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

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 Tw