Professional Documents
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Chapter 5
Drug classes (MOA, side effects)
Opioids—respiratory depression, CNS depression, constipation, urinary retention
NSAIDs—(Ibuprofen, naproxen, Tordol)
Aspirin (ASA)
Acetaminophen
Tricyclic antidepressants (adjuvant)
Non-pharmacological treatments
Why does pain go untreated?
Table 5-7: effects from different drugs/intoxication
Chapter 6: Nutritional Support
Definitions
Malnutrition: change in body composition and diminished function.
Undernutrition: arises when body’s minimum nutritional requirements of CHS, PRO, lipids and
other essential nutrients are not met.
Starvation: Severe malnutrition condition characterized by failure to meet the minimum body
requirements. During times of metabolic stress, increased energy expenditure and
gluconeogenesis. Stored glycogen gone within 24 hours….moves on to fatty acids mobilized.
Marasmus: Often associated with altered GI functioning, severe cachectic process. Wasting.
Kwashiorkor: caused by prolonged protein malnutrition.
Protein-calorie malnutrition commonly seen in acute/chronic illness due to depletion of fat,
muscle wasting, and micronutrient deficiencies.Discuss enteral nutrition, including benefits,
potential complications, barriers
Explain nutritional alterations associated with selected disease states.
Liver: High CHO, normal to moderate protein, low-fat diets
Lung: Lower CHO with adequate protein to maintain nutritional needs
Kidney: Protein restriction until on dialysis (nitrogenous waste products = raised BUN and
creatinine). Extra CHO for calories. Low calcium/high phosphorus = supplement calcium
Heart: Can become cachectic. Fluid restriction.
GI: SNS slows down the gut.
Burns: CALORIES CALORIES CALORIES + fluids
Traumatic Brain Injury: VERY HIGH ENERGY NEEDS – risk of catabolic state
Discuss enteral nutrition, including benefits, potential complications, barriers
Using the gut via G-tube, PEG, NG, etc.
Start within 24-48 hours
Contraindications—bowel obstruction
Benefits include reduced risk of sepsis/infection, lower inflammation, more effective absorption,
much cheaper than TPN
Complications—aspiration, diarrhea
Can be placed post-pyloric if vomiting/delayed gastric emptying is an issue
o Only continuous feeds with jejunum
Discuss parenteral nutrition, including potential complications.
Generally given via central line
o Infection risk d/t high sugar content of solution
o Watch for fever, chills, hypotension, tachycardia
o Risk of air embolism if port is left open when inserting (treat with left side
trendelenburg)
Describe refeeding syndrome and management strategies.
In Starvation, body uses stored fats.
Huge release of insulin.
Leads to major electrolyte abnormalities.
Patients at risk: cancer, cachexia, HIV/AIDS, chronic alcoholism, anorexia
REFEED SLOWLY!! Initially only 20 cals/kg
Chapter 11: Determinants and Assessment of Pulmonary Function
Explain the conducting airway and the concept of ventilation.
o Conducting (trachea, nose: moving air, no gas exchange)—humidifying, filter, warming
the air, mucociliary blanket to trap debris and microbes
o Ventilation—air in and out
o Compliance—how easy it is to inflate and deflate lungs
(change in volume / change in pressure)
Discuss external vs. internal respiration and pulmonary gas diffusion.
o Respiration—gas exchange
o External = between blood and alveoli (external air)
o Internal = between blood and tissues
Describe pulmonary perfusion and its components.
o Affected by cardiac output, gravity, V:Q, Pulmonary Vascular
Resistance (PVR)
o Alveoli ventilation = 4L/min
o Perfusion = 5L/min
o V:Q ratio = 0.8
o Ventilation (V) problem = low V:Q ratio = shunting
o Perfusion problem (Q) = high V:Q ratio
Interpret ABGs, including compensation.
o Resp = CO2 vs. metabolic = bicarbonate
Conduct a focused respiratory nursing history and assessment.
o Sputum—yellow/green vs white vs frothy
o Breath sounds—abnormal (wheezing, crackles, rhonchi (bigger
airways, probably secretions)
o Vesicular breath sounds in peripheral lung fields = normal
o Dyspnea (shortness)/PND (sudden shortness of breath at
night)/Orthopnea (can’t lay flat)
o Chest pain—respiratory or cardiac? Resp. might change with
inhale/exhale
Describe tests used to evaluate pulmonary function.
o FEV1 (Forced expiratory volume over 1 second)
Discuss noninvasive and invasive methods of monitoring gas exchange.
o Pulse ox relies on hemoglobin binding—lower hemoglobin doesn’t show change in
saturation.
o CO poisoning—binds to hemoglobin, will show normal saturation
o Capnography—monitoring exhaled CO2
How to diagnose?
o Physical Exam—listen to heart tones
o Echo – 2D or TEE: usually 2D is enough but TEE gives better view of posterior of heart
o Risk factors—endocarditis/sepsis, cardiac surgery, IV drug users, rheumatic fever,
congenital heart disease, elderly patients (especially those with HTN)
o How to treat? Depends on severity—monitoring; treat it medically (treat heart failure or
replace valve)
Medically: abx, furosemide, HTN meds, weight monitoring
Low Na+ diet, frequent breaks/space out activities, maybe on
anticoagulants
Replacement: biological or mechanical
Apply knowledge of heart failure to the assessment and management of the high-acuity patient.
o Risk factors—valvular disorders (aortic, mitral = left sided failure), (tricuspid, pulmonic =
right sided failure); genetics; chronic HTN (left sided HF); diet (coronary heart disease);
chronic lung disease (right sided HF/cor pulmonale); persistent left sided failure can lead
to right sided failure
o Clinical Manifestations
Left side—crackles, shortness of breath, fatigue, hypoxia; S3 heart tone
Right side—edema, JVD, weight gain
o Classification—Class I (mild) to IV (severe)
o Pathophysiology—problem with a pump(s)
Decreased CO; RAAS activation = vasoconstriction and fluid retention (increasing
afterload and preload respectively; SNS activation = vasoconstriction; ventricle is
getting overstretched
BNP think HF
o Assessment and Diagnosis—echo to find ejection fraction (55%-70%); chest x-ray; ECG
o Treatment: Control risk factors, Pharmacology, Invasive
CO = HR x SV
Reduce preload (furosemide, spironolactone, ACE inhibitor/ARBs, beta
blockers), afterload (ACE inhibitors/ARBs, calcium channel blockers,
vasodilators) and improve contractility (inotropes, digoxin, dobutamine)
Control risk factors via lifestyle, statins, HTN meds, DM2 meds
o Weight gain limits for HF: 1-2lb/day or >3lb in a week
o Urine output: 30mL/hr is okay for 2-3 hours
o Normal is at least 60mL/hr
Demonstrate the ability to assess and manage care of patients with hypertension.
o Normal: <120 / <80
o Elevated: 120–129 / <80
o Stage 1: 130-139 / 80-89
o Stage 2: >140 / > 90
Apply knowledge of hypertensive crises to the assessment and management of the high-acuity
patient.
o Any target organ damage + >180 / 110 = inpatient treatment
o Only drop 20% in first hour to reduce risk of organ ischemia; 160 / 100 in 2-6 hours
Demonstrate the ability to assess and manage the patient with aortic aneurysm.
o Classification—saccular, dissecting, ruptured fusiform, false aneurysm
o Risk Factors—hyperlipidemia, HTN, stress on vessel walls, plaques
o Pathophysiology
Dissecting—blood in tunica media
Rupture—drop in BP, ripping/tearing sensation
o Clinical Manifestations
o Diagnosis: CT, TEE
o Management
Medical management—if it’s small and not a rupture risk
= watch BP, treat hyperlipidemia, manage DM2, quit
smoking
Surgical management—repair via open chest arterial
graft; endovascular repair