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Unit I Flashcards

1
Q

Sedation

A

Analgesics AND sedative needed for patient and safety

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2
Q

Excessive sedation can cause…

A

Prolonged ventilation

Physical/psychological dependence

Increased length of hospital stay

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3
Q

Motor Activity Assessment Scale (MAAS)

A

0-6, 0 being unresponsive and 6 being dangerously agitated

6 would be great risk to themselves

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4
Q

Richmond Agitation-Sedation Scale (RASS)

A

Scale from -5 to +4

-5 is unresponsive, +4 is combative

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5
Q

Drugs for Short-Term Sedation

A

Benzodiazepines

Propofol

Dexmedetominde (Alpha-2 Receptor Agonist)

Ketamine

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6
Q

Drug for Intermediate Term Sedation

A

Lorazepam

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7
Q

Drug for Long Acting Sedation

A

Diazepam

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8
Q

Lorazepam

A

Ativan

Side effect: hypotension

Used for mechanically ventilated patients

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9
Q

Midazolam

A

Versed

Side effects: hypotension, respiratory depression, amnesia

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10
Q

Diazepam

A

Valium

Shorter acting; used for patients in alcohol withdrawal

Side effects: hypotension, respiratory depression

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11
Q

Antidote for Benzodiazepines

A

Romazicon, Flumazenil

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12
Q

Propofol Effects

A

Used for deep sedation

Rapid onset, rapid elimination

No amnesia effect

Use only on mechanically ventilated patients

Adverse Effects: elevated triglycerides, pancreatitis

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13
Q

Propofol Infusion Syndrome

A

Rare, usually in pediatrics over 48 hours

Cardiac arrest, metabolic acidosis, rhabdomyolysis

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14
Q

Propofol Characteristics

A

Lipid soluble solution (risk for infection)

IV use only

Change IV tubing every 12 hours

Rapid IV may precipitate hypotension

Dose range 5-80mcg/kg/min

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15
Q

Dexmedtomidine

A

Approved for short term use (< 24 hours)

Does NOT produce respiratory depression

Patients are arousable and alert when stimulated

Sympatholytic, sedative, analgesic, and opioid sparing properties

50% of patients not able to achieve therapeutic goal

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16
Q

Sedation Vacation (Spontaneous Awakening Trial)

A
  1. Discontinue sedation at the same time each day until patient wakes up (every shift)
  2. Assess patient’s level of alertness
  3. Resume sedation according to unit’s protocol
  4. Monitor patient closely to prevent harm from sedative withdrawal or agitation
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17
Q

Neuromuscular Blocking Agents (Paralytics)

A

Block transmission of nerve impulses by blocking cholinergic receptors

Muscle paralysis occurs

MUST have sedation and pain medication as well

Used in severe situations when sedatives are not enough to ensure ventilatory synchrony and patient safety

AMNESIA is desired outcome

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18
Q

Short Term NMB

A

Mivacurium (IVP)

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19
Q

Intermediate NMB

A

Vecuronium (IVP and infusion)

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20
Q

Long Acting NMB

A

Pancuronium (intermittent IV bolus)

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21
Q

Agitation

A

Psychomotor disturbance

Marked increase in both motor and psychological activities

Loss of control of action

Disorganization of thought

RASS scores +1 to -4

Use of restraints predictor

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22
Q

Delirium

A

Acute fluctuations in mental status

Rapid onset, reversible

Inattention

Cognitive changes

Perceptual differences

Hyperactive or hypoactive

Results in systemic illness, pain, sleep deprivation

Caused by infection, fever, metabolic fluctuations, electrolyte disturbances, medications

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23
Q

Risk Factors for Delirium “ICU Psychosis”

A

Prolonged ICU hospitalization

Sleep deprivation/disruption of circadian rhythm

Mechanically ventilated parents

Low arterial pH

Elevated serum creatinine

CURRENT USE OF BENZODIAZEPINES/OPIOIDS

Severity of illness

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24
Q

Delirium Manifestations

A

SUDDEN DECLINE FROM PREVIOUS MENTAL STATUS

Disorientation to time

Hallucinations

Auditory, tactile, or olfactory misperceptions

Hyperactive behaviors like agitation

Hypoactive behaviors like withdrawn/lethargic

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25
Q

CAM-ICU Assessment of Delirium

A
  1. Acute onset of mental status change
  2. Visual (picture) or Auditory (letter) Attention Screening Tool
  3. Altered LOC (RASS Score)
  4. Disorganized thinking (4 yes/no questions)
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26
Q

Treatment of Delirium

A

Nonpharmacologic first

Correct physiological problems (O2, pain, BUN, electrolytes, blood glucose, benzodiazepine adverse effects)

Pharmacological measures

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27
Q

Nonpharmacologic Management of Delirium

A

Noise reduction, light reduction, cluster cares, promote sleep, back massage, music, calm voice, visual cues to orientation

MINIMIZE SLEEP DEPRIVATION

EARLY MOBILIZATION

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28
Q

Pharmacologic Management of Delirium

A

Give Haloperidol

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29
Q

Neuroleptic Malignant Syndrome

A

Muscular rigidity, hyperthermia, sweating, fluctuations in VS

Critical crisis

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30
Q

Treatment for Neuroleptic Malignant Syndrome

A
  1. Dantrolene as muscle relaxant
  2. Management of fever
  3. Fluid volume replacement as needed
  4. Discontinue neuroleptic drug
  5. Bromocriptine for CNS toxication
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31
Q

Adverse Effects of Haloperidol

A

Orthostatic hypotension

Anticholinergic symptoms

Sedation

Prolonged QT interval, risk for dysrhythmias

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32
Q

ABCDE Bundle

A

A: Sedation Awakening Trial

B: Spontaneous Breathing Trial

C: Coordination

C: Choice of Analgesia and Sedation

D: Delirium Prevention and Management

E: Early Physical Mobility

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33
Q

Test Used Prior to ABGs

A

Allen’s Test

Compress radial and ulnar artery to blanch hand, release ulnar artery and make sure hand pinks up again

Draw from radial artery

Must be put on ice to prevent metabolism

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34
Q

In order for perfusion to happen…

A

Adequate O2 moving from lungs to body cells

Lungs must receive enough O2 to be perfused and ventilate

O2 must be transported via blood

Tissue demand for O2 determines how much O2 unloads from hemoglobin

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35
Q

PaO2

A

Partial pressure of oxygen in arterial blood

Dissolved and not bound to hemoglobin

80-100

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36
Q

SaO2

A

Arterial saturation of hemoglobin

Oxygen bound to hemoglobin

95-97%

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37
Q

PaCO2

A

Partial pressure of CO2 in arterial blood

CO2 dissolved in the blood

35-45

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38
Q

SpO2

A

Saturation of hemoglobin in peripheral capillaries

Noninvasive measurement

Estimate of SaO2

Greater than 93%

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39
Q

Oxyhemoglobin Curve–Right Shift

A

Caused by: Hypermetabolic states, decreased perfusion, decreased pH, acidosis, fever

Results in: decreased affinity of O2 for hemoglobin, increase in amount of O2 available for tissues

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40
Q

Oxyhemoglobin Curve–Left Shift

A

Caused by: decreased temperature, alkalosis, high pH

Results in: increased affinity of O2 for hemoglobin, but decreased amount of O2 released to tissues, less cellular activity

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41
Q

2,3-DPG

A

Phosphate that forms when red blood cells break down glucose to make ADT–measure of metabolism

Increased production by: thyroxine, HGH, epinephrine, testosterone, high altitudes

Decreased production by: aging

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42
Q

Carbonic Anhydrase Buffer System

A

H20 + CO2 (lungs) = H+ - HCO3 (kidneys)

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43
Q

Normal ABG Values

A

pH: 7.35-7.45

PCO2: 35-45

PO2: 80-100

HCO3: 22-26

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44
Q

Analysis of ABGs

A

Oxygenation Status: PaO2, SaO2, FiO2

Acid-Base Status: pH, pCO2, HCO3

ROME (Respiratory Opposite, Metabolic Equal)

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45
Q

Compensation

A

Body attempts to maintain homeostasis

When pH is WNL, but CO2 + HCO3 are not

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46
Q

Metabolic Alkalosis

A

Caused by steroid therapy, vomiting, GI suction, diuretic therapy, NA Bicarb intake

Loss of acid or gain of bicarb

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47
Q

Metabolic Acidosis

A

Gain of H+, increase in lactic acid, DKA, hypermetabolic state, intake acid (ASA), renal failure

Loss of HCO3, diarrhea

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48
Q

Respiratory Acidosis

A

Gain of CO2

Oversedation, hypoventilation, drug overdose, COPD, mechanical ventilation, head-spinal trauma, neuromuscular disease

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49
Q

Respiratory Alkalosis

A

Loss of CO2

Pregnancy, high altitude, PE, hypoxia, fever, increased metabolic state, anxiety/fear

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50
Q

Rationale for Mechanical Ventilation

A

Respiratory arrest

Procedure anesthesia/analgesia

Post-operative recovery

Poor ABGs

Deteriorating respiratory status

Airway protection

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51
Q

Types of Mechanical Ventilation

A

Negative Pressure Ventilation

Positive Pressure Ventilation

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52
Q

Negative Pressure Ventilation

A

Used for atelectasis

Air is pulled out of the lungs

Iron Lung

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53
Q

Positive Pressure Ventilation

A

Used for respiratory failure

Air is pushed into the lungs

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54
Q

High Frequency Jet Ventilation

A

Used for pediatrics and barotrauma patients

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55
Q

Neutrally Adjusted Ventilator Assistance

A

Used for pediatrics and barotrauma patients

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56
Q

Respiratory Volumes

A

Tidal volume

Inspiratory reserve volume

Expiratory reserve volume

Minute volume

Residual volume (dead space)

Sigh

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57
Q

Types of Breaths for Ventilated Patient

A

Controlled (by the ventilator; positive pressure)

Assisted (initiated by patient but delivered by the ventilator; positive pressure, little dips of negative pressure)

Spontaneous (regulated by the patient; negative pressure)

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58
Q

Normal Inspiration/Expiration Ratio

A

1 inspiration to 2 expiration

Exhalation 2x as long as inspiration

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59
Q

Tidal Volume

A

Volume of gas inhaled or exhaled

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60
Q

Minute Volume

A

Volume of gas entering or leaving the lungs per minute

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61
Q

Continuous Mandatory Ventilation (CMV)

A

All breaths controlled by the ventilator

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62
Q

Assisted Mandatory Ventilation

A

All breaths initiated by patient but delivered by the ventilator

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63
Q

Assist/Control Mandatory Ventilation (A/C)

A

Minimum number of controlled breaths plus any additional assisted breaths initiated by patient

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64
Q

Synchronized Mechanical Ventilation (SIMV)

A

Minimum number of controlled/assisted breaths

Additional spontaneous breaths by patient’s own effort and tidal volume

Insures that ventilated breaths occur at end-expiratory phase of respiratory cycle

No stacking of ventilated breaths on already inhaled chest volume

Facilitates ventilator tolerance

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65
Q

Continuous Positive Airway Pressure (CPAP)

A

All spontaneous breaths by patient

Slight elevation of airway pressures

NO MECHANICAL VENTILATION

MUST HAVE THE DRIVE TO BREATHE

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66
Q

Ventilator Settings

A

Mode: CMV, A/C, SIMV, CPAP

FiO2: % Oxygen

Respiratory Rate

Tidal Volume (volume per ventilated breath)

Positive End-Expiratory Pressure (PEEP)

Pressure Support Ventilation (PSV)

SIGHS and frequency

SENSITIVITY: 3-5 mm H2O negative pressure

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67
Q

Modes of Mechanical Ventilation for Servo 300

A

Pressure Controlled (PC)

Volume Controlled (VC)

Volume Support (VS)

Pressure Support (PS)

Pressure Regulated Volume Controlled (PRVC)

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68
Q

Pressure Controlled

A

Pressure cycled ventilations

Decelerating inspiratory flow

Pre-set rate and time

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69
Q

Volume Controlled

A

Similar to CMV

Volume cycled ventilations

Higher airway pressures than PC

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70
Q

Volume Support

A

Patient must trigger each breath

Spontaneous breaths with inspiratory pressure support until minimum tidal volumes and minute volumes are achieved

Tidal volumes adjusted if minute volumes below preset levels

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71
Q

Pressure Support

A

Patient must trigger each breath

Spontaneous breaths assisted with preset inspiratory pressures

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72
Q

Pressure Regulated Volume Controlled

A

Inspiratory pressures of ventilations are minimized to what is necessary for chest expansion

Insures tidal volume of ventilations

Preset rate; best for patients with ARDS

Minimizes inspiratory pressures and barotrauma

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73
Q

NAVA

A

A mode where the patient, specifically the brain, not us, decides when and how to breathe

Can be used invasively or non-invasively

Ultimate in synchronization–reduces barotrauma and overassist, and eases transition to nonventilated breathing

Better sleep quality, lung protective, less sedation needed

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74
Q

Who Can Use NAVA

A

Spontaneously breathing patients

Must have a working diaphragm

Patients greater than 500 grams

Ability to place either an NG or OG catheter

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75
Q

Who Can’t Use NAVA

A

Patients with an absent electrical signal from brain to diaphragm

Patients with paralysis/neuromuscular blockade

Esophageal bleeding

Inability to place an NG/OG tube

Actively used cardiac pacemaker

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76
Q

Noninvasive Positive Pressure Ventilation

A

Alternative to invasive MV

Indicated for respiratory distress with respiratory drive

Rationale: reduces workload of breathing, decreased number of ventilator days, decreased ICU days, decreased length of stay in hospital

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77
Q

Ideal Patients for Noninvasive Positive Pressure Ventilation

A

Nocturnal hypoventilation (sleep apnea)

Chronic hypoventilation (neuromuscular disease, COPD)

Acute hypoventilation

Acute cardiogenic pulmonary edema

Conscious and cooperative

Able to protect airway

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78
Q

Contraindications to Noninvasive Positive Pressure Ventilation

A

Respiratory arrest

Cardiovascular shock

Risk for aspiration

Severe hypoxemia, acidemia

Uncooperative patient (agitation)

Facial, esophageal, or gastric surgery

Cranial trauma or burns

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79
Q

Initiation of NPPV–Settings

A

Interface (mask & face)

Machine

Mode

Trigger, cycle, rise time

IPAP (inspiratory pressure)

EPAP (PEEP)

FiO2

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80
Q

Steps for Initiation of NPPV

A
  1. Explain process, select mask/ventilator
  2. Fit mask
  3. Initiate NPPV while holding mask in place
  4. Titrate inspiratory pressure to patient comfort and titrate upward
  5. Secure mask
  6. Monitor O2 saturation, titrate FiO2 for O2 sat > 90%
  7. Titrate EPAP to minimize trigger effort and increase O2 sat
  8. Check for air leaks
  9. Avoid peak airway pressures > 20 cm H2O
  10. Continue to coach patient
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81
Q

NPPV Nursing Care

A

Skin breakdown

Gastric insufflation with IPAP > 20 cm H2O

Air leaks

Conjunctival irritation

Nasal or oral dryness

Claustrophobia

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82
Q

Outcome for Dysfunctional Ventilatory Weaning Response

A

Wean from ventilator with IER ABGs

Remain free from unresolved dyspnea

Effectively clear airway

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83
Q

Interventions for Dysfunctional Ventilatory Weaning Response

A

Exercise respiratory muscles

Reduce oxygen consumption

Maintain adequate oxygenation

Pressure support ventilation as needed

Maintain adequate rest and nutrition prior to weaning

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84
Q

Readiness to be Weaned from Mechanical Ventilation

A

PEEP < 5

FiO2 < 40-50%

pH > 7.25

PaO2/FiO2 ratio > 200

Negative inspiratory force of -20 cm H2O or more

Hemodynamic stability

Patient is adequately nourished, rested, not sedated

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85
Q

PaO2/FiO2 Ratio

A
  1. Obtain PaO2 value (mmHg)
  2. Convert FiO2 to decimal (e.g. 32% –> 0.32)
  3. Divide PaO2 by FiO2 (e.g. 92 mmHg / 0.32 == 287.5)
  4. Criterion for weaning if ratio > 200
  5. Normal is about 300
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86
Q

Expected PaO2/FiO2 Ratio

A

FiO2 x 5 == estimate of expected value if lungs were functioning normally

The larger the distance from the expected value, the worse the lung function

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87
Q

Ventilator Nursing Diagnoses

A

Impaired spontaneous ventilation

Ineffective airway clearance

Ineffective breathing pattern

Impaired verbal communication

Impaired gas exchange

Fear

Powerlessness

Social isolation

Risk for infection

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88
Q

Communication with Patients on Ventilator

A

Patients are not hard of hearing

Patients usually are not unconscious

Verbal communication: written on paper, signs

Nonverbal communication: nodding yes/no to questions, gestures with hands

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89
Q

Complications of Mechanical Ventilation

A

Pulmonary: barotrauma, damage to nasal/oral mucosa, oxygen toxicity

Acid/base imbalances

Aspiration

Ventilation associated pneumonia

Ventilator dependence

Cardiovascular: decreased CO

GI: stress ulcers

Endocrine: fluid retention = ADH

Psychosocial: loss of control, anxiety

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90
Q

Ventilator Alarms

A

Disconnect; check patient, check connections from patient to ventilator, Ambu bag at bedside, use if malfunction of ventilator

Low-pressure alarm: leaks, decreased compliance

High-pressure alarm: pressure exceeds selected threshold

Causes: secretions, tubing condensation, biting ET tube, increased resistance (bronchospasms), decreased compliance (pulmonary edema)

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91
Q

Ventilator Induced Lung Injury

A

VILI is due to volume, overdistention of lung

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92
Q

Ventilator Associated Pneumonia

A

Artificial airway associated pneumonia (AAAP)

Risk of VAP among intubated patients: 8-25%

Consequences: increased length of stay, increased cost, mortality up to 27%

Never Event: hospital eats cost of treatment

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93
Q

Interventions to Decrease Risk of VAP

A

Proper handwashing

HOB > 30 degrees

Frequent/careful oral hygiene

Proper ET cuff inflation

Stress ulcer prophylaxis

Increase use of NPPV

Insure assessments of daily spontaneous breathing trials

Oral tracheal instead of nasotracheal intubation

Decrease frequency of ventilator circuit tubing changes

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94
Q

Definition of ARDS

A

Within one week of injury or new or worsening respiratory symptoms

Imaging with bilateral opacities (not fully explained by nodules, effusions)

Edema not explained by cardiac issues

Mild/moderate/severe p/f ratio abnormalities

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95
Q

Pathophysiology of Acute Lung Injury

A

Systemic Inflammatory Response Syndrome

Release of mediators such as histamine, leukotrienes, TNF-a –>

Increased alveolar-capillary permeability –>

Diffuse pulmonary edema, impaired gas exchange –>

Destruction of surfactant –>

Decreased compliance, increased resistance –>

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96
Q

Direct Risk Factors for ALI

A

Pulmonary infections

Toxic inhalation

Aspiration

Pneumonia

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97
Q

Indirect Risk Factors for ALI

A

Shock, sepsis

Hypothermia, hyperthermia

Drug overdose

DIC

Multiple transfusions

Burns

Eclampsia

Trauma

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98
Q

Severe Sepsis

A
  1. Known or suspected infection
  2. Two signs of SIRS
  3. At least 1 organ failing or dysfunctional
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99
Q

SIRS

A
  1. Core temperature > 100.4
  2. HR > 90
  3. RR > 20 or paCO2 < 32mmHg
  4. WBC > 12,000 or < 4,000, or > 10% immature neutrophils/bands
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100
Q

Transfusion-Related ALI (TRALI)

A

Most common cause of transfusion-associated mortality

Potentially preventable

Improved antigen screening

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101
Q

Ventilator-Induced Lung Injury (VILI)

A

Ventilator pressures

Lung strain

Inflammation

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102
Q

LIPS

A

Lung Injury Prediction Score

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103
Q

LIPS Risk Factors

A

High risk trauma

High risk surgery

Aspiration

Sepsis, shock

Pneumonia

Pancreatitis

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104
Q

LIPS Risk Modifiers

A

Alcohol abuse

Hypoalbuminemia

Tachypnea

O2 supplementation

Chemotherapy

Obesity, diabetes

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105
Q

Checklist for Lung Injury Prevention (CLIP)

A

Respiratory support

Aspiration precautions

Infection control

Fluid management

Transfusion

Structured handoff

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106
Q

Physiology of ALI

A

Exudative Phase

Fibroproliferative Phase

Resolution Phase

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107
Q

Exudative Phase of ALI

A

First 72 hours

Increased capillary permeability (leakage of fluids into interstitial tissues, compression of terminal bronchioles)

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108
Q

Fibroproliferative Phase of ALI

A

Gas exchange compromised

Hypoxemia from atelectasis, decreased diffusion

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109
Q

Resolution Phase of ALI

A

Recovery over several weeks

Reestablish a/c membrane

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110
Q

Goals of Therapy for ALI

A

Recruitment (opening) of collapsed alveoli

Prevent barotrauma by tolerating “permissive hypercarbia” (slight respiratory acidosis)

Oxygenation: ratio of paO2/FiO2 > 200 (ratio of paO2/FiO2 = 300 is normal)

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111
Q

Investigational Interventions for ALI

A

Synthetic surfactant instilled via ET tube

Extra-corporeal gas exchange (ECMO)

Inhaled liquid nitric oxide with HFJV

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112
Q

Oxygenation (SpO2)

A

O2 for metabolism

Measures percentage of oxygen in RBCs

Changes within 5 minutes

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113
Q

Ventilation (Capnography)

A

CO2 from metabolism

EtCO2 measures exhaled CO2 at point of exit

Changes within 10 seconds

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114
Q

Capnography

A

Available for spontaneously breathing and for intubated patients

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115
Q

Capnography Waveforms

A

The higher the waveform, the more CO2

Normal EtCO2 is 35-45

Length of waveform corresponds to respiratory rate

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116
Q

Shark Fin in Capnography

A

Possible causes include partially kinked airway, presence of foreign body, obstruction of expiratory limb of vent circuit, BRONCHOSPASM

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117
Q

Curare Cleft in Capnography

A

Appears when NMBAs begin to wear off

Depth of cleft inversely proportional to degree of blockade

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118
Q

EtCO2 > 45

A

Hypoventilation

Respiratory acidosis

Fever

Bronchospasms

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119
Q

EtCO2 < 35

A

Hyperventilation

Respiratory alkalosis

Partial airway obstruction

PE

Cardiac arrest

Hypotension, hypothermia, hypovolemia

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120
Q

Acute Kidney Injury

A

An abrupt reduction in kidney function, leading to retention of nitrogenous and other waste products normally eliminated by the kidneys

High incidence in the aging population with greater susceptibility and illness severity, comorbidities

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121
Q

Acute Kidney Injury Statistics

A

1% of acute hospital admissions

Complicates 7% of inpatient episodes

Increases mortality rate to 38-80%

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122
Q

Pre-renal Acute Kidney Injury

A

Hypo-perfusion of the kidneys

Caused by shock states (hypovolemia, cardiogenic, distributive), sepsis, occlusion of renal arteries, altered auto-regulatory capability

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123
Q

Intra-renal Acute Kidney Injury

A

Damage to renal parenchyma

Caused by nephrotoxic antibiotics (aminoglycosides), heavy metal poisoning, hemolysis, organic solvents, fungicides/pesticides, radiopaque contrast agents, NSAIDS

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124
Q

Post-renal Acute Kidney Injury

A

Reflux of urine flow due to obstruction beyond the kidneys

Caused by kidney stones, UTIs, BPH, anticholinergics, tumors, blood clots

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125
Q

Urinalysis for Prerenal AKI

A

Na: < 5 mEq/L

SpecGrav: > 1.020

BUN:CR: > 20:1

Urine is concentrated, kidneys are hanging on to water

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126
Q

Urinalysis for Intrarenal AKI

A

Na: 10-40 mEq/L

SpecGrav: 1.010

BUN:Cr: 10:1

Urine is dilute, kidneys are damaged and unable to concentrate urine, water is spilling out

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127
Q

RIFLE Criteria

A

Severities: RISK, INJURY, FAILURE

Outcomes: LOSS of renal function, ESKD

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128
Q

RIFLE-Risk

A

Rise in SCr level of at least 0.3

0r increased 1.5x normal

Urine output reduction to 0.5 for more than 6 hours

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129
Q

RIFLE-Injury

A

SCr increased 2x normal

Urine output reduction to 0.5 for more than 12 hours

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130
Q

RIFLE-Failure

A

SCr increased 3x normal

0r > 4 or acute rise > 0.5

UO < 0.3 for 24 hours or anuria for 12 hours

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131
Q

RIFLE-Loss

A

AKI > 4 weeks

132
Q

Diagnostic Criteria for AKI

A

SCr end-product of muscle breakdown

Freely filtered glomerulus

Not metabolized or reabsorbed

AKI: SCr level 50% higher than baseline within 24-48 hour period

133
Q

Primary Prevention for AKI

A
  1. Maintain adequate hydration
  2. Monitor UO if patient is receiving meds that may cause urinary retention
  3. Watch urine output if patient is receiving nephrotoxic antibiotics (aminoglycosides)
134
Q

Phases of AKI

A

Onset

Oliguric or Non-Oliguric

Diuretic

Recovery

135
Q

Onset Phase of AKI

A

Initial insult–cell injury

Hours to days

Goal is to determine cause

136
Q

Oliguric or Non-Oliguric Phase of AKI

A

Oliguric: fluid overload

Non-Oliguric: cause is usually toxic injury, decreased fluid complications

137
Q

Period of Oliguria

A

Initiation period from Insult to Oliguria

Urine output < 400ml/day

10-30 days duration

Azotemia: increase in BUN (BUN: 25-30, SCr: 1.5-2)

138
Q

Complications of AKI

A

Cardiovascular (fluid overload, CHF, edema, MI, hyperkalemia)

Respiratory (mechanical ventilation)

GI bleeding

Metabolic acidosis

Neurological (uremic symptoms: lethargy, altered mental status, cognitive deficits, itching, breath odor, N/V, HA, seizures, coma)

139
Q

Treatment of AKI

A

Restore adequate renal blood flow

Treat cause (hypovolemia–rapid fluid infusion, remove nephrotoxins, remove obstruction, renal replacement therapy RRT)

140
Q

Assessment of Fluid Overload

A 
Daily weights
Strict I&amp;O
Edema (sacral, pretibial)
Vital signs
CVP
Skin turgor/membranes
141
Q

Implementation for Fluid Overload

A

Regulate IV fluids according to urine output and daily weights

Diuretics (mannitol, furosemide, ethacrynic acid)

Dialysis

142
Q

Assessment of Hyperkalemia in AKI

A

Serum potassium (> 5.5)

Irritability and restlessness

N/V, abdominal cramps

Weakness, distal numbness and tingling

ECG: peaked T wave, prolonged PR and QRS, tachy-brady patterns

143
Q

Implementation for Hyperkalemia in AKI

A

Restrict potassium

Kayexolate Resin PO or PR with Sorbitol

Glucose and regular insulin IVP

NaHCO3 IVP

Dialysis

144
Q

Period of Diuresis

A

Gradual increase in urine output (up to 4L/day)

Lab values stop rising, begin to decline

Potential for dehydration, electrolyte depletion

145
Q

Period of Recovery

A

3-12 months

Return of serum values to normal levels

1%-3% loss of renal function

146
Q

Initial Stage of Chronic Renal Failure

A

Loss of renal reserve

40-75% loss of nephron function

Normal renal function

147
Q

Second Stage of Chronic Renal Failure

A

75-80% loss of nephron function

Elevated BUN and creatinine

Polyuria, dilute urine

148
Q

Etiologies of ESKD

A

Diabetes mellitus

Uncontrolled HTN

Chronic glomerular nephritis

Unresolved AKI

Polycystic kidney disease

Systemic lupus eryhtematosus

Sickle cell disease

149
Q

Uremic Syndrome

A

Elevation of blood nitrogens

Signs–

Early: N/V, anorexia

Late: stupor, seizures, coma

Chronic: pericarditis, pleuritis

Rare: uremic frost

150
Q

Hypernatremia

A

Thirst, fever, dry membranes, altered consciousness, seizures

REDUCE SODIUM INTAKE

DIALYSIS

151
Q

Hypocalcemia

A

Phosphorus-Calcium Balance

Decreased vitamin D synthesis

Irritability, muscle tetany, Chvostek sign, bone disorders

CALCIUM SUPPLEMENT

VITAMIN D SUPPLEMENT

152
Q

Hyperphosphatemia

A

N/V, anorexia

Bone wasting

Hemolysis, bleeding tendencies

PHOSPHATE BINDERS WITH DIET

DIALYSIS

153
Q

Hypermagnesemia

A

Use of antacids

CNS depressed, lethargy, coma

Bradycardias

Prolonged PR, QRS complex

Tall T waves, AV blocks

DIALYSIS AND DIET

154
Q

Anemia

A

Reduced production of EPO

SHORTER LIFE SPAN OF RBCs

Fatigue, activity intolerance

EPOGEN THERAPY IV POST DIALYSIS

MONITOR SERUM IRON AND TRANSFERRIN

DIETARY SUPPLEMENT OF IRON

155
Q

Bone Disorders

A

Osteomalacia and osteoporosis

Hyperphosphatemia and hypocalcemia

Parathyroid hormone secretion

Vitamin D not converted by kidneys

Poor absorption of calcium

RESTRICT PHOSPHATES

PHOSPHATE BINDERS IN DIET

CALCIUM AND VITAMIN D SUPPLEMENTS

156
Q

Cardiovascular Problems with ESKD

A

Accelerated atherosclerosis

Pericarditis

Congestive heart failure, fluid overload

Potential for dysrhythmias secondary to electrolyte imbalances

157
Q

Nursing Diagnoses for Chronic Renal Failure

A

Fluid volume excess

Altered nutrition

Knowledge deficit

Activity intolerance

Self-esteem disturbance

158
Q

Alteration in Nutrition, Less than Body Requirements (Chronic Renal Failure)

A

Restrict protein intake

Sodium, potassium, and phosphate restriction

High carbohydrates

Fluid restriction

Calcium and vitamin supplements

159
Q

Fluid Volume Excess (Chronic Renal Failure)

A

Fluid restriction (500-600 mL + volume of urine output)

Diuretics (sometimes)

Daily weights

Maintenance of dry weight

Dialysis

160
Q

Treatment Options for Chronic Kidney Failure

A

Conservative treatment

Intermittent hemodialysis

Peritoneal dialysis

Transplant

161
Q

Treatment Options for Acute Kidney Injury

A

Intermittent hemodialysis

Continuous renal replacement therapy

162
Q

Hemodialysis

A

Artificial kidney function by circulation of blood through dialyzer with semipermeable membrane and dialysate bath

163
Q

Functions of Hemodialysis

A

Dialysis: removal of wastes

Ultrafiltration: removal of fluid volume

164
Q

Components of Hemodialysis

A

Dialyzer, Dialysate, Extracorporeal circulation, and Venous Access Device

165
Q

Access Sites for Hemodialysis

A

AV fistula

AV graft

Dual lumen central catheter

166
Q

Care for Hemodialysis Access Devices

A

Do not use the extremity for BP, IVs, tourniquets

Wear shirts with sleeves unbuttoned or with loose sleeves

Auscultate for bruits

Possible anticoagulant therapy

Avoid cold exposure to extremity

Good body hygiene

167
Q

Central Line Associated Bloodstream Infection (CLABSI)

A

Daily assessment is necessary

NURSE SENSITIVE INDICATOR

Maximal sterile barrier on insertion

Hand hygiene

Scrub ports, tubing changes

168
Q

Problems with Hemodialysis

A

Hypovolemia

Air embolism

Dialysis Disequilibrium Syndrome

Painful muscle cramping

Nausea/Vomiting

Infection

Blood clots

169
Q

New Patient Receiving Hemodialysis

A

May require catheter until AV access site is healed

More prone to dialysis disequilibrium syndrome

Blood chemistry and hydration more imbalanced

170
Q

Dialysis Disequilibrium Syndrome

A

Cerebral dysfunction (N/V, agitation, confusion –> seizures, HTN)

Caused by too rapid removal of fluid resulting in osmolarity shifts

Slow down rate of dialysis

Phenytoin for seizures

171
Q

Air Embolism During Hemodialysis

A

Caused by break in the extracorporeal circulation

Prevention with foam air detectors

Critical complication; life-threatening

Dyspnea, chest pain, anxiety, low O2 sats, tachycardia

Position on LEFT side in Trendelenburg

172
Q

Painful Muscle Cramping during Hemodialysis

A

Caused by excessive removal of sodium or drop in osmotic pressure in blood

Reduce flow rate, bolus with hypertonic solution

173
Q

Hypotension during Hemodialysis

A

Related to too rapid fluid removal, bleeding from tubing connection

Lightheadedness, confusion, cramps, N/V

Position supine with legs elevated, bolus with NS, slow rate

174
Q

Peritoneal Dialysis

A

Replace kidney function by the instillation of dialysate into the peritoneal cavity

Dialysis occurs by diffusion and osmosis across the peritoneal membrane

Peritoneal cavity and catheter, dialysate solution, timed cycles

175
Q

Intermittent Peritoneal Dialysis

A

Infusion: 2 L of dialysis over 5-10 minutes, sterile technique

Maximum diffusion first 5-10 minutes

Dwell time: 30-45 minutes

Drain for 10-30 minutes, should be clear

176
Q

Continuous Ambulatory Peritoneal Dialysis

A

Dialysate infused into peritoneum

Catheter clamped, bag kept under clothing

Effluent drained and new dialysate infused 4x a day

More freedom for client

Removal of larger molecule wastes

177
Q

Peritoneal Dialysis: Incomplete Recovery of Fluid

A

Monitor fluid return closely

Assess for fluid retention (edema, ABD distention, WEIGHT GAIN)

Turn client from side to side

Heparin may need to be added to dialysate

178
Q

Peritoneal Dialysis: Leakage Around the Catheter

A

Common with new catheter

Start with lower volumes of diaysate and increase slowly

Change dressing frequently with sterile technique

Reduce intra-ABD pressure

179
Q

Peritoneal Dialysis: Blood Tinged Effluent

A

Common with new catheter, should clear up after a couple of days

May occur in menstruating women

Heparin may be added

Assess for other possible causes

180
Q

Peritoneal Dialysis: Peritonitis

A

Common complication

Potential for sepsis

Sterile technique with dialysis treatment dressing changes

Signs: cloudy effluent, ABD pain, ABD rigidity

Culture effluent

Antibiotics in dialysate and PO

181
Q

Peritoneal Dialysis Components

A

Access: Catheter

Length: Continuous

Complications: peritonitis, dialysate leaks, hernias

Advantages: continuous removal, home maintenance, fewer dietary restrictions

Disadvantages: not with history of abdominal surgery, waste removal slow

Heparinization: not indicated

182
Q

Hemodialysis Components

A

Access: AV site

Length: 3 per week, 4 hours per treatment

Complications: hypotension, muscle cramps, bleeding, clotting, machine malfunction

Advantages: quick removal, useful for overdose

Disadvantages: vascular access device strain, potential for blood clots

Systemic heparinization

183
Q

Continuous Renal Replacement Therapy

A

Use of extracorporeal circuit

Purpose: fluid and solute removal

Regulated by patient’s own MAP, assisted with a roller pump

Usually started when BUN > 60 but before BUN > 90 and SCr > 9

184
Q

Positive Aspects of CRRT for AKI

A

Safer for patients with hemodynamic instability

Less intense fluctuation of fluid and electrolyte levels

Most resembles normal kidney function

185
Q

Drawbacks of CRRT for AKI

A

Use of large catheter in major artery

Risk for infections

Distal thrombosis formation

Disconnection

Exsanguination

186
Q

Diffusion with CRRT

A

Movement of solutes along a concentration gradient from high to low, across a semipermeable membrane

Main mechanism in hemodialysis

Solutes: creatinine, urea

Fluid also removed

187
Q

Convection with CRRT

A

Pressure gradient is set up so water is pushed/pumped across dialysis filter

Molecules dragged with fluid

188
Q

Absorption with CRRT

A

Filter attracts solute

Molecules absorb with the dialysis filter

189
Q

Ultrafiltrate Volume for CRRT

A

Fluid removed each hour

190
Q

Replacement Fluid for CRRT

A

Some ultrafiltrate is replaced through the circuit

Increase volume of fluid passing through filter

Improves convection

191
Q

Five CRRT Methods

A

Slow continuous ultrafiltration

Continuous arteriovenous hemofiltration

Continuous arteriovenous hemodiafiltration

Continous venovenous hemofiltration

Continuous venovenous hemodiafiltration

192
Q

Slow Continuous Ultrafiltration

A

Removes fluid slowly (100-300 ml/hour)

Minimal impact on solutes

Only driving force is blood pump and blood pressure

More likely to clot filter

193
Q

Continuous Arteriovenous Hemofiltration

A

Semipermeable filter

Propelled by MAP

Ultrafiltrate to gravity bag

Convention

Simple technology

Remove and replace fluid effectively

194
Q

Continuous Arteriovenous Hemodiafiltration

A

Semipermeable filter

Dialysate used

Ultrafiltrate to gravity bag

Convention

Diffusion

Results in more rapid solute reduction (BUN, creatinine)

195
Q

Continous Venovenous Hemofiltration

A

Semipermeable filter

Propelled by roller pump

Convection

Solute removal

Replacement fluid added to facilitate convection

196
Q

Continuous Venovenous Hemodiafiltration

A

Semipermeable filter

Dialysate used

Propelled by roller pump

Convection

Diffusion

Increased solute removal

Fluid removal

197
Q

Complications with CRRT

A

Dehydration and hypotension

Electrolyte imbalances

Acid/base imbalances

HYPOTHERMIA

Hyperglycemia

Inadequate blood flow through hemofilter, clotted hemofilter

Sepsis

198
Q

Nursing Management of CRRT

A

Surveillance for side effects of dialysis

Monitoring fluid balance, accurate I&O

Prevention and detection of complications

Trends electrolyte laboratory values

Patient and family education

Lab values every 6 hours

199
Q

Catheter Associated Urinary Tract Infection

A

Daily assessment of need

Aseptic insertion

Closed drainage

Securement device

Automatic discharge orders

Hygiene

200
Q

Contractility

A

Shortening of heart muscle in response to stimuli

201
Q

Excitability

A

Irritability ability to respond to stimuli influenced by: neural, hormonal, nutritional balance, O2 supply, drug therapy

202
Q

Conductivity

A

Ability to transmit electrical impulses

203
Q

Automaticity

A

Ability to beat spontaneously and repetitively without external neurohormonal control

204
Q

Parasympathetic Effects on Heart

A

DECREASE automaticity, contractility, conduction, rate

205
Q

Sympathetic Effects on Heart

A

INCREASE automaticity, contractility, conduction, rate

206
Q

Refractoriness

A

The period of recovery that cells need after being discharged before they are able to respond to a stimulus

207
Q

Absolute Refractory Period

A

Cells cannot be stimulated to conduct an electrical impulse, no matter how strong the stimulus

Onset of QRS to peak of T

208
Q

Relative Refractory Period

A

Cardiac cells can be stimulated to depolarize if stimulus is strong enough

Downslope of T wave

209
Q

Supernormal Period

A

Weaker than normal stimulus can cause cardiac cells to depolarize

Corresponds with end of T wave

210
Q

Primary Pacemaker of the Heart

A

Sinoatrial node

211
Q

Atria

A

Fibers of SA node connect directly with fibers of atria

Impulse leaves SA node

Spreads from cell to cell across atrial muscle

212
Q

Internodal Pathways

A

Impulse is spread to AV node via internodal pathways

Merge gradually with cells of AV node

213
Q

AV Junction

A

Area of specialized conduction tissue

Provides electrical links between atrium and ventricle

214
Q

AV Node

A

Located in floor of right atrium

Delays conduction of impulse from atria to ventricles (allows for atria to empty into ventricles)

215
Q

Bundle of His

A

Connects AV node and bundle branches

Conducts impulse to right and left bundle branches

216
Q

Purkinje Fibers

A

Receives impulse from bundle branches

Relays to ventricular myocardium

217
Q

Nervous Influences on Pacemaker

A

Parasympathetic (Vagal): slows heart rate at the SA node

Sympathetic (Beta Adrenergic): increases HR at SA node, increases conductivity and automaticity

218
Q

Baroreceptor Influences on Pacemaker

A

Aortic arch, carotid sinuses

Influenced by blood pressure

Stimulates/inhibits nervous system influences

219
Q

P Wave

A

Atrial depolarization and the spread of the impulse throughout the right and left atria

Influx of Na+ and/or Ca++ cations

220
Q

QRS Complex

A

Ventricular depolarization

Influx of Na+ and/or Ca++ cations

221
Q

T Wave

A

Ventricular repolarization

Restabilization of cell membrane

222
Q

What Can an ECG Tell Us?

A

Orientation of the heart in the chest

Conduction disturbances

Electrical effects of medications/electrolytes

Mass of cardiac muscle

Presence of ischemic damage

223
Q

Lead I

A

Records difference in electrical potential between left arm (+) and right arm (-) electrodes

Views lateral wall of left ventricle

224
Q

Lead II

A

Records difference in electrical potential between left leg (+) and right arm (-) electrolodes

Views inferior surface of left ventricle

225
Q

Lead III

A

Records difference in electrical potential between left leg (+) and left arm (-) electrodes

Views inferior surface of left ventricle

226
Q

Leads II, III, aVF

A

Inferior heart surface

227
Q

V1, V2

A

Septal heart surface

228
Q

V3, V4

A

Anterior heart surface

229
Q

I, aVL, V5, V6

A

Lateral heart surface

230
Q

Baseline

A

Isoelectric line

A straight line recorded when electrical activity is not detected

231
Q

Waveform

A

Movement away from the baseline in either a positive or negative direction

232
Q

Segment

A

A line between waveforms, named by the waveform that precedes or follows it

233
Q

Interval

A

A waveform and a segment

234
Q

Complex

A

Several waveforms

235
Q

Factors for Rhythm Strip Analysis

A 
Rate
Rhythm
P waves
PR interval
QRS Complex
QT interval and T wave -- ST segment
236
Q

Rate Assessment

A

Number of complexes in 6 seconds and multiply by 10

237
Q

Assessment of Rhythmicity

A

Measure R-R interval–Ventricular

Measure P-P interval–Atrial

Origin of Impulse: sinus, atrial, junctional, ventricular

238
Q

Essentially Regular Rhythm

A

If the variation between the shortest and longest R-R intervals is less than four small boxes

239
Q

Irregular Rhythm

A

If the shortest and longest R-R intervals vary by more than 0.16 seconds

240
Q

Regularly Irregular Rhythm

A

When the R-R intervals are not the same, the shortest and longest R-R intervals vary by more than 0.16 seconds, and there is a repeating pattern of irregularity

241
Q

Irregularly Irregular Rhythm

A

When the R-R intervals are not the same, there is no repeating pattern of irregularity, and the shortest and longest R-R intervals vary by more than 0.16 seconds

242
Q

PR Segment

A

Horizontal line between end of P wave and beginning of QRS complex

243
Q

PR Interval

A

P wave + PR segment = PR interval

Begins with the onset of the P wave and ends with the onset of the QRS complex

Normally measures 0.12-0.20 seconds

244
Q

Long PR Interval

A

Greater than 0.20 seconds

Indicates the impulse was delayed as it passed through the atria or AV junction

245
Q

Short PR Interval

A

Less than 0.12 seconds

May be seen when the impulse originates in the atria close to the AV node or in the AV junction

246
Q

QRS Complex

A

Normally follows each P wave

Represents spread of electrical impulse through the ventricles (ventricular depolarization)

247
Q

Q Wave

A

First negative, or downward, deflection following the P wave

Always a negative waveform

Represents depolarization of the interventricular septum

248
Q

R Wave

A

The first positive, or upward, deflection following the P wave

Always positive

249
Q

S Wave

A

A negative waveform following the R wave

Always negative

R and S waves represent depolarization of the right and left ventricles

250
Q

Normal QRS Complex

A

Measure the QRS complex with the longest duration and clearest onset and end

Normal QRS duration is 0.10 seconds or less

251
Q

QT Interval

A

Represents total ventricular activity–the total from ventricular depolarization to repolarization

Measured from beginning of QRS complex to end of T wave

Duration varies according to age, gender, and heart rate

Normal does not exceed 0.42 seconds

Prolonged QT associated with risk of ventricular dysrhythmias and sudden death

252
Q

T Wave

A

Represents ventricular repolarization

Slightly asymmetric

T Wave following an abnormal QRS is usually opposite direction of QRS

253
Q

Negative T Waves

A

Myocardial ischemia

254
Q

Peaked T Waves

A

Hyperkalemia

255
Q

ST Segment

A

Portion of the ECG between QRS and T wave

Represents early part of repolarization of right and left ventricles

256
Q

ST Segment Depression

A

MI or hypokalemia

257
Q

ST Segment Elevation

A

Normal variant, myocardial injury, pericarditis, or ventricular aneurysm

258
Q

7 H’s of Dysrhythmias

A 
Hypovolemia
Hypoxia
Hypothermia
Hypokalemia
Hypocalcemia
Hypoglycemia
Hydrogen ions
259
Q

6 T’s of Dysrhythmias

A 
Toxins/tablets
Tamponade
Tension pneumothorax
Thrombus (cardiac)
Thrombus (pulmonary)
Trauma
260
Q

Rhythm

A

P-P interval regular, R-R interval regular

261
Q

SA Node Electrical Impulses Affected by…

A

Medications

Diseases or conditions that cause the heart rate to speed up, slow down, or beat irregularly

Diseases or conditions that delay or block the impulse from leaving the SA node

Diseases or conditions that prevent an impulse from being generated in the SA node

262
Q

Sinus Bradycardia

A

If the SA node fires at a rate slower than normal for the patient’s age

In adults and adolescents, HR < 60

263
Q

Sinus Bradycardia ECG Characteristics

A

Rhythm: PP and RR regular

P waves: Positive, one precedes each QRS, P waves look alike

PR Interval: 0.12-0.20 seconds and constant from beat to beat

QRS duration: 0.10 second or less

264
Q

Normal Causes of Sinus Bradycardia

A

Occurs during sleep

Common in well-conditioned athletes

Present in up to 35% of people under 25 years of age while at rest

265
Q

Abnormal Causes of Sinus Bradycardia

A

Inferior/Posterior MI

Disease of SA node

Hypoxia, hypothermia, hypokalemia, hypothyroidism

Increased ICP

Sleep apnea

CCBs, digitalis, beta-blockers, amiodarone, sotalol

266
Q

Treatment of Sinus Bradycardia

A

No treatment if not symptomatic

Oxygen, IV access, atropine, TCP

267
Q

Signs and Symptoms of Hemodynamic Compromise Related to Sinus Brady

A

Changes in mental status

Low blood pressure

Chest pain, SOB, signs of shock

CHF, pulmonary congestion, decreased urine output

Cold, clammy skin

268
Q

Sinus Tachycardia

A

Looks like sinus rhythm only faster

At very fast rates, it may be hard to tell the difference between a P and T wave

QT interval normally shortens as HR increases

269
Q

ECG Characteristics of Sinus Tachycardia

A

PP regular, RR regular

P waves: positive, one precedes each QRS, P waves look alike

PR: 0.12-0.20 seconds

QRS duration: 0.10 seconds or less

270
Q

Causes of Sinus Tachycardia

A

Exercise, fever, pain, fear, hypoxia

CHF, acute MI, infection, shock

PE

Epinephrine, atropine, dopamine, nicotine, cocaine

271
Q

Treatment of Sinus Tachycardia

A

Fluid replacement

Relief of pain

Removal of offending medications or substances

Reducing fever or anxiety

272
Q

Sinus Arrhythmia

A

When the SA node fires irregularly

273
Q

Respiratory Sinus Arrhythmia

A

Associated with the phases of respiration and changes in interthoracic pressure

274
Q

Nonrespiratory Sinus Arrhythmia

A

Not related to the respiratory cycle

275
Q

ECG for Sinus Arrhythmia

A

Rate: 60-100

Rhythm: irregular, phasic with respiration, HR increases gradually with inspiration (RR shortens) and decreases with expiration (RR lengthens)

P waves: normal

PR interval: 0.12-0.20

QRS duration: 0.10 seconds or less

276
Q

Atrial Dysrhythmias

A

Lose the “atrial kick”

Some are associated with extremely fast ventricular rates

An excessively rapid HR may compromise cardiac output

Affects P wave

277
Q

Premature Complexes

A

Pairs: two beats in a row

“Runs”: three or more in a row

Bigeminy: every other beat is premature

Trigeminy: every third beat is premature

Quadrigeminy: every fourth beat is premature

278
Q

Premature Atrial Complexes

A

Occur when an irritable site within the atria discharges before the next SA node impulse is due to discharge

P wave of a PAC may be biphasic, flattened, notched, pointed, or lost in the preceding T wave

279
Q

How to Recognize PACs

A

Irregular rhythm

May occur because of emotional stress, CHF, fatigue, atrial enlargement, digitalis toxicity, hypokalemia

280
Q

Atrial Flutter

A

Ectopic atrial rhythm in which an irritable site fires regularly at an extremely rapid rate

281
Q

ECG for Atrial Flutter

A

Rate: atrial rate 250-450 bpm

Rhythm: atrial regular, ventricular regular or irregular depending on AV conduction

P waves: no identifiable P waves

PR interval: not measurable

QRS: 0.10 seconds or less

282
Q

Atrial Fibrillation

A

Can occur in patients with or without detectable heart disease or related symptoms

Increased stroke risk

283
Q

ECG for Atrial Fibrillation

A

Rate: atrial rate 400-600

Rhythm: ventricular rhythm usually irregularly irregular

P waves: no identifiable P waves; erratic, wavy baseline

PR interval: not measurable

QRS: 0.10 seconds or less

284
Q

Conditions Associated with Atrial Fibrillation/Atrial Flutter

A

HTN, ischemic heart disease, CHF, pericarditis

Diabetes, stress

Hypoxia, hypokalemia, hypoglycemia

285
Q

What to do with Atrial Fibrillation/Atrial Flutter

A

Cardiologist consult

If rapid ventricular rate, control ventricular response

If rapid ventricular rate and serious signs and symptoms, synchronized cardioversion

Anticoagulation recommended if AFib has been present for > 48 hours

286
Q

Supraventricular Tachycardia

A

Begin above the bifurcation of the bundle of His

Includes rhythms that begin in the SA node, atrial tissue, AV junction

Also referred to as NARROW COMPLEX Tachycardia

287
Q

ECG for Supraventricular Tachycardia

A

Rate: 150 or greater

Rhythm: regular or irregular

P waves: unable to identify

PR interval: unable to measure

QRS: 0.10 seconds or less

288
Q

Causes of Supraventricular Tachycardia

A

Acute illness with excessive catecholamine release

Digitalis toxicity

Heart disease

Infection

Hypoxia

PE

Stimulant use

289
Q

Supraventricular Tachycardia Assessment Findings

A

Acute changes in mental status

Asymptomatic

Dizziness, dyspnea, fatigue

Fluttering in the chest

Hypotension

Palpitations

Signs of shock

290
Q

Interventions for Supraventricular Tachycardia

A

Apply pulse oximeter and administer oxygen if indicated

Obtain vital signs

Establish IV access

Obtain 12-lead EKG

291
Q

ECG for Junctional Rhythm

A

Rate: 40-60

Rhythm: very regular

P waves: may occur before, during, or after the QRS; may be inverted

PR interval: if shown, 0.12 seconds or less

QRS: usually 0.10 seconds or less

292
Q

Causes of Junctional Rhythm

A

Increases parasympathetic tone

Immediately after cardiac surgery

Digitalis, Quinidine, Beta-Blockers, CCBs

Acute myocardial infarction

Rheumatic heart disease

SA node disease

Hypoxia

293
Q

Interventions for Junctional Rhythm

A

Patient may be asymptomatic or may experience signs/symptoms associated with the slow heart rate and decreased cardiac output

If the patient’s S/S are related to the slow heart rate, consider atropine and/or transcutaneous pacing, dopamine infusion, epinephrine infusion

294
Q

Ventricular Rhythms

A

Ventricles assume responsibility if:

SA node fails to discharge

Impulse from SA node is generated by blocked

Rate of discharge of SA node is slower than that of ventricles

Irritable site in either ventricle produces an early beat or rapid rhythm

295
Q

Premature Ventricular Contractions

A

Arise from an irritable focus within either ventricle

Occurs earlier than the next expected sinus beat

QRS is typically 0.12 seconds or greater

T wave is usually in the opposite direction of the QRS complex

296
Q

ECG for PVCs

A

Ventricular/Atrial Rhythm: essentially regular with premature beats

Ventricular/Atrial Rate: usually within a normal range

P waves: usually absent

PR interval: none

QRS duration: usually 0.12 seconds or greater, wide and bizarre

297
Q

Patterns of PVCs

A

Pairs: two sequential PVCs

Runs or bursts: 3 or more sequential PVCs

Ventricular bigeminy: every other beat is a PVC

Ventricular trigeminy: every 3rd beat is a PVC

Ventricular quadrigeminy: every 4th beat is a PVC

298
Q

Uniform/Monomorphic PVCs

A

Premature ventricular beats that look the same in the same lead and originate from the same anatomical site

299
Q

Multiform/Polymorphic PVCs

A

PVCs that appear different from one another in the same lead

Often arise from different anatomical sites

300
Q

R-on-T PVCs

A

Occur when the R wave of a PVC falls on the T wave of the preceding beat

A PVC occurring during this period of the cardiac cycle can cause VT or VF

301
Q

Causes of PVCs

A

LOW POTASSIUM, LOW MAGNESIUM

Acid-base imbalances

Acute coronary syndromes

Cardiomyopathy

Digitalis toxicity

Electrolyte imbalances

Exercise

Heart failure

Hypoxia

Stimulants

Ventricular aneurysm

302
Q

Ventricular Tachycardia

A

VT exists when three or more PVCs occur in a row at a rate of more than 100 beats per minute

303
Q

Nonsustained VT

A

A short run lasting less than 30 seconds

304
Q

Sustained VT

A

Persists for more than 30 seconds

305
Q

ECG for Ventricular Tachycardia

A

Ventricular/Atrial Rhythm: essentially regular

Ventricular/Atrial Rate: 101-250

P waves: usually not seen

PR interval: none

QRS duration: 0.12 seconds or greater

306
Q

Causes of Ventricular Tachycardia

A

Acid-base imbalances

Acute coronary syndromes

Cocaine abuse

Electrolyte imbalances

Mitral valve prolapse

Trauma

Tricyclic antidepressant overdose

307
Q

Interventions for Pulseless Patient with VT

A

CPR and defibrillation

308
Q

Interventions for Patient with a Pulse and VT

A

Stable: oxygen, IV access, ventricular antidysrhythmics

Unstable: oxygen, IV access, sedation, defibrillation, CPR

309
Q

Polymorphic VT

A

QRS complexes vary in shape and amplitude from beat to beat and appear to twist from upright to negative or negative to upright and back

Resemble a spindle

310
Q

Causes of Polymophic VT

A

Magnesium deficiency

Congenital

Hypokalemia

311
Q

Ventricular Fibrillation

A

Chaotic rhythm that begins in the ventricles

No organized depolarization of the ventricles

Ventricular myocardium quivers, no effective myocardial contraction and no pulse, no normal-looking waveforms are visible

312
Q

ECG for VF

A

Ventricular/atrial rhythm: rapid and chaotic with no pattern or regularity

Ventricular/atrial rate: cannot be determined

P waves, PR interval, QRS duration not discernible

313
Q

Causes of Ventricular Fibrillation

A

Acute coronary syndromes, dysrhythmias, electrolyte imbalances, hypertrophy, severe heart failure, vagal stimulation

314
Q

Pulseless Electrical Activity

A

Organized electrical activity is observed on the cardiac monitor but the patient is unresponsive, is not breathing, and has no pulse

315
Q

Interventions for Pulseless Electrical Activity

A

CPR, oxygen, start an IV

Advanced airway

316
Q

Asystole

A

Total absence of ventricular electrical activity

There is no ventricular rate or rhythm, no pulse, and no cardiac output

317
Q

ECG of Asystole

A

Ventricular/Atrial Rhythm: ventricular not discernible, atrial may be discernible

Ventricular/Atrial Rate: ventricular not discernible, but atrial activity may be observed

P waves: usually not discernible

PR interval and QRS duration absent

318
Q

PATCH-4-MD

A 
PE
Acidosis
Tension pneumothorax
Cardiac tamponade
Hypovolemia

Hypoxia
Heat/cold
Hypokalemia
Hyperkalemia

MI
Drug overdose

319
Q

Normal BUN

320
Q

Normal Creatinine

321
Q

Normal Glucose

322
Q

Normal Calcium

323
Q

Normal Magnesium

324
Q

Normal Phosphate

325
Q

Normal Sodium

326
Q

Normal Hemoglobin

A

13-17 in men

12-15 in women

327
Q

Normal Hematocrit

A

40-52% in men

36-47% in women

Critical Care (3 decks)

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