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Winter 2024 Cardiopulmonary > Unit 3 Most Important Things > Flashcards

Unit 3 Most Important Things Flashcards

1
Q

Causes of Dyspnea

A
  1. Ventilatory pump failure- hypoxia- not enough O2 is in the blood and likely CO2 build up
  2. Cardiac Pump/supply failure- ischemic hypoxia- typical of someone having an MI b/c the vessels are occluded also happens in strokes + PVD
  3. Blood’s O2 carrying capacity- anemic hypoxia - if the blood isn’t able to carry enough O2 even though the heart + lungs are functioning properly
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2
Q

What are the 3 main causes of breathing disorders?

A
  1. Damage to the breathing control mechanism within the brainstem - restrictive disease can’t inhale well
  2. Difficulty in generating the differential pressure required to create airflow - obstructive disease can’t exhale well
  3. Difficulty in generating airflow for a given differential pressure between the atmosphere and alveoli
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3
Q

Restrictive Disease

A
  • Cannot fully fill their lungs with air b/c their lungs feel like they are restricted from fully expanding/breathing is restricted as if the movement of the chest is restricted
  • Greater effort to move chest to breathe regardless of strength of muscle

2 types
1. Normal strength but to stiff
2. Normal stiffness but to weak
- Restrictive disease includes diseases of muscle, lung tissue, soft tissue, nervous system, edema,

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4
Q

T/F All spirometry volumes are reduced in restrictive disease

A

True

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5
Q

Obstructive Disease

A
  • Shortness of breath due to difficult exhaling air from their lungs
  • Exhaled air comes out more slowly due to damage or narrowing of the airways
  • Characterized as: Increased FRC (functional residual capacity), marked increase in A-P diameter of chest (barrel-chest), and slow expiration
  • Can be acute and Chronic
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6
Q

What is the most efficient way to breathe with Obstructive Disease

A

Long slow breathing

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7
Q

What are the 2 causes of Obstructive Disease

A
  1. increased airway resistance
  2. Decreased elastic recoil; diminished ability to expire has same consequences as physical obstruction
    - Elasticity of the alveoli helps push the air out if they lose their elasticity they become like a deflated balloon that is limp and has no air in it and end up collapsing on themselves

-Emphysema primarily loss of elastic recoil; can have some airway obstruction
- Cystic fibrosis results in obstructive disease ; either bronchiectasis or chronic bronchitis

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8
Q

Equal Pressure point
Why do airways collapse in obstructive disease?

A
  • Point in airway anatomy where the outside compressive pressure equal the inside elastic pressure
  • In obstructive disease loss of pressure moving air through obstruction moves the equal pressure point distally because the decrease in elasticity
    –> Forced expiration, couching, ect becomes less effective as small airways collapse, trapping air and mucus behind
  • If this happens in smaller airways they will collapse during forced expiration
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9
Q

T/F COPD is a category of diseases

A

True

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10
Q

COPD

A

Chronic Obstructive Pulmonary Disease
- Category of diseases
- Usually a combination of emphysema and chronic bronchitis
- Also denoted as COLD Chronic obstructive lung disease

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11
Q

Emphysema

A
  • Abnormal, permanent enlargement of air spaces distal to bronchioles with destruction of their walls
  • Elastic fibers in alveolar walls destroyed
  • Lack of alveolar recoil necessary for expiration
  • Lungs increase in size until recoil sufficient to drive air out *****
  • FRC increases, resulting in barrel chest
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12
Q

What are the 4 diseases that make up COPD

A
  1. Asthma
  2. Bronchiectasis
  3. Chronic bronchitis
  4. Emphysema
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13
Q

Pathophysiology of COPD

A
  • Mostly caused by smoking
  • Which tissue is damaged determines whether emphysema, chronic bronchitis or both occur
  • usually insidious because but perceived as acute because they will not notice without exertion and blame it on things like being out of shape
  • Small airways are involved first in COPD
  • Respiratory reserve dwindles progressively
  • Loss of reserve becomes evident during illness or extraordinary exertion
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14
Q

Pathophysiology of Emphysema

A

-Smoking irritates the lining of the lungs and causes the white blood cells and neutrophils to accumulate in the walls of the alveoli
- Smoking increases the level of lung proteases and impairs the action of antiproteases
–> Protease are found through out the body especially in neutrophils and macrophages and they serve to digest the conductive tissue elements when needed to destroy foreign bodies
–> Normally antiproteases protect living tissue but b/c the smoking inhibits that we actually get damage to the connective tissue

  • Smoking –> neutrophils accumulate in alveolar walls–> release of proteolytic enzymes–> Alpha 1 Antitrypsin activity critical (type of antiprotease)–>normally inhibits proteolysis
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15
Q

Signs and Symptoms of Emphysema

A
  • Barrel Chest
  • Emaciated
    -FEV1/FVC ration <0.6
  • Pink Puffer
  • Tripod position
  • hypertrophied SCM and scalenes
  • Prolonged Expiration

Can progress to: LHF, Corpulmonale- right sided HF, cyanosis

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16
Q

Pulmonary Hypertension

A

-Pulmonary hypertension is a type of high blood pressure that affects the arteries in the lungs and the right side of the heart.

-In one form of pulmonary hypertension, called pulmonary arterial hypertension (PAH), blood vessels in the lungs are narrowed, blocked or destroyed. The damage slows blood flow through the lungs. Blood pressure in the lung arteries goes up. The heart must work harder to pump blood through the lungs. The extra effort eventually causes the heart muscle to become weak and fail.

  • Untreated Pulmonary hypertension is the most common cause of RHF b/c the gas exchange abnormality, destruction of the pulmonary vascular bed –> when the alveoli are destroyed the vascular bed is also destroyed as well which causes a decrease in surface area in which the blood flow therefore increases the pressure in the pulmonary system
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17
Q

Barrel Chest

A
  • Less surface area for gas exchange
  • Less vascular bed for gas exchange
  • COMPENSATE BY HYPERVENTILATION
  • Low cardiac output and develop muscle wasting and weight loss b/c they are working so hard to breathe
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18
Q

Hypoxemia

A

Hypoxemia is a low level of oxygen in the blood. It starts in blood vessels called arteries. Hypoxemia isn’t an illness or a condition. It’s a sign of a problem tied to breathing or blood flow. It may lead to symptoms such as:

Shortness of breath.
Rapid breathing.
Fast or pounding heartbeat.
Confusion.

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19
Q

Medical & Surgical Management of Emphysema

A
  • Bronchodilators = increase airway size and improves air movement and decrease resistance to expiration
  • Supplemental O2= improves the perfusion of the available exchange of O2 ; it gives the air higher percentage of O2 and makes it less difficult for a person to breathe
  • Lung reduction surgery
  • Airway clearance not specifically needed for pure emphysema
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20
Q

Lung Volume Reduction Surgery
LVRS

A
  • procedure that removes approximately 20%-35% of the poorly functioning space occupying lung tissue from each lung
  • By reducing the lung size the remaining lung and surrounding tissue like the intercostals and diaphragm are able to work more efficiently; should make breathing easier
  • Lungs regain dome shape
  • Significant improvements in exercise capacity
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21
Q

Chronic Bronchitis

A
  • Excessive sputum production on most days for at least 3 months of the year for at least 2 consecutive years
  • Airway is swollen so its size is diminished
    Presents with:
    –>Impaired mucus clearance
    –> Chronic rattling cough
    –> inflamed bronchial tube
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22
Q

Progression of Chronic Bronchitis

A
  • Smoking predisposes to infection
    -Primary and secondary Bronchi are continuously inflamed and irritation of the airways cause hyperplasia of the mucus glands b/c they are constantly scus in response to irritation
  • Decreased ciliary clearance
  • Damaged epithelium
  • Interference with WBC function
  • Irritation of airways
  • Hyperplasia of mucus glands in large airways
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23
Q

Blue Bloater

A
  • Chronic bronchitis
  • Greater obstruction than one with empysema
  • Overwight and cyanotic
  • Hypercapnic
  • -> lose responsiveness to CO2 becomes less senstitive causing control of ventilation to be controled more by[ PaCO2
  • Cor Pulmonale
    –> RHF caused by respiratory disease –> cor pulmonale can cause LHF
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24
Q

Hypercapnic

A

Hypercapnia is the increase in partial pressure of carbon dioxide (PaCO2) above 45 mm Hg

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25
Q

Cor Pulmonale

A

Cor pulmonale is an enlarged right ventricle in your heart that happens because of a lung condition. Pushing against high pressure in your pulmonary artery can cause your right ventricle to fail.

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26
Q

Medical Management of Chronic Bronchitis

A
  • frequently co-morbid with emphysma
  • Bronchodilators
  • Supplmental O2
  • Antibiotics
  • Airway clearance
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27
Q

Bronchiectasis

A
  • Chronic and permanent dilation of bronchi due to inflammation of infection
  • Copious amounts of foul smelling sputum
  • Dilated, obliterated, damaged bronchi in dependent airways
  • mucus plugging of bronchi
  • Common problem in CF
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28
Q

Bronchiectasis Signs and Symptoms

A
  • Chronic coughing
  • Coughing blood
  • coughing up large amounts of mucus
  • abnormal sounds or wheezing in the chest on breathing
  • Shortness of breath
  • chest pain
  • daily bad breath
  • skin has a blue apperance
  • weight loss
  • fatigue
  • thickening of the skin under your nails and toes
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29
Q

Causes of Bronchiectasis

A
  • Idopathic
  • Obstruction by tumor or foriegn object
  • Immotile cilia
  • Congenital
  • Post-infective/cystic fibrosis
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30
Q

Medical/Surgical Management of Bronchietasis

A
  • Antibiotics
  • airwayclearance
  • Surgical removal of affected area
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31
Q

Ventilation is driven by>

A

Driven by levels of CO2 in the body not O2 ***
- ventilation regulated to rid the body of CO2
- CO2 is a volatile acid

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32
Q

What is the mechanism of ventialtion?

A
  • Primary mechanism is negative feed back loop between pH of CSF and ventilation
  • pH of CSF is primarily determined by paCO2

Secondary mechanism includes: arterial PO2 and pH, negative feedback loop

Feedforward mechanism: limb movements

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33
Q

When there is a decrease in pH what happens to ventilation?

A
  • Ventilation increases in order to blow off the excess CO2 and to normalize the pH
    -Chronically, kindey and buffering systems respond to eliminate fixed acid= they do this by increasing the rate hydrogen ion secreations and increacease reabsorption of bicarbonate ions to increase plasma and HCO3
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34
Q

What is the response to increased pH?

A
  • Ventilation is slowed
  • CO2 accumulates
  • pH is normalized
  • CHronically, kidneys and buffering systems respond
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35
Q

T/F ventilations affects are on CO2 and not on how fast/slow you breathe

A

true

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36
Q

Euventilation

A

produces normal PaCO2

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37
Q

Hyperventilation

A

Decreased PaCO2

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38
Q

Hypoventilation

A

Increased PaCO2

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39
Q

Effects of CO2 on the Brain

A
  • Hgih CO2 depresses cerebral function
    * Giddy–> somnolent–>unconscious–> dead*
  • Cerebral blood flow rids the brain of CO2 by negative feedback loop –> if there is high CO2 in the brain the body will react by increasing blood flow ot the brain to normalize the CO2 by taking it away faster
  • Headache from increased blood volume in the skull
    Hyperventilation
    –> decreased cerebral blood flow
    –> Compromise Cerberal function
  • ->Lightheaded, dizzy, ataxic, other
  • ->Mechanical ventilation used to decrease cerebral edema post- CVA, head injury
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40
Q

Hypercapnia

A

Hypercapnia (hypercarbia) is when you have high levels of carbon dioxide in your blood. Carbon dioxide is a waste product that your body gets rid of when you exhale. If you can’t get rid of it, it can build up in your blood. COPD and conditions that affect your lungs, brain, nerves and muscles are the most common causes.

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41
Q

T/F breathing to maintain blood in PO2 at high altitudes results in hyperventilation

A

True

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42
Q

Supplemental O2

A
  • Normal air has 21% O2 (FIO@ = 0.21)
  • Spplemental oxygen is measured as FIO2 (fraction of inspired air)

FIO2 Increases by:
- increasing flow rat
- increasing % of O2
- Usually by incresing flow rat of 100% O2

Changing the dose of O2 must be ordered by a physician

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43
Q

If low PaO2 is driving low ventilation excessive FIO2 causes…..

A

hypoventilation/slow breathing allowing PaO2 to fall to regulated level

(hypoventilation is an accumulation of CO2/retnetion of CO2 causes respiratory acidiosis)

44
Q

1.Atmosphere has — PO2 and very — PCO2

  1. Venous blood has — PO2 and —PCO2
A
  1. high : low
  2. Low : High
45
Q

V/Q (V Q ratio) The Primary

A
  • Determinant of oxygenation of the blood
  • Increasing V/Q increases PaO2 and lowers PaCO2
  • Decreasing V/Q decreases PaO2 and increases PaCO2
46
Q

Effects of V and Q

A

O2 molecures back up and wait at the alveoli for the hemoglobin to pick them up–> the VQ ratio is to high or greater than 0.8 –> when some RBC’s have hemoglobin that leave the alveoli without 4 molecles of O2 attached to them the vVQ ratio is to low or less than 0.8 –>when O2 is picked up by hemoglobin of the RBCs at the same rate it is used by the body the VQ ratio is just right 0.8 with about 100% O2 saturation

-Ventilation brings O2 molecules into the alveoli
- Perfusion carries them away from the alveoli to be used by the body
- VQ follows a Goldilocks process
–> O2 molecules back up and wait at the alveolus for hemoglobin to pick them up (V/Q 0.8 too much)
–> SOme Hb leaves the alveolus without 4 molecules of oxygen (V/Q <0.8 too little)
–> Oxygen is picked up by the Hb at the same rate it is used by the body ( V/Q = 0.8 just right with nearly 100% Hb saturation leaving the alveoli

47
Q

Low V/Q

A
  • Low ventilation relative to perfusion results in low PaO2 unloaded Hb leaving the alveolar capilaries (known as hypoxic hypoxia)
  • Resultant arterial blood gases the same reguarless of whether low ventilation of high perfusion
48
Q

High V/Q

A
  • High ventilation relative to perfusion causes PO2 to rise and PCO2 to fall
  • Perfusion is a function of cardiac out put and local vascular status/ bloodflow to area
  • Things like clot or cardiac can cause VQ to rise
49
Q

How does V/Q behave during normal resting conditions

A
  • Slow ventilation of 4L/min
  • slow pulmonary blood flow of 5L/min
    -V/Q = 0.8
  • oxygen enters alveoli due to breathing as fast as pulmoney blood flow removes it
  • CO2 removed from blood at the same rate as it is produced
50
Q

How V/Q behaves during exercise

A
  • Pulmonary blood flow (cardiac output) may increase 4-5x resting blood flow
  • Ventilation increases in proportion to pulmonary blood flow
  • Beyond the anerobic threshold:
    –> ventilation increases out of proportion
    –> Oxygen rises slightly not really significant
    –> carbon dioxide falls to help maintain arterial pH
51
Q

Wasted Ventilation

A
  • As V/Q exceeds 0.8 PO2 increases but oxyegn content changes in very little —> its already 100% saturated —> more oxygen is used by muscles of ventilation than what is added by increasing V/Q above 0.8 –> less oxygen is avalible for rest of the body because ventilatory muscles are taking all the O2 –> Arterial CO2 falls respiratory alkalosis results
52
Q

Slower blood flow increase—–

A

PaO2

53
Q

What happens when ther is very low cardiac output but normal PaO2

A
  • If someone has ver low cardiac output but normal PaO2 there will be limited amounts of O2 delivered to the tissue b/c of low flow as a result the body will try to extract the max amount of O2 as possible venous PO2 will become–> since there is such low flow of blood tissue hypoxia, acidosis and multisystem organ failure can occur
54
Q

Comparing 2 Processes
1. If cardiac output is low and V/Q is normal (or high) it may—–
2. If cardiac output is normal and V/Q is Low it may result in—–

A
  1. Result at tissue level is ischemic hypoxia and cellular injury : PaO2 may be high
  2. Results in hypoxic hypoxia and cellular injury : PaO2 beocmes low

Both can result in cyanosis and cellular injury

55
Q

Pulmonary Function Tests (PFTs)

A
  • How well you are able to breath and how effective your lungs work
  • Cna diagnose either obsturctive or restrictive diseases
    1. Lung volumes
    2. Gas flow rates
    3. Diffusion
    4. Flow volume loop

Interpertations are based on norms for sex, height and age

56
Q

Flow Volume Loop Interpretation:
- Low volumes=
-Scooped out =

A
  • Low volumes= restrictive disese
  • Scooped out = obstructive disease
57
Q

Diffusion Capacity of Lung for CO2

A
  • The ability of lungs to trnasfer gas from inhaled air to the RBC’s in the pulmonary capillaries

Diffusion decreased by :
- Anemia
-Increased diffusion distance
- Decreased exchange area
- Poor perfusion

58
Q

Predictive walking speeds

A

1.<0.59m/s increased risk of adverse outcomes such as falls
2. <0.4m/s (10m/25s) less likely to be discharged to home from acute care, limited home ambulation, requires assistance to exit and enter, difficulty wit stairs
3. 0.4-0.8 m/s limited community ambulation
4. >0.8 unlimited communit ambulation can ambulate through crowds and in shopping cneters (10m/12.5s)

59
Q

Restrictive Lung Disease

A
  • group of conditions
  • Difficulty in bringing O2 in due to decreased lung compliance or impaired ability of the thorax to expand
  • Increased stiffness of lungs or chest wall
  • Respiratory muscle weakness
  • Pulmonary edema

3 Main Characteristics of RLD :
1. Decreased pulmonary compliance, resistance to lung expansion decreased
2. increased work breathing (WOB)
3. On PFT all lung volumes and capacities are DECREASED

60
Q

RDL changes with aging

A
  • Usually no problems until 60’s-70’s
  • Exacterbated by smoking
  • Changes in control ventilation
    —> decreased sensitivity: peripheral to hypoxia and central receptors to hypercapnia
  • Changes in bony thorax-arthritis, kyphosis : decreased compliance of chest/decreased strength and endurance of respiratory muscles
  • increased WOB (work of breathing)
  • Decreased pulmonary compliance - changes in lung tissue
  • Decreased max. voluntary ventilation
  • decreased vital capacity
  • sleep apnea
61
Q

RDL Cancer

A
  • Leading cause of cancer deaths
  • Medical treatments: surgery, radiation, chemo PT is mostly supportive care
  • movility-manual therapy
  • ADLs
  • strengthening
  • breahting ect
62
Q

Pulmonary Fibrosis

A
  • RDL
  • Directly involves lungs
  • Inflammatory process of alveolar wall
  • Etiology= unknown/maybe viral, genetic or immune mediated
  • Patchy focal infiltrates throughout the lung, may become fibrotic or scarred
  • decreased lung compliance
  • decreased lung volume
  • increased V/Q mismatch
  • Decreased surface area for gas exchange
  • decreased diffusion area
  • increased work of right ventricle
  • inceased work of breathing
63
Q

Pulmonary Fibrosis Signs and Symptoms

A
  • CRX show reticulonodualr pattern
  • ABGs= PO2 decreased, PCO2 normal
  • Breath sounds are decreased
  • Cor pulmonale, clubbing, cyanosis
  • DOE then SOB at rest
  • Non-productive cough
  • Weight loss
64
Q

Treatment for Pulmonary Fibrosis

A
  • corticosteroids usueful only for acute inflammatory stage
  • O2
  • Nutrition
  • Pulmonary rehab
65
Q

Pneumonia

A

RLD
- Inflammatory process of lung parenchyma
- Can be viral, bacterial, mycoplasma protozoa

Defined by:
- type of pneumonia
- site of pneumonia
- where the pneumonia is acquired

66
Q

Pneumonia Signs and Symptoms / Treatment/Interventions

A
  • crackls over consolidation
  • Infiltrate on CXR (chest radiography)
  • Hyporesonance on percussion
  • DOE/SOB
  • Tacypnea

Treatment:
- antibiotics
- broncodilators/steroids

PT Interventions:
- breathing exercises
- Mobilization
- Strengthening
- PD/Chest PT

67
Q

Obstructive Vs Restrictive

A
68
Q

Upper Respiratory Infection

A

Vast Majority of respiratory infections
- Mostly viral URI
- Accounts for largest number of lost workdays
- Cna lead to LRI

69
Q

Lower Respiratory Infection

A

-Pneumonia –> inflammaton and consolidation of lung tissue filled with either fluid, mucus, pus

  • Lung abscesses
  • Airways –> bronchitis—> bronchiolitis
70
Q

Atypical Pneumonia

A
  • caused by mycoplasma, viruses, chlamydia or rickttsia
71
Q

” walking pneumonia”

A

Infection by mycoplasma pneumoniae

  • watery sputum and substernal burning and coughing
  • person does not feel very ill and cna continue to function to a large degree
  • requires an antibiotic
72
Q

Lobar Pneumonia

A

Limited to a lobe or segment of the lung

73
Q

What is being shown ?

A

R UL Pneumonia

74
Q

Bronchopneumonia

A
  • Affects 1 or more lobes and is frequently bilateral and basilar in nature
  • Characterized by wiespread inflammation of distal airways
75
Q

Lung Abscesses

A

Aspiration of infected material due to dysphagia caused by:
- CVA or other NM injury
- ETOH abuse
- septic embolism into the lungs
- traumatic perforation

76
Q

Epiglottitis

A
  • When tissue protecting the windpipe becomes inflamed and the resulting inflammation causes swelling which can eventually block the air to the lungs
  • Life threatening infection in young children
  • Obstruction, cyanosis and stridor
  • Hemophilus B is usual cause ( influenza type)
77
Q

Croup

A
  • upper airway infection that blocks the breathing and has a distractive barking cough
  • young children
  • Subglottic narrowing
  • Inpriatory stridor, cough, and hoarseness, labored, noisy breathing
  • Occurs secondary to epiglottitis or laryngotracheobronchitis in children

Steeple like shape: starts big and gets smaller

78
Q

Respiratory Syncytial Virus (RSV)

A
  • Most common cause of viral pneumonia in children under 2
  • Common cause of death in infants
  • passed by nurses not washing hands
79
Q

Restrictive lung Dysfunction: Classic signs and symptoms

A
  • tachypnea
  • cyanosis
  • dry cough
  • dyspnea
    -Alveolar hyperventilation/decreased CO2
  • V/Q mismatch
  • Hypoxemia
  • Clubbing
  • Decreased lung volumes and capacities
  • decreased diffusion capacity
  • Pulmonary hypertension
80
Q

Treatment of RLD

A
  • Supplemental O2
  • Antibiotics for infections
  • Chest tube if pneumothorax
  • Breathing exercises, chest expansion
  • postural correction
  • conditioning: mobility and strengthening
81
Q

Pursed-Lip breathing Exercising

A
  • Indicated for dyspnea at rest or with exertion,wheezing
  • Decreased symptoms of dyspnea, slowed RR, improved activity tolerance, reduced wheezing
  • Creates positive pressure splinting open airways allowing for more gas exchange and increased time frame
  • keeps airways from collapsing—> important to use pursed lip breathing in patients with COPD b/c airwya collapse during expiration in advanced stages of COPD
  • Inhale 2 seconds- Exhale 4 seconds
82
Q

Paced Breathing

A
  • volitional coordination of breahting during activity
  • most used with walking and ADLs
  • exhale slowly and comfortably not forcibly breathing out twice as long as you breath in
  • start with a 2:4 ration
  • Can combine with pursed lip or diaphragmatic breathing
83
Q

Inspiratory Muscle Training

A
  • Indicated for patients w/decreased strength or endurance of the diaphragm and intercostal muscles

Goal= to increase ventilatory capacity and decrease dyspnea

  • Incentive Spirometry
  • Diaphragmatic breathing
  • Stacked Breaths
  • Progressive Volume Breaths
  • Segmental Breathing
84
Q

Incentive Spirometer

A
  • Can be used to practice Diaphragmatic breathing, prevent or reverse ateleccasis and stimulate a cough
  • Breathing exercises are indicated for patients with ectasis which caused by hypoventilation and collapse of the alveoli of the lungs
85
Q

atelectasis

A

Atelectasis, the collapse of part or all of a lung, is caused by a blockage of the air passages (bronchus or bronchioles) or by pressure on the lung

86
Q

Why use incentive spirometry

A
  • To prevent atelectasis and promote diaphragmatic breathing
87
Q

For which patients is incentive spirometry best utilized?

A
  • Post surgical patients reluctant to take deep breaths d/t pain
  • Can be used for patients having difficulty getting air in
88
Q

Diaphragmatic Breathing

A
  • observation or measure abdominal excursion
  • Used to control dyspnea, reduce atelectasis and increase oxygenation
  • Facilitates outward motion of abdominal wall while reducing upper rib cage motion during inspiration
89
Q

Stacked breathing

A
  • Gradually increases breathing
  • w/o expiration up to max. volume tolerated
  • Used for hypoventilation, atelectasis, ineffective cough, pain, uncoordinated breathing pattern
  • improved ventilation and perfusion matching, resolution of atelectasis, reduced pain, improved cough effectiveneess
90
Q

Progressive VOlume Breaths

A
  • Increased inhalation
  • Series of breaths that are progressively increasing in depth
    Assists with increasing inspiratory volume
91
Q

Counter rotation and Butterfly Rotation

A
  • Both increase tidal volume and decrease RR by reducing tone and increasing thoracic mobility
92
Q

Effective Cough Consists of 4 Stages:

A
  1. as inspiration greater than tidla volume
  2. Closure of the glottis
  3. OCntraction of abdnominal and intercostal muscles, producing positive intrathoracic pressure –> builds force behind the cough
  4. sudden opening of the glottis and forceful expulsion of inspired air
93
Q

If someone is having a problematinc inhale what does it mean and what intervention will you choose?

A

Means they are not getting a large enough volume of air in
- Pick an intervention that primarily focuses on inspiratory breathing exercises

94
Q

Sputum colors:
1. white
2. Yellow
3. Green
4. Brown
5. Red

A
  1. normal, allergies or viral infection
  2. Developing infection
  3. Viral or bacterial infection
  4. Dried blood or heavy smoking
  5. Bleeding in respiratory tract
95
Q

When is huffing used?

A
  • Post op. when coughing is to painful
  • Sitting postiion the pt. takes feep breath and holds it and forcefully exhales 2-3 bursts of air without glottis closure
96
Q

Medium Volume Vs High volume Huffing

A

Medium Volume= Helps move secretions lower down in your airways : normal breath and long

High volume = helps move secretions in your upper airways : deep breath and quick

97
Q

Autogenic Drainage

A
  • pattern of controlled breathing inn 3 differnet volumes to mobilize secretions
  • 3 different volumes until crackles are heard
    bottom
    middle
    top
98
Q

Contraindications & precautions to Postural drainage and percussion

A
  • over fractured ribs
  • flail segments
  • over metastatic bone concer
  • over osteoporotic regions
  • Unstable cardiovascular conditions
  • Untreated pulmonary embolism
  • Subacute emphysema within the neck/head
  • Over a recent skin graft
  • Over a fragile wound
  • Over conditions where in poistioning for treatment is contraindicated : spinal surgeries, significant hemorrhage risk
  • over regions wiht lung neoplasms
99
Q

Upper Lobe Posterior segment Postural Drainage position

A
100
Q

Upper Lobe Anterior Apical Segment Postural Drainage position

A
101
Q

Upper Lobe Anterior Segment Postural Drainage Position

A
102
Q

Lingula or R middle lobe Postural Drainage Position

A
103
Q

Lower Lobe Lateral Segment (Basilar) Postural Drainage

A
104
Q

Lower Lobe posterior segment (basilar)

A
105
Q

Lower Lobe Posterior Superior Segment

A
106
Q

Lower Lobes Anterior basal segments

A
107
Q

What are the 2 forms of suctioning ?

A
  1. Inline suctioning
  2. Sterile catheter technique
    - suctioning reserved as a last resort

Winter 2024 Cardiopulmonary (4 decks)

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