21 – Pathophysiology: Respiratory System Flashcards
What are the 3 body systems that sustain life min-by-min?
- CNS
- Respiratory system
- CV system
- *if stop working=life threatening!
Upper airways include
- Nose, nasal cavity and sinuses, nasopharynx
- Mouth, oropharynx, larynx
Lower airways (lungs) zones
- Conducing zone
a. Trachea, bronchi, bronchioles, tertiary bronchi - Respiratory zone
a. Tertiary bronchi, alveoli
Upper airway functions
- Thermoregulation
- Filtration
- Humidification
- Olfactory
- Air conduction
- Phonation
- Swallowing (airway protection)
What are the 2 main functions of the lower airways?
- Non-respiratory
- Respiratory
Non-respiratory functions of the lower airways
- Immunological (mucociliary)
- Acid-base regulation
- Vascular, metabolic, endocrine, etc.
Respiratory functions of the lower airways
- GAS EXCHANGE
o Works closely with CV system - Surfactant synthesis
What is ventilation primarily controlled by?
- CO2
Respiratory center provides
- Slow, steady ventilation control
2 areas of the respiratory center
- Medulla oblongata
- Pons
Medulla oblongata (respiratory centre)
- Dorsal and ventral respiratory groups
o Control inspiration and expiration
Pons (respiratory center)
- Pneumotaxic center and apneustic center
o Adjust ventilation controlled by medulla oblongata respiratory groups
Central chemoreceptors
- Min-by-min changes in ventilation
- Floor of ventral medulla
- Dissolved CO2 passed through semipermeable membrane (BBB) and enters CSF
What is the normal CSF pH and what happens if it changes?
- 7.32
- If changes=control breathing
- Increased CO2=decrease pH=STIMULATE breathing
- *less buffering capacity than blood=greater changes in pH based on PCO2
Peripheral chemoreceptors
- Rapid, fine-tunning ventilation
- Aortic and carotid bodies!
- Sense PaCO2, PaO2, pH and perfusion of carotid/aortic bodies
- *overrides ventilation controlled by respiratory center
When do you get an increased ventilation from the peripheral chemoreceptors in response?
- Increased PaCO2
- Decreased blood pH
- Decreased PaO2
What are the positives of endotracheal intubation?
- Prevent aspiration of gastric contents
- Prevent upper airway obstruction (due to muscle relaxation of laryngeal muscles=sedatives and tranquilizers)
- Ability to manually ventilate for patient experiencing hypoventilation or apnea
What are the negatives of endotracheal intubation?
- Bypass humidification and heating mechanisms of upper airways
- Increased resistance to breathing
o if too small tube, connectors or one-way valves in breathing circuit
What are ways to treat for heat and water losses with endotracheal intubation?
- Passive: COMMON
- Active
- Active warming
Passive ways to treat heat and water losses with endotracheal intubation?
- Implement low fresh gas flow rates
- Use HME filters
Active ways to treat heat and water losses with endotracheal intubation?
- Humidifiers/nebulizers
- Heated anesthesia breathing circuits
How can you treat for increased resistance to breathing with endotracheal intubation?
- Choose largest tube possible
o *Poiseuille’s’ law: airway resistance through a tube is INVERSELY proportional to radius to the power of 4
What is the normal PaCO2?
- 35-45 mmHg
When awake, alveolar ventilation changes _______with changes in PaCO2
- LINEARLY
o Max response at PaCO2=100mmHg
What is involved with hypoventilation?
- Inadequate CO2 elimination detected by increased PaCO2 or ETCO2
- *PaCO2 is MORE THAN 45mmHg
Anesthesia effects: progressive dose-dependent decrease in spontaneous ventilation leads to
- Blunted peripheral and central chemoreceptor responses to increased PaCO2
- Muscle relaxation (respiratory muscles)
What is the normal PaO2?
- 80-100mHg on room air (=21% of inspired O2)
- 5x inspired O2
What does hypoxemia trigger?
- Peripheral chemoreceptors to cause a STEEP INCREASE in ventilation
o NON-LINEAR response of alveolar ventilation to changing PaO2 - *when less than 60mmHg
What is ‘hypoxic drive’?
- Overrides normal CO2 driven ventilation
Inhalant anesthetics have dose-dependent inhibition of peripheral chemoreceptor response, causing a
- DECREASED ventilation response to hypoxemia
Apnea
- Complete absence of breathing
o Extreme end point of respiratory depression
When is the most common stage of anesthesia for apnea?
- Induction (75% incidence)
o Potent IV anesthetics (propofol/alfaxalone) agent used with high respiratory depressant effects
What can induction apnea lead to?
- Hypoxemia
Who are high risk patients of induction apnea?
- *those with reduced functional residual capacity (FRC)
o Increased intra-abdominal pressure (ex. pregnancy)
o Lung disease
o Obesity
o Age (pediatrics and geriatrics)
o Anesthesia (decreases FRC by 15%)
How can you prevent induction apnea?
- Titrate induction agent
o Use lowest does possible to allow intubation
How can you prevent hypoxemia?
- Pre-oxygenate for 3-7 mins PRIOR to induction
What does pre-oxygenating for 3-7mins prior to induction do?
- Increases PaO2 and oxygen reserve
- De-nitrogenize system
- Provides extra time (~3mins) before patient will DESATURATE after becoming apneic
What are some other causes of apnea?
- Equipment failure (incompetent one-way flow)
- Deep anesthesia levels with inhalant anesthetics
When is the max response of chemoreceptors and what happens?
- PaCO2=100mH
- Ventilation DECLINES
o Can become apneic and may not restart breathing at deep planes of anesthesia
Anesthetic index
- Ratio of end-tidal anesthetic where animals becomes APNEIC, divided by MAC
- *inverse relationship
- Ex. sevoflurance (3.45) < Halothan < Isoflurane (2.5)
What does a lower apnetic index mean?
- Drug is MORE respiratory depressant
When does/what is the equation for respiratory arrest?
- Respiratory arrest = 1.5-3.0 x MAC
Normal breathing creates a
- NEGATIVE intra-thoracic pressure
o Expands lungs
o Expands vascular structures (improves venous return)
What happens with mechanical/manual ventilation?
- Creates POSITIVE intra-thoracic pressure
o Used to support ventilation and assess airway patency
o Expands lungs
o COMPRESSES vascular structures
What are the effects of positive pressure ventilation?
- Reduced venous return (preload) leads to reduced SV=decreased CO
- *result=lower BP and possible hypotension
- Can be seen as increased PP variation on arterial wave form
How do you fix positive pressure induced hypotension?
- Increase venomotor tone (ephedrine: alpha1 agonist causing venoconstriction)
- Increase venous return=IV fluid bolus OR adjust ventilatory settings to reduce pressure within the chest
Atelectasis
- Complete/partial collapse of entire or an area of a lung
o Unable to participate in gas exchange=reduced ventilation and oxygenation
What does atelectasis create?
- R-to-L circulatory SHUNT
R-to-L circulatory SHUNT
- De-oxygenated blood bypasess lung -> re-enters arterial system=reduces PaO2
- *can lead to hypoxia
3 types of atelectasis
- Compression
- Resorption
- Contractions
Compression atelectasis
- Weight of internal organs on lungs
o Affected by posture/recumbency - *Fasting
How does fasting help with compression atelectasis?
- Reduces intra-abdominal pressure
- Increases functional residual capacity by 16%
What gas is responsible for keeping alveoli open?
- Nitrogen
What is de-nitrogenization (resorption atelectasis)?
- Provide 100% O2 for anesthesia=it removes all nitrogen
o Result=small alveoli collapse
How does airway blockage by secretions contribute to resorption atelectasis?
- Reduced mucociliary action during anesthesia and NO coughing reflex=build up of secretions
- O2 in alveoli taken up by Hgb -> collapse
Lung zone 1
- Upper lung region
- Ventilation>perfusion=high V/Q ratio
Lung zone 2
- Middle lung region
- Ventilation=perfusion
- IDEAL
Lung zone 3
- Lower lung region
- Ventilation<perfusion=low V/Q ratio
How can you improve V/Q mismatch?
- Choose best position
- Use high fraction inspired O2 (will loose N scaffold)
- Ventilate to maintain normal PaCO2
- Maintain stable BP (perfusion)
- Use bronchodilators (ex. inhaled salbutamol)
- *Perform recruitment maneuver=open collapsed alveoli
Choose the best position to improve V/Q mismatch
- Sternal > left lateral > right lateral > dorsal > Trendelenburg (‘head stand’)
o R. lung field is larger - Tilt surgical table
- Avoid changing sides
How can you perform recruitment maneuver=open collapse alveoli?
- Manually squeeze re-breathing bag
- Hold peak inspiratory pressure (PIP) of 20-30cm H2O (small) 40-50cm H2O (large) for 20-30s
- WILL reduce venous return (watch BP)
- Can repeat as needed
What is a common anesthetic period to experience hypoxemia due to hypoventilation?
- Recovery
o Switch from 100 to 21% O2
o Still experiencing respiratory depression from anesthesia and atelectasis
o Most important in patients with lung disease or reduced functional residual capacity
How can you improve hypoxemia due to hypoventilation during recovery
- Provided supplemental O2 (increased FiO2)
o Improve PaO2 until patient recovers more and stops hypoventilation
o Monitor SpO2 with pulse oximeter
