Exam 2: NSG 430/ NSG430 (NEW 2026/ 2027 Update) Adult Health Nursing II Complete Guide| Comprehensive Questions & Answers| Grade A| 100% Correct (Verified Solutions)- GCU

Exam 2: NSG 430/ NSG430 (NEW 2026/ 2027 Update) Adult Health Nursing II Complete Guide| Comprehensive Questions & Answers| Grade A| 100% Correct (Verified Solutions)- GCU Q. S/S of ADHF ANSWER Fluid overload, SOB, fatigue Q. What can rheumatic heart disease result in ? ANSWER Mitral valve stenosis Q. What happens in mitral valve stenosis? ANSWER Stiff valave is unable to open sufficiently during left atrial systole (ejection) Q. What is main symptom of mitral valve stenosis? ANSWER Exertional dyspnea (shortness of breath on exertion) Q. Why do you do prophylactic antibiotic therapy for mitral valve stenosis? ANSWER Prevent recurrent rheumatic fever and infective endocarditis Q. What drug do you teach benefits and side effects for in mitral valve stenosis ? ANSWER ACE inhibitors Q. Surgical therapy for mitral valve stenosis ANSWER Valve replacement or valvuloplasty Q. What do you need to tell patients about after getting a valve replacement? ANSWER Patient will need to be on lifelong anticoagulant therapy because clots form more easily in artificial replacement valves Q. What is pericarditis? ANSWER inflammation of the pericardium Q. What does the pericardium do? ANSWER Holds serious fluid and anchors and provides lubrication to decrease friction between heart contractures Q. What is the most common cause of pericarditis? ANSWER Infectious (viral & bacterial) Q. Main s/s of pericarditis ANSWER Pericardial friction rub and fever Q. How do you assess pericardial friction rub? ANSWER Auscultate on lower left sternal border Q. What s/s needs to be reported immediately with pericarditis? ANSWER Jugular venous distention to jaw level Q. What are other s/s of pericarditis? ANSWER Progressive frequent severe, sharp chest pain (worse when lying flat) Q. Drug treatment for pericarditis ANSWER NSAIDs (usually indocin), antibiotics to treat bacterial, and corticosteroids Q. What are two types of infective endocarditis? ANSWER Acute and subacute Q. What is acute infective endocarditis? ANSWER Affects those with health valves and staph is usually the bacteria most common; likely from IV drug use Q. What is subacute infective endocarditis? ANSWER Affects those with preexisting valve disease or congenital and strep is usually the bacteria Q. What is the assessment finding of nursing diagnosis of decreased cardiac output related to valvular insufficiency for a patient with IE? ANSWER Urine output less than 30 ml/hr Q. When do you give prophylactic antibiotics for patients with IE ANSWER Dental procedures, respiratory tract incisions, tonsillectomy, and adeniodectomy Q. If the IE is from strep, what do you need to tell the patient? ANSWER They need to be arranged for placement of long-term IV catheter Q. What are the 3 types of cardiomyopathy? ANSWER hypertrophic dilated restrictive Q. What is hypertrophic cardiomyopathy? ANSWER Obstructed LV outflow and most common in young/atheletes Q. What will you want to know with hypertrophic cardiomyopathy? ANSWER You will want to know if there is a history in the family of cardiac arrest Q. S/S of cardiomyopathy ANSWER Dry cough, palpitations, abdominal bloating, N/V, anorexia, S3, S4 murmurs, pulmonary crackles, edema, pallor Q. What are interventions for cardiomyopathy? ANSWER Beta blockers, prepare for cardiac Cath, instruct client to avoid strenous exercise Q. What is the main sign of acute coronary syndrome? ANSWER Angina-chest pain Q. What is stable angina? ANSWER Resolves with rest and lasting less than 20 minutes Q. What is unstable angina? ANSWER Does not resolve with rest Q. Management for angina ANSWER Morphine, oxygen, nitro, and aspirin Q. What is a STEMI? ANSWER Heart attack where there is a total occlusion of coronary artery Q. What can a stemi result in? ANSWER Vtach, Vfib, and pericarditis Q. Main s/s of STEMI ANSWER Angina Q. What do you always ask with a patient with chest pain? ANSWER What time did your chest pain begin? Q. What is the main intervention for a STMI? ANSWER Emergent PCI Q. What is the goal for PCI? ANSWER 90 minutes from door to Cath laboratory (open the blocked artery) Q. What if your hospital does not have a Cath lab, what do you do next for a STEMI? ANSWER Thrombolytic therapy; given IV within 30 minutes of arrival to the ED Q. What is a patient at risk for with PCI and what should the nurse assess? ANSWER Risk for hemmorage; assess BP, pulses, and access site immediately after Q. Risk factors for bradycardia ANSWER Calcium channel blockers, beta blockers, athletes, hypothermia Q. Medication treatment for bradycardia ANSWER Atropine (anticholinergic drug) What do you do for unstable bradycardia? Transcutaneous (external) pacing Risk factors for tachycardia Stressors, hyperthyroidism, hypovolemia (dehydrated), heart failure Medication for tachycardia Metoprolol Intervention for tachycardia Vagal maneuvers What are premature ventricular contractions premature occurrence of a QRS complex that is wide and distorted; looks like an extra QRS that does not belong Risk factors with PVCs Stimulants, electrolyte imbalances (hypokalemia), hypoxia, exercise, fever, emotional stress Management of PVCs Dont really treat unless symptomatic; correct the cause (electrolyte imbalance, oxygen for hypoxia); assess hemodynamics status is important if you need drug therapy Drug for PVCs Amiodarone What is ventricular tachycardia? Run of three or more PVCs with ventricular rate at 150-250 bpm Treatment of v-tach with pulse Amiodarone or cardio version if more unstable Treatment of v-tach with no pulse same manner as v-fib with CPR and rapid defibrillation Treatment of ventricular fibrillation Immediate CPR and ACLS: defibrillation and drug therapy (epinephrine, vasopressin) What does a patient look like in v fin Unresponsive, pulses, and apenic When do we use defibrillation? Fib and pulseless tach What is the difference of procedure in defibrillation and cardio version? In cardio version, the sync button is turned ON What is post procedure education of pace makers? Patient can be out of bed once stable; keep arm down until they see the doctor; monitor insertion site for bleeding and infection and keep it clean and dry; report any pulse rate lower than what its set at; no MRI What is AKI? Rapid loss of kidney function accompanied by a rise in creatinine and BUN, reduction in urine output, low GFR, and high potassium What is pre-renal failure? Causing reduction in blood flow to kidneys Factors of pre renal failure Severe dehydration, trauma, hemorrhage, hypotension, heart failure, decrease in CO What does pre renal azotemia result in? Oliguira, reduction in excretion of sodium, increased salt and water retention What is acute tubular necrosis? Blood flow to kidneys is poor/poor oxygenation and most common cause of infrarenal kidney injury Causes of acute tubular necrosis Trauma, massive blood transfusion, nephrotoxins What is post-renal injury? Involves mechanical obstruction in the outflow of urine Causes of post-renal ? Benign prostatic hyperplasia, prostate cancer, calculi, trauma, obstruction What is RIFLE classification? Risk, Injury, Failure, Loss, & end-stage renal disease If a patient is admitted to the hospital with severe renal colic, what is the first priority ? Administer opioids What type of diet are AKI patients on? Increase dietary fat & carbs, restrict sodium, restrict fluids, enteral nutrition First step to produce the greatest reduction in risk for CAD. 1. First, assess for the readiness to change and health literacy. 2. Then, help the patient select the lifestyle changes acute coronary syndrome (ACS) chest pain from ischemia is prolonged and not immediately reversible (STEMI and NSTEMI) Unstable angina (UA) chest pain that is new in onset, occurs at rest. The pain usually lasts 10 minutes or more myocardial infarction (MI) occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation. STEMI occlusive thrombus, results in ST-elevation. The artery must be opened within 90 minutes of presentation to restore blood and O2 to the heart muscle (by PCI or thrombolytic therapy) PCI Done in Cath lab. first-line treatment for MI. It confirms which artery has the occlusive thrombus so it can be opened with a balloon and stent - performed with local anesthesia - patient is ambulatory shortly after the procedure - hospital stay is about 3 to 4 days after MI Thrombolytic therapy done in hospitals that do not have a catheterization laboratory for PCI for a pt with STEMI. - limit the infarction size by dissolving the thrombus in the coronary artery - give the thrombolytic within 30 minutes of the patient's arrival to the ED - All thrombolytics (e.g., tenecteplase, alteplase) are given IV Not candidates for PCI (CABG surgery used instead) diabetes, left ventricle dysfunction, chronic kidney disease, failed PCI with ongoing chest pain, blockages are long or difficult to access CABG (coronary artery bypass graft) placement of arterial or venous grafts to provide blood from the aorta to the heart muscle distal to blocked coronary arteries. Requires: - sternotomy (opening of the chest cavity) - cardiopulmonary bypass (blood is diverted from the patient's heart to a machine where it is oxygenated and returned) The Internal hammer artery (IMA) is the most common artery used for bypass graft. CABG medications Perioperative calcium channel blockers and long-acting nitrates can control the spasms Minimally invasive direct coronary artery bypass (MIDCAB) does not involve a sternotomy and CPB. off-pump coronary artery bypass (OPCAB) requires sternotomy but no CPB performed on a beating heart Totally endoscopic coronary artery bypass (TECAB) uses a robotic technology to perform CABG surgery. No CPB. PCI and thromolytic therapy pallitative or cure? palliative. Not a cure procedure of thombolytic therapy 1. draw blood to obtain baseline laboratory values 2. start 2 or 3 lines for IV therapy. perform all invasive procedures before giving thrombolytic therapy - therapy is given in 1 IV bolus or over time (30 to 90 minutes) Signs that repercussion occurred 1. return of the ST segment to baseline on the ECG 2. resolution of chest pain 3. rapid rise of the serum cardiac biomarkers within 3 hours of therapy (necrotic heart cells release proteins into the circulation after perfusion is restored to the area) NSTEMI nonocclusive thrombus, does not cause ST segment elevation. patients usually undergo catheterization within 12 to 72 hours. Thrombolytic therapy is not indicated diabetics with MI may have silent (asymptomatic) MIs because of cardiac neuropathy or have atypical symptoms (e.g., shortness of breath). NOT candidates for PCI= CABG surgery Initial phase of MI sympathetic NS release (norepinephrine and epinephrine) = diaphoresis, increased HR and BP (later drops from decreased CO) and vasoconstriction of peripheral blood vessels, Fever (up to 100.4, 38 in first 24-48 hrs) patient’s skin may be ashen, clammy, and cool to touch. After MI - increased BG (glycogenolysis occurs) - by 6 wks heart muscle is considered healed (scar tissue has replaced necrotic tissue) - Dysrhythmias are the most common complication after an MI - acute pericarditis (2 or 3 days after) = friction rub (diaphragm of stethoscope, mid to lower left sternal border) - Nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids are avoided in the first 4 weeks after MI because they can interfere with myocardial scar formation - NPO (except water) until stable necrotic zone after MI within a day or two proteolytic enzymes of the neutrophils and macrophages begin to remove necrotic tissue and necrotic muscle wall is thin. = identified by ECG: lowering ST segements, T wave inversion, pathologic Q wave biomarker highly specific indicators of MI Troponin (increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days) patient with a STEMI must undergo cardiac catheterization within 90 minutes of presentation or receive thrombolytic therapy within 30 minutes in agencies without PCI capability When developing a teaching plan for risk factors associated with MI focus on modifiable risk factors (lowering LDLs) Characteristic of acute MI chest pain greater than 20 min the first line of treatment for patients with confirmed STEMI Emergent PCI: open the blocked artery within 90 minutes of arrival when a patient should stop exercise after MI - chest pain - change in heart rate of more than 20 beats over the resting heart rate thrombolytic therapy cautions change in level of consciousness (intracranial bleeding) minor bleeding is expected: surface bleeding from IV sites or gingival bleeding (apply manual pressure or ice packs) Major bleeding: drop in BP, increase in HR, sudden change in the patient’s mental status, blood in the urine or stool. stop the drug and notify the HCP. after thrombolytic therapy concern 1. bleeding 2. reocculusion of the artery: IV heparin is started Contraindications for Thrombolytic Therapy - Intracranial or intraspinal surgery within 2 mo - Recent (within past 3 mo) ischemic stroke - closed-head or facial trauma within past 3 mo - Active internal bleeding - Major surgery (3 wks) - Severe uncontrolled hypertension pericarditis complication after MI chest pain increases when taking a deep breath and is relieved by leaning forward assess: pericardial friction rub Emergency Management Chest Pain 1. Assess ABCs 2. Position Pt upright 3. Give O2 by nasal cannula or nonrebreather mask. 4. Obtain 12-lead ECG, Insert 2 IV catheters. 5. Start continuous ECG monitoring and identify underlying rhythm 6. Obtain baseline blood work ST segment changes on ECG indicated reinfarction (After MI) or ischemia in patient silent ischemia- noted by ST segment changes can occur with no symptoms Notify the HCP if you see ST segment changes with or without clinical symptoms. Monitoring for signs of early HF after MI dyspnea, tachycardia, pulmonary congestion, distended neck veins Phases of Rehabilitation After Acute Coronary Syndrome 1- Hospital: may rest in a chair within 8 to 12 hours after the event. ROM excersizes. Prolonged bed rest is not recommended 2- After discharge: 2-12 wks, outpatient facility. gradual increase (walking program) 3- Long term: lifestyle changes should become lifelong habits Education after MI - Tell the patient that more complete teaching will begin once the patient is feeling stronger - it is helpful for you to start a conversation by remarking that fear of dying is a common concern among most patients who have had ACS. ONAM O- Position patient upright unless contraindicated. • Give O2 by nasal cannula or nonrebreather mask. N- Sublingual first until IV nitro is ready. Monitor BP A- aspirin (chewable). Aspirin should never be stopped. M- Morphine: decreases cardiac workload by lowering myocardial O2 consumption, reduce fear and stress Drug therapy after MI indefinitely Aspirin Beta Blockers- reduces the risk for reinfarction and the development of HF ACE inhibitors and ARBS- should be started within the first 24 hours if the BP is stable Lipid-Lowering Drugs- Statins indefinitely (atorvastatin) Statins AE and nursing considerations taken indefinitely after MI AE: rhabdomyolysis, report to HCP Rhabdomyolysis: high creatine kinase levels and muscle pain pt with STEMI, most important to report to HCP Bilateral crackles are auscultated in the mid-lower lobes early sign of HF (complication of MI) Chest pain priority intervention Oxygen, ECG HDL and LDL LDL less than 100 mg/dL HDL greater than 40 mg/dL nutrition to prevent CAD rich in omega-3 fatty acids: walnuts, tofu, tuna NOT red meats, whole milk If a patient has chest pain, the nurse should institute the following measures 1) administer supplemental oxygen and position the patient in upright position unless contraindicated, (2) assess vital signs, (3) obtain a 12-lead ECG, (4) provide prompt pain relief first with a nitrate followed by an opioid analgesic if needed, and (5) auscultate heart sounds women SS in CAD fatigue Fatigue, rather than pain or shortness of breath, may be the first symptom of impaired cardiac circulation Neck, throat, or back pain may be symptoms experienced by women clinical manifestation with MI Ashen skin Diaphoresis Nausea and vomiting S3 or S4 heart sounds ECG represent electrical activity of depolarization and repolarization produced by the movement of ions across the membranes of heart cells Automaticity Ability to initiate an impulse spontaneously and continuously Excitability Ability to be electrically stimulated Conductivity Ability to transmit an impulse along a membrane in an orderly manner Contractility Ability to respond mechanically to an impulse SA node spontaneously fires 60 to 100 times per minute P Wave Represents time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction). Should be upright 0.06–0.12 PR Interval time taken for impulse to spread through the atria, AV node and bundle of His, bundle branches, and Purkinje fibers, to a point immediately before ventricular contraction 0.12–0.20 QRS Interval Represents time taken for depolarization (contraction) of both ventricles (systole) 0.12 ST Segment Represents the time between ventricular depolarization and repolarization (diastole). Should be isoelectric (flat) 0.12 T Wave Represents time for ventricular repolarization. Should be upright 0.16 electrophysiologic study (EPS) can identify the causes of heart blocks, tachydysrhythmias, bradydysrhythmias, and syncope. Determine effectiveness of antidysrythmIc drugs Sinus Bradycardia sinus rhythm, but the SA node fires at a rate less than 60 beats/min SS: pale, cool skin; hypotension; weakness; angina; dizziness or syncope; confusion or disorientation; and shortness of breath. Tx: IV atropine, dopamine or epinephrine may need a permanent pacemaker Sinus Tachycardia the HR is 101 to 180 beats/min and rhythm is regular SS: dizziness, dyspnea, and hypotension because of decreased CO, angina Tx: IV β-blockers (e.g., metoprolol), adenosine (Adenocard), or calcium channel blockers (e.g., diltiazem) clinical patients- synchronized cardioversion possible causes of sinus tachycardia exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear. over-the-counter cold remedies Premature Atrial Contraction (PAC) contraction starting from an ectopic focus in the atrium sooner than the next expected sinus beat. Distorted P wave shape. SS: report palpitations or a sense that the heart "skipped a beat." Tx: withdrawal sources of stimulation (caffeine or drugs), B-blockers (reduce irritation of heart) PAC causes stress, fatigue, caffeine, tobacco, alc, hypoxia, electrolyte imbalances, disease Paroxysmal Supraventricular Tachycardia (PSVT) 151–220 beats/min and regular rhythm. dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His. PAC triggers a run of repeated premature beats, termination is followed by a brief period of asystole. P wave Abnormal shape, may be hidden in the preceding T wave Cause: overexertion, emotional stress, deep inspiration, and stimulants, rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale. Tx: IV adenosine, IV B-Blockers, Calcium Channel Blockers, Amiodarone, unstable= synchronized cardioversion Adenosine nursing considerations 1. Lay patient down BEFORE giving drug (apply O2) 2. push rapidly (over 1 to 2 sec), follow with a rapid 20-mL normal saline flush 3. Brief period of asystole is common HR 180 = decreased CO and stroke volume Atrial Flutter atrial tachydysrhythmia, recurring, regular, sawtooth-shaped flutter waves. Atrial rate = 200 to 350 beats/min ventricular rate =150 beats/min Tx: Radiofrequency catheter ablation in an EPS laboratory, electrical cardioversion (in emergency) , antidystryhtmic drugs (amiodiorone), calcium channel blockers, B-blockers (NO adenosine, its coming from the atria) Atrial flutter means risk for stroke because thrombi (clots) can form in the atria from the stasis of blood Atrial Fibrillation total disorganization of atrial electrical activity because of multiple ectopic foci = loss of atrial contraction. Irregular QRS complex atrial rate- 350-600 bpm ventricular rate- 60-100 bpm (controlled) 100+ (rapid ventricular response) decrease in CO because of ineffective atrial contractions, thrombi in atria from stasis = anticoagulants Atrial Fibrillation Treatment Tx: amiodarone, electrical conversion, If a patient is in atrial fibrillation for longer than 48 hours, anticoagulation therapy with warfarin is needed for 3 to 4 weeks before the cardioversion. If drugs or cardioversion does not convert atrial fibrillation to normal sinus rhythm, the patient needs long-term anticoagulation therapy 1st Degree AV block every impulse is conducted to the ventricles, but the time of AV conduction is prolonged = The PR interval is prolonged (greater than 0.20 second). . Cause: hypokalemia, rheumatic fever, hyperthyroidism no Tx 3rd degree AV Heart Block no impulses from the atria are conducted to the ventricles. Atria are stimulated and contract independently of the ventricles Atrial rate- 60 to 100 beats/min Ventricular rate: 40 to 60 beats/min (AV node), 20 to 40 beats/min (His-Purkinje system). SS: reduced CO with subsequent ischemia, HF, and shock, syncope Tx: Pacemaker. transcutaneous pacemaker until a temporary transvenous pacemaker can be inserted. dopamine and epinephrine as an interim measure NO atropine. Premature Ventricular Contractions (PVC) contraction coming from an ectopic focus in the ventricles = premature (early) occurrence of a QRS complex. Irregular rhythm, nursing- we don't count PVCs as HR cause: stimulants Tx: relates to the cause of the PVCs (e.g., O2 therapy for hypoxia, electrolyte replacement) β-blockers, lidocaine, or amiodarone PVC nursing Take the patient’s apical-radial pulse rate and determine the pulse deficit, since PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse. 6 or more PVC per minute is very dangerous (not enough CO) Ventricular Tachycardia ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker = three or more consecutive PVCs Ventricular rate: 150-250 bpm SS: hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest VT treatment stable (has a pulse): procainamide, lidocaine, or amiodarone are options. Cardioversion is used if drug therapy is ineffective unstable (no pulse): Cardiopulmonary resuscitation (CPR) and rapid defibrillation are the first lines of treatment Monomorphic VT QRS complexes that are the same in shape, size, and direction Polymorphic Tachycardia OR Torsades de Points QRS complexes gradually change back and forth from one shape, size, and direction to another over a series of beats Polymorphic VT with a prolonged baseline QT interval Tx IV magnesium (reduces irritability), isoproterenol, phenytoin, or antitachycardia pacing Drugs that prolong the QT interval (dofetilide [Tikosyn]) should be stopped Ventricular Fibrillation ventricle is simply "quivering," with no effective contraction, and so no CO occurs Cause: acute MI and myocardial ischemia and in chronic diseases such as HF and cardiomyopathy, electric shock, hyperkalemia, hypoxemia, acidosis, and drug toxicity SS: unresponsive, pulseless, and apneic state V fib Tx immediate initiation of CPR defibrillation epinephrine, amiodarone, vasopressin Pulseless Electrical Activity electrical activity is seen on the ECG, but there is no mechanical heart activity and the patient has no pulse Cause: Hs and Ts Tx: begins with CPR, followed by drug therapy (e.g., epinephrine) and intubation Hs and Ts H: Hypovolemia, Hypoxia, Hydrogen (acidosis), Hyper/Hypokalmeia, Hypoglycemia, Hypothermia T: Toxins, Tamponade (cardiac), Tension pneumothorax, Trauma Asystole total absence of ventricular electrical activity Tx: CPR with ACLS measures. epinephrine and intubation. (NO DEFIB) Nursing- Always assess the rhythm in more than 1 lead. Defibrillation and Cardioversion • Check that the synchronizer switch is OFF for defibrillation. • Turn the synchronizer switch ON for a cardioversion. • Never apply defibrillator pads over a pacemaker or implantable cardioverter-defibrillator. • Be certain that personnel are "all clear" before discharging the device Defibrillation Biphasic- 120 to 200 joules Monophasic- 360 joules After the first shock, start CPR immediately Steps: 1. Start CRP 2. Turn on and select energy 3. Sync button OFF 4. Apply Gel pads 5. Charge 6. Position paddles on chest 7. All Clear! 8. Dleiver charge Synchronized Cardioversion - non-emergent basis: we sedate the patient with IV agents (e.g., midazolam, fentanyl) beforehand. - Remove all metallic objects, dentures, and transdermal patches. Clipping or removing chest hair may be needed. - Becomes pulseless, switch to OFF and defibrillator - initial energy for synchronized cardioversion at 50 to 100 joules (biphasic defibrillator) and 100 joules (monophasic defibrillator) Teaching Implantable Cardioverter-Defibrillator (ICD) - Keep incision dry for 4 days after insertion or as instructed - Avoid lifting arm on ICD side above shoulder until approved - It is usually safe to resume sexual activity once your incision is healed. - Do not drive until cleared by your HCP - Avoid large magnets and strong electromagnetic fields (MRIs - Travel is NOT restricted, just down stand near anti left devices in doorways - If your ICD fires once, call your HCP right away - Medic wristband Teaching Pacemaker - Keep incision dry for 4 days after implantation, or as ordered. - Avoid lifting arm on pacemaker side until approved - Microwave ovens are safe to use and do not interfere with pacemaker function. - No MRIs - Avoid standing near antitheft devices in doorways - Travel is not restricted. transcutaneous pacemaker noninvasive, temporary procedure (emergency) Position 1 pad on the anterior part of the chest, usually on the V4 lead position, and the other pad on the back between the spine and left scapula at the level of the heart provide analgesia and/or sedation while the TCP is in use. pacemaker spike P-R interval is 0.24 seconds 1st degree heart block (PR interval .20 sec), document findings no need to call HCP Radiofrequency catheter ablation therapy uses electrical energy to burn or ablate areas of the conduction system as definitive treatment of atrial flutter (i.e., restore normal sinus rhythm) and tachydysrhythmias. A patient has ST segment changes that support an acute inferior wall myocardial infarction. Which lead would be best for monitoring the patient? II ST depression and T wave inversion on the ECG myocardial ischemia irregular R-R intervals and small fibrillatory (f) waves. There are no normal P waves A fib education to patient before initiating emergency transcutaneous pacing "The device delivers a current through your skin that can be uncomfortable rate of 150 to 250 beats/min; the P wave is not normally visible Vtach atrial fibrillation with a rapid ventricular response synchronized cardioversion Acute kidney injury (AKI) develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium with or without a reduction in urine output azotemia accumulation of nitrogenous waste products (urea nitrogen, creatinine) in the blood AKI diagnostic criteria Acute reduction in urine output AND/OR Elevation in serum creatinine Prerenal Causes AKI Decreased Cardiac Output • Cardiogenic shock • Dysrhythmias • HF • MI Decreased Peripheral Vascular Resistance • Anaphylaxis • Neurologic injury • Septic shock Decreased Renovascular Blood Flow • Bilateral renal vein thrombosis • Embolism • Hepatorenal syndrome • Renal artery thrombosis Hypovolemia • Burns • Dehydration • Excessive diuresis • GI losses (diarrhea, vomiting) • Hemorrhage • Hypoalbuminemia Intrarenal causes of AKI Interstitial Nephritis • Allergies: antibiotics (sulfonamides, rifampin), NSAIDs, ACE inhibitors • Infections: bacterial (acute pyelonephritis), viral (Epstein-Barr), fungal (candidiasis) Nephrotoxic Injury • Chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride • Contrast media • Drugs: aminoglycosides (gentamicin, amikacin), amphotericin B • Hemolytic blood transfusion reaction • Severe crush injury Other Causes • Acute glomerulonephritis • Malignant hypertension • Prolonged prerenal ischemia • Thrombotic disorders • Toxemia of pregnancy • Systemic lupus erythematosus Post renal causes of AKI • BPH • Bladder cancer • Calculi formation • Neuromuscular disorders • Prostate cancer • Spinal cord disease • Strictures • Trauma (back, pelvis, perineum) Pre renal AKI factors that reduce systemic circulation, causing a reduction in renal blood flow = glomerular perfusion and filtration of the kidneys pre renal to intra renal pre renal conditions contribute to infrarenal disease if renal ischemia is prolonged. decreased perfusion for extended time = damage to kidney parenchyma itself = intra renal damage auto regulatory mechanisms in pre renal AKI decrease circulatory BV= body increased angiotensin ii, aldosterone, norepinephrine, ADH (attempt to preserve BF to essential organs) Pre renal azotemia reduction in sodium excretion (less than 20 mEq/L), increased sodium and water retention, and decreased urine output intra renal AKI conditions that cause direct damage to the kidney itself = impaired nephron function Acute tubular necrosis (ATN) most common intrarenal cause of AKI cause: ischemia, nephrotoxins, or sepsis nephrotoxins penicillins, cephalosporins, sulfonamides, thiazides dietetics, furosemide, NSAIDS, rifampicin, IV contrast, amnioglycocides, amphortercin, cyclosporin Right after dialysis pt received really high dose of medication (because dialysis takes all the drug levels away) SO the next day you maybe wouldn't give the drug because the previous dose is still circulating in blood stream (dialysis hasn't occurred yet so nothing filtered out the med) post renal AKI mechanical obstruction of outflow Oliguric Phase oliguria: a reduction in urine output to less than 400 mL/day lasts on average 10 to 14 days Fluid retention: distended neck veins, bounding pulse, edema, HTN hypovolemia: exacerbates AKI metabolic acidosis (kidney can't excrete H+, HCO3 decreased) = Kussmaul hyponatremia (cerebral edema) hyperkalemia Therapies for High Potassium Levels Calcium Gluconate IV, Dietary Restriction (K+ of 40 mEq/day), Hemodialysis (most effective), Regular Insulin IV, Sodium Bicarbonate, Sodium Polystyrene Sulfonate (Kayexalate) (excretes K+ in stool, causes osmotic diarrhea) urinary specific gravity (concentration of solutes in urine) urine osmolarity (number of dissolved particles in urine) urine specific gravity: 1.003-1.030 Urine osmolarity: 300-1300 The best serum indicator of AKI creatinine Diuretic Phase daily urine output is usually around 1 to 3 L but may reach 5 L or more last 1 to 3 weeks monitor for: hyponatremia, hypokalemia (now we want to give K+), and dehydration but can't concentrate urine Recovery phase GFR increases, allowing the BUN and serum creatinine levels to decrease Kidney function may take up to 12 months to stabilize Contraindications for pt with AKI MRI w Gadolinium contrast medium Magnetic resonance angiography (MRA) with gadolinium contrast medium metformin and contrast medium drug should be held for 48 hrs prior to contrast media diagnostic studied AKI kidney ultrasound: avoids nephrotoxic dyes renal biopsy: best method for confirming intrarenal causes of AKI. calculating the fluid restriction add all losses for the previous 24 hours + plus 600 mL for insensible losses Nutritional Therapy AKI adequate caloric intake: from carbohydrate and fat sources to prevent ketosis Sodium is restricted limit protein (adds to BUN) Dietary fat intake is increased so that the patient receives at least 30% to 40% of total calories from fat. AKI nursing don't give nephrotoxic meds! (NSAIDS) Peritoneal Dialysis (PD) Home dialysis possible obtained by inserting a catheter through the anterior abdominal wall- Once the catheter incision site is healed, the patient may shower and then pat the catheter and exit site dry Hemodialysis arteriovenous fistula (AVF) is usually created in the forearm or upper arm with an anastomosis between an artery and a vein Continuous renal replacement therapy (CRRT) method for treating AKI: dialyze patients in a more physiologic way (over 24 hours), just like the kidneys - CRRT can be continued as long as 30 to 40 days. hemofilter should be - changed every 24 to 48 hours - ultrafiltrate should be clear yellow - there should be little change in mean arterial pressure or cardiac output. - Once the patient's AKI is resolved or there is a decision to withdraw treatment, CRRT is stopped and the needle(s) removed. CRRT ultra filtrate becomes blood tinged suspect a rupture in the filter membrane. Stop treatment to prevent blood loss. CRRT is contraindicated if life-threatening manifestations of uremia (hyperkalemia, pericarditis) that need rapid treatment To assess the patient with pericarditis for evidence of a pericardial friction rub, the nurse should auscultate by placing the diaphragm of the stethoscope on the lower left sternal border. post op kidney care a sudden decrease in U/O is a concern Could be due to clot = keep urinary catheter clear and patent (stays fro 3-5 days to allow the ureter-bladder anastomosis to heal) hallmark of systolic HF decreased ejection fraction (normal 50%) universal finding of ADHF pulmonary and systemic congestion due to elevated left-sided and right-sided filling pressures. BNP levels correlate positively with the degree of LV failure Indicators of decreased perfusion hypotension, decreased urine output, cool extremities, altered mentation, heart murmur, dysrhythmias, and worsening renal and liver function tests PAWP 6 to 15 mm Hg PAWP is an indirect measurement of LA filling pressure measured from the tip of the PA catheter when inflated in a capillary artery. tamsulosin (Flomax) relax the smooth muscle in the ureter, can help stone passage urinary calculi meds NSAIDS opioids Lithotripsy eliminate stones from the urinary tract. (breaking them into smaller pieces for them to pass) Left flank pain, bruising, and hematuria are common after lithotripsy report: decrease in U/O (could indicate obstruction) To prevent recurrence of uric acid renal calculi, the nurse teaches the patient to avoid eating sardines and liver. best way to prevent renal calculi fluids! 2-3 L priority nursing intervention with renal calculi analgesic Administration arteriovenous graft (AVG) placement and pt complains of coldness in fingers report to HCP (SS of inadequate perfusion to extremity) demonstrates latency of fistula The presence of a thrill (feel) and bruit (auscultate) indicates adequate blood flow through the fistula temporary vascular access catheter in the left femoral vein bed rest (prevent trauma to vein) heart failure medication dobutamine and dopamine: • Increase contractility (positive inotropic effect) • Increase CO • May reduce PAWP • May cause dysrhythmias • Increase myocardial O2 demand ACE Inhibitors: • Dilate venules and arterioles • Reduce afterload and SVR • Improve renal blood flow • May relieve HF symptoms • Promote reverse remodeling • May reduce morbidity, mortality, and HF hospitalizations in patients with chronic HF complications of pericarditis pericardial effusion (build-up of fluid in the pericardium) and cardiac tamponade SS pericardial effusion: cough, dyspnea, and tachypnea hiccups (Phrenic nerve compression) hoarseness (Compression of the laryngeal nerve) distant and muffled heart sounds SS cardiac tamponade: chest pain, confusion, jugular venous vein distention, large decrease in systolic BP during inspiration (Pulsus paradoxus) Mitral valve regurgitation- where do we listen? mitral valve: apex of the heart, fifth intercostal space, midclavicular line. risk for infective endocarditis (IE) with regurgitation Dental work. take antibiotics prophylacticly prior to going to dentist infective endocarditis inflammation of the endocardium vegetations on the valves prevent valve closure = new regurgitant murmur Tx: 4 to 6 weeks of IV antibiotic therapy in order to eradicate the bacteria, which will require a long-term IV catheter such as a peripherally inserted central catheter (PICC) line. nursing intervention pericarditis place the patient in Fowlers position, leaning forward (pain worse lying down) When caring for a patient with mitral valve stenosis, it is most important that the nurse assess for shortness of breath upon exertion accurate indicators of kidney function serum creatinine clearance determinations (calculated GFR) kidney transplant concerns - central venous pressure - decreased U/O - rejection RIFLE classifies AKI Risk, Injury, Failure, Loss, End-stage renal disease cause of dysrhythmias -Thyroid disease -Alcohol Intoxication -Caffeine Use -HTN or Vascular Disease aortic valve stenosis caution with what med nitroglycerin