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week 3 Flashcards

1
Q

Anatomy of the Lower Airway

A

Function
Exchange oxygen and carbon dioxide
Location
Externally, it extends from the fourth cervical vertebra to the xiphoid process.
Internally, it spans the glottis to the pulmonary capillary membrane.

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2
Q

Anatomy of the Lower Airway trachea

A

Serves as a conduit for air entry into the lungs
Tubular structure, approximately 10 to 12 cm in length and consists of a series of C-shaped cartilaginous rings
Begins immediately below the cricoid cartilage
Descends anteriorly down the midline of the neck and chest to the level of the fifth or sixth thoracic vertebra
Divides into the right and left main stem bronchi at the level of the carina

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3
Q

Anatomy of the Lower Airway hilum

A

Point of entry for blood vessels and the bronchi on each lung
Lungs consist of the entire mass of tissue that includes the smaller bronchi, bronchioles, and alveoli.

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4
Q

Anatomy of the Lower Airway lungs

A

Right lung has three lobes.
Left lung has two lobes.
Visceral pleura- lines the lungs
Parietal pleura- lines the thoracic cavity
Small amount of fluid is found between the pleurae.

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5
Q

Anatomy of the Lower Airway bronchus

A

Divides into increasingly smaller bronchi once it enters the lungs
Further divide into smaller bronchioles
Smaller bronchioles branch into alveolar ducts that end at the alveolar sacs.

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6
Q

Anatomy of the Lower Airway alveoli

A

Balloon-like clusters of single-layer air sacs
Functional site for the exchange of oxygen and carbon dioxide with the pulmonary capillaries
Surfactant decreases surface tension to keep alveoli open
Atelectasis-when alveoli collapse

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7
Q

Total Lung Capacity

A

Average adult man
6 litres
Only a fraction of this capacity is used during normal breathing.
Most of the gas exchange occurs in the alveoli.

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8
Q

Tidal Volume (VT)

A

Measure of the depth of breathing
Volume of air that is inhaled or exhaled during a single respiratory cycle
Normal tidal volume 5 to 7 ml/kg (approx 500ml)
In children 6 to 8 ml/kg
Inspiratory reserve volume- amount of air that can be inhaled in addition to normal Vt (typically around 3000ml)

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9
Q

Dead Space (Vd)

A

Anatomical
Includes trachea and larger bronchi. Air lingers but does not take place in gas exchange (typically 150 ml or 30% of normal Vt)
Physiological
Created by intrapulmonary obstructions or atelectasis (alveolar collapse)

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10
Q

Alveolar Volume

A

Volume of air that reaches the alveoli and participates in gas exchange
Equal to tidal volume(Vt) minus dead space volume (Vd)
Approx 350 ml in average adult man

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11
Q

Minute Volume (Vm)

A

Amount of air that moves into and out of the respiratory tract per minute
Multiply the tidal volume by the respiratory rate (Vt x RR)
Will increase if either the tidal volume or the respiratory rate increases
Will decrease if either the tidal volume or the respiratory rate decreases

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12
Q

Minute Alveolar Volume (Va)

A

Amount of air that actually reaches the alveoli per minute and participates in gas exchange
Multiply the tidal volume (minus dead space volume) by the respiratory rate (Vt– Vd x RR)
Will increase if either the tidal volume or the respiratory rate increases
Will decrease if either the tidal volume or the respiratory rate decreases

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13
Q

Functional Residual Capacity

A

Volume of gas remaining in lungs at the end of normal tidal volume exhalation.
PEEP limits exhalation, Ie. Increases FRC and keeps alveoli from collapsing

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14
Q

Expiratory reserve volume

A

The amount of air that can be exhaled following a normal (relaxed) exhalation, approx 1200ml
Residual volume
Cannot completely empty your lungs
Amount of air that remains in the lungs after maximal expiration, also approx 1200ml

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15
Q

VENTILATION VOLUMES AND CAPACITIES

A

Tidal Volume - The amount of air inhaled and exhaled during a normal breath.
+
Inspiratory Reserve Volume - The amount of air that can be inspired with maximum inspiration.

Expiratory Reserve Volume - The amount of air that can be expired with maximum expiration.

Vital Capacity - The sum of the tidal volume, inspiratory reserve volume and the expiratory reserve volume.

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16
Q

Fraction of Inspired Oxygen (FIO2)

A

Percentage of oxygen in inhaled air
Increases when supplemental oxygen is given to a patient
May decrease at altitude, in confined spaces, chemical vat
Expressed as decimal
Ie. breathing room air, 21% O2 (Fio2 0.21%)

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17
Q

Ventilation

A

Process of moving air into and out of the lungs
Two phases
Inspiration (inhalation): process of moving air into the lungs
oxygenation- bringing in O2

Expiration (expiration): process of moving air out of the lungs
removal of CO2- byproduct of cellular metabolism

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18
Q

Ventilation cycles

A

Cycle
One inspiration and one expiration
Inspiration: one third of the ventilation cycle
Expiration: two thirds of the ventilation cycle

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19
Q

Regulation of Ventilation

A

Body’s need for oxygen is dynamic and constantly changing
Respiratory system must be able to accommodate those changes by altering the rate and depth of ventilation.
Ventilation is primarily regulated by the pH of the Cerebral Spinal Fluid – directly related to the amount of CO2 dissolved in the blood (PaCO2)
Regulation of ventilation involves a series of receptors and feedback loops to sense concentrations of CO2, pH and O2 in the blood and plasma.
These receptors send signals to the respiratory centre of the brain to alter ventilations accordingly

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20
Q

Control of Ventilation

A

Neural control of ventilation
Involuntary control of breathing originates in the brain stem, in the pons and medulla
Impulses descend through the spinal cord and can be overridden by voluntary control, ie. Breath holding

Two motor nerves affect breathing
Phrenic nerve- innervates the diaphragm
Intercostal nerve- innervate the external intercostal muscles between the ribs

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21
Q

Respiratory Center

A

Respiratory center in medulla is divided into 3 regions:
Respiratory rhythmicity center
Apneustic center
Pneumotaxic center

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22
Q

Respiratory rhythmicity center

A

Sets the respiratory rate
During normal, quiet breathing, it increases its stimulation for inhalation for approximately 2 seconds, then relaxes for 3 seconds, allowing passive exhalation
Cycle then repeats, this results in a resting respiratory rate

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23
Q

Apneustic Center

A

Receives signals from the chest wall (from mechanical stretch receptors) and bronchioles via the vagus nerve to inhibit inhalation and thus expiration occurs.
This feedback loop which combines neural and mechanical control, is called Hering-Breuer reflex. Serves to prevent overexpansion
Influences respiratory rate by increasing number of inspirations per minute

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24
Q

Pneumotaxic Center

A

Working opposite the apneustic center, it inhibits inspiration.
In times of increased demand, pneumotaxic center decreases its influence, thereby increasing respiratory rate

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25
Q

Chemical control of ventilation

A

The respiratory system helps to keep the concentration of O2 & CO2 in blood, a component of acid-base balance, within a very narrow range
Carbon dioxide is the most powerful stimulant to affect the respiratory center.
Small increases, as little as 1% can increase minute volume, whereas small change in PO2 has almost no effect
Primary stimulus to breathe is termed HYPERCARBIC DRIVE
Chemoreceptors
monitor levels of CO2, O2 and the pH of the CSF and provide feedback to the respiratory center to modify rate and depth of respiration based on the body’s current needs

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26
Q

Hydrogen ions
regulation of ventillation

A

The pH of blood also has a powerful effect on respiratory center
CO2 and pH levels inversely rise and fall together causing a combined effect in the control of respirations
CO2 + H20 = H2CO3 = H + HCO3

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27
Q

Central chemoreceptors
regulation of ventillation

A

Are located adjacent to the respiratory center in the medulla
Monitor and sense minute changes in the pH of the CSF (Hydrogen ions)
An increase in hydrogen ion concentration results in a decrease in pH, causing an excitatory response in the central chemoreceptors to increase the rate and depth of breathing
Help maintain acid-base balance

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28
Q

Peripheral chemoreceptors
regulation of ventillation

A

Located in the carotid bodies and aortic arch
Monitor and sense reduction in levels of O2 and to a lesser degree, CO2 and pH, in arterial blood
Aortic arch detect levels of O2 and CO2 but not pH. Carotid bodies detect all 3

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29
Q

Control of ventilation by other factors

A

Body temperature-fever = increased metabolism
Medications
Hypoxia (increased respirations=more O2)
Acidosis (increased respiratory rate and volume to blow off more C02)
Metabolic rate

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30
Q

The Mechanics of Ventilation

A

Accomplished
Pressure changes brought about by contraction and relaxation of the intercostal muscles and diaphragm
Inhalation
Active process
Initiated by contraction of the respiratory muscles
Net effect is to increase the volume of the chest.
Lungs undergo a comparable increase in volume.
Negative-pressure ventilation-air flows into the expanded lungs because pressure inside less than outside

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31
Q

Exhalation

A

Passive process
At the end of inhalation, the respiratory muscles relax.
Natural elasticity of the lungs passively exhalesthe air.

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32
Q

MECHANICS OF VENTILATION relaxation inspiration expiration

A

RELAXATION:No movement of the muscles of ventilation
INSPIRATION:The chest expands and the diaphragm contracts.
EXPIRATION:The chest contracts and the diaphragm relaxes.

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33
Q

Respiration

A

Mechanism to ensure a constant oxygen supply and the removal of excess carbon dioxide
External respiration (pulmonary respiration)
Internal respiration (cellular respiration)

34
Q

CIRCULATORY SYSTEM

A

Pulmonary Artery
Pulmonary Vein
Venous System
Arterial System

35
Q

OVERVIEW OF THE TRANSPORT OF O2 AND CO2 to lungs

A

The majority of carbon dioxide transported to the lungs is in the form of carbonic acid (H2CO3), where the CO2 is excreted and the water (H2O) is retained.

36
Q

OVERVIEW OF THE TRANSPORT OF O2 AND CO2 in capillaries

A

Arriving back in the pulmonary capillaries, hemoglobin releases any carbon dioxide for excretion and picks up available oxygen molecules for transport.

37
Q

OVERVIEW OF THE TRANSPORT OF O2 AND CO2 3

A

Hemoglobin molecules returning to the lung carry minor amounts of carbon dioxide and a percentage of residual oxygen, depending upon the current needs of the tissues.

38
Q

how many oxygen molecule can hemoglobin molecule transport to peripheral tissue

A

Each hemoglobin molecule is capable of transporting up to four (4) oxygen molecules to peripheral tissues.

39
Q

what alveoli do

A

Clear and functional alveoli allow for the rapid exchange of gases:

O2 moves into the lungs on inspiration.

CO2 moves out of the lungs on expiration.

40
Q

Factors Affecting Affinity of Oxygen to Hemoglobin

A

3 main components that affect hemoglobin’s affinity for O2
Temp (increase temp, decreased affinity)
pH (increase in H+ ions, decrease affinity)
Carbon dioxide (increase CO2, decrease affinity

41
Q

Bohr Effect

A

The Bohr effect describes the changes in the affinity of oxygen to bind to hemoglobin as a result of the shift in blood pH that occurs on a breath by breath basis. Changes in hemoglobin to oxygen affinity occur at both the level of the lungs and the tissues.
Think of hemoglobin as a MAGNET that’s affected by blood pH.

42
Q

Bohr Effect exhalation

A

when we exhale, we blow off CO2 and a shift of the blood’s pH toward the alkaline side occurs
when the blood is more alkaline, hemoglobin has a greater affinity (stronger magnet) for O2 and thus O2 is drawn toward hemoglobin at the alveolar/capillary level.
when the blood reaches the tissue level, CO2 , a by-product of cellular metabolism, diffuses from the tissue to the capillary blood
this shifts the blood pH toward the acidic side which weakens hemoglobin’s hold on oxygen (weaker magnet)
blood (hemoglobin) that shifts toward the acidic side of pH gives up O2 readily to the tissues

43
Q

ACIDOTIC STATE

A

when the blood is acidic, hemoglobin becomes a weak magnet and does not pick up O2 as readily
we attempt to compensate for this by providing the patient with supplemental oxygen which increases the amount of O2 dissolved in blood plasma for transport.
if blood is acidic at the tissue level, O2 bound to hemoglobin is released to the tissue easily.

43
Q

ALKALINE STATE

A

hemoglobin becomes a stronger magnet, drawing O2 toward it
if the blood remained alkaline at the tissue level, it would not release O2 to the tissues readily (e.g. hyperventilation makes the blood alkaline, as does administering sodium bicarbonate, excessive vomiting, etc)

44
Q

PULSE OXIMETRY false readings

A

Falsely low O2 Sat. readings can be caused by:
- Cold extremities
- Nail polish
- Inflating BP cuff
- Ambient lighting
- States of decreased perfusion

Falsely high O2 Sat. readings can be caused by:
- Anemia
- Carbon Monoxide (CO) poisoning

45
Q

Troubleshooting SPO2 why not getting enough oxygen

A

Is there adequate FiO2 and PAO2 (atmospheric O2 in inspired air) ?

stretcher wheel is overtop of the oxygen tubing, or the O2 tank has run dry or has not been turned on.
at high altitude there is a lower PAO2

46
Q

Troubleshooting SPO2 2

A

Is there adequate diffusion of O2 across the alveolar-capillary membrane?
a shunt, such as exudate from pneumonia, pulmonary edema, bronchospasm and mucous plugs, is impairing gas diffusion and exchange.

47
Q

Troubleshooting SPO2 acidotic/alkalotic state

A

in an acidotic state, oxygen doesn’t bind as well to hemoglobin
in an alkalotic state, oxygen binds very tightly to hemoglobin but does not release easily at the tissue level
carbon monoxide (CO) has a greater affinity to hemoglobin than oxygen, approx. 200 times greater. Hemoglobin preferentially binds to CO which reduces the oxygen carrying capacity

48
Q

Troubleshooting SPO2 carrying capacity

A

Is there adequate O2 carrying capacity?

remember, 98% of oxygen transported in the blood is bound to hemoglobin.
A patient who is anemic or hypovolemic may have a saturation (SpO2) of 100%, but their oxygen carrying capacity is low. Therefore, a patient may be hypoxic despite a normal to high saturation reading.
(CO) will also bind preferentially to hemoglobin. This not only impairs the body’s oxygen carrying capacity, but because a pulse oximeter cannot differentiate between O2 and CO, you are likely to see a falsely high SpO2 reading.

49
Q

Troubleshooting SPO2 perfusion

A

Is there adequate perfusion ?
shock states or conditions such as a pulmonary embolus reduce or stop blood flow to the lungs resulting in hypoxia
Is there adequate release of O2 at the cellular level ?
a patient may have an SpO2 of 100%, but if the hemoglobin is not releasing oxygen at the tissue level, hypoxia results. This occurs when blood pH is alkalotic.

50
Q

Troubleshooting SPO2 ability of cell to use 02

A

ability of the cell to utilize the O2 that is delivered

Cyanide poisoning prevents the utilization of O2 at the cellular level.
CO, in addition to its affinity for hemoglobin, also impairs the utilization of O2 at the cellular level.

51
Q

OXYGENATION

A

Oxygenation of the patient simply means to provide oxygen. To hyperoxygenate a patient is to provide supplemental oxygen in a high concentration.
Providing supplemental oxygen affects the PaO2 level. Supplemental O2 also affects SpO2 or the amount of oxygen bound to hemoglobin

52
Q

Oxygenation - Sequence of events

A

When we inhale atmospheric gas, oxygen diffuses across the alveolar-capillary membrane and dissolves in blood plasma
98% of it is quickly then taken up and bound to hemoglobin, while the rest remains dissolved in plasma
at the tissue level, oxygen bound to hemoglobin is released, dissolves in plasma, then diffuses into the tissues

53
Q

Ventilation

A

Refers to the movement of air into and out of the lungs. It depends on the following:

Neurological control must be able to initiate ventilation.
The nerves between the brain stem and the muscles of respiration must be intact (chiefly the diaphragm).
There must be functional diaphragm and intercostal muscles.
The upper airway must be patent
The lower airways must be functional.
The alveoli must be functional.

54
Q

PAC02

A

breathing affects primarily the PaCO2 level (partial pressure exerted by carbon dioxide in arterial blood plasma) – ETCO2 is an approximation of PaCO2
normal PaCO2 is 35-45 mmHg
hyperventilation blows off CO2 and therefore may result in PaCO2 (or ETCO2) level of less than 35 mmHg

55
Q

Hyperventilation

A

Hyperventilation is not defined by the respiratory rate. i.e. a patient who is breathing at a faster than “normal” rate (e.g. an adult breathing at 40 breaths per minute), is not necessarily hyperventilating; they may be experiencing tachypnea but not excessive ventilation
Hyperventilation is defined as a Minute Volume (rate x tidal volume) that exceeds the body’s metabolic demands.

56
Q

Hyperventilation 2

A

an adult who is breathing at a rate of 40 BPM with a very low tidal volume (shallow breathing) may in fact be hypoventilating and in need of ventilatory assistance.
When encountering a patient who is breathing fast, it’s important to not assume that they’re hyperventilating. It’s equally important not to assume that their breathing needs to be coached, as their breathing pattern and minute volume may likely be a compensatory response to an underlying disorder.

57
Q

Impaired Ventilation

A

Upper airway obstruction- foreign body obstruction
- epiglottitis
- swelling

Lower airway obstruction - asthma
- bronchospasm

Chest wall impairment -pneumo/tension pneumothorax
- flail chest

Neurogenic dysfunction - CNS depressant drugs
- cervical spinal trauma
- CVA

58
Q

week 3 page 63

A

lol

59
Q

Diffusion

A

Refers to the exchange of gases (O2 and CO2) between the alveoli and the pulmonary capillaries. Gas moves from an area of high to low concentration.
Dissolved O2 crosses the pulmonary capillary membrane and binds to the hemoglobin molecule of the red blood cell
Approximately 98% of body’s total O2 is bound to hemoglobin

60
Q

FOR Diffusion to occur

A

For diffusion to occur the following must be intact:

The alveolar and pulmonary capillary walls must not be thickened.

The interstitial spaces between the alveoli and the pulmonary capillaries must not be enlarged or filled with fluid.

61
Q

Impaired Diffusion

A

Inadequate oxygen in the air - Smoke inhalation
- CO poisoning

Alveolar / bronchial pathologies - emphysema
- bronchitis

Interstitial space pathologies- pulmonary edema
- submersion aspiration
- interstitial lung disease

Capillary bed pathologies- severe atherosclerosis
- PE

62
Q

Perfusion

A

Refers to the circulation and oxygenation of blood as it circulates through the pulmonary capillary bed. The following must be intact for perfusion to occur:

There must be adequate blood volume.
There must be adequate hemoglobin within the blood.
The pulmonary capillaries must not be occluded.
There must be a functional left ventricle that allows for the smooth flow of blood through the pulmonary capillary bed.

63
Q

Impaired Perfusion

A

Inadequate blood volume - shock

Inadequate hemoglobin - anemia

Impaired circulation or flow - pulmonary embolus
- myocardial infarction

64
Q

The General Signs And Symptoms Of Respiratory Distress:

A

Stridor - partial obstruction of the upper airway.
Wheezing - bronchospasm / bronchoedema.
Crackles - Pulmonary edema / consolidation of pus.
Decreased LOC - cerebral hypoxia
Accessory muscle use
Tripod positioning
Diminished breath sounds
Tachycardia
Tachypnea
Pale, cool diaphoresis
Bradycardia - late hypoxia (pre-arrest)

65
Q

Oxygen Therapy

A

The purposes O2 therapy are to
Increase the PO2 in the alveoli and blood
Reduce ventilatory workload
Reduce myocardial workload

66
Q

NRB

A

Estimated NRB Flow Rates

6 lpm 60%
7 lpm 70%
8 lpm 80%
9 lpm 90%
10-15 lpm 95+%

67
Q

Nasal Cannula Flow Rates

A

1 lpm 24%
2 lpm 28%
3 lpm 32%
4 lpm 36%
5 lpm 40%
6 lpm 44%

68
Q

Simple Face Mask Flow Rate

A

@ 10 lpm 40%-60%

In Thunder bay we utilize with pediatric population

69
Q

Nebulizer

A

Typically ran at 8 lpm and used to deliver medications such as bronchodilators and epinephrine

70
Q

BVM

A

at 15 lpm 100% O2 supplied

Indicated for apneic pts and those with inadequate respirations

71
Q

METHOD OF USE BVM

A

High flow oxygen (e.g. 15L/min) is attached to the system and it is attached to a mask or tube
appropriate mask size
place over mouth and nose
tight fit/good seal

72
Q

Method of Use bvm2

A

open airway using two-handed thumbs down technique (with an assistant bagging) in preference to the less effective one-handed C-E grip to ensure airway patency (best if OPA and NPAs in situ too)
compress to manually ventilate them via a mask or tube (an assistant can provide ventilations)

73
Q

BVM Technique- JAWS

A

Remember JAWS for the two-handed two-thumbs down two person technique:
Jaw thrust
Airways (oral/nasal)
Work together
Slow, small squeeze — 5-7 cc/kg, over 1-2 seconds, at 10-12/min, using low pressure

74
Q

Difficulties With BVM

A

Mask seal- diff to get good seal ie. Blood, facial injuries and beards
Obese- due to increased body weight
Age- >55, loss of bony structure and connective tissue
No teeth- mask seal problems with loss of teeth
Stiff lungs- require increased ventilatory pressures, may be difficult to achieve

75
Q

ppt 84

A

a

76
Q

Complications bvvm

A

Poor compliance
Gastric insufflation
Barotrauma
t.co/8KwJc6WYgl

Atelectasis improvement with BVM ventilations and PEEP

77
Q

Hyperoxia

A

Oxygen use in the hypoxic pt is vital, however studies are showing too much may have deleterious effects on the body
Hyperoxia and oxygen toxicity may increase production of free radicals

78
Q

Hyperoxia 2

A

Result in decrease surfactant production, leading to atelectasis
Result in CNS toxicity leading to seizure and coma
affect vision
Vasoconstriction in vessels throughout the body including brain, heart, and retina
PNS activation resulting in slow HR and decreased CO to compensate for arterial vasoconstriction

79
Q

Calculation of Tank Duration

A

Duration of Flow (minutes) =
Gauge Pressure (psi ) – Safe Residual Pressure (SRP )x constant factor
Flow Rate (L/minute)
CONSTANT FACTOR
D-0.16
E-0.28
M-1.56

79
Q

sp02

A

measurement of how much oxygen your blood is carrying as a percentage of the maximum it could carry

patient care (7 decks)

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