Unit I Flashcards
(327 cards)
1
Q
Sedation
A
Analgesics AND sedative needed for patient and safety
2
Q
Excessive sedation can cause…
A
Prolonged ventilation
Physical/psychological dependence
Increased length of hospital stay
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
4
Q
Richmond Agitation-Sedation Scale (RASS)
A
Scale from -5 to +4
-5 is unresponsive, +4 is combative
5
Q
Drugs for Short-Term Sedation
A
Benzodiazepines
Propofol
Dexmedetominde (Alpha-2 Receptor Agonist)
Ketamine
6
Q
Drug for Intermediate Term Sedation
A
Lorazepam
7
Q
Drug for Long Acting Sedation
A
Diazepam
8
Q
Lorazepam
A
Ativan
Side effect: hypotension
Used for mechanically ventilated patients
9
Q
Midazolam
A
Versed
Side effects: hypotension, respiratory depression, amnesia
10
Q
Diazepam
A
Valium
Shorter acting; used for patients in alcohol withdrawal
Side effects: hypotension, respiratory depression
11
Q
Antidote for Benzodiazepines
A
Romazicon, Flumazenil
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
13
Q
Propofol Infusion Syndrome
A
Rare, usually in pediatrics over 48 hours
Cardiac arrest, metabolic acidosis, rhabdomyolysis
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
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
16
Q
Sedation Vacation (Spontaneous Awakening Trial)
A
- Discontinue sedation at the same time each day until patient wakes up (every shift)
- Assess patient’s level of alertness
- Resume sedation according to unit’s protocol
- Monitor patient closely to prevent harm from sedative withdrawal or agitation
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
18
Q
Short Term NMB
A
Mivacurium (IVP)
19
Q
Intermediate NMB
A
Vecuronium (IVP and infusion)
20
Q
Long Acting NMB
A
Pancuronium (intermittent IV bolus)
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
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
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
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
25
CAM-ICU Assessment of Delirium
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)
26
Treatment of Delirium
Nonpharmacologic first
Correct physiological problems (O2, pain, BUN, electrolytes, blood glucose, benzodiazepine adverse effects)
Pharmacological measures
27
Nonpharmacologic Management of Delirium
Noise reduction, light reduction, cluster cares, promote sleep, back massage, music, calm voice, visual cues to orientation
MINIMIZE SLEEP DEPRIVATION
EARLY MOBILIZATION
28
Pharmacologic Management of Delirium
Give Haloperidol
29
Neuroleptic Malignant Syndrome
Muscular rigidity, hyperthermia, sweating, fluctuations in VS
Critical crisis
30
Treatment for Neuroleptic Malignant Syndrome
1. Dantrolene as muscle relaxant
2. Management of fever
4. Fluid volume replacement as needed
4. Discontinue neuroleptic drug
5. Bromocriptine for CNS toxication
31
Adverse Effects of Haloperidol
Orthostatic hypotension
Anticholinergic symptoms
Sedation
Prolonged QT interval, risk for dysrhythmias
32
ABCDE Bundle
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
33
Test Used Prior to ABGs
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
34
In order for perfusion to happen...
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
35
PaO2
Partial pressure of oxygen in arterial blood
Dissolved and not bound to hemoglobin
80-100
36
SaO2
Arterial saturation of hemoglobin
Oxygen bound to hemoglobin
95-97%
37
PaCO2
Partial pressure of CO2 in arterial blood
CO2 dissolved in the blood
35-45
38
SpO2
Saturation of hemoglobin in peripheral capillaries
Noninvasive measurement
Estimate of SaO2
Greater than 93%
39
Oxyhemoglobin Curve--Right Shift
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
40
Oxyhemoglobin Curve--Left Shift
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
41
2,3-DPG
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
42
Carbonic Anhydrase Buffer System
H20 + CO2 (lungs) = H+ - HCO3 (kidneys)
43
Normal ABG Values
pH: 7.35-7.45
PCO2: 35-45
PO2: 80-100
HCO3: 22-26
44
Analysis of ABGs
Oxygenation Status: PaO2, SaO2, FiO2
Acid-Base Status: pH, pCO2, HCO3
ROME (Respiratory Opposite, Metabolic Equal)
45
Compensation
Body attempts to maintain homeostasis
When pH is WNL, but CO2 + HCO3 are not
46
Metabolic Alkalosis
Caused by steroid therapy, vomiting, GI suction, diuretic therapy, NA Bicarb intake
Loss of acid or gain of bicarb
47
Metabolic Acidosis
Gain of H+, increase in lactic acid, DKA, hypermetabolic state, intake acid (ASA), renal failure
Loss of HCO3, diarrhea
48
Respiratory Acidosis
Gain of CO2
Oversedation, hypoventilation, drug overdose, COPD, mechanical ventilation, head-spinal trauma, neuromuscular disease
49
Respiratory Alkalosis
Loss of CO2
Pregnancy, high altitude, PE, hypoxia, fever, increased metabolic state, anxiety/fear
50
Rationale for Mechanical Ventilation
Respiratory arrest
Procedure anesthesia/analgesia
Post-operative recovery
Poor ABGs
Deteriorating respiratory status
Airway protection
51
Types of Mechanical Ventilation
Negative Pressure Ventilation
Positive Pressure Ventilation
52
Negative Pressure Ventilation
Used for atelectasis
Air is pulled out of the lungs
Iron Lung
53
Positive Pressure Ventilation
Used for respiratory failure
Air is pushed into the lungs
54
High Frequency Jet Ventilation
Used for pediatrics and barotrauma patients
55
Neutrally Adjusted Ventilator Assistance
Used for pediatrics and barotrauma patients
56
Respiratory Volumes
Tidal volume
Inspiratory reserve volume
Expiratory reserve volume
Minute volume
Residual volume (dead space)
Sigh
57
Types of Breaths for Ventilated Patient
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)
58
Normal Inspiration/Expiration Ratio
1 inspiration to 2 expiration
Exhalation 2x as long as inspiration
59
Tidal Volume
Volume of gas inhaled or exhaled
60
Minute Volume
Volume of gas entering or leaving the lungs per minute
61
Continuous Mandatory Ventilation (CMV)
All breaths controlled by the ventilator
62
Assisted Mandatory Ventilation
All breaths initiated by patient but delivered by the ventilator
63
Assist/Control Mandatory Ventilation (A/C)
Minimum number of controlled breaths plus any additional assisted breaths initiated by patient
64
Synchronized Mechanical Ventilation (SIMV)
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
65
Continuous Positive Airway Pressure (CPAP)
All spontaneous breaths by patient
Slight elevation of airway pressures
NO MECHANICAL VENTILATION
MUST HAVE THE DRIVE TO BREATHE
66
Ventilator Settings
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
67
Modes of Mechanical Ventilation for Servo 300
Pressure Controlled (PC)
Volume Controlled (VC)
Volume Support (VS)
Pressure Support (PS)
Pressure Regulated Volume Controlled (PRVC)
68
Pressure Controlled
Pressure cycled ventilations
Decelerating inspiratory flow
Pre-set rate and time
69
Volume Controlled
Similar to CMV
Volume cycled ventilations
Higher airway pressures than PC
70
Volume Support
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
71
Pressure Support
Patient must trigger each breath
Spontaneous breaths assisted with preset inspiratory pressures
72
Pressure Regulated Volume Controlled
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
73
NAVA
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
74
Who Can Use NAVA
Spontaneously breathing patients
Must have a working diaphragm
Patients greater than 500 grams
Ability to place either an NG or OG catheter
75
Who Can't Use NAVA
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
76
Noninvasive Positive Pressure Ventilation
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
77
Ideal Patients for Noninvasive Positive Pressure Ventilation
Nocturnal hypoventilation (sleep apnea)
Chronic hypoventilation (neuromuscular disease, COPD)
Acute hypoventilation
Acute cardiogenic pulmonary edema
Conscious and cooperative
Able to protect airway
78
Contraindications to Noninvasive Positive Pressure Ventilation
Respiratory arrest
Cardiovascular shock
Risk for aspiration
Severe hypoxemia, acidemia
Uncooperative patient (agitation)
Facial, esophageal, or gastric surgery
Cranial trauma or burns
79
Initiation of NPPV--Settings
Interface (mask & face)
Machine
Mode
Trigger, cycle, rise time
IPAP (inspiratory pressure)
EPAP (PEEP)
FiO2
80
Steps for Initiation of NPPV
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
81
NPPV Nursing Care
Skin breakdown
Gastric insufflation with IPAP > 20 cm H2O
Air leaks
Conjunctival irritation
Nasal or oral dryness
Claustrophobia
82
Outcome for Dysfunctional Ventilatory Weaning Response
Wean from ventilator with IER ABGs
Remain free from unresolved dyspnea
Effectively clear airway
83
Interventions for Dysfunctional Ventilatory Weaning Response
Exercise respiratory muscles
Reduce oxygen consumption
Maintain adequate oxygenation
Pressure support ventilation as needed
Maintain adequate rest and nutrition prior to weaning
84
Readiness to be Weaned from Mechanical Ventilation
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
85
PaO2/FiO2 Ratio
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
86
Expected PaO2/FiO2 Ratio
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
87
Ventilator Nursing Diagnoses
Impaired spontaneous ventilation
Ineffective airway clearance
Ineffective breathing pattern
Impaired verbal communication
Impaired gas exchange
Fear
Powerlessness
Social isolation
Risk for infection
88
Communication with Patients on Ventilator
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
89
Complications of Mechanical Ventilation
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
90
Ventilator Alarms
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)
91
Ventilator Induced Lung Injury
VILI is due to volume, overdistention of lung
92
Ventilator Associated Pneumonia
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
93
Interventions to Decrease Risk of VAP
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
94
Definition of ARDS
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
95
Pathophysiology of Acute Lung Injury
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 -->
96
Direct Risk Factors for ALI
Pulmonary infections
Toxic inhalation
Aspiration
Pneumonia
97
Indirect Risk Factors for ALI
Shock, sepsis
Hypothermia, hyperthermia
Drug overdose
DIC
Multiple transfusions
Burns
Eclampsia
Trauma
98
Severe Sepsis
1. Known or suspected infection
2. Two signs of SIRS
3. At least 1 organ failing or dysfunctional
99
SIRS
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
100
Transfusion-Related ALI (TRALI)
Most common cause of transfusion-associated mortality
Potentially preventable
Improved antigen screening
101
Ventilator-Induced Lung Injury (VILI)
Ventilator pressures
Lung strain
Inflammation
102
LIPS
Lung Injury Prediction Score
103
LIPS Risk Factors
High risk trauma
High risk surgery
Aspiration
Sepsis, shock
Pneumonia
Pancreatitis
104
LIPS Risk Modifiers
Alcohol abuse
Hypoalbuminemia
Tachypnea
O2 supplementation
Chemotherapy
Obesity, diabetes
105
Checklist for Lung Injury Prevention (CLIP)
Respiratory support
Aspiration precautions
Infection control
Fluid management
Transfusion
Structured handoff
106
Physiology of ALI
Exudative Phase
Fibroproliferative Phase
Resolution Phase
107
Exudative Phase of ALI
First 72 hours
Increased capillary permeability (leakage of fluids into interstitial tissues, compression of terminal bronchioles)
108
Fibroproliferative Phase of ALI
Gas exchange compromised
Hypoxemia from atelectasis, decreased diffusion
109
Resolution Phase of ALI
Recovery over several weeks
Reestablish a/c membrane
110
Goals of Therapy for ALI
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)
111
Investigational Interventions for ALI
Synthetic surfactant instilled via ET tube
Extra-corporeal gas exchange (ECMO)
Inhaled liquid nitric oxide with HFJV
112
Oxygenation (SpO2)
O2 for metabolism
Measures percentage of oxygen in RBCs
Changes within 5 minutes
113
Ventilation (Capnography)
CO2 from metabolism
EtCO2 measures exhaled CO2 at point of exit
Changes within 10 seconds
114
Capnography
Available for spontaneously breathing and for intubated patients
115
Capnography Waveforms
The higher the waveform, the more CO2
Normal EtCO2 is 35-45
Length of waveform corresponds to respiratory rate
116
Shark Fin in Capnography
Possible causes include partially kinked airway, presence of foreign body, obstruction of expiratory limb of vent circuit, BRONCHOSPASM
117
Curare Cleft in Capnography
Appears when NMBAs begin to wear off
Depth of cleft inversely proportional to degree of blockade
118
EtCO2 > 45
Hypoventilation
Respiratory acidosis
Fever
Bronchospasms
119
EtCO2 < 35
Hyperventilation
Respiratory alkalosis
Partial airway obstruction
PE
Cardiac arrest
Hypotension, hypothermia, hypovolemia
120
Acute Kidney Injury
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
121
Acute Kidney Injury Statistics
1% of acute hospital admissions
Complicates 7% of inpatient episodes
Increases mortality rate to 38-80%
122
Pre-renal Acute Kidney Injury
Hypo-perfusion of the kidneys
Caused by shock states (hypovolemia, cardiogenic, distributive), sepsis, occlusion of renal arteries, altered auto-regulatory capability
123
Intra-renal Acute Kidney Injury
Damage to renal parenchyma
Caused by nephrotoxic antibiotics (aminoglycosides), heavy metal poisoning, hemolysis, organic solvents, fungicides/pesticides, radiopaque contrast agents, NSAIDS
124
Post-renal Acute Kidney Injury
Reflux of urine flow due to obstruction beyond the kidneys
Caused by kidney stones, UTIs, BPH, anticholinergics, tumors, blood clots
125
Urinalysis for Prerenal AKI
Na: < 5 mEq/L
SpecGrav: > 1.020
BUN:CR: > 20:1
Urine is concentrated, kidneys are hanging on to water
126
Urinalysis for Intrarenal AKI
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
127
RIFLE Criteria
Severities: RISK, INJURY, FAILURE
Outcomes: LOSS of renal function, ESKD
128
RIFLE-Risk
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
129
RIFLE-Injury
SCr increased 2x normal
Urine output reduction to 0.5 for more than 12 hours
130
RIFLE-Failure
SCr increased 3x normal
0r > 4 or acute rise > 0.5
UO < 0.3 for 24 hours or anuria for 12 hours
131
RIFLE-Loss
AKI > 4 weeks
132
Diagnostic Criteria for AKI
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
Primary Prevention for AKI
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
Phases of AKI
Onset
Oliguric or Non-Oliguric
Diuretic
Recovery
135
Onset Phase of AKI
Initial insult--cell injury
Hours to days
Goal is to determine cause
136
Oliguric or Non-Oliguric Phase of AKI
Oliguric: fluid overload
Non-Oliguric: cause is usually toxic injury, decreased fluid complications
137
Period of Oliguria
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
Complications of AKI
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
Treatment of AKI
Restore adequate renal blood flow
Treat cause (hypovolemia--rapid fluid infusion, remove nephrotoxins, remove obstruction, renal replacement therapy RRT)
140
Assessment of Fluid Overload
```
Daily weights
Strict I&O
Edema (sacral, pretibial)
Vital signs
CVP
Skin turgor/membranes
```
141
Implementation for Fluid Overload
Regulate IV fluids according to urine output and daily weights
Diuretics (mannitol, furosemide, ethacrynic acid)
Dialysis
142
Assessment of Hyperkalemia in AKI
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
Implementation for Hyperkalemia in AKI
Restrict potassium
Kayexolate Resin PO or PR with Sorbitol
Glucose and regular insulin IVP
NaHCO3 IVP
Dialysis
144
Period of Diuresis
Gradual increase in urine output (up to 4L/day)
Lab values stop rising, begin to decline
Potential for dehydration, electrolyte depletion
145
Period of Recovery
3-12 months
Return of serum values to normal levels
1%-3% loss of renal function
146
Initial Stage of Chronic Renal Failure
Loss of renal reserve
40-75% loss of nephron function
Normal renal function
147
Second Stage of Chronic Renal Failure
75-80% loss of nephron function
Elevated BUN and creatinine
Polyuria, dilute urine
148
Etiologies of ESKD
Diabetes mellitus
Uncontrolled HTN
Chronic glomerular nephritis
Unresolved AKI
Polycystic kidney disease
Systemic lupus eryhtematosus
Sickle cell disease
149
Uremic Syndrome
Elevation of blood nitrogens
Signs--
Early: N/V, anorexia
Late: stupor, seizures, coma
Chronic: pericarditis, pleuritis
Rare: uremic frost
150
Hypernatremia
Thirst, fever, dry membranes, altered consciousness, seizures
REDUCE SODIUM INTAKE
DIALYSIS
151
Hypocalcemia
Phosphorus-Calcium Balance
Decreased vitamin D synthesis
Irritability, muscle tetany, Chvostek sign, bone disorders
CALCIUM SUPPLEMENT
VITAMIN D SUPPLEMENT
152
Hyperphosphatemia
N/V, anorexia
Bone wasting
Hemolysis, bleeding tendencies
PHOSPHATE BINDERS WITH DIET
DIALYSIS
153
Hypermagnesemia
Use of antacids
CNS depressed, lethargy, coma
Bradycardias
Prolonged PR, QRS complex
Tall T waves, AV blocks
DIALYSIS AND DIET
154
Anemia
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
Bone Disorders
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
Cardiovascular Problems with ESKD
Accelerated atherosclerosis
Pericarditis
Congestive heart failure, fluid overload
Potential for dysrhythmias secondary to electrolyte imbalances
157
Nursing Diagnoses for Chronic Renal Failure
Fluid volume excess
Altered nutrition
Knowledge deficit
Activity intolerance
Self-esteem disturbance
158
Alteration in Nutrition, Less than Body Requirements (Chronic Renal Failure)
Restrict protein intake
Sodium, potassium, and phosphate restriction
High carbohydrates
Fluid restriction
Calcium and vitamin supplements
159
Fluid Volume Excess (Chronic Renal Failure)
Fluid restriction (500-600 mL + volume of urine output)
Diuretics (sometimes)
Daily weights
Maintenance of dry weight
Dialysis
160
Treatment Options for Chronic Kidney Failure
Conservative treatment
Intermittent hemodialysis
Peritoneal dialysis
Transplant
161
Treatment Options for Acute Kidney Injury
Intermittent hemodialysis
Continuous renal replacement therapy
162
Hemodialysis
Artificial kidney function by circulation of blood through dialyzer with semipermeable membrane and dialysate bath
163
Functions of Hemodialysis
Dialysis: removal of wastes
Ultrafiltration: removal of fluid volume
164
Components of Hemodialysis
Dialyzer, Dialysate, Extracorporeal circulation, and Venous Access Device
165
Access Sites for Hemodialysis
AV fistula
AV graft
Dual lumen central catheter
166
Care for Hemodialysis Access Devices
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
Central Line Associated Bloodstream Infection (CLABSI)
Daily assessment is necessary
NURSE SENSITIVE INDICATOR
Maximal sterile barrier on insertion
Hand hygiene
Scrub ports, tubing changes
168
Problems with Hemodialysis
Hypovolemia
Air embolism
Dialysis Disequilibrium Syndrome
Painful muscle cramping
Nausea/Vomiting
Infection
Blood clots
169
New Patient Receiving Hemodialysis
May require catheter until AV access site is healed
More prone to dialysis disequilibrium syndrome
Blood chemistry and hydration more imbalanced
170
Dialysis Disequilibrium Syndrome
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
Air Embolism During Hemodialysis
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
Painful Muscle Cramping during Hemodialysis
Caused by excessive removal of sodium or drop in osmotic pressure in blood
Reduce flow rate, bolus with hypertonic solution
173
Hypotension during Hemodialysis
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
Peritoneal Dialysis
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
Intermittent Peritoneal Dialysis
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
Continuous Ambulatory Peritoneal Dialysis
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
Peritoneal Dialysis: Incomplete Recovery of Fluid
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
Peritoneal Dialysis: Leakage Around the Catheter
Common with new catheter
Start with lower volumes of diaysate and increase slowly
Change dressing frequently with sterile technique
Reduce intra-ABD pressure
179
Peritoneal Dialysis: Blood Tinged Effluent
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
Peritoneal Dialysis: Peritonitis
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
Peritoneal Dialysis Components
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
Hemodialysis Components
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
Continuous Renal Replacement Therapy
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
Positive Aspects of CRRT for AKI
Safer for patients with hemodynamic instability
Less intense fluctuation of fluid and electrolyte levels
Most resembles normal kidney function
185
Drawbacks of CRRT for AKI
Use of large catheter in major artery
Risk for infections
Distal thrombosis formation
Disconnection
Exsanguination
186
Diffusion with CRRT
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
Convection with CRRT
Pressure gradient is set up so water is pushed/pumped across dialysis filter
Molecules dragged with fluid
188
Absorption with CRRT
Filter attracts solute
Molecules absorb with the dialysis filter
189
Ultrafiltrate Volume for CRRT
Fluid removed each hour
190
Replacement Fluid for CRRT
Some ultrafiltrate is replaced through the circuit
Increase volume of fluid passing through filter
Improves convection
191
Five CRRT Methods
Slow continuous ultrafiltration
Continuous arteriovenous hemofiltration
Continuous arteriovenous hemodiafiltration
Continous venovenous hemofiltration
Continuous venovenous hemodiafiltration
192
Slow Continuous Ultrafiltration
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
Continuous Arteriovenous Hemofiltration
Semipermeable filter
Propelled by MAP
Ultrafiltrate to gravity bag
Convention
Simple technology
Remove and replace fluid effectively
194
Continuous Arteriovenous Hemodiafiltration
Semipermeable filter
Dialysate used
Ultrafiltrate to gravity bag
Convention
Diffusion
Results in more rapid solute reduction (BUN, creatinine)
195
Continous Venovenous Hemofiltration
Semipermeable filter
Propelled by roller pump
Convection
Solute removal
Replacement fluid added to facilitate convection
196
Continuous Venovenous Hemodiafiltration
Semipermeable filter
Dialysate used
Propelled by roller pump
Convection
Diffusion
Increased solute removal
Fluid removal
197
Complications with CRRT
Dehydration and hypotension
Electrolyte imbalances
Acid/base imbalances
HYPOTHERMIA
Hyperglycemia
Inadequate blood flow through hemofilter, clotted hemofilter
Sepsis
198
Nursing Management of CRRT
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
Catheter Associated Urinary Tract Infection
Daily assessment of need
Aseptic insertion
Closed drainage
Securement device
Automatic discharge orders
Hygiene
200
Contractility
Shortening of heart muscle in response to stimuli
201
Excitability
Irritability ability to respond to stimuli influenced by: neural, hormonal, nutritional balance, O2 supply, drug therapy
202
Conductivity
Ability to transmit electrical impulses
203
Automaticity
Ability to beat spontaneously and repetitively without external neurohormonal control
204
Parasympathetic Effects on Heart
DECREASE automaticity, contractility, conduction, rate
205
Sympathetic Effects on Heart
INCREASE automaticity, contractility, conduction, rate
206
Refractoriness
The period of recovery that cells need after being discharged before they are able to respond to a stimulus
207
Absolute Refractory Period
Cells cannot be stimulated to conduct an electrical impulse, no matter how strong the stimulus
Onset of QRS to peak of T
208
Relative Refractory Period
Cardiac cells can be stimulated to depolarize if stimulus is strong enough
Downslope of T wave
209
Supernormal Period
Weaker than normal stimulus can cause cardiac cells to depolarize
Corresponds with end of T wave
210
Primary Pacemaker of the Heart
Sinoatrial node
211
Atria
Fibers of SA node connect directly with fibers of atria
Impulse leaves SA node
Spreads from cell to cell across atrial muscle
212
Internodal Pathways
Impulse is spread to AV node via internodal pathways
Merge gradually with cells of AV node
213
AV Junction
Area of specialized conduction tissue
Provides electrical links between atrium and ventricle
214
AV Node
Located in floor of right atrium
Delays conduction of impulse from atria to ventricles (allows for atria to empty into ventricles)
215
Bundle of His
Connects AV node and bundle branches
Conducts impulse to right and left bundle branches
216
Purkinje Fibers
Receives impulse from bundle branches
Relays to ventricular myocardium
217
Nervous Influences on Pacemaker
Parasympathetic (Vagal): slows heart rate at the SA node
Sympathetic (Beta Adrenergic): increases HR at SA node, increases conductivity and automaticity
218
Baroreceptor Influences on Pacemaker
Aortic arch, carotid sinuses
Influenced by blood pressure
Stimulates/inhibits nervous system influences
219
P Wave
Atrial depolarization and the spread of the impulse throughout the right and left atria
Influx of Na+ and/or Ca++ cations
220
QRS Complex
Ventricular depolarization
Influx of Na+ and/or Ca++ cations
221
T Wave
Ventricular repolarization
Restabilization of cell membrane
222
What Can an ECG Tell Us?
Orientation of the heart in the chest
Conduction disturbances
Electrical effects of medications/electrolytes
Mass of cardiac muscle
Presence of ischemic damage
223
Lead I
Records difference in electrical potential between left arm (+) and right arm (-) electrodes
Views lateral wall of left ventricle
224
Lead II
Records difference in electrical potential between left leg (+) and right arm (-) electrolodes
Views inferior surface of left ventricle
225
Lead III
Records difference in electrical potential between left leg (+) and left arm (-) electrodes
Views inferior surface of left ventricle
226
Leads II, III, aVF
Inferior heart surface
227
V1, V2
Septal heart surface
228
V3, V4
Anterior heart surface
229
I, aVL, V5, V6
Lateral heart surface
230
Baseline
Isoelectric line
A straight line recorded when electrical activity is not detected
231
Waveform
Movement away from the baseline in either a positive or negative direction
232
Segment
A line between waveforms, named by the waveform that precedes or follows it
233
Interval
A waveform and a segment
234
Complex
Several waveforms
235
Factors for Rhythm Strip Analysis
```
Rate
Rhythm
P waves
PR interval
QRS Complex
QT interval and T wave -- ST segment
```
236
Rate Assessment
Number of complexes in 6 seconds and multiply by 10
237
Assessment of Rhythmicity
Measure R-R interval--Ventricular
Measure P-P interval--Atrial
Origin of Impulse: sinus, atrial, junctional, ventricular
238
Essentially Regular Rhythm
If the variation between the shortest and longest R-R intervals is less than four small boxes
239
Irregular Rhythm
If the shortest and longest R-R intervals vary by more than 0.16 seconds
240
Regularly Irregular Rhythm
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
Irregularly Irregular Rhythm
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
PR Segment
Horizontal line between end of P wave and beginning of QRS complex
243
PR Interval
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
Long PR Interval
Greater than 0.20 seconds
Indicates the impulse was delayed as it passed through the atria or AV junction
245
Short PR Interval
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
QRS Complex
Normally follows each P wave
Represents spread of electrical impulse through the ventricles (ventricular depolarization)
247
Q Wave
First negative, or downward, deflection following the P wave
Always a negative waveform
Represents depolarization of the interventricular septum
248
R Wave
The first positive, or upward, deflection following the P wave
Always positive
249
S Wave
A negative waveform following the R wave
Always negative
R and S waves represent depolarization of the right and left ventricles
250
Normal QRS Complex
Measure the QRS complex with the longest duration and clearest onset and end
Normal QRS duration is 0.10 seconds or less
251
QT Interval
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
T Wave
Represents ventricular repolarization
Slightly asymmetric
T Wave following an abnormal QRS is usually opposite direction of QRS
253
Negative T Waves
Myocardial ischemia
254
Peaked T Waves
Hyperkalemia
255
ST Segment
Portion of the ECG between QRS and T wave
Represents early part of repolarization of right and left ventricles
256
ST Segment Depression
MI or hypokalemia
257
ST Segment Elevation
Normal variant, myocardial injury, pericarditis, or ventricular aneurysm
258
7 H's of Dysrhythmias
```
Hypovolemia
Hypoxia
Hypothermia
Hypokalemia
Hypocalcemia
Hypoglycemia
Hydrogen ions
```
259
6 T's of Dysrhythmias
```
Toxins/tablets
Tamponade
Tension pneumothorax
Thrombus (cardiac)
Thrombus (pulmonary)
Trauma
```
260
Rhythm
P-P interval regular, R-R interval regular
261
SA Node Electrical Impulses Affected by...
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
Sinus Bradycardia
If the SA node fires at a rate slower than normal for the patient's age
In adults and adolescents, HR < 60
263
Sinus Bradycardia ECG Characteristics
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
Normal Causes of Sinus Bradycardia
Occurs during sleep
Common in well-conditioned athletes
Present in up to 35% of people under 25 years of age while at rest
265
Abnormal Causes of Sinus Bradycardia
Inferior/Posterior MI
Disease of SA node
Hypoxia, hypothermia, hypokalemia, hypothyroidism
Increased ICP
Sleep apnea
CCBs, digitalis, beta-blockers, amiodarone, sotalol
266
Treatment of Sinus Bradycardia
No treatment if not symptomatic
Oxygen, IV access, atropine, TCP
267
Signs and Symptoms of Hemodynamic Compromise Related to Sinus Brady
Changes in mental status
Low blood pressure
Chest pain, SOB, signs of shock
CHF, pulmonary congestion, decreased urine output
Cold, clammy skin
268
Sinus Tachycardia
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
ECG Characteristics of Sinus Tachycardia
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
Causes of Sinus Tachycardia
Exercise, fever, pain, fear, hypoxia
CHF, acute MI, infection, shock
PE
Epinephrine, atropine, dopamine, nicotine, cocaine
271
Treatment of Sinus Tachycardia
Fluid replacement
Relief of pain
Removal of offending medications or substances
Reducing fever or anxiety
272
Sinus Arrhythmia
When the SA node fires irregularly
273
Respiratory Sinus Arrhythmia
Associated with the phases of respiration and changes in interthoracic pressure
274
Nonrespiratory Sinus Arrhythmia
Not related to the respiratory cycle
275
ECG for Sinus Arrhythmia
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
Atrial Dysrhythmias
Lose the "atrial kick"
Some are associated with extremely fast ventricular rates
An excessively rapid HR may compromise cardiac output
Affects P wave
277
Premature Complexes
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
Premature Atrial Complexes
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
How to Recognize PACs
Irregular rhythm
May occur because of emotional stress, CHF, fatigue, atrial enlargement, digitalis toxicity, hypokalemia
280
Atrial Flutter
Ectopic atrial rhythm in which an irritable site fires regularly at an extremely rapid rate
281
ECG for Atrial Flutter
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
Atrial Fibrillation
Can occur in patients with or without detectable heart disease or related symptoms
Increased stroke risk
283
ECG for Atrial Fibrillation
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
Conditions Associated with Atrial Fibrillation/Atrial Flutter
HTN, ischemic heart disease, CHF, pericarditis
Diabetes, stress
Hypoxia, hypokalemia, hypoglycemia
285
What to do with Atrial Fibrillation/Atrial Flutter
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
Supraventricular Tachycardia
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
ECG for Supraventricular Tachycardia
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
Causes of Supraventricular Tachycardia
Acute illness with excessive catecholamine release
Digitalis toxicity
Heart disease
Infection
Hypoxia
PE
Stimulant use
289
Supraventricular Tachycardia Assessment Findings
Acute changes in mental status
Asymptomatic
Dizziness, dyspnea, fatigue
Fluttering in the chest
Hypotension
Palpitations
Signs of shock
290
Interventions for Supraventricular Tachycardia
Apply pulse oximeter and administer oxygen if indicated
Obtain vital signs
Establish IV access
Obtain 12-lead EKG
291
ECG for Junctional Rhythm
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
Causes of Junctional Rhythm
Increases parasympathetic tone
Immediately after cardiac surgery
Digitalis, Quinidine, Beta-Blockers, CCBs
Acute myocardial infarction
Rheumatic heart disease
SA node disease
Hypoxia
293
Interventions for Junctional Rhythm
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
Ventricular Rhythms
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
Premature Ventricular Contractions
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
ECG for PVCs
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
Patterns of PVCs
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
Uniform/Monomorphic PVCs
Premature ventricular beats that look the same in the same lead and originate from the same anatomical site
299
Multiform/Polymorphic PVCs
PVCs that appear different from one another in the same lead
Often arise from different anatomical sites
300
R-on-T PVCs
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
Causes of PVCs
LOW POTASSIUM, LOW MAGNESIUM
Acid-base imbalances
Acute coronary syndromes
Cardiomyopathy
Digitalis toxicity
Electrolyte imbalances
Exercise
Heart failure
Hypoxia
Stimulants
Ventricular aneurysm
302
Ventricular Tachycardia
VT exists when three or more PVCs occur in a row at a rate of more than 100 beats per minute
303
Nonsustained VT
A short run lasting less than 30 seconds
304
Sustained VT
Persists for more than 30 seconds
305
ECG for Ventricular Tachycardia
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
Causes of Ventricular Tachycardia
Acid-base imbalances
Acute coronary syndromes
Cocaine abuse
Electrolyte imbalances
Mitral valve prolapse
Trauma
Tricyclic antidepressant overdose
307
Interventions for Pulseless Patient with VT
CPR and defibrillation
308
Interventions for Patient with a Pulse and VT
Stable: oxygen, IV access, ventricular antidysrhythmics
Unstable: oxygen, IV access, sedation, defibrillation, CPR
309
Polymorphic VT
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
Causes of Polymophic VT
Magnesium deficiency
Congenital
Hypokalemia
311
Ventricular Fibrillation
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
ECG for VF
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
Causes of Ventricular Fibrillation
Acute coronary syndromes, dysrhythmias, electrolyte imbalances, hypertrophy, severe heart failure, vagal stimulation
314
Pulseless Electrical Activity
Organized electrical activity is observed on the cardiac monitor but the patient is unresponsive, is not breathing, and has no pulse
315
Interventions for Pulseless Electrical Activity
CPR, oxygen, start an IV
Advanced airway
316
Asystole
Total absence of ventricular electrical activity
There is no ventricular rate or rhythm, no pulse, and no cardiac output
317
ECG of Asystole
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
PATCH-4-MD
```
PE
Acidosis
Tension pneumothorax
Cardiac tamponade
Hypovolemia
```
Hypoxia
Heat/cold
Hypokalemia
Hyperkalemia
MI
Drug overdose
319
Normal BUN
8-21
320
Normal Creatinine
0.8-1.3
321
Normal Glucose
65-110
322
Normal Calcium
8.5-10.2
323
Normal Magnesium
1.5-2
324
Normal Phosphate
0.8-1.5
325
Normal Sodium
135-145
326
Normal Hemoglobin
13-17 in men
12-15 in women
327
Normal Hematocrit
40-52% in men
36-47% in women
