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YEAR 3 > NURS 332 > Flashcards

NURS 332 Flashcards

1
Q

Trauma Process Steps

A
  1. Prep and triage
  2. General impression
  3. Primary survey
  4. Secondary survey
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2
Q

Primary Survey

A

A: Alertness & airway
B: Breathing & ventilation
C: Circulation & control of hemorrhage
D: Disability (neuro status)
E: Exposure & environment control
F: Full set of vitals and family presence
G: Get adjuncts & give comforts

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3
Q

Secondary Survey

A

H: History
H: Head-to-toe assessment
J: Just keep re-evaluating

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4
Q

AVPU

A

Alert, Verbal, Pain, Unresponsive

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5
Q

A: Alertness & airway - Assessment

A

AVPU, airway patency, cervical spine immobilization

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6
Q

A: Alertness & airway - Interventions

A

Jaw-thrust maneuver, oro/nasopharyngeal airway (OPA/NPA), endotracheal tube (ETT)

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7
Q

Ensuring ETT placement

A

1) CO2 detector (purple = good, 35-45mmHg)
2) Chest rise/fall observation
3) Auscultate epigastrium & bilateral breath sounds

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8
Q

B: Breathing & Ventilation

A

Breath sounds, depth, rate and pattern, work of breathing, dyspnea, spontaneous breathing, subcut emphysema (rice krispy), tracheal deviation (LATE)

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9
Q

C: Circulation and control of hemorrhage - Assessment

A

Color, temp, central pulse, control hemorrhage

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10
Q

C: Circulation and control of hemorrhage - Interventions

A

Torniquet, multiple IV’s running WARM fluids

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11
Q

D: Disability (neurological status)

A

GCS - eyeopening, verbal response, motor response
AVPU
Pupils
Glucose (BGM)

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12
Q

E: Exposure & environment control

A

Remove clothing (injuries), warming measures (blankets, increased room temp, warm fluids)

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13
Q

G: Get adjuncts & give comfort

A

L: Lab analysis
M: Monitor cardiac - 12-lead ECG
N: Naso/Orogastric tube to pump stomach
O: Oxygenation & capnography
P: Pain

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14
Q

H: History

A

S: S&S
A: Allergies
M: Meds
P: Past medical hx
L: Last oral intake/LMP
E: Event leading up

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15
Q

H: Head-to-toe Assessment

A

Optimize resps & cardiac function
Anterior and posterior assessment

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16
Q

J: Just keep re-evaluating

A

V: VS
I: Injury & Interventions
P: Primary survey
P: Pain

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17
Q

CTAS Triage

A

1) Resuscitation
2) Emergent
3) Urgent
4) Less Urgent
5) Non-Urgent

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18
Q

1: Resuscitation

A

Threats to life or limb that need immediate interventions - trauma, car accident, heart stopped

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19
Q

2: Emergent

A

Potential threats to life or limb/require rapid interventions (trauma, suspected MI, trouble breathing)

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20
Q

3: Urgent

A

Potentially lead to a serious problem (fainting, mod trauma, head injury, asthma attack, seizures, temp > 40)

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21
Q

4: Less Urgent

A

Relate to a potential deterioration (minor trauma, sore eye/ear/throat, stitches, small fracture)

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22
Q

5: Non-Urgent

A

May be acute but non-urgent. Interventions can be safely delayed (minor trauma, prescription renewal, cold)

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23
Q

Disaster Management

A

RPM-30-2-Can-Do

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24
Q

RPM-30-2-Can do

A

R: Resps < 30
P: Perfusion - cap refill <2
M: mental status - can do commands

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25
Q

Black Triage Tag

A

Expectant - unlikely to survive

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26
Q

Red Triage Tag

A

Need immediate intervention, compromised ABC’s

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27
Q

Yellow Triage Tag

A

Can be delayed, potentially life threatening

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28
Q

Green Triage Tag

A

“Walking wounded”, unlikely to deteriorate

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29
Q

Normal pH

A

7.35-7.45

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30
Q

Normal PCO2 (partial pressure of CO2)

A

35-45mmHg

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31
Q

Normal Bicarbonate (HCO3-)

A

22-28mmol/L

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32
Q

Normal PaO2 (partial pressure of oxygen)

A

80-100mmHg

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33
Q

Low pH

A

Acidic

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34
Q

High pH

A

Alkalotic

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35
Q

Low PaCO2

A

Alkalotic

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36
Q

High PaCO2

A

Acidic

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37
Q

Low HCO3-

A

Acidic

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38
Q

High HCO3-

A

Alkalotic

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39
Q

Low PaO2

A

Hypoxemic

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40
Q

Respiration

A

Sequence of events that results in exchange of O2 & CO2 between atmosphere and body cells = WHOLE PROCESS

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41
Q

Ventilation

A

Flow of air in & out of alveoli (mechanical aspect)

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42
Q

Ventilation 3 Components

A

1) Mechanical movement
2) Air flows from higher-lower pressure
3) Dependent upon volume, disease, and position

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43
Q

Capnography

A

ETCO2 - measures “end-tidal” CO2 exhaled

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44
Q

Diffusion

A

Movement of gases (O2 & CO2) across permeable membrane from high-low pressure
Dependent upon pressure difference, SA, and wall thickness

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45
Q

Hemoglobin Components

A

Heme, protein, iron

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46
Q

Hemoglobin function

A

Carries oxygen in blood - has a high affinity (attraction) to O2

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47
Q

Normal Hemoglobin in Female

A

120-150mg/dl

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48
Q

Normal Hemoglobin in Male

A

135-170mg/dl

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49
Q

SpO2

A

% of oxygen-saturated HGB in capillary bed (>94%)

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50
Q

SaO2

A

% of oxygen-saturated HGB in arterial blood (>95%)

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51
Q

PaO2

A

Partial pressure of oxygen (amount of O2 dissolved in plasma) (80-100mmHg)

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52
Q

Hypoxemia

A

Low blood PaO2 level (<50mmHg)

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53
Q

Hypoxia

A

Inadequate cellular O2 = anaerobic metabolism

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54
Q

Oxyhemoglobin dissociation curve

A

Relationship between PaO2 and HGB molecule sat
When HGB is 50% saturated with oxygen, PaO2 is 27mmHg

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55
Q

LEFT shift on dissociation curve

A

Haldane: HGB holding oxygen TOO TIGHT - tissues are not getting enough

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56
Q

RIGHT shift on dissociation curve

A

Bohn: HGB not holding oxygen tight enough - tissues are getting oxygen, but SpO2 is falsely low

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57
Q

Perfusion

A

Arterial blood flow (peripheral or central)

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58
Q

3 P’s of Perfusion

A

PUMP (heart)
PIPES (vasculature)
PLASMA (blood)

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59
Q

VQ mismatch

A

When ventilation (V) does not match perfusion (Q) - ex. lung receives oxygen without blood flow OR lung receives blood flow but no oxygen

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60
Q

Oxygenation

A

The result of perfusion, ventilation, and diffusion

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61
Q

FiO2

A

Fraction of Inspired Oxygen
RA: 0.21 (21%)

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62
Q

Nasal Prong oxygen delivery

A

Adds 3% FiO2 (0.24), up to 6L/min

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63
Q

Simple mask oxygen delivery

A

Adds 40-60% FiO2 (0.61-0.81), up to 8-10L

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64
Q

Non-re-breather oxygen delivery

A

Adds 80-95% FiO2, 10-15L/min

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65
Q

High Flow & ETT ventilation oxygen delivery

A

Adds 21-100% FiO2

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66
Q

Respiratory Acidosis ABG Characteristics

A

CO2 HIGH

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67
Q

Metabolic Acidosis ABG Characteristics

A

HCO3- LOW

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68
Q

Respiratory Alkalosis ABG Characteristics

A

CO2 is LOW

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69
Q

Metabolic Alkalosis ABG Characteristics

A

HCO3- HIGH

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70
Q

Respiratory Acidosis

A

Retention of CO2 - CNS depression, neuromuscular disorder, obstructive lung disease

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71
Q

Metabolic Acidosis

A

Gain of Acid (H+) - DKA, lactic acidosis
Loss of base (HCO3-)
Inability to excrete acid

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72
Q

Respiratory Alkalosis

A

Excretion of CO2 - CNS hyperactivity (anxiety, fever, pain), hypoxemia increased ICP

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73
Q

Metabolic Alkalosis

A

Loss of acid (H+) - vomiting, increased aldosterone, total volume loss, admin of NaHCO3

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74
Q

Acidosis Effects on Heart

A

Decreased contractility = decreased CO = hypotension
Increased vasodilation = hypotension
Increase HR = vtach arrhythmia

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75
Q

Alkalosis Effects on Heart

A

Increased vasoconstriction
Increased HR = vtach arrhythmias, vfib, SVT

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76
Q

Acidosis Effects on Lungs

A

Increased RR - increased WOB = fatigue

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77
Q

Alkalosis Effects on Lungs

A

Decreased RR = hypoxemia

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78
Q

Acidosis Effects on Metabolic

A

Increased H+ move into cells - increase K+ (arrhythmias)
H+ alter ability of insulin on tissues (increase resistance, increased BGM)

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79
Q

Alkalosis Effects on Metabolic

A

Decreased K+ and Mg

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80
Q

Acidosis Effects on CNS

A

Altered mental status - COMA

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81
Q

Alkalosis Effects on CNS

A

Altered mental status - COMA
Seizures, tetany

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82
Q

Lung compensation for acidosis

A

Increased rate and depth of ventilation - attempt to rid body of CO2

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83
Q

Lung compensation for alkalosis

A

Decreased rate and depth of ventilation - retain CO2

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84
Q

Kidney compensation for acidosis

A

Kidney’s excrete H+ and conserve HCO3-

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85
Q

Kidney compensation for alkalosis

A

Kidney’s retain and excrete HCO3-

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86
Q

Uncompensated ABG Characteristics

A

pH normal, 1 abnormal and 1 normal value (opposite system has NOT compensated)

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87
Q

Partially compensated ABG characteristics

A

pH abnormal, 2 abnormal values (opposite system attempting to compensate)

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88
Q

Fully compensated ABG characteristics

A

pH normal, 2 abnormal values (opposite system has compensated enough to normalize pH)

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89
Q

Restrictive Pulmonary Disorder

A

Reduced total lung capacity = loss of lung volume = compromised oxygenation

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90
Q

Extra-pulmonary causes

A

obesity, flail chest, muscular dystrophy

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91
Q

Internal-pulmonary causes

A

pneumonia, HF, pneumothorax

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92
Q

Obstructive Pulmonary Disorder

A

Air moves in and out at a reduced rate = air trapped = compromised oxygenation

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93
Q

Flow of Obstructive Disorders

A
  1. air flows into lungs & gets trapped
  2. difficult to exhale because alveoli can’t empty, CO2 trapped in lungs
  3. Airway narrowing
  4. Airway obstruction
  5. Hyper-inflated lungs & decreased elastic recoil
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94
Q

Cues of Obstructive Disorders

A

Increased lung expansion, decreased expiratory flow, decreased FEV, normal to increased TLC, increased FRV, decreased VS, chronic abnormal ABG’s (increased PCO2, normal HCO3-, normal pH or slightly acidic, decreased PO2)

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95
Q

Asthma Control Steps

A
  1. SABA
  2. SABA, daily LTRA and SLIT
  3. SABA, ICS, LTRA, or SLIT
  4. SABA, medium dose ICS, LAMA, SLIT
  5. SABA, further assessment, LAMA, ICS, LTRA
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96
Q

Status Asthmaticus Cues

A

Unable to speak, drowsy/coma, poor respiratory effort, bradycardia, paradoxical thoracoabdominal breathing, silent chest, cyanosis and O2 sats < 92%

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97
Q

Major features of status asthmaticus

A

Pulsus paradoxus, accessory muscle use (labored), lung hyperinflation, ABG showing hypoxemia (low PO2), sudden decrease of wheezing or decreased breath sounds

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98
Q

Acute exacerbation of COPD Symptoms

A

Worsened dyspnea, cough of sputum production - decreased SpO2

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99
Q

Primary causes of acute exacerbation of COPD

A

Infection (viral or bacterial) vs non-infective (environmental trigger)

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100
Q

Secondary causes of acute exacerbation of COPD

A

Pneumonia, PE, CHF, pneumothorax, rib fractures, opioid/sedative use, beta-blockers

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101
Q

Management of COPD exacerbation

A

Systemic corticosteroids

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102
Q

Pneumonia

A

Acute infection of pulmonary parenchyma that is associated with:
at least 2 symptoms (fever, chills, new cough, CP, SOB) AND crackles/bronchial lung sounds AND new opacity/consolidation on CXR

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103
Q

Treatment of Impaired gas exchange

A

antibiotics, support O2 needs, support cardiac status, remove exudate

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104
Q

Complications of pneumonia and impaired gas exchange

A

Empyema, pleural effusion, atelectasis, delayed resolution, abscess, pericarditis/endocarditis, sepsis/bacteremia

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105
Q

Empyema

A

Collection of puss

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106
Q

Pleural Effusion

A

Collection of fluid in pleural cavity

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107
Q

Atelectasis

A

Collapse in certain areas of the lungs

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108
Q

Complications of COVID pneumonia

A

Sepsis, thrombotic event, ARDS, myocardial injury, hypoxic resp failure, AKI, multisystem organ failure

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109
Q

Acute PE

A

Condition of impaired perfusion
large thrombi obstruct perfusion in pulmonary artery - blockage - increased pressure and resistance - increased RV workload - decreased lung perfusion

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110
Q

Diagnosis of PE

A

D-dimer, CT, MRI, VQ scan, CXR, TTE, ABG’s

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111
Q

D-dimer

A

Indicates clot but does not show where it is

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112
Q

Virchow’s Triad

A

1) Hypercoaguable state
2) Venous stasis
3) Vessel Injury

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113
Q

Treatment of PE

A

High-flow O2, mechanical ventilation, vena-cava filter (for prevention if at high risk), embolectomy, anticoagulants, thrombolytic/fibronolytic

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114
Q

Respiratory failure

A

When compensation STOPS working
1) Resp distress/insufficiency
2) Acute resp failure (2 types)
3) Respiratory arrest

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115
Q

Types of Acute resp failure

A
  1. Oxygenation failure (PO2 < 60)
  2. Ventilation failure (PCO2 > 50 and pH <7.35)
    Usually a mix of BOTH types
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116
Q

Whole Process of resp distress and failure

A

1) disease process affects normal lung function
2) VQ mismatch and decreased PaO2
3) Body increases RR and depth
4) Increased PaO2 and decreased PaCO2
5) Compensation increases metabolic rate = increased oxygen consumption and decreased CO2 production

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117
Q

Clinical criteria of Resp failure

A

PaCO2 > 50 AND pH < 7.30, PaO2 < 60

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118
Q

Oxygen Failure Pulmonary Cues

A

Dyspnea, tachypnea, increased PVR

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119
Q

Oxygen failures CV cues

A

Increase BP & HR, dysrhythmias, weak thready pulse, cyanosis

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120
Q

Oxygen failure CNS cues

A

Altered LOC, restlessness, confusion

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121
Q

Ventilation failure pulmonary cues

A

Tachypnea OR bradycardia

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122
Q

Ventilation failure CV cues

A

Bounding pulse, increase BP & HR

123
Q

Ventilation failure vascular cues

A

Headache, flushed & wet skin

124
Q

Ventilation failure CNS cues

A

Lethargy, drowsiness, coma

125
Q

Color of Pt in Resp failure

A

Cyanotic, grey, mottled

126
Q

RR of Pt in resp failure

A

high (to compensate) and then low when tired

127
Q

Breath sounds of pt in resp failure

A

None = WORST - no O2 flow

128
Q

BP of pt in resp failure

A

high to compensate, then low when tired

129
Q

HR of pt in resp failure

A

high to compensate, then low when tired

130
Q

Interventions for Resp failure

A

maintain airway oxygenate, correct acid-base imbalances, support systems (fluids and electrolytes), treat the cause, control complications

131
Q

Acute Respiratory Distress Syndrome (ARDS)

A

Lung damage causes sudden onset of resp failures

132
Q

ARDS criteria

A
  1. Within 1 week of insult/worsened resp symptoms
  2. Bilateral opacities with no explanation
  3. Resp failure NOT explained by cardiac/fluid overload
  4. PEEP > 5, hypoxemia even with 100% FiO2
133
Q

Bipap

A

Non-invasive positive pressure vent, 2 pressure settings

134
Q

CPAP

A

continuous positive airway pressure, 1 pressure setting

135
Q

Pericardium

A

Outermost layer, protects the heart. 2 layers - fibrous and serous

136
Q

Epicardium

A

Visceral surface of the pericardium

137
Q

Myocardium

A

Middle layer of thick muscular tissue. Does the major pumping action

138
Q

Endocardium

A

Thin layer of endothelium and connective tissue - lines the valves

139
Q

4 Chambers of the Heart

A

Right atrium, Right ventricles, left atrium, left ventricle

140
Q

4 Valves

A

AV: tricuspid and mitral (atria to ventricle)
SL: pulmonic and aortic (ventricle to body)

141
Q

Coronary Arteries

A

Supplying and draining surfaces of the heart.

142
Q

Major Coronary Arteries

A

Right coronary artery (RCA)
Left main/Left coronary artery
- Left anterior descending (LAD)
- Left circumflex (LCX)

143
Q

Hemodynamics

A

Study of flowing blood and of all the solid structures (such as arteries) through which it flows

144
Q

Cardiac Output

A

Amount of blood the heart pumps each minute
= HR x SV

145
Q

Components of stroke volume

A

Preload
Contractility
Afterload

146
Q

Stroke Volume

A

Amount of blood ejected from the heart (LV) with each pump

147
Q

Preload

A

Filling - pressure in the myocardial fibers at end of diastole

148
Q

Contractility

A

Force/strength of the myocardial contraction

149
Q

Afterload

A

Pressure/resistance which the ventricles pump to eject blood

150
Q

Ejection Fraction

A

Amount of blood expelled with each contraction (50-80%)

151
Q

Frank Starling Law

A

The more the heart is filled during diastole, the more forcefully it contractions
More fill = stronger contraction

152
Q

What Systems regulate CO?

A

Autonomic nervous system (ANS) and Kidneys (RAAS)

153
Q

MAP

A

Mean Arterial Pressure - high BP = high map because of increased afterload
CO x SVR

154
Q

Arterial Line indications

A

Need for continuous BP monitoring (hemodynamic instability, vasopressor requirement)
Frequent ABG draws

155
Q

Arterial Line complications

A

Hemorrhage, hematoma, thrombosis, embolization, infection

156
Q

Measuring Preload

A

Right-sided heart pressure
CVP/RAP: amount of fluid in the right side of the heart, can be measured through a CVL
NORMAL = 2-5mmHg

157
Q

Pulmonary Artery Catheter

A

Measures CVP, PAP, PAWP, CO - very invasive, not used often

158
Q

PAS

A

Higher pressure in systole (contracting)
normal: 20-30mmHg

159
Q

PAD

A

Lower pressure in diastole (relaxing)
Normal: 10mmHg

160
Q

Pulmonary Artery Wedge Pressure (PAWP)/Pulmonary Artery Occlusion Pressure (PAOP)

A

Reflects pressure in the left side of the heart (left filling)
Normal: 5-12mmHg

161
Q

S&S of decreased CO

A

Delayed cap refill, tachycardia, weak pulses, hypotension, decreased urinary output, altered LOC

162
Q

Types of Heart Failure

A

Left-sided (CHF)
Right sided
High-Ouptut

163
Q

Typical causes of HF

A

Cardiomyopathy (HTN, diabetes, valve disease, PV disease), CAD, dysrhythmias, rheumatic fever, cardiotoxic agents, substance misuse

164
Q

Left-Sided HF - Systolic

A

LV not sending much blood through, causing pooling and backup in aorta (blood “backs up” into pulmonary system)

165
Q

Left-Sided HF diastolic

A

The LV loses ability to relax - STIFF (cannot fill)

166
Q

Right-Sided HF

A

Result of Left HF, increases lung pressure (pulmonary HTN) or RV problems, blood flow backs up into peripheral system - right side gets tired

167
Q

Compensatory Mechanism - SNS stimulation

A

Decreased CO stimulates increased HR and increase BP by vasoconstriction

168
Q

Compensatory Mechanism - RAAS activation

A

NOT HELPFUL - senses decreased CO, increases preload and afterload which affects contraction - BAD because there is not enough blood to be pumped effectively

169
Q

HF affects on heart itself

A

Muscle layer increases to try to compensate - hypertrophy. This is temporarily effective, BUT oxygen needs of the heart increase and needs more blood. If not getting blood, it causes cell death and the heart fails again.

170
Q

BNP in HF

A

Release from ventricles when overloaded/stretched - KEY

171
Q

Serum Electrolytes in HF

A

Fluid shifts, diuretics - increase Na

172
Q

Urea and Creatinine in HF

A

RAAS - kidneys become damaged - urea and creatinine increase

173
Q

HGB/HCT in HF

A

Effect on kidneys lead to reduced erythropoietin albuminuria - lower RBC’s and HGB

174
Q

Albuminuria in HF

A

Decrease heart compliance

175
Q

Echocardiogram in HF

A

Visualizes valves, pericardial effusion, chamber enlargement, thickness of walls, ejection fraction

176
Q

CXR in HF

A

Cardiomegaly (enlargement of the heart, pulmonary edema)

177
Q

ABG in HF

A

Hypoxemia - impaired diffusion

178
Q

HF Acute Management - A&B

A

Intubation, Oxygenation (FiO2, increased pressure, and diuretics), Diuresis (removed excess fluid)

179
Q

HF Acute Management - C

A

Optimize hemodynamics
Increase contractility
Vasodilation - reduce afterload/preload
Regulate HR

180
Q

Reducing Preload in HF

A

Fluid management - fluid and salt restrictions , serum electrolytes, BUN, creatinine, positioning. Diuretics (loop - furosemide, thiazide - spironolactone, SGLT2i - sodium glucose cotransporter - 2 inhibitors)

181
Q

Reducing Afterload

A

Improving contractility - ACE/ARB (stop RAAS from being activated), beta blockers (increase contractility and decrease HR), Nitrates (vasodilate), inotropes (increase contractility - digoxin), amiodarone (HR control and arrhythmias control), ICN (decrease HR)

182
Q

Ventricular Assist Device - LVAD

A

Used as a bride to transplant - external pump/ventricle (circulates blood externally)

183
Q

S&S of Pulmonary Edema

A

Pink frothy sputum, acute resp deterioration, decreases sats, SOB

183
Q

Treatment of Pulmonary Edema

A

IVP furosemide - works quickly

184
Q

S&S of RIGHT sided failure

A

Peripheral Edema, JVD

185
Q

Biventricular failure S&S

A

JVD, 2+ edema in feet and ankles, swollen hands and fingers, distended abdomen, bibasilar crackles, productive cough with pink-tinged sputum

186
Q

Endocarditis

A

Disease of the valves and chambers

187
Q

Causes of infective endocarditis

A

Microbial infection - IV drug use, valve replacements, altered immunity, structural heart defects, dental procedures, hemodialysis, infections

188
Q

Infective Endocarditis Pathophysiology

A

1) organism adheres to valve surface - disturbed surface of endothelium attracts platelets
2) introduction of bacteria in blood
3) bacteria settle on thrombi of heart valve
4) Forms vegetations (become like emboli)
5) Vegetations enlarge and alter valve function

189
Q

IE - Septic vegetations on right side of heart

A

Lodged in pulmonary system - PE

190
Q

IE - septic vegetations on left side of heart

A

Lodged all over body - brain, liver, etc.

191
Q

Types of Valvular disease

A

Stenosis, insufficiency, prolapse

192
Q

Stenosis in Valves

A

tissue thickening narrows valve opening - risk of clots

193
Q

Insufficiency in valves

A

allows for backflow /regurgitation - incomplete valve closure

194
Q

Causes of Valvular disease

A

degeneration (weakens with age), calcific degeneration, IE, CAD, MI

195
Q

Potential Complications of valvular disease

A

Arrhythmias, CMO, HF, thrombotic disorders

196
Q

Mitral Valve Prolapse

A

Usually benign - can progress to regurgitation
One of the mitral leaflets is slightly curved the wrong way and allows some back flow

197
Q

S&S Mitral Valve Prolapse

A

“Click murmur” - systolic murmur
Palpitations or chest pain

198
Q

Aortic valve prolapse

A

Valve doesn’t close completely during diastole, so back flow into LV happens
diastolic murmur

199
Q

Stenosis of a valve

A

Hardening/thickening of the valve caused by fibrosis or calcification - valve leaflets fuse (stiff and narrow)

200
Q

Mitral Valve stenosis

A

Narrow valve opening obstructs BF from LA to LV (pressure increases, left atrium dilates, PAP increases, rt ventricle hypertrophy)
- rt HF, diastolic murmur

201
Q

Aortic Valve stenosis

A

narrow valve opening obstructs BF from LV to aorta during systole
“wear and tear”
Left HF, systolic murmur

202
Q

Treatment of valve stenosis

A

Valve repair/replacement, medication for symptoms, management of HF

203
Q

Bicuspid aortic valve

A

Most common congenital cardiac malformation - 2 leaflets instead of 3

204
Q

Complications of bicuspid aortic valve

A

HF, aortic aneurysm and dissection, stenosis or regurgitation

205
Q

3 main cues of IE

A

Fever, NEW murmur, fatigue

206
Q

Evidence of systemic embolization

A

Petechiae, janeway lesions (flat, painless reddened maculae on hands and feet) , splinter hemorrhages (nail beds), osler nodes (painful on palms of hands and soles of feet), roth spots (hemorrhagic lesions that appear as round or oval spots on retina)

207
Q

Prosthetic (synthetic/artificial) valve replacement

A

Lifelong anticoagulation with warfarin

208
Q

Bioprosthetic (tissue)

A

No long-term anticoagulation, not as durable (last about 7-8yrs)

209
Q

2 types of myocardial cells

A

electrical (pacemaker), mechanical cell

210
Q

Electrical (pacemaker) cells

A

Generation and conduction of electrical impulses

211
Q

Mechanical cell

A

do actual pumping by contracting and relaxing - dependent on electrical stimulus

212
Q

Sinoatrial (SA) node

A

Primary pacemaker cell - responds to needs of body and controls beat based on info it receives from nervous, circulatory, and endocrine systems

213
Q

AV node

A

Receives signal from SA node (through 3 pathways) and slows the conduction from the atria to the ventricles long enough for atrial contraction (supplied by RCA)

214
Q

Bachmans bundle

A

Bundle in LA

215
Q

SA node intrinsic rate

216
Q

AV junction intrinsic junction

A

40-60 (if SA fails)

217
Q

Purkinje fibers instrinsic rate

A

20-40 (if AV fails)

218
Q

Cardiac conduction

A

calcium, magnesium, potassium, sodium are used to develop “electricty”

219
Q

Phase 0 of cardiac conduction

A

Depolarization, influx of Ca and Na

220
Q

Phase 1 of cardiac conduction

A

Na channels close, hits “peak”

221
Q

Phase 2 cardiac conduction

A

Influx of Ca, K slowly trickles out - prolonged depolarization

222
Q

Phase 3 of cardiac conduction

A

rapid depolarization, decrease in K and Ca channels close - back to resting potential

223
Q

Phase 4 cardiac conduction

A

Resting potential - leaky K channels, can not be activated again - negative

224
Q

Phase 0-3 of cardiac conduction

A

Positive - in refractory period, cannot be activated

225
Q

Depolarized

A

Stimulation - negative space letting positives in

226
Q

Repolarizing

A

Resting - becomes more negative - when negative enough, it can be stimulated again

227
Q

ECG paper

A

Small box = 0.04 seconds
Big box (5 little ones) = 0.2 seconds
Each lead = 2.5 seconds, full ECG = 10 seconds

228
Q

Isoelectric line

A

Baseline of ECG

229
Q

P wave

A

ATRIAL DEPOLARIZATION - atrial filling
0.08-0.11 seconds, spread of electrical impulse that depolarizes atria

230
Q

PR Interval

A

0.12-0.2 seconds

231
Q

PR segment

A

AV node delaying electrical impulse

232
Q

QRS

A

VENTRICAL DEPOLARIZATION
<0.12 seconds
Spread of electrical impulse that depolarizes ventricles, atria repolarizes during this time

233
Q

J point

A

Where S stops and ST segment begins

234
Q

ST segment

A

Should be neutral (on isoelectric line)

235
Q

T wave

A

VENTRICULAR REPOLARIZATION
ventricles relax

236
Q

QT interval

A

total time of ventricular depolarization and repolarization - we only care if this is too long

237
Q

6 Step ECG reading

A

1: rate (fast/slow?, intervals?)
2: rhythm (regular? wide/narrow WRS? p-wave?)
3: p=waves (upright? uniform? prior to WRS?)
4: PR interval (0.12-0.20 seconds, prolonged = blockage)
5: QRS (< 0.12 seconcds, wide ventricles = bad)
6: interpret

238
Q

R-R interval

A

Ventricular BPM

239
Q

Sequence Method

A

Select R wave on dark pink line - next dark line as shows 300, 150, 100, 75, 60 and 50 (where next r wave finds, that is the HR)

240
Q

Bundle Branch Block

A

Functional or pathological block in one of the major branches of intraventricular conduction system - ventricles NOT depolarized simultaneously (using detour because main highway is blocked)

241
Q

Hypokalaemia on ECG

A

T-wave inversion, ST depression, prominent U wave

242
Q

Hyperkalemia on ECG

A

Peaked T waves, P wave flattening, PR prolongation, wide QRS

243
Q

S&S of Dysrrhythmias

A

Vitals: fluctuating HR, increased RR, low SpO2
Lungs: crackles if fluids backed up
Heart sounds: may hear S3 and S4
PV: slow CO (> cap refill, weak pulses)
Pulse deficit: difference in apical and radial pulse

244
Q

SINUS

A

Originates from SA node

245
Q

Normal Sinus Rhythm

A

Rate: atrial and ventricular rates 60-100
Rhythm: atrial and ventricle rhythms regular
P waves: present, upright, consistent configuration, 1 p-wave before each QRS
PR interval: 0.12-0.2 seconds, constant
QRS duration: 0.06-0.12 seconds, constant

246
Q

Sinus Bradycardia

A

Everything normal on ECG EXCEPT HR is < 60 BPM

247
Q

Sinus Tachycardia

A

Everything normal on ECG EXCEPT HR >100BPM

248
Q

Premature Atrial Contraction (PAC)

A

Atrial tissue fires an impulse before the next sinus impulse is due - triggers ventricles responding sooner than expected (QRS fires too fast on ECG)

249
Q

Causes of PAC

A

Stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, drugs.

250
Q

Atrial Flutter

A

Too many P waves - saw-toothed /flutter waves - atrium continuously contracting, ventricles always getting a stimulus but only contract (QRS) when they are repolarizedT

251
Q

Treatment of atrial flutter

A

Beta-blockers, ca channel blockers, cardiovert, ablations

252
Q

Biggest Complication of atrial flutter

A

risk of clot due to stasis.

253
Q

ECG characteristics of atrial fibrillation

A

rate - hard to calculate
rhythm - irregular
ration - multiple p waves

254
Q

What is the most common sustained arrhythmias

A

Atrial fibrillation

255
Q

Atrial fibrillation ECG

A

Indiscernible P waves (no PR interval, normal QRS, ventricles are irregular rhythm)

256
Q

Atrial fibrillation Complications

A

decreased SV by 25%, potential for clots and HF

257
Q

Treatment for atrial fibrillation

A

Anticoagulants, beta-blockers, ca channel blockers, antiarrhythmics (digoxin)

258
Q

Supraventricular Tachycardia (SVT)

A

Originated in AV node, NO P waves (can’t see them) - AV getting stimulated too fast, normal QRS, rate 150-250

259
Q

Treatment for SVT

A

Modified valsava maneuver, beta blockers, ca channel blockers, antiarrhythmics, IV adenosine

260
Q

IV Adenosine

A

Stop electrical impulses in the heart to allow SA to start firing again

261
Q

Premature Ventricular Contraction (PVC)

A

Result of increased irritability of ventricular cells - signal coming from ventricles instead of atria
NO p waves before QRS

262
Q

R-on-T phenomenon

A

BAD - v-tach from improperly timed electrical impulses on later part of the T wave (ventricular repolarization)

263
Q

PVC bigeminy

A

Every second (normal, PVC)

264
Q

PVC trigeminy

A

Every third (normal, normal, PVC)

265
Q

Unifocal PVC

A

Single irritable focus - all look the same

266
Q

Multifocal PVC

A

Multiple irritable foci - all look different

267
Q

Ventricular Tachycardia

A

3 or more consecutive PVCs occurring rapidly, 100-200bpm, no P waves

268
Q

Torsades de points

A

Polymorphic - smaller and bigger pattern (not consistent) - give IV magnesium

269
Q

Sustained V tach

A

If for > 30 seconds

270
Q

Non-sustained v tach

A

anything less than 30 seconds

271
Q

Treatment for v tach

A

CPR and defibrillation if pulse is lost, antiarrhythmics

272
Q

Ventricle Fibrillation

A

Electrical chaos in ventricles

273
Q

Course v fib

A

Bumpy on ECG

274
Q

Fine v fib

A

smoother on ECG

275
Q

Asystole

A

Cardiac standstill, complete stop of electrical impulses (no rate or rhythm or CO or pulse)

276
Q

Pulseless Electrical Activity (PEA)

A

Any organized rhythm without a central pulse (pt always unresponsive)

277
Q

S&S of decreased CO due to arrhythmias

A

Weak, lightheaded, chest pain, delayed cap refill, palpitations, change in LOC, resp distress or apnea

278
Q

Algorithm for symptomatic bradycardia

A

HR <60 AND S&S
1) ABC - O2, IV
2) 12 lead ECG
3) treat the cause
4) decide if pt has adequate CO

279
Q

Algorithm for Tachycardia

A

1) ABCs - O2, IV, pulse
2) 12-lead ECG
3) unstable - cardiovert (defibrillate)

280
Q

H’s of Lethal arrhythmias

A

Hypoxia, Hypothermia, Hyper/hypokalemia, Hypovolemia, Hydrogen ion (acidosis)

281
Q

T’s of Lethal arrhythmias

A

Toxins, Tamponade, Trauma, Thrombosis, Tension pneumothorax

282
Q

Defibrillation

A

Delivery of an electrical current across the heart muscles over a very brief period to terminate an abnormal heart rhythm

283
Q

Cardiac Arrest Algorithm

A

1) Check central pulse - if nothing call code blue
2) call for help/code, get AED and defibrillator
3) Start CRP
4) Start IV, get O2 on (BVM)
5) Treat H’s and T’s or cause if known

284
Q

Algorithm if VF/PVT

A

Assess rhythm - shockable - defibrillation, clear patient for 360J/AED shock (<10 seconds)

285
Q

Algorithm for PEA/Asystole

A

Assess rhythm - not shockable
CPR
Drugs

286
Q

Types of Acute Coronary Syndrome

A
  1. Stable Angina
  2. Unstable Angina
  3. NSTEMI
  4. STEMI
287
Q

Stable Angina

A

Angina pain develops when there is increased demand in the setting of stable atherosclerotic plaque - vessel unable to dilate enough to allow adequate blood flow to meet myocardial demand - normal ECG

288
Q

Unstable Angina

A

Plaque ruptures and a thrombus forms around the ruptured plaque, causing partial occlusion of the vessel. Angina pain occurs at rest or progressed rapidly over a short period of time. ECG - normal OR inverted T waves OR ST depression

289
Q

NSTEMI

A

The plaque ruptures and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium. ECG - normal OR inverted T waves OR ST depression

290
Q

STEMI

A

Complete occlusion of the blood vessel lumen resulting in transmural injury and infarct to the myocardium, troponin changes. ECG - hyperacute T waves OR ST elevation

291
Q

S&S of ACS

A

Pain/discomfort/pressure, PSNS (N/V), diaphoresis, SOB/dyspnea, anxiety, fatigue, signs of impaired CO

292
Q

Hyperacute Phase

A

Tall T wave

293
Q

Early Acute phase

A

Tall T wave, elevated ST-segment

294
Q

Later acute phase

A

Inverted T wave, elevated ST segment

295
Q

Fully evolved phase

A

Inverted T wave, elevated ST segment

296
Q

Management of ACS

A

Heparin IV infusion, DAPT (ASA, clopidogrel or ticagrelor)

297
Q

Troponin function

A

Protein in muscles - decrease shows a problem with the heart

298
Q

CK-MB Function

A

Increased when there is heart damage

299
Q

Myoglobin Function

A

protein in the muscles that supply oxygen - means low red blood cells

300
Q

CRP function

A

protein synthesized by the liver, marker for inflammation or infection

301
Q

Lipid profile (cholesterol, LDL, triglycerides, HDL) Functions

A

Plaque in vessels

302
Q

INR/PT/aPTT Function

A

Ability of blood to clot

YEAR 3 (14 decks)

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