Exam 1 review sheet Flashcards
(119 cards)
1
Q
Insulin drip
A
atlanta multiplier methodstarting rate units/hour = (BG - 60) x .02
2
Q
blood sugar 226
A
(226-60) x .02 = 3.32 …. 3 units/hour
3
Q
correction bolus forumula
A
current BG - Ideal BG——————————–glucose correction factor
4
Q
Ideal blood glucose
A
100
5
Q
example:250-100————–30
A
= 5.0u
6
Q
fasting glucose is 326ideal is 100correction factor of 30
A
326-100———–30 = 7.53 or 8 units
7
Q
Notes
A
Will be given glucose correction factorIdeal is always 100Round up if the decimal is 5 or greater
8
Q
hypoglycemia
A
glucose is 40how much d50 iv push should mrs. jones receive
9
Q
D50 formula
A
= (100-bg) x 0.4 ml IV
10
Q
(100-40) x 0.4 ml IV
A
24ml/IV
11
Q
40 glucose is considered
A
a severe hypoglycemia
12
Q
ABG Analysisph 7.35, pao2 60, paco2 50, hco3 30
A
compensated respiratory acidosis
13
Q
ph 7.50, pao2 75, paco2 40, hco3 32
A
uncompensated metabolic alkalosis
14
Q
ph 7.6, pa02 80, paco2 30, hco3 24
A
uncompensated respiratory alkalosis
15
Q
ph 7.3 pa02 75, paco2 32, hco3 19
A
partially compensated metabolic acidosis
16
Q
ph 7.45, pa02 75, paco2 28, hco3 20
A
fully compensated respiratory acidosis
17
Q
Two challenge rule
A
f you call the provider and you don’t get a reasonable solution, restate what you think is approrpriate, restate why you think it’s appropriate, and if you still don’t get what you need, contact another provider
18
Q
Compassion fatigue
A
Intrusive ThoughtsBlending of RolesLowered ToleranceDreadDepressionSelf-destructive ActionsHyper-vigilanceDecreased FunctioningLoss of Hope
19
Q
Best level for hospital and NICU
A
Level 1 hospital: good. Teaching hospital with multiple care pathways and can handle multiple patients. NICU: level 3 is the best
20
Q
Open vs. Closed unit
A
Open:-multiple staff is coming and going, physicians, ancilary staff, nurses, all managing a patient-most typically usedClosed:certain staff including an intensivist who managed your patient. Great, unless the intensivist missing something, or something special happens that’s not in the intensivists realm of specialty.
21
Q
VAP bundle includes?
A
prevent ventilator associated pneumonia*head of bed elevated 30*oral care every 2 hours*turn Q2*sedation vacation every 24 hours*peptic ulcer prphylaxis within the first 24 hours of mechanical ventilation*DVT thrombosis w/i 24 hours on vent (DVT precautions)
22
Q
Biggest problems for critical care patients
A
-they are vulnerable-communication issues-technology-complex, multiple-step process
23
Q
Safe Medical Device Act
A
-Require that hospitals report serious or potentially serious device-related injuries to the U.S. Food and Drug Administration (FDA).-All implantable devices must be documented and tracked with the FDA
24
Q
Weaning of morphine per london health center guidelines
A
Morphine: If dose is less than 4mg per hour , then decrease by half every six hours. If dose is more than 4mg an hour, decrease by 25% every 6 hours until less than 4
25
Most beneficial in reducing pain in patients
Touch and family
26
To provide adequate pain control, first rule out?
→ hypoxia→ hypoglycemia→ withdrawal→ sleep deprivation→ immobility→ fear
27
Three purposes of sedation
Amnesia: to forget what's going onAgitation: Anxiety: go to sedation as last resort
28
Neonatal: Mother-Driven Interventions for pain
breastfeedingskin-to-skin carematernal voice, maternal heartbeat with NNSolfactory, aromatherapy recognition
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Neonatal: Sensorial Interventions for pain
containment & swaddlingfacilitated tuckingvestibular stimulation (rocking)orotactal stimulation: non-nutritive sucking (NNS) sweet solutionsCombining interventions offers additional benefits
30
Delirium classifications
-Hyperactive (agitated): Most common. sudden change, hallucinated, hyperactive-Hypoactive (quiet) – often misdiagnosed as depression, become nonresponsive and sluggish-Mixed: Second most common, bipolar-ish
31
Treat Cause of Delirium Acronym
THINK-Toxic situations and medication: CHF, shock, dehydration, organ failure. Benzodiazepines, anticholinergics, and steroids-Hypoxemia-Infection/sepsis, inflammation, immobilization-Nonpharmacological interventions: sleep, reorientation/reassurance, familiar people/objects-K+ (potassium) or other electrolyte imbalance
32
Delirium
-Common in critically ill patients (esp. on ventilator)-Caused by neurotransmitter imbalance in brainPredisposing factors-Patient (age, substance use, sensory impairment)-Illness (infection, electrolyte imbalance, low HCT)-Iatrogenic (polypharmacy, sleep disruption, immobility)-causes hospitals not to get reimbursed
33
Sedation med used for long term, or low level sedation
Lorazepam (Ativan): benzodiazepine \* intravenous onset: 15 to 30 minutes, duration ~8 hours \* intermittent or continuous-can only be mixed with d5w-can cause renal tubular necrosis
34
When you want a sedation medication that acts rapidly and ends rapidly?
Propofol (Diprivan): short-acting general anesthetic agent \* onset: 40 seconds, duration 3 to 5 minutes \* sedation is necessary with rapid awakening \* bolus, then continuous-usually on ventilated patients-containers it's in can only be used for 12 hours-(lipid) generally used through central line or used large bore peripherally because it's very irritating-if drip is stopped, expect them to wake up in 8
35
Ventilation vs. Respiration
Ventilation is the rate at which gases enter or leave the lungs whereas respiration is the transport of oxygen from the outside air to the cells within tissues, and the transport of carbon dioxide in the opposite direction
36
the volume of air breathed in or out of the lungs during normal respiration0.5
tidal volume
37
The Ventilation-Perfusion (V/Q) ratio (normal?)
The V/Q ratio is the ratio between the amount of air getting to the alveoli (the alveolar ventilation, V, in ml/min) and the amount of blood being sent to the lungs (the cardiac output or Q - also in ml/min).V/Q = (4 l/min)/(5 l/min)V/Q = 0.8
38
Shunt Unit
Inadequate ventilation to an alveolusExample: Pneumonia
39
Dead Space Unit
Alveolar cluster where perfusion failsExample: Pulmonary embolism
40
Normal ABG's
PaO2: 80-100SaO2: 93-99pH: 7.35-7.45PaCO2: 35-45HCO3: 22-26
41
Type?Impaired Gas Exchange-Pneumonia-Pulmonary edema-ARDS-AtelectasisNursing Interventions?
Type I- HypoxemiNursing Interventions:-Cough and deep breathe-HOB elevated-administering of meds such as diuretics-Add some ventilator peep-incentive spirometry-Get up to allow lung expantion
42
Ineffective Breathing Pattern-COPD-Neurological Respiratory Failure-Muscular FailureType?Nursing Interventions?
Type II- HypercapneicNursing interventions:-Bipap-ventilate them and change inspiratory expiratory ratio to allow more time to breathe in (add paralytics)-mechanical ventilation-change position Q2-HOB elevated
43
Difference between CPAP and BIPAP
CPAP-Continuous Positive Airway Pressure-for patients who need continuous low pressure to keep lungs openBIPAP-Bilevel Positive Airway Pressure-can assist with low level pressure at inspiration and expiration to help lungs stay open
44
Volume Control
controlling the volume on the ventilator
45
pressure control
delivers volume until a certain pressure is acheived
46
synchronized intermitted mandatory ventilation
on the breaths that the ventilator is going to deliver, it will deliver the settings. Won't assist on their own breaths
47
What is ECMO and how does it work?
-extracorporeal life support-De-saturated blood is drained via a venous cannula, CO2 is removed, O2 added through an “extracorporal” device (often misnamed an oxygenator), and the blood is then returned to systemic circulation via another vein (VV ECMO) or artery (VA ECMO)
48
Patho of ALI/ARDS phases
-Phase 1: (inflammation and exudation) Capillary membranes are compromised and alveoli begin to fill with protein rich fluid. Type I alveolar cells are destroyed. Hyaline membranes are formed.-Phase 2: (proliferation) Type II alveolar cells are damaged & surfactant production declines. Inspiratory pressures increase as compliance decreases resulting in a ventilation/perfusion mismatch.-Phase 3: (resolution) Fibrotic tissue develops resulting in increased pulmonary pressures and ventilation dead space.
49
NON-PHARMACOLOGICAL interventions for ALI/ARDS
-Nutrition Support-Prone positioning: Guérin et al (2013) found early prone positioning decreased 30 & 90 day mortality-Mechanical Ventilation: Low VT and high PEEP,FiO2 below 60%, High Frequency Oscillation-Extracorporeal Life Support (ECLS): Lung bypass, ECMO
50
Pharmacological interventions for ARDS/ALI
Anti-Inflammatories: Cases of hypoxia \>7Days & started before Day 14VasodilatorsSurfactantB-AgonistsCytokine InhibitorsColloidsParalyticsOxygen
51
-Leading cause of cancer deaths in the US-Main Types: SCLC, NSCLC (small cell: agressive & paliate care starts at the begginning, nonsmall cell is the other)
Lung Cancer
52
Treatment options for lung cancer
-Proton therapy: A type of radiation that uses high energy beams.-Chemotherapy:The most commonly used drugs to treat small cell lung cancer are cisplatin or carboplatin with etoposide.-Brachytherapy: radiation beads or rods are inserted at the cancer site.
53
-One of the most common congenital abnormalities-Incidence 1 in 2000 to 5000 births-One third of infants with this are stillborn, usually due to associated fatal anomalies like neural tube defects and cardiac defects-Defects are common on left side (80%) compared to right (20%)-expected risk in a 1st degree relative is 1 in 45combo with karyotype is associated with poor outcome-Bilateral is very rare
Congenital Diaphragmatic Hernias (CDH)
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two main CDH
-Bochdalek: most common-Morgani: much less common
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How to diagnose/treat CDH
-CXR showing displaced organs into the chest cavity-diagnosed with ultrasound usually in utero, can be diagnosed 1st day of life-EKG shows stress to heart-surgical treatment: Laparotomy, thoracotomy, laparoscopy and thoracoscopy. When diaphragmatic tissue is adequate, primary repair with nonabsorbable suture can be done. If the defect is too large, prosthetic material can be used for a tension-free repair-Meds: nitros oxide in lung and htn medicine
56
RSD risk factors
-Develops in ~ 50% of infants born between 28-32 weeks gestation-Inversely related to prematurity-Males-Second born twins-C-section-Caucasian race
57
RDS: Treatment
-Maintain FRC (CPAP vs. intubation)-Surfactant replacement (with temporary intubation)-Exogenous surfactants (if they don't have any)-Survanta 4cc/kg-Infasurf 3cc/kg
58
-Diffuse reticular granular or “ground glass”pattern-Air bronchograms (bronchi visible)-Underaeration
alveolar disease
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-(beta cells)-stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose
insulin
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-(alpha cells)-stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose
glucagon
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Functions of insulin
-Enables glucose to be transported into cells for energy for the body-Converts glucose to glycogen to be stored in muscles and the liver-Facilitates conversion of excess glucose to fat-Prevents the breakdown of body protein for energy
62
-Usually under 30-Rapid onset-Normal or underweight-Little or no insulin-Ketosis common-Autoimmune plus environmental factors-Genetic Propensity possible-Treated with insulin, diet and exerciseType 1 or type 2?
Type 1
63
-Usually over 40-Gradual onset-Most have insulin resistance-Ketosis rare-Part of metabolic insulin resistance syndrome-Strongly hereditary-Obesity in 80% of Cases-Diet & exercise, progressing to tablets, then insulinType 1 or type 2?
Type 2
64
-Polydipsia – increased thirst-Polyuria – increased urine-Polyphagia – increased hunger-Fatigue-Blurred vision-Slow healing infections-Impotence in menType 1 or 2 clinical manifestations?
Type 2
65
Major defect in individuals with type 2 diabetesReduced ability of beta-cells to secrete insulin in response to hyperglycemia
beta cell dysfunction
66
-Most common form of diabetes (90%+ of all cases)-Risk factors: Obesity, Family history, Sedentary lifestyle, Ethnicity (African American, Hispanic, and Native Americans), Hypertension, Hyperlipidemia, --Over the age of 45 years-Combination of physiological factors contribute: ---Impaired insulin production,-Insulin resistance-These individuals may have both-Hyperinsulinemia-Hyperglycemia
Type 2
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-Polyuria – increased urine-Polydipsia – increased thirst-Polyphagia – increased hunger-3 ‘Ps”-Weight loss-Fatigue-Nausea, vomiting-Ketoacidosis may be a presenting signclinical manifestations for?
Type 1
68
-Not fully understood-Current thoughts-Viral exposure triggers immune response that also attack the beta cells in the Islets of Langerhans. -Genetic propensity also believed to be involved.-Some drug therapies destroy the beta cells-Pyrinuron (no longer used in the US)-Zanosar (used in the treatment of pancreatic cancer)
Type 1 diabetes
69
AACE/ADA Recommended Target Glucose Levels in ICU Patients
ICU setting:-Starting threshold of no higher than 180 mg/dL-Once IV insulin is started, the glucose level should be maintained between 140 and 180 mg/dL-Lower glucose targets (110-140 mg/dL) may be appropriate in selected patients -Targets 180 mg/dL are not recommended 180: NOT RECOMMENDED
70
AACE/ADA Target Glucose Levels in Non–ICU Patients
Non–ICU setting:-Premeal glucose targets \<40
71
Severe hypoglycemia is defined as a blood glucose level?
less than 40, less than 50 = decrease in cerebral glucose availability
72
Events Triggering Hospital Hypoglycemia
-Transportation off ward, causing meal delay-Failure to measure blood glucose before insulin doses-New NPO status-Interruption of: IV dextrose therapy, Total parenteral nutrition, Enteral feedings, Continuous venovenous hemodialysis
73
Features Increasing the Risk of Hypoglycemia in an Inpatient Setting
-Concurrent illness (cerebral vascular accident, congestive heart failure, shock, sepsis)-Concurrent medications (Beta-blockers, quinolones, epinephrine)-Advanced age-Renal failure-Liver disease-Ventilator use
74
Continuous Variable Rate IV Insulin DripAtlanta Multiplier Method
-\*(formula on test) Starting Rate Units / hour = (BG – 60) x 0.02, where BG is current Blood Glucose and 0.02 is the multiplier-Check glucose every hour and adjust drip-Adjust Multiplier to keep in desired glucose target range (90 to 120 in ICU; 100 to 140 on floor)
75
Converting to SC insulin from IV protocol? What's the exception?
-If More than 0.5 u/hr IV insulin required with normal BG, start long-acting insulin (glargine). -------Exception: if no prior DM and normal A1C, may not need SC insulin-Must start SC insulin at least 1 to 2 hours before stopping IV insulin-Some centers start long-acting insulin on initiation of IV insulin or the night before stopping the drip
76
Correction Bolus Formula
Current BG - Ideal BG/ Glucose Correction factorExample:Current BG: 250 mg/dlIdeal BG: 100 mg/dlGlucose Correction Factor: 30 mg/dlso 250-100/correction factor of 30= 5 units\* ON TEST\*Add that correction factor to current dose to calculate how much you're giving
77
-A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone.-Can occur in both Type I Diabetes and Type II Diabetes: In type II diabetics with insulin deficiency/dependence-The presenting symptom for ~ 25% of Type I Diabetics.
Diabetic Ketoacidosis (DKA)
78
-An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia.-Occurs predominately in Type II DiabeticsA few reports of cases in type I diabetics.-The presenting symptom for 30-40% of Type II diabetics.
Hyperosmolar Hyperglycemic State (HHS)
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Severe DKA vs HHS. Which is which? ? ?Plasma glucose level: \>250 \>600Arterial pH: 7.30Sodium Bicarb: 15Urine Ketones: positive smallSerum Ketones: positive smallSerum Osmolality variable \>320Anion Gap: \>12 variableMental Status: Stupor/Coma
DKA HHSPlasma glucose level: \>250 \>600Arterial pH: 7.30Sodium Bicarb: 15Urine Ketones: positive smallSerum Ketones: positive smallSerum Osmolality variable \>320Anion Gap: \>12 variableMental Status: Stupor/Coma
80
Treatment of DKA
HYDRATION!!!Normal Saline:500-1000 cc/hr for 4 hours, then 250 – 500 cc/hr for 4 hours, then 125-250 cc/hrOnce glucose is \< 200, should change fluids to D5 ½ NS until insulin drip is stoppedInsulin-Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hrIdeally should decrease glucose 50-100 mg/dL per hourIn DKA: Change to subcutaneous regimen once anion gap has closed and patient is ready to eat.Need to give long-acting insulin dose several hours prior to stopping insulin drip.AccuchecksEvery 1 hour initially, then every 2 hours, and so on.Serial ElectrolytesPotassium repletionShould add potassium to IV fluids once potassium \< 5
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Treatment of HHS
-Hydration!!!: Even more important than in DKA-Find underlying cause and treat!-Insulin drip: Should be started only once aggressive hydration has taken place. Switch to subcutaneous regimen once glucose \< 200 and patient eating.-Serial Electrolytes: Potassium replacement.
82
Five H's of Pheochromocytoma
-hypertension, headache, hyperhidrosis (excessive sweating), hypermetabolism, and hyperglycemia.-Absence of hypertension excludes diagnosis.
83
Primary- Decreased thyroid hormone production, most commonCauses:Hashimoto’s thyroiditisResult of thyroid surgeryRadioactive iodine treatment of hyperthyroidism Overtreatment of hyperthyroidismIodine deficiencySecondary- Originates from anterior pituitary gland not producing TSHMyxedema Coma- rare, serious complication
hypothyroidsm
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SUBJECTIVE:Weakness, fatigue, lethargyHeadachesSlowed memory, psychotic behaviorLoss of interest in sexual activityMenstrual disturbancesDepressionOBJECTIVE:NeurologicalCVPulmonaryMetabolicGIIntegumentaryPsychologicalReproductiveGoiter
Hypothyroid
85
Clinical syndrome caused by excessive circulating thyroid hormonesAKA Thyrotoxicosis , Graves’ DiseaseGraves’ disease, the most frequent cause. Signs: goiter, exophthalmos, pretibial edemaThyroid scanUltrasonographyElectrocardiography
Hyperthyroidsm
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Graves’ Disease is most common causePossible autoimmune repsonseOccurs in 3rd or 4th decadeAffects women \> menEmotional trauma, infection, increased stressOverdose of meds to tx hypothyroidismUse of certain weight loss products
Risk factors of hyperthyrodism
87
Nervousness, mood swings, irritability, hyperactivity, decreased attention spanInsomnia, interrupted sleepIncreased appetite, weight lossPalpitations, widened pulse pressure, increased SBPHeat intolerance, increased perspirationDyspneaWeakness, exercise intoleranceVision changes, exophthalmos, staring gazeGoiterBruits over thyroid glandIrregular mensesS&S of?
Hyperthyroidism
88
Exopthalamus treatment
Provide symptomatic treatment.Treatment of hyperthyroidism does not correct eye and vision problems of Graves’ disease.Elevate the head of bed at night.Instill artificial tears.Treat photophobia with dark glasses/patchesGive steroid therapy.Provide diuretics.
89
postop treatment of thyroidectomy
HemorrhageRespiratory distress AIRWAY, SUCTION AND TRACH SET AT BEDSIDEHumidified O2Semi-fowlers with pillows on either side of neckHypocalcemia and tetanyLaryngeal nerve damage
90
What are the Nurse-Patient Relationship Phases
Pre-interaction phaseIntroductory/orientation phaseworking phasetermination phase
91
Pre-interaction Phase
initial task: self-exploration, self-analysischallenges of psychiatric setting may cause stress and fears,Analyze strengths, limitationsGather data about patientPlan for first interaction
92
Introductory/orientation phase
Find out why patient sought helpExplore patient’s feelings, identify problemsEstablish trust, understanding, acceptance, open communicationEstablish goal consensus, collaborationFormulate contract, explaining roles, confidentiality, responsibilities, expectations of patient and nurse
93
Working phase
Nurse and patient explore stressors Promote development of insight by linking perceptions, thoughts, feelings, actionsTranslate insight into action/behavior changeMaster anxieties, increase self-responsibility, develop constructive coping mechanismsStandoff, impasse, or plateau may develop if patient resists moving forward
94
Termination phase
Learning maximized because of higher levels of trust, intimacyExchange feelings and memories to evaluate patient progress, goal attainmentEstablish reality of separation; explore feelings of rejection, loss, sadness, anger Make referrals if needed for continued care or treatment
95
Therapeutic communication techniques
Listening is the foundationUse broad openings to encourage patient to communicate what is important to him/herRestate part of patient’s statementClarify vague ideas, thoughtsReflect on/validate patient’s behavior, feelings
96
Authenticity
Comes with awareness of self. Helps with therapeutic alliance so the patient is more comfortable opening up to the provider.
97
Nurse patient interactions
?????????
98
Phases of schizophrenic disorder
Acute Relapsing: reduce stimulationStabilizing: Titration of medicationsStable: symptoms controlledRecovery: psychosocial goalsRefractory: cope with level of symptomsPersistent psychotic symptoms
99
Schizophrenia Positive Symptoms
HallucinationsDelusionsIllusionsParanoiaSleep DisordersDisorganized SpeechLooseness of AssociationBizarre Behavior
100
Schizophrenia Negative Symptoms
Poverty of SpeechAffective BluntingAnhedoniaSocial WithdrawalApathyAvolitionPoor GroomingAttentional ImpairmentAsocial behavior
101
Alogia
lack of speech
102
Anergia
lack of energy
103
Anhedonia
lack of ability to experience pleasure
104
Avolition
Cannot initiate or persist in goal-directed activities
105
Laboratory tests for schizophrenia
complete blood count (CBC), other blood tests to rule out other conditions with similar symptoms, screening for alcohol and drugs, and imaging studies, such as an MRI or CT scan.Metabolic issues...lipid profile, HA1C, track weight.
106
Medications for Schizophrenia
AtypicalTypical
107
Atypical medications
treat both positive and negative symptoms. Risks:Metabolic syndrome...increased appetite, increased blood sugar, increased lipids.examples; Abilify, zypraxa, invenga, paloperidone, respridol, resperidone, clozaril
108
Typical medications
As good as atypical for positive symptoms, but does not treat negative. Cheaper, but more side effects.examples; halidol, perfenazine, prolixine, trilifon
109
Somatization Disorder
Physical complaintsCannot be explained medicallyUsual onset before age 30Extends to a period over yearsPain, GI, Sexual, Neuro symptomsSymptoms are not intentionally produced0.2-2% women, 0.2% men, prevalence
110
Conversion Disorders
Voluntary motor/sensory functionsSymptom is initiated or exacerbated by stressorSymptoms not intentionally producedSymptoms cannot be explained medicallyImpaired social, occupational, or role functioning“La belle indifference”
111
“La belle indifference”
Inappropriate lack of emotion
112
Body Dysmorphic Disorder
Unrealistic focus regarding a deformed or defective featureExcessive grooming to disguiseClinically significant impairment of social, occupational or role functionNot better accounted for by another disorder
113
Depersonalization disorder
persistent or recurrent feelings of depersonalization and/or derealization.
114
Depersonalization
sense of personality is lost
115
Derealization
external world is not real...a dream
116
D50 coverage for hypoglycemia calculation
(100 (ideal BS) - actual BS) x 0.4
117
emergency equipment for artificial airways
Ambu Bag, Obturator, Suction Equipment, Extra Tubes
118
Cam ICU 4 sections
1. Acute onset or fluctuating course: is pt. different from baseline, or had fluctuation in mental status last 24 hrs2. Inattention: letter attention test squeezing only on A's3. Altered level of consciousness: present if RASS is anything other alert and calm (zero)4. Disorganized thinking: yes/no questions, commands
119
How to tell if CAM ICU is positive for delirium?
Feature 1+ 2, and EITHER 3 OR 4 present = positive
