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NSG430 Exam 2 Broad Topic List NOTES
broad topics list expanded with notes on each topic // 2023
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NSG430 Broad Topic List Exam 2
Cardiovascular System
★ Acute Decompensated HF = pulmonary venous pressure increases d/t the left ventricle failing; results in engorgment of
pulmonary vascular system → lungs become less compliant → increased resistance in small airways → compensation = lymphatic
system increases flow = maintain constant volume of pulmonary extravascular fluid
○ Diagnotic
■ Determine + treat underlying cause
■ Echocardiogram → provides info on LVEF, heart valves, presence of effusion or thrombus → help differentiates
between HFpEF and HFeEF
■ ECG
■ Ambulatory heart monitors
■ Chest x-ray
■ 6 min walk test
■ Multi-gated acquisition (MUGA) scan
■ Cardiac MRI
■ Cardiopulmonary exercise stress test
■ Cardiac catheterization/angiogram
■ Endomyocardial biopsy (EMB) → for selective acutely ill patients w/ sudden + unexplained HF unresponsive to
usual care
■ Serum electrolytes (BUN, creatinine/LFTs)
■ NT-proBNP or BNP → may be high in chronic stable HF or other conditions like PE, renal failure, acute
coronary syndrome
■ Chest x-ray
■ Echocardiogram, ECG-O2 sat
○ Manifestations
■ Early S/S
● Increased pulmonary venous pressure
● Mild increase in the respiratory rate
● Decreased PaO 2
■ Later S/S
● Interstitial pulmonary edema
● Tachypnea
● Shortness of breath → Further progression = RBCs w fluid move into alveoli = alveolar edema
● Respiratory acidosis (as result from alveolar edema)
■ Pulmonary edema → LIFE-THREATENING b/c alveoli fills w/ fluid; usually associated w left-sided HF
● Anxious, pale, cyanotic
● Dyspnea (difficult labored breathing)
● Orthopnea (shortness of breath lying down)
● Tachypnea (fast breathing)
● Paroxysmal nocturnal dyspnea
● Accessory muscles use
● Cough w/ frothy, blood-tinged sputum
● Crackles + wheezes
● Tachycardia
● Hypo/hypertension
● Abnormal S 3 or S 4
○ Heart Failure Manifestations
■ Fatigue
■ Dyspnea
■ Orthopnea
■ Paroxysmal nocturnal dyspnea
■ Cough
■ Tachycardia
■ Palpitations
■ Edema (in Dependent, liver, abdominal cavity, lungs//may be pitting)
■ Changes in urine output (like Nocturia)
■ Skin changes
■ Neurological manifestations
■ Mental status and behavioral changes
■ Sleep problems
■ Chest pain
■ Weight changes
○ Interventions/Treatments
■ Assess always! = Subjective + Objective data, PMH, medications for coexisting conditions
■ Current meds that may cause co-existing conditions → OTC causing Na retention (NSAIDs, high dose aspirins,
ephedrine, pseudoephedrine, diet pills)
■ Low sodium diet w cultural considerations (2d/day)
■ Fluid restrictions for stage D HF pts
■ Review of Systems
● Resp = Dyspnea, orthopnea, cough, PND
● GI = Nausea/vomiting/anorexia-Stomach
bloating
● CV = Fluid status---Weight gain-Ankle
swelling-Palpitations-Dizziness, fainting-chest
pain
● VS = Tachypnea, tachycardia, HTN or Low BP
■ Treatment Groups categorized into: dry-warm, dry-cold,
wet-warm, and wet-cold.
● most common presentation is the wet and warm
patient.
○ patient is “wet” due to volume overload
(congestion, dyspnea), but “warm” due
to adequate perfusion (warm skin,
positive pulses)
■ Ongoing monitoring and assessment
● VS, O 2 saturation, weight, mentation, ECGs, indicators of volume overload
■ High/Semi Fowler’s position
■ Hemodynamic monitoring if unstable
■ Daily weights (same time, same clothes), I&Os, monitor edema
● Weight gain 3lbs over 2 days or 3-5 over wk → report to HCP!
■ Alternate rest w activity + diversional activities → monitor responses to activity
■ Collab w OT/PT
■ Reduce anxiety if possible
■ Supplemental oxygen, BiPaP
■ Mechanical ventilation if unstable
■ Ultrafiltration (aquapheresis) for patients with volume overload and resistance to diuretics
■ Mechanical cardiac assist devices for patients with deteriorating HF
● IABP—VADs---ECMO
○ Medication Therapy
■ Diuretics = Decrease volume overload (preload) → Loop diuretics—Furosemide
■ Vasodilators = Reduce circulating blood volume and improve coronary artery circulation
● IV nitroglycerin
● IV sodium nitroprusside
● Aortic stenosis
● Genetic (autosomal dominant)
● Hypertension
■ Restrictive-impaired diastolic filling and stretch (uncommon) → Exercise intolerances
○ Impaired diastolic filling and stretch with normal systole
○ Unknown cause
● Amyloidosis
● Endomyocardial fibrosis
● Neoplastic tumor
● Post-radiation therapy
● Sarcoidosis
● Ventricular thrombus
○ Diagnotics
■ History and physical examination
■ Electrocardiogram
■ b-Type natriuretic peptide (BNP)
■ Chest x-ray
■ Echocardiogram
■ Nuclear imaging studies
■ Heart catheterization
■ Endomyocardial biopsy
○ Manifestations → Progresses to Heart Failure → assess s/s
■ Decreased exercise capacity, Fatigue
● Dyspnea at rest and PND and Orthopnea
● Dry cough
● Palpitations
■ Abdominal bloating, hepatomegaly, JVD → nausea vomiting anorexia
■ S3, S4, murmurs
● Dysrhythmias
● Pulmonary crackles
● Edema, Weak peripheral pulses, Pallor
■ Blood flow stasis → lead to embolization
○ Interventions/Treatments
■ Drug therapy
● Nitrates (except in hypertrophic CMP)
● β-Blockers
● Antidysrhythmics
● ACE inhibitors
● Diuretics
● Digitalis (except in hypertrophic unless atrial fibrillation)
● Anticoagulants (if indicated)
■ Surgical intervention and devices
● Ventricular assist device
● Cardiac resynchronization therapy
● Implantable cardioverter-defibrillator
● Surgical repair
● Heart transplantation
● Cardiac rehabilitation
■ Palliative + hospice care
★ Chest Pain = chronic unstable angina or MI; intermittent chest pain that occurs over long period of time
similar onset, duration, and symptom intensity
○ Common locations + Patterns
■ Onset: physical exertion, stress, or emotional upset
■ Accurate assessment important: PQRST
■ May deny pain; have pressure, heaviness, or discomfort in chest; may be accompanied by
dyspnea or fatigue; no change with position or breathing
■ Some patients, especially women and older adults, report atypical symptoms of angina,
including dyspnea, nausea, mid-epigastric discomfort, and/or fatigue. We refer to this as an
angina equivalent.
○ Angina
■ Pain Duration = few minutes
● Subsides when cause is resolved
● Rest, calm down, SL nitroglycerin
● Generally predictable + controlled w drugs
■ 12 Lead ECG → shows ischemic changes → ST segment depression OR T wave inversion
● Returns to normal when blood flow restored + pain relieved
○ Types
■ Silent = asymptomatic ischemia, associated w diabetic neuropathy; confirm w ECG changes
■ Prinzmetal’s = AKA variant angina, vasospastic angina; rare, occurs at rest w w/o increased
physical demand, Spasm of a major coronary artery with or without CAD
● Hx: migraine headaches, Raynaud’s phenomenon, and heavy smoking
● Contributing factors: increased levels of certain substances, exposure to medications
that narrow blood vessels, or exposure to cold weather
● Treatment = Moderate exercise, calcium channel blockers and/or nitrates, stop use of
offending substances
● May disappear spontaneously
■ Microvascular = Coronary microvascular disease or dysfunction (MVD); Chest pain occurs
in the absence of significant CAD or coronary spasm of a major coronary artery
● R/t myocardial ischemia from atherosclerosis or spasm of distal coronary branches
● More common in women; physical exertion
● Prevention and treatment follows CAD recommendations
○ Diagnostics
■ 12-lead ECG
■ Laboratory studies: cardiac biomarkers, lipid profile, CRP
■ Chest x-ray
■ Echocardiogram
■ Exercise stress test
■ Electron beam computed tomography
● Post procedure drugs = Prevent platelet aggregation + stent thrombosis
● During PCI = heparin or LMW heparin, DTI and/or GP IIb/IIIa inhibitor
● After PCI → dual antiplatelet therapy (DAPT) = Aspirin + clopidogrel
■ Post-op PCI
● Compare assessments to preprocedure
● Assess catheter insertion site for hematoma, bleeding, bruit every 15 minutes for first
hour, then agency policy
● ECG for dysrhythmia; chest pain or other pain
● IV infusion of antianginals
● Monitor for complications
● Education: discharge care and drugs; signs and symptoms to report to HCP
■ Coronary artery bypass graft (CABG) Surgery for patients who:
● Do not respond well to medical management
● Have left main coronary artery or 3-vessel disease
● Are not candidates for PCI OR Continue to have chest pain after PCI.
● may be an option for patients with diabetes, LV dysfunction, and/or CKD
■ Other surgical interventions = MIDCAB, Off-Pump CABG, TECAB-Endoscopic, Laser
Revascularization
★ Endocarditis = diseased of the endocardium (inside of heart) + valves; prognosis = poor + decreased life
expectancy
○ Cause = increased prevalence d/t IV drug use
■ Risks include: Hx of infective endocarditis, IV drug use, prosthetic valve, health care
associated infections from intravascular device (MRSA), renal dialysis
■ Bacterial IE is most commonly d/t staph aureus (50%), step viridans, coagulase negative staph
■ Colonizing of the oropharnyx → d/t HACEK organisms = Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, Kingella
○ Classifications of Endocarditis
■ Cause → IV drug use = IVDA IE, fungal = fungal IE
■ Site of involvement → prosthetic valve endocarditis = PVE
■ Severity/occurence → subacute forms affect preexisting valve disease, while acute form
affects healthy valves
○ Etiology + Patho
■ 3 stages = bacteremia, adhesion, vegetation
● Vegatation
○ Fibrin, leukocytes, platelets, and microbes → stick to valve or endocardium →
Parts break off → enter circulation (embolization)
○ Left-sided vegetation can move to brain, kidneys, spleen, and extremities
○ Right-sided vegetation can move to lungs (PE)
○ Diagnotic
■ Health history-3-6 months/dental, surgical, gyn, IVDA, implants, infections, dialysis
■ Laboratory tests
● Blood cultures-multiple sites
● CBC with differential
● ESR, C-reactive protein (CRP)
■ Echocardiography
■ Duke criteria for major and minor critieria
■ Assessment = subjective + objective (clinical manifestations present?)
● Subjective = hx of IV drug use, alcohol use, meds/drugs, immunosuppressive therapy,
weight changes, chills, night sweats, hematuria, exercise intolerances, weakness,
fatigue, cough, dyspnea on exertion, orthopnea, palpitations, pain, headache, joint, or
muscle tenderness
○ Manifestations → can be nonspecific + involve multiple organ systems
■ Fever
■ Chills
■ Weakness + malaise + fatigue
■ Anorexia
■ Subacute form
● Arthralgias
● Myalgias
● Back pain
● Abdominal discomfort
● Weight loss
● Headache
● Clubbing of fingers
■ Vascular manifestations
● New/worse systolic murmur
● Heart failure
■ Manifestations secondary to septic embolism
● Splinter hemorrhages in nail beds
● Petechiae
● Osler’s nodes on fingertips or toes
● Janeway’s lesions on fingertips, palms, soles of feet, and toes
● Roth’s spots
○ Interventions/Treatments → dependent on what conditions they have
■ Prophylactic antibiotics = high risk
● Heart conditions: CHD, Valvular disease, Hx of IE, Prosthetic Valve
● Procedures
○ Certain dental procedures
○ Respiratory tract incisions
○ Tonsillectomy and adenoidectomy
○ Surgical procedures involving infected skin, skin structures, or musculoskeletal
tissue
■ Active infection treatment
● Blood cultures → Accurate identification of organism
● IV antibiotics (long-term)
● Repeat blood cultures
● Valve replacement if needed
● Antipyretics + Fluids + Rest
● Anticoagulation therapy for A-fib
■ Surgical
● Percutaneous transluminal balloon valvuloplasty (PTBV) = Split open fused
commissures to treat mitral, tricuspid, and pulmonic, and AS → Balloon-tipped
catheter inserted via femoral artery → Inflated to separate valve leaflets
● Valve repair (Commissurotomy (valvulotomy), Valvuloplasty, Annuloplasty) =
Preferred surgical procedure lowering operative mortality rate than replacement, but
may not restore total valve function
● Valve replacement (can be Mechanical or Biological) = Transcatheter aortic valve
replacement (TAVR) used for severe AS and is a transfemoral approach
○ Mechanical (artificial)
■ More durable, last longer
■ Risk of thromboembolism → Require long-term anticoagulation
○ Biologic (tissue) → can be Bovine, porcine, and human
■ More natural blood flow
■ No anticoagulation required
■ Less durable
○ Nursing Considerations
■ Health promotion
● Early treatment of streptococcal infections
● Prophylactic antibiotics for patients with history
● Discourage tobacco use
● Need for Medical-alert device or bracelet d/t anticoag therapy
■ Individualize rest and exercise = Limit activities
■ Monitoring drug effectiveness
■ Monitor INR if on anticoagulants
■ Notify HCP for: Signs of infection, HF, or bleeding + Planned invasive or dental work
★ Pacemaker = paces heart when normal conduction pathway is damaged, will appear as “spikes”
○ Pacing circuit consists of Power source (can be battery powered pulse generator) + Programmable circuitry
○ “Dual Chamber” = pacing atrium and/or one ventricles
■ Fixed = always paced, no underlying complexes
■ On demand = fires only when HR drops below preset
rate, sensing device will stop pacemaker when HR is
acceptable range, pacing device triggered when no
QRS complex in set time frame
○ Types
■ Transcutaneous = through skin-chest placement
● For emergency pacing needs
● Noninvasive
● Bridge until transvenous pacer can be inserted
● Use lowest current that will “capture”
● Patient may need analgesia/sedation
■ Transvenous = through Central line
■ Epicardial = through chest wall-Post cardiac surgery
■ Permanent
○ Interventions + Management
■ Monitor for other complications
● Infection
● Hematoma formation
● Pneumothorax
● Atrial or ventricular septum perforation
● Lead misplacement
■ Postprocedure care
● Out of bed once stable
● Limit arm + shoulder activity
● Observe insertion site for bleeding and infection
■ Patient and Caregiver Teaching
● Follow-up appointments for pacemaker function checks
● Incision care
● Arm restrictions
● Avoid direct blows
● Avoid high-output generator
● No MRIs unless pacer approved
● Microwaves OK
● Avoid antitheft devices
● Travel not restricted
● Monitor pulse
● Pacemaker ID card + Medic Alert ID
★ Pericarditis = inflamed pericardial sac + fluid accumulation (normal is 10-15mL volume)
○ Cause
■ Infectious-Bacterial, fungal, viral
■ Noninfectious-MI, Cancers, Aortic Dissection, renal
failure, trauma
■ Autoimmune-Meds, Post-Op, RF, RA, SLE,
Scleroderma, AS
■ Dressler Syndrome = Post MI irritation and fluid 4-
weeks after
○ Diagnotic
■ EKG—diffuse ST segment elevation-not like an MI
■ CXR-enlargement of silouette
■ Echocardiogram
■ CT MRI
■ Labs
● CBC, CRP, ESR, Troponin
● Pericardial fluid testing, cultures and biopsy
○ Manifestations
■ Chest Pain → Worse with deep inspiration and lying flat
■ Radiation arm, neck, shoulder, upper back
■ Degree of LV dysfunction depends on area of heart and size of infarction
■ Cardiac Biomarkers
● Proteins released after MI
● Cardiac-specific troponin T (cTNT)
● Cardiac-specific troponin I (cTNI)
○ Increased 4 to 6 hours after onset of MI
○ Peak at 10 to 24 hours
○ Return to baseline over 10 to 14 days
○ Note: Cardiac-specific troponins are better indicators of MI than CK-MB or myoglobin
● Biomarkers negative for UA; positive for NSTEMI
■ Cardiac catheterization
● STEMI: within 90 mins
● UA or NSTEMI: within 12-72 hrs
● Can get thrombolytic therapies within 30 mins (if no PCI available)
○ Manifestations
■ Severe chest pain not relieved by rest, position change, or nitrate admin
● May feel like heaviness, pressure, tightness, burning, constriction, crushing
● Common locations = substernal or epigastric (but can radiate to neck, lower jaw, arms,
back
● Occur in morning greater than 20 mins
● Note: women feel MIs differently → may feel anxious or sense of doom, something
not right
● No pain if there is cardiac neuropathy (diabetes)
■ Diaphoresis
■ Increased HR + BP → then reduced BP d/t decrease in CO
■ Ashen, clammy, cool skin
■ Decreased urine output d/t dec renal perfusion
■ Crackles d/t LV dysfunction
■ Jugular vein distention, hepatic engorgment, peripheral edema (RV dysfunction)
■ Abnormal heart sounds → S3 or S4, murmurs holosystolic
■ N/V → d/t reflex stimulation of vomit center from severe pain
■ Fever → up to 100/38C in first 24-48 hrs up to 4-5 days; from systemic inflammation d/t heart cell death
○ Interventions
■ Emergency care → ONAM = (oxygen, nitro, aspirin, morphine)
● 12-lead ECG
● Upright position
● Oxygen—keep O 2 sat > 93%
● IV access
● Nitroglycerin (SL) and ASA (chewable)
● Morphine
● Statin
■ ST elevation = cardiac cath lab for PCI or thrombolytic therapy
■ ST depression or inversion = critical care or tele unit
■ Monitor dysrhythmias and serum biomarkers
● UA, NSTEMI = heparin, glycoprotein IIb/IIIa inhibitors before, during PCI
● STEMI = glycoprotein IIB/IIA inhibitors during PCI
■ Admit to ICU/tele unit → monitor vitals, pulse ox, cont. ECG, serial 12 leads, serial cardiac
biomarkers, bed rest/limit activity for 12-24hrs then increase gradually
■ PCI → opens blocked arteries
● Severe LV dysfunction? → IABP and/or inotropes
● Emergency CABG
■ Thrombolytic therapy if less than 12 hrs → STEMI only
● Advantages: availability and rapid administration (if not PCI-capable)
● May transfer if PCI can be done within 120 minutes
● Goals: Limit size of infarction + Administer IV within 30 minutes of arrival
■ IV heparin when concerned for reocclusion
■ Drug therapy
● Suspected ACS = Antiplatelet therapy, IV NTG, atorvastatin
● NSTEMI or UA = Anticoagulation and glycoprotein IIb or IIIa
● MI = DAPT, Aspirin, b-blockers, calcium channel blockers, ACE inhibitors, and/or
nitrates
● IV nitroglycerin (NTG) → for pain too
● Morphine → for pain
● β-Adrenergic blockers
● ACE inhibitors and ARBs
● Antidysrhythmic drugs
● Lipid-lowering drugs
● Aldosterone antagonists
● Stool softeners
■ Physical activity
● Increase activity gradually; check HR; FITT formula
● Limit isometric exercise; Valsalva maneuver
● Women; less adherence due to caregiver role; also consider fatigue and depression
■ Cardiac rehab → restore physio, psycho, mental, spiritual, economic, vocational function
(outptaitne or home-based)
■ Sexual counseling = ED drugs contraindicated w nitrates, prophylactic nitrates before sex,
avoid sex 7-10 days post MI or when able to climb 2 flights stairs
○ Complications
■ Dysrhythmias = Most common complication
■ Heart failure = decreased pumping power → L-HF or R-HR
■ Papillary muscle dysfunction or rupture → causes acute + massive mtral valve regurg + new
murmurs = aggravates already compromised LV + decreases CO
■ Left Ventricular Aneurysm = Myocardial wall is thin; bulges out during contraction
■ Ventricular septal wall rupture and left ventricular free wall rupture → emergency repair +
high death rate, but RARE
■ Pericarditis = Inflammation of visceral and/or parietal pericardium
● Delayed is called Dressler syndrome
● Treat w high dose aspirin
● Hypoxia
● Hydrogen ion (acidosis)
● hyper/hypokalemia
● Hypoglycemia
● Hypothermia
■ T
● Toxins
● Tamponade (cardiac)
● Thrombosis (MI + pulmonary)
● Tension penumothorax
● Trauma
★ Paced Rhythms = medical emergency if CO is decreased!
○ Troubleshooting Pacemakers
■ Failure to sense = not reading rhythm + causes
inappropriate firing
● Manifests as pacer spikes that are too close
to patients own rhythm
■ Failure to capture = not stimulating muscle; Lack
of pacing when needed leads to bradycardia or
asystole
■ Failure to pace = not firing; Pacemaker does not
initiate electrical stimulus when it should fire
★ PAC = AKA premature atrial contraction; a type of supreventricular dysrhythmia
○ Contraction starts form ectopic focus in atrium in a place other than SA node
■ Travels thru atria by abnormal pathway → creates distorted P waves
■ Can be stopped, delayed, or conducted normally at AV node
○ Causes → many different → must find out cause
■ Emotional stress
■ Fatigue
■ Caffeine
■ Tobacco
■ Alcohol
■ Hypoxia
■ Electrolyte imbalances
■ Disease states-hyperthyroidism, chronic obstructive pulmonary disease (COPD), and heart
disease, including CAD and valvular disease.
■ In persons with healthy hearts, isolated PACs are not significant.
○ Manifestations = palpitations, heart “skips a beat”
○ Interventions/Treatments
■ Treat cause
■ Monitor for MORE serious dysrhythmias
■ Withhold stimulation sources
■ Beta blockers
★ PVC = AKA premature ventricular contraction; contraction coming
from ectopic focus in ventricles, is premature/early QRS occurrence
○ Appearance
■ QRS may appear wide + distorted in shape
■ T wave large + opposite inn direction of QRS complex
○ Types
■ Multifocal PVCs = PVCs w different points w different
shapes form each other
■ Unifocal PVCs = PVCs w same shapes
■ Ventricular Bigeminy = PVCs occurs every other beat
■ Ventricular Trigeminy = PVCs every THIRD beat
■ Couplet = two consecutive PVCs
○ Considerations
■ Ventricular tachycardia results w/ three or more consecutive PVCs
■ R-on-T phenomenon → occurs when PVC falls on T wave of preceding beat (see pic below)
○ Manifestations
■ Dizziness
■ Near-fainting
■ Anxiety
■ Pounding sensation in neck
○ Interventions/Treatments → correct the cause + medications
■ Causes
● caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin
● electrolyte imbalances, hypoxia, fever, exercise, and emotional stress
● MI, mitral valve prolapse, HF, cardiomyopathy, and CAD.
■ Medications = Beta blockers, lidocaine, amiodarone
★ Normal Sinus Rhythm
○ 60-100bpm ← fired by SA node
○ Normal conduction pattern
○ P wave normal, precede QRS
○ QRS normal shape + duration
○ PR interval normal
○ *sinus arrhythmia = conduction
pathway same, but SA fires irregulary
★ Sinus Bradycardia → can occur normally in aerobically trained athletes + sleep; may occur in response to
PSN stimulation, drugs (B-adrenergic blockers/Beta-blockers, calcium channel blockers), carotid sinus
★ Ventricular Tachycardia = can be monomorphic, polymorphic, sustained, or nonsustained; stable (pulse) or
unstable (pulseless)!; Life threatening d/t decreased CO + possible ventricular fibrillation
○ Ectopic foci came to take over as pacemaker
○ Shown A = v tach (monomorphic) // B = torsades de pointes
(polymorphic)
○ Associated w/ HD, long QT syndrome, electrolyte imbalances,
drug toxicity, CNS disorders
○ Manifestations
■ Decreased CO →
● Hypotension
● pulmonary edema
● decreased cerebral blood flow
● cardiopulmonary arrest
○ Interventions/Treatments → treat root cause (like hypoxia)
■ VT w/ pulse/stable → treat w/ antidysrhythmics or cardioversion
■ Polymorphic VT w prolonged baseline QT → IV magnesium, isoprotenrenol, phenytoin, or
antitachycardial pacing
■ Pulseless/unstable VT = LETHAL→ CPR, rapid defibrillation, followed w/ vasopressors
(epinephrine) + antidysrhythmics (amiodarone) if defibrillation unsucessful
Renal System
★ Acute Renal Failure/Injury = ranges from partial/complete impairment of kidney fxn resulting from
inability to excrete metabolic waste products and water → affects ALL body systems
○ Rapid loss of kidney fxn w/
■ Rise in creatinine and/or urine output
■ Elevated BUN + K
■ Azotemia = accumulation of nitrogenous waste products
○ Prognosis = high mortality rate w other life-threatneing conditions
○ Phases + Etiology/Pathophysiology
■ Prerenal = d/t factors reducing systemic circulation → reduces renal blood flow → leads to oliguria
● S/S: Severe dehydration, heart failure, decreased CO
● Autoregulatory mechanisms → tries preserving blood flow
● Prerenal azotemia = Na excretion → increased Na + H2O retention + decreased urine output
■ Intrarenal = d/t problems causing damage to kidney tissue + acute tubular necrosis
● Causes → prolonged ischemia, nephotoxins, hemoglobin released from hemolyzed RBCs, myoglobin
released form necoritc muscle cells, kidney disease (acute glomerulonephritis + SLE)
● Acute Tubular Necrosis → results form ischemia, nephrotoxins, or sepsis → is potentially reversible
○ Severe ischemia → disrupts basement membrane + causes pathy destruction to tubular
epithelium
○ Neprhotic agents cause necrosis of tubular epithelial cells → clogs tubules
■ Postrenal = d/t mechanical obstruction of outflow → refluxes into renal pelvis → impairs kidney fxn
● Causes = Benign prostatic hyperplasia, prostate cancer, calculi, truma, + extrarenal tumors
● Bilateral ureteral obstruction = hydronephrosis; must relieve the obstruction in 48 hrs for potential
recovery!!
○ Cause/Risk Factors
■ Most commonly caused by hypervolemia (too much fluid in body) leading to HTN
■ Gerontologic
■ MRI/MRA w contrast causes induced nephropathy
■ T2 DM and metformin use → hold 48hrs prior to contrast admin
○ AKI vs CKD
○ Diagnotic
■ Thorough history
■ Serum labs = GFR, Creatinine Clearance, creatinine, BUN, electrolytes
■ Urinalysis
■ Renal ultrasound
■ Renal scan
■ CT scan
■ Renal biopsy
■ Contraindications for contrast medium
● MRI or MRA with gadolinium contrast medium—may be fatal
● Contrast-induced nephropathy (CIN)
● Diabetics taking metformin: hold 48 hours before and after use of contrast medium; risk of lactic
acidosis
● If contrast is needed for high-risk patients—use low-dose and optimal hydration
○ Manifestations → depend on the three phases (oliguric, diuretic, and recovery)
■ Oliguric = urinary changes characterized by oliguria (abnormal small amt urine); about 50% pts are nonoliguric
= more than 400mL urine/day
● Criteria
○ Urine output < 400 mL/day
○ Occurs 1-7days after injury
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NSG430 Exam 2 Broad Topic List NOTES
Course: Adult Health Nursing II (NSG-430)
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NSG430 Broad Topic List Exam 2
Cardiovascular System
★Acute Decompensated HF =pulmonary venous pressure increases d/t the left ventricle failing; results in engorgment of
pulmonary vascular system → lungs become less compliant → increased resistance in small airways → compensation = lymphatic
system increases flow = maintain constant volume of pulmonary extravascular fluid
○Diagnotic
■Determine + treat underlying cause
■Echocardiogram → provides info on LVEF, heart valves, presence of effusion or thrombus → help differentiates
between HFpEF and HFeEF
■ECG
■Ambulatory heart monitors
■Chest x-ray
■6 min walk test
■Multi-gated acquisition (MUGA) scan
■Cardiac MRI
■Cardiopulmonary exercise stress test
■Cardiac catheterization/angiogram
■Endomyocardial biopsy (EMB) → for selective acutely ill patients w/ sudden + unexplained HF unresponsive to
usual care
■Serum electrolytes (BUN, creatinine/LFTs)
■NT-proBNP or BNP → may be high in chronic stable HF or other conditions like PE, renal failure, acute
coronary syndrome
■Chest x-ray
■Echocardiogram, ECG-O2 sat
○Manifestations
■Early S/S
●Increased pulmonary venous pressure
●Mild increase in the respiratory rate
●Decreased PaO2
■Later S/S
●Interstitial pulmonary edema
●Tachypnea
●Shortness of breath → Further progression = RBCs w fluid move into alveoli = alveolar edema
●Respiratory acidosis (as result from alveolar edema)
■Pulmonary edema → LIFE-THREATENING b/c alveoli fills w/ fluid; usually associated w left-sided HF
●Anxious, pale, cyanotic
●Dyspnea (difficult labored breathing)
●Orthopnea (shortness of breath lying down)
●Tachypnea (fast breathing)
●Paroxysmal nocturnal dyspnea
●Accessory muscles use
●Cough w/ frothy, blood-tinged sputum
●Crackles + wheezes
●Tachycardia
●Hypo/hypertension
●Abnormal S3or S4
○Heart Failure Manifestations
■Fatigue
■Dyspnea
■Orthopnea
■Paroxysmal nocturnal dyspnea
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