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Flashcards in respiratory integration Deck (37)
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1
Q

what does low Sa02 and high CO2 cause

A

Hypoxaemia
Hypercapnia = hypercarbia
Poor Tissue Perfusion
Poor Oxygen Capacity

2
Q

what does respiratory failure cause

A

Due to resp. path.
compensation
Cardiac Failure- Low Output
Anaemia

3
Q

what is the difference between dyspnoea, apnoea, hypopnea and bradypnoea

A

Dyspnoea – difficulty or discomfort in breathing
Hypopnoea – low minute ventilation, low tidal volume (Overly shallow breathing)
Bradypnoea – Low breathing rate
Apnoea – breathing stops, muscles of resp stop

4
Q

what is narcosis

A

a state of confusion, stupor, unconsciousness or euphoria (like drunkenness)

5
Q

what are narcotic drugs

A

opioids: morphine & heroine, reduce respiratory drive

6
Q

what are the types of narcosis

A

N2 Narcosis – during scuba diving, high partial pressure of N2 in blood leads to impairment of judgment. Can be relieved by ascending to less depth (i.e. toward surface)
CO2 Narcosis – when plasma CO2 is chronically high, body reduces homeostatic response to CO2 (ie less respiratory drive)

7
Q

is it possible to have a high PaO2 but a low SaO2

A

yes - Hb pathologies, other gases (CO) & poisons interfering with Hb binding to O2, etc
but not high SaO2 and low PaO2 - High SaO2 will unload O2 into solution until equilibrium is reached
so SaO2 is main measure of oxygen delivery to tissues

8
Q

what is clubbing

A

growth of nail beds due to chronic hypoxia

9
Q

what causes respiratory failure

A

Must be due to respiratory pathology

Cannot be due to homeostatic respiratory compensation for kidney or liver pathologies

10
Q

what causes respiratory failure type 1

A

Hypoxaemia, normal arterial CO2
breathing appropriately
Inspired O2 does not arrive inside capillaries of perfused alveoli (or at high concentration inside aorta)
eg V-Q mismatch, diffusion problems, shunt,
Transfer factor (DLCO)

11
Q

what causes respiratory failure type 2

A

Hypoxaemia with pathologically elevated CO2 due to respiratory causes
hypoventilation

12
Q

what is anatomical dead space

A

no gas exchange occurs
In adult: 150 ml, of tidal volume of 500 ml
While exhaling, this air is identical to atmospheric air
Physiological Dead Space = anatomical dead space + alveolar dead space

13
Q

what is residual volume

A

amount of gas remaining in the lungs after maximal expiratory effort
While inhaling, this air is identical to expired (ie high CO2, lower O2) alveolar air. Arrives from deepest recesses of alveoli.

14
Q

what is infection of airways

A
Airways have mucus and cilia to protect alveoli
When airways collapse or clog, CO2 builds up behind obstruction
makes breathing (moving air in and out of lungs) difficult
15
Q

what is infection of alveoli

A

When alveoli collapse or clog, no CO2 can leave blood: alv dead sp
This is the reason pneumonia causes V-Q mismatch

16
Q

what results in type 2 respiratory failure

A

acidosis
Increased airways resistance (COPD, asthma, suffocation)
Reduced breathing effort (e.g. narcotic drugs, opiates)
Partial closure of airways (e.g. chronic bronchitis)
Neuromuscular problems (e.g. myasthenia gravis)
Chest defects that interfere with breathing

17
Q

what are types of type 2 respiratory failure

A

obstructive and restrictive

18
Q

what is obstructive lung disease

A

An obstruction (or ubiquitous obstructions) in airways increase resistance to air flow
Typically more difficult to exhale
Rate of exhalation (FEV1) is smaller
But in many cases the total volume is preserved

19
Q

what is restrictive lung failure

A

Lung/chest stiffness (or neuromuscular dysfunction) limit ability of lung/chest to drive airflow
more difficult to inhale
TOTAL VOLUME of exhalation, FVC, is smaller
So is the RV and the FRC (and thus the TLC)

20
Q

what are examples of obstructive airways

A

COPD
Asthma
Bronchiectasis
CF

21
Q

what is COPD

A

Often a mixture of emphysema and chronic bronchitis
Chronic bronchitis – airways narrow, mucus, cough
Emphysema – alveolar walls destroyed, making big air spaces that cannot be emptied, shortness of breath and fatigue

22
Q

What are blue bloaters in COPD

A

air trapping (large chest), cyanotic. Mostly Bronchitis

23
Q

What are pink puffers in COPD

A

Not cyanotic, increase internal airway pressure during exhalation to keep alveoli and airways open. Mostly Emphysema
CO2 retention – COPD patients who receive excessive supplemental O2 lose respiratory drive

24
Q

why are pressure-volume curves are important in intubated (mechanically-ventilated) patients

A

Increases in impedance can be due to an increase in airway resistance, or a decrease in compliance
Airway Resistance is NOT measured at equilibrium

25
Q

what is hysteresis in compliance

A

Normal. Slope of pressure vs volume is 1 / Impedance. Low slope = high impedance. Hysteresis is caused by finite delay of airflow due to friction in airway
Restriction. Increased impedance due to decreased compliance.
Obstruction. Increased impedance due to airway obstruction.

26
Q

what is air trapping in obstructive disease

A

When increased air (with expiratory levels of O2 & CO2) remains in the lungs at the end of expiration.
Caused by increased airway resistance (R)
Results in Increased Residual Volume

27
Q

what happens if air trapping is chronic

A

lungs remodel such that
Total Lung Capacity is Increased
Thoracic cavity may change shape
Detected as increase in Residual Volume

28
Q

what is spirometry like normal, obstructive and restrictive

A
A = Normal, late breath is convex
B = obstructive, late breath is concave
C = restrictive, late breath is convex like normal, but maximal volume is low b/c had less inspired air to start
29
Q

what are restrictive pulmonary diseases

A
Difficulty with inhalation
Interstitial lung disease 
e.g. pulmonary fibrosis
Autoimmune diseases that reduce lung compliance
Obesity 
e.g. obesity hypoventilation syndrome
Scoliosis
Neuromuscular disease
E.g. muscular dystrophy or amyotrophic lateral sclerosis (ALS)
30
Q

what is hypoventilation as a compensatory breathing change

A
Hypoventilation to acidify
In metabolic alkalosis
Vomitting
Antacids
Dehydration>Aldosterone
Result: High CO2 levels
31
Q

what is hyperventilation as a compensatory breathing change

A
Hyperventilation to de-acidify
In metabolic acidosis
Diabetic Ketoacidosis
Chronic kidney disease (“kidney failure”)
Also psychogenic
Pain
Anxiety
Result: Low CO2 levels
32
Q

what is respiratory failure type 1

A

Low PiO2 (e.g. at high altitude)
V-Q mismatch (e.g. pulmonary embolism)
Diffusion problem (e.g. Pulmonary Hypertension)
Shunt (when some non-oxygenated blood is mixed with oxygenated blood in aorta blood)

33
Q

Why does type 1 resp failure lead to hypoxaemia but not hypercapnia?

A

excess of O2 in compared to what blood can take up and excess CO2 in blood compared to expired air
the airways remain patent, there is a homeostatic increase in minute ventilation to dispose of the extra CO2

34
Q

what is an extreme type of V/Q mismatch

A
Physiological dead space
Ventilation occurs, but NOT perfusion
Example: pulmonary embolism
Shunt
Perfusion occurs, but NOT ventilation
Examples: complete airway obstruction, lobar pneumonia
True shunt does *not* respond to breathing 100% O2
VQ mismatch will benefit from 100% O2
35
Q

what causes V-Q Mismatch, Perfusion with impaired Ventilation

A
Conditions that cause changes in or collapse of a subset of the alveoli
such as 
Lobar Pneumonia 
Asthma
Pulmonary oedema
36
Q

what causes Ventilation with impaired Perfusion

A

pulmonary embolus or
decreased cardiac output
Shock

37
Q

Extreme V-Q Mismatch: How does Alveolar Collapse lead to Low O2 Saturation

A

pneumonia - lungs filled with with fluid but other lobes ventilate normally
CO2 high - vasoconstriction stops perfusion
alveolus collapses, CO2 does NOT build up as cannot unload where liquid is
So this region of lung is perfused, but blood gets no O2
Air sacs downstream of blocked airway accumulate CO2