RESPIRATORY PHYSIOLOGY Flashcards
Laryngospasm treatment
- 100% Fi O2
- Remove noxious stimuli
- Deepen anesthetic
- CPAP 15 - 20 cmH2O
- Open airway (head extension, chin lift)
- Larson’s maneuver
- Succinylcholine (or roc if pt can’t have sux, can be given IM)
Describe how the respiratory muscles function during the breathing cycle
Contraction of the inspiratory muscles reduces thoracic pressure and increases thoracic volume.
Example of Boyles Law (Pressure and Volume are inversely proportional)
Describe how respiratory muscles function during inspiration
- Diaphragm and external intercostals contract during tidal breathing
- Diaphragm increases the superior-inferior dimension of the chest
- External intercostals increase the anterior-posterior diameter
- accessory muscles include the sternocleidomastoid and scalene muscles
Describe how respiratory muscles function during expiration
Exhalation is usually passive, driven by chest wall recoil
Abdominal musculature (rectus abdominis, transverse abdominis, internal obliques, and external obliques) assist in ACTIVE exhalation
What is minute ventilation
Ve is the amount of air (Vt) in a single breath multiplied by the number of breaths per minute
Ve = Vt x RR
What is alveolar ventilation
VA only measures the fraction of Va available for gas exchange.
VA = (Vt - anatomic dead space) x RR
What is the difference between minute ventilation and alveolar ventilation
Alveolar ventilation measures the fraction of Ve available for gas exchange. It removes anatomic dead space gas from the minute ventilation equation.
How is alveolar ventilation related CO2 & PaCO2
VA is DIRECTLY proportional to CO2 production
VA is INDIRECTLY proportional to PaCO2
VA = (CO2 production)/PaCO2
What are 4 types of deadspace
Anatomic
Alveolar
Physiologic
Apparatus
Define the 4 types of deadspace
ANATOMIC = air in conducting airway
ALVEOLAR = alveoli that are ventilated but NOT perfused
PHYSIOLOGIC = Anatomic Vd + alveolar Vd
APPARATUS = Vd added by equipment
Give an example for each type of deadspace (4)
ANATOMIC = nose/mouth to terminal bronchioles
ALVEOLAR = DEC pulmonary BF (i.e. DEC CO)
PHYSIOLOGIC = anything that increases anatomic or alveolar Vd
APPARATUS = facemask, HME, limb of circle system w/ incompetent valve
What does the alveolar compliance curve tell you?
Alveolar ventilation is a function of alveolar size and its position on the alveolar compliance curve.
- Best ventilated alveoli are the MOST compliant (steep slope)
- Poorest ventilated alveoli are the LEAST compliant (flat slope)
State the alveolar gas equation?
Alveolar Oxygen = FiO2 x (Pb - PH2O) - (PaCO2/RQ)
What variables are included in the alveolar gas equation?
FiO2 Pb=Barometric pressure PH2O = humidity of inhaled gas (47 mmHg) PaCO2 RQ = Respiratory quotient (0.8)
What is the purpose of the alveolar gas equation?
To estimate the partial pressure of O2 in the alveoli
How is the alveolar gas equation useful
It can tell us the maximal PAO2 that can be achieved at a given FiO2
Define Henry’s Law.
The solubility of a gas in a liquid is directly proportional to the partial pressure of the gas above the liquid
How is oxygen content calculated.
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)
What is the difference between CaO2 & DO2
CaO2 is how much O2 is in the blood
DO2 is how much O2 is delivered to tissue per minute
How is DO2 calculated?
DO2 = CaO2 x CO x 10
What does CaO2 measure
Oxygen content in 1 deciliter (100 mL) of blood
How is O2 consumption calculated?
VO2 = CO x (CaO2 - CvO2) x 10
What 2 ways is O2 carried in the blood
- Reversibly binds with Hgb (97%)
2. Dissolves in plasma (3%)
Equation for O2 bound to Hgb
(1.34 x Hgb x SaO2)
Equation for O2 dissolved in plasma
PaO2 x 0.003
What is the Fick principle
Oxygen consumption is the difference in oxygenated arterial blood and returning pulmonary venous blood. Thus flow (CO) can be calculated
What is the Bohr effect
An increased partial pressure of CO2 and decreased pH causes hgb to release O2.
CO2 and hydrogen ions cause a conformational change in the hgb molecule which causes hgb to release O2
What does the oxyhemoglobin dissociation curve describe?
The tendency of hgb to bind O2
What is 2,3-DPG
It is produced during RBC glycolysis and stabilizes the deoxygenated form of hgb facilitating O2 release at tissues
(2,3 diphophoglyceric acid)
How is 2,3-DPG & the Oxyhemoglobin dissociation curve affected by banked blood
The concentration of 2,3-DPG falls and shifts the dissociation curve left, reducing the amount of O2 available at the tissues
How does Hgb F respond to 2,3-DPG and the associated effect on the oxyhemoglobin dissociation curve
Hgb F doesn’t respond to 2,3-DPG which is why there is a left shift (P50 = 19)
How does hypoxia affect 2,3-DPG
It increases 2,3-DPG production and facilitates O2 offloading (right shift)
What is the Hamburger shift?
Chloride(-) shift into the deoxygenated erythrocyte to maintain neutrality w/ H+. It replaces HCO3-
What is the Bohr effect?
Hgb-O2 binding affinity is inversely related to acidity and CO2 concentration
High acidity = low affinity = release(right)
Low acidity = high affinity = lock(left)
What is the Haldane effect?
Effect of O2 on CO2 transport
Deoxygenated blood can carry increasing amounts of CO2, whereas oxygenated blood has reduced CO2 capacity
Produces left shift (venous blood becomes more acidic)
How is carbonic acid produced in the RBC?
Carbonic anhydrase is an enzyme that facilitates formation of carbonic acid (H2CO3).
Carbonic anhydrase is only found in the erythrocyte
What is the result of carbonic acid
rapid dissociation into H+ & HCO3-
3 ways that CO2 is transported in the blood. From greatest to least
Bicarbonate (70%) Carbamino compounds ( (23%) Dissolved CO2 (7%)
What is CO2 solubility compared to O2
CO2 solubility = 0.067 mL/dL/mmHg
It is 20x more soluble than O2
O2 solubility = 0.0031 mL/dL/mmHg
How does the CO2 dissociation curve shift in the presence of oxygenated hgb and why?
RIGHT SHIFT
- blood has decreased affinity for CO2
- facilitates CO2 unloading in lungs
How does the CO2 dissociation curve shift in the presence of DEOXYgenated hgb and why?
LEFT SHIFT
- Blood has increased affinity for CO2
- Facilitates CO2 loading in systemic capillaries
Where in the body is the CO2 dissociation curve right-shifted?
Lungs to facilitate CO2 offloading from Hgb
Where in the body is the CO2 dissociation curve left-shifted?
Systemic capillaries to facilitate CO loading on Hgb
3 categories of hypercapnia
Increased CO2 production
Decreased CO2 elimination
Rebreathing
Examples of reasons for hypercapnia d/t increased CO2 production
sepsis overfeeding MH Intense shivering Prolonged seizure Thyroid storm Burns
Examples of reasons for hypercapnia d/t decreased CO2 elimination
Airway obstruction Increased DS Increased Vd/Vt ARDS COPD Respiratory center depression Drug OD Inadequate NMB reversal
Examples of reasons for hypercapnia d/t rebreathing
Exhausted soda lime
incompetent unidirectional valve in circle system
inadequate FGF
Hypercapnia effects on P50
RIGHT shift
Release more O2
Hypercapnia effect on cardiac and smooth muscle depression
CO2 is myocardial depressant and directly dilates peripheral vasculature
It activates SNS, increasing catecholamine release from adrenal medulla
Result of hypercapnia on cardiac rate and rhythm changes
Tachycardia, increasing myocardial O2 consumption and decreasing O2 delivery
Dysrhythmias
Prolonged QT interval
Hypercapnia effect on pulmonary vascular resistance
Increases PVR
CO2 constricts pulmonary vasculature, increasing PVR and workload of right heart
Hypercapnia effect on alveolar ventilation
Increases alveolar ventilation d/t CO2 stimulating effects and increases in Ve
Hypercapnia effect on K+
INCREASES K+
d/t activation of H+/K+ pump
Buffers CO2 acid in exchange for releasing K+ into plasma
Hypercapnia effect on Ca++
INCREASES Ca++
iCa++ competes w/ H+ for binding sites on plasma proteins
Acidosis/Alkalosis effects on Ca++/H+ binding
Acidosis = plasma proteins buffer H+ and release Ca++ (increase inotropy)
Alkalosis = plasma proteins release H+ and bind Ca++ (decrease inotropy)
Hypercapnia effect on ICP
INCREASES
Decreased CSF pH leads to decreased cerebrovascular resistance and increased CBF/volume
Hypercapnia effect on LOC
CO2 narcosis
How do the kidneys handle acidosis
Kidneys excrete H+ and conserve HCO3- to return pH to normal
How much does acute respiratory acidosis decrease pH
For every 10 mmHg >40 mmHg, pH decreases by 0.08
How much does chronic respiratory acidosis decrease pH, and why is this different than acute?
For every 10 mmHg >40 mmHg, pH decreases by 0.03.
d/t HCO3- retention by the kidneys
What does a right shift of the CO2 response curve demonstrate?
What are contributing examples?
That the respiratory center is LESS sensitive to CO2
Sevoflurane s/p CEA Opioids NMBs Metabolic alkalosis
What does a left shift of the CO2 response curve demonstrate?
What are contributing examples?
That the respiratory center is MORE sensitive to CO2
Hypoxemia Salicylates Surgical stimulation Intracranial HTN Metabolic acidosis
What does the CO2 ventilatory response curve describe?
The relationship between PaCO2 and minute ventilation
Where is the primary monitor of PaCO2 and what type is it?
Where = Medulla
Type = central chemoreceptors
What is the apneic threshold?
It is the highest PaCO2 which a person will not breathe
When PaCO2 is greater than apneic threshold, the patient will begin to breathe
What locations play a secondary role in monitoring in monitoring PaCO2
Carotid bodies
Transverse aortic arch
Peripheral chemoreceptors
What does the slope of the CO2 ventilatory response curve indicate
The sensitivity of the entire respiratory apparatus to PaCO2
At what level (mmHg) does CO2 become a respiratory depressant?
PaCO2 >80-100 mmHg
How is minute ventilation affect by shifts in the CO2 ventilatory response curve?
Left shift = Ve is higher than expected for a given PaCO2, creating respiratory alkalosis
Right shift = Ve is lower than expected for a given PaCO2, creating respiratory acidosis
How does the CO2 ventilatory response curve impact apneic threshold
Left shift = apneic threshold is decreased
Right shift = apneic threshold increased
What is the pacemaker for normal breathing?
Dorsal respiratory center
What is the role of the pneumotaxic center
To inhibit DRC, the pacemaker for breathing
What is the role of the apneustic center
To stimulate the DRC
What does the ventral respiratory center control
Responsible for expiration
Where is the respiratory center located and what is the primary job?
In the reticular activating system in medulla and pons
Job = to determine how fast and deep you breath. REgulation of PaCO2 and PaO2
Describe the afferent input, integration and modifier of the respiratory center
Afferent input = from central and peripheral chemoreceptors, lung stretch receptors
Integration = incoming signals w/ intrinsic respiratory pattern and sending a coordinated response to muscles of respiration
What are the medullary respiratory centers
Dorsal respiratory group
Ventral respiratory group
What are the pontine respiratory centers
Pneumotaxic center (UPPER pons)
Apneustic center (LOWER pons)
What are the 4 determinants of respiratory rate and pattern
- Neural control in respiratory center - Medulla
- Chemical control in the central chemoreceptors - medulla
- Chemical control in peripheral chemoreceptors - carotid bodies, aortic arch
- Baroreceptors - lungs
Where does the respiratory center receive afferent input from
Central and peripheral chemoreceptors
Lung stretch receptors
What does new evidence report is the respiratory pacemaker
The central pattern generator, which includes:
DRG
pre-Botzinger complex (in VRG)
Other medullary structures
What stimulates the central respiratory chemoreceptors and where is this located
pH changes in the CSF and PaCO2
location = ventral surface of medulla
What byproduct freely diffuses across BBB
CO2
Which ions do not freely diffuse across the BBB in relationship to respiration
H+ and HCO3-
How does H+ and HCO3- enter CSF
CO2 dissociates into H+ and HCO3-
How does H+ concentration in CSF affect respiration
Increases rate and depth of respirations until new steady state is achieved
How long do effects of hyperventilation reduce ICP
a few hours to 2 days
What substances can freely diffuse across CSF
Some gases and lipid soluble molecule
The concentration of which ion in the CSF is most important for stimulating the central chemoreceptors of the respiratory center?
H+
What type of relationship does H+ CSF concentration have with respiratory rate and depth
Direct relationship, as H+ rises so do rate and depth of respirations
How doe ions, glucose and amino acids travel across the BBB
Active transport mechanisms
What is the difference in response of central versus peripheral chemoreceptors
Central chemoreceptors respond to PaCO2
Peripheral chemoreceptors respond to PaO2
What type of cells mediate peripheral chemoreceptor hypoxic ventilatory drive ?
How?
Type 1 Glomus cells
sense and transduce PaO2 into an action potential
What nerve makes up the AP of the afferent limb of the peripheral chemoreceptor response
AP is propagated along the afferent limb of Hering’s nerve and glossopharyngeal nerve (CN 9)
How does CEA affect peripheral chemoreceptor function?
It impairs function on the ipsilateral side
What is the chief responsibility of the carotid bodies
To monitor hypoxemia
Do the carotid bodies or transverse aortic arch chemoreceptors respond to SaO2 or CaO2?
No
Why aren’t bilateral CAE performed simultaneously?
Because CEA severs the afferent limb of the hypoxic ventilatory response and takes time for recalibration
Where are the carotid bodies located
at the bifurcation of the common carotid artery
What are secondary responsibilities of the carotid bodies
Monitoring PaCO2, H+, perfusion pressure
What layer are the carotid bodies located?
Adventitia
Describe the hypoxic ventilatory response to hypoxemia (5)
- Decreased PaO2 closes O2-sensitive K+ channels in Type 1 glomus cells
- Resting membrane potentials rise d/t altered K+, Ca++ channels open and increase NT release of Ach and ATP
- An AP is propagated via Hering’s nerve and glossopharyngeal nerve (CN 9)
- The afferent path terminates in the inspiratory center of medulla (DRG)
- Ve increase to restore PaO2
Conditions that impair hypoxic ventilatory response
CEA
Sub-anesthetic doses of inhalation and IV anesthetics
What is the Hering-Breuer inflation reflex
lung hyperinflation turns off the respiratory drive to avoid overinflation
Hering-Breuer deflation reflex
Activates the respiratory drive when lung volume is too small to prevent atelectasis
What are J receptors
Pulmonary C-fiber receptors
Increases the respiratory rate in the setting of PE or CHF
How is ventilation controlled in the lungs
Stretch receptors in the smooth airway muscles which transduce pressure conditions inside the airway
What nerve transduces the pressure conditions inside lung smooth muscle and to where
Vagus nerve (CN 10) To the dorsal respiratory center (DRG, respiratory PM)
