Pathophysiology of Anesthesia: Respiratory System Flashcards
Which 3 body systems sustain life minute-by-minute?
- CNS
- respiratory system
- cardiovascular system
If the 3 body systems that sustain life stop working, what happens?
- this can be life threatening
- all other systems are supported by good function of these!
What are the upper airways of the respiratory system?
- nose, nasal cavity & sinuses, nasopharynx
- mouth, oropharynx, larynx
What two zones are there in the lower airways?
- conducting zone
- respiratory zone
what is the conducting zone?
- trachea, bronchi, bronchioles, tertiary bronchi
What is the respiratory zone?
- tertiary bronchi, alveoli
What are the functions of the upper airways?
- thermoregulation
- filtration
- humidification
- olfactory
- air conduction
- phonation
- swallowing (airway protection)
What are the respiratory & non respiratory functions of the lower airways?
- non-respiratory: immunological (mucocilliary, etc.; acid-base regulation; vascular, metabolic, endocrine, etc.)
- respiratory: GAS EXCHANGE (O2 & CO2 movement - works closely w/ cardiovascular system); surfactant synthesis
How is ventilation controlled?
primarily by CO2
What is the respiratory center?
for slow, steady ventilation control
- medulla oblongata = dorsal & ventral respiratory groups (control inspiration & expiration)
- pons = pneumotaxic center & apneustic center (adjust ventilation controlled by medulla oblongata respiratory groups)
what are central chemoreceptors?
minute by minute changes in ventilation
- floor of ventral medulla
- dissolved CO2 passes through semipermeable membrane (BBB) & enters CSF
- CSF pH = 7.32 (changes in pH = control breathing; increased CO2 = decreased pH -> stimulates breathing
- less buffering capacity than blood = greater changes in pH based on PCO2
what are peripheral chemoreceptors?
rapid, fine-tuning ventilation
- sense PaCO2, PaO2, pH, & perfusion of carotid/aortic bodies (increase ventilation in response to increased PaCO2, decreased blood pH, and decreased PaO2)
- overrides ventilation controlled by respiratory center (rapid, breath-by-breath control of ventilation)
- GOAL: maintain normal CO2 & O2 levels in blood (PaCO2 = 35-45 mmHg, PaO2 = 80-100 mm Hg)
What is good about endotracheal intubation?
- prevent aspiration of gastric contents
- prevent upper airway obstruction (sedatives & tranquilizers cause muscle relaxation of laryngeal muscles -> predispose to AIRWAY OBSTRUCTION)
- able to manually ventilate for patient experiencing hypoventilation or apnea
What is potentially bad about endotracheal intubation?
- bypass humidification & heating mechanisms of upper airways
- increased resistance to breathing if using too small of an ET tube, connectors, & one-way valves in breathing circuit
How do your treat for heat and water loss with endotracheal intubation?
- passive: implement low fresh gas flow rates & use HME filters
- active: humidifiers/nebulizers, heated anesthetic breathing circuits
- active warming (ex: Bair Hugger, HotDog)
How do you treat for increased resistance to breathing with endotracheal intubation?
- choose largest endotracheal tube possible: Poiseuille’s Law: airway resistance through a tube is INVERSELY proportional to its radius, to the power of 4; ex: halving diameter -> 16- FOLD INCREASE in airflow resistance through the tube
What is general respiratory depression?
- Normal PaCO2 = 35-45 mmHg
- awake: alveolar ventilation changes LINEARLY w/ changes in PaCO2 (max response at PaCO2 100mmHg)
- hypoventilation: inadequate CO2 elimination detected by increased PaCO2 or ETCO2
- HYPOVENTILATION: PaCO2 > 45 mm Hg
Anesthetics and general respiratory depression?
- all anesthetics cause respiratory depression which can lead to hypoventilation (inhalant anesthetics: decrease tidal volume at low dosage & respiratory rate at high doses; IV anesthetics: decrease tidal volume and respiratory rate; tranquilizers, sedatives, & hypnotics: decrease respiratory rate; opioids: change CO2 response trigger to a higher value)
- anesthesia effects: progressive dose-dependent decrease in spontaneous ventilation (esp. when drugs are used in combination): blunted peripheral & central chemoreceptor responses to increase PaCO2; muscle relaxation (respiratory muscles)
Oxygen, inhalant anesthetics, and general respiratory depression:
- normal PaO2 = 80-100 mmHg in room air (FiO2 21%)
- hypoxemia: triggers peripheral chemoreceptors to cause a STEEP increase in ventilation (NON-LINEAR response of alveolar ventilation to changing PaO2 levels; “hypoxic drive” = overrides normal CO2 driven ventilation)
- inhalant anesthetics: dose-dependent inhibition of peripheral chemoreceptor response -> DECREASED VENTILATORY RESPONSE TO HYPOXEMIA
what is apnea?
- apnea = complete absence of breathing (extreme end-point of respiratory depression)
- most common stage of anesthesia for apnea = induction (75% incidence): potent IV anesthetic (propofol/alfaxalone) agent used w/ high respiratory depressant effects
What can induction apnea lead to?
HYPOXEMIA
Which patients are at high risk for apnea?
those w/ reduced functional residual capacity (FRC):
- increased intra-abdominal pressure (Ex: GDV, pregnancy)
- lung disease (Ex: pneumonia, asthma)
- obesity
- age (pediatrics & geriatrics)
- anesthesia (decreases FRC by 15% in NORMAL patients)
How can you prevent induction apnea?
titrate the induction agent (use lowest dose possible to allow intubation)
how can you prevent hypoxemia?
pre-oxygenate for 3-7 mins prior to induction:
- increases PaO2 & oxygen reserve
- de-nitrogenizes system
- provides extra time (~3 mins) before patient will desaturate after becoming apneic
what are other causes of apnea?
- equipment failure = incompetent one-way valves on rebreathing system leading to excessive CO2
- deep anesthesia levels w/ inhalant anesthetics
what is the maximum response of chemoreceptors to apnea?
PaCO2 100 mmHg, then ventilation starts to DECLINE
- can become apneic & may not restart breathing at deep planes of anesthesia
What is the anesthetic index?
= ratio of end-tidal anesthetic where animal becomes apneic, divided by minimum alveolar concentration (MAC)
- INVERSE RELATIONSHIP: lower apneic index means drug is MORE respiratory depressant
- cant compare respiratory depression to potency of inhalation anesthetics
- SEVOFLURANE (3.45) < HALOTHANE (2.9) < ISOFLURANE (2.51)
- as anesthetic depth increases, so does the agent’s respiratory depressant effects
- 1.5 - 3.0 x MAC = RESPIRATORY ARREST
What is positive pressure ventilation?
- normal breathing: creates NEGATIVE intra-thoracic pressure (expands lungs; expands vascular structures (improves venous return))
- mechanical/ manual ventilation: creates POSITIVE intra-thoracic pressure (used to support patient ventilation & to assess airway patency/security; expands lungs; COMPRESSES vascular structures (reduces venous return))
what are the effects of positive pressure ventilation?
- reduced venous return (preload) -> reduced stroke volume- > reduced cardiac output
- RESULT = LOWER BP & POSSIBLE HYPOTENSION
- can be seen as increased pulse pressure variation on arterial waveform
How do you fix positive pressure induced hypotension?
- increase venomotor tone (ephedrine = a1 agonist causing venoconstriction)
- increase venous return = IV fluid bolus, adjust ventilator settings to reduce pressure w/in chest
What is atelectasis?
- complete/partial collapse of entire or area (lobe) of a lung (unable to participate in gas exchange -> reduces ventilation & oxygenation)
- creates right-to-left circulatory SHUNT (de-oxygenated venous blood bypasses lung -> re-enters arterial system -> reduces PaO2; can lead to hypoxemia)
what are the 3 types of atelectasis?
- COMPRESSION
- RESORPTION
- contraction
What is compression atelectasis?
- weight of internal organs on lungs (affected by posture/recumbency; FASTING = reduces intra-abdominal pressure & increases FRC by 16%)
- anesthesia effects: general muscle relaxation includes respiratory muscles (diaphragm, intercostal muscles, etc.) -> unable to normally expand lungs; loss of ‘deep sigh’
What is resorption atelectasis?
- gas responsible for keeping alveoli open = NITROGEN
- de-nitrogenization = provides 100% O2 as medical gas for anesthesia, removes all nitrogen (result = small alveoli collapse; Hgb remove all oxygen from within the alveoli -> little gas remains in alveoli -> collapse)
- airway blockage by secretions: reduced mucociliary action during anesthesia & no coughing reflex -> can build up secretions; O2 in alveoli is taken up by Hgb -> collapse
What is V/Q mismatch?
- distribution of blood flow depends on GRAVITY -> promotes perfusion (Q) to dependent lung field
- ventilation / perfusion (V/Q) relationship changes over different lung zones
- normal ventilation distribution (standing position): zone 1: upper-most lung region (ventilation > perfusion = high V/Q ratio); zone 2: middle lung region (ventilation = perfusion (IDEAL AREA)); zone 3 = lower-most lung region (ventilation < perfusion = low V/Q ratio)
How does position effect the V/Q mismatch?
anesthesia patients are usually in lateral or dorsal recumbency (changes physiological zones of the lung)
What are the anesthetic drug effects on V/P mismatch?
- reduced cardiac output -> reduced perfusion
- atelectasis: ventilation preferentially goes to upper-most lung region
- loose spontaneous ‘sigh’ reflex
how is mechanical ventilation related to V/Q mismatch?
mechanical ventilation = reduces venous return + atelectasis worsens
What is the result of V/Q mismatch?
can lead to lower PaO2 & higher PaCO2
How do you improve V/Q mismatch?
- choose best position (keep weight off diaphragm): sternal > left lateral > right lateral > dorsal > Trendelenburg; tilt the surgical table; avoid changing sides
- use high FiO2 (but will loose nitrogen scaffold)
- ventilate to maintain normal PaCO2
- maintain stable BP (perfusion)
- use bronchodilators (ex: inhaled salbutamol)
- perform recruitment maneuver: open collapsed alveoli (manually squeeze re-breathing bag; hold peak inspiratory pressure (PIP) of 20-30 cmH2O (small animal) or 40-50 cmH2O (large animal) for 20-30 seconds; WILL reduce venous return -> watch BP!; can repeat as needed
What is recovery?
- common anesthetic period to experience hypoxemia due to hypoventilation: switch from 100% -> 21% FiO2 (room air); still experiencing respiratory depression effects from anesthesia & atelectasis; most important in patients w/ lung disease or reduced FRC
- how to fix this: provide supplemental O2 (increase FiO2; improve PaO2 until patient recovers more & stops hypoventilation; monitor SpO2 w/ pulse oximeter)
