Pathophysiology of Respiratory Disorders Flashcards

1
Q

Obstructive disease

A

can’t get air out

Occurs when the positive pressure of exhalation causes the small airways to pinch shut trapping gas in the alveoli

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2
Q

Signs of obstructive disease

A

Pursed lip breathing

Increased inspiratory to expiratory ratio

Abdominal muscle use

Jugular venous distention

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3
Q

Asthma Name from Greek work meaning

A

panting

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4
Q

Asthma is characterized by

A

an inflammation in the bronchiole airways due to a variety of stimuli.

Is a common chronic inflammatory disease of the airways.

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5
Q

Hallmark of Asthma is

A

Airway Diameter Reduction

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6
Q

key points of asthma

A

Reversible

Must be triggered

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7
Q

normal levels of C02 in blood

A

35-45mmhg

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8
Q

CPAP rule

A

must have neb running

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9
Q

Hypoxia

Hypoxemia

A

Hypoxia: area of the body that is short of oxygen

Hypoxemia: entire body is short of oxygen

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10
Q

Only way to fix Hypoxemia aka low spo2

A

02 and PEEP

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11
Q

Bronchospasm/ Bronchoconstriction

A

Caused by the construction of smooth muscle that surrounds the larger bronchi in the lungs

When air is forced through the constricted tubes it causes them to vibrate which creates wheezing

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12
Q

The primary treatment of bronchospasm

A

is the administration of bronchodilator medication ex: Ventolin

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13
Q

3 main symptoms of asthma

A

bronchoconstriction
mucous production
inflammation

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14
Q

Signs and Symptoms of asthma

A

SOB

Increase Work of Breathing

Accessory Muscle use

SPO2 abnormalities

Adventitious lung sound, especially wheezing

Decreased air entry

Pallor or cyanosis

ETCO2 reveals signs of bronchoconstriction

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15
Q

treatment for asthma

A

Ventolin(Salbutimol)

Atrovent(Ipratropium Bromide)

epinephrine

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16
Q

Potentially Fatal Asthma

A

Severely compromised ventilation all of the time

Be alert for silent chest syndrome

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17
Q

Potentially Fatal Asthma

Ask if pt:

A

Previous intubation for respiratory failure or respiratory arrest

2 or more admissions to hospital despite oral corticosteroid use

2 or more episodes of pneumothorax

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18
Q

Status asthmaticus

A

severe prolonged asthmatic attack that cannot be broken with conventional treatment

Patient physically tired: accessory muscle use, cyanosis, chest hyperinflatedA despite treatment already given

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19
Q

when is epinephrine used for asthma

A

silent lungs

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20
Q

Mild asthma

A

Can form sentences

Lungs: clear
-Expiratory wheezes

  1. 5-5.0mg Ventolin
    - Contra: tachy arrythmia

250-500mcg Atrovent *won’t do anything after 2 doses (1000mcg)

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21
Q

moderate asthma

A

Can speak few words at a time, tripod position

Inspiratory and expiratory wheezes through all 4 lobes

O2 immediately

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22
Q

Severe asthma

A

Stridor
—Upper airways already 50% closed

wheezing upper lobes, silent lower lobes

02

5.0/500 Combivent- Atrovent and Ventolin

CPAP: must have neb running

  1. 5mg EPI when you hear Silent chest
    - –Call ALS
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23
Q

Anaphylaxis

A

Serious allergic reaction that is rapid in onset and may cause death

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24
Q

Risk factors: Anaphylaxis

A

Predisposition

Substance

Route and dosage

Time between exposure

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25
Q

Allergen

Antibody (immunoglobulin)

Antigen

Hypersensitivity

A

Allergen: antigen

Antibody (immunoglobulin): attach to surface of mast cell and

Antigen: proteins found on surface of cells

Hypersensitivity: results from immune response to antigens

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26
Q

Allergic Reaction vs Anaphylaxis

A

Allergic Reaction
1 body system

Anaphylaxis
2 body systems
EPI!!

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27
Q

Sensitization

A

over production of IgE (antibodies)

First exposure

Antibodies attach to MAST cells and basophils
–Mast cell: part of immune system and fights off stuff

Release of chemical mediators

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28
Q

Anaphylaxis Common causes

A

Drugs

Foods and Additives

Hymenoptera Stings

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29
Q

Chemical Mediators cause and result in

A

Causes inflimation, bronchonstriction and mucous

These substances result in bronchoconstriction, peripheral vasodilation and increased capillary permeability.

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30
Q

Mediators that are stored include

A

*histamine, heparin and chemotactic factors.

Other mediators are formed during degranulation such as prostaglandins, leukotriene’s, bradykinins and interleukins.

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31
Q

Histamine Receptors

H1

A

Bronchospasm

increased peristalsis

Vessel dilation

Post capillary venule permeability

Increases heart rate

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32
Q

Histamine Receptors

H2

A

Gastric acid secretion

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33
Q

Anaphylaxis Presentation initial response

A

which occurs within the first 30 minutes after exposure and resolves within one hour consists of vasodilation, vascular leakage, and smooth muscle spasm

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34
Q

Anaphylaxis Presentation delayed response

A

which can occur hours later and last for days consisting of more intense infiltration of tissues with inflammatory cells and more severe symptoms

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35
Q

Anaphylaxis Presentation

skin

A

Urticaria (Hives)
Pruritus(itching)
Angioedema (Swelling)

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36
Q

Criteria for anaphylaxiss exist when one of the following are met:

A
  1. Acute onset symptoms involving hives, flushing, swelling of the mouth and throat, with at least one of the following:

Respiratory concerns or distress, including difficulty breathing or speaking or decrease peak expiratory flow

Declining blood pressure

Symptoms of end organ disfunction

  1. Rapid occurrence of two or more of the following after exposure to likely Allergan:

Skin and mucosal tissue symptoms including hives itchy and flushed skin and or swelling of the face and body

respiratory concerns or distress including difficulty breathing or speaking or decreased peak expiratory flow

Declining blood pressure

Symptoms of an organ disfunction

Severe gastrointestinal symptoms

  1. Exposure of known allergin causing a decline in blood pressure
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37
Q

COPD

A

General term (umbrella term): contains emphysema and chronic bronchitis

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38
Q

copd spo2

A

Spo2 always lower than normal

Goal is 94 but COPD pts goal is 90-92

Do not get COPD pt into 98

Too much O2 will lower respiratory rate

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39
Q

copd CO2

A

CO2 is always higher 50-60 mmhg

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40
Q

Common Pathologies of COPD

A

Airflow obstruction

Bronchospasm/bronchoconstriction

Increased mucous production

Impaired elasticity of airways

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41
Q

Emphysema

A

is a long-term, progressive disease of the lungs that primarily causes shortness of breath due to over-inflation of the alveoli.

Emphysema patients have damage to lung tissue in alveoli, which causes thickening and delays, or block entirely, the oxygen/carbon dioxide exchange.

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42
Q

Pulmonary Emphysema (Pink Puffers)

A

Abnormal, permanent enlarged air spaces distal to terminal bronchiole

Usually a non-productive cough

Increased Anterior/Posterior diameter (barrel chest) due to hyperinflation and increased lung volume

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43
Q

Emphysema Pathologies

A

 Destruction of alveoli walls

Weakening and destruction of bronchioles

Decreased alveoli surface area

Decreased gas exchange

44
Q

Emphysema – Signs and Symptoms

A

“pink puffer”- respiratory distress: exhalation

Pink color

Pursed lip breathing

Leaning forward

Use of accessory muscles

Tachypnea

Distended neck veins

Barrel chest

Tachypneic

Thin because they burn calories trying to breath

45
Q

Chronic Bronchitis

A

Inflammation, swelling and excessive mucous production in the bronchial tree.

Minimal alveoli involvement

Decreased ventilation of alveoli due to airflow obstruction

46
Q

Chronic Bronchitis - Signs and Symptoms

A

“blue bloater”- respiratory distress: inhalation

Cyanotic

Sweating

Leaning forward

Use of accessory muscles

Tachypnea

Distended neck veins

47
Q

COPD with right heart failure

A

Very difficult to push the patients thick blood through lungs destroyed by emphysema and through capillaries squashed by hyperinflated alveoli

48
Q

COPD with right heart failure Signs and symptoms

A

Peripheral edema
JVD
End inspiratory crackles

49
Q

Hypoxic Drive

A

Rare phenomenon that affects only a very small percentage

Pts whose respiratory drive can be decreased by high levels of oxygen

50
Q

Bagging someone with COPD

A

Pts who have severe asthma or copd should be ventilated 4-6 breaths per pin to avoid bagging them to death

51
Q

Management of COPD

A

Primary goal is to reverse airflow obstruction through bronchodilation

This is accomplished through use of sympathomimetics and
anticholinergics.

CPAP, if indicated, helps with medication administration

PEEP: Positive End Expiratory Pressure

52
Q

Pleural effusion

A

is when fluid collects between the visceral and parietal pleura.

53
Q

Effusions can be caused by

A

infections, tumors, CHF, trauma

54
Q

what do pleural Effusions cause

A

can contain several litres of fluid, which can decrease lung
capacity and cause dyspnea.

They impair breathing by limiting lungs expansion and can cause partial or complete lung collapse.

55
Q

where do P effusions happen

A

Happens in pleural space

56
Q

what will you hear with a pleural effusion

what will the spo2 be

A

When you listen you won’t hear anything

SPO2 will be low (hypoxemic)

57
Q

P effusions Treatment

A

Prehospital treatment should consist of proper positioning, high fowlers most often, aggressive supplemental oxygen if required.

58
Q

Bronchitis

A

Is an inflammation of the mucous membranes of the bronchi

59
Q

bronchitis Is characterized by

A

development of cough or small sensation in the back of the throat, with or without production of sputum

60
Q

bronchitis Divided into two categories:

A

Acute

Chronic

61
Q

bronchitis treatment

A

treat symptomatically

62
Q

Laryngitis

A

inflammation of voice box due to overuse, irritation or infection

63
Q

Croup

A

is the inflammation of the larynx and airwaves just below it

it primarily affects children five years or younger

it comes on strongest in the night time in the last 3 to 7 days

64
Q

symptoms and cause of croup

A

symptoms include loud harsh barking cough, fever, noisy inhalations, hoarse voice and dyspnea

caused by a virus

65
Q

Pneumonia

A

Is an inflammatory condition of the lung, affecting primarily the alveoli

66
Q

Viral Pneumonia

A

In adults, viruses account for approximately a third and in children for about 15% of pneumonia cases

Commonly implicated agents include rhinoviruses, coronaviruses, influenza viruses, respiratory syncytial virus (RSV)

67
Q

Pneumonia signs and symptoms

systemic:
skin:
lungs;
muscular:
central
vascular
heart
gastric
joints
A

Systemic:

  • High fever
  • Chills

Skin:

  • Clamminess
  • Blueness

Lungs:

  • Cough with sputum or phlegm
  • SOB
  • Pleuritic chest pain
  • Hemoptysis

Muscular:

  • Fatigue
  • Aches

Central:

  • Headaches
  • Loss of appetite
  • Mood swings

Vascular:
-Low bp

Heart:
-High hr

Gastric:

  • Nausea
  • Vomiting

Joints:
-Pain

68
Q

Pneumonia treatment

A

treat symptomatically

69
Q

V:Q normals and normal ratio

A

Ventilation 4l/min

Perfusion 5l/min

0.8 is normal VQ ratio

70
Q

Pulmonary Embolism

A

is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism).

71
Q

P embolism most commonly results from

A

deep vein thrombosis (a blood clot in the deep veins of the legs or pelvis) that breaks off and migrates to the lung, a process termed venous thromboembolism (VTE)

72
Q

Pulmonary embolism Risk Factors

A

Estrogen-containing hormonal contraception

Cancer (due to secretion of pro-coagulants)

Alterations in blood flow: immobilization after surgery, injury, pregnancy, obesity (also procoagulant), cancer (also procoagulant)

Smoking

Travel

73
Q

Signs and Symptoms of pulmonary embolism

A

Dyspnea

Short of breath but clear and equal lung sounds think pulmonary embolism

Pleuritic chest pain on inspiration

Pin point chest pain

Low oxygen saturation

Cyanosis

Tachypnea

Hemoptysis

Usually clear sounding lung sounds

About 15% of all cases of sudden death are attributable to PE

Severity of symptoms depend on the vessel size and location

74
Q

pulmonary embolism treatment

A

symptomatically

high O2

75
Q

Normal co2 levels

A

35-45 mmhg

76
Q

Acute Respiratory Failure

A

Respiratory failure is inadequate gas exchange by the respiratory system, with the result that levels of arterial oxygen, carbon dioxide, or both cannot be maintained within there normal ranges.

77
Q

hypoxemia

A

A drop in blood oxygenation

78
Q

hypercapnia

A

a rise in arterial carbon dioxide level

79
Q

Type 1 Respiratory Failure

A

Oxygenation Failure

hypoxia without hypercapnia, and indeed the PaCO2 may be normal or low

80
Q

ventilation/perfusion (V/Q) mismatch

A

; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs

81
Q

the 5 causes of Type 1 Respiratory Failure

A
  1. V:Q mismatch
  2. Low inp fiO2= 21%
  3. Alveolar wall disease
  4. Low resp rate
  5. Shunt
82
Q

Type 1 Respiratory Failure treatment

A

oxygen

83
Q

conditions that affect oxygenation

A

Parenchymal disease (V/Q mismatch)

Diseases of vasculature and shunts: right-to-left shunt

Pulmonary embolism

Interstitial lung diseases: ARDS, pneumonia, emphysema

84
Q

Type 2 Acute Respiratory Failure

A

Ventilation CO2

Failure to compensate: hypercapnia

They will be breathing like 35 times per minute but their end tidal will still be high

85
Q

inadequate ventilation defined

A

the build up of carbon dioxide levels (PaCO2) that has been generated by the body

86
Q

Type 2 Acute Respiratory Failure underlying causes include

A

Increased airway resistance( COPD, Asthma, Suffocation)

Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)

A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis).

Neuromuscular problems (GB syndrome., myasthenia gravis, motor neurone disease)

 Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.

87
Q

Respiratory failure resulting from hypoventilation

A

Conditions and impair lung function

Conditions that impair mechanisms of breathing

Conditions are impaired the neuromuscular apparatus

Conditions that reduce respiratory drive

88
Q

Acute Respiratory Distress Syndrome

A

Is a life-threatening reaction to injuries or acute infection to the lung.

nflammation of the lung parenchyma leads to impaired gas exchange with systemic release of inflammatory mediators, causing inflammation, hypoxemia and frequently multi organ failure

89
Q

Acute Respiratory Distress Syndrome death rate

A

This condition has a 90% death rate in untreated patients

90
Q

Acute Respiratory Distress Syndrome symptoms

A

People usually present with shortness of breath, tachypnea leading to hypoxia and providing less oxygen to the brain, occasionally causing confusion

91
Q

Aspiration

A

Is the inhalation of either oropharyngeal or gastric contents into the lower airways

92
Q

Aspiration Pneumonia

A

Migration of fluids and inflammatory cells into the area of irritation

Fever, productive cough, radiographic findings

Immunocompromised patients may not present the inflammatory response

93
Q

most common area if aspiration occurs in the sitting position

Aspiration in supine position

A

Right lower lobe

may produce infection in any lobe

94
Q

The severity of the symptoms of Aspiration Pneumonia is related to :

A

Volume of aspirant

Amount of bacterial contamination

Oropharyngeal contents with anaerobic bacteria

pH of material

pH less than 2.0 are associated with a much higher mortality rate

95
Q

Aspiration Pneumonia Management

Acute symptomatic Aspiration

A

Remove airway obstruction

Monitor CO2/SpO2

Correct hypoxia

Ventilate as required

Bronchodilators
–Aspiration-induce bronchospasm

Bronchoscopy

96
Q

Aspiration Pneumonia Treatment

A

Aggressively reduce the risk of aspiration by avoiding gastric distension when ventilating and by decompressing the stomach with an NG tube whenever appropriate

Aggressively monitor the patient’s ability to protect his or her own airway and seek to protect the patient’s airway with an advanced airway if this is impossible

Aggressively treat aspiration to suction and airway control if steps one and two fail

97
Q

BVM: ROMAN

A

restriction

obesity

mask seal

age over 55 (loss of muscle tone/ increase risk for disease)

no teeth

98
Q

SGA: RODS

A

restriction

obesity

deformed anatomy

stiff neck

99
Q

nasal O2

A

1-6lpm

24-44%

100
Q

simple o2

A

6-12lpm

24-50%

101
Q

nrb o2

A

10-15lpm

90-100%

102
Q

bvm 02

A

15lpm

100%

103
Q

o2 consumption constant
D
E
H

A
D= 0.16
E= 0.28
H= 3.14
104
Q

o2 consumption formula

A
       flow rate
105
Q

fiO2

A

fraction of inspired oxygen

106
Q

Hyperventilation

A

Hyperventilation Syndrome is a respiratory disorder, psychologically or physiologically based, involving breathing too deeply or too rapidly.

The hyperventilation is self-promulgating as rapid breathing causes carbon dioxide levels to fall below healthy levels, and respiratory alkalosis (high blood pH) develops.

107
Q

Hyperventilation Signs and symptoms

A
Palpation 
Chest pain 
Paresthesia hand and muscle 
Light headed 
Weak 
Dizzy 
Carpo-pedal spasm