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Patient Care > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Components of Upper Respiratory Tract

A

Sinus, nasal cavity, external nose, nostril, tongue, larynx, esophagus, trachea, pharynx, glottis, epiglottis, opening of eustachian tube

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2
Q

Components of Lower Respiratory Tract

A

Larynx, Trachea, Bronchi, Lungs

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3
Q

Central Chemoreceptors

A

In brain, respond to changes in H and arterial Co2 in CSF
Positive feedback loop

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4
Q

Dorsal and ventral respiratory neurons

A

In medulla
Control rhythm of respiration

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5
Q

Apneustic and Pneumotaxic centres

A

In pons
Affect rate and depth of respiration

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6
Q

Activation of muscles of respiration

A

Phrenic nerve

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7
Q

Peripheral Chemoreceptors

A

In carotid and aortic bodies, respond to changes in CO2, pH and O2 levels
Secondary drive

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8
Q

Low pO2 in peripheral chemoreceptors

A

Increase ventilation

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9
Q

Inspiratory muscles

A

Increase thoracic cage volume –> decreased intrathoracic pressure

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10
Q

Expiratory muscles

A

Decrease thoracic cage volume –> increased intrathoracic pressure

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11
Q

Tidal volume

A

500mL
Amount of air moved in or out each breath

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12
Q

Inspiratory Reserve Volume

A

3000mL
Max volume inspired above normal inspiration

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13
Q

Expiratory Reserve Volume

A

1100mL
Max volume expired below normal expiration

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14
Q

Residual Volume

A

Volume of air left in the lungs after maximum expiratory effort

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15
Q

Surfactant

A

Produced by type II alveolar epithelial cells
Reduces surface tension by forming a layer between aqueouss fluid lining alveoli and air

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16
Q

Bronchial Sounds

A

Heard over trachea
I:E ratio 2:3 or 1:3
Loud, harsh, high pitched

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17
Q

Broncho-vesicular sound

A

Anteriorly near 1st and 2nd IC space
Soft/breezy

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18
Q

Vesicular Sounds

A

Lungs, peripheral
Lower pitch

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19
Q

Adventitious sounds

A

Crackles, wheeze, stridor, pleural rub

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20
Q

Pulmonary Oxygen Toxicity

A

Cellular injury to lung parenchyma and airway epithelium
O2 causes thickening of intra-cellular space, loss or inhibition of surfactant
Results in ARDS, fluid leaking, and atelectasis
Depends on O2 concentration, length of exposure, underlying condition

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21
Q

Nitrogen Washout

A

Damage from deficiency of nitrogen. High concentrations of O2 causes nitrogen to be exhaled and replaced by O2 in the alveoli. Removal of O2 causes alveolar collapse and hypoxemia

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22
Q

Oxygen Induced Hypercarbia/Apnea

A

Extended time to occur
Affects pts that utilize peripheral chemoreceptors to breath
Affects hypoxic drive
COPD pts

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23
Q

Retinopathy of Prematurity

A

Insult to developing retinal vasculature from elevated PaO2 leading to abnormal blood vessel growth
Leads to separation of retina, visual impairments, blindness
Oxygen radical attack incompletely developed retinal tissue
Premature infants

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24
Q

Factors influencing affinity of HgB for O2

A

Acidity
Partial pressure of CO2
Temperature
2,3 BPG

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25
Q

Right Shift

A

Acidosis
Hyperthermia
Hypercapnia
Hypoxia
Anemia
Increased 2,3 BPG

More oxygen available to the tissues, high affinity at lungs

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26
Q

Shift Left

A

Alkalosis
Hypothermia
Hypocapnia
Decreased 2,3 BPG
Carboxyhemaglobin

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27
Q

V<Q

A

Wasted perfusion
Anything that decreases or completely stops O2 from reaching alveoli
Pulmonary oedema, COPD, asthma, FBAO

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28
Q

V>Q

A

Dead space, wasted ventilation
Oxygen present but no pulmonary capillaries/blood for diffusion

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29
Q

Hypoxic Hypoxia

A

Lack of oxygen diffusion into pulmonary circulation
Decreased amount inhaled
Pulmonary oedema, COPD, ARDS, FBAO, drowning, high altitude

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30
Q

Anemic Hypoxia

A

Lack of RBC to transport O2
Will not respond to O2 therapy
Low HgB, sickle cell anemia, hemorrhage, CO poisoning

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31
Q

Histotoxic Hypoxia

A

Inability to offload oxygen from hemoglobin
Inability for cells to utilize oxygen
Requires treatment of underlying cause to respond to O2
Metabolic alkalosis, cyanide poisoning

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32
Q

Stagnant Hypoxia

A

lack of circulating O2
Blood flow insufficient to supply tissues
Treat the cause
Angina, MI, crush injury, poor circulation

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33
Q

Asthma

A

Hyper-reactive airway to stimuli resulting in inflammation, swelling, and narrowing of trachea and bronchi

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34
Q

3 main insults causing asthmatic respiratory distress

A

Inflammation
Bronchoconstriction
Excess mucus Secretion

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35
Q

Asthma Triggers

A

Allergens
Exercise
Respiratory infeciton
Nose + sinus problems
Drug and food additives
GERD
Emotional stress

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36
Q

Early Phase Asthma

A

30-60 min post exposure, subsides 30-90 min late
Bronchospasm
Release of histamine and leukotrienes
Release of inflammatory cytokines

Wheezing, cough, chest tightness, dyspnea

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37
Q

Late Phase Asthma

A

Inflammation
Histamine causes hyper-responsive airways
Increased resistance causes air trapping and hyperinflation of lungs
Can cause lung damage
Peaks in 5-6 hours with infiltration of eosinophils, and neutrophils
Within 1-2 day infiltration with monocytes and lymphocytes occurs

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38
Q

Medication Therapy of Asthma

A

Bronchodilators
Longer acting bronchodilator
Anti-inflammatory drugs
Leukotriene Modifiers

39
Q

Dexamethasone Indications

A

Hx of asthma/COPD or 20 pack/year Hx of smoking

40
Q

Contraindications dexamethasone

A

Allergy to steroids
Steroids in last 48 hours

41
Q

Treatment Dexamethasone

A

PO/IM/IV
0.5mg/kg up to 8mg
1 dose

42
Q

Permissive Hypercapnia

A

Tolerating higher ETCO2 instead of attempting to decrease value with aggressive ventilation

43
Q

COPD

A

Chronic inflammatory lung disease causing obstructed airflow from lung

44
Q

Chronic Bronchitis

A

Mucus plugging/inflammatory edema
Increased airflow resistance leads to alveolar hypoventilation
Increased secretions due to ongoing mucus + phlegm
Hypoxemia and Hypercarbia

45
Q

Hypoxemia

A

Increased RBCs without oxygen
Cyanosis (blue bloater)

46
Q

Hypercarbia

A

Pulmonary vascular constriction
Increased RV work
Right heart failure
For Pulmonale

47
Q

Emphysema

A

Excess loss of elastin causing lung tissue to lose elastic recoil
Destruction of alveolar septum
Neutrophils produce elastase that destroy elastin
Pink Puffer

48
Q

Pathology of Emphysema

A

Destruction of alveolar walls/septum
Destruction of gas exchange surface area
Distension or pulmonary air space
Loss of elastic recoil

49
Q

Emphysema vs Bronchitis

A

Bronchitis: irritation + inflammation of upper and lower air tracts
Emphysema: alveoli, destruction of elastin, loss of ability to recoil

50
Q

Factors affecting CO

A

HR
Preload
Afterload
Contractility

51
Q

Preload

A

Volume of blood in LV at diastole

52
Q

Starlings Law

A

Greater the stretch, greater the contraction

53
Q

Increases of preload

A

Fluid increase
Vasoconstriction

54
Q

Decreases of Preload

A

Fluid loss
Vasodilation
Loss of atrial kick

55
Q

Afterload

A

Resistance LV must pump against

56
Q

Increases of Afterload

A

HTN
Vasoconstriction

57
Q

Decreases of Afterload

A

Vasodilation

58
Q

Contractility

A

Ability of heart to squeeze, strength of contraction and ejection fraction

59
Q

Ejection fraction

A

Amount of blood as percent that LV pushes
50-70%

60
Q

Decreases of Contractility

A

Infected tissue
Ischemic tissue
Acid-base imbalance
Negative inotropes

61
Q

Increases of Contractility

A

Sympathetic stimulation
Positive inotropes (digoxin)

62
Q

Compensatory mechanisms of CHF

A

SNS stimulation
Myocardial hypertrophy
Hormonal response

63
Q

Left sided heart failure

A

Blood backs up through left atrium and into pulmonary system
Pulmonary HTN
Biventricular failure

64
Q

Causes of LSHF

A

HTN
MI
Dysrhythmias
Valvular disorder

65
Q

Right Sided Heart Failure

A

Dereased RV
Blood backs up into right atrium and venous circulation
Can lead to venous congestion

66
Q

Causes of RSHF

A

LVF
For pulmonal
RV infarction

67
Q

Clinical Manifestations of Acute CHF

A

Pulmonary edema
Agitation
Pale/cyanosis
Cold, clammy skin
Severe dyspnea
Tachypnea
Pink, frothy sputum

68
Q

Clinical Manifestations of Chronic CHF

A

Fatigue
Dyspnea
Tachycardia
Edema
Nocturia
Behavioural changes
Chest pain
Weight change
Skin changes

69
Q

Drug Therapy Chronic CHF

A

ACE inhibitors
Diuretics
Inotropic drugs
B-adrenergic drugs

70
Q

Goal of Initial CHF therapy

A

Decrease intravascular volume
Decrease venous return
Decrease afterload
Increase gas exchange and oxygenation
Increase cardiac function
Decrease anxiety

71
Q

Nitroglycerin

A

Relaxes vascular smooth muscle
Peripheral venodilation
Dilation of arteriolar resistance vessels of peripheral circulation
Decrease MVO2

72
Q

Side effects of Nitro

A

Headache
Dizziness
Weakness
Tachycardia
Hypotension
Orthostasis
Skin rash
Dry mouth
N/V

73
Q

Causes of PE

A

Trauma/travel
Hypercoagulability or hormone replacement
Recreational drugs
Older
Malignancy
Birth control
Obesity/obstetrical
Surgery
Immobilization
Sickness

74
Q

3 Types of PE

A

Massive
Submassive
Low Risk

75
Q

Etiology of PE

A

DVT moves to pulmonary arterial tree causing V/Q mismatch. Increase pulmonary artery resistance leads to right ventricular failure

76
Q

Clinical Manifestation PE

A

Tachypnea
SOB
Hypotension
Tachycardia
Altered LOC
Anxiety
Pale
Cough
Central cyanosis
Leg pain
Cardiovascular collapse
S1Q3T3

77
Q

S1Q3T3

A

S Wave in lead 1
Q wave in lead 3
T wave inversion lead 3

78
Q

Immunologic Anaphylaxis

A

Allergen enters system and interacts with B cells, creating antibodies for the allergen

79
Q

Non-Immunologic Anaphylaxis

A

Allergen interacts directly with receptors on mast cells

80
Q

Epinephrine

A

Antagonist for Histamine
Alpha and Beta effects
Relaxes smooth muscle in GI and GU

81
Q

Benadryl

A

H1 receptor antihistamine
Competes for histamine receptors in CNS and PNS
Sedative properties due to competitive antagonism in CNS
Also acts as anti-muscarinic

82
Q

Epiglottitis

A

Swelling of supraglottic area of epiglottis and pharyngeal structures
Often bacterial

83
Q

S/Sx epiglottitis

A

Sniffing position with inability to swallow, high fever, inspiratory stridor, retractions

Children 2-6yo
Quick progression

84
Q

Croup

A

Inflammation of entire airway, edema in subglottic area
Bacterial or viral, usually viral

85
Q

Croup S/Sx

A

URTI, barking cough, low fever
Children 6mth to 3 years

86
Q

Spontaneous Pneumothorax

A

Sub-pleural bleb ruptures allowing air to enter pleural space

87
Q

Simple Pneumothorax

A

No communication with atmosphere
No mediastinum shift or hemi-diaphragm

88
Q

Mechanism of Simple Pneumothorax

A

Fracture rib
Increased intrathoracic pressure with closed glottis

89
Q

Open Pneumothorax

A

Open defect in chest wall
If >2/3 diameter of trachea then path of least resistance
Paradoxical motion of affected lung
Large dead space

90
Q

Tension Pneumothorax

A

Trapping of air created by one way valve

91
Q

S/Sx of Tension Pneumothorax

A

Decreased BS or hyper-resonance on one side
Distended neck veins
Hypotension
tachycardia

92
Q

Needle decompression current site

A

2nd intercostal space, superior aspect of 3rd rib mid clavicular line

93
Q

PCS 5 Needle decompression

A

Patch removed
Site anterior axilla

Patient Care (11 decks)

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