Gas Exchange Flashcards

1
Q

Acid base balance is regulated to maintain

A

Normal ph

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2
Q

Two forms of body acids

A

Volatile and nonvolatile

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3
Q

Volatile

A

Carbonic acid H2CO3

Eliminated as CO2 gas and water

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4
Q

Nonvolatile

A

Sulfuric, phosphoric, and other organic acids
Eliminated by renal tubules
Regulated by bicarbonate HCO3

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5
Q

What is a buffer

A

Chemical that can bind to excess H or OH without large change to ph

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6
Q

Most important plasma buffering system

A

Carbonic acid bicarbonate pair

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7
Q

Protein buffering system

A

Proteins have negative charge

Can buffer H+

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8
Q

Renal buffering

A

Secretion of H+ in the urine and reabsorption of HCO3-

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9
Q

Where does carbonic acid bicarbonate pair happen

A

Lungs and kindeys

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10
Q

Greater partial pressure of CO2 =

A

More carbonic acid H2CO3 formed

Both can increase but the ratio must be maintained

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11
Q

Respiratory system compensation with carbonic acid bicarbonate pair

A

Increase ventilation to get rid of CO2
Or
Decrease ventilation to retain CO2

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12
Q

Renal system compensation with carbonic acid bicarbonate pair

A

Produces acidic or alkaline urine

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13
Q

Normal arterial blood ph

A

7.35-7.45

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14
Q

Acidosis

A

System increase in H+ concentration or decrease in bicarbonate

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15
Q

Alkalosis

A

System decrease in H+ or increase in bicarbonate

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16
Q

Normal pCO2

A

35-45

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17
Q

Normal HCO3

A

22-26

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18
Q

Resp acidosis

A

High paco2
Ventilation depression
Low ph high paco2

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19
Q

Resp alkalosis

A

Low paco2
Alveolar hyperventilation
High ph low paco2

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20
Q

Metabolic acidosis

A

Low HCO3 or increase in noncarbonic acids

Ph low HCO3 low

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21
Q

Metabolic alkalosis

A

High HCO3
Excessive loss of metabolic acids
Ph high HCO3 high

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22
Q

Fully compensated

A

Ph normal

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23
Q

Partially compensated

A

All 3 abnormal

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24
Q

Uncompensated

A

PCO2 or HCO3 is normal, other is abnormal

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25
Q

Causes of impaired gas exchange

A

Ineffective ventilation
Reduced capacity for gas transport (reduced hemoglobin/RBC)
Inadequate perfusion

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26
Q

COPD diagnostic studies

A

Chest X-ray
Spirometry
History
Physical exam

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27
Q

COPD spirometry findings

A

Reduced FEV1/FVC ratio

Increased residual volume

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28
Q

COPD ABG findings

A

Low PaO2
High PaCo2
Low ph
High bicarbonate (late stage)

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29
Q

COPD oxygen therapy used for

A

Reduce work of breathing
Maintain PaO2
Reduce cardiac work load

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30
Q

COPD oxygen therapy humidification

A

Use humidifiers because O2 dries mucosa

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31
Q

Complication of oxygen therapy

A
Combustion 
CO2 narcosis 
O2 toxicity 
Absorption atelectasis 
Infection
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32
Q

What do bronchodilators do

A

Relax bronchial smooth muscles causing bronchodilation

33
Q

Three classes of bronchodilator

A

Beta-adrenergics agonists
Anticholinergics
Xanthine derivatives

34
Q

Beta adrenergic agonists action

A

Dilate airways

Stimulate beta 2 adrenergic receptors in lungs

35
Q

Beta adrenergic agonists adverse effects

A
Insomnia 
Restlessness 
Anorexia 
Heart stimulation 
Hyperglycemia 
Tremor 
Vascular headache 
Tachycardia 
Angina pain 
Hyper/hypotension
36
Q

Beta agonists bronchodilator drugs

A
Ephedrine
Epinephrine 
Fenoterol 
Formoterol 
Isoproterenol 
Salbutamol 
Salmeterol
Terbutaline
37
Q

Salbutamol sulphate

A
Ventolin 
Short acting 
Most common 
Route: inhalation 
Onset: immediate 
Peak: 10-25 min
Half life: 3-4 hours
Duration of action: 3-4 hours
38
Q

Anitcholinergics action

A

Prevents ACh from binding to receptors
Allows bronchodilation
Reduce secretions in people with COPD

39
Q

Anticholinergics adverse effects

A
Dry mouth/throat 
Nasal congestion 
Heart palpitations 
GI distress 
Urinary retention 
Increased intraocular pressure 
Headache 
Cough 
Anxiety
40
Q

Ipratropium bromide

A
Atrovent 
Anticholinergic
Oldest most common 
Liquid aerosol and inhaler 
Route: inhalation 
Onset: 5-15 min 
Peak: 1-2 hours 
Half life: 1.6 hours 
Duration of action: 4-5 hours
41
Q

Xanthine derivatives action

A

Cause bronchodilation
Increase levels of cAMP
Stimulates CNS which I handles respiratory drive

42
Q

Xanthine derivatives adverse effects

A
Nausea 
Vomiting 
Anorexia 
Gastroesophogeal reflux 
Tachycardia 
Extrasytole 
Palpitations 
Ventricular dysrhythmias
43
Q

Corticosteroids action

A

Reduced inflammation

Enhance activity of B-agonists

44
Q

Fluticasone propionate

A

Flovent
Route: inhalation
Half life 3 hours
Duration: up to 24 hours

45
Q

Antitussives action

A

Suppress cough reflex
Act directly on cough Center in the CNS
Reduce runny nose and post nasal drop by drying mucosa

46
Q

Expectorants action

A

Reduce the thickness of bronchial secretions

Increases mucous flow so it can be easily removed by coughing

47
Q

What is asthma

A

Chronic inflammation disorder of the airways

48
Q

Asthma triggers

A
Allergens
Exercise
Respiratory infection 
Nose and sinus problems 
Drug and food additives
GERD 
Air pollutants 
Emotional stress
49
Q

Early phase of asthma

A

Bronchospasm
Increased mucous secretions, edema formation, increased amounts of tenacious sputum
Peaks in 30-60 mins after exposure
Subsides in about 30-90 mins

50
Q

Asthma late phase response

A
More severe 
Primary response is inflammation 
Peaks 5-12 hours 
Can last hours to days 
Corticosteroids effective
51
Q

asthma inspiration expiration ratios

A

1: 2
1: 3
1: 4

52
Q

Asthma complications

A

Severe acute attack

Severe asthma attack

53
Q

Severe acute attack causes

A
Viral illness 
Ingestion of aspirin or other NSAIDS 
increased environmental pollutants 
Allergen exposure 
Discontinuation of drug therapy
54
Q

Severe asthma attack clinical manifestation

A

Similar to non severe asthma

More serious and prolonged

55
Q

Severe asthma attack

A

Pneumothorax
Pneumomediastinum
Acute cor pulmonale with right ventricular failure
Severe respiratory muscle fatigue that leads to respiratory arrest

56
Q

Asthma diagnostic studies

A
History 
Physical exam 
Pulmonary function test 
Peak flow monitoring 
Chest X-ray 
ABG 
Oximetry 
Allergy testing 
Blood levels of eosinophils 
Sputum culture and sensitivity
57
Q

Three categories of medication used to treat asthma

A

Mast cell stabilizers
Leukotrine modifiers
Glucocorticoids

58
Q

Mast cell stabilizers action

A

Inhibit release of inflammatory chemicals (histamines) from mast cells
Makes airways less likely to construct
Anti-inflammatory in nature

59
Q

Mast cell stabilizers indication

A

Prevent but do not treat attacks

Help people with exercise induced asthma

60
Q

Mast cell stabilizers prototypes

A

Cromolyn (crolomintal) and nedocromil (alocril)

61
Q

Leukotriene modifiers/antagonists

A

Anti-inflammatories that prevent the action/synthesis of leukotrienes
Prevent inflammation, bronchoconstriction and mucous production
Can be used during an attack

62
Q

Leukotriene modifiers/antagonists prototypes

A

Monetelukast (singulair)
Zarfirlukast (accolate)
Zileuton (zyflo)

63
Q

Leukotriene modifiers/antagonists action

A

Bund to D4 leukotriene receptor subtypes in the respiratory tract
Prevent leukotrienes from attaching to receptors on immune cells

64
Q

Montelukast sodium

A
Singulair 
Approved use in children 2+
Fewer side effects 
Route: PO
Onset: 30 mins
Peak: 3-4 hours 
Half life: 2.7-5 hours 
Duration of action: 24 hours
65
Q

Status asthmaticus

A

Severe attack that does not reposed to pharmacotherapy

Life threatening

66
Q

What happens during status asthmaticus

A
Bronchospasm not reversed 
Hypoxemia develops 
Hypercapnea (respiratory acidosis) develops 
Silent chest (no audible air movement)
paCO2 greater than 70
67
Q

Status asthmaticus symptoms

A
Decreased consciousness 
Use of accessory muscles 
Increased respiratory rate 
Wheezing 
Increased fatigue 
Increased heart rate 
Inflammation if airway 
Decreased oxygen level
68
Q

Status asthmaticus first line of treatment

A

Beta antagonists
Rapid relief of bronchospasms
Provide immediate bronchodilation

69
Q

Status asthmaticus second line of treatment

A

IV corticosteroids

Highly effective anti inflammatory drugs

70
Q

Status asthmaticus third line of treatment

A

Theophylline
Smooth muscle relaxation causing optimal bronchodilation
Ensuring optimal cardiac functioning

71
Q

Status asthmaticus other medications

A

Anticholinergics: decrease mucous production and increase bronchodilation
Sedatives: calms anxiety
Anesthetics: relaxes smooth muscle

72
Q

Status asthmaticus additional treatment

A

IV fluid
Monitor oxygen level via ABG
Oxygen support
If oxygen support not enough, may need to be ventilated

73
Q

Inhalation of pulmonary drugs

Aerosol methods

A

Nebulizers
Dry powder inhaler
Metered dose inhaler

74
Q

Advantages of inhaled pulmonary drugs

A

Delivers drug to immediate site of action

Reduces systemic effects

75
Q

Disadvantages of inhaled pulmonary drugs

A

Precise dosing is difficult

People dont use device and spacer correctly

76
Q

Acute intervention

A
Monitor respiratory and cardiovascular system
Kung sounds 
Respiratory rate 
Pulse 
BP
77
Q

Peak flow

Green zone

A

80-100% of personal best

Remain on medication

78
Q

Peak flow

Yellow zone

A

50-79% of personal best
Indicates caution
Something is triggering asthma

79
Q

Peak flow

Red zone

A

56-60% of personal best
Indicates serious problem
Action to be taken with health care provider