Respiratory Emergencies Flashcards
Stertorous respirations
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
Stridorous:
high pitch on inspiration associated with obstructive disease of larynx or trachea
potential complication associated with upper airway obstruction that affects the parenchyma
noncardiogenic pulmonary edema and aspiration pneumonia
Paradoxical laryngeal motion
inward movement of the arytenoids secondary to negative pressure generated upon inspiration
Complications of upper airway obstructions
hyperthermia resulting from failure to dissipate heat Severe hyperthermia can induce additional derangements.
Noncardiogenic pulmonary edema
Grading Tracheal collapse
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
Tracheal stent complications
- Tracheal stent fractures (historically catastrophic) - improvements with stent design so complication is infrequent and readily manageable.
- Tracheal stent migration: usually early complication and promptly recognized
- Inflammatory (granulation) tissue formation - nonobstructive –> immunosuppressive steroid therapy. obstructive –> repeat tracheal stenting, steroids, antimicrobials
Bronchopulmonary disease in cats divided into 2 categories
- asthma
- chronic bronchitis
Feline asthma
hyperreactive airway with reversible bronchoconstriction.
Chronic bronchitis
characterized by thickening of the airways and excessive mucus production.
Dyspnea
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
tachypnea
rapid breathing
hyperpnea
increase rate and depth of breathing
Normal pleural space pressure
-5cm H2O
Tidal volume
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
Functional residual capacity
volume of air left in lungs after passive expiration
residual volume
The remaining air in lungs if individual expired as much as possible
Vital capacity
maximum volume of air a patient can consciously control on inhale
Total lung capacity
vital capacity + residual capacity
Minute volume (Ve)
Total ventilation x rate of breathing (Vf)
Alveolar ventilation
proportion of inspired air that actually makes it to the alveoli
Medullary respiratory center
Contains pre-botzinger complex - generates respiratory rhythm
Dorsal respiratory group
inspiration
ventral respiratory group
expiration
pneumotaxic center in Pons
regulate volume and rate
Central chemoreceptors
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
Peripheral chemoreceptors locations
Carotid and aortic bodies
responds to decrease in PaO2 and increases in PaCO2
Stretch receptors
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
Irritant receptors
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
Bronchoconstriction Innervated by _____________ __________
Results in _____________ airway resistance
vagus nerve
increased
What are the class of drugs that contribute to bronchodilation? Give two examples.
Beta 2 agonist
albuterol, terbutaline
Juxtacapillary or J receptors
Location
Results in what when stimulated?
suspected to be located in alveolar walls
results in rapid shallow breathing - plays a role in patients with dyspnea
Haldane Effect
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.
Bohr Effect
explains how carbon dioxide and hydrogen ions influence hemoglobin’s oxygen affinity.
Right shift of oxygen dissociation curve
Promotes offloading of oxygen from hemoglobin.
Occurs with increased CO2, increase in acidity (decrease in pH), increase in temperature
Left shift of Oxygen dissociation curve
Increases affinity of oxygen to hemoglobin
Occurs with decrease in CO2, alkalosis (increase in pH), decrease in temperature.
CO2 respirations
explain pathophysiology of CO2
bicarbonate is carried by plasma to alveoli, where it is converted back to CO2 and diffuses across alveolar capillary membrane by passive diffusion.
Hypoxia
inadequate delivery of oxygen (DO2) to meet tissue metabolic demand (VO2) caused by inadequate tissue perfusion, metabolic disturbances, lack of O2 supply.
Define: Hypoxemia
Provide PaO2 value
abnormally low concentration of oxygen in blood
PaO2 <80mmHg
Severe hypoxemia
Provide PaO2 value and clinical sign
PaO2 <60mmHg
Cyanotic
5 Types of hypoxia
- Hypoxemic hypoxia
- hypemic hypoxemia or Anemic hypoxia
2a. hemoglobinopathy caused by: carboxyhemoglobin, methemoglobinemia - Stagnant or circulatory hypoxia
- histiotoxic hypoxia
- metabolic hypoxia
hypoxemic hypoxia
inadequate oxygen carrying capacity of blood (CaO2) secondary to hypoxemia
hypemic hypoxemia
AKA: anemic hypoxia: anemia caused decrease in circulating hemoglobin, reducing the oxygen carrying capacity o blood (CaO2)
hemoglobinopathy
patient not anemic, but limited hemoglobin available to transport O2
Stagnant or circulatory hypoxia
caused by decreased cardiac output and poor tissue perfusion
histiotoxic hypoxia
when tissues are unable to extract and utilize O2 appropriately
metabolic hypoxia
when there is an increase in cellular consumption of oxygen (VO2)
Causes of hypoxemia
- decreased fractional inspired oxygen concentration
- 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)
Four causes for venous admixture
- low ventilation perfusion regions
- small airway and alveolar collapse or infiltration (no ventilation-perfusion regions)
- diffusion defects
- anatomic right to left shunts
methods to assess severity of hypoxemia
A:a gradient
PaO2: FiO2 ratio
SaO2:FiO2 ratio
oxygenation index
oxygen saturation index
decreased fractional inspired [O2]
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
Hypoventilation defined by PaCO2, EtCO2, venous PCO2
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
How do you prevent hypoxemia secondary to hypoventilation?
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
Mechanism of hypoxemia
- low inspired oxygen (e.g. problem with mechanical apparatus, high altitude)
- hypoventilation (PaCO2 greater or equal to 45mmHg)
- 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 - d. anatomical right to left shunts.
V/Q mismatch
regions of low ventilation, high perfusion
0 = dead space
Causes of V/Q mismatch
- small airway narrowing
- fluid accumulation
- 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
cause, effects and treatment of zero v/q regions
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
Cause, effects and treatment of diffusion impairments
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
Treatments for anatomic shunts
right to left shunt bypass lungs
nonresponsive to oxygen therapy or positive pressure ventilation
Correct with surgery
Patm at sea level
760mmhg
PH2O at sea level
45mmHg
Respiratory quotient
0.8
PAO2 calculation
[(Patm - Ph2O)(FiO2)] - (PaCO2/RQ)
A:a gradient
what is normal?
A-a
Normal <10mmHg
120 rule
PaCO2 = 40mmHg
PaO2 = 80mmHg
Sum = 120mmHg
<120mmHg suggest presence of venous admixture
The greater the discrepancy, the greater the lung dysfunction
PaO2:FiO2 ratio (AKA P/F ratio)
Normal P/F ratio is approximately 500
e.g. PaO2 = 100mmHg
FiO2 = 0.21
100mmHg/0.21 = 500mmHg
Disadvantage of P/F ratio
does not account for PaCO2; therefore inaccurate if PaCO2 values are abnormal
Dead space subdivided into three regions
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
Methods for measuring dead space
Fowler’s method
Bohr’s method
Bohr’s method:
measures volume of he lung that does not eliminate CO2
Also measures physiologic dead space
Fowler’s method:
measure the concentration of a tracer gas (usually nitrogen) when given with 100% oxygen
Normal PaCO2 for Dog and Cat
Dog: 30-42mmHg
Cat: 25-36 mmHg
PaCO2 levels to indicate hypoventilation and hyperventilation
Hypoventilation: > 40-45mmHg
Hyperventilation: <30-35mmHg
Mechanism and etiology of hypercapnia
- increased inspired CO2
- increased CO2 production
- impaired CO2 excretion
causes of increased inspired CO2
- faulty circuits
- excessive dead space
- inadequate fresh gas flow
- exhausted absorptive agents
causes for increase CO2 production with fixed minute ventilation
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.
causes for impaired CO2 excretion
global hypoventilation or increased dead space
systemic effects of hypercapnia and respiratory acidosis
alterations to autonomic nervous system
cardiorespiratory
neurologic
metabolic functions
decrease in myocardial contractility
decrease in systemic vascular resistence
Effects of elevated PCO2 on cardiorespiratory
vasoconstriction of pulmonary circulation
bronchodilation
decrease in diaphragmatic contractility
Effects of hypercapnia on neurologic system
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
effects of hypercapnia on metabolic and endocrine functions
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
Effects of respiratory acidosis
cardiovascular instability
altered mentation
electrolyte abnormalities
Why is sodium bicarbonate contraindicated for correcting respiratory acidosis.
Because of the carbonic anhydrase equation - increase in bicarbonate can shift to increase in CO2, which will exacerbate hypercapnia.
What are three respiratory stimulants?
Doxapram
Methylxanthine (aminophylline, theophylline, caffeine)
Progesterone
Methylxanthine
(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.
Doxapram
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
Progesterone
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
Anticipated Compensation for Acid-Base Disorders
P:F ratio normal values
P:F ration abnormal value indications
Normal 400-500
acute lung injury <300
ARDS <200
Why is sodium bicarbonate contraindicated in respiratory acidosis?
Carbonic anhydrase equation.
Bicarbonate may worsen hypercapnia.
What are five determinant factors for transvascular fluid flux?
- capillary hydrostatic pressure
- interstitial hydrostatic pressure
- capillary colloid osmotic pressure (COP)
- COP beneath the endothelial glycocalyx
- reflection/filtration coefficients
What are the two main pathophysiologic forms for pulmonary edema?
- high hydrostatic pressure
- increased permeability
Pathophysiology of pulmonary edema as a result of high hydrostatic pressure
increase in pulmonary capillary pressure –> fluid extravasation that eventually overwhelms the lymphatic removal capacity
What are three causes for hypoxemia?
- low inspired FiO2
- hypoventilation
- venous admixture
+/- 4. reduced venous oxygen content secondary to low cardiac output or slow peripheral blood flow *(shock) or high extraction by tissues (seizures)
Causes for low inspired O2
If attached to mechanical apparatus and fault with machine or circuit
high altitude
Define hypoventilation
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
Treatment for hypoxemia as a result of hypoventilation
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
4 Causes of venous admixture
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
Explain pathophysiology of low V/Q. What are some causes and is it responsive to oxygen?
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.
Regions of zero V/Q
explain pathophysiology and potential causes. Is it responsive to oxygen therapy?
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
