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Emergency Critical Care VTS > Respiratory Emergencies > Flashcards

Respiratory Emergencies Flashcards

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1
Q

Stertorous respirations

A

characterized by low pitch snoring; can be heard on inspiration and expiration. Indicative of disease in rostral region of upper airway, nasal passages, choanae, nasopharynx

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2
Q

Stridorous:

A

high pitch on inspiration associated with obstructive disease of larynx or trachea

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3
Q

potential complication associated with upper airway obstruction that affects the parenchyma

A

noncardiogenic pulmonary edema and aspiration pneumonia

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4
Q

Paradoxical laryngeal motion

A

inward movement of the arytenoids secondary to negative pressure generated upon inspiration

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5
Q

Complications of upper airway obstructions

A

hyperthermia resulting from failure to dissipate heat Severe hyperthermia can induce additional derangements.

Noncardiogenic pulmonary edema

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6
Q

Grading Tracheal collapse

A

Graded I-IV with each grade 25% progressive reduction in tracheal diameter lumen and flattening of the tracheal cartilages and dorsal tracheal membrane.

Grade IV: Inversion of ventral tracheal cartilages

Gold standard for grading severity: tracheobronchoscopy

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7
Q

Tracheal stent complications

A
  1. Tracheal stent fractures (historically catastrophic) - improvements with stent design so complication is infrequent and readily manageable.
  2. Tracheal stent migration: usually early complication and promptly recognized
  3. Inflammatory (granulation) tissue formation - nonobstructive –> immunosuppressive steroid therapy. obstructive –> repeat tracheal stenting, steroids, antimicrobials
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8
Q

Bronchopulmonary disease in cats divided into 2 categories

A
  1. asthma
  2. chronic bronchitis
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9
Q

Feline asthma

A

hyperreactive airway with reversible bronchoconstriction.

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10
Q

Chronic bronchitis

A

characterized by thickening of the airways and excessive mucus production.

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11
Q

Dyspnea

A

uncomfortable awareness of breathing
e.g. shortness of breath
inability to take a breath
chest tightness
Appears as difficult/labored breathing; subjective experience
not to be confused with tachypnea, hyperpnea, hyperventilation

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12
Q

tachypnea

A

rapid breathing

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13
Q

hyperpnea

A

increase rate and depth of breathing

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14
Q

Normal pleural space pressure

A

-5cm H2O

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15
Q

Tidal volume

A

amount of air that moves in and out of lung with each respiratory cycle
approximately 10-20ml/kg
slightly less in cat
Vt = VA + VD (tidal volume = alveolar ventilation + deadspace

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16
Q

Functional residual capacity

A

volume of air left in lungs after passive expiration

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17
Q

residual volume

A

The remaining air in lungs if individual expired as much as possible

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18
Q

Vital capacity

A

maximum volume of air a patient can consciously control on inhale

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19
Q

Total lung capacity

A

vital capacity + residual capacity

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20
Q

Minute volume (Ve)

A

Total ventilation x rate of breathing (Vf)

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21
Q

Alveolar ventilation

A

proportion of inspired air that actually makes it to the alveoli

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22
Q

Medullary respiratory center

A

Contains pre-botzinger complex - generates respiratory rhythm

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23
Q

Dorsal respiratory group

A

inspiration

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24
Q

ventral respiratory group

A

expiration

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25
Q

pneumotaxic center in Pons

A

regulate volume and rate

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26
Q

Central chemoreceptors

A

responds to pH in extracellular fluid
decrease in pH = increase in respiration
increase in pH = decrease in respiration
Does not respond to arterial oxygen content

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27
Q

Peripheral chemoreceptors locations

A

Carotid and aortic bodies
responds to decrease in PaO2 and increases in PaCO2

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28
Q

Stretch receptors

A

Located in lung and airway smooth muscle.

When distended (ie giving a breath under anesthesia) will initiate a brief period of decreased respirations +/- apnea

Known as Hering Breur Reflex

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29
Q

Irritant receptors

A

Also known as rapidly adapting pulmonary stretch receptors
located in airway epithelia cells
stimulated by irritants (e.g. smoke, cold air, noxious gas)
results in rapid bronchoconstriction and hyperpnea

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30
Q

Bronchoconstriction Innervated by _____________ __________
Results in _____________ airway resistance

A

vagus nerve
increased

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31
Q

What are the class of drugs that contribute to bronchodilation? Give two examples.

A

Beta 2 agonist
albuterol, terbutaline

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32
Q

Juxtacapillary or J receptors
Location
Results in what when stimulated?

A

suspected to be located in alveolar walls
results in rapid shallow breathing - plays a role in patients with dyspnea

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33
Q

Haldane Effect

A

oxygenation of blood in lungs displaces carbon dioxide from hemoglobin which increases removal of carbon dioxide

explains how oxygen concentrations influence hemoglobin’s carbon dioxide affinity.

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34
Q

Bohr Effect

A

explains how carbon dioxide and hydrogen ions influence hemoglobin’s oxygen affinity.

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35
Q

Right shift of oxygen dissociation curve

A

Promotes offloading of oxygen from hemoglobin.
Occurs with increased CO2, increase in acidity (decrease in pH), increase in temperature

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36
Q

Left shift of Oxygen dissociation curve

A

Increases affinity of oxygen to hemoglobin
Occurs with decrease in CO2, alkalosis (increase in pH), decrease in temperature.

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37
Q

CO2 respirations

explain pathophysiology of CO2

A

bicarbonate is carried by plasma to alveoli, where it is converted back to CO2 and diffuses across alveolar capillary membrane by passive diffusion.

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38
Q

Hypoxia

A

inadequate delivery of oxygen (DO2) to meet tissue metabolic demand (VO2) caused by inadequate tissue perfusion, metabolic disturbances, lack of O2 supply.

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39
Q

Define: Hypoxemia

Provide PaO2 value

A

abnormally low concentration of oxygen in blood
PaO2 <80mmHg

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40
Q

Severe hypoxemia

Provide PaO2 value and clinical sign

A

PaO2 <60mmHg
Cyanotic

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41
Q

5 Types of hypoxia

A
  1. Hypoxemic hypoxia
  2. hypemic hypoxemia or Anemic hypoxia
    2a. hemoglobinopathy caused by: carboxyhemoglobin, methemoglobinemia
  3. Stagnant or circulatory hypoxia
  4. histiotoxic hypoxia
  5. metabolic hypoxia
42
Q

hypoxemic hypoxia

A

inadequate oxygen carrying capacity of blood (CaO2) secondary to hypoxemia

43
Q

hypemic hypoxemia

A

AKA: anemic hypoxia: anemia caused decrease in circulating hemoglobin, reducing the oxygen carrying capacity o blood (CaO2)

44
Q

hemoglobinopathy

A

patient not anemic, but limited hemoglobin available to transport O2

45
Q

Stagnant or circulatory hypoxia

A

caused by decreased cardiac output and poor tissue perfusion

46
Q

histiotoxic hypoxia

A

when tissues are unable to extract and utilize O2 appropriately

47
Q

metabolic hypoxia

A

when there is an increase in cellular consumption of oxygen (VO2)

48
Q

Causes of hypoxemia

A
  1. decreased fractional inspired oxygen concentration
  2. hypoventilation

3.venous admixture

+/-4. reduced venous oxygen content secondary to low cardiac output or slow peripheral blood flow (shock) or high extraction from tissue (seizures)

49
Q

Four causes for venous admixture

A
  1. low ventilation perfusion regions
  2. small airway and alveolar collapse or infiltration (no ventilation-perfusion regions)
  3. diffusion defects
  4. anatomic right to left shunts
50
Q

methods to assess severity of hypoxemia

A

A:a gradient
PaO2: FiO2 ratio
SaO2:FiO2 ratio
oxygenation index
oxygen saturation index

51
Q

decreased fractional inspired [O2]

A

No changes in A-a gradient
Tx: increase FiO2

Can occur at high altitudes or when there is an interruption and inadequate amount of O2 spplementation

52
Q

Hypoventilation defined by PaCO2, EtCO2, venous PCO2

A

PaO2 greater or equal to 40mmHg
ETCO2 is usually 5mmHg lower than PaCO2, so when ETCO2 is greater or equal to 40mmHg = hypoventilation
Central venous PCO2 is approximately 5mmHg higher than PaCO2, so when PCO2 is greater or equal to 50mmHg = hypoventilation

53
Q

How do you prevent hypoxemia secondary to hypoventilation?

A

Increase FiO2

Alveolar oxygen is a balance between oxygen delivered to alveoli and amount of oxygen removed from alveoli

The amount of oxygen delivered to alveoli = alveolar minute ventilation + inspired FiO2
hypoventilation = decline in alveolar minute ventilation
decrease in oxygen delivery to alveoli = decrease in delivery to blood = hypoxemia.
Therefore increase FiO2 can prevent hypoxemia

54
Q

Mechanism of hypoxemia

A
  1. low inspired oxygen (e.g. problem with mechanical apparatus, high altitude)
  2. hypoventilation (PaCO2 greater or equal to 45mmHg)
  3. Venous admixture
    3.a. low ventilation/perfusion regions in the lungs
    3.b. Regions of zero V/Q; small airway and alveolar collapse (atelectasis or no ventilation, but well perfused lung unit)
    3.c. diffusion impairments
  4. d. anatomical right to left shunts.
55
Q

V/Q mismatch

A

regions of low ventilation, high perfusion
0 = dead space

56
Q

Causes of V/Q mismatch

A
  1. small airway narrowing
  2. fluid accumulation
  3. increase in perfusion (pulmonary thromboembolism)

1+2 can be caused by bronchospasms, fluid accumulation/epithelial edema

Poorly oxygenated blood in these regions is mixed with blood from normal functioning regions and dilutes/reduces the net oxygen concentration. –> regional hypoventilation -> is also responsive to O2 therapy

57
Q

cause, effects and treatment of zero v/q regions

A

occurs in diseases associated with accumulation of fluids or alveolar collapse
if animals recumbent for prolonged periods of time
absence of deep breath
(Atelectasis)
Condition = physiologic shunt

Hypoxemia due to zero V/Q is not responsive to oxygen therapy
Must treat by increasing airway or transpulmonary pressure –> positive pressure ventilation

58
Q

Cause, effects and treatment of diffusion impairments

A

diffusion impairments are uncommon
results from thickened respiratory membranes secondary to remodeling of pulmonary structures

flat type I alveolar pneumocytes damaged by inhalation or inflammatory injury
healed –> type II cuboidal alveolar pneumocytes
This can occur with O2 toxicity or ARDS

diffusion defect will be present until type II mature to type I pneumocytes
Diffusion defects only partially responsive to O2 therapy

59
Q

Treatments for anatomic shunts

A

right to left shunt bypass lungs
nonresponsive to oxygen therapy or positive pressure ventilation
Correct with surgery

60
Q

Patm at sea level

A

760mmhg

61
Q

PH2O at sea level

A

45mmHg

62
Q

Respiratory quotient

A

0.8

63
Q

PAO2 calculation

A

[(Patm - Ph2O)(FiO2)] - (PaCO2/RQ)

64
Q

A:a gradient

what is normal?

A

A-a
Normal <10mmHg

65
Q

120 rule

A

PaCO2 = 40mmHg
PaO2 = 80mmHg

Sum = 120mmHg

<120mmHg suggest presence of venous admixture

The greater the discrepancy, the greater the lung dysfunction

66
Q

PaO2:FiO2 ratio (AKA P/F ratio)

A

Normal P/F ratio is approximately 500
e.g. PaO2 = 100mmHg
FiO2 = 0.21
100mmHg/0.21 = 500mmHg

67
Q

Disadvantage of P/F ratio

A

does not account for PaCO2; therefore inaccurate if PaCO2 values are abnormal

68
Q

Dead space subdivided into three regions

A

anatomic: upper airway; trachea, lower levels to the terminal bronchioles
alveolar: gas in alveoli but does not participate in exchange with pulmonary capillaries
physiologic = anatomic + alveolar dead space
apparatus dead space

69
Q

Methods for measuring dead space

A

Fowler’s method
Bohr’s method

70
Q

Bohr’s method:

A

measures volume of he lung that does not eliminate CO2
Also measures physiologic dead space

71
Q

Fowler’s method:

A

measure the concentration of a tracer gas (usually nitrogen) when given with 100% oxygen

72
Q

Normal PaCO2 for Dog and Cat

A

Dog: 30-42mmHg
Cat: 25-36 mmHg

73
Q

PaCO2 levels to indicate hypoventilation and hyperventilation

A

Hypoventilation: > 40-45mmHg
Hyperventilation: <30-35mmHg

74
Q

Mechanism and etiology of hypercapnia

A
  1. increased inspired CO2
  2. increased CO2 production
  3. impaired CO2 excretion
75
Q

causes of increased inspired CO2

A
  1. faulty circuits
  2. excessive dead space
  3. inadequate fresh gas flow
  4. exhausted absorptive agents
76
Q

causes for increase CO2 production with fixed minute ventilation

A

Rare, but reasons can include:
thyrotoxicosis
fever
sepsis
malignant hyperthermia
overfeeding
exercise

This is uncommon because a compensatory increase to minute ventilation restores PaCO2 to normal.

77
Q

causes for impaired CO2 excretion

A

global hypoventilation or increased dead space

78
Q

systemic effects of hypercapnia and respiratory acidosis

A

alterations to autonomic nervous system
cardiorespiratory
neurologic
metabolic functions
decrease in myocardial contractility
decrease in systemic vascular resistence

79
Q

Effects of elevated PCO2 on cardiorespiratory

A

vasoconstriction of pulmonary circulation
bronchodilation
decrease in diaphragmatic contractility

80
Q

Effects of hypercapnia on neurologic system

A

Neurologic sequelae depends on magnitude and duration of hypercapnia and concurrent hypoxemia
increase PCO2 can increase cerebral blood flow because of vasodilation
increases systemic and intracranial pressure
CO2 narcosis seen at PCO2 >90mmHg - likely due to alterations in intracellular pH and changes in cellular metabolism

81
Q

effects of hypercapnia on metabolic and endocrine functions

A

constriction of renal afferent arterial result in AKI and decreased urine output
sodium and water retention –>hyperkalemia
increase in CO2 stimulate anterior pituitary –> increase adrenocorticotropic hormone secretions

82
Q

Effects of respiratory acidosis

A

cardiovascular instability
altered mentation
electrolyte abnormalities

83
Q

Why is sodium bicarbonate contraindicated for correcting respiratory acidosis.

A

Because of the carbonic anhydrase equation - increase in bicarbonate can shift to increase in CO2, which will exacerbate hypercapnia.

84
Q

What are three respiratory stimulants?

A

Doxapram
Methylxanthine (aminophylline, theophylline, caffeine)
Progesterone

85
Q

Methylxanthine

A

(aminophylline, theophylline and caffeine)
shown to improve ventilation
Beneficial effects:
bronchodilation
central respiratory center stimulation
improved skeletal muscle and diaphragmatic contractility
enhance mucociliary clearance
effects vary between types of methylxanthine
Theophylline - more potent cardiac stimulant, greater diuretic and bronchodilator but higher incidence of tachycardia
Caffeine stimulate CNS and penetrates CSF.

86
Q

Doxapram

A

stimulates respiratory via activation of peripheral chemoreceptors
higher doses stimulate medulla respiratory center causing increase tidal volume and increase respiratory rate
side effects: systemic catecholamine release and CNS stimulation; may increase work of breathing thereby increasing O2 consumption

87
Q

Progesterone

A

Progesterone acts as trigger of the primary respiratory centre by increasing the sensitivity of the respiratory centre to carbon dioxide, as indicated by the steeper slope of the ventilation curve in response to alveolar carbon dioxide changes

88
Q

Anticipated Compensation for Acid-Base Disorders

A
89
Q

P:F ratio normal values
P:F ration abnormal value indications

A

Normal 400-500
acute lung injury <300
ARDS <200

90
Q

Why is sodium bicarbonate contraindicated in respiratory acidosis?

A

Carbonic anhydrase equation.

Bicarbonate may worsen hypercapnia.

91
Q

What are five determinant factors for transvascular fluid flux?

A
  1. capillary hydrostatic pressure
  2. interstitial hydrostatic pressure
  3. capillary colloid osmotic pressure (COP)
  4. COP beneath the endothelial glycocalyx
  5. reflection/filtration coefficients
92
Q

What are the two main pathophysiologic forms for pulmonary edema?

A
  1. high hydrostatic pressure
  2. increased permeability
93
Q

Pathophysiology of pulmonary edema as a result of high hydrostatic pressure

A

increase in pulmonary capillary pressure –> fluid extravasation that eventually overwhelms the lymphatic removal capacity

94
Q

What are three causes for hypoxemia?

A
  1. low inspired FiO2
  2. hypoventilation
  3. venous admixture
    +/- 4. reduced venous oxygen content secondary to low cardiac output or slow peripheral blood flow *(shock) or high extraction by tissues (seizures)
95
Q

Causes for low inspired O2

A

If attached to mechanical apparatus and fault with machine or circuit
high altitude

96
Q

Define hypoventilation

A

elevated PaCO2: greater or equal to 45mmHg
ETCO2 (usually 5mmHg lower than PaCO2): greater or equal to 4mmHg
Central venous PCO2 (approx 5mmHg higher than PaCO2): greater or equal to 50mmHg

97
Q

Treatment for hypoxemia as a result of hypoventilation

A

Increase FiO2

Alveolar oxygen is a balance between the amount of O2 delivered to the alveol and the amount of O2 removed from th alveoli

A decrease in alveolar minute ventilation (hypoventilation) results in decrease oxygen delivery to alveoli, which decreases delivery to blood, resulting in hypoxemia

98
Q

4 Causes of venous admixture

A

1) Low ventilation - perfusion regions in the lungs
2) small airway and alveolar collapse (atelectasis or no ventilation but perfused lung units)
3) diffusion defects
4) anatomical right to left shunts

99
Q

Explain pathophysiology of low V/Q. What are some causes and is it responsive to oxygen?

A

Low VQ = low ventilation with or without high perfusion. V/Q drops with more perfusion.

Poorly oxygenated blood in the regions of low V/Q admixes (regional hypoventilatio) with blood from normal funtioning regions resulting in a dilute and reduced net concentration of oxygen.

This is responsive to ventilation.

100
Q

Regions of zero V/Q

explain pathophysiology and potential causes. Is it responsive to oxygen therapy?

A

Occurs with diseases associated with accumulation of fluids or alveolar collapse.

Condition refered to as physiologic shunt - blood flowing past these areas but no oxygen change.

Areas of zero V/Q are not responsive to oxygen therapy.

Tatment is to reactive by increasing airway or transpulmonary pressure with positive pressure ventilation

101
Q
A

Emergency Critical Care VTS (21 decks)

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