Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PCE STUDY > Cardiorespiratory > Flashcards

Cardiorespiratory Flashcards

1
Q

Name all the components of a cardiorespiratory assessment

A

IPPA
1. Inspection
a. vital signs
b. mechanisms of ventilation
c. thoracic shape
d. head, neck and extremities
e. speech, cough and sputum

  1. Palpation
    a. chest wall expansion
    b. diaphragmatic excursion
    c. edema
    d. pain and crepitus
    e. tracheal positioning
    f. tactile fremitus
  2. Percussion
    a. diagnostic percussion
    b. diaphragmatic excursion
  3. Auscultation
    a. breath sounds
    b. voice sounds
    c. heart sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are normal values for HR, SPo2, BP and RR

A

HR - 60-100bpm
BP- 120/80mmHg
Spo2- >94%, below 88% requires O2
RR - 12-20 breaths/minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do you determine HR?

A

Radial pulse with index and middle (not thumb - has own pulse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When do you determine RR?

A

Inspect covertly
Right after doing HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where do you determine BP?

A

Brachial artery pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do you determine systolic and diastolic BP?

A

Systolic - when the sound is first hear, diastolic - when the sound first disappears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is orthostatic hypotension?

A

Drop in greater than 20mmHg when going from lying to upright

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is normal breathing pattern?

A

70% diaphragmatic, 30% lateral costal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are abnormal breathing patterns?

A

Apical - breathing through shoulders and chest
Paradoxical - opposite of typical, on inspiration - chest contracts
Flail - separate rib segments
Use of abdominal muscles on exhale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the normal and abnormal inspiration:expiration ratios?

A

Normal 1:2, 1:3 - obstructive, 1:1 - restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 4 types of thoracic shape?

A
  1. Pectus excavatum
  2. Pectus carinatum
  3. Kyphoscoliosis
  4. Barrel chest (hyperinflated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you know if someone has finger clubbing

A

Positive Schamroth’s Sign
Normal fingers 160 deg with schamroth’s window
Clubbing has >180 deg finger angle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What sign do you look for with head, neck and extremities?

A

Head - nasal flaring, cyanosis, colour
Neck - jugular distention, accessory muscle use
Extremities - colour, edema, capillary refill, muscle wasting, clubbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is indicative of clubbing?

A

Hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is indicative of jugular vein distension/edema?

A

Right sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the sputum colours?

A

Clear - Saliva
White - Normal (asthma)
Yellow - Mucopurulent: Infected (chronic bronchitis, CF, pneumonia)
Green - Purulent (emphysema, advanced pneumonia, bronchiectasis, lung abscess)
Brown Flecks - Carbon particles (smoker, smoke inhalation)
Pink frothy - Pulmonary edema
Frank blood - Hemoptysis (TB, lung cancer, pulmonary infarction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do you look for in a cough? Sputum?

A

Cough: Effective, productive, wet/dry, persistent. Sputum: Quantity, colour, consistency, odour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Methods to determine chest wall expansion

A

Manual (3 lobes), circumferential (axilla, 10th rib)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Methods to determine diaphragmatic excursion

A

manual ,circumferential, percussions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Common conditions with edema

A

Right sided heart failure
Pregnancy
Lymphedema
Other systemic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does pitting edema mean?

A

Water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can you know something is pain vs. organic in nature?

A

Palpation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does the trachea normally sit

A

Between the sterno-costal joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is subcutaneous emphysema and how do you tell it is that? Plus causes

A

Feels like bubble wrap, sounds like rice krispies - it is air bubbles under the skin. Causes - air leak in chest tube, pneumothorax, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you palpate for tactile fremitus

A

Place palm of hand or ulnar borders for hand to feel for vibrations from sound transmission as a pt loudly repeats 99

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does the trachea move?

A

increase pressure = move away
decrease pressure = move towards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tactile fremitus results

A

increase in sound = increased density
decrease in sound = decreased density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Types of percussion

A

Diagnostic percussion
Diaphragmatic percussion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does diagnostic percussion tell us?

A

ventilation and change in density up to 5 cm in depth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do you perform diagnostic percussion?

A

Place finger with extended DIP on chest wall with firm pressure
Strike the DIP with middle finger of other hand (quick snap of wrist)
Perform 2-3 strikes on exposed skin and listen to resonance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Percussion sounds

A

Resonant - normal,
dull- less aerated (e.g., atelectasis, organs, pneumonia, tumour),
hyper-resonant - more aerated (pneumothorax, COPD, empty stomach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name all the lobes of the lungs

A

RUL, RML, RLL (10 segments)
LUL, LLL (8 segments)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Is the base of the Diaphragm symmetrical?

A

Dome shaped and higher on right than left due to the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Normal value for diaphragmatic excursion and outwith causes

A

3-5cm. (If reduced DE = hyperinflation / other conditions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When should you use the bell or diaphragm or bell for auscultation?

A

Bell for low frequency sounds (BP)
Diaphragm for high frequency sounds (pulmonary Ax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are normal breath sounds

A

Vesicular, bronchovesicular, bronchial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is vesicular breath sounds

A

3:1 I:E, soft, low pitched - typically in peripheries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is bronchovesicular breath sounds

A

1:1, mix of the two, in between 1-2nd intercostals and scapula
Inspiration is soft/low pitched
Expiration is loud/high pitched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Bronchial breath sounds

A

1:1,1:2, loud, high, pitched - over trachea and manubrium. louder on exhale.
Pause between inhalation and exhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Other name for abnormal breath sounds

A

Adventitia, or adventitious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Types of abnormal breath sounds

A

Crackles, wheezing, stridor, pleural rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What do the different types of crackles mean?

A

Early - pulmonary edema,
late - atelectasis,
coarse - sputum,
fine - fluid or atelectasis/fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What do the different types of wheezing mean?

A

High - bronchospasm,
Low - secretions - more oscillations=more pitch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is stridor?

A

Loud, musical high constant pitch, audible w/o stethoscope - during inspiration, due to turbulent air flow (upper airway obstruction or narrowed airways) - could be medical emergencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

You hear a low-pitched, leathery creaking sound. Differentiate between two possibilities.

A

pleural friction rub
pericardial rub: If pt holds breath and sound continues it is this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is pleural friction rub?

A

Long, low, leathery creaking sound. Friction between layers. Usually only hear with pleural effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe Bronchophony

A

Increased intensity and clarity of vocal resonance = consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe whispered pectoriloquy

A

Whispered words change from muffled over normal lung tissue to clearer over areas of consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe egophony

A

Pt repeats “E” while being auscultated, if “A” is heard it indicates consolidation (mucus or lung tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Types of voice sounds

A
  1. egophony
  2. whispered pectriloqy
  3. bronchophony
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the clinical utility of PFTs?

A

Determine if have respiratory condition
Determine severity
Determine response to broncho dilators
Outcome measure for progression, effectiveness of treatment and medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Explain different static lung volumes

A

Tidal volume = normal
Inspiratory reserve volume - max inhale after normal
Expiratory reserve volume - max exhale after normal
Residual volume - air remaining in lungs after max exhale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What would have decreased tidal volume

A

Restrictive disease, lung cancer, atelectasis, MSK impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What would residual volumes show if increased / decreased

A

Increased - obstructive
Decreased - restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What would inspiratory reserve volumes show if increased / decreased

A

Increased - obstructive
Decreased - restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What would expiratory reserve volumes show if decreased

A

pleural effusion, pneumothorax. ascites - restrictive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Explain different lung capacities

A

Total lung capacity - volume of gas at end of max inhale
Vital capacity - max amount expired following max inspiration
Inspiratory capacity - max inspired from resting expiratory level
Functional residual capacity - amount of gas remaining at respiratory expiratory level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Low FVC

A

Restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Low FEV1

A

Obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Low FEV1/FVC

A

Obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is gold classification for COPD

A

mild - >80, mod 50-80, severe 30-50, very severe <30 or <50 with chronic respiratory condition of FEV1 %. FEV1/FVC = <70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Diffusion studies

A

Low DLCO - circulatory and pulmonary, High = circulatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Indications for respiratory muscle strength tests

A

Weakness, prescribing IMT, OM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Normal values for ABGs

A

pH 7.35-7.45, PaCO2 - 35-45, HCO3- 22-26, SpO2- 95-100, PaO2 - 80-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Explain different conditions for ABGs (e.g., respiratory alkalosis)

A

Respiratory acidosis - decrease pH, increase in PaCo2
Respiratory alkalosis - increase pH, decrease in PaCo2
Metabolic acidosis - decrease pH, decrease HCo3
Metabolic alkalosis - increase pH, increase HCo3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Explain compensations for ABGs

A

Uncomp - pH and one
Partially comp - all
Fully comp - pH normal, others not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Conditions with obstructive lung disease

A

Chronic Bronchitis
Asthma
Emphysema
Bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Causes of Obstructive lung disease

A

Smoking
Inhalation
Genetics - alpha antitrypsin
Aging
Allergies
Air pollutants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Physical Exam of Chronic Bronchitis

A

Blue bloater - obese and cyanotic
Ankle edema and JVD
Tactile fremitus - decreased in areas of air trapping, increase with consolidation
Percussion - dull in consolidation, hyper-resonant with air trapping
Decreased breath sounds, early inspiration wet crackles, wheezing
Decrease PaO2 and increase PaCO2
CXR: cardiomegaly and white haziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Chronic Bronchitis pathophysiology

A

Increase mucus cell production, decreased cilia motility with inflammation of bronchial walls and decreased gas exchange (enlarged and misshapen alveoli) = chronic bronchitis
Productive cough for more than 3 months/ year for 2 years
From smoking and pollutant inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Emphysema pathophysiology

A

Bullar forms. From backpressure due to obstruction within airways, creators hyperinflated alveoli and destructs walls which leads to a decrease elastic recoil, increase in dead space and decreased area for gas exchange (malformed and large alveolar, destroy capillaries)
From smoking, air pollutants and genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Types of emphysema

A

Centrilobar
-Just respiratory inflammation
-Smokers, men, common with bronchitis
Panlobar - terminal and respiratory inflammation
-Genetic component

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Emphysema physical exam

A

Pink puffer - thin and wasted
Barrel chest
1:3
PLB
Accessory muscle use
Respiratory distress - leaning forward on a table
Palpation - tactile fremitus - decreased, decreased chest wall expansion
Percussion - hyperresonant
CXR - blackened areas, no rib angle, flattened diaphragm, thin heart mediastinum
ABGs - decrease PaO2, increase in PaCO2
Auscultation - decreased BS, dry crackles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Asthma pathophysiology

A

Decreased threshold to stimulant leading to bronchospasm, edema and inflammation and increased secretion causing airway resistance
Causing are idiopathic (EIA, weather, stress, drugs) or allergies (dust, pollen, food)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Asthma physical exam

A

Dyspnea, chest tightness, increase accessory muscle use, respiratory distress - leaning forward
Palpation - decreased tactile fremitus, decrease chest expansion
Percussion - hyperresonant
Auscultation - decreased BS, wheezing, crackles
ABGs - decrease PaO2, increased PaCO2 (decreased pH severe)=

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Bronchiectasis/ causes pathophysiology

A

Irreversible, dilation of median sized airways leading to increased secretion (cilia replaced with non-cilia) retention and airway obstruction and more at risk for recurrent infections. May cause atelectasis if severe
Post-infection (necrotizing bacterial pneumonia), congenital (CF, cilia dysfunction, airway defects), bronchial obstruction (aspiration, tumour) and other (connective disorder disease, system disorders, immunodeficiencies. idiopathic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Bronchiectasis physical exam

A

Clubbing
Signs of respiratory distress
Accessory muscle use
Foul smelling sputum
Severe cough
Thin and fatigued
Palpation - decreased tactile fremitus, decreased chest expansion
Percussion - hyperresonant
Auscultation - decreased breath sounds, wheezing, coarse crackles
CXR - blackened airspace, flattened diaphragm, dilated airways, consolidation or atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Types of restrictive lung disease

A

Parenchymal disease, pleural disease, chest wall deformities and neuromuscular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Explain restrictive lung disease

A

Inhalation disorder, decreased compliance = decrease in negative pressure = decrease in air entry - decreased ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What happens with an increased WOB with restrictive diseases

A

Increased WOB = increased RR, increase pressure to keep airways open, increased fatigue, increased accessory muscle use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are they 4 parenchymal diseases

A

Interstitial lung disease, sarcoidosis, ARDS, atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is interstitial lung disease?

A

Disease causing fibrosis around the interstitium of the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the pathophysiology of interstitial lung disease?

A

Decreased compliance= increased air way resistance, increased elastic recoil, increased fibrosis, decreased diffusion capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the cause of interstitial lung disease?

A

Idiopathic, environment toxins, genetics, connective tissue disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the physical exam findings for interstitial lung disease?

A

Inspection - dyspnea, increased RR, dry unproductive cough, clubbing, cyanosis, decreased chest expansion
Palpation - increased tactile fremitus
Percussion - Dull
Auscultation - late fine inspiratory crackles
ABGs - decreased PaO2, decreased PaCO2
CXR - small contracted lungs, diffuse reticular markings, raised diaphragm,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is sarcoidosis?

A

Granuloma formation on lungs - which are inflammatory cells that gather

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is atelectasis?

A

Collapse of alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Causes of atelectasis

A

Obstruction, compression, hyper/hypoventilation, decreased nitrogen, decreased surfactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the clinical presentation of atlectasis

A

Inspection - dyspnea, increased RR / shallow breathing, shift of trachea towards collapse, cyanosis
Palpation - decreased tactile fremitus, deceased chest wall expansion (affected side)
Percussion - Dull
ABGs - decreased PaO2
Auscultation - decreased or absent breath sounds, dry inspiratory crackles
CXR - darkened area of collapse, mediastinum shifting ipsilaterally, elevated hemi-diaphragm (tenting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is ARDS?

A

Acute lung injury characterized by increased permeability, respiratory distress and hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is the pathophysiology of ARDS?

A

Increased permeability = edema, fibrotic scarring as progression in the disease, V/Q mismatch= shunting = arterial hypoxemia, decreased surfactant = decreased lung compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the etiology of ARDS?

A

Shock, severe pneumonia, severe trauma, sepsis, aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the clinical presentation of ARDS?

A

Inspection - cyanosis, severe dyspnea, increased RR and shallow breathing
Palpation - increased tactile fremitus
Percussion - dull
ABGs - decreased PaO2, decreased PaCO2
Auscultation - diffuse wheezing, inspiratory crackles
CXR - patchy infiltrate in peripheries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the two pleural disease?

A

Pneumothorax
Pleural effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is a pneumothorax?

A

Air in pleural space causing collapse of lung or causing rib cage expansion

96
Q

What is the etiology of pneumothorax?

A

Idiopathic
Infection of pleura
Complication of mechanical ventilation
Complication of procedure
Rupture of respiratory structure
Trama

97
Q

What are the three types of pneumothorax?

A

Spontaneous, Trauma and Tension

98
Q

Describe the types of pneumothorax

A

Spontaneous - primary (rupture of blebs) or secondary
Traumatic - penetrating vs. non-penetrating
Tension - medical emergency - can decrease venous return leading to decreased CO and eventually shock and death - one way valve

99
Q

What is the clinical presentation of pneumothorax?

A

Inspection - chest pain, dyspnea, signs of respiratory distress, dry cough, increased RR
Palpation - decreased tactile fremitus
Percussion - hyper-resonant
ABGs- decreased PaO2
Auscultation - decreased or absent breath sounds
CXR - darkened area over collapse, flattened hemi-diaphragm

100
Q

What is pleural effusion?

A

Increased accumulation and decreased clearance within the pleural space

101
Q

What are the types of pleural effusion?

A

Exudative - increased permeability from infection, tumour, inflammation, cloudy fluid
Transudative - from increased hydrostatic pressure, clear fluid

102
Q

Etiology of pleural effusion?

A

Secondary to infection, cancer, inflammation - kidney disease, liver disease, CHF, TB, PE , trauma, pneumonia

103
Q

Clinical presentation of pleural effusion?

A

Inspection - dyspnea, chest pain, increased RR, dry cough
Palpation - decreased tactile fremitus (increased above when tissue is compressed), decreased chest wall expansion on side of effusion
Percussion - dull
ABGs - decreased PaO2 and PaCO2
Ausculation - pleural friction rub, decreased or absent breath sounds
CXR - fluid surrounding lungs - white area, contralateral tracheal deviation, potentially elevated diaphragm

104
Q

Types of bony deformities

A

AK
Kyphosis
Kyphoscoliosis
Pectus excavatum / carinatum
Congenital deformities

105
Q

Causes of bony deformities

A

idiopathic, congenital, NM

106
Q

Clinical presentation of bony deformities

A

Inspection - SOBOE, dyspnea, abnormal thoracic shape
Palpation - decreased tactile fremitus
Percussion - normal
Auscultation - normal
ABGs - decreased PaO2, decreased PaCO2
CXR - abnormal thoracic shape

107
Q

What happens with NM disoders?

A

Affecting the muscles of respiration in some way or another

108
Q

What innervates diaphragm

A

C3, C4, C5 - phrenic nerve

109
Q

What nerve do you need to keep diaphragm without mechanical ventilation

A

C4

110
Q

What does the diaphragm rely on

A

Abdominal and intercostals

111
Q

What innervates the intercostals

A

T1-T12

112
Q

What intercostals are responsible for breathing

A

Inhale - external intercostals
Exhale - internal intercostals

113
Q

What innervates the abdominals

A

T6-L1

114
Q

What is the purpose of the abdominals

A

Increase intra-thoracic pressure for strong cough

115
Q

What are accessory muscles for respiration

A

ES, Pectoralis, SCM, Scalenes, SA, Trapezius

116
Q

What is cystic fibrosis?

A

A systemic, hereditary disease of the exocrine glands that results in thick secretions

117
Q

What is the pathophysiology of cystic fibrosis?

A

-Imbalance of ion transport of Na/ Cl
-Thick secretions leading to recurrent infections, fibrosis/scarring, cystic dilations of bronchi
-Malabsorption of nutrients

118
Q

What is the etiology of cystic fibrosis?

A

-Autosomal recessive gene affecting the exocrine glands
-Affects growth and development - diagnosed in childhood

119
Q

What areas are commonly affected for cystic fibrosis?

A

Liver, Sinuses, Kidney, Skin, Reproductive organs, Intestines, Pancreas, Lungs

120
Q

How do you diagnose CF?

A

Genetic testing, Chloride sweat test

121
Q

What is the clinical presentation of CF?

A

Inspection - Increased RR, barrel chest (if obstructive), clubbing, chronic productive cough, sputum either yellow or green - if infected or blood, low weight
Palpation, Percussion - depends if obstructive, restrictive or mixed
Auscultation - decreased breath sounds, inspiratory/expiratory crackles, wheezing

122
Q

What are the two infectious lung diseases?

A

Pneumonia
Tuberculosis

123
Q

What is pneumonia?

A

Acute lung inflammatory response leading to consolidation within the alveoli

124
Q

What is the pathophysiology of pneumonia?

A

Infectious agent, irritant or auto-immune disorder trigger inflammatory response

125
Q

What is the etiology of pneumonia?

A

Hematogenous (circulation), inhalation (droplet), contact (trauma, chest tube), aspiration

126
Q

Who are the at -risk populations for pneumonia?

A

infants, elderly, chronic respiratory and heart conditions, immunocompromised individuals

127
Q

What is the clinical presentation for pneumona?

A

depends if bacterial, fungal or viral

Inspection - productive (if bacterial) cough, fever (if bacterial), dyspnea, increased RR, cyanosis
Palpation - increased tactile fremitus
Percussion - dull
Auscultation - bronchial or bronchovesicular breath sounds, wet inspiratory crackles
ABGs - decreased PaO2, may have decreased PaCO2
CXR - air brochograms, opacities around alveoli

128
Q

What is tuberculosis?

A

An infectious systemic inflammatory disease affecting primarily the lungs

129
Q

What is the pathophysiology of TB?

A

Mycobacterium tuberculosis - leads to latent TB (dormat) or post-primary TB - targeting weakened immune systems (e.g., developing countries, immunocompromised)

130
Q

What is the clinical presentation of TB?

A

Respiratory - dry cough (early), then productive (with blood)
Systemic - fatigue, malaise, fever, weight loss, swollen lymph nodes, night sweats

131
Q

How do you diagnose TB?

A

TB blood test or skin test. When active - CXR (looking for infiltrate or cavitation, or pleural involvement/parenchymal fibrosis), sputum sample, medical history or physical exam

132
Q

What are the intervention of TB?

A

Medication, negative pressure room, sputum clearance techniques, deep breathing exercises, coughing

133
Q

What is acute coronary syndrome?

A

Impairment of blood flow to the heart

134
Q

What is myocardial ischemia?

A

Insufficient blood flow to the myocardium typically resulting in angina pectoris symptoms

135
Q

What is asymptomatic myocardial ischemia called?

A

Silent myocardial ischemia

136
Q

What is angina? How to do know it is angina?

A

Tightness, heaviness, restriction in chest behind sternum from reduced blood flow. Presents with Levine’s sign - closed fist over sternum.

*may radiate to left jaw, left arm and between scapula

137
Q

What are the types of angina?

A

Stable angina, Unstable angina, Variant angina

138
Q

What is stable angina? What is unstable angina?

A

Stable - Brought on by activities that increase oxygen demand of myocardium.
Unstable - Not precipitated by activities that increase demand. Could come on at rest or minimal activity.

139
Q

What activities bring on stable angina and why?

A

-Physical activity, sexual activity - increased demand, not enough supply
-Cold, emotional stress - Emotional stress - increase cortisol = increase BP = (or cold now) vasoconstriction leading to increased heart contraction (because of increased resistance) + decreased supply to coronary arteries (and therefore heart muscles) cause they are vasoconstricted too
-Meals - N/A
-Laying supine - increase venous return = increased pre-load. increased EDV = increased SV = increased contraction (Frank Starling principle) therefore if preload, then increased contraction

140
Q

What relieve stable angina vs. unstable angina?

A

Stable - rest and NTGs - allow demand = supply, also vasodilation with NTGs
Unstable - may be NTGs, not rest = medical attention required!!

141
Q

What is variant angina?

A

Vasospasm of the coronary arteries (no occlusive disease). Sometimes relieved by NTGs short term, long term need calcium channel blockers.

142
Q

What is the best positioning with someone with chest pain?

A

Sitting with pillows under legs and behind back / neck. Reduces oxygen demand of muscles while NOT increasing venous pressure. Can also use your knee to support their back but still monitor their face.

143
Q

What is myocardial infarction?

A

Sudden complete occlusion of coronary arteries causing death of cardiac muscle due to the complete reduction of blood flow. Piece of plaque breaks off - platelets come to fix it and causes block.

Injury - reversible, injury from the MI
Infarction - complete death, irreversible - can see later as doesn’t heal

144
Q

What is the evaluation triad for acute coronary syndrome?

A

Symptoms, ECG changes, blood markers

145
Q

What are the symptoms of acute coronary syndrome?

A

Fatigue, Nausea, Angina pectoris, Anxiety, Dizziness, Diaphoresis, Dyspnea

146
Q

What are the ECG changes for acute coronary syndrome that occur and describe a normal ECG

A

Injury to myocardium - depressed ST segment, inverted T- wave
Small MI - no changes (NSTEMI, NQMI)
Large MI - elevated ST segment (goes away after acute phase over), pathological Q-wave (stays forever) (STEMI / QMI)

Normal:
P-wave - depolarization of atrium
Then isoelectric period at AV node
QRS - depolarization of ventricles (*repolarization of atrium happen here)
T-wave- repolarization of ventricles

147
Q

What are the cardiac biomarkers found for acute coronary syndrome?

A

Troponin I, Troponin T, Myoglobin and Creatine Kinase- Myocardial band (CK-MB)

148
Q

What is the medial management for acute coronary syndrome?

A

Surgery - PTCA - stent, CABG - bypass with donor vessel (saphenous vein, internal thoracic artery, radial artery - non-dominant)
Medication (*all reduce BP)
-Beta blockers - decrease HR and contractility = decrease BP (and decrease energy from heart)
-Calcium channel blockers - prevent spasm from decreased workload - decrease BP
-Nitrates - vasodilator = increased BF and decrease BP
-ACE-inhibitors - inhibit vasoconstriction
-ARB - inhibit vasoconstriction and sympathetic activity
-supplemental O2- giving to all not receiving enough O2

149
Q

What are the phases of cardiac rehab?

A

Phase 1 - acute/inpatient - low level intensity, education on adverse effects, monitor vitals, assess hemodynamic response and independence in functional mobility
-1 MET - bed rest, AROM for upper and lower, deep breathing, 24 hour since medically clear
-2 MET - walk up to 50 ft to bathroom ,ADLs, sitting up to eat
-3 MET - ambulate up to 250 ft
-4 MET - ambulate to 1000 ft, 1 flight of stairs, independent ADLs
Phase 2 - subacute / conditioning
-Monitor vitals closely
-Outpatient setting
Phase 3 - intensive rehab phase
-Resistance training starts - group setting
Phase 4 - maintenance
-Continue exercise with group or self-monitored

150
Q

What categories of education can you provide for cardiac rehab patients?

A

Activity guidelines
Self-monitoring
Symptom recognition and response
Nutrition
Medication
Sexual activity
Psychological / Social issues

151
Q

What is congestive heart failure?

A

Failure to pump blood throughout the heart (specifically the ventricles that typically fail)

152
Q

What are the types of CHF and what is the pathophysiology?

A

RHF
-RV stops working, backflow in to RA and then to interstitum of blood vessels within body = peripheral edema and JVD
LHF
-LV stops working, backflow to LA, then to pulmonary vein (increased pressure in pulmonary vein therefore capillary pressure) moves to interstitum and then to lungs
Biventricular heart failure
-LV stops working, backup right to lungs and then all the way through to the pulmonary artery = RV overworking = RHF

153
Q

What is the pathophysiology of CHF?

A

LHF –> decreased SV = increased LVEDV = increased LV pressure = increased LA pressure = increased pulmonary vein pressure = fluid in interstitum and then lungs = pulmonary edema

LHF –> decreased SV –> increased SNS activity –> increased HR –> myocardial fatigue

decreased CO –> decrease arterial blood flow –> decraesed perfusion to kidneys –> Kidney failure (look for BUN and plasma creatine levels)

inactivity/ bed rest –> myopathy, osteoporosis, muscle wasting

*can be compensation (increased SNS, medication or hypertrophy) or uncompensated
-don’t push too hard with compensated or can lead to active failure

154
Q

What is the etiology of CHF?

A

-Long term CAD (damage of ventricles - alter contractility), cardiomyopathy, cardiac muscle dysfunction, cardiac dysrhythmia, hypertension (increase pressure on LV = LHF), valve abnormality, pericardial pathology (pericardium pushing on ventricles = failure)

155
Q

What is the clinical presentation of CHF?

A

RHF - COR PULMONALE
-dyspnea, fatigue, weakness
-peripheral edema
-ascities
-JVD
- fluid weight gain (kidneys retain)
-pitting edema

LHF -
-dyspnea, fatigue, weakness
-orthopnea - based on number of pillows - want in semi-fowler position (30 degrees)
-paraoxymal noctural dyspnea
-pulmonary edema

156
Q

What are the interventions of CHF?

A

-Graded exercise and early mobilization
-Positioning to reduce orthopnea
-cardiac rehabilitation program
-supplemental oxygen

157
Q

What is pulmonary edema?

A

Abnormal collection of fluid within the lungs

158
Q

What is the pathophysiology of pulmonary edema?

A

Increased capillary permeability
Increased capillary hydrostatic pressure
Decreased capillary osmotic pressure - want to move where there is increased pressure
Lymphatic insufficiency

159
Q

What are the types of pulmonary edema? And the pathophysiology?

A

Cardiogenic
-Increased hydrostatic pressure (e.g., LHF, kidney failure, heart muscle or valve damage) -increasing accumulation in pulmonary capillaries- creates flow of fluid to lower pressure space (within interstitium and then lungs)
Non-cardiogenic
-Inflammation (from trauma or toxins) creates increased permeability within the pulmonary capillaries. Decreased osmotic pressure. Fluid moves easier and to where there is higher osmotic pressure.

160
Q

What is the clinical presentation of pulmonary edema?

A

-Dyspnea, pink frothy sputum, increased WOB, cyanosis, orthopnea, swelling in extremities if severe
-Palpation - normal or increased TF
-Percussion - dull
-ABGs - decrease PaO2
-Ausculatation - decreased or absent, fine inspiratory crackles
-CXR - cardiomeagly, increased pulmonary vessles, white hazy/foggy airspce, kerley B lines

161
Q

What is PE?

A

Blood clot that can travel to lungs (pulmonary artery) and block blood flow - can become complete blocked causing infarction and necrosis of lungs
-most common DVT
-large pulmonary resistance increased –> increase R ventricle –> RHF

162
Q

What are the risk factors to PE?

A

Immobilisation
Increase in coagulation
Other

163
Q

What is the clinical presentation of PE?

A

-Acute onset of dyspnea, increased RR, chest pain, blood in sputum (hemoptysis)
-ABGs - decreased PaO2, decreased PaCO2, increased pH
-CXR - infarcted area may appear white (rare_
-Dignosed with CT scan or V/Q

164
Q

What is the management of PE?

A

Prophylactic
-Anti-coagulants
-Compression
-Bed mobility and early mobilization
If suspected
-Don;t move them
-Tell someone
-Document
-Anticoagulants and thrombolytics

165
Q

What is PVD?

A

Disorder of blood vessels - primarily from atherosclerosis
Significant narrowing of vessels need to happen first before full occlusion

166
Q

What are the S + S of PVD?

A

Leg pain, numbness, coldness, decrease hair, decrease pulses (anaerobic as not enough O2 = build up of lactic acid)
decreased mobility and function due to pain
skin breakdown, gangrene, ulceration
-pain and paleness with elevation (buergers sign) or redness (roberton dependencies) with gravity dependence

167
Q

What is intermittent claudication?

A

Increased pain with increased activity due to poor circulation - anaerobic as not enough O2 demand = increased lactic acid
Decrease pain at rest (even standing)

168
Q

How do you differentiate between IC and neurogenic claudication?

A

In standing - better for IC not NC
Flexed when walking - better for NC not IC
Both better when sitting
Bicycle test - flex when cycling - better for NC

presents same as both up and walking

169
Q

What is the intervention of IC?

A

Progressive increase in activity and aerobic exercise - stimulate collateral blood vessels
Education on risk factors and self management
Self assessment of skin and education on skin care

170
Q

What are the categories of infectious agents?

A

Bacterial, Virus, Fungi ,Protozoa

171
Q

Is PPE determined by diagnosis?

A

No

172
Q

What are the 5 key moments of hand hygiene?

A

Before touching a patient
Before cleaning/aseptic procedures
After body fluid exposure and risk
After touching patient’s surroundings
After touching a patient

*take at least 15 secs - e.g., taking patient to bathroom

173
Q

When do you wear each PPE?

A

Gloves - contact with blood or body fluids may occur or non- intact skin or contaminated items
Gowns - If clothing may get soiled
Mask and eye protection - for all coughing patients, procedures with splashing

174
Q

What is the order you don PPE?

A

Sanitize, Gown, Mask, Eye protection, Gloves

175
Q

What is the order you doff PPE?

A

Gloves, Gown, Sanitize, Eye protection, Mask, Sanitize

176
Q

What are the three types of transmission?

A

Airborne, Contact, Droplet

177
Q

What is contact transmission? What are examples?

A

Transmission through skin to skin contact or indirectly through infected surfaces

-MRSA, C-diff, Norovirus, uncontained diarrhoea or drainage, VRA, ESBL

178
Q

What is droplet transmission? What are examples?

A

Transmission through droplets (travelling short distances and settle on surfaces) generated from the respiratory tract and land on nasal or oral mucus of new host

-Mumps, Rubella, Pertussis, Influenza, Pneumonia, Meningitis, Acute respiratory illness

179
Q

What is airborne transmission? What are examples?

A

Transmission of organisms that have become aerosolized and remain suspended - inhaled by host

-TB, disseminated shingles, measles, SARS, varicella

*negative pressure room

180
Q

What are the different types of thoracic surgery?

A

Pneumonectomy - removal of a lung
Lobectomy - removal of a lobe of the lung
Segment resection - removal of a segment of the lung
Wedge resection - removal of an area, not anatomically defined
Bullectomy / lung volume reduction - removal of large emphysematous tissue (done with bullae as risk of pneumothorax and with COPD patient to improve needed oxygenation within the area)

181
Q

What are the two types of thoracic incisions?

A

Median sternotomy and thoracotomy

182
Q

Describe the procedure of a thoracotomy, including muscles affected and post-op positioning

A

Typically posterolateral, going through the 4th intercostal space

Muscle incised - SA, Lats, Traps, Internal/external intercostals, rhomboids

Positioning - can lie on chest tube, just make sure it isn’t kinked / you won’t pull it out. Pneumonectomy - make sure bad lung is down (prevent atlectasis). Change positions to not get pressure sores.

183
Q

What education is needed pre/post op for thoracic surgery?

A

Deep breathing, coughing (splinting/ huff if needed), early mobilisation, transfers, bed mobility, positioning, relaxation, lines, scar management

184
Q

What are the potential complications of thoracic surgery?

A

Atelectasis (from not deep enough breaths, mucus plug or phrenic nerve impairment), Aspiration, increase pain, phrenic nerve impairment (leads to diaphragm elevation unilaterally), ulcers and DVT

185
Q

What is a Deep Vein Thrombosis? What are the risk factors?

A

A blood clot formed in the deep vein that may travel to the lungs (PE), heart or brain and cause a full or partial blockage of blood flow. Most common is in the legs.

Risk factors - venous stasis, hypercoagulation and blood vessel changes

186
Q

What are the signs and symptoms of DVT?

A

Leg pain, tenderness, ankle edema, swollen calf, dilated vessels and positive Homan’s sign (DF with SLR)

187
Q

What is the prevention of DVT? What to do if you suspect one?

A

Early mobilisation, graduated compression stockings, ankle pumps, anti-coagulants

Stop all exercise/ treatment, tell someone, document (IN THAT ORDER)

188
Q

What are the common cardiovascular surgeries?

A

CABG - usually saphenous vein (limited LL exercise until dr. clearance), internal thoracic (ant. chest wall or breast tissue) and radial artery
Value replacement (mitral or atrial)
Heart replacement - need to have caution as denervation happens and parasympathetic dysfunction increases HR (90-100bpm) and sympathetic dysfunction doesn’t increase HR during exercise as much (still some for epinepherine - exercise is good but should use RPE instead of HR monitoring

Aortic aneurysm or abdominal aortic aneurysm

189
Q

What are the sternal precautions after surgery?

A

Takes 6-8 weeks to heal

No pushing (e.g., transferring, lying to sit, sit to stand - do without hands and with pillow splint), pulling, lifting one arm about 90 degrees, hand behind back, driving for 4 weeks, lifting more than 10 pounds for 6 weeks.
*anything that gets pect activation as attachment to sternum and does adduction and internal rotation (just the clavicular part does flexion to 90 degrees, sternocostal part can bring it back to neutral)

190
Q

What are the benefits of early mobilisation?

A

Sputum clearance, improve breathing, chest mobility, assists GI function/ bowel motility, improves conditioning and activity tolerance, allowed increased independence, improve mood. Prevents - aspiration, thrombus formation, muscle atrophy, contractures, pressure sores, neuropathy

191
Q

What are the types of ventilation? And when do we use them?

A

Negative (SUCK) - like normal breathing, just using for the iron lung these days. On inspiration there is an increased space (by diaphragm, intercostals and accessory muscles) which leads to less resistance in the lung causing the air to move in
Positive (PUSH) - WHAT IS USED - pushing the air in to the lungs

192
Q

What is the administrative types in mechanical ventilation?

A

Invasive (intubation) - endotracheal tube, tracheostomy
Non-invasive - face mask, nasal mask

193
Q

What are the indications for mechanical ventilation?

A
  1. Hypoventilation, hypoxemia, hypoxia
    -Apnea
    -Hypercarbia
    -PaO2 <50mmHg with supplemental O2
    -Vital capacity <10L/ minute
    -RR >30 breaths/minute
    - Inspiratory force <-25 H20
  2. Central depression
    -Sedation or anesthesia, head injury, drug overdose, decreased LOC
  3. Decrease WOB and respiratory muscle fatigue
  4. Poor pulmonary hygiene (increased secretions)
194
Q

What are the complications of mechanical ventilation?

A

Barotrauma - alveolar rupture (can lead to atelectasis and then pneumothorax)
Volutrauma - Alveolar distension
Ventilator acquired pneumonia
Diaphragm atrophy
Hemodynamic compromise - overinflated, lead to compression of great vessels, leading to decrease venous return, decreased pre-load, decrease stroke volume (FRANK STARLING), decreased CO

195
Q

What are the types of mechanical ventilation breaths?

A

Mandatory - all done by ventilator
Assisted - initiated by patient, controlled and ended by ventilator
Spontaneous - all done by patient (except if patient isn’t doing enough volume and pressure)

196
Q

What are the modes of ventilation?

A

CMV - continuous mandatory ventilation
-All ventilator - no control by patient
ACV - assist control ventilation
-Patient initiates, ventilator provides set tidal volume and minimum number of breaths (minimum minute ventilation)
SIMV - Synchronized intermittent mandatory ventilation
-Patient initiates and controls and ends but if doesn’t then ventilator provides for them synchronized to them (with RR and tidal volume)

CPAP (non-invastive with mask)
-Constant inspiratory pressure (positive) augmenting spontaneous breathing, used for weaning or postponing intubation
-Used for those with obstructive apnea, adults with NM conditions, children with acute respiratory distress, acute and chronic ventilatory failure
-Benefits - keeps airways inflated, improving FRC and preventing alveolar collapse, enhances oxygenation

197
Q

What are the ventilator adjuncts?

A

PEEP
-On exhalation, positive pressure to keep airways open and reduce shunting (keeping -adequate ventilation)
-Complications - increases dead space, decrease CO, VAP, barotrauma and volutrauma
PSV - pressure support ventilation
-Positive pressure with inhalation - augmenting the amount of air in on spontaneous respiration
-Decreases WOB
-Complication - if increase in RR ventilator doesn’t know = too much air

198
Q

What is pre-exercise testing? And what does it consist of?

A

Pre-exercise Testing - need test to determine if at risk for adverse event to see if they need further assessment
-Medical history
-Physical exam
-Laboratory testing
-Risk stratification
-Test selection

199
Q

Explain risk stratification for pre-exercise testing

A

If have health history of CV disease, metabolic disease or pulmonary disease = high risk
If have current signs and symptoms of CV/pulmonary or metabolic disease = high risk
If have risk factors (>=2 = moderate risk, <2 = low risk)

200
Q

What are the risk factors for exercise determine in pre-exercise testing?

A

Age
-Men >45, Female >55
Family History
-Family member who is male before 55, female before 65 - sudden death, MI or coronary revascularisation
Physical activity levels
-Not exercising moderately 30 minutes/ day, 3x/week for last 3 months
Obesity
-BMI >=30 kg/M2
-Waist circumference - Male >102cm, Females >88cm
Pre-diabetes
-Glucose in urine/ blood tests taken, history of diabetes
-If unsure, age >45 and BMI >25kg/m2 - assume pre-diabetes
Dyslipidemia
-HDL >130 mg/dl
-LDL <40 or if >60mg/dl is protection
-On statin medication
-Total serum cholesterol count >200mg/Dl
Hypertension
-Systolic >140 or diastolic <90
-On hypertensive medication
Stress / Psychological
-SF-36 QOL, Beck Depression Inventory : Depression
Smoker
-Current or quit in last 6 months, exposure to 2nd hand smoke
Alcohol
-Men >14, Women >9
Diet

201
Q

How to you determine if patient’s need pre-exercise screening, exercise testing or medical supervision throughout exercise?

A

Low risk - no screening, testing or monitoring
Moderate risk - during vigorous exercise requires a screen
High risk - requires all

*Moderate exercise - 40-60 % VO2 or 2-6 METs, Vigorous >60% VO2 or >6 METs

202
Q

What are the indication for exercise testing?

A

Diagnostic
-Maximal testing
-Sub maximal testing
-Endurance
-Movement economy
-Onset of exertional symptoms (Subjective - dyspnea, chest pain, leg pain, cerebral symptoms, Objective - EKG changes, HR, BP)
-Effect of meds
-Evaluate progress
Prognostic
-Likelihood of adverse event
-Surgical risk
Prescription
-Medications
-Exercise program

203
Q

What are the absolute contraindications to exercise testing?

A

Recent change in resting ECG - suggesting significant ischemia, recent MI (within 2 days), or other acute cardiac events
Acute pulmonary embolism or pulmonary infarction
Acute myocarditis or pericarditis
Acute systemic infection - with fever, body aches or swollen lymph nodes
Unstable angina
Uncontrolled cardiac dysrhythmia - causing symptoms or hemodynamic compromise
Uncontrolled symptomatic heart failure
Symptomatic severe aortic stenosis
Suspected or known dissecting aneurysm

204
Q

What are the relative contraindications to exercise testing?

A

Left main coronary stenosis
Moderate stenotic valvular heart disease
Electrolyte abnormalities
Severe arterial hypertension at rest (SBP >200mmHg, >110 mmHg DBP)
Tachydysrhythmia or bradydysrhythmias
Hypertrophic cardiomyopathy and other forms of outflow tract obstruction
Neuromotor, MSK or rheumatoid disorder exacerbated by exercise
High degree AV block
Ventricular aneurysm
Uncontrolled metabolic disease (DM)
Chronic infectious disease (HIV)
Mental or physical impairment leading to inability to exercise adequately

205
Q

What is maximal exercise testing?

A

AKA STRESS TEST
Done by GP - due to adverse events occurring and prescription of medication
Used to determine through graded exercise testing predicted VO2 max
Use Bruce Protocol - treadmill testing

206
Q

What is submaximal exercise testing?

A

Determined by PT
Evaluative - 6MWT - can do 2 practice trials, take frequent breaks - distance travelled in 6 minutes
-Good since easy to administer and minimal equipment. Disadvantage since motivation based and no measures of HR, BP, etc
Predictive (predicting Vo2 max) - modified Bruce protocol - treadmill test or cycle erogometer testing (astrand- rhyming test)

207
Q

What are the indications to prematurely terminate exercise testing?

A

General
-Fatigue (vocal or physical)
-Decreased perfusion - lightheadedness, confusion, pallor, cyanosis, ataxia, nausea, cold or clammy
-SOB
-wheezing
CVD
-angina or angina like symptoms
-leg cramps or claudication
-no increase in HR
-Drop in SBP on >10 mmHg
-Increase in SBP >250mmHg and DBP>115 mmHg
-Cardiac dysrhythmia by palpation or auscultation
Other
-Patient request
-Failure of equipment

208
Q

What are the components of exercise prescription

A

-Exercise selection
-Exercise parameters
-Monitoring
-Safety
-Indications to stop exercise

209
Q

What is exercise selection based on?

A

-Goals, ability, safety, preference

210
Q

What are exercise parameters?

A

Based on goals, guidelines, evaluation, safety
-FITT

211
Q

What are the FITT principles for exercise prescription?

A

Frequency
-How often per day or week to do exercise
-3-5 days/week for moderate to vigorous exercise for aerobic
Intensity
-Typical - 60-85%, High risk 50-75%
-Can be measured by: (*ALL GET A RANGE)
–>RPE - 6-20 or modified 0-10
–>HR Max (220-age=HRR Max), Target HR = HRR x % intensity
–>HR Reserve = [(HRR x Resting HR) x %intensity] + resting HR - KARVONEN
–>Target VO2 Max = VO2 Max x %intensity
–>VO2 Max Reserve = [(VO2 Max x VO2 rest) x % intensity] + VO2 rest
–>Maximal Metabolic Equivalents (METs Max) - 1 MET = 3.5 ml/kg/min = VO2 max/3.5 mg/l/min x % intensity = METs max
Time
-30-60 min / day (150 min/week) of moderate
-20-60 min / day (75 min/ week) of vigorous
-20 mins for sedentary is still fine, best in 10 minutes bouts - continous or intermittent
Type
-Aerobic
-Resistance - power, endurance, strength

212
Q

What are the Canadian Physical Activity Guidelines?

A

150 minutes moderate - vigorous exercise - 10 min bouts or more
2x / week for strength

213
Q

What are some safety tips for exercise prescription?

A

C/I to exercise testing apply here
Don’t use valsalva maneuver
Don’t do upper body with those who are hypertensive as increase SBP
Appropriate screening and testing should take place prior to beginning of exercise program

214
Q

What are reasons to terminate exercise session?

A

S + S
-Angina or angina like symptoms
-Leg pain or claudication
-Excessive Fatigue
-Lightheadedness, dizziness, ataxia
-cyanosis or pallor
-Marked dyspnea
Other
-no rise SBP
-Rise in SBP >200 mmHg, DBP >110mmHg
-Drop in 10-15 mmHg for SBP
-Cardiac dysrythmia on palpation or ECG (arrthymias, ST changes)

215
Q

What are 5 possible interventions?

A

-Positioning
-Breathing exercises
-Airway clearance
-Forced expiratory techniques
-Exercise

216
Q

What is the end goal of CRT interventions?

A

Optimizing gas exchange - improve patient’s condition, optimize function and decrease symptoms

should be assessed prior (through testing, notes and talking to medical staff) and after intervention

217
Q

Explain the positioning intervention for CRT

A

V/Q matching
-Unilateral - good lung down -Send the blood where the better oxygenation is
-Bilateral - prone- Thorax at a mechanical advantages and this improve oxygenation
-Pneumonectomy - good lung up
-ARDS - prone

Decrease dyspnea in those with COPD
-Forward leaning standing against wall
-Forward leaning against a table
-Forward lean on elbows
-Forward lean with head done on table

*all offloading thorax, relaxing postural muscles (not using as much O2 and energy, decreases SOB) and putting accessory muscles in mechanical advantageous position for breathing

218
Q

Explain the breathing exercise intervention for CRT

A

Deep diaphragmatic breathing
-Decrease energy cost (O2), promote relaxation, decrease use of accessory muscles
-*only do with COPD NOT DEEP, because relaxation and decrease energy of accessory muscles
-Can do quick stiff or hand on belly for prompting

Pursed lip breathing
-GOOD FOR COPD
-1:3 inhale:exhale through pursed lips
-Good to decrease RR, promote relaxation, use positive backflow to keep airways open, decrease hyperinflation, improves gas exchange

Inspiratory muscle training
-Resistve exercises - increasing strength and endurance
-Can use inspiratory muscle trainer (IMT device)
-Strength - 2-4x/week, 60-85% PIMax (find out through MIP/MEP manometer), 8-12 reps, 1-3 sets
-Endurance - 4-6x/week, 40-85% PIMax, >15 minutes (as tolerated)

Segmental breathing
-Use tactile input to get an area of a lung to expand requiring greater expansion or ventilation

Sustained maximal inspiration (SMI)
-Incentive spirometer increases compliance and motivation through visual feedback - go to TLC 3-5sec holds
-Flow meter - maintain level balls on inspiration, volume - maintain marker through a specific range
-*GOOD POST OP - prevent atelectasis and airway closure

219
Q

What are the 6 types of airway clearance techniques? What are the indications and complications?

A

Vibrations, Percussion, Postural drainage, PEP devices independent breathing techniques, suctioning

*want to decrease secretions - ciliary defect, asthma, respiratory muscle weakness, prevent atelectasis (mucus plug), mechanical ventilator

Hypoxemia/hypoxia, O2 desaturation, bronchospasm, cardiac dysrhythmia

220
Q

Explain postural drainage

A

Putting people in position that would best get drainage to central airways based on where their secretions are and is gravity dependent - keep in position for 5-10 minutes (or longer if tolerated)

Signs of treatment intolerance - SOB, hypertension, bronchospasm, nausea, anxiety, dizziness

See book for photo - left posterior lobe, superior lobe and posterior segments are the weird ones

*can be modified if C/I to just lay flat

221
Q

What are the contraindications for postural drainage? For trendelenberg position?

A

Increase ICP >20mmHg
Head or neck injury (spinal instability) not stabilized yet
Recent spinal surgery or acute spinal injury
Active hemorrhage or hemodynamic compromise
Active hemoptysis
Empyema
Bronchopleural fistula
Pulmonary edema (associated with LHF)
Pulmonary embolism
Large Pleural effusion
Untreated pneumothorax
Rib fracture (initially)
Surgical wounds or healing tissue (initially)
Elderly, confused or anxious

Trendelenberg
-Increased ICP
-Uncontrolled hypertension
-Uncontrolled airway at risk for aspiration
-GERD or recent esophageal surgery
-Recent gross hemopytsis from lung carcinoma
-Distended abdomen

222
Q

What are percussions?

A

Using cupping technique to dislodge secretions towards central airways to be coughed up and exporated (should sound hollow - not slap, rhythmic and equal, bony prominences, breast tissue and direct over heart avoided and patient should be appropriately draped) - mechanical and self percussions could also be performed

can be on inhale or exhale

223
Q

What are the contraindications for percussions?

A

-Increased ICP
-Pulmonary embolism
-Pneumothorax
-Subcutaneous emphysema
-Rib fracture
-Severe osteoporosis
-GI bleeding
-Burns/skin graft
-Open wound
-Malignancy
-Anticoagulation medication

224
Q

What are vibrations?

A

Use hands to create vibratory force to dislodge secretions - helps to stretch respiratory muscles (improving volume and inspiratory effort) and enhance mucociliary transport. Can use mechanical vibration devices

Types -
-Fine - small amplitude, high frequency better tolerated
-Coarse - large amplitude, low frequency

*only on exhale

225
Q

What are the contraindications for vibrations?

A

Increased ICP
Pulmonary embolism
Pneumothorax
Subcutaneous emphysema
Rib fracture
Severe osteoporosis
GI bleeding
Open wound
Severe burns/ skin graft
Malignancy
Anticoagulation medication

226
Q

What is a PEP device and what are the different types?

A

Device used on exhalation that creates back pressure to splint open aways, pass through inter-alveolar connections and dislodge/move mucus proximally
>=15 mins per session 2-3x/day
Types
-Low pressure - 10-20cm H2O, same effectiveness as high pressure (50-120 cm H2O) but without the risk of pneumothorax
-Non-oscillating - smooth, same as PLB
-Oscillating - accelerated expiratory flow rates and interrupts airflow through oscillations
-Flutter - only one position dependent, look up = more pressure, down = less

227
Q

What are the advantages and disadvantages of PEP?

A

-Advantages - portable, easy to use, passive technique, promotes independents, no risks such as bronchospasm or aspiration
-Disadvantages - stigma around use, have to use a device

228
Q

What are the independent breathing techniques?

A

ACBT
-10 min segments, 10-30 sessions
-BC - tidal breath, TE - deep breaths (with vibrations and percussion if needed), huff/cough all rotating in cycles
-Can be in sitting or a postural drainage position

AD
-30-45 min treatment time
-Breathing at different lung volumes to mobilise secretions
-Stages - unstick - low levels, collect - mid levels (around TV), and evacuate - high levels, followed by 2-3 cough/huff and some deep diaphragmatic breathing (not for COPD patients)
-Do 5-6 reps, 3 sec holds

229
Q

What are the advantages and disadvantages of independent breathing techniques?

A

ACBT
-Advantages - promotes independent, easy to use and no equipment required, no risk of O2 desaturation, bronchospasm, aspiration
-Disadvantages - takes a long time, active participation

AD
-Advantages - no complications (bronchospasm, aspiration), free, independent techniques
-Disadvantages - takes a long time, need active involvement, need cognitive capacity, need proprioception, tactile and auditory capacity

229
Q
A
230
Q

What is suctioning?

A

10-15 sec per pass, 30 sec rest between (5-10 sec if TBI)
Inset through nose/mouth, nose/mouth with artificial airway or endotracheal tube or tracheostomy tube
ONLY USE WHEN INDICATED - remove secretions when patient can not do independently
-Visible secretions
-crackles (inspiratory/expiratory) on auscultation
-patient describes feelings or you feel consolidation in chest (increase tactile fremitus)
-Suspect aspiration of gastric or upper airway secretion
-Clinical apparent SOB or increased WOB
-ABGs showing hypoxemia or hypercarbia
-CXR showing consolidation

231
Q

What are the contraindication to suctioning?

A

Increase ICP
Severe O2 desaturation (<92%)
Hemoptysis
Malignant arrhythmia
Hyperinflation post CABG and head injury

232
Q

What are the complications of suctioning?

A

Increased ICP
Hypoxia/hypoxemia
Hemodynamic instability
Mucosal (tracheal and bronchial) trauma
Laryngospasm / bronchospasm
Pneumothorax
Atelectasis
Infection
Pain
Anxiety

233
Q

How do you minimze complications of suctioning?

A

Infection control measures
Hyperoxygenation
Hyperinflation
Limit suction time and allow recovery time
Medication and sedation prior

234
Q

How do you assess the outcome of suctioning?

A

Improved breath sounds, removal of secretions, improve blood gas data or pulse oximetry, decreased WOB (decreased RR or dyspnea)

235
Q

What are the forced expiratory techniques?

A

Cough
-Stages - 1/ inspiration - adequate is 60% of VC, 2/ glottal closure, 3/compression - increases intra-thoracic pressure, 4/ expulsion - open glottis and air is forced out
Huff
-Open glottis, mid-low is peripheral, mid to high is proximal airways
-Less effective than cough but might be good if pain post-op or in obstructive lung disease due to risk of small airway collapse from high intra-thoracic pressure
Assisted cough
-Costophrenic assist - hands on costophrenic angle on exhale, then quick release and then again after 3 sec hold the patient coughs
-Hemilich-Type assist - using heel of hand of epigastric area - deep breath in for 3 sec then cough with assisted J-stroke
do not use for those with GERD and recent abdominal surgery

PCE STUDY (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions