chest CT with IV contrast, venography, angiography, and radionuclide scans were necessary. ▪ Currently, the spiral CT scan with contrast, which provides accurate information about tumor location and involvement of the vena cava, may be the only diagnostic test performed. ▪ However, biopsy or cytologic tests may be required to establish a diagnosis in many patients because this syndrome is the presenting symptom at the time of diagnosis of cancer. o Management ▪ Treatment is determined by the severity and rapidity of symptom onset. ▪ As many as 31% of patients experienced symptoms less than 2 weeks prior to presentation for evaluation and hence require emergent antineoplastic therapy as well as urgent diversive procedures ; the mean time to presentation in one study was 34 days. ▪ The primary treatment of choice for SVCS caused by a tumor is radiation therapy ▪ Radiation therapy is initially given in high daily fractions (total dose of 300 to 500 cGy) for 2 to 4 days followed by 100 to 200 cGy for an additional 14 to 21 days. ▪ Symptom relief occurs in 7 to 14 days. 127 Radiation therapy is given with palliative intent for SVCS in advanced cancer with little hope of total resolution. ▪ Radiation of the mediastinal, hilar, and supraclavicular lymph nodes and any adjacent parenchymal lesions is appropriate in patients with locally advanced non–small cell lung cancer. ▪ Patients who receive radiation therapy experience increased cough within 3 days of the start of therapy. ▪ During the initial 7 to 10 days, secretions are increased because of inflammation, but a dry irritation then develops, resulting in a dry, hacking cough with few secretions but possible bleeding. ▪ Chemotherapy may be the treatment of choice for SVCS in patients with disseminated disease, such as small treatment of SVCS caused by a thrombus around a central venous catheter may include intravenous or catheter-directed antifibrinolytics or anticoagulants and possibly surgical removal of the catheter. ▪ In any case, chest and neck central venous catheter placements should be avoided until effective treatment has been delivered. ▪ In some circumstances, the placement of stents or vascular grafts in the superior vena cava provides immediate symptomatic relief while patients receive definitive therapy. ▪ It is unclear whether long-term anticoagulation is required. Supportive care is essential. ▪ Maintenance of a patent airway is of the highest priority. ▪ Because many patients have severe dyspnea, they are unable to lie flat for their radiation therapy, and short-term airway intubation may be necessary. ▪ Clinicians may prescribe oxygen therapy, diuretics, steroids, and heparin, and their administration requires careful observation of patient response. If necessary, administration of corticosteroids for 3 to 7 days to decrease the edema associated with the disease and treatment is warranted. ▪ The nurse teaches the patient not to bend over and to avoid Valsalva maneuvers. ▪ When the patient is in bed, the head should be at least in a semi-Fowler position. ▪ Elevation of the arms on pillows helps alleviate swelling; however, elevation of the legs is not helpful because this increases fluid volume in the torso. o Complications ▪ Several complications may occur in patients with SVCS. Right-sided heart failure is the most common. ▪ Such heart failure is usually self-limiting and is treated symptomatically with fluid restrictions, diuretics, and digoxin. ▪ Vessel rupture in SVCS when a tumor invades the vena cava is a great risk because the tumor shrinks with treatment. ▪ The incidence of vessel rupture is highest in patients with esophageal and lung cancer; peak incidence is 3 to 4 weeks after initiation of therapy. ▪ Warning signs of vessel rupture are acute and sudden dyspnea, hypoxia, cough, and vascular collapse. ▪ Radiation pneumonitis, an inflammatory response in the radiation field that correlates with breath sound and radiographic changes reflective of alveolar capillary permeability, may occur 2 to 8 weeks after start of therapy in patients who receive chest radiation for SVCS. ▪ Treatment of radiation pneumonitis involves corticosteroids and supportive therapy. ▪ SVCS recurs in 10% to 30% of patients. ▪ Severe obstruction results in impaired cardiac filling, and the venous congestion has also been associated with tracheal obstruction and cerebral edema. ▪ Long-term obstruction has also been associated with portal hypertension and esophageal varices. o Pleural effusion (p. 972) o Pathophysiology ▪ There is normally 30 to 150 mL of fluid between the visceral and parietal pleura that helps maintain a negative pleural pressure to facilitate lung expansion with minimum work of breathing. ▪ A pleural effusion is excess accumulation of fluid in the pleural space with subsequent impaired lung expansion and hypoxemia. ▪ When lymphatic obstruction (particularly of the thoracic duct), venous congestion, pleural inflammation, or excess capillary permeability occurs, the amount of fluid increases or does not drain properly. ▪ Although many nonmalignant conditions (e.g., congestive heart failure, hypothyroidism) may cause pleural effusion, malignant conditions involving lymphatic obstruction or infiltration with malignant cells may also be the cause. ▪ Pleural effusions that result from volume overload, capillary permeability, or lymphatic obstruction produce a transudate characterized by the presence of albumin and the absence of cell fragments or enzymes in the pleural fluid. ▪ Malignant cell infiltration or pleuritic infection causes pleural inflammation and exudates characterized by the release of red blood cells, WBCs, and lactate dehydrogenase into the pleural fluid. ▪ Unilateral pleural effusions occur when the tumor is located in a single lung, but bilateral effusions are more common with abdominal cancers (e.g., ovarian, pancreatic), hematologic malignancies, or when accompanied by ascites. ▪ The presence of pleural effusion is associated with a shorter life expectancy, averaging 3 to 12 months after diagnosis. ▪ Accumulation of pleural fluid leads to increased (more positive) pleural pressure. Higher pleural pressures increase the work of breathing, and collapsed alveoli cause decreased gas exchange and hypoxemia. o Assessment ▪ The clinical findings in pleural effusion are related to the two major physiologic mechanisms: increased work of breathing and alveolar collapse. ▪ Excess pleural pressures decrease lung compliance (“stiff lungs”). ▪ Patients feel short of breath and must use their accessory muscles to breathe, and chest excursion on the affected side is reduced. ▪ When patients are in an upright position, the force of gravity pulls down the fluid, and breath sounds are diminished to the level of fluid. The pleural fluid takes up space in the chest, impeding lung expansion with consequent alveolar collapse. ▪ Symptoms that relate to this pathologic process are persistent cough and dyspnea, diminished breath sounds, unequal chest excursion, tracheal shift away from the effusion, and signs of hypoxemia (e.g., dyspnea, anxiety, confusion, oliguria, decreased bowel sounds). ▪ The first diagnostic test performed to confirm the presence of pleural effusion is an upright chest radiograph or CT. ▪ Lateral x-rays may be more sensitive that upright x-rays in small effusions. ▪ The fluid accumulates in the lower lung, causing a blunted diaphragmatic dome and decreased radiolucence in the lower lung. Fluid accumulation often produces a meniscus of decreased radiolucence and a thickened lateral pleural lining, indicating fluid tracking up the side. ▪ When alternative diagnoses such as hemothorax, infection, or tumor infiltrates are possible, the CT scan may be more accurate. ▪ After a pleural effusion is confirmed, a cytologic evaluation, which involves extraction of a sample of fluid and sending it for fluid chemistry and cytology, is necessary. ▪ Pleural fluid is categorized as transudative or exudative, which provides clues to the cause of the effusion. ▪ Multiple specimens may be necessary to confirm malignancy; it is estimated that cytology may be positive only half of the time when malignant cells are present. 149 When fluid cytology is inconclusive, pleural biopsy may be helpful in diagnosis of malignant infiltration. o Management ▪ The treatment of pleural effusion depends on the etiologic mechanism, rapidity of symptom onset, degree of respiratory compromise, and overall goals of care. ▪ Because many patients with malignant pleural effusion have limited survival, the selection of treatment that enhances quality of life with minimal time required for recovery is optimal. ▪ When pleural effusions are small or have a nonmalignant cause, observation without definitive treatment may be indicated. ▪ Aggressive antineoplastic therapy may be indicated when a large tumor causes lymphatic obstruction, heart failure, or pneumonitis that in turn causes pleural effusion. ▪ When malignant cells are present in the pleural fluid, management may be determined by overall treatment goals. ▪ Repeated therapeutic thoracenteses are often the preferred initial choice; this assumes that the ultimate cause of the pleural effusion is being treated or that the patient’s life expectancy does not warrant more interventional measures. ▪ When the patient’s life expectancy is longer, and pleural effusions do not resolve with anticancer therapy and intermittent thoracenteses, treatment includes long-term chest catheter drainage or pleurodesis. ▪ Long-term pleural drainage via a soft tunneled catheter allows patients to have a means of draining excess fluid while remaining at home. ▪ When drainage slows and patients become a good candidate for pleurodesis, they are admitted to the hospital for this procedure, although spontaneous pleural adherence has occurred. ▪ Alternatively, patients may be admitted for placement of a traditional chest catheter, and once drainage slows, pleurodesis may be performed. ▪ Pleurodesis, also called pleural sclerosing, involves intrapleural administration of a chemical (e.g., doxycycline, bleomycin) or a mechanical agent (e.g., talc slurry) to alter the pH of the pleural fluid and cause inflammatory adherence of the visceral and parietal pleura to each other. ▪ Sclerosed pleura do not have the normal lubricating pleural fluid, and restrictive lung disease is the long-term consequence. ▪ Pleurectomy is a thoracic surgical procedure that removes the entire pleura. Pleurectomy is effective but can be difficult to perform when long-term inflammation and pleurodesis attempts cause a friable pleura that is not easily separated. ▪ Chronic, long- term pleuroperitoneal shunts or implanted access devices have been used, but development of fibrin sheaths on the catheters often causes occlusion. ▪ In cases where catheter drainage is unsuccessful, intracavitary chemotherapy with cisplatin, interferon, or pemetrexed have been used with moderate success. o Complications ▪ Untreated pleural effusions that continue to accumulate lead to clinically significant alveolar collapse and respiratory failure, which may be caused by loss of gas-exchanging airways or mediastinal shifting with major airway obstruction. ▪ Progressive hypoxemia leads to profound respiratory acidosis and ischemic organ failure. ▪ Evacuation of an extensive and long-standing pleural effusion may result in re-expansion pulmonary edema or hypotension from fluid shifts. o Tracheobronchial obstruction (p. 975) • Pathophysiology ▪ Obstruction of the trachea or major branches of the bronchi with tumor results in respiratory distress and hypoxemia. ▪ The severity of symptoms depends on the rapidity of obstruction and degree of closure. ▪ Tumors most likely to cause airway obstruction are lung cancer and lymphoma, although other metastatic tumors (e.g., head and neck cancer, melanoma, thyroid, renal or breast cancer) and nonmalignant disorders (e.g., amyloidosis, bronchomalacia) may also cause airway obstruction ▪ left mainstem bronchus obstruction, poor performance status, and high anesthesia risk category are poor prognostic factors in outcomes for patients with central airway obstruction. o Assessment ▪ Patients with tracheobronchial obstruction present with varying degrees of dyspnea depending on the amount and location of the obstruction and the rapidity of onset. ▪ Some patients with slowly developing tumors have compensated respiratory acidosis and minimal symptoms even with nearly complete obstruction. ▪ Other patients, especially those with lymphoma or small cell lung carcinoma, have rapidly growing tumors and severe symptoms even when the airway is less than 75% obstructed. ▪ Stridor is present in tracheal obstruction, and wheezing with unequal chest excursion is seen with bronchial obstruction. ▪ Some patients presenting with severe respiratory distress actually have only partial airway obstruction, but the resultant narrowed airway leads to concomitant atelectasis or trapped secretions with pneumonia that may be mistaken as more severe tumor obstruction. ▪ Bronchoscopy makes it easy to detect tracheal or bronchial obstruction and grade its severity. ▪ However, bronchoscopy does not always reveal whether the airways are compressed extrinsically or invaded with tumor. ▪ Bronchoscopy is used with spiral CT scans to provide a comprehensive description of the obstructive process that is used to guide therapy. o Management ▪ Clinically significant obstruction of the major airways always necessitates immediate treatment, although the therapeutic plan varies according to tumor-specific factors and therapeutic goals. ▪ Emergent treatment of airway occlusion–induced hypoxemia or hypercapnia may require nasal inhalation or heliox-based nebulizer treatments. ▪ A combination of oxygen and helium that is lighter than pure oxygen, heliox enhances movement of the air beyond the area of obstruction and provides palliative relief until more aggressive operative measures are possible. ▪ If air movement is adequate, bronchodilators and corticosteroids are administered to enhance ventilation, and if simultaneous pneumonia is suspected, antimicrobial therapy is instituted. ▪ Effective treatment for endobronchial tumors includes laser, cautery, photodynamic therapy, and endobronchial brachytherapy. ▪ These therapies for tumors invading the major airways are highly successful for prolonging life as well as improving its quality. ▪ Most procedures entail use of a rigid bronchoscope under anesthesia, and patients usually experience a rapid recovery with little more than a sore throat and annoying cough for a few days afterward. ▪ Airway opening with tracheal or bronchial stents may provide temporary symptomatic relief while definitive anticancer treatment is implemented for palliative relief of symptoms. ▪ For insertion of an airway stent, a rigid bronchoscope and light anesthesia are necessary, and multiple bronchoscopic procedures to assess or adjust placement are required. ▪ The most common problem with stents, especially if placed before shrinking the tumor, is displacement, because the airway naturally opens with the reduction of tumor. ▪ Displaced stents usually cause severe and sudden respiratory distress and require immediate interventional adjustment. ▪ Chronic lung infections after stent placement may occur, and are associated with high risk of occlusion and long-term stenosis. o Complications ▪ Two severe complications that may occur are total airway occlusion and hemorrhage caused by tumor erosion into the nearby pulmonary vessels. ▪ Treatment of total obstruction is the same as that of partial obstruction when an improvement in symptoms can be reasonably expected as a result of therapy. ▪ Emergent extracorporeal membrane oxygenation (ECMO) has also been used to bridge until the tumor shrinks. ▪ Treatment of hemorrhage, when recognized before massive bleeding occurs, may involve embolization. ▪ If severe hemorrhage occurs, it is necessary to insert a dual-lumen endotracheal tube or single- sided intubation and occlude the bleeding lung while ventilating the good lung until surgical repair can be performed. ▪ Airway obstruction may also lead to erosion through the airway and accompanying pneumothorax. In these circumstances, supportive therapy, such as chest tube insertion, may be used but is rarely helpful. o Hypercalcemia (p. 976) • Hypercalcemia exists when the corrected serum calcium level is above 11 mg/dL (normal range, 8.5 to 10.5 mg/dL). • This is the most common metabolic oncologic emergency that develops when the bones release more calcium into the extracellular fluid than can be filtered by the kidneys and excreted in the urine. • In the advent of effective prevention of bone demineralization using bisphosphonates, this complication has greatly reduced in incidence, and now most commonly a manifestation of refractory and end-stage malignancy. • Pathophysiology ▪ Ninety-nine percent of the calcium in the body is in an insoluble form in the bones. ▪ The remaining 1% is freely exchangeable calcium. The calcium of importance is the ionized calcium, which must be maintained within a precise range. ▪ Free total calcium levels may be affected by albumin, other serum proteins, or vascular volume status, and are most likely to be underestimated, even with standardized correction formulas. ▪ Serum calcium levels are regulated by parathyroid hormone and calcitonin. release of parathyroid hormone from the parathyroid glands stimulates an increase in serum calcium levels, whereas the release of calcitonin produces a decrease in serum calcium levels. ▪ The three primary etiologies of hypercalcemia are (1) excessive quantities of intact parathyroid hormone (parathyroid origin) or humoral- mediated (malignant production) parathyroid-related hormone (2) osteolysis with bone demineralization (3) excessive vitamin D activation. ▪ Ectopic parathyroid hormone (PTH) may occur with primary parathyroidism (incidence less than 20% of cases), or with PTH or PTH-like substance production by tumor cells (44% to 60% of cases). ▪ Destruction of the bone by metastatic invasion was once believed to be the most common cause of malignant hypercalcemia; however, reduction of skeletal events with prophylactic bisphosphonates has reduced the incidence of this etiology. ▪ In patients with multiple myeloma, the abnormal plasma cells produce osteoclast-activating factor (OAF); however, hypercalcemia rarely develops in these patients unless they have inadequate renal function. ▪ Patients with T-cell lymphoma have severe hypercalcemia related to the ectopic production of OAF, colony-stimulating factor, interferon-γ, and an active vitamin D metabolite. o Assessment ▪ The severity of signs and symptoms of hypercalcemia often correlates with the serum calcium level. ▪ Mild calcium elevations may be asymptomatic or present as anorexia, constipation, fatigue, or malaise. ▪ Moderate hypercalcemia has presenting symptoms such as abdominal pain, nausea, bone pain, polyuria, and mental status changes. ▪ Most patients presenting with severe calcium elevations demonstrate dysrhythmias or neurologic symptoms such as somnolence, combativeness, confusion, or coma. ▪ Elevated serum calcium and elevated ionized calcium are the hallmark diagnostic findings in hypercalcemia. ▪ After initial assessment of increased calcium levels, the specific etiology should be determined. ▪ Intact PTH is analyzed; when elevated, it is indicative of primary or secondary parathyroidism. ▪ A normal intact PTH or elevated immunofluorescence PTH-related peptide may indicate humoral-mediated PTH elevations ▪ Bone demineralization is characterized by normal PTH levels with low phosphorous and elevations in alkaline phosphatase. ▪ Hyperphosphatemia in the presence of hypercalcemia, especially in the absence of kidney dysfunction, suggests vitamin-D mediated disease. ▪ Symptomatic patients usually have ECGs that show a bradycardia and prolonged PR, QRS, and QT intervals. o Management ▪ Medical management of hypercalcemia involves the use of IV fluids and drug therapy to enhance renal excretion of calcium and to decrease bone resorption. ▪ Acute hypercalcemia is initially treated with IV normal saline (0.9% NaCl) solution to dilute calcium levels and increase urinary calcium excretion. ▪ When hypercalcemia is life-threatening, aggressive hydration (250 to 300 mL/h) and IV loop diuretics such as furosemide are necessary. ▪ Hemodialysis with calcium-free dialysate has been used successfully for emergency management of life-threatening hypercalcemia. ▪ In most patients, treatment with hydration, diuretics, appropriate antitumor therapy, and mobilization is effective ▪ Patients who do not respond to these therapies require hypocalcemic therapy indefinitely. ▪ Bisphosphonates are most frequently used. ▪ Currently, the most potent bisphosphonate available is zoledronic acid. It is administered as an 8-mg 15-minute IV infusion daily for 3 days unless serum calcium levels decrease before that time. ▪ Alternatively, bisphosphonate therapy with pamidronate may be given as a 90 mg infusion over 90 to 120 minutes. ▪ Denosumab, an FDA-licensed monoclonal antibody targeting rank ligand for prevention of bone breakdown, is also available to prevent skeletal related events, but its use in hypercalcemia has been limited. 180,185 In cases unresponsive to bisphosphonates, calcitonin, corticosteroids, or strontium-98 may be useful. ▪ If possible, patients should ambulate to prevent osteolysis. It is necessary to eliminate constipation, which is usually caused by an increased level of calcium in the blood. ▪ Reduced oral intake of calcium or increased salt intake may be of some help. ▪ Patients should not take medications, such as thiazide diuretics and vitamins A and D, because they elevate the calcium level. ▪ Close monitoring of fluid status is essential. Patients may receive up to 10 L of IV fluids daily, and the nurse should carefully measure intake and output. In addition, careful observation for overhydration is important. Potassium supplements may be necessary. ▪ Hypercalcemia is a common oncologic emergency that can be prevented or diminished in a large number of patients with the appropriate prophylactic bisphosphonates, education, and precautions. o Complications ▪ Permanent renal tubular abnormalities may develop in patients with prolonged hypercalcemia. ▪ Sudden death from cardiac dysrhythmias may result from an acute increase in serum calcium. ▪ Long-term bisphosphonate use has been associated with severe osteonecrosis of the jaw. Specific risk factors for this complication are not yet clear. o Tumor lysis syndrome (p. 979) • A metabolic imbalance caused by rapid cancer cell death • Most patients with chemosensitive or radiosensitive tumors experience this complication 1 to 5 days after initiation of therapy. • There are documented instances of tumor lysis syndrome in rapidly proliferating disease such as acute leukemia or high-grade lymphoma even before treatment initiation. • Patients at greatest risk for tumor lysis syndrome are those with bulky tumors that have a high growth rate (e.g., acute leukemia or Burkitt lymphoma) and those with highly radiosensitive or chemosensitive tumors, such as small cell lung cancer and most malignant lymphomas • Patients with preexisting renal dysfunction may be at greatest risk owing to their difficulty in clearing the metabolic waste products fast enough to prevent clinical complications. • Other patients at high risk are those with Merkel tumor, testicular cancer, hepatoblastoma, and medulloblastoma. • Pathophysiology ▪ Rapid cell death causes the release of intracellular contents (potassium, phosphorus, and nucleic acids) into the circulating serum. ▪ The normal filtration mechanisms in the kidneys should immediately detect the levels of metabolic waste products and attempt to excrete them. ▪ If production is more rapid than excretion or renal insufficiency is present, accumulation of electrolytes and uric acid occurs in the serum. The most common abnormalities include hyperkalemia, hyperphosphatemia, and hyperuricemia. ▪ High phosphorus causes the kidneys to excrete calcium, causing hypocalcemia. ▪ Hyperuricemia causes deposition of uric acid crystals in the urinary tract and may lead to renal failure. o Assessment ▪ Signs and symptoms of tumor lysis syndrome are related to the specific electrolyte imbalances involved and renal dysfunction. Hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acidosis may occur. ▪ The electrolyte panel analysis is used to identify key abnormalities in patients at risk for tumor lysis syndrome. ▪ Elevated serum potassium, phosphate, uric acid, blood urea nitrogen, and creatinine, with low calcium, are reported. ▪ Acidosis may be present in patients with severely compromised renal function. ▪ The urinary uric acid/creatinine ratio is greater than 1 ▪ Renal ultrasonography is used to exclude ureteral obstruction. o Management ▪ Treatment involves recognition of high-risk patients and promoting prevention through aggressive hydration, as well as administration of phosphate-binding agents and allopurinol for at least 48 hours before beginning chemotherapy ▪ It is necessary to avoid agents that block tubular reabsorption of uric acid (e.g., aspirin, radiographic contrast, probenecid, thiazide diuretics). The goal is to keep the serum uric acid level within normal limits. ▪ Electrolyte disturbances are specifically treated as needed. ▪ IV fluids are given to ensure a urine volume of more than 3 L/d. In the past, IV sodium bicarbonate (4 g initially, then 1 to 2 g every 4 hours) has been administered to alkalinize the urine and reduce uric acid crystallization in the kidney tubules. ▪ Clinicians are now less likely to initiate alkalinization if the phosphate is high because calcium phosphate precipitation is equally likely to cause renal failure. ▪ To measure urine output more accurately, insertion of a Foley catheter into the bladder is usually necessary. ▪ If oliguria or anuria develops, ureteral obstruction must be excluded. ▪ Phosphate-binding agents such as aluminum hydroxide are given every 2 to 4 hours in an effort to keep phosphate levels below ▪ Concomitant diuresis or medications such as Kayexalate that enhance gastrointestinal excretion of potassium may effectively manage elevated serum potassium levels not prevented with hydration. ▪ Allopurinol, a xanthine oxidase inhibitor that blocks uric acid production, is administered in doses ranging from 300 to 900 mg/d. ▪ Rasburicase (Elitek) acts like the natural enzyme urate oxidase to oxidize uric acid to allantoin for excretion. ▪ If diuresis does not occur within a few hours after the initiation of treatment, renal replacement therapy is needed. ▪ An initial hemodialysis treatment usually reduces the patient’s uric acid levels by 50%, but most patients then receive several additional days of continuous renal replacement therapy (CRRT) until electrolyte abnormalities and hyperuricemia resolve. ▪ A low-calcium dialysate is used to prevent calcium phosphate precipitation. ▪ If peritoneal dialysis is used, albumin is added to the dialysate to increase uric acid protein binding and removal. ▪ The focus of nursing care is on careful monitoring of fluid therapy, intake and output, and electrolyte balance. ▪ The use of prophylactic allopurinol, aggressive hydration, and early intervention with CRRT has reduced the incidence and severity of tumor lysis syndrome [Show More]

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