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✽ Heart Failure Review
○ Pathophysiology: insufficient blood supply/oxygen to body
- key manifestations: diastolic dysfunction (vent. fill)/(HFpEF) or systolic dysfunction (vent. ejection)/(HFrEF)
- Ejection fraction (EF): blood pumped out by LV with heartbeat ○ Risk factors: HTN, CAD ○ End-stage: heart transplant
- Immunosuppressive therapy: steroids, calcineurin inhib, antiproliferative drugs
- Monitor infection
- Endomyocardial biopsy (EMB) - detect rejection
✽ Acute Decompensated Heart Failure
✽ HF exacerbation usually related to pulmonary/systemic congestion and volume overload
- Early response - inc. pulmonary nervous pressure: RR inc., PaO2 dec.
- Later - interstitial edema: tachypnea
- Further - alveolar edema: respiratory acidosis ✽ Complication: pulmonary edema ✽ Hemodynamic Monitoring: Swanz Ganz/pulmonary artery catheter; normal 2-8 mmHg ✽ Drug therapy: diuretics, vasodilators (nitrogly, nitropruss, nesiri), morphine, digoxin, beta agonist (dopamine, dobutamine, norepin)
- key manifestations: diastolic dysfunction (vent. fill)/(HFpEF) or systolic dysfunction (vent. ejection)/(HFrEF)
✽ Chronic Heart Failure
○ Dx: echocardiogram, BNP (normal<100), Stress test, 6 minute walk, EF (55-70% norm, 40% or less bad) ○ Clinical Manifestations: Left Sided Right Sided
● Pulmonary edema ○ Peripheral edema
tering discomfort in neck, fatigue, possible RUQ pain
- Peripheral edema, loud S3 (loud holosystolic murmur at apex to left axila) ○ Treatment: surgery
✽ Mitral Valve Prolapse
○ Pathophysiololgy: leaflets open/buckle backwards during systole ○ RF: Genetic link ○ Dx: M-mode, 2-D ECG ○ Clinical manifestations: regurgitaion murmur louder during systole, dysrhythmia (PVC, PSVT, VT) - palpitation, lightheadness, syncope; clustered chest pain (stress) ○ Beta blockers - palpitation/chest pain ○ Hydration, exercise regularly, avoid caffeine, antibiotic prophylaxis for endocarditis, avoid OTC stim
✽ Aortic Valve Stenosis
○ Congenital AS or Rheumatic Fever ○ Pathophysiology: obstruct blood flow from left ventricle to aorta during systole ○ LV hypertrophy, reduced CO, pulmonary HTN, HF ○ Clinical Manifestations (occur when valve is one-third its normal size): classic trid (angina, syncope, exertional dyspnea)/LV failure, soft S1, decreased/absent S2, crescendo-decrescendo systolic murmur to cartotids ○ Nitroglycerin - angina, caution as it dec BP/worsen chest pain
✽ Aortic Valve Regurgitation
○ Acute: IE, truma, aortic dissection - medical emergency! ○ Chronic: rheumatic heart disease, congenticl bicuspid aortic valve, syphilis, connective tissue problem, postsurgical cause ○ Pathophysiology: backward blood flow froma ascending aorta into LV during diastole - volume overload, LV hypertrophy/dilation - lead to pulmonary HTM, and RV failure ○ Manifestations:
- Acute: severe dyspnea. Chest pain, hypotension indicating LV failure and cardiogenic shock
- Chronic: water-hammer pulse (strong, quick beat that collapses immediately), soft or absent S1, S3, S4, soft, high-pitche diastolic murmur; exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea after considerable heart dysfunction, angina
✽ Tricuspid and Pulmonic Valve Disease
○ Tricuspid regurgitation: IE, RV dilation from pulm. HTN/cor pulmonale/pulm. outflow obstruction; manifestations - JVD, enlarged liver, peripheral edema only when severe ○ Tricuspid stenosis: always RF
○ Pulmonary regurgitation: pulm. HTN, surgical repair of TOF, congenital - lead to RV dilation, usually asymp. ○ Pulmonary stenosis: always congenital with TOF, RV HTN/hypertrophy, S/S - syncope, dyspnea, angina
✽ Interprofessional Care
○ RF & IE prophylactic antibiotic ○ Prevent exacerbation of HF, pulm. Edema, thromboembolism, recurrent endocarditis ○ Atrial dysrhythmia common; anticoagulant for atrial fibrillation ○ Sodium restriction ○ Percutaneous Transluminal Balloon Valvuloplasty (PTBV) - stenosis ○ Surgery:
- Valve Repair: usually in mitral/triscupid
- Open valvuloplasty: sutures torn parts, treat mitral/tricuspid regurgitation
- Minimally invasive
- Commissurotomy (valvulotomy)
- Annuloplasty
- Valve Replacement - both subject to leaking and risk of IE
- Mechanical
- Durable, last longer but increase risk for thromboembolism - need anticoagulation therapy
- Biological valves
- Less durable, no anticoagulation therapy, early calciication, tissue degen., stiffening ○ Nursing:
- Early tx of strep inf., prophylactic antibiotics, rest
- If on anticoagulants (warfarin) - INR 2.5-3.5 normal, even green leafy veggies
- Avoid dental procedures 6 mo after surgery, take antibiotics before
✽ Cardiomyopathy (CMP)
○ All low CO = low blood/O ○ Primary cause: idiopathic, heart muscle is only part of heart involved ○ secondary: myocardial disease is know and due to other disease process ○ 3 types: dilated, hypertrophic, restrictive ○ Dx: echocardiogram/EF, angiography (rule out blockages), BNP ○ Clinical manifestations: low oxygen, restlessness, agitation, altered LOC, syncope, dizzy, fatigue, HF, embolism
Per an Car
○ Classic s/s: fatigue, exercise intolerance, dyspnea; angina, HF, atrial fib/AV block
✽ Pericarditis
○ Inflammation of pericardial sac (outside) with fluid accumulation, compressing the heart and cant pump; normally has 10-15 mL serous fluid; pericardium lubes to decrease friction with heart contractions ○ Etiology: MI, autoimmune (RA/scleroedema, lupus), infection (HIV/herpes/bactrial (TB)), renal failure (uremia/high BUN)
- Most common: idiopathic or viral - coxsackievirus B ○ Dx: EKG (ST elevation), echo, leukocytosis, increased CRP/ESR ○ Clinical manifestations: precordial chest pain, elevated WBC, CRP, cardiac tamponade (JVD, muffled heart sounds, pulsus paradoxus/sys. BP drop by 10)
- Hallmark: pericardial friction rub best heard at lower left sternal border of the chest with patient leaning forward; ask to hold breath and if u still hear it - cardiac and not pleural rub
- Progressive, severe, sharp chest pain that’s worse with deep inspiration and supine
- Relieved when sitting and leaning forward, may radiate to similar places like angina
- Distinction: spreads to trapezius muscle (shoulder, upper back)
- Dyspnea with rapid/shallow breaths, fever, anxiety ○ Complication- cardiac tamponade, pericardial effusion, phrenic nerve compression lead to hiccups and compressed laryngeal nerve (hoarseness)
- Cardiac tamponade: chest pain, confused, anxious, restless, muiffled heart sounds, narrowed pulse pressure, tachypnea, tachycardia, JVD, pulsus paradoxus (large decrease in BP during inspiration)
- Position the patient in a semirecumbent position.
- Have patient breathe normally.
- Using a manually operated BP cuff, measure systolic BP.
- Inflate BP cuff at least 20 mm Hg above systolic BP.
- Deflate cuff slowly until you hear sounds throughout the respiratory cycle (inspiration and expiration) and note the pressure.
- Determine the difference between the measurements taken in steps 4 and 5. This will equal the amount of paradox: ○ Treatment: NSAIDS (indomethacin), steroids (prednisone), pericardiocentesis (needle in heart to drain fluids), antibiotics, antiinflammatory drug (colchicine), pericardial window for dx/fluid drainage, HOB>45/table for support ○ Chronic constrictive: rigid pericardium, JVD, pulsus para. Uncommon, tx: pericardiectomy
✽ Infective Endocarditis
○ Inflammation inside heart, valves can’t fully close
- Bacteria (mold on heart valves), noninfective ○ Etiology: dirty needles, dental visits, heart surgery (valve replacements, CABG), untx. strep throat
Niacin: vitamin B, lower LDL and triglyceride, inc. HDL, SE: flushing, pruritus, G
- S. aureus, strep., coag. Staph ○ Main risk factors: age, IV drug use, prosthetic valve, hemodialysis ○ Stages: bacteremia, adhesion, vegetation
- Vegetation: fibrin, leukocytes, plt, microbes stick to valve/endocardium
- Parts break off and enter circulation (embolization)
- Left side: brain, kidneys, spleen; Right side: lungs ○ Dx: 3 blood cultures over 1 hr from 3 sites (+), ESR, CRP, Duke criteria ○ Clinical manifestations: clots in heart and brain (stroke - agitation, altered LOC/ splinter hemorrhages under fingernails), crackles, fever, clubbed fingers
- Roth spots (hemorrhagic retinal lesions), Osler’s nodes (painful, tender, red or purple, pea sized lesion on fingertips and toes), Janeway lesions (flat, painless, small, red spots on fingertips, palms, soles, toes) (immune response) - Fever , chills, weakness, malaise, fatigue, anorexia - HF, systolic murmur, septic embolism! ○ Monitor infection, oral care (2x/day no floss), dental visits/surgery - antibiotic adherence! ○ Prophylactic antibiotic: dentist, respiratory, tonsillectomy, adenoidectomy ○ 2 sets of blood culture every 24/48 hrs until clear, follow up echo and markers 1, 3, 6, 12 mo ○ Valve replacement, antipyretics (aspirin, acetam), fluids, rest
✽ Coronary Artery Disease (CAD)
○ Etiology: atherosclerosis - characterized by lipid deposits within artery intima ○ CRP inc ○ Fatty streaks - lipid filled smooth muscle cells, earliest lesions, yellow tinge ○ Cardiac cath - gold ○ Collateral circulation: angiogenesis and presence of chronic ischemia ○ No early signs ○ Care:
- Avoid red meat, egg yolks, whole milk
- Drugs:
- Lipid lowering
- Statin: inhibit cholesterol, dec. LDL, inc. HDL - monitor liver dmg and myopathy that can progress to rhabdomyolysis (skeletal muscle breakdown)
- I, ortho. hypoTN
✽ Percutaneous Coronary Intervention (PCI)
○ Local anesthesia, ambulatory shortly postop, CABG (6-8 wks before going back to work) ○ Postop: Neurovascular status q 15 for 1st hr, bleeding at site ○ Stents: heparin, post - dual antiplt therapy (DAPT - aspirin/clopidogrel) for min. 12 mo, aspirin - lifetime ○ CABG post op
- Arterial line for BP, pleral/mediastinal chest tube for drainage, ET to vent, foley cath, NG for gastric decompression, afib is common
- Extubated within 6 hours
- Beta blockers reduce afib
- Nurse: chest incision dressing removed after 24 hours
✽ Acute Coronary Syndrome
○ Chest pain from ischemia is prolonged/not immediately reversible
- Difference with UA and NSTEMI - cardiac biomarkers
- Irreversible heart damage after 20 minutes if no collateral circulation ○ Caused by rupture of atheroscleros plaque ○ Unstable angina: last over 10 min and unrelieved with NTG ○ UA/NSTEMI: DAPT, heparin, cardiac cath with PCI once stable ○ Myocardial Infarction (STEMI, NSTEMI)
- Tx within 90 min (door to cath): PCI, thrombolytic therapy (30 min)
- Thrombolytic: given with heparin, minor bleeding expected, pressure with dressing or ice packs
- Absolute contraindicationL active bleeding (excluding menstruation), hx of intracranial hemorrhage, recent (3mo) ischemic stroke, severe uncontrolled HTN, trauma within past 3 mo
- Inclusion: chest pain less than 12 hours with EKG of STEMI, no absolute contraindications
- NSTEMI: cath within 12-72 hrs, thrombolytic therapy not indicated
- Both - hypokinesis (worsened myocardial contractility), akinesis
- If total occluded and not tx - entire necrosis 4-6 hrs
- Clinical manifestations: severe chest pain unrelieved by rest, position change, NTG; heavy, pressure, crushing feeling, substernal/epigastric area, last 20 min or longer, cool/clammy/ash skin, dysrhythmia ○ Tx: MONA, antiplt/IV NTG/atorvastatin, PCI
✽ EKG
○ PR interval: 0.12 - 0.
At Dy
○ QRS interval: <0. ○ QT interval: 0.34-0. ○ PDA: connects aorta and pulmonary artery
✽ Sinus Bradycardia
○ NSR for athletes and when sleeping ○ Manifestations: pale, cool skin, hypotension, weakness, angina, dizziness, syncope, SOB, confusion ○ Tx the cause: if due to drugs, then held; IV atropine, if ineffective: transcutaneous pacing, dopamin, epinephrine, possible permanent pacemaker
✽ Sinus Tachycardia
○ Caused by vagal inhibition or sympathetic stimulation ○ Manifestations: dizziness, dyspnea, hypotension ○ Tx cause: analgesic, vagal manueuver, IV beta blockers, adenosine, calcium channel blockers (diltiazam); unstable - sync. cardioversion
✽ Premature Atrial Contraction (PAC)
○ Contraction from ectopic focus in atrium sooner than next beat ○ Rhythm is irregular, P wave diff. or hidden in T wave, PR shorter or longer but still normal ○ Causes: stress, fatigue, caffeine, tobacco, alc, hypoxia, COPD, heart disease ○ Manifestations: palpitations, skipped beat ○ Tx: withdrawal of stim./drugs (epi, dopamine), betablockers
✽ Paroxysmal Supraventricular Tachycardia (PSVT)
○ Ectopic focus above bifurcation of bundle of His ○ Cause: reentrant phenomenon (rexcitation of atria with 1 way block) ○ PAC triggers run of repeated beats; abrupt onset and ending, brief period of asystole ○ Causes: overexertion, stress, deep inspiration, stimulants, heart disease, digoxin toxicity ○ HR: 151 - 220, regular or slightly irreg rhythm, P wave abnormal or hidden ○ HR>180 -low CO and SV, hypotension, palpitations, dyspnea, angina ○ Tx: vagal stimulation, drug
- Valsalva, carotid massage, coughing
- IV adenosine (1st line): may feel chest pressure, site should be close to heart as possible, give over 1- sec followed with NS, stopcock, brief asystole common; assess flushing, dizziness, chest pain, palpitations
- IV beta blockers, calcium channel blockers; if unstable - sync. Cardioversion
- Recurrent PSVT - radiofreq. cath. ablation
○ Bigeminy- every other beat; trigeminy- every third beat; couplet- two consecutive ○ Unifocal - same shape/focus; multifocal- differs; Vtach when 3 in a row ○ Causes: stimulants, stress, electrolyte imbalances, fever, disease (mitral prolapse, HF) ○ Take apical-radial pulse and determine difference - not enough vent. contraction for peri. pulse ○ S/S: reduced CO leading to angina and HF ○ Tx: cause, drug - beta blocker, lidocaine, amiodarone
✽ Ventricular Tachycardia
○ Run of 3 or more PVCs; ectopic focus fire repeatedly and ventricle takes control as pacemaker ○ Torsades-poly VT with prolonged QT interval ○ May be sustained (longer than 30 sec) or nonsustained and is ominous ○ Causes: MI, CAD, electrolyte magnesium, cardiomyopathy, CNS ○ V. rate: 150-250 beats ○ Stable or unstable, stable causes low CO due to low diastolic filling ○ S/S: hypotension, pulmonary edema, decreased cerebral blood flow ○ Tx:
- Stable, monomorphic, presered LV fxn: IV procainamide, lidocaine, amiodarone
- Polymorphic VT with prolonged QT interval: IV magnesium, isoproterenol, phenytoin, antitachycardia
- Cardioversion
- VT w/o pulse: CPR, defib, epi (vasopressor), amiodarone (antidysrhythmics)
✽ Ventricular Fibrillation
○ Irregular waveforms, multiple ectopic foci firing - ventricles quivering - no CO ○ Causes: HF, cardiomyopathy, MI, myocardial ischemia, drug toxicity, etc ○ Unresponsive, pulseless, apneic state ○ Tx: CPR, ACLS with defib and definite drug (epi, amio)
✽ Pulseless Electrical Activity
○ EKG electrical activity, no mechanical activity, NO PULSE ○ Common after defibrillation ○ Tx: CPR, epi, intubation
✽ Asystole
○ Total absence of ventricular electrical activity; pulseless, unresponsive, apneic ○ Tx: CPR, ACLS, epi, intubation
✽ Pacemakers
○ Antitachycardia pacing: stimulus to ventricle to end tachydysrhythmias (VT)
○ Overdrive pacing: pacing atrium at rates of 200 to 500 impulses per min to stop atrial tachycardias ○ Permanent: SQ over pectoral muscle on nondominant side ○ Temporary:
- Transvenous: emergency, lead to perma. PM. or until tx cause; central line
- Epicardial: prophylaxis for brady/tachydysrhythmia occurs in early postop; chest wall postop
- Transcutaneous: adequate HR/rhythm in emergency; emergency ○ Failure to sense: doesn’t sense activity and fires inappropriately; can cause VT ○ Failure to capture: electrical charge is not enough to produce contraction; brady, asystole ○ Failure to pace: does not fire when it should ○ Teaching: limit affected arm movement, incision dry for 4 days, avoid direct blows to sit, MRI must be approved, can use microwaves, avoid standing near anti-theft store devices, travel is okay/wand should not be placed directy over pacemaker
✽ Acute Kidney Injury
○ Definite increased Cr and reduced urine output - rapid loss of kidney fxn ○ Most common cause: acute tubular necrosis ○ Dx: MRI with contrast is contraindicated, hold metformin 48 hrs prior ○ Azotemia: accumulation of urea nitrogen, cr in blood ○ Prerenal: reduce systemic circulation and renal blood flow; cardiogenic shock, burn, FVD, HF
- Prerenal oliguria: no kidney damage, caused by decreased blood volume
- Prerenal azotemia: reduced sodium excretion, increased water/retention, decrease UO ○ Intrarenal: direct kidney damage
- Prolonged ischemia - blood deficiency in one or both kidneys
- Acute tubular necrosis (ATN): result of ischemia, nephrotoxins, sepsis, nonoliguric ○ Postrenal: mechanical obstruction in urine outflow
- Urine reflux into renal pelvis
- Most common causes: benign prostatic hyperplasia (BPH), prostate cancer, stones, trauma, extrarenal tumors ○ Stages:
- Oliguric
- UO<400 mL/day, UA may inc. RBC/WBC
- Hypovolemia, metabolic acidosis (Kussmaul), sodium intake (hyponatremia - cerebral
Ren Dy
○ Surgery: Laparoscopic donor nephrectomy; open nephrectomy (side by side, incision at 11th rib)
- Recipient: urinary cath placed with antibiotic, placed in iliac fossa ○ Care:
- Preop: review immunosuppresive drugs, prevent infection, dialysis may be needed before.after
- If on PD: empty peritoneal cavity of all dialysate
- Postop:
- Live donor: renal fxn, hct for bleeding, usually feel more pain, work in 6-8 weeks
- Recipient: priority-fluid/electrolyte balance, inc. UO after transplant normal and replaced with fluids for first 24 hours, monitor hyponatremia/kalemia, if metabolic acidosis - IV sodium bicarbonate, ATN may occur - dialysis - stops when UO inc and Cr/BUN normalize
- Sudden decrease UO in early postop - possible blood clot in urinary cath, patency must be maintained since cath is in bladder for 3-days, gentle cath irrigation (ordered)
- Immunosuppressive therapy
- Cancers: skin (basal, squamous, melanoma), posttransplant lymphoproliferative disorder (hodgkin/non)
- Steroids: affect bones
- Calcineurines: cyclosporine, tacrolimus (no grapefruit)
- Prophylaxis antibiotics: HSV - acyclovir months postop, antiviral (clotrimazole, fluconazole)
✽ Urinary Tract Calculi/Nephrolithiasis
○ Types: calcium oxalate, cal. phosphate, cystine, struvite (mag. ammonium phos.), uric acid ○ Clinical manifestations: severe, sharp, and sudden pain in flank, back lower abdomen aka renal colic (first sign), colicky pain, n/v, kidney stone dance due to renal colic, mild shock with cool/moist skin
- If obstruction at calyx or UPJ, dull costovertebral flank pain or renal colic
- As stone nears ureterovesical junction (UVJ), pain moves from abdomen to lower quadrant
- testicular/labial pain; groin pain
- UTI like-dysuria, fever, chills ○ Dx: noncontrast helical/spiral CT/US, complete UA (hematuria, crystalluria, urinary pH)
- 24 hour urinary measurement ○ Care:
- Acute attack: tx pain/inf/obstruction, opioid, NSAID if no contraindi. w/renal fxn
- Alpha adrenergic blockers - tamsulosin or terazosin relax muscle/men with BPH
- Hydration, sodium restriction
- Struvite stone- control infection, acetohydroxamic acid, surgery
- Endourology, lithotripsy, open surgical removal: too large, symptomatic inf., impaired renal fxn, paralytic ileus, only 1 kidney - Endourology: cystoscopy, cystolitholapaxy, cystoscopic lithotripsy, flexible ureteroscopes, percutaneous nephrolithotomy - Lithotripsy: hematuria common postop, gradually to dark red/smoky., antibiotics, experience severe colicky pain; self-retaining ureteral stent then removed 2 wks after
- Don’t force fluids, 3L/day, at least 2.5L/day UO, strain all urine ○ Pathophysiology: infection causing increased mucus production + inflammation - cold-like symptoms ○ RN interventions: heated high flow nasal cannula (humidified O2 + CPAP), pulsox + supp. O2 <90%, suctioning/NS in bulb syringe (esp. before feeding/bedtime), IV fluids, contact+droplet precautions, 5 - 10 mL fluids/10 min ○ Prevention: breastfeeding, avoid smoke, handwashing, palivizumab vacc. - high risk infants
